Jaw pain - in the middle of a meal is characteristic for temporal arteritis.

The lumen of the arteries narrow and cannot respond to increased blood requirement during the meal. Tongue pain during meals (tongue claudication) may also occur. -Temporal arteritis presents in elderly patients (mean age of onset is 65 years old). The most common symptom is headache. It can be accompanied by scalp tenderness, especially pronounced during hair combing. The inflamed temporal artery can sometimes be palpated as a firm, painful subcutaneous cord in the temporal region. Jaw and tongue claudication, fever, malaise and weight loss may be present. 50% of patients also complain of muscle pain and morning stiffness (due to polymyalgia rheumatica). -The index of suspicion for temporal arteritis should be high. Treatment should be started as soon as possible to prevent vision loss. The vision loss is painless, monocular and may lead to permanent blindness. Erythrocyte sedimentation rate (ESR) should be determined if temporal arteritis is suspected. It is almost always significantly elevated (often > 100 mm/hr). -Temporal artery biopsy is necessary for definitive diagnosis. -Corticosteroid treatment should be started ASAP to prevent possible vision loss. http://video.google.com/videoplay?docid=-2645662225255385165#

Aortic stenosis =systolic diamond-shaped (crescendo-decrescendo) murmur - The most common cause of this valvular disease is degenerative (senile) calcification of the aortic valve leaflets. Calcific aortic stenosis is a result of prolonged hemodynamic stress on the aortic valves leading to inflammation of the valvular tissue overtime. It is common in patients older than 65 years old. -Physical examination of the patient with aortic stenosis reveals small and slow rise in the carotid pulse during systole (pulsus parvus et tardus), a diminished aortic component of S2 sound, and a harsh systolic crescendo-decrescendo murmur. The murmur is best heard at the right upper sternal border. http://www.merck.com/mmpe/multimed...peed=256&Plugin=WMP&Error=

Burkitt lymphoma - EBV causes latent infection and immortalization of B-cells. A crucial step in the transformation of infected cells is the balanced t(8:14) translocation, which generally requires a background of immunodeficiency (e.g. immunosuppressive medications, HIV infection). -The histology for Burkitt lymphoma: diffuse medium-sized lymphocytes producing the characteristic “starry sky” appearance, a high proliferation index represented by the high Ki-67 fraction (99%), and increased apoptosis. - The EBV genome is identified in 50% of all systemic B-cell lymphomas and almost all primary CNS lymphomas occurring in HIV patients. There is little evidence of a direct effect of HIV in AIDS-associated lymphomas. http://www.webpathology.com/image.asp?n=14&Case=389

Angiogenesis in neoplastic and granulation tissue - The key growth factors that promote angiogenesis in neoplastic and granulation tissue are vascular endothelial growth factor (VEGF) and fibroblast growth factor (EGE). - Proinflammatory cytokines (like IL-1 and INF-y) can indirectly promote angiogenesis through increased vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF). Proinflammatory cytokines (like IL-1 and INF-y) can indirectly promote angiogenesis through increased VEGF expression. The laminin in basement membranes may pose a physical barrier to the sprouting of new blood vessels. http://www.researchvegf.com/researchvegf/images/VEGF-ligand.jpg http://www.nature.com/nrc/journal/v6/n4/images/nrc1836-f4.jpg

Invasive breast carcinoma - typically presents as a mammographic finding or a palpable mass. Larger tumors may be adherent to the chest wall. Nipple inversion is observed when the tumor invades the central region of the breast, and skin retraction is identified when the cancer infiltrates the suspensory Cooper ligaments. Should the lymphatic drainage become impeded by tumor, lymphedema and pitting and thickening of the skin-- such that it adopts the appearance of an orange peel (peau d’orange) -- may occur. The peau d’orange finding is particularly common in patients with inflammatory breast cancer. http://ocbreastcare.com/mediac/400_0/media/10302.jpg http://tgmouse.compmed.ucdavis.edu...MM2000/BRCA-1/slide158.jpg

Carbon tetrachloride (CCl4) =causes free radical injury. Like many other toxic substances CCl4 is oxidized by the P450 oxidase system in the liver. The result is the formation of the free radical CCl3, which reacts with structural lipids of cell membranes. The result is lipid degradation and hydrogen peroxide (H202) formation. This process is called lipid peroxidation. The peroxides go on to form new radicals, continuing the vicious circle of lipid degradation. Carbon tetrachloride cell injury develops rapidly and leads to swelling of the endoplasmic reticulum, destruction of mitochondria, and increased permeability of cell membranes. These processes culminate in hepatocyte necrosis. - Mitochondrial dysfunction occurs in CCl4 intoxication as a result of free radical injury

Catecholamine-secreting tumors = repeated paroxysmal episodes, which resolve without intervention, are characteristic of pheochromocytoma, a catecholamine producing tumor of the adrenal medulla. It is unclear why the catecholamine-secretion by pheochromocytomas is so often episodic. -Classically, a patient with pheochromocytoma will present with intermittent headaches, hypertension, diaphoresis and pallor or flushing. In between these episodes, blood pressure maybe normal. Episodic hypertension is a very important clinical clue in the diagnosis of pheochromocytoma. The differential diagnosis includes autonomic dysfunction, cocaine abuse, withdrawal from clonidine and beta-blockers, and panic attacks. - The Rule of 10s is helpful in remembering the features of pheochromocytoma. Roughly 10% of pheochromocytomas occur as part of hereditary syndromes (e.g. MEN 2 A and B, von Hippel Lindau disease), 10% of pheochromocytomas are bilateral, and 10% are extra-adrenal. Only 10% of pheochromocytomas are malignant; the majority =benign. http://www.healcentral.org/content...ma%20pheochromocytoma3.JPG

Panic attacks = episodic symptoms including apprehension, shortness of breath, chest pain ,diaphoresis, tremors and a feeling of impending doom. However affected individuals typically experience their first panic attacks at an earlier age (mean age at first presentation is around 24 years). Additionally panic attacks are twice as common in females as compared to males. - Furthermore the rise in blood pressure seen in panic attacks is typically an isolated systolic increase rather than the combined systolic and diastolic hypertension

Carcinoid syndrome = results from excessive production of 5-hydroxytryptamine, usually from a metastatic mid-gut neuroendocrine tumor. These patients typically present with facial flushing bronchospasm and diarrhea. Hypotension is present rather than hypertension. http://www.pathconsultddx.com/pathCon/largeImage?pii=S15598675(06)70133-4&figureId=fig1 http://www.pathconsultddx.com/pathCon/largeImage?pii=S15598675(06)70133-4&figureId=fig4

Congenital QT-interval prolongation = often the result of mutations of the genes coding for cardiac cell potassium or sodium channels. Various congenital long-OT syndromes are recognized, with Jervell and Lange-Nielsen syndrome as one of the most prominent. - This autosomal recessive condition is accompanied by congenital neurosensory deafness. The QT-interval prolongation predisposes the patient to syncopal episodes and possible sudden cardiac death due to torsades de pointes (a ventricular tachyarrhythmia). http://www.geneticheartdisease.org/jpegs/lqts_four.gif http://www.mykentuckyheart.com/images/pictures/qt_syndrome.gif

Kartagener’s syndrome =A familial syndrome associated with bronchiectasis = immotile cilia due to a microtubular dynein arm defect. Infertility, recurrent sinusitis, and bronchiectasis result. Although this syndrome is sometimes associated with situs inversus, there are no associated cardiac electrophysiological abnormalities. http://www.mypacs.net/cases/DEXTRO...ENERS-SYNDROME-632514.html

Syndactyly= failure of the digits to separate =the most common congenital upper limb deformity. The second most common deformity is a constriction band syndrome which interrupts the fetal blood supply to the distal limbs and causes amputation of fingers (or toes). Most upper-limb deformities are the result of developmental accidents of unknown etiology and are non-syndromic, i.e. not associated with congenital abnormalities in other organ systems. http://upload.wikimedia.org/wikipe...two_fingers_right_hand.JPG http://www.handsport.us/images/constriction-bands.jpg

Multiple telangiectasias = Osler-Weber-Rendu disease (aka Hereditary Hemorrhagic Telangiectasia), an autosomal dominant condition in which vascular telangiectasias are found in the skin and mucous membranes of the lips, oronasopharynx, and respiratory, gastrointestinal, and urinary tracts. -Their rupture may cause epistaxis, GI bleeding, or hematuria.

and osseous lesions. . legs. axillary or inguinal freckling.html Neurofibromatosis type 2 (the more “central” form) = bilateral acoustic neuromas..com/issues/articles/2005-08_09. cutaneous neurofibromas. MEN is not associated with thyroid cancer or perioral nodules. and fingers.brighamandwomens. optic glioma. http://www. This constellation of clinical findings is consistent with multiple endocrine neoplasia type 2B (MEN 2B). tall and slender with disproportionately long arms. http://www.http://www. thickened proliferations of neural tissue.. Demyelination of the dorsal columns in the spinal cord causes a loss of vibratory and position senses.ispub.com/eye/journal/v19/n3/fig_tab/6701478f1.nature.asp MEN 2B = multiple endocrine neoplasia type 2B = Marfanoid habitus.th_keloids/keloid-fig2.estibular%20Schwannoma.jpg http://cnx.jpg Multiple endocrine neoplasia type 1 (MEN 1)= the “3 Ps.residentandstaff. http://www. iris hamartomas... -The flesh-colored nodules on his lips and tongue are likely mucosal neuromas. -The history of total thyroidectomy is suggestive of a thyroid malignancy.occurs 20-30 years after an untreated syphilis infection.” =autosomal dominant condition characterized by tumors of the parathyroid gland tumors of the anterior pituitary gland. and tumors of the pancreas. Neurosyphilis =a condition that occurs in less than 10% of patients with tertiary syphilis. which are unencapsulated.org/ne. because benign thyroid masses are usually treated medically or with partial thyroidectomy. but sensory ataxia prevails in the dark (demonstrated by this patient’s frequent . Loss of these senses is usually compensated for by visual clues.org/content/m14901/latest/ Neurofibromatosis type 1 = multiple café-au-lait spots. brain meningiomas.com/ispub/ijd/vol. and schwannomas of the dorsal roots in the spinal cord.

Sorbitol increases cell osmolarity and facilitates water influx into the cell. Accumulating glucose is converted into sorbitol and fructose by aldose reductase.gr2.. hyalinization. It can also affect the nerves that serve the heart and control blood pressure. Autonomic neuropathy can also cause hypoglycemia unawareness. and narrowing of the walls of the arteries. such as components of the thick or thin filaments. -Peripheral neuropathy.jpg Peripheral neuropathy . harsh systolic murmur.diabetes mellitus . Non-enzymatic glycosylation of proteins leads to increased thickness. as well as nerves in the lungs and eyes.Most cases of HCM are thought to result from mutations in genes for cardiac sarcomere proteins. paresthesias. . sexual response.org/caseoftheweek/2008/case08-21.mt/showdoc.50441-2. Intracellular hyperglycemia occurs in peripheral nerves. Ischemic nerve damage follows. a condition in which people no longer experience the warning symptoms of low blood glucose levels. the most common type of diabetic neuropathy.stumbling at night). On echocardiography.. Areflexia and loss of bladder function can also occur. -Autonomic neuropathy causes changes in digestion.Dynamic ventricular out flow tract obstruction is seen in about 25% of patients with HCM. bowel and bladder function. and arms. http://www.mdconsult.html http://www. The result is osmotic damage to axons and Schwann cells.0-2450-7.scmr. The magnitude of the abnormal systolic LV to aorta pressure gradient correlates with the degree of SAM of the anterior mitral leaflet. The bulging is the result of asymmetric septal hypertrophy (ASH). 2. Argyll Robertson pupil and positive Romberg sign are found. These changes lead to diabetic microangiopathy of endoneural arterioles.. -Involvement of the dorsal roots causes loss of pain sensation. hands. causes pain or loss of feeling in the toes. legs. and perspiration..com/das/book/.ilesource=4&file=fig03.It occurs in both type 1 and 2 diabetes and is associated with poor glycemic control and/or long duration of the disease. The most important mechanisms of the development of diabetic neuropathy are the following: 1.. On physical examination. there is systolic anterior motion (SAM) of the anterior leaflet of the mitral valve such that it comes abnormally close to the interventricular septum as it bulges into the left ventricular (LV) outflow tract.gov. and painful crises.sahha.as. and asymmetric septal hypertrophy in a young man = an autosomal dominant Mendelian-inherited condition in at least 50% of cases . feet. Hypertrophic cardiomyopathy (HCM) = idiopathic hypertrophic subaortic stenosis = exertional syncope.. The systolic murmur heard in patient with HCM is a systolic ejection murmur produced by the LV out flow tract obstruction. .jpg http://www.

-Focal neuropathy results in the sudden weakness of one nerve or a group of nerves.. after the neuronal death.gif http://www.iu. astrocytes proliferate at the site of injury. Lambert-Eaton syndrome is a paraneoplastic condition associated with antibodies against presynaptic calcium channels. http://hdroster. or buttocks and leads to weakness in the legs. http://www5. such as the lower back or leg(s) chest or abdominal pain that is sometimes mistaken for another condition such as heart attack or appendicitis Focal neuropathy is painful and unpredictable. vesicular and display prominent nucleoli. Antibodies against acetylcholine receptors of the neuromuscular junction are the cause of myasthenia gravis. Segmental demyelination is another typical pathologic finding. This process is called astrocytosis (or gliosis) and is a universal response of the CNS to severe damage.cubital-tunnel. Any nerve in the body can be affected.Entrapment of a nerve within an anatomic compartment leads to compression neuropathy. hips.pyroenergen. it tends to improve by itself over weeks or months and does not tend to cause long-term damage.aaos.org/oko/description. a so-called “neural form” of muscular atrophy. however. Charcot-MarieTooth disease often presents with weakness of foot dorsiflexion due to involvement of the common peroneal nerve.Symptoms may include: double vision eye pain paralysis on one side of the face (Bell's palsy) severe pain in a certain area. causing muscle weakness or pain. Proliferating astrocytes are enlarged and contain a large number of fibrils and glycogen granules.jpg http://www. -The mutation of a myelin protein gene is the pathogenesis of Charcot.com/article.. Later.One of the main functions of astrocytes is participation in tissue repair.carpal-tunnel-syndrome. Their nuclei are large.com/cms/. http://www. which occurs due to compression of the median nerve at the wrist.com/hha/b_15_3_2a.-Proximal neuropathy causes pain in the thighs./stories/cubitaltunnel. Proliferated astrocytes replace lost neurons and compensate for their volume.. astrocytic processes form a closely connected firm meshwork called a gliotic scar.asp . In an event of irreversible neuronal damage and neuronal death.Tooth disease..edu/AboutHD/brainAndHD. CNS damage .jpg -Abnormal signal transmission at the neuromuscular junction is characteristic of myasthenia gravis and Lambert-Eaton syndrome. .cfm?topic=FOO027 DIFF: -Endoneural inflammatory infiltration of the peripheral nerves is characteristic of Guillain-Barre syndrome. The most common example is carpal tunnel syndrome.hughston.

htm Potter syndrome =pulmonary hypoplasia. infantile polycystic kidney disease http://www. C-reactive protein.Neither vascular hyalinization nor amyloid deposition is a component of normal tissue repair.ist..Fibroblast migration to a site of injury occurs in the peripheral nervous system.gif http://www. Renal defects that lead to Potter syndrome are usually profound (and would be easily seen on ultrasound) bilateral renal agenesis.foxhallmri.renal_dysplasia_03_1-2.humpath. Potter facies (flattened nose.ch/genetic_diseas. Both of these processes are pathologic. the lower poles) -The isthmus of renal tissue is anterior to the great vessels and is easily detected on abdominal ultrasonography. serum amyloid P. Multicystic kidney dysplasia = multiple cysts of varying size in the kidney and the absence of a normal pelvocaliceal system. IL-1 and IL-6 into circulation. prominent epicanthal folds. and cardiovascular abnormalities. serum amyloid A. local neutrophils and macrophages release tumor necrosis factor-alpha (TNF-α).php?offset=45&cat3=661 Systemic inflammatory response .edu/staff/nlillega/phil%20350_files/image005..gfmer.com/sol/01368.com/case/horseshoe. These particular cytokines mediate systemic inflammatory response. in part by stimulating hepatic production of acute phase reactants (eg. http://www. . Abdominal ultrasound of fetus or newborn is diagnostic. not in the CNS where tissue repair is a function of astrocytes. Fibrinogen. limb defects. Many acutephase proteins bind to microbes and fix complement. complement factors).. ferritin. http://www.http://www.jpg DIFF: .jpg Horseshoe kidney =The abnormal fusion of kidneys at poles (usually.com/IMG/jpg/bil.pathguy.utm.When an injury occurs. recessed chin. The condition is associated with ureteral or ureteropelvic atresia and the affected kidney is nonfunctional. When increased the acutephase protein fibrinogen causes erythrocytes to form stacks (rouleaux) that .. and low-set ears).

nature. (Later. -Muscular dystrophy is a term that applies to the various diseases that manifest with progressive muscular weakness. A further increase in blood pressure ensues.) Gower’s sign and calf enlargement in a male child between 3 and 6 years of age indicates Duchenne muscular dystrophy. X-linked and . or ESR.jp/fulltext/048020103/img/048020103_f01. http://doctorxdrive2. Hyperplastic arteriolosclerosis which can result from diastolic pressures >120—130 mmHg.html Gower’s sign = Using the support of one’s hands to raise from a squat or from a chair (because of proximal muscle weakness) .jsaweb. chemotaxis. fat and connective tissue contribute to the enlargement.. PAF also enhances leukocyte adhesion to endothelium. therefore.gif Hypertensive crisis = persistent diastolic pressure exceeding 130 mmHg that is often associated with acute vascular damage.jeeran.Distal muscle hypertrophy. irritability.com/images/0016.. This aggregation rate is termed the erythrocyte sedimentation rate.malignant hypertension is present. and degranulation.. such as the calf enlargement . Patients may also have hypertensive encephalopathy characterized by headache._data/Rouleaux%20Blood. phagocytosis.allows affected children to overcome proximal muscle weakness.jpg http://www.com/pshin.ntlworld.sediment at a faster rate than do individual erythrocytes. accelerated. -When the rise in pressure causes retinal hemorrhages exudates. The renal arteriolar stenosis of hyperplastic arteriolosclerosis decreases glomerular perfusion and GFR thus activating the renin-angiotensin aldosterone system. alterations in consciousness.com/nrrheum/jour. The genetic basic of Duchenne muscular dystrophy is mutation or deletion of the gene that codes for the protein dystrophin. and platelet stimulation. and other signs of central nervous dysfunction. or papilledema. In very small amounts PAF causes vasodilation and increased vascular permeability. producing a vicious cycle and malignant nephrosclerosis. Duchenne muscular dystrophy is. presents as onion-like concentric thickening of the walls of arterioles as a result of laminated smooth muscle cells (SMC) and reduplicated basement membranes. Duchenne muscular dystrophy is the most common form.JPG Platelet-activating factor (PAF) -typically causes vasoconstriction. http://ai. This gene is located on the X chromosome. bronchoconstriction.g_tab/ncprheum0268_F6.. http://homepage. and is a non-specific marker of inflammation.

contaminated soil. http://www. ora motor vehicle accident.edu/.ualberta.pathguy.html Tetanus . booster immunization is recommended every 10 years. In addition. so a recent history of a penetrating trauma is important to elicit.JPG http://www. -On history it is important to determine the immunization status of the patient and the length of time since the last tetanus vaccine. which is represented by increased BUN and creatinine and oliguria (low urine output). remember that C.gif http://neuropathology. and subsequent cell necrosis and denudation of tubular basement membrane (TBM). these portions of nephron will suffer first.... Some fibers have centrally located (internalized) nuclei. Muddy brown casts which are pathognomonic for ATN are a variant of granular pigmented casts. Loss of dystrophin results in cellular injury (myonecrosis).rier/Vol1/Fig. the proximal tubules and ascending limb participate in the active (ATP-consuming) transport of ions. a burn.com/lectures/atn. -Histologically overt ATN is characterized by flattening of the epithelial cells.com/DMD/dystrophin. -Dystrophin is a structural component of skeletal muscle fibers.com.....Culture of various specimen types does not frequently yield the organism and may take several days. extension of truncal muscles resulting in .org/wikipe. only males are affected.washington. Proximal tubules and the thick ascending limb of Henle’s loop are located in the outer medulla of the kidney. Additionally the route of entry of C.jpg http://cnserver0. Physical exam may reveal masseter muscle spasm (“trismus” or “lockjaw”).is also recessive. http://jennyndesign.neoucom./QuizPics51-75/68M-dmd.med. On light microscopy. Ischemic injury is often not universal: some parts of the nephron are physiologically more susceptible to hypoxia than others. loss of the brush border in proximal tubular cells. It links a component of the cytoskeleton (actin) to transmembrane proteins (α. while females are carriers. In adults.9_031103/byr10494_fm-1. variation of muscle fiber size and angulated fibers are seen.JPG http://upload. for example a piercing wound. facial grimacing “risus sardonicus”).%2010-10. Generally. illicit drug use. When oxygen delivery to the kidney is compromised.. tetani will only be found locally at the wound into which they were inoculated. an area that even under normal conditions has a low blood supply. tetani is usually trauma. muscle spasms.nne-muscular-dystrophy.edu/hubio562/urinaly/mb1..and βdystrophiglycans) that are connected to the extracellular matrix.jpg http://courses.jpg Acute tubular necrosis (ATN) -ischemic injury to the kidneys.mja. The histologic presentation of Duchenne muscular dystrophy is widespread muscle necrosis.nkf.wikimedia.au/public/issue.

The organism is infrequently isolated from the blood.edu/pedisurg/imag.brown.airahospital.” http://www.residentandstaff. http://www. Migratory superficial thrombophlebitis is “Trousseau’s sign..com/issues/articles/2007-06_05..learningradiology.opisthotonos. The result is secretion of abnormally viscous mucus into the small bowel.asp Communicating hydrocephalus =Symmetrical enlargement of the ventricles . this infant is suffering from meconium ileus.jpg Migratory thrombophlebitis . Thus.g.should always make you think “cancer.l/MeconiumIleusPellets. http://www. Meconium ileus =Bilious vomiting. sodium.. air fluid levels.com/Hydrocephalus/Commun_Med.htm http://bms.. and when it does grow it will take 2. In 5-10% of patients with CE the diagnosis is made soon after birth because of this complication.usually occurs secondary to dysfunction or obliteration of subarachnoid villi. cardiorespiratory complications (e.09/06/risus-sardonicus. -Cystic fibrosis (CE) is the most common cause of meconium ileus. This dysfunction is usually a sequelae of meningeal infection (including tuberculosis meningitis) or subarachnoid intra ventricular hemorrhage. The intraoperative finding of an inspissated green mass suggests that the distal ileum has been obstructed by dehydrated meconium. abdominal distention.com/diseases_images/tetanus.” .. and cor pulmonale) account for 80% of deaths due to CE. http://neuroanimations. or lung. -Hypercoagulability occurs because adenocarcinomas produce a thromboplastinlike substance that is capable of causing chronic intravascular coagulations that are both disseminated and tend to migrate.html .gif .0Ileus/mecileuscorrect. bronchitic obstructive pulmonary disease. and water transport by the ductal epithelium of intestinal mucous glands cause isotonic dehydration of the lumen contents.org/wp-con.medical-look.. and small bowel dilatation all indicate small bowel obstruction (SBO).3 days to identify.com/a. Abnormalities in chloride. pneumonia bronchiectasis.jpg http://www.Hypercoagulability is a very common paraneoplastic syndrome seen most commonly in adenocarcinomas of the pancreas. colon. Patients with tetanus require immediate treatment based on a presumptive diagnosis based on history and physical. In the US.Blood cultures are not of much use in the diagnosis of tetanus as the disease is caused by toxin released from a local wound infection.

Hypokalemia and metabolic alkalosis are common. Villous adenomas may secrete large amounts of mucus.The path of CSI flow is as follows: lateral ventricles — interventricular foramen of Monro —the third ventricle — cerebral aqueduct — the fourth ventricle — the foramina of Luschka and Magendie — subarachnoid space. which causes diuresis and eventual compensatory sodium loss. Hypernatremia.Communicating hydrocephalus is far more common than choroid plexus papilloma Villous adenoma -Although most of colon adenomas are asymptomatic.flickr.plasma renin activity is suppressed and plasma aldosterone is likely to be elevated. The bleeding is usually unknown to the patient.static. while those below the obstruction are normal. the obstacle to CSF flow exists within the ventriculi. DIFF . cause non-communicating hydrocephalus. because of the phenomenon of “aldosterone escape” whereby increased sodium and chloride absorption leads to intravascular hypervolemia that in turn causes release of atrial natriuretic peptide. For this reason these patients do not typically have edema on physical examination. -In summary. hypokalemia. Partial intestinal obstruction can manifest with bowel habit changes. -Congenital anomalies. Arnold-Chiari or DandyWalker malformations. The dynamic balance between production and absorption of CSF allows stable intracranial volume (120-150 ml) and pressure (50-180 mm H20). and abdominal distention. . 2. diarrhea may cause hypovolemia and electrolyte imbalances. but overt bleeding may also occur. larger ones can cause a number of symptoms: 1. suppressed renin and non-suppressible aldosterone. In the subarachnoid space CSF is absorbed by arachnoid granulations and then enters the venous sinuses. non-communicating hydrocephalus occurs. leading to secretory diarrhea . is rare. Lower intestinal bleeding causes guaiac-positive stool (fecal occult blood testing) and microcytic hypochromic anemia. 4. however. In all cases. these patients have hypertension. Villous adenomas have a high risk of progression to adenocarcinoma.jpg Primary hyperaldosteronism and "aldosterone escape" =primary mineralocorticoid excess . 3. potassium loss. http://farm4. such as aqueductal stenosis. If the stool volume is large. crampy abdominal pain. Excessive mineralocorticoid secretion from tumors or hyperplasia of the zona glomerulosa leads to sodium retention. and bicarbonate retention. If the normal flow of CSF from the ventriculi to the subarachnoid space is disrupted.com/3103/2653200355_9502991760.. constipation. Ventriculi above the obstruction are enlarged.

.com/hypothyroidismafter4.pathguy. usually present over the tibia associated primarily with Graves disease. characterized by cystic dilatations of the medullary collecting ducts. Diuretics lead to urinary losses of sodium potassium and chloride. The renal cortex is typically spared.Hyponatremia and hypokalemia with metabolic alkalosis are suggestive of diuretic use. which causes alkaline phosphatase levels to increase. such as a toxic multinodular goiter or a toxic thyroid nodule.jpg Graves disease -Infiltrative dermopathy (i. and heat intolerance can be present in hyperthyroidism from any etiology.e.some patients develop kidney stones. or urinary tract infections secondary to this condition. .however. Most patients are asymptomatic.“pretibial myxedema” describes a diffuse. such as an intravenous pyelogram . . Medullary sponge kidney (MSK) = relatively common and benign congenital disorder.Normal serum sodium. When MSK patients do develop CRF..jcrows. Atrial fibrillation.info/g. Remember also that the antithyroid drug methimazole can lead to cholestasis. non-pitting edema and thickening of the skin.The hepatic inflammation associated with Graves disease causes an additional slight increase of alkaline phosphatase.. . http://www. hand tremors. hypokalemia and metabolic acidosis are suggestive of renal tubular acidosis. http://www. hypochloremia. hematuria. pretibial myxedema) and proptosis are quite specific for Graves disease.kidneys rarely progress to CRF. .primary adrenocortical insufficiency= hyponatremia.com/sol/25472. .jpg -Exophthalmos and pretibial myxedema are not seen with other causes of hyperthyroidism. Kidney stones are the most common complication of the disease. and metabolic acidosis. (60% of MSK patients have kidney stones. increased alkaline phosphatase. the term “myxedema” describes the overall disease process of hypothyroidism. . 12% of patients with kidney stones have MSK.Isolated hyponatremia in the setting of normal potassium and bicarbonate is most likely the result of SIADH (the syndrome of inappropriate ADH secretion). hyperkalemia. it is usually due to recurrent urinary tract infections or obstruction.edullary_sponge_kidney.) .. The disease is usually identified during a routine imaging procedure. http://www. -The etiology of this disorder is not known.aboutkidneystone. as well as increased absorption of bicarbonate due to volume contraction (“contraction alkalosis”).jpg .

. .med. Only a lymph node biopsy can definitively distinguish this malignancy from benign causes of lymphadenopathy...JPG Hodgkin’s disease (HD) =either nontender lymphadenopathy or have lymphadenopathy incidentally detected on routine chest x-ray -many patients develop associated systemic symptoms (B symptoms).HD has a bimodal age distribution with one peak in the second and third decades of life and another peak in the fifth decade.gov/medlineplus/ency/imagepages/2534. The key to diagnosing HD .jpg . parathyroid gland.blogspot. These microemboli tend to localize to the palms and soles. http://www. http://4.FR8c/s400/osler_s_node.ated_cutaneous_lesions. neutrophils..info/encyclopedia/K/Kaposis_sarcoma.blogspot. -The complete blood count and peripheral blood smear are usually unremarkable in most patients..jpg Hypercalcemia . On histologic examination..A neoplastic proliferation of cells of vascular origin = Kaposi’s sarcoma http://www.Granulomatous inflammation can produce cutaneous lesions in miliary tuberculosis.Bacterial endocarditis . macules on the sole of the foot are likely Janeway lesions. and the resultant lesions are painless.The most common cause of hypercalcemia in the outpatient setting is primary hyperparathyroidism secondary to a benign parathyroid adenoma.com/_nFuCC8zh. sarcoidosis.org/wikipe.EY/s400/janeway_lesion.jpg http://2. and leprosy.ohio-stat.nlm.com/_nFuCC8zh.pathology.med.wikimedia.A hypersensitivity-type vasculitis (microscopic polyangiitis) could cause cutaneous purpuric maculopapule or nodules (palpable purpura) http://vasculitis. subcutaneous microabscesses are apparent. sometimes hemorrhagic.the differential diagnosis must include multiple endocrine neoplasia (MEN) syndrome.daviddarling.erythematous. -Janeway lesions are composed of bacteria.jpg DIFF: . and pancreas (the “3 Ps”)./Images/10531/PAXIT017.. http://www. Janeway lesions are the result of septic embolization from infected cardiac valve vegetations. MEN 1 is characterized by tumors of the pituitary.htm http://upload.bp. necrotic material. -In contrast to Janeway lesions Osler nodes are painful papulopustules found in the pulps of the fingers and toes.edu/typesof/images/purpura_MPA. and subcutaneous hemorrhage. .nih..bp.jhu.html .

and inclusion-like eosinophilic nucleoli. a condition that takes months or years to develop. and tricuspid stenosis. RS cells have ample cytoplasm. RS cells are seen against a background of lymphocytes.selargeb-celllymphomadlbcl Pericarditis -The chest pain of pericarditis is sharp and pleuritic in nature.ocyte_nci-vol-7172-300.. bibbed or double nuclei.files. and the pericardial friction rub is the most striking physical finding.. http://gemininotcancer. rheumatic fever. http://www.jpg Large B-cell lymphoma = diffuse sheets of large lymphocytes with nuclei at least 5x the size of small lymphocytes.com/images/po. Gastrinomas = neuroendocrine tumors that are most commonly located in the pancreas. In fact the presence of jejunal ulcers is strongly suggestive of a diagnosis of ..gkins-disease-pictures.gif Kussmaul’s sign . http://www. The gastrin produced by these tumors stimulates gastric acid production. or the duodenum.jpg http://www. this type of pericarditis is caused by myocardial infarction..wordp.. In most instances. resulting in gastrointestinal ulcerations.mabthera. -Fibrinous or serofibrinous pericarditis is the most common variant. restrictive cardiomyopathy. severe right-sided heart failure. histiocytes and eosinophils in classic HD. Kussmaul’s sign is a paradoxical increase in the jugular venous pressure with inspiration.com/media/mmpe/figures/MMPE_07CVS_78_01_eps. oftentimes in unusual locations such as the jejunum.During inspiration the jugular venous pressure and level of distension normally decrease.. and characteristically decreases when the patient sits up and leans forward.is detection of the characteristic Reed-Sternberg (PS) cell on H&E preparation. though a viral infection may occasionally cause a fibrinous exudate to accumulate in the pericardial space.healthoma. the peripancreatic tissue around the head of the pancreas. Kussmaul’s sign is found most often in patients with chronic constrictive pericarditis. or uremia.com/portal/eip.merck. -The differential diagnosis for Kussmaul’s sign includes cardiac tamponade.

comprised of the actual tumor cells. -The diagnosis of gastrinoma is made by measuring basal and stimulated gastrin levels. reaching > 90% in the ninth decade. or IAA) is due to deposition of abnormally folded (β-pleated sheet conformation) atrial natriuretic peptide-derived proteins. -Typically. as well as the skin. Together. It is detected in the pancreatic islets of more than 90% of patients with type 2 diabetes. remnants of Rathke’s pouch cells can remain in the diencephalon (the posterior region of the forebrain).org/cgi/content/full/179/2/536/FIG2 http://www.cell proliferations (e.Localized amyloidosis confined to the cardiac atria (isolated atrial amyloidosis.com/amyloid_pop2. because of the association with MEN-I.proteotech. Proton pump inhibitors are the first-line therapy for most gastrinomas. The posterior pituitary gland arises from an extension of the hypothalamic neurons. the anterior and posterior pituitary glands lie in the sella turcica at the skull base. and a calcified component. . β-amyloid protein is also found in localized amyloid deposits in the walls of cerebral blood vessels of Alzheimer patients as well as in patients with cerebral amyloid angiopathy (CAA). The incidence of IAA increases with age. Neoplastic transformation of these “pouch cells” is called a craniopharyngioma. -During the time of pituitary development. tongue. -Patients with gastrinomas also often complain of diarrhea and abdominal pain. Workup of all patients with newly diagnosed gastrinoma should include measurement of serum calcium PTH and pituitary hormones. DIFF: -Deposition of immune globulin light chains. .ajronline.β-amyloid protein is the 4000 Dalton peptide found in the core of the cerebral plaques of Alzheimer disease. especially 1-light chains and their fragments is responsible for primary systemic (not localized) amyloidosis. kidney. The anterior pituitary is formed from an out-pouching of the pharyngeal roof and is called Rathke’s pouch. Primary systemic amyloidosis arises in association with monoclonal B.gastrinoma.g. This is a form of senile cardiac amyloidosis which may increase the risk of atrial fibrillation. cystic filled with “machinery oil” liquid. . gastrointestinal tract.Islet amyloid protein (amylin) is usually found in patients with localized pancreatic amyloidosis. craniopharyngiomas have three components: solid. Isolated amyloidosis . multiple myeloma) and causes systemic amyloid deposition involving the heart. Immunoglobulin light chains of either the Y or the K variety (Bence Jones proteins) may also be found in the serum and urine. http://www. Any suprasellar mass with three components is highly suggestive of craniopharyngioma. and peripheral nerves.html Craniopharyngiomas = tumors arising from remnants of Rathke’s pouch.

Ultimately. It results from brain injury sustained during multiple cerebral infarcts. compression of the pituitary stock by craniopharyngioma leads to hyperprolactinemia by loss of dopaminergic inhibition.org/content/26/5/1517/F1. thus resulting in a narrowed ventricular cavity size. http://www.-Craniopharyngioma symptoms include headaches.cns.gif Vascular dementia (also called multi-infarct dementia) =the second most common cause of dementia after Alzheimer disease.org/uploads/images/0000/0781/Craniopharyngioma.org/wiki/images/9/9c/CAA2.Concentric hypertrophy uniformly thickens the ventricular wall while the outer dimensions of the ventricle remain almost unchanged.clc.edu/Fankhauser/Labs/Anatomy_&_Physiology/A&P202/Endo crine_System/histology_jpgs/pituitary_40x_P2252250lbd.jpg http://radiographics.jpg http://radiopaedia. Concentric hypertrophy results from chronic elevation of the ventricular pressure during systole (pressure overload). Vascular dementia is associated with hypertension.com/lectures/craniopharyngioma.thumb. visual field defects. 1. multiple ischemic strokes and systemic atherosclerosis. http://www.annals-general-psychiatry. The presence of amyloid is not characteristic. and hypopituitarism.com/content/2/1/8/figure/F1 Hypertensive heart disease = concentric hypertrophy .jp g http://biology. stenosis of the vessel lumen and fragmentation of the internal elastic lamina. Craniopharyngiomas are usually tumors of childhood.expansion?ck=nck http://wiki.JPG Amyloid associated with Alzheimer disease = is called A3 amyloid. as is .pathguy. -Both senile plaques and amyloid angiopathy may also be seen in the brain tissue of healthy elderly individuals. APP is a normal component of neuronal membranes. These deposits damage the media and adventitia of cerebral vessels and cause thickening of the basal membrane.uc. 2. http://www. The core of these structures is composed of A3 amyloid.rsna. which is a product synthesized by the cleavage of APP (amyloid precursor protein). evidenced by growth retardation. being most frequently discovered between the ages of 5 and 10 years of age. Amyloid deposits in brain parenchyma form senile plaques.com/images/stories/conditions/amyloid-plaqueformation. Amyloid deposits in vascular walls lead to amyloid angiopathy.elements4health.

3x. http://omeweb2.S checkpoint.typically seen in hypertension due to the increased LV afterload.nature.nature.S phase transition. activation of cyclin D. cyclin E and the corresponding cyclin kinases (CDK 4 and 6) occurs and the Rb protein is hyper phosphorylated (rendering it inactive).ro/eng/tulbritmeng.edu/pmd/robbins/cvd5/cvd530. Cells with damaged DNA are not allowed to enter the S phase. -Retinoblastoma (Rb) protein is a regulator of the G1 —. When the cell is stimulated by growth factor. http://www. The transition from GI to S phase is one of the two primary cell cycle checkpoints that ensure “quality control” of the DNA. 2.html Bullous pemphigoid =Primarily a disease of the elderly =autoimmune condition characterized by antibodies that attack hemidesmosomes along the basement membrane of the dermal-epidermal junction.com/emboj/journal/v23/n24/fig_tab/7600481f2. If the Rb protein is hypo phosphorylated (active).gif Rb protein An increase in the activity of enzymes responsible for DNA synthesis signifies that the cell is in the S phase of the cell cycle. These patients have accessory pathways which directly connect the atria and ventricles and bypass the AV node. and . Active Rb protein.com/nrc/journal/v3/n7/images/nrc1123-f3.gif Wolff—Parkinson—White syndrome =an electrophysiological abnormality of atrioventricular cardiac conduction. This results in pre-excitation and arrhythmias.htm http://firstaidteam.com/usmlerximages/d/613/USMLERxConcentric+left+ventricular+hypertrophy. http://rezidentiat. The activity of these autoantibodies results in complement fixation.files/image034. The resting cells in the G0 phase contain active (hypo phosphorylated) Rb protein. Hyper phosphorylated Rb releases E2F transcription factor.ucdavis. 1. therefore serves as a “brake” that stops the cell from dividing. it binds to the E2F transcription factor. The Rb protein is present in one of two forms: active (hypo phosphorylated) or inactive (hyper phosphorylated). which allows the cell to progress through the G1 —.gif http://www. This complex inhibits the transcription of genes necessary for G1 —S transition.

and mitosis. Quantitative analysis for fecal fat is used to confirm the diagnosis (>7gm/day of excreted fat is diagnostic for malabsorption).edu/lm/DermatologyGlossary/img/Dermatology %20Glossary/Glossary%20Histo%20Images/bullous_pemphigoid_low_power. It consists of an inactive phase.ucsf. 2. Bacteria compete for nutrients causing relative nutrient deficiency. axillae. and E) may also be lost. 3. non acantholytic blister appears in conjunction with superficial edema and perivascular lymphocytic infiltrate. -Fat-soluble vitamins (K.jpg http://missinglink. -The first step in screening for malabsorption is Sudan lll stain . -Clinically. and tetany (due to hypocalcaemia) can occur.jpg Malabsorption . groin.org/directory/ABIM/GRS/Fig56_4. and lower abdomen. Intestinal mucosal defects: examples are celiac disease. -Vacuolations in the basal cell layer coalesce to form the fluid-filled blisters that are the hallmark of bullous pemphigoid. tropical sprue Whipple disease. Bacterial proliferation in the small bowel occurs in afferent loop syndrome diverticulosis.edu/lm/DermatologyGlossary/img/Dermatology %20Glossary/Glossary%20Histo %20Images/bullous_pemphigoid_higher_power_thumb. Eventually. Cell cycle =the sequence of events that separates one cell division from the next. A. Crohn disease and many others. a subepidermal. and diabetic neuropathy. the lesions of bullous pemphigoid are serous fluid-filled. -Anemia may result from iron folate. interphase. Excess fat content will cause the stool to float in the toilet bowl.ucsf. D. http://www. -Multiple disorders that cause malabsorption are divided into the following major groups: 1. Structural defect or injury to the intestinal epithelial cells hampers nutrient transport from the intestinal lumen and/or from intestinal cells to peripheral organs. 1. G 0 phase is the stage in which the cell cycle is suspended. Further diagnostic steps are then taken to identify the primary cause of malabsorption. Diminished production of digestive pancreatic enzymes leads to impaired hydrolysis of nutrients in the small intestine.americangeriatrics. -Decreased calcium and vitamin D absorption leads to bone pain. The most common sites of involvement on the body include the inner thighs. flexor aspects of the forearms.the recruited neutrophils and eosinophils can cause significant tissue injury. -Muscle wasting and edema (protein deficiency) hyperkeratosis (vitamin A deficiency). greasy stool that contains large amounts of fat. tense bullae on bases of normal to erythematous skin typically measuring 2 cm in diameter. Weight loss and symptoms of various nutritional deficiencies are common.jpg http://missinglink. The cells are . Vitamin K deficiency may cause petechiae and easy bruising.The main clinical manifestation of this syndrome is steatorrhea: foul-smelling bulky. Pancreatic exocrine insufficiency: chronic pancreatitis and cystic fibrosis belong to this group of disorders. and/or vitamin B12 deficiency.

. Upper respiratory tract ulceration is not characteristic. sinusitis hemoptysis) and rapidly progressive glomerulonephritis—producing a variable degree of renal failure—is characteristic of Wegener’s granulomatosis. C-ANCA may also be useful as a quantitative measure of disease activity. http://www.html http://brighamrad.html DIFF: . At both the G1 to S phase transition and the G2 to M phase transition. Cells with normal DNA are allowed to proceed through the checkpoint.jpg Wegener’s granulomatosis = Necrotizing vasculitis of the upper and lower respiratory tract (causing nasal ulcerations.resting and do not divide.nature. synthesis of RNA protein. lipid. the cell undergoes apoptosis.L2060/BIOL2060-19/1936. in contrast. with a better than 90% specificity and sensitivity. .edu/Cases/bwh/images/344/path1.com/ki/journal/v64/n6/fig_tab/4494120f3. Interphase comprises 90% of the cell cycle and is the stage in which the cell prepares for division. and the G2 phase (ie. 3. -The Rb (retinoblastoma) tumor suppressor gene located on chromosome 13q14 encodes a nuclear phosphoprotein that regulates the G1 —S checkpoint.tulane. while cells with damaged DNA trigger DNA repair mechanisms. 2. Interphase is subdivided into the G1 phase (ie.edu/classwar. Presenting clinical manifestations of Goodpasture syndrome are hemoptysis.jpg http://www. Abnormal phosphorylation of Rb protein results in its inactivation. osteosarcoma. These stages are called “checkpoints” and are regulated by cyclins and cyclin-dependent kinases that screen for DNA damage or abnormalities.8/Lung_Review/Lung-56. The activated Rb protein.harvard.Goodpasture syndrome is sometimes called anti-glomerular basement membrane (GBM) antibody disease.mun.. The inactivated Rb protein allows the cell to proceed through the G1 —.Cytoplasmic staining antineutrophil cytoplasmic antibodies (c-ANCAs) are virtually pathognomonic for Wegener’s. Mutations of the Rb protein have been linked to retinoblastoma.S checkpoint. breast adenocarcinoma.som.. DNA replication). the cell cycle can be stopped. thereby allowing cells with damaged DNA to proceed through the G1 —S checkpoint and then divide. http://www.. If the DNA damage is too substantial to be repaired. ATP synthesis). This disease is associated with C-ANCAs. S phase (ie. small cell carcinoma of the lung. Mitosis (M) is the stage in which the cell divides into two daughter cells.ca/biology/desmid/b. -Rb protein can be in an active (Hypophosphorylated) state or an inactive (hyperphosphorylated) state. which may target neutrophil proteinase 3. stops the cell cycle. and carbohydrate). . radiographic focal pulmonary consolidations and a glomerulonephritis that may rapidly progress to renal failure. and bladder carcinoma.

-The adrenals are the most common site of hematogenous spread of lung cancer. weakness.Size selectivity is a feature of the dimensions of the pores.6 nm. -Other common sites of lung cancer metastases include: bone. . hypotension) occur only with extensive bilateral metastases. Selective proteinuria =Albumin loss with minimal loss of the more bulky proteins (such as lgG and macroglobulin) . They repel negatively charged molecules such as albumin. Peripheral smear shows fragmented RBCs (microangiopathic hemolytic anemia) and thrombocytopenia. The GBM and slit diaphragms are. factor V. They may be unilateral or bilateral and are almost always asymptomatic. therefore. and decreased fibrinogen. Between the foot processes of epithelial cells there is a thin membrane (a slit diaphragm) with pores the same size as those in the GBM. Symptoms of hypoadrenalism (dizziness. GBM pores have a radius of 4 nm. the glomerular basement membrane (GBM) and epithelial cells. The presence of adrenal metastases indicates stage IV disease. which should be treated with chemotherapy. which contains three components: fenestrated endothelium. Since albumin is small enough to fit through pores in the GBM the . DIC results from activation of the coagulation cascade by bacterial endotoxins. and burn injury. In gram-negative sepsis. DIC = common complication of gram-negative bacterial sepsis.Albumin is a protein with molecular weight of 70000 daltons. Adrenal metastases account for more than half of all metastases of lung neoplasms. Lab tests show prolongation of PT. and a radius of 3. Early detection of adrenal metastases is important because it determines the treatment strategy. . The barrier is selective to size and charge. the most selective determinant of particle penetrance with regard to size. and factor VIII levels. brain. and the contralateral lung.Charge selectivity is provided by negatively charged anions (ie. -Liver metastases represent about 30% of the metastases of lung cancers. PTT. heparan sulfate and other proteoglycans) located on endothelial cells and the GBM. causing the formation of microemboli.Lung cancer -One reason for this high mortality rate is the early hematogenous spread of the tumor.A filtration barrier to protein molecules is provided by the glomerular capillary wall. acute pancreatitis. . Endothelial cells have fenestrations with an approximate radius of 40 nm.

upmc.jpg Functional proteinuria =caused by a change in blood flow through the glomerulus.htm DIFF: .f1/medium http://path.Tubular proteinuria= associated with the presence of low molecular weight proteins such as b2. high fever. It is a common cause of proteinuria in young adults with normal renal function and disappears on repeated testing. immunoglobulin light chains.predominantly occurs in older tall thin adolescents and is characterized by increased protein excretion in the upright position but normal protein excretion in the supine position. anorexia.barrier to its excretion is provided mostly by charge selectivity. . and right upper quadrant tenderness. Subsequently albumin is lost via the urine. dark colored urine. http://pathcuric1. These are normally filtered by the glomerulus and almost completely reabsorbed in the proximal tubule. renal function is normal and overnight collection of urine reveals normal albumin excretion (less than 50 mg during 8 hour period).org/articles/view/36150/files/JCI0836150. . some of the negatively charged molecules that provide charge selectivity are lost from the glomerular basement membrane.. emotional stress or cold exposure. nausea. Isolated proteinuria = usually an incidental finding in an asymptomatic individual with normal renal function and normal urinary sediment. Albuminuria is usually less that 1. amino acids and retinol-binding protein. http://www.0 g/day.edu/PathDemo/kid1/kid170. They appear in urine when the proximal tubular function is disrupted for instance in tubulointerstitial nephritis.jci..HAV is the most common cause of acute viral hepatitis in young adults.htm http://sinoemedicalassociation.edu/cases/case41/images/micro14.microglobulin.swmed.org. Orthostatic proteinuria . In minimal change disease (MCD). Precipitating factors include exercise. No manifestations of systemic disease are present. Acute viral hepatitis = low-grade fever.gery/kidney%20diseases.

Prevailing clinical symptom: slow. Biochemical abnormalities: decreased acetylcholine levels in the hippocampus and nucleus basalis of Meynert.edu/WirSe..) http://www..jpg http://www. 1-2 y/o =retroperitoneal mass + HTN + anorexia. Microscopic brain changes: neurofibrillary tangles.jpg http://focosi. (Liver biopsy is not needed to make the diagnosis of HAV infection..med. 2.blastoma/Neuroblastoma./image/dementia/tangle. Another involved structure is the hippocampus: the major function of the hippocampus is formation of new memories..ahaf.. and amyloid angiopathy. however.cancer. It has the following characteristic features: 1. weight loss =solid sheets of small cells with dark nuclei and scant cytoplasm (small blue round cells) =high catecholamines in urine =increased number of copies of the N-myc gene =paraneoplastic sd: opsoclonus. http://www. truncal ataxia http://www.govt. This occurs due to the deficiency of choline acetyltransferase.gov/pr. progressive memory loss. senile plaques.jpg Alzheimer disease =the most common cause of dementia.org/alzheimers/abo. 3.nz/newborn/Te. mononuclear cell infiltrates.. myoclonus.edu/Lumen/meded/orfpath/images/8-4-4.harvard. which participates in memory and cognition.In all cases of acute viral hepatitis.jpg http://visualsonline.jpg http://www.g/plaques-and-tangles.. -The most important biochemical abnormality noted in Alzheimer disease is a decrease in acetycholine level.jpg .html http://www.meddean.edu/AANLIB/cases/case3/mr1/040..anatomyatlases.org/apoptoticbodies.natomy/Images/Plate361.mageid=2593&fileformat=jpg Medulloblastoma = the second MC brain tumor in children =arises in the cerebellum and causes gait and limb ataxia http://www.html neuroblastoma = MC extracranial childhood cancer..adhb.com/sciencenews/images/imscn051606_02_01.luc.. 4. The decline in acetylcholine levels is most notable in the basal nucleus of Meynert.sflorg. This nucleus is located at the base of the forebrain and widely projects to the neocortex.vcu.org/Micr. Macroscopic brain appearance: mild-to-moderate generalized brain atrophy.pathology. and Councilman bodies (eosinophilic apoptotic hepatocytes) are seen histologically. diffuse ballooning degeneration (hepatocyte swelling).altervista.

-High levels of dietary aflatoxin exposure is associated with a G:C — T:A transversion in codon 249 of the p53 gene a mutation thought to greatly increase the risk of developing hepatocellular carcinoma http://www. writer’s cramp Chorea: Huntington disease Hemiballism: contralateral injury in or near the subthalamic nucleus Aflatoxins are categorized as A1.sflorg. B2. Oropharyngeal: Erythema of the palatine mucosa. Generalized rash: Polymorphous (usually urticarial) erythematous rash beginning on the extremities and moving to the trunk (centri petal spread) There are two types of membranoproliferative glomerulonephritis. . Fever 2. .ohio-stat. Bilateral conjunctivitis 3. with aflatoxin B1 the most common and most toxic. Symptoms of Kawasaki disease include: 1. “strawberry” tongue 2.Type I = with upper respiratory tract infections and causes a nephrotic sediment .. The most serious complication =coronary artery involvement leading to the development of coronary artery aneurysms.med.JPG Kawasaki disease= vasculitis of medium-sized arteries that affects very young children (12-24 months of age). Peripheral extremities: Edema of hands and feet. Lymphadenopathy 4.Type II = also called "dense deposit disease"= nephritic sediment..pathology. Cutaneous involvement: 1. -Both are caused by immune complex deposition in the glomerular basement membrane.jpg Dystonias= impaired function of the basal ganglia -MC focal dystonia = spasmodic torticollis -blepharospasm.http://www. erythema of palms and soles. and G2./Images/10534/PAXIT025.com/sciencenews/images/imscn051606_02_02. desquamation of the fingertips (periungual) 3. G1. fissured erythematous lips.

= decreased platelet adhesion and aggregation .Diffuse carcinoma (linitis plastica) infiltrates the stomach wall and displays a signet-ring pattern on light microscopy. Primary ciliary dyskinesia =autosomal recessive mutation in the microtubule-associated protein dynein. http://web2. can cause Kartagener’s syndrome in about 50% of patients (variable penetrance). Blood products containing vWF are used in severe forms of von Willebrand disease. =abnormal menstrual bleeding/Bleeding of the gums/Bruising/Nose bleeds/Skin rash =more common and milder than hemophilia -definitive diagnosis of von Willebrand disease = measuring the levels of different fractions of vWF factor.net/uthman/specimens/images/gastcarc_enface. Kartagener’s syndrome is characterized by male infertility._diffuse_type_mucinous.pathologyatlas. When the vWF level is decreased. .iadfw. Deficiency of thromboxane A2= with aspirin treatment..jpg http://www.ro/patho..jpg Von Willebrand disease (vWF deficiency) = impairments of platelet function and coagulation pathway abnormalities. situs . there is poor platelet aggregation in the presence of ristocetin. due to irreversible inactivation of COX in platelets.Gastric adenocarcinoma: .The ristocetin aggregation test is normal. = prolonged bleeding time and decreased platelet aggregation in response to ristocetin -the ristocetin aggregation test is used to measure vWF-dependent platelet aggregation. but is decreased with addition of ADP.Intestinal type forms a solid mass that projects into the stomach lumen and is composed of glandular-forming cuboidal or columnar cells. -Rx= desmopressin (DDAVP)I which stimulates vWF release from endothelium. Hereditary deficiency of GP lIb-Illa receptors=Glanzmann thrombasthenia = mucocutaneous bleeding and increased bleeding time. Ristocetin activates Gp Ib-IX receptors on platelets and makes them available for vWF binding. Platelet aggregation in response to ristocetin is normal.

very aggressive. a primary abnormality in a development process.Potter syndrome = a sequence. The rates of mitosis and apoptosis in the cancerous tissue are high. high-dose chemotherapy -endemic (African type) Burkitt lymphoma: jaw involvement. -Congenital hip dislocation. short-term.com/lectures/l3. Almost all cases of Burkitt lymphoma are associated with translocations of the C-MYC gene on chromosome 8. and bronchiectasis.com/handcloseup. responds well to intensive. accounting for 10% of patients on dialysis in the United States = autosomal dominant.inversus. usually onto the Ig heavy chain region of chromosome 14 [t(8:14)]. .amnioticbandsyndrome. . clubbed feet and flat facies (Potter syndrome) are deformations (secondary to extrinsic compression). asso/w EBV infection http://www. http://www. -Amniotic band syndrome = disruption (secondary destruction of a previously well-formed tissue or organ). recurrent sinusitis.jpg Autosomal Recessive (infantile) Polycystic Kidney Disease (ARPKD) manifests in infants. Trinucleotide repeat mutations = three-nucleotide sequence is abnormally repeated.pathguy.jpg Holoprosencephaly = from failure of forebrain cleavage into cerebral hemispheres= congenital malformation. Most of these patients die shortly after birth or during the first years of their lives. Such mutations cause . ADPKD = the most frequent genetic cause of renal failure in adults. Most cases of hypertrophic cardiomyopathy = mutations in the genes encoding cardiac sarcomere proteins Burkitt lymphoma =“starry sky” appearance due to the presence of macrophages and apoptotic bodies in a sea of medium-sized lymphocytes.

jpg Thromboangiitis obliterans (Buerger’s disease) = vasculitis of medium and small-sized arteries. = large collagen bundles lying in parallel with one another and excess cellular connective tissue. =soft or firm nodules that grow beyond the borders of the wounds within which they form with claw-like extensions onto normal tissue.fragile X syndrome. veins. . and nerves) in fibrous tissue.uiowa.Lipid-filled intimal plaques that bulge into the arterial lumen= atherosclerosis.Onion-like concentric thickening of arteriolar walls = malignant hypertension -Granulomatous inflammation of the media= temporal (giant cell) arteritis . Mitochondrial disease: Myoclonic epilepsy with ragged red fibers syndrome. Leber’s hereditary optic neuropathy = bright red irregular (moth eaten) subsarcolemmal depositions with Gomori trichrome on frozen sections http://webeye. normal fibrinogen.edu/eyef. = acute and chronic inflammation of the arterial walls. PT. which can undergo organization and recanalization.ophth. PTT Keloids =excessive collagen formation during tissue repair in susceptible individuals. The inflammatory phase consists of movement of neutrophils (within first 24 .Unlike keloids. principally the tibial and radial arteries. hypertrophic scars are limited to the area of the wound and may regress spontaneously though this is uncommon..ggedredfibers_03252005. This segmental thrombosing vasculitis often extends into contiguous veins and nerves (a feature rarely seen in other types of vasculitis). Wound healing= three phases: 1.. . myotonic dystrophy. DIC : =bleeding +PT and PTT are prolonged +Low fibrinogen and increased FDP TTP/HUS: -no bleeding. often with thrombosis of the lumen. The inflammatory process may eventually encase all three structures (arteries.Transmural inflammation of the arterial wall + fibrinoid necrosis = polyarteritis nodosa. Kearns-Sayre syndrome . . and Huntington disease.

Infectious endocarditis (IE) is the usual source of such microemboli.jpg Bronchioloalveolar carcinoma = is a variant of adenocarcinoma.mesothelioma-asbestos-l. the uterus is enlarged out of proportion to the gestational age. During this phase active fibroblasts synthesize collagen elastin and other components of the connective tissue matrix. The proliferative phase begins 3-5 days after the injury. The maturation phase is characterized by fibrosis (scar formation) and starts during the second week after the injury. slender microvilli and abundant tonofilaments. 3.hours) and macrophages (2-3 days) to the damaged area and phagocytosis of necrotic debris and bacterial contaminants.jpg http://www. During this phase.. Partial mole =69 XXX or XXY.au/gfx/pubs/-1843038135_r0. bunch of grapes appearance. 2. http://health. It almost always arises at the periphery of the .. hyperthyroidism and theca-lutein cysts as well.Hemorrhagic pleural effusions and pleural thickening are characteristic. Complete mole =46 XX or XY (paternal origin). Janeway lesions (small. Fibroblasts and endothelial vascular cells proliferate to form connective tissue and blood vessels (neovascularization) respectively. revealing tumor cells with numerous.formation/images/meso9. 15% risk of malignant trophoblastic disease. low risk of malignancy Malignant mesothelioma = rare neoplasm that arises from the pleura or peritoneum = strongly associated with asbestos exposure . erythematous or hemorrhagic macular. -Electron microscopy is the gold standard for diagnosis. By 6-8 weeks initial scar formation is complete and the wound reaches 30-40% of normal tensile strength during this time.act. nontender lesions on the palms and soles) are a sign of microembolism as well. granulation tissue looks pink. Maturation of the scar continues for the next several months with a slowly progressive increase in tensile strength occurring over that span of time. long. Subungual splinter hemorrhages: splinter. friable and edematous. There may be pre-eclampsia.gov.or flame-shaped hemorrhagic streaks in the nailbed that appear as a consequence of microemboli. normal villi and fetal tissue are also present.

Neuroendocrine markers such as chromogranin and synaptophysin are usually positive. tubular atrophy with decreased tubular epithelial size. and fibrosis of the interstitium and glomerular atrophy would be seen... Angiotensin II is a potent vasoconstrictor and also releases aldosterone.ro/patho.flickr. persistently circulating factor Va Leiden results in increased thrombin production Renal artery stenosis (RAS) =is most often caused by atherosclerotic plaques at the junction of the aorta and the renal artery -On light microscopy of the smaller kidney.jpg Squamous cell carcinoma also arises from the major bronchi. patchy inflammation. http://www. This tumor can sometimes present as a cavitary lung lesion. Imaging will show a hilar mass. -Factor V Leiden is the most common cause of inherited thrombophilia.edu/Courses/Digit.emic_path/pulmonary/L4. On chest imaging it is seen as a hilar mass. http://www.jpg The major clinical manifestations of factor V Leiden = deep vein thrombosis (DVT). cerebral vein thrombosis. with the heterozygote prevalence of this genetic mutation ranging from 1-9% in Caucasian populations worldwide. Histologically. This .renal blood flow is normally 3-5 times greater than that of blood flow in other organs.jpg Small cell carcinoma = usually arises from the major bronchi. tubuloclerosis.com/3146/2921388243_e748573afe. Heterozygote carriers of factor V Leiden have five to ten times the risk of developing a thrombosis. and recurrent pregnancy loss. while homozygote carriers of factor V Leiden have fifth to one hundred times the risk of developing a thrombosis.brown. it is characterized by keratinization and intercellular bridges. http://farm4.static.pathologyatlas. ._carcinoma_skin_detail. On chest x-ray it appears as a peripheral mass or as an area of pneumonia-like consolidation.. which is then converted to angiotensin II.lung and has a characteristic distribution along the alveolar septa without vascular and lymphatic spread.. -Because factor Va is a cofactor in the conversion of prothrombin to thrombin. When renal perfusion pressure decreases to 70-85 mm Hg for any reason renin-secreting cells of the juxtaglomerular apparatus are stimulated to convert angiotensinogen to angiotensin l.

and advanced age may also contribute to the tendency toward thrombosis in cancer patients. especially patients with adenocarcinomas of the pancreas. and the ears. Both are rare diagnoses. colon. -A glomangioma is a tumor of the modified smooth muscle cells of a glomus body.davidlnelson. The vasoconstriction that occurs causes hypertension. hepatic involvement and dysfunction. which is then connected to an efferent vein. None of these mechanisms/factors directly promotes activated protein C resistance in the aPTT coagulation test. http://www.ajronline. =the presence of antiphospholipid antibodies (lupus anticoagulant and/or anticardiolipin antibodies) plus one or more of the following: venous thromboembolism. and a sudden decrease in renal function may develop. . muscular arteriovenous anastomosis. .ge/09_07_2426_14_cmyk.org/content/v. Modified smooth muscle cells are arranged in layers around these vascular channels.proceed cautiously with ACE inhibitors when RAS is present because elevated levels of angiotensin II are necessary to maintain glomerular filtration in these patients. The role of the glomus body is to shunt blood away from the skin surface in cold temperatures in order to prevent heat loss. A bluish neoplasm occurring underneath the nail bed = may be either a glomus tumor (glomangioma) or a subungual melanoma..md/images/Glomus_2. The mechanism of cancer-induced hypercoagulability is thought to involve release of procoagulant tumor products. sepsis. encapsulated neurovascular organs found in the dermis of the nail bed. http://www. the pads of the fingers and toes. patient immobility. Lupus anticoagulants are the most common cause of aPTT prolongation. Vascular stasis due to obstruction of blood flow by the tumor. or frequent fetal loss. Paraneoplastic syndrome of hypercoagulability = in some patients with cancer.patients with antiphospholipid antibody syndrome typically have a prolonged baseline aPTT.jpg . or lung.vasoconstriction is necessary to maintain glomerular filtration.jpeg Antiphospholipid antibody syndrome = common immune cause of hypercoagulability.. Each glomus body is composed of an afferent arteriole connected to a richly innervated. arterial thromboembolism. Glomus bodies are numerous small. and to direct blood flow to the skin surface in hot environments to facilitate the dissipation of heat.

. Diverticula may be asymptomatic or may manifest with painless rectal bleeding or acute diverticulitis. They consist of networks of endothelium-lined lymph spaces.Lymphangiomas = occur subepidermally. Because they do not contain pigmented cells or red blood cells. in the head. The defective receptor does not allow PTH to be appropriately suppressed by an increase in serum calcium level. In familial hypocalciuric hypercalcemia. These patients have excellent long-term prognoses. Familial hypocalciuric hypercalcemia = autosomal disorder caused by a defective calcium-sensing receptor on the parathyroid cells. Urinary calcium excretion is the key feature that differentiates the familial disease from hyperparathyroidism. neck. Meckel diverticulum = an example of both a true and congenital diverticulum. Chronic constipation is a risk factor for this condition. lymphangiomas would be unlikely to have a bluish appearance. submucosa and muscular layer). Traction diverticula = occur due to inflammation and subsequent scarring and are true by structure (consist of mucosa. Example of traction diverticula are midesophageal diverticula. It results from an abnormality that occurs during fetal development and it consists of all layers of the intestinal wall. mild to moderate hypercalcemia is accompanied by normal to high serum PTH levels.The most common site is the sigmoid colon. which occur due to mediastinal lymphadenitis and periesophageal scarring. and axilla. . Colonic diverticula = usually develop due to increased intraluminal pressure and are composed of mucosa and submucosa. as both conditions have elevated calcium and PTH levels.

even when the disease is localized.edu/DPT/Hist/Tzanck01. =poor signal transmission at the neuromuscular junction. as can paralysis of cranial nerves. Surgery is usually not a treatment option. -average lifespan following diagnosis is less than one year Lambert-Eaton myasthenic syndrome = paraneoplastic disorder. -Antibodies to voltage-gated presynaptic calcium channels are found in these patients.lmp. such as CN VII . Dermal inflammatory infiltration and leukocytoclastic vasculitis may be present. -weakness improves during the day and with exercise -nerve stimulation studies = incremental response -no improvement after tensilon test Varicella-zoster virus (VZV) = enveloped double-stranded DNA virus -Weakening of cellular immunity leads to reactivation of the virus that manifests as herpes zoster (shingles). = painful vesicular rash in a dermatomal distribution -Light microscopy of a sample from a vesicle base reveals intranuclear inclusions in keratinocytes and multinucleated giant cells (positive Tzanck smear).ages/Images-T/000p028w.jpg http://tray.cause hypercalcemia (and hypocalciuria) increasing the distal tubular reabsorption of filtered calcium. http://www.dermatology.jpg Guillain-Barre syndrome =acute demyelinating disease with an immune-mediated pathogenesis. Paralysis of respiratory muscles may occur. This tumor is sensitive to chemotherapy and radiation. Skin biopsy would show acantholysis (loss of intercellular connections) of keratinocytes and intraepidermal vesicles.ca/resourc.HCTZ .ualberta.. most commonly associated with small cell lung cancer that clinically resembles myasthenia gravis.uiowa. Demyelination causes ascending flaccid paralysis and areflexia. -Antibodies against infectious antigens are thought to cross-react with the myelin of the spinal roots and peripheral nerves. segmental demyelination of peripheral nerves is seen. -On light microscopy. Small cell carcinoma =the most aggressive type of lung cancer. The increased serum calcium levels usually suppress PTH.. Demyelination is accompanied by an “endoneural inflammatory infiltrate” consisting of lymphocytes and macrophages. Most patients have distant metastases at the time of diagnosis.

and vision loss. MAP-kinase pathway 2.jpg Giant cell (temporal) arteritis =the most common form of systemic vasculitis in adults =Granulomatous inflammation of the media with fragmentation of the internal elastic lamina of branches of the carotid artery = patients older than 50: headache. physicians may wait to obtain ESR. cAMP pathway .Another contributing factor of diabetic neuropathy= accumulation of sorbitol and fructose in nerve axons. Phosphoinositide-3-kinase pathway 3./diabetic-neuropathy-1. -CSF =increased protein with normal or only slightly elevated cell count (albumino-cytologic dissociation). http://www.because of the segmental nature of the disease.jpg Polymyositis = “Endomysial” inflammatory infiltration =bilateral.(Bell’s palsy). Inositol-lipid pathway 4..edu/neurology/images/nmus16. biopsy may not show inflammation -prevent blindness by prompt initiation of prednisone therapy. After the growth factor binds its cell membrane receptor. signal transduction systems transfer the signal to the nucleus. Examples of signal transduction systems include: 1.com/wp-con. jaw claudication. and elevation of the erythrocyte sed rate . facial pain. rather than nerves. http://diabetesinfodesk. symmetric weakness of proximal muscles. but should not wait for biopsy results before starting highdose prednisone Growth factors = stimulate cell proliferation by altering the expression of certain genes in the nucleus.. .bcm. as polymyositis involves the muscles. Reflexes are normal. Diabetic microangiopathy =Hyalinization of nerve arterioles = narrowing of the arterial lumen and ischemic nerve injury.

JAK/STAT pathway MAP-kinase pathway : http://www. Inactive (GDP-containing) Ras is activated by a signal from the receptor tyrosine kinase. In frozen sections.edu/news/sr/sr2007/images/Sun. Inactive Ras contains GDPI while the active form is bound to GTP.vener_GCN2_OilRedLiver.abnormally ..nature.science.edu/instruction/bb450/stryer/ch15/Slide60.jpg Polycystic ovarian syndrome 1. An increased LH/FHS ratio (>3) is characteristic. the resultant permanently activated Ras stimulates cell proliferation and can lead to cancer.png http://www. leading to Ras activation. lipids can be demonstrated by staining with oil red O or sudan black. Mutation of Ras can lead to an inability to split GTP.. Active (GTP-containing) Ras is inactivated by GAP (GTPase-activating protein).riken.youtube. Activated Ras transmits the signal to MAP (mitogen-activated protein) kinase.jpg http://www.jpg http://oregonstate.5.edu/alert/i.com/watch?v=bYioSvT33cA Growth factor binding to the receptor tyrosine kinase leads to auto phosphorylation of the receptor. which induces the hydrolysis of GTP into GDP. alcohol dehydrogenase and aldehyde dehydrogenase. acyclic estrogen production.psu.com/onc/journal/v26/n22/images/1210394f1.go. due to anovulation.jpg Hepatic steatosis = nonspecific condition = triglyceride accumulation within the hepatocellular cytoplasm =decrease in free fatty acid oxidation secondary to excess NADH production by the two major alcohol metabolism enzymes. and elevated LH ). http://www.Fig1.brc. 2. Ras is a G-protein that exists in active and inactive forms. -fatty tissue = cytoplasmic vacuoles because the lipid is dissolved during histologic processing. Menstrual irregularity (most often oligomenorrhea) and infertility. Hormonal dysregulation (progesterone deficiency. which enters the nucleus to influence gene transcription. -The alteration of the hepatic NAD/NADH ratio in alcoholics induces fatty liver through inhibition of gluconeogenesis and fatty acid oxidation.scripps. http://www. Additional pathogenetic factors include impaired lipoprotein assembly and secretion and an increase in peripheral fat catabolism. The Ras protein exists in a balance between its active and inactive forms. Phosphotyrosine produced in this reaction interacts with a number of proteins (such as 3H2-domain proteins and SOS protein).MB.jp/lab/dna/en/GENESETBANK/mapk_ras.

“foamy” cytoplasm. 3. cystic follicles. 5. Abdominal U/S =bilateral ovarian enlargement.. = triad of acute renal failure. microangiopathic hemolytic anemia..ftheweekpix2006/cow190. sclerotic.high levels of unopposed estrogen on the endometrium = long-term risk of endometrial hyperplasia and endometrial adenocarcinoma.jpg Xanthomas = suggestive of hyperlipidemia.com/co. Henoch-Schonlein purpura (HSP) = systemic hypersensitivity (leukocytoclastic) vasculitis that can be induced by numerous bacterial and viral pathogens as well as a number of medications. =palpable purpura on the buttocks and lower extremities.learningradiology. and triglycerides.. Histologic = multiple enlarged.com/watch?v=cUQNoAK9OUs&feature=channel Hemolytic-uremic syndrome (HUS) =common cause of acute renal failure in children.. -yellow nodules composed of lipid-laden histiocytes in the dermis -eruptive xanthomas =yellow papules that abruptly appear when plasma triglycerides and lipids increase -tuberous and tendinous xanthomas often present on Achilles tendons and the extensor tendons of the fingers . This cytoplasm contains high levels of cholesterol.plane xanthomas =linear lesions in skin folds that are strongly associated with prima biliary cirrhosis . phospholipids.com/c. Patients with PCOS have a higher risk of developing type 2 DM 4.residentandstaff. coli 0157:H7 and Shigella dysenteriae. It is caused by immune complex (classically IgA) deposition in affected tissues. The lipid-laden macrophages are frequently also . Increased insulin resistance leads to obesity.xanthelasma =soft eyelid or periorbital plaques with no associated lipid abnormalities in 50% of affected individuals Histologically xanthomas = benign macrophages packed with finely vacuolated. http://www. especially when present in conjunction with a family history of early cardiac death.youtube. arthralgias and acute glomerulonephritis http://www.jpg http://www. It is associated with shiga toxin-producing organisms like E.06/11/img/RSP200611f21. and thrombocytopenia. abdominal pain. Changes of lipid metabolism= increased risk for atherosclerosis and CAD 6. Hirsutism and acne due to increased androgen levels.

. Nonspecific symptoms and paraneoplastic syndromes are common. http://www. and a positive heterophile antibody reaction =most commonly caused by EBV. due to secretion of erythropoietin-like substance. The classic triad of hematuria. atypical lymphocytosis.g. and hypercalcemia is common as well.cjp.. due to synthesis of PTH-related peptide. the small aggregates of dermal foam cells are present without any surrounding inflammation or fibrosis.microscopyu. this neoplasm is often golden-yellow on macroscopic examination..hepatonet. -The lung= most common site for metastasis.jpg http://renis. For the same reason.ges/mononucleosis40x02.org/Division/c/photo/cmv1. pharyngitis. multiple nucleoli) in these cells distinguishes them from the immature blast forms found in various hematologic malignancies. CMV can also cause retinitis in immunocompromised (especially HIV+) patients.com/img/imagenes8.com/slides. = classic atypical lymphocytes on the peripheral smear. The abundant cytoplasm and lack of bizarre nuclear changes (e. With xanthelasmas.can cause a mononucleosis-like syndrome in immunocompetent patients. flank pain and palpable mass occurs in a minority of patients. CMV infection is sometimes associated with the presence of atypical lymphocytes but these cells are less prominent than in EBV infection. http://www.idney_RCC_Chromophobe4.registry.. The cytoplasm appears clear due to the high lipid content of the tumor.enclosed by inflammatory cells and fibrotic stroma. lymphadenopathy.jpg Renal cell carcinoma = large cells with clear cytoplasm and eccentric nuclei.webpathology. erythrocytosis can occur. hepatosplenomegaly. EBV infection is also associated with an increased incidence of Burkitt’s lymphoma and nasopharyngeal carcinoma.com/images/image/0147056.cz/res/image/renal-cell-ca-nephrectomy.jpg Infectious mononucleosis =Fever.jpg .jpg Cytomegalovirus (CMV) infection .asm.com/galleri.jpg http://www. http://www. http://mmserver.

Dilated cardiomyopathy (DCM) = dilatation of all four chambers of the heart. making it prone to rupture.jpg Toxic megacolon = complication of ulcerative colitis. Temporal sequence of the major histologic changes: 0-4 hrs :minimal change 4-12 hrs: early coagulation necrosis.ajronline. Barium contrast studies and colonoscopy are contraindicated due to risk of perforation. On light microscopy. Perforation is a life-threatening complication of megacolon. http://www. .gif Acute myocardial infarction -changes on light microscopy are usually not apparent until 4 hours after the onset of severe ischemia. Rapid colonic distention ensues.com/galleri. and signs of shock are typical..microscopyu.. Although a variable waviness of myofibrils at border of the infarct (due to myofibril relaxation) might be observed before this more definite signs of early coagulative necrosis such as cytoplasmic eosinophilia and nuclear pyknosis take at least 4 hours to develop.microscopyu.If improvement does not follow within 24-48 hours surgery should be considered (total colectomy with ileostomy). hemorrhage wavy fibers 12-24 hrs: coagulation and marginal contraction band necrosis 1 to 5 days:coagulation necrosis and neutrophilic infiltrate 5 to 10 days: macrophage phagocytosis of dead cells 10 to 14 days:granulation tissue and neovascularization 2 weeks to 2 months:collagen deposition / scar formation http://www. due to exogenous cardiotoxic agents) DCM may exist in the absence of coronary artery disease.. Abdominal pain and distention. -Complete cessation of neuromuscular activity in the intestinal wall is the first step in the pathogenesis of toxic megacolon. with a mortality rate > 50%. segmental necrosis may be seen.myocardialinfarct20x02.jpg http://www.daviddarling.g. which thins the intestinal wall.com/galleri. http://www.info/images/cardiomyopathy. -Both primary (idiopathic) and secondary (e.org/cgi/content-nw/full/188/6/1604/FIG21 . edema. Plain abdominal X-ray should be used for diagnosis. along with fever. systolic dysfunction and myocardial failure..myocardialinfarct10x03. diarrhea.

CBC. diffuse. and reticulocyte count are normal. Janeway lesions — small.These changes disrupt the flow of potassium ions in the inner ear and in cardiac muscle. and other tissues. leading to the hearing loss and irregular heart rhythm Arrhythmogenic right ventricular cardiomyopathy (ARVC) =progressive fibrofatty replacement of the right ventricular myocardium of uncertain pathogenesis. kidneys. -Acute. -no QT prolongation =Mutations of a calcium-binding sarcoplasmic reticulum protein Bacterial endocarditis (BE) . but liver function tests. proliferative glomerulonephritis secondary to circulating immune complexes may complicate BE and can result in acute renal insufficiency. with neurosensory deafness) and the more common Romano-Ward syndrome (autosomal dominant. it is unlikely to cause glomerulonephritis. Gilbert syndrome = familial disorder of bilirubin glucuronidation that typically presents with mild unconjugated hyper bilirubinemia thought to be provoked by one of the classic triggers. nontender lesions on the palms and soles — are an example of this process.Microemboli from endocardial vegetations in BE can produce systemic thromboembolic events in the brain. blood smear. Both may predispose to torsades de pointes at a young age.Jervell and Lange-Nielsen syndrome (autosomal recessive. no deafness).Congenital syndromes that cause QT prolongation: . 75% of all renal glomeruli would have to be affected. -while endotoxin production can cause acute tubular necrosis as part of sepsis. macular. = from mutations in a K channel protein that contributes to the delayed rectifier current K of the cardiac action potential. -In order to decrease GFR by5O%. erythematous or hemorrhagic. causing syncopal episodes and possible sudden cardiac death. myocardium. -unconjugated hyperbilirubinemia persists with repeat testing. Hepatitis B virus infection = associated with a serum-sickness like syndrome in the prodromal .

The presence of thyroid nodules may be an indication for fineneedle aspiration biopsy to rule out malignancy.pathology. =symptoms of thyrotoxicosis and a painful. http://medsci.edu/WebPath/ENDOHTML/ENDO018. and right upper quadrant pain may ensue.jpg http://www. suggesting an autoimmunity role in the development of Riedel’s thyroiditis. skin rash pruritus.the thyroid has intense mononuclear infiltration consisting of lymphocytes and plasma cells. patients afflicted with subacute thyroiditis usually attain euthyroidism.indiana. Occasionally. lymphadenopathy.med. and very high titers of anti-thyroid peroxidase antibody.edu.edu/c602web/602/C602web/liver/slide132. cellular infiltration with occasional multinuclear giant cells -The original insult to the thyroid may be a viral infection.htm http://www. Eventually.pathconsultddx.onlab/Acutehep-diffuse.jpg Hashimoto’s thyroiditis =symptoms of hypothyroidism.com/pathCon/diagnosis?pii=S1559-8675(06)715510 . tender thyroid gland. The thyroid follicular epithelial cells undergo a metaplastic change. presence of hypothyroidism (elevated TSH and low T4/T3) and elevated antithyroid peroxidase antibody. leading to the formation of large oxyphilic cells with granular cytoplasm. There are several germinal centers also present.utah. Anorexia nausea jaundice.jpg http://www.A biopsy is typically not required. and joint pain. http://www. .. the thyroid gland is nodular on examination.pathconsultddx. A hard.period:experiencing malaise. http://library. called “Hurthle cells. fever. a diffusely enlarged thyroid gland. fixed thyroid gland can simulate a malignancy.html de Quervain’s thyroiditis=granulomatous thyroiditis=subacute thyroiditis =Mixed. ..com/pathCon/diagnosis?pii=S1559-8675(06)715509 Riedel’s thyroiditis = extensive fibrosis of the thyroid gland extending into the surrounding structures. After a brief thyrotoxic phase.com/ctrls/atlas/Images/153. patients often develop transient hypothyroidism.med.edu/greensonlab/Lyticdeath.” -diagnosis of Hashimoto’s thyroiditis= clinical examination. -significant elevations in ALT and AST (with ALT> AST) followed by rises in bilirubin and alkaline phosphatase.umich. A large proportion of patients with Riedel thyroiditis have positive antithyroid peroxidase antibody titers.med.egyhep.pathology.umich. http://www.

th/acamed/kanchana/p27.class.tulane. http://home. -They occur in microangiopathic hemolytic anemias (DIC.som.hakeem-sy.jpg Erythroid precursors . -Haptoglobin is a serum protein that binds free hemoglobin and promotes its excretion by the reticuloendothelial system. UP) and due to RBC destruction by prosthetic cardiac valves. In intravascular hemolysis.hmc. This variant of papillary thyroid cancer is seen in older individuals and carries a relatively worse prognosis when compared to welldifferentiated papillary thyroid cancer.ac. a condition characterized by erythropoietin-stimulated. HUS.tw/ch10/Slide98.edu/classwar.Psammoma bodies = typical of papillary thyroid cancer.kku.jpg http://www. Extramedullary hematopoiesis is most frequently caused by severe chronic hemolytic anemias.kmu. the amount of free hemoglobin in the serum exceeds the binding capacity of haptoglobin thereby decreasing the level of haptoglobin http://www.org. http://pathology. such as β-thalassemia.qa/hmc/qmj/images/813%20Fig%201.htm . http://www. -Hemolytic anemias = decreased serum haptoglobin level as well as an increased LDH and bilirubin. -Intravascular erythrocyte destruction results in hemoglobinemia and hemoglobinuria as well as increased LDH.html Megaloblastic anemia = hypersegmented neutrophils (> 5 nuclear lobes) and enlarged ovoid erythrocytes (oval macrocytes). and hyperplastic marrow cell invasion of extramedullary organs.jpg Schistocytes (helmet cells) = fragmented erythrocytes. Another characteristic feature of papillary thyroid cancer is the ground-glass nucleus with intranuclear grooving.in organs such as the liver and spleen is indicative of extramedullary hematopoiesis.normalRBC/AbnormalRBC. lined by tall epithelial cells.com/main/files/pasomma..edu. The tall cell variant of papillary thyroid cancer is characterized by follicular hyperplasia..

or less well-differentiated consisting of sheets of follicular cells or large cells with eosinophilic cytoplasm (Hurthle cells). the semiliquid exudate within will partially drain creating an air-containing cavity that can be identified on chest radiograph. http://radiology. http://www.med.miami. simulating normal thyroid morphology. The 1-2 year mortality approaches 100% given the tendency of this tumor to invade nearby structures and metastasize to distant sites. -no psammoma bodies and no ground glass nuclei of PTC . = secondary to the release of lysosomal enzymes by neutrophils and macrophages.xml IEN. To be called FTC the lesion must show capsular and vascular invasion. inducible nitric oxide synthase release. FTC is distinguished from benign follicular adenomas by its capsular and vascular invasion. Follicular adenomas = benign thyroid tumors that can be very difficult to distinguish from well differentiated FTC.y production = responsible for phagolysosome formation. FTC = the second most common thyroid cancer. FTC may be welldifferentiated. = large pleomorphic cells and large multinucleated osteoclast-like cells. FTC and PTC are differentiated based on the presence of ground glass nuclei and psammoma bodies in PTC. Occasionally small cells mixed with spindle cells are seen as well. and the development of granulomas and caseous necrosis.pathologystudent. Histologically.Pulmonary abscesses = local suppurative collections within lung parenchyma -if the abscess cavity communicates with an air passage.edu/x40.com/?tag=follicular-thyroid-carcinoma Anaplastic thyroid carcinoma = very aggressive tumor with a poor prognosis.

lmp.ualberta.pathconsultddx. Cushing sd 2.ualberta. Treatment= discontinuing warfarin and administering fresh frozen plasma to replenish protein C content..L/000p045b.. Following the initiation of warfarin.. early local and distant spread.. and large cell carcinoma..http://www. Small cell (oat cell) carcinoma= aggressive behavior=rapid growth.. and poor prognosis =treated with chemotherapy and radiation. Non-small cell carcinoma is far more common = adenocarcinoma. causing a relative hypercoagulable state with thrombotic occlusion of the microvasculature and skin necrosis. .es/Images-K. If a protein C deficiency is present.jpg Mitral valve prolapse (MVP) = defects in mitral valve connective tissue proteins which predispose to myxomatous degeneration and stretching of the valve leaflets by chronic hemodynamic stress. cavitation is common.lmp.lmp.ualberta. squamous cell carcinoma. asso/w hypercalcemia http://www. asso/v gynecomastia.jpg http://www. http://upload. SIADH.ca/resourc.Adenocarcinoma=peripheral =MC subtype of non-small cell carcinoma. .ages/Images-S/000p026k.lmp. the transient procoagulant/anticoagulant imbalance is further exaggerated.ages/Images-S/000p026r.ca/resourc. http://www. asso/w Lambert-Eaton Sd.ualberta. a rapid drop in factor VII and protein C levels occurs. -central..ca/resourc.org/wikipe. Protein C is natural anticoagulant (as is protein S)..jpg -squamous cell ca = central.jpg -squamous cell carcinoma and small cell carcinoma have a strong association with smoking. Warfarin-induced skin necrosis = in patients with a protein C or S deficiency who are started on warfarin..wikimedia.. asso/w clubbing and hypertrophic osteoarthropathy = tumor cells that form glandular or papilla structures. It is also the MC subtype in women and non-smokers.ages/Images-A/000p032y.jpg -large cell ca = peripheral.-induced_skin_necrosis.ca/resourc. galactorrhea http://www.com/pathCon/diagnosis?pii=S1559-8675(06)715625 Lung cancer 1.

medskool. enlarged liver. -Histologically= attenuation of the fibrosa layer of the valve and thickening of the spongiosa layer by deposition of mucoid (myxomatous) material. a systolic ejection murmur is heard at the right second intercostal space (aortic area) and may radiate to the carotids. whereas the AS associated with congenitally bicuspid aortic valves tends to present by the 6th decade.ucla. Aortic valve infective endocarditis tends to cause aortic regurgitation.Rheumatic aortic heart disease usually produces combined AS and aortic regurgitation. showing: .html Hepatic angiosarcoma =exposure to carcinogens such as arsenic. Marfan and Ehlers-Danlos syndromes are examples of connective tissue disorders promoting MVP. and polyvinyl chloride.htm Aortic stenosis Severe aortic stenosis = exertional syncope. Laboratory findings =increased levels of direct bilirubin. http://www.. Liver biopsy is usually diagnostic.Senile calcific aortic valve degeneration usually becomes clinically apparent in the 7th decade of life. -MCC= Senile calcific aortic valve degeneration ..wilkes. Tumor cells express CD 31. angina and dyspnea (SAD). impairing proper coaptation of the valve margins during systole. . and gamma-glutamyl transferase.jpg http://www. Affected children will have the characteristic cholestatic picture of acholic (light) stools and dark urine.mitral incompetence = due to elongation and redundancy of the valve leaflets and possibly also the chordae tendineae. =cells that express CD 31. Thus.. alkaline phosphatase. The chordae tendineae may have an attenuated collagenous structure and may be elongated. On physical examination there is a firm.blaufuss. the patient most likely has mitral valve prolapse (MVP) at low LV volumes but fewer prolapses as LV EDV is increased.edu/Systolic.org/tutorial/index2. By the 3rd week of life there is total obstruction. In AS.ral%20valve%20prolapse. an endothelial cell marker.med. thorotrast.net/images/cir. Under these circumstances an increase in left ventricular end diastolic volume (EDV) could facilitate proper closure of the otherwise oversized mitral valve leaflets. which is PECAM (platelet endothelial cell adhesion molecule) Extrahepatic biliary atresia = a congenital obstruction of extrahepatic bile ducts. -MVP is thought to be caused by subtle defects in connective tissue proteins that predispose connective tissues rich in microfibrils and elastin (such as cardiac valves) to damage by chronic hemodynamic stress. = A mid-systolic click followed by a systolic murmur http://www.

jpg Gilbert syndrome =famlial disorder of bilirubin glucuronidation. Portal tract edema and fibrosis 3. Chronic lymphocytic thyroiditis=Hashimoto’s thyroiditis =Diffuse mononuclear infiltration with formation of germinal centers is a very characteristic feature . An antithyroid peroxidase antibody titer is not elevated in these patients. bile stasis will cause development of biliary cirrhosis by 6 months of life. The thyrotoxic phase is followed by a hypothyroid phase for few months.. and multinucleated giant cells surround the fragmented colloid. possibly viral. and multinucleated giant cells. Marked intrahepatic bile ductule proliferation 2. These patients do not develop liver disease.medscape.. Most patients respond to non-steroidal anti. Reduced production of UDPglucuronyl transferases causes a mild unconjugated hyperbilirubinemia during times of stress (fasting. Most patients eventually recover without any residual thyroid dysfunction. -Patients with Hashimoto’s thyroiditis present with thyroid enlargement .edu/WebPath/jpeg4/LIVER049. Subacute granulomatous thyroiditis = de Quervain’s thyroiditis = granulomatous thyroiditis. α1-antitrypsin deficiency = oval-to-round intracytoplasmic hepatocyte inclusions that appear eosinophilic on H&E stain and are strongly PAS positive. subacute thyroiditis does not cause excessive production of thyroid hormone which is why iodine uptake is decreased. possibly caused by a viral infection. Parenchymal cholestasis If biliary drainage is not restored surgically. -Thyrotoxicosis in subacute thyroiditis= by release of stored thyroid hormones secondary to thyroid inflammation. increased ESR. The thyroid follicles become disrupted.jpg http://img. The patient has had a recent illness. and also has various features of thyro toxicosis tenderness over the thyroid gland. illness). and a markedly reduced radioactive iodine uptake.com/pi/emed/ck.med.inflammatory drugs for thyroid pain and inflammation. -The involvement of thyroid gland in subacute thyroiditis can be patchy. http://library.The infiltrate consists of lymphocytes and plasma cells. Initial neutrophil infiltration predominance is followed by infiltration of lymphocytes. histiocytes.utah.ogy/336139-406335-9293.1.

type columnar cells .jpg http://www.(goiter) and/or hypothyroidism.epWatershedInfarct1_21. . resulting in weakening of the wall and predisposition to rupture. They are found in the arterioles that supply the basal ganglia.org/wp-content/uploads/2007/07/internal-wsi.Can be differentiated from other thyroid dysfunction by the following: a relatively normal erythrocyte sedimentation rate.edu/neurorad/webpage/cya. features of hypothyroidism. http://www. They are usually located in the cerebral hemispheres (lobar strokes) and involve smaller areas of brain parenchyma.edu/lm/ids. -is associated with advanced age and is not related to systemic amyloidosis.jpg Charcot-Bouchard aneurysms = small in size (<1 mm in diameter) and occur in patients with longstanding hypertension. “Watershed infarcts” wedge-shaped areas of necrosis on the border of distribution between the anterior and medial cerebral arteries are common sequelae. and high titers of antithyroid peroxidase autoantibody.med.ncvc.can rupture and cause intracerebral hemorrhage. Unlike cerebral hemorrhages caused by hypertension amyloid-associated strokes are less severe.uc.jpg Barrett esophagus =metaplasia = replacement of squamous cells by intestinal. http://www. Conversely hypertensive hemorrhagic strokes are larger and tend to involve the basal ganglia. and deep white matter. -Recurrent hemorrhagic stroke is the most common presentation of cerebral amyloid angiopathy.nl/en/484b8328cb6b2#p484bc1fd1c74d http://www. internal capsule. Usually. a nontender thyroid gland with a rubbery texture.. the presentation of Hashimoto’s thyroiditis is chronic.NAME=S2004081257570005.jpg http://missinglink.html Hypoxic encephalopathy = from global interruption of the cerebral blood supply.radpod.jp/cgi-bin/.. http://medirec. with symptoms gradually worsening over several weeks or months. Cerebral amyloid angiopathy = β-amyloid is deposited into the arterial wall.ucsf.go.. .ca/pathol/cases/Neuro/neuro53.uwo..radiologyassistant.

kmu. Most of the transmitted cases are iatrogenic. http://203.131.gif Old cerebral infarct = liquefactive necrosis .class.troke/mca-o-infarct03a..130/neurosurger.jpg Caseous necrosis =Granulomatous reactions. This predilection for liquefactive necrosis is thought to be associated with large amounts of lipids and lysosomal enzymes in the nervous cells.tw/ch14/Slide114.209.jhu.edu.Interruption of blood supply to an area of the brain (by thrombosis or embolism) induces irreversible ischemic changes in the neurons. Complete digestion of necrotic tissue with the formation of a cavity is known as liquefactive necrosis.utah. and astrocytes proliferate around the necrotic area with the formation of a scar (gliosis).htm Creutzfeldt-Jakob disease =a rare disorder that can be sporadic or infectious. http://pathology. Adenocarcinomas develop through the progression from intestinal metaplastic epithelium to dysplasia to malignancy. Phagocytic cells migrate into the area and remove the necrotic tissue leaving a cavity.edu/WebPath/jpeg1/LUNG031. -Non caseous granulomatous inflammation occurs in sarcoidosis. Release of lysosomal enzymes from these ischemic neurons results in degradation of the tissue in the ischemic region . http://library.med. -CJD is included in a group of rare prion diseases. seen in patients that received contaminated corneal transplants.edu/beWeb/images/beprog.= believed to be a compensatory reaction as intestinal epithelium is resistant to acid. Mycobacterial infections -cheesy appearance and is surrounded by histiocytes and multinucleated giant cells. implantable electrodes or preparation of growth hormone.. (Chronic gastroesophageal reflux disease) =is a pre-malignant condition that increases the risk of adenocarcinoma of the esophagus by 30-40 times. = relative preservation of the architecture of the necrotic tissue.jpg Coagulative necrosis = most commonly seen type of necrosis. http://pathology2. Liquefactive necrosis is characteristic for hypoxic injury to the CNS. Kuru (a type of transmissible spongiform encephalopathy in cannibals of New Guinea that eat infected human brain) and fatal familial insomnia are the other examples of prion disorders that .

spiculated.htm Gallstones = aggregation of bile constituents and are categorized as cholesterol stones.com/image. sickle cell anemia. However they are rapidly progressive after the onset of clinical symptoms. Grossly. As the disease progresses. Vacuoles form in the cytoplasm of the neutrophils and neurons. Elevated levels of circulating unconjugated bilirubin are primarily associated with chronic intravascular hemolysis (eg. with an increased incidence in women and the elderly.. This protein is normally present in host neurons.gov/ncidod/eid/vol6no4/bonthius1G. Characteristic morphologic changes in brain are described as spongiform encephalopathy.edu/mhunt/pml2.msu. or mixed stones. =linked to an abnormal measles virus that persists in the CNS of these patients for years after recovery from measles infection. Patches of demyelination due to the preferential infection of oligodendrocytes is the primary pathologic effect.affect humans. These diseases have long incubation periods.. Because these stones contain high amounts of calcium carbonates and phosphates. the vacuolated areas transform into cysts. http://pathmicro. Microscopic examination shows myelin degeneration and viral inclusions.jpg Subacute sclerosing panencephalitis = progressive dementia. A change in its secondary structure renders it resistant to enzymatic digestion by proteases and leads to its accumulation. All prion diseases have a number of common features: 1. http://graphics8. =caused by JC polyoma virus. and hereditary spherocytosis). There is no treatment for prion diseases. 3.edu/WebGraphics/Pathgraph/31957.sc. black pigment stones are usually present in significant numbers and are small. spasticity and seizures. -Pigment stones are most common in rural Asian populations (accounting for only 10-25% of gallstones in the United States).8/01/health/adam/17146. Black pigment stones form within the gallbladder when increased unconjugated bilirubin precipitates in bile as calcium bilirubinate. No inflammatory changes are present. 4. pigment stones.jpg Progressive multifocal leukoencephalopathy = usually seen in immunocompromised (HIVI lymphoma or leukemia) patients. β-thalassemia.med. . and crumbly. 5O-75% of them are radioopaque and will appear on x-ray. These conditions are invariably fatal. http://www. They are associated with an abnormal prion protein (PrP).nytimes.cdc.jpg http://kobiljak. 2.

jpg Normal pressure hydrocephalus = decreased absorption of CSF leads to increased CSF volume.thebarrow..com/k/-/-/qjyFwIjC/PyLeBQ/pigment%20stone.LU/xdFxVJWAWwI/s320/04.jpg Micturition reflex is regulated by the following centers: 1.http://1. The patient has no sensation of bladder fullness and no control over bladder function. . -On light microscopy.. then dementia. Myotonic dystrophy =autosomal-dominant disorder =caused by an increased number of trinucleotide repeats on myotonia-protein kinase gene. The bladder fills with urine and empties reflexively when full. -Later in the disease process..blogspot.ts/webcontent/bqjpg141. lack of inhibition from the cerebral cortex leads to frequent and uncontrolled micturition. 3. It coordinates relaxation of external urethral sphincter with bladder contraction during voiding.google. Unlike Duchenne muscular dystrophy. =triad of ataxic gain and urinary incontinence. causing increasingly severe disease in each generation (anticipation). Sustained muscle contraction (myotonia). -Myotonic muscular dystrophy is the second most common inherited muscle disorder (Duchenne muscle dystrophy is the most common). -Age of presentation varies from early childhood to late adulthood. Pontine micturition center— located in the pontine reticular formation. 2. Cataracts are seen in almost all patients. This traction disrupts the periventricular pathways that transmit impulses from the cortex to the sacral micturition center. http://www.org/stellent/. along with weakness and atrophy. which is accommodated by ventricular enlargement. Frontal balding and gonadal atrophy are other common features. Cerebral cortex — inhibits sacral micturition center. is common.The number of repeats increases with subsequent generation.bp. Parasympathetic fibers travel from S2-S4 ventral white matter within pelvic nerves and stimulate cholinergic receptors in the bladder wall. necrosis of muscle fibers and fibrofatty replacement are not common in myotonic dystrophy. Voluntary relaxation of the urethral sphincter remains intact. Expanded ventriculi place traction on cortical efferent and afferent fibers (corona radiata). atrophy of muscle fibers is prominent.com/_0yn9eo5n. -DM1=DMPK (Dystrophia myotonica protein kinase) gene on chromosome 19 -DM2=Znf9 (Zinc finger 9) gene on chromosome 3 . or urge incontinence. These symptoms are explained by distortion of periventricular white matter. Sacral micturition center— located in S2-S4 level and responsible for bladder contraction.JPG http://knol..

Somatotroph adenomas= increase growth hormone production= acromegaly in . -Pituitary tumors typically arise from one of the five major cell types of the anterior pituitary gland. Diminished urinary excretion of radiolabeled vitamin B12 is a sign of impaired intestinal absorption. Pituitary tumors can grow beyond the limits of the sella turcica. Pituitary tumors . Vitamin B12 deficiency = may occur due to low dietary intake of this vitamin. bacterial overgrowth. If the pituitary tumor grows superiorly it erodes the optic chiasm. weak muscle tone (hypotonia). The urinary excretion of radioactive B12 is then measured. it grows into the sphenoid sinus.Compression of the optic chiasm by suprasellar extension of pituitary tumors causes the characteristic bitemporal hemianopsia. breathing problems. Prolactin also suppresses gonadotrophinreleasing hormone (GnRH) production from the hypothalamus which causes decreased libido. Administration of vitamin B12 without intrinsic factor will show low urinary radioactive B12 excretion on the Schilling test. and infertility. or malabsorption. Normal excretion after the addition of intrinsic factor is diagnostic of pernicious anemia.Pernicious anemia is associated with atrophic gastritis and the presence of antibodies against gastric parietal cells and intrinsic factor. and B12 deficiency in this setting is most likely due to poor intake of Vitamin B12 in the diet . A growing pituitary tumor can also compress normal pituitary cells causing hypopituitarism. Prolactinomas stimulate inappropriate milk production in non postpartum females (galactorrhea). inferiorly. Normal urinary excretion of radiolabeled vitamin B12 suggests normal absorption. Headache is likely caused by an increase in intracranial pressure. . . The patient is first given a dose of radiolabeled oral vitamin B12 and an intramuscular injection of unlabeled Vitamin B12. Approximately 60% of pituitary tumors are prolactinsecreting adenomas. The signs and symptoms include generalized weakness. amenorrhea. To differentiate between pernicious anemia and malabsorption. caused by mass effect of the tumor. club foot. laterally it invades the cavernous sinus. causing compression and erosion of surrounding structures. Low excretion of B12 after administration of intrinsic factor rules out pernicious anemia and suggests a malabsorption syndrome such as pancreatic insufficiency. developmental delays. The primary physiologic action of prolactin is preparation of the breasts for milk production/lactation in the postpartum period.-congenital myotonic dystrophy= noted at birth. the presence of antibodies against intrinsic factor (pernicious anemia). or short gut syndrome. the next dose of radiolabeled B12 is given with intrinsic factor. Prolactin is a 199 amino acid peptide hormone secreted from lactotrophs of the pituitary gland. The Schilling test helps differentiate between these causes. and intellectual disability.

. . In addition. which may represent fibrosis .Gonadotroph adenomas usually do not produce intact follicle-stimulating hormone (ESH) or luteinizing hormone (LH). iron (in hemochromatosis).. heterozygotes enjoy relative protection from Plasmodium falciparum (malaria). they are generally protected from sickle cell crises aplastic crises and sequestration crises by the presence of> 50% normal hemoglobin (Hb A).il/hcm/sarcomere. Approximately 5O% of cases HCM are familial. Hypertrophic cardiomyopathy (HCM) = myocyte hypertrophy (relatively large transverse diameter of myocytes) and haphazardly arranged myocytes and myocyte bundles. The exact mechanism is not known: proposed mechanisms include increased sickling of .adults and gigantism in children. the interstitial spaces are particularly prominent. or doxorubicin may cause dilated cardiomyopathy which may occasionally progress to sudden cardiac death.. A high incidence of UTI and splenic infarction at high altitude has also been reported.images/medium/coverfig.or. -although homozygotes for the sickle cell trait are often very ill.Corticotroph adenomas produce adrenocortical-stimulating hormone (ACTH) which causes Cushing’s disease.org. such as components of the thick or thin filaments (most commonly beta-myosin heavy chain). inheritance is autosomal dominant with variable expression. -Patients with sickle cell trait are usually asymptomatic. These tumors typically over produce alpha subunits of these glycoprotein hormones and present with mass effects and hypogonadism. http://eurheartj. . The histologic changes seen in DCM are non-specific. Most nonsecretory adenomas arise from the gonadotrophs. cocaine. Sickle cell trait (Hb AS) = hemoglobin composed of 35 to 40% hemoglobin S (Hb S). patients with homozygous SS have severe disease with >80 % Hb S. These tumors tend to grow slowly. Thyrotroph adenomas are very uncommon.oxfordjournals. potentially including interstitial fibrosis and variable myocyte hypertrophy or thinning. -In contrast. although they may develop hematuria and a limited ability to concentrate urine.Thyrotroph adenomas produce thyroid-stimulating hormone (TSH) leading to thyrotoxicosis.jpg Dilated cardiomyopathy (DCM) -Toxic agents like alcohol.gif http://gilead.In most cases HCM is the result of mutations in the genes coding for cardiac sarcomere proteins.

have shown increased activity of enzyme cyclooxygenase-2 (COX-2) in some colon adenocarcinomas and in inherited polyposes syndromes.rsna. Recent studies.parasitized sickle-cell trait red blood cells and accelerated removal of these cells by the splenic monocyte macrophage system. First.jpg http://radiology.gov/health/fhs/sicklecell/images/inheritance. The risk of hepatocellular carcinoma. red cell indices and red cell morphology are normal. patients with sickle cell trait are asymptomatic. http://pathmicro. it causes chronic liver cell injury and regenerative hyperplasia. Generally. full-blown sickle cell anemia).org/wikipe. http://www. Patients taking NSAIDs regularly have been shown to have a lower incidence of adenomas compared to the general population. irreversibly sickled cells are not seen.wikimedia. However.e.mons/4/44/Colon_cancer.med. increasing the number of hepatocytes susceptible to genetic mutations. HBx protein also binds to p53 apparently impeding its growth-suppressing activities. Infectivity ceases and liver damage tapers off when the host’s antiviral antibodies appear and viral replication stops. They tend to develop in people older than 50 years old as a result of APC gene mutation. -The best prevention of malignant transformation of adenomatous polyps = regular screening and timely excision of adenomas. HBV DNA is incorporated into the host genome of those hepatocytes that survived the immune response. p53 and DCC. Stepwise progression to adenocarcinoma may follow. This integration of HBV DNA into the host genome is thought to have multiple implications.gif . remains elevated because of the HBV DNA that has been integrated into the host genome. which represents intracellular dehydration. perhaps because of the COX-2 inhibitory effect of NSAIDs. a substance that disrupts growth control of infected cells by activating multiple growth-promoting genes. Furthermore. however. Increased MCHC. the reticulate count is not elevated. the sickling test will be positive (RBCs will sickle when sodium metabisulfite is added).org/cgi/content-nw/full/244/2/471/F2C Hepatocellular carcinoma .edu/virol/hep-bstruct. except perhaps for hematuria.nj.In the integrative phase of hepatitis B infection.. such as R-ras.. This accumulation of gene mutations is called the “adenoma-to-carcinoma sequence”.gif Adenomatous polyps = dysplastic mucosa and are considered premalignant. however. Second HBV encodes for HBx protein.sc. http://upload. is seen only with homozygous SS (i. -Peripheral smears are usually normal in sickle cell trait patients. It is unlikely that patients will develop painful crises as they are protected by the 60% Hb A (normal hemoglobin). This progression includes a series of other gene mutations.

which are cell-surface proteins that help inactivate complement. The OPI anchor is necessary for the attachment of CD55 and CD59. http://www. and rye. flatulence. This misnomer originated because the primary clinical manifestation of PNH is dark-colored urine (hemoglobinuria from hemolysis) in the morning. -Anti-gliadin.pathguy. where the concentration of gluten is the highest.nih.alxn.com/images/diag_comp_activation. and anti-endomysial antibodies are found in patients with celiac sprue. -Common symptoms = those of malabsorption: diarrhea.free diet if celiac disease is present. Histologic changes and clinical symptoms will disappear after a period of gluten. http://www. including BuddChiari syndrome. as well. It was once believed that the complement that hemolyses red blood cell membranes was activated by sleepassociated acidosis. and symptoms of nutrient deficiencies. Know that the deficiency of CD 55 and CD 59 proteins is diagnostic of PNH and that this deficiency disallows the inactivation of complement.pnhsource.Ironically PNH is neither paroxysmal. Since PNH is a stem cell disorder. and chronic inflammation of the lamina propria.ncbi. therefore commonly develop thrombosis: recurrent venous thrombosis is common.eu/styles/images/sidebar.jpg Gallbladder hypomotility . a protein found in wheat.org/afp/20071215/afp20071215p1795-u3.aafp.nlm.gif http://www. .http://www.eu.gov/ICTVdb/WIntkey/Images/em_hepad.jpg Celiac sprue (gluten-sensitive enteropathy) =caused by hypersensitivity to gluten.com/lectures/hepatocellular_carcinoma. Without CD59 and CD55. nor nocturnal. atrophy of villi. barley. it is often associated with pancytopenia. anti-reticulin. Patients with PNH. -diagnosed by small bowel biopsy = flattening of the mucosa. complement stays activated and hemolysis of the cell results .PNH is a condition in which there is mutation of the PIG-A gene that codes for the glycosylphosphatidylinositols (OPI) anchor. These changes are most commonly seen in the duodenum and proximal jejunum.gif http://www. and thrombosis the commonest cause of death in these patients. steatorrhea.jpg Paroxysmal nocturnal hemoglobinuria (PNH) . We now know that hemolysis only appears to be nocturnal/paroxysmal because urine collects and concentrates overnight causing a dramatic color change in the morning—hemolysis in PNH has been demonstrated to occur all throughout the day.

com/a.jpg http://www. only the mucosa and submucosa are inflamed.JPG Crohn’s disease =abdominal pain and diarrhea in a 20-30 year old patient.” -Clinically=abdominal pain and bloody diarrhea.diagnosticimaging. -One of the more frequent consequences of gallbladder hypomotility is the formation of biliary sludge. Ulcers can penetrate the entire thickness of the affected intestinal wall. ascending colon and most of the transverse colon are supplied by branches of the superior mesenteric artery (SMA). The cecum.edu/lectures/gi/s-int-b/16. calcium bilirubinate. and high spinal cord injuries. and mucus and is a known precursor to stone formation.htm Ischemic colitis = Low perfusion to the bowel can cause ischemia and necrosis of the intestinal wall.proctosite. prolonged use of total parenteral nutrition or octreotide. The distal sigmoid colon lies between the areas supplied by IMA and hypogastric arteries.. Weight loss.onteudo/Crohn_surgical..jpg http://www.id=1384330&t=1236110195004 http://www.. and aphthous ulcers of the oral mucosa are also common. . Biliary sludge typically contains cholesterol monohydrate crystals. in ulcerative colitis..Toxic megacolon is a potentially life-threatening complication of both Crohn’s disease and ulcerative colitis.g%20Sign/stringcorrect.htm http://www.Crohn’s disease causes transmural inflammation of any area of the gastrointestinal tract -Transmural inflammation explains the two most common complications of Crohn’s disease: strictures.learningradiology.com/images/biliary%20tract. however the splenic flexure and distal sigmoid colon are the most susceptible. http://www. rapid weight loss.com/i. hepatic flexure. It occurs due to neuromuscular degeneration of the intestinal wall and its rapid dilatation. and fistulas.Risk factors= pregnancy... fatigability.medgadget. so strictures and fistulas are not common. Hence ischemia affects these areas first and is called “watershed infarction. -The splenic flexure is a “border” area between the distribution of the superior mesenteric (SMA) and inferior mesenteric (IMA) arteries. Inflammation and necrosis of the intestinal wall causes ulcer formation.com/newslett. leading to the formation of a fistula. Complications such as acute cholecystitis occur in up to 2O% of patients with biliary sludge. Mesenteric . Any area of the bowel maybe affected. Remember.pitt. .com/archives/img/crohn. low grade fever. which results from bile precipitation.. Chronic inflammation causes edema and fibrosis leading to narrowing of the intestinal lumen (strictures). http://gallstoneflush. Toxic megacolon is associated with bowel perforation.pathology. Abdominal pain and distention are common symptoms.

edu/bio203/s20.gastro. However. and there is little/no suppression of cortisol release on the overnight dexamethasone suppression test. serum cortisol levels drop significantly in the evening hours as a function of normal circadian rhythm. An alkaline (pink) color persisting more than five minutes is considered a positive test for H. Although the pink color typically develops within 30 minutes when H. pylori. then the cause of the Cushing syndrome is likely ectopic ACTH production. the Cushing syndrome likely stems from some primary adrenal process. pylori is present.gif http://www.In normal individuals. Helicobacter pylori infection -the rapid urease test is able to make a relatively quick diagnosis from tissue samples. the sample should be observed for 24 hours before being considered negative..m. . alone is not a very sensitive or specific screening test for Cushing syndrome. and there is no decrease in evening cortisol levels. hence the use of a urea solution in this test. however. If the a.or.loads/2008/06/h-pylori. causing a pH increase and resultant color change of the phenol red pH indicator.ischemia can occur in any of these areas although ischemia there occurs less frequently than in “watershed areas. In normal individuals. In endogenous Cushing syndrome.clinicalcorrelations. to a level <5O% of baseline) in the setting of elevated baseline ACTH levels then the cause of the Cushing syndrome is likely a pituitary adenoma.. pylori produces large amounts of extracellular urease enzyme. cortisol level is moderately suppressed (i.e.m. Thus. this normal circadian rhythm is lost. measuring cortisol at 8 a.jpg Cushing syndrome The overnight dexamethasone suppression test is commonly used in the workup of Cushing syndrome. http://bioweb..uwlax. Urease converts urea to carbon dioxide and ammonia.. patients with endogenous Cushing syndrome do not show complete suppression of cortisol and ACTH production. If there is low baseline ACTH and little/no cortisol suppression with the overnight dexamethasone test.pylori%20scott%20smith. If the baseline ACTH is high. .com/Gastro/images/ischemic_colitis1_img.” http://www.a sample from the gastric mucosa is added to a solution containing a pH indicator and urea -H.jpg Cystinuria . administration of this potent glucocorticoid causes suppression of ACTH and cortisol production.

scalp and the dorsa of the arms and hands. The most commonly affected areas are the face. causing a purple discoloration in 2-10 minutes. Actinic keratosis is regarded as either a premalignant condition or a carcinoma in situ. Keratinocytes display various degrees of atypia.jpg Pityriasis rosea = pink or brown scaly plaque with central clearing and a collarette of scale . The cyanide added to the urine converts cystine to cysteine.= from a defect in the renal proximal tubules. Mitoses and an inflammatory infiltrate are present. Hyperkeratosis in such lesions may become prominent and turn into “cutaneous horns”.scopnetwork. and hyperkeratosis (thickening of stratum corneum). -The detection of cystine in urine is important not only for establishing a diagnosis. as these are relatively soluble..com/imag.GIF http://www. Increased excretion of these amino acids does not result in stone formation.visualdxhealth. beginning at a young age. -On light microscopy. http://www. -Patients with cystinuria experience recurrent kidney stones. http://www. -The sodium cyanide-nitroprusside test detects sulfhydryl groups. but also for monitoring treatment effects and for predicting the rate of stone formation.thiola. ears.org/images/actinic_keratosis_th. affected areas show acanthosis (thickening of the epidermis) parakeratosis (retention of nuclei in the stratum corneum).com/gfx/stones/MS/27_cystine_crystals. which causes decreased reabsorption of the amino acid cystine. and is a rapid qualitative determinant of the presence of urine cystine. ornithine. The increased cystine excretion can precipitate stone formation. -Hexagonal cystine crystals on urinalysis are pathognomonic. but less than 1% of AKs will evolve into frank squamous cell carcinoma.A “sandpaper-like” texture on palpation of the affected areas= typical . Usually their size does not exceed 10 mm in diameter. These crystals are relatively radiopaque due to the density of sulfur-containing compounds. upper chest) can be involved. The cystine transporter also contributes to the reabsorption of other dibasic amino acids (arginine. .jpg Actinic keratoses (AK) = erythematous papules with a central scale due to hyperkeratosis. however. -Treatment of cystinuria = hydration and alkalinization of urine. They form in acidic urine (pH < 6). dyskeratosis (abnormal keratinization). and lysine).. back.The lesions are small and flat at first but may enlarge and become elevated.larKeratosis_51744_med. but any other chronically sun-exposed site (legs. The nitroprusside then binds cysteine. -Actinic keratoses develop in genetically predisposed individuals 40-60 years of age under the influence of excessive sun exposure.

its deficiency leads to failure to lactate.usuhs. which has important symptomatic and diagnostic significance. It is a medical emergency. http://rad. Patients suffering from Sheehan syndrome also commonly have hypothyroidism and hypercortisolism. and altered sensorium.com/imag.mil/derm/lecture_notes/Images/sebK2. causing it to both enlarge and become more vascular. Autoimmune hypophysitis = sometimes seen during late pregnancy or the early postpartum period. If significant hypotension occurs while the pituitary is still enlarged (the most common cause is postpartum hemorrhage) ischemic necrosis of the pituitary occurs.colored lesions with velvety or “greasy” surface.tyriasisRosea_42641_lg.. http://www. A high index of suspicion is required. A deficiency of multiple pituitary hormones (panhypopituitarism) follows this ischemia. Both the anterior and posterior pituitary become inflamed.(herald patch) on the trunk neck or extremities. http://radiographics. As prolactin is responsible for milk secretion from the breast. severe headache. ophthalmoplegia.JPG Sheehan’s syndrome High estrogen levels during pregnancy stimulate growth of the pituitary. Pituitary apoplexy = hemorrhage into a preexisting pituitary adenoma.rsna.jpg Seborrheic keratoses = in elderly individuals and presents with “stuck-on” deeply pigmented or flesh. visual field defects and cortisol deficiency. Prolactin deficiency is one sequelae of the necrosis. The patient usually presents with acute. It is followed by development of maculopapular rash classically in a “Christmas tree” pattern along the skin tension lines.org/cgi/content-nw/full/27/1/95/F8 Abdominal aortic aneurysm (AAA) .. For unknown reasons cortisol deficiency develops more commonly than other hormonal deficiencies. The presentation is acute with headaches.visualdxhealth. Hypophysitis differs from Sheehan syndrome in the presence of visual field deficits and the acuity of presentation. The patients require urgent neurosurgical consultation and stress doses of glucocorticoids.

plasma cells.. Age: The highest incidence is in the 65-75 age groups. Adenocarcinoma at the head of the pancreas =The palpable but non-tender gallbladder (Courvoisier sign). and pale stools)= common bile duct compression signs . macrophages.vasa vasorum endarteritis in the thoracic aorta—is thought to be the mechanism by which syphilis produces thoracic aortic aneurysms. Chronic pancreatitis: The risk of pancreatic cancer increases with the duration of the disease. These complexes then insudate into the intima through an injured leaky endothelium. 2. A palpable abdominal mass need not be present.jpg Vasa vasorum obliteration . Atherosclerotic atheromas can sufficiently progress enough to weaken the underlying media of the aortic wall. syphilis rarely progresses to this stage in the United States. Intimal (fatty) streaks. Genetics: Hereditary pancreatitis. Aortic dissections can rupture and are therefore considered medical emergencies. Diabetes mellitus: The risk of pancreatic cancer increases with the duration of diabetes. It doubles the risk. weight loss. predominantly LDL.An intimal tear is thought to be the process that initiates formation of a dissecting aortic aneurysm. are composed of intimal lipid-filled foam cells. dense periaortic fibrosis with an inflammatory reaction— characterizes an unusual variant of AAA.com/MediaServer/MediaItems/MediaItem_237. . An aortic dissection generally results in severe chest and/or back pain. and often giant cells. http://www. The inflammatory reaction is known to be rich in lymphocytes. Because pancreatic cancer is a malignancy that manifests late most tumors are unresectable at the time of diagnosis. 4. which may extend as the dissection progresses distally. The risk is highest after 20 years of chronic pancreatitis.The major cause of AAA is atherosclerosis. the earliest lesion of atherosclerosis. dark urine. which are derived from macrophages and smooth muscle cells that have engulfed lipoproteins. -The following are risk factors for this malignancy: 1. Smoking is the most important environmental risk factor for pancreatic cancer.Cancers of the body and tail of the pancreas usually do not become symptomatic until they invade the splanchnic plexus and cause midepigastric abdominal pain. although the cause of such inflammatory AAAs is uncertain. Currently. -Perivascular fibrosis—more specifically. since the dissecting intramural hematoma is often contained within an intact adventitial layer of the aorta. MEN syndromes. and obstructive jaundice (associated with pruritus. the major cause of AAA is atherosclerosis. Nonetheless. 5. HNPCC (hereditary nonpolyposis colon cancer) and familial adenomatous polyposis syndromes can all be . 3.cvtsa.

.luc. tuberculosis. tuberculosis allows for intracellular bacterial proliferation.homestead. tuberculosis organisms spread widely through out the body in small. It is not a risk factor for pancreatic cancer. In the lung. calcineurin inhibitors (eg. resulting in caseating necrosis where the organisms are present. http://granuloma. the lumbar spine (Pott disease).edu/LUMEN/m. Patients who take chronic corticosteroids.Secondary M. while smaller droplets are carried to the alveoli and can establish infection. tuberculosis enters the lymphatic circulation. Langhans giant cells (with a horseshoe-shaped arrangement of nuclei). M. The caseating granulomas consist of T lymphocytes. or who are HIV positive are at increased risk for reactivation tuberculosis. and the sulfatide virulence factor expressed by M..meddean. Classic locations of extrapulmonary tuberculosis include the basal meninges (tuberculous meningitis).a lower lobe lung lesion (Ghon focus) accompanied by ipsilateral hilar adenopathy is described as a Ghon complex. scattered. dormant M. -M. organism-laden droplets into the lower lung fields. it can seed organs throughout the body. able to later cause secondary tuberculosis during periods of immunosuppression. and serous membranes such as the pericardium and pleura. In this condition the M. Most droplets of infectious size carry approximately five organisms. epithelioid activated macrophages. infliximab or etanercept). -Alcohol consumption increases the risk of the malignant tumors of the head.com/files/tb_gross_lung26. These droplets are of varying sizes: larger droplets make contact with the tracheal and bronchial epithelium and are typically removed by mucociliary motion.Hematogenous dissemination of M. While nestled within these macrophages. http://www. tuberculosis is TH1 cell-mediated. Pulmonary tuberculosis infection is first established after the gravi-assisted entry of small.chanisms/pancreas_mass. esophagus and liver.jpg . the psoas muscle (psoas abscess). The most extreme case of extra pulmonary tuberculosis is miliary tuberculosis. The immune reaction to M. Although eliminated in 95% of cases. The Ghon complex occurs during initial infection with M. tuberculosis infection occurs when patients who have been primarily infected incompletely eliminate the M. . The mycobacteria are phagocytosed by alveolar macrophages. tuberculosis bacilli are still present within the larger granulomas of many patients. tuberculosis is associated with extrapulmonary tuberculosis. anti-TNF agents (eg..associated with an increased risk of pancreatic cancer. seed-like foci of infection. tuberculosis is passed from person to person through the transmission of aerosolized airway secretions. neck. cyclosporine). The organisms that remain then mobilize from these foci during periods of immunosuppression to cause active disease.htm TB . Eventually. The net result of this response is a “walling off” of the organisms within a fibrous capsule. tuberculosis bacilli within Ghon foci or extrapulmonary sites. and proliferating fibroblasts that actively synthesize collagen. the typical pathologic finding associated with secondary infection is an apical cavitary lesion.

) However. the (15.org/governme.. It presents with lymphadenopathy.In acute promyelocytic leukemia (APL)I type M3 of acute myelogenous leukemia in the FAB classification system..ewashtenaw.healthsystem.wadsworth.com/2008/10/atra-syndrome.homestead.jpg http://tbfreeindia.blogspot. APL results from that (15.org/chemheme/heme/microscope/cll. Neoplastic cells resemble mature B-lymphocytes.. 17) mutation produces an abnormal retinoic acid receptor that is unable to signal for the differentiation of myeloid precursors.gif Acute myelogenous leukemia .com/files/tb_gross_lung50.com/xar. http://www.17) mutation where by the gene for the retinoic acid receptor alpha (RARa) is transferred from chromosome l7 to chromosome 15 where it fuses with the promyelocytic leukemia (PML) gene.wadsworth.html Chronic lymphocytic leukemia = is frequently seen in elderly patients.jpg Acute lymphocytic leukemia = predominantly affects children.. (The receptor interacts with retinoic acid to effect transcription of genes required for maturation. Normally the retinoic acid receptor plays a role in the proper differentiation of myeloid precursors.virginia.c_health/phcontent/xray_tb http://brighamrad.htm http://renalfellow. and has an indolent course.http://granuloma. white blood cells produce an aberrant protein with an affinity for retinoic acid. resulting in the formation of new gene called PML/RARα. Blast cells positive for the CD1O antigen (CALLA) suggest a good prognosis.htm . -Treatment with all-trans-retinoic acid (ATRA) stimulates differentiation of myeloblasts into mature granulocytes and induces remission in about 90% of patients with acute promyelocytic leukemia.jpg http://www.harvard. hepatosplenomegaly and anemia.html http://www.ukemia-m2-100x-website. http://www.e.edu/fireCases/images/41/cxr. http://rebeccanelson.com/leukemia/all.org/chemheme/heme/microscope/auerrod.

and sore throat even though they don’t feel heartburn. . http://www.myeloid precursors in different stages of differentiation proliferate.. erosions or ulcerations may be seen. Asian and Mediterranean descent. antimalarials. and is more common in patients of African. This disease is caused by at (9. and bisphosphates Glucose-6-phosphate dehydrogenase (G6PD) deficiency =X-linked disorder that affects mostly males. 22) translocation that forms the bcr-abl fusion gene which codes for an abnormal tyrosine kinase. -G6PD is an enzyme of the pentose phosphate pathway that in erythrocytes is essential for maintaining adequate concentrations of NADPH. nocturnal cough.pathologystudent. hemoglobinemia and hemoglobinuria (dark-red urine). dapsone.jpg Gastrointestinal reflux disease (GERD) = heartburn and regurgitation.Chronic myeloid leukemia .com/wp. This increases the vulnerability of erythrocytes to oxidative stress and manifests with hemolysis induced by infection. leading to an inflammatory reaction and epithelial repair. elongation of lamina propria papillae. -Hemolytic episodes= malaise and pallor. Bactrim. mucosal erythema or edema in the distant esophagus is seen: in severe cases. Basal zone hyperplasia. and inflammatory cells (eosinophils. nitrofurantoin). Macroscopically. potassium chloride. The level of serum haptoglobin decreases and a reticulocytosis develops to compensate for the increased destruction of RBC. patients can have “silent GERD. Gastroesophageal junction incompetence is the primary pathophysiologic mechanism responsible for GERD. neutrophils and lymphocytes) are characteristic histologic findings Pill-induced esophagitis = commonly seen with tetracycline antibiotics. drugs (e. This incompetence is most commonly caused by transient lower esophageal sphincter relaxations and a hypotensive lower esophageal sphincter (LES). or other oxidants (e.However.” which means they may have symptoms like dysphagia.9/04/cml-blood-better7.g. indirect bilirubinemia (jaundice). Patients are generally asymptomatic between .g.. fava beans). Insufficient NADPH results in an inability to maintain glutathione in the reduced state. Acidic gastric contents reflux back into the esophagus and irritate the esophageal mucosa.

or protein 4. The patient also has a megaloblastic anemia which in alcoholics typically stems from folic acid deficiency. component of the virus.edu/Faculty/bcup.mc. Alcohol-associated hepatic steatosis is probably the cause of his hepatomegaly. http://pathology.. The missing antigen causes failure of the measles virus to be cleared by the immune system and allows its persistence in the CNS. In the CSF antibodies are found as oligoclonal bands of immunoglobulins. Affected children may have various neurological deficits and progressive dementia. and gliosis in many cerebral areas.edu/neuro.. Scientists hypothesize that subacute sclerosing encephalitis is caused by a certain type of measles virus that is missing an antigen (M protein).ecture2/sspeinclusions. enveloped RNA virus.edu/medicine/web/Smearreview/img024.png Hereditary spherocytosis = autosomal dominant defect in RBC structural proteins (spectrin.indwes.diseaseaday. conjunctivitis. ankyrin. cough coryza (runny nose).. primary measles pneumonia. Measles manifests with prodromal fever. which is a member of Paramyxoviridae family. . -Subacute sclerosing encephalitis is a rare complication of measles.. It occurs in children who appear to have recovered from measles infection several years earlier. but is fatal.jpg Chronic pancreatitis =recurrent abdominal pain...Complications include acute encephalitis. Note that there are no antibodies to M.com/wp-cont. Neurons and glial cells display viral nuclear inclusions.s/Blood/spherocytes_nw. http://www.1) characterized by increased erythrocyte osmotic fragility and MCHC (mean corpuscular hemoglobin concentration) increased above 36 g/dL.med. and secondary bacterial infections (pneumonia and acute otitis). hepatomegaly and pancreatic calcifications . The disease is slowly progressive.duke.jpg Measles virus = helical. and erythematous maculopapular rash. .the most common cause= ethanol abuse.unc. demyelination. -High titer of antibodies to the measles is found in the serum and CSF of these patients./g6pddeficiencyprocess. Most American children are vaccinated against measles.episodes. http://www. This retained virus causes inflammation.jpg http://www.

including subcutaneous nodules (erythema nodosum).. 3. Its incidence increases with age. erythematous plaques.org/content/24/1/e18/F1. Mutation of the K-ras protooncogene is thought to facilitate this step. The initial appearance of small adenomatous polyps is attributed to the mutation of the APC tumor suppressor gene./n8/fig_tab/3800613f1. -Liver biopsy shows changes in up to 75% of cases. Increase in the size of the polyps.. Sometimes called a “molecular policeman” p53 is an anti-oncogene. Certain diseases (such as inflammatory bowel disease) and genetic factors also play an important role in the development of this malignancy.medscape.com/sol/13889. This mutation is considered the last “hit” in the adenoma-to-carcinoma sequence. Scattered granulomas are . -Most cases of sporadic colon adenocarcinoma arise from preexisting adenomatous polyps.-The underlying biochemical feature of megaloblastosis is a defect in DNA synthesis.com/pi/emed/ck.nature.html http://www. and it affects males and females equally. It codes for protein p53. RNA and protein synthesis may continue relatively unaltered. 2..Sarcoidosis can cause arthralgias and skin changes occur in 30-50%. Malignant transformation of adenoma into carcinoma requires mutation of two genes: p53 and DCC. and its mutation leads to uncontrolled cell proliferation.gery/188616-190486-676.jpg Colon cancer = third most common malignancy in the United States (lung and breast cancers occur more often). Mutation of p53 allows cells with genomic errors to enter the cell cycle.large.jpg http://radiographics. The transformation of normal mucosal cells into malignant ones is caused by a series of gene mutations called the “adenoma-tocarcinoma sequence” which includes the following steps: 1.pathguy. leading to a state of unbalanced cytoplasmic growth with impaired cell division. A diet that is high in cholesterol and carbohydrates and low in fiber increases the risk. http://www. Folic acid is a single carbon donor required for the synthesis of purine and pyrimidine bases. APC is located on chromosome 5.. http://img. Progression from normal mucose to a small polyp.rsna. or macules that are slightly reddened and scaling. This mutation leads to the appearance a protein that stimulates unregulated cell growth.com/modpathol/jo.jpg Sarcoidosis = chest x-ray findings and elevated serum ACE level . which triggers apoptosis of cells with damaged DNA. A variety of skin lesions are possible.

scaling and thickening of the skin (erythroderma) may result . http://www. Some individuals also appear to develop lactase deficiency secondary to injury of the gastrointestinal mucosa.the most common liver pathology finding.gif http://www. This condition manifests with plaques that may be confused with eczema or psoriasis. which can progress to cor pulmonale. Generalized erythema.Distended macrophages in the intestinal lamina propria= Wipple disease. Follicular lymphoma = most common non-Hodgkin lymphoma in adults..jpg http://www. Proliferating CD4+ lymphocytes infiltrate the dermis and epidermis where they form Pautrier microabscesses. Liver granulomas affect the portal triads to a greater degree than the lobular parenchyma.yale. Native Americans. The congenital variant is a rare autosomal recessive condition caused by a gene near (but separate from) the lactase gene.coidosis/graphics/rad1. The acquired variant typically arises in certain races (eg.8/Lung_Review/Lung-53.edu/intmed/car. -Mycosis fungoides is a cutaneous T-cell lymphoma. It derives from follicular Bcells and has an indolent clinical course marked by remissions and recurrences. -Collections of neutrophils within the crypt lumina =ulcerative colitis..html Lactase deficiency =classified as congenital (rare) or acquired (common). It presents with a large lymph node or extranodal mass. -Light and electron microscopic examination of the bowel mucosa in lactasedeficient patients has never demonstrated an identifiable abnormality. DIFF: . African Americans) that cease producing lactase by midchildhood. .edu/classwar. -Diffuse large cell lymphoma is an aggressive non-Hodgkin lymphoma of B-cell origin.Burkitt lymphoma is associated with EBV infection and is an aggressive tumor (short doubling time) that is yew susceptible to chemotherapy. This condition most often presents with painless lymph node enlargement or abdominal discomfort from an abdominal mass. The Waldeyer ring (oropharyngeal lymphoid tissue) and GI tract are commonly involved.aafp.som. -Intestinal inflammation with scattered noncaseating granulomas= Crohn disease. -Massive infiltration of the intestinal lamina propria with atypical lymphocytes = gastrointestinal lymphomas. so normal intestinal mucosa would be the expected finding in this patient population.. DIFF: .med.The major cause of morbidity in sarcoidosis is pulmonary fibrosis..org/afp/20020415/1581_f5.tulane.

. Night blindness (nyctalopia) implies degeneration and/or functional impairment of the retinal rods. Diabetic retinopathy This patient also has dry skin.asp?case=389&n=3 http://courseweb. syphilis. and/or tachykinins by carcinoid tumors. nausea.. histamine prostaglandins.eatment/gep_4. and is thought to be due to production of serotonin. vomiting. -Although the most common cause of night blindness is hereditary retinitis pigmentosa. http://www. The degree of endocardial fibrosis seen in this syndrome correlates with plasma levels of serotonin and urinary excretion of the serotonin metabolite 5hydroxyindoleacetic acid. Pulmonic stenosis and restrictive cardiomyopathy may ultimately result from this condition. Carcinoid syndrome . Vitamin A deficiency 3.gif Night blindness This patient describes symptoms consistent with decreased visual acuity and tunnel vision in low ambient light.webpathology. It is of B-cell origin and presents with painless “waxing and waning” lymphadenopathy. kallikrein. abdominal cramping. bradykinin. Toxic retinopathy due to phenothiazines or chloroquine 2.. this patient has acquired nyctalopia. -This fibrosis is generally limited to the right heart because both serotonin and bradykinin in the blood are inactivated distally by pulmonary vascular endothelial monoamine oxidase.. or other infections 4.com/images/. Congenital rubella.icular%20lymphoma%20lp.uottawa. Tunnel vision predisposes to motor vehicle accidents.http://www. The cytogenetic change (14:18) is characteristic and results in overexpression of the bcl-2 oncogene. the differential diagnosis of which includes: 1..carcinoid heart disease= fibrous intimal thickening with endocardial plaques limited to the right heart . and diarrhea.com/image.edteched.0_image1.classically produces episodes of skin flushing.jpg So:Follicular lymphoma is the most common non-Hodgkin lymphoma in adults.sandostatin. which suggests vitamin A deficiency (from biliary obstruction leading to cholestasis and fat soluble vitamin malabsorption) Hemophilia A .

which usually affects the lower lung lobes most severely.ucsf. Panacinar emphysema is thought to be caused by excess neutrophil elastase activity inside alveoli. not hyperplasia or hypertrophy. -A1-antitrypsin is the major serum inhibitor of neutrophil elastase. a1-antitrypsin deficiency .= X-linked recessive disorder that develops due to mutations of the gene that codes for factor VIII. Destructive proteases released by both macrophages and neutrophils cause the acinar wall destruction in this type of emphysema. The predilection of this type of emphysema for upper lung segments may reflect the relatively low perfusion and therefore low presence of serum α1-antitrypsin. .edu/case25/image253.Factor VIII is synthesized by hepatocytes and stored in the endothelium of blood vessels. Desmopressin is a synthetic analog of vasopressin (ADH) and is also used for treatment of diabetes insipidus because it increases reabsorption of water in the collecting tubules. . DDAVP is used for the treatment of mild-to. typically measuring less than 5 cm in width.Deficiency of a1-antitrypsin can cause panacinar emphysema (a form of COPD). -Hemangiomas may occur singly or in multiples and are well-circumscribed masses of spongy consistency.html#answer2 http://pathhsw5m54. an X-linked recessive defect in factor IX. allowing a greater rate of neutrophil infiltration. -Symptoms= prolonged bleeding after tooth extractions and surgeries. Lower lung fields maybe affected most severely because they receive relatively greater perfusion. but no petechial lesions are present because petechiae are characteristic of platelet disorders. Spontaneous bleeding into the joints (hemarthrosis) is typical for hemophilia and may lead to inflammation and deformity of affected joints.moderate hemophilia A and has no effect in hemophilia B.Centriacinar emphysema =predominantly upper lung lobe distribution and a strong association with smoking. If the concentration of this pro-coagulant is greater than 5% of normal then the bleeding disorder is mild.html#answer3 Cavernous hemangioma = most common benign liver tumor typically presenting in adults aged 30-50 years.html#answer http://pathhsw5m54. These benign tumors are thought to be congenital malformations that enlarge by ectasia. DIFF: .ucsf. http://pathhsw5m54.edu/case25/image253.ucsf. -Desmopressin acetate (DDAVP) stimulates release of factor VIII from endothelial cells and can temporarily increase plasma factor VIII levels by two to three-fold.edu/case25/image253. Easy bruising maybe seen.

Chronic asthmatics with extrinsic allergic asthma =bronchial wall pathology (remodeling) which includes thickening of the bronchial epithelium.. blood. intermittent abdominal pain. Chronic irritation by other inhaled environmental substances. although some will complain of abdominal pain and right upper quadrant fullness. basement membrane.jpg DIFF: . In patients older than 2 years of age. Intussusception leads to impaired venous return from the invaginated segment of the bowel which can cause ischemia and subsequent necrosis of the intestinal wall.vcu.learningradiology. a lead point.med.uk/smd.edu/pedia.filled vascular spaces of variable size lined by a single epithelial layer. or intestinal tumor. Prognosis is usually excellent.. and bronchial smooth muscle . nausea. -The most typical location for intussusception is at the ileocolic junction. -Most patients are asymptomatic.sepics/images/broncrbr. such as Meckel diverticulum. http://surgery. neutrophil infiltration. it often occurs without any structural cause (sometimes associated with viral infection).. foreign body.htm http://www. should be sought.j. Collagenous scars or fibrous nodules may be seen in association with thrombosis. In this age group. with surgical resection an option for those patients who are symptomatic or who have compression of adjacent structures. vomiting..mages/intussusception3. these tumors consist of cavernous.ac. Barium enema is diagnostic and may be therapeutic..pathology.com/a.-Microscopically.edu/education/gi/lab3. https://courses. surgical intervention is mandated. mucous gland enlargement and patchy squamous metaplasia of the bronchial mucosa are features of chronic bronchitis.jpg Chronic bronchitis -The leading cause of chronic bronchitis is cigarette smoking. A tubular mass may be palpable in the lower right abdominal quadrant. and “currant jelly” stools (that contain blood and mucus). If the intussusception does not resolve with barium enema. -Clinical presentation is colicky. inflammatory infiltrates submucosal mucous gland enlargement..stu. The size differences in the adjacent segments of the intestine allow the small bowel to invaginate into the cecum.qmul. -Intussusception is most common in children younger than 2 years old.umich. and bronchial walls as well as edema.iver/hemangiomacorrect.html Intussusception = an invagination of a portion of the intestine into the lumen of the adjacent intestinal segment (imagine a collapsed telescope).Thickened bronchial walls. . http://www. such as air pollutants and grain cotton. or silica dusts may also be a contributing factor.

. The resultant architecture is . Furthermore.Medullary carcinoma = by solid sheets of vesicular pleomorphic.tw/ch10/Slide86.. Most cases have a mixture of patterns. As the malignant cell membranes become necrotic they calcify. DCIS now represents 15-30% of all carcinomas and 5O% of mammogram-identified carcinomas. In mammographically screened populations.jpg http://pathology. chronic asthmatic bronchitis.rsna.htm . while asthma can cause chronic bronchitis (e..com/slides/invsl25. Comedocarcinoma (DCIS)Ductal carcinoma in situ = precancerous breast lesion characterized by a malignant clonal cell proliferation contained by the surrounding ductal basement membrane.ages/Images-C/000p039q.jpg . Sclerosing adenosis is a common finding in fibrocystic change. far more extensive DCIS lesions can occur.ca/resourc. http://www. http://www. .ualberta. The (basal) myoepithelial layer of the duct is preserved and uninvolved. cigarette smoking is a much more common cause. If the comedocarcinoma is extensive the lesion maybe palpable as a poorly defined nodule.lmp.Sclerosing adenosis=central acinar compression and distortion (by surrounding fibrotic tissue) and peripheral ductal dilation.Paget disease of the nipple= rare form of breast cancer in which malignant cells spread from superficial DCIS into nipple skin without having crossed the basement membrane. allowing mammographic detection of microcalcification clusters. inspissated breast secretions and chronic granulomatous inflammation in the periductal and interstitial areas. However.hypertrophy. chronic eosinophilic bronchitis). and micropapillary.breastdiseases.org/cont..Phyllodes tumors= similar to fibroadenomas but have increased cytological atypia and stromal cellularity and overgrowth. Usually only a single ductal system appears to have DCIS.Mammary duct ectasia= ductal dilation.kmu. However. = identified as solid sheets of pleomorphic. solid cribriform.htm DIFF: .g. papillary. Chronic inflammation and periductal concentric fibrosis are additional findings. mitotically active cells with a significant lymphoplasmacytic infiltrate around and within the tumor and a pushing noninfiltrating border. Physical examination reveals unilateral erythema and scale crust around the nipple.large.class. with widespread involvement of the breast parenchyma occasionally identified. .edu. -Comedocarcinoma. high-grade cells with central necrosis./suppl_1/S65/F32. -Classically DCIS is divided into five different subtypes: comedocarcinoma. the infiltrate will consist predominantly of eosinophils and mast cells. http://radiographics.

3. -Damage to mamillary bodies (foci of hemorrhage and necrosis) is characteristic of Wernicke encephalopathy. thiamine tends to be deficient because of liver dysfunction among other things. ataxia and ophthalmoplegia f = occurs in the setting of chronic thiamine deficiency (usually due chronic alcoholism or severe malnutrition). Preformed antibodies are the cause.. 2. and disorientation indicate the development of encephalopathy..com/wikip. Perivascular infiltration with lymphocytes. This is a cellmediated immune response. Acute rejection causes vascular damage. Confusion. Always give thiamine supplementation with glucose in patients suspected of having thiamine deficiency (patients who abuse alcohol and patients with a poor diet). and low-grade fever. Ocular irregularities are the first to respond to thiamine infusion. Ataxia is a manifestation of cerebellar damage (degeneration of all layers of the cortex).described as “leaflike. and complete ophthalmoplegia. It represents the recipient’s reaction to the HLA antigens of the graft.” http://wpcontent. Acute rejection occurs 1-2 weeks after receiving a transplant.answers. . hyperacute rejection is sometimes called “white graft” reaction. Hyperacute rejection = occurs within minutes of transplantation. infusion of glucose will exacerbate the pre-existing thiamine deficiency.Pulmonary and bronchial vessels are the main targets of acute rejection. There may be perihilar and lower lobe opacities on chest x-ray. Damage can be irreversible. inattentiveness. dry cough.190px-Phyllodes_tumour.jpg Wernicke encephalopathy =Confusion. 2. For this reason. macrophages and plasma cells is characteristic. Immunosuppressants can successfully treat acute rejection. Hyperacute rejection is rare. Hallmark ocular findings include horizontal nystagmus. often precipitating Wernicke encephalopathy. On light microscopy perivascular and peribronchial lymphocytic infiltrates are seen. CD8 I-cells play a central role. acute rejection manifests with dyspnea. The clinical presentation of thiamine-deficient (Wernicke) encephalopathy: 1. Because thiamine is a cofactor of the enzymes responsible for glucose metabolism. In alcoholics. 1. apathy. There is graft blood vessel spasm and resultant ischemia. In lung transplant patients. bilateral abducens palsy. Rejection reactions -The severity of the rejection depends on the degree of difference between the donor and recipient MHC (major histocompatibility complex) antigens.

ankylosing spondylitis. 2. the reticulocyte count increases dramatically. however. Loss of bile acids cause impaired fat absorption. .com/slides/PHE1608. episcleritis. Skin: erythema nodosum. pyoderma gangrenosum. inadequate intrinsic factor production. 4. and gallstones.jpg DIFF: .Vitamin B12 deficiency is associated with increased serum levels of methylmalonic acid and homocysteine. Chronic rejection occurs months or years following transplantation. Liver: primary sclerosing cholangitis. and elevated serum gastrin and methylmalonic acid (MMA) levels. In Crohn’s disease calcium binds instead to lipids making it unavailable for oxalate binding. anemia. is commonly involved. The excess lipids in the bowel lumen bind calcium ions.3. Joints: arthritis. It is the major cause of mortality in lung transplant patients. increased risk of cholangiocarcinoma. “recycled” in the liver. . . most bile acids are lost with feces. 5. increased risk of adenocarcinoma. Malabsorption: oxalate kidney stones. In the healthy bowel.uveitis. megaloblastic anemia. enabling oxalate excretion. Clinically bronchiolitis obliterans presents with dyspnea. The terminal ileum.worldofstock. Crohn’s disease may involve any area of the gastrointestinal tract. and then reused in the absorptive process. When the wall of the terminal ileum is inflamed. Eyes: iritis . B12 and folate deficiencies. Alveolar walls and pleura are not affected in chronic rejection. and this complex is excreted with feces. strictures. Atrophic gastritis -can result in profound hypochlorhydria. As a result oxalate is absorbed and forms urinary stones. Crohn’s disease Complications: 1. Hemoglobin and RBC count levels gradually rise while the methilmalonic acid level decreases. Normally bile acids which are necessary for the absorption of fat and other nutrients are reabsorbed in the terminal ileum. http://www. a process called bronchiolitis obliterans. abscesses perianal disease. 6.Once vitamin B12 replacement therapy is initiated in an individual with atrophic gastritis. dietary calcium binds dietary oxalate. The levels of these substances should gradually fall in accordance with effective vitamin B12 replacement. non-productive cough and wheezing. 3. hypoproteinemia. Intestinal: fistulas. vitamin B12 deficiency. Chronic rejection causes inflammation of the small bronchioles.Increased intestinal calcium absorption= in sarcoidosis and certain lymphomas. Inflammation and fibrosis of the bronchiolar walls lead to narrowing and obstruction of the affected bronchioli.

calculilab. leading to hypercalcemia. http://www. but the physician examination will usually appear benign.hopkinsbreastcenter. As well-demarcated spherical nodules ranging in size . often myxoid stroma that encircles epithelium-lined glandular and cystic spaces. -Histologically = a cellular.breastpathology. palpable mass. http://www.org/pathology/benign/1r.hopkinsbreastcenter. many patients avoid the pain associated with eating. Epigastric or periumbilical abdominal pain occurs 30-60 min after food intake.org/pathology/benign/1u.It is caused by excess synthesis of 25-dihydroxy vitamin D. Patients report severe pain.jpg Medullary carcinoma=solid sheets of vesicular pleomorphic. http://www. in older women. fibroadenomas can occur in both breasts. mitotically active cells with a significant lymphoplasmacytic infiltrate around and within the tumor and a pushing noninfiltrating border. -Struvite stones (not oxalate) are associated with chronic urinary tract infection.jpg DIFF intraductal papilloma http://www. -On light microscopy hypoperfused areas of intestine show mucosal atrophy and loss of villi. Atherosclerotic arteries are not able to dilate in response to increased blood flow requirements during the digestion and absorption of food. Weight loss is common. This triad of symptoms characterizes the disease: 1.jpg fat necrosis with microcalcifications http://www. this epithelium atrophies and the stroma becomes more hyalinized.html#Inv Medullary Like Ca . -In younger women= freely movable. 2. As women age. Fibroadenomas may increase in size during the luteal phase of the menstrual cycle or during lactation. Angiography is the gold standard but this method is invasive and expensive. The epithelium of a fibroadenoma can be compressed by the surrounding stroma. Mesenteric duplex ultrasonography is a non-invasive alternative in assessing intestinal blood Fibroadenoma =the most common benign tumor of the breast typically arising in young adult women in their twenties or thirties. the tumor generally is identified as a mammographic density.org/pathology/benign/1k. -Correctly diagnosing chronic mesenteric ischemia is difficult.info/Special%20Types.hopkinsbreastcenter.jpg Chronic mesenteric ischemia =most often caused by atherosclerotic narrowing of the celiac trunk SMA and IMA. Atherosclerotic plaques are found in the intestinal vessels.com/art/pix/struvite.

medic.ac. DCM is characterized by ventricular dilatation contractile dysfunction and oftentimes symptoms and signs of CHF (as is chronic ischemic heart disease). the peripartum state or genetic mitochondrial or cytoskeletal defects. DCM is the most common form of cardiomyopathy.uk/illingworth/myopath/postmort.cardiotoxic substances such as alcohol.Possible causes of CHF=diffuse ischemic heart disease or dilated cardiomyopathy (DCM).Type 2 RPGN is immune-complex mediated. but can also be idiopathic.Type 1 RPGN is characterized by anti-glomerular basement membrane (antiGBM) antibodies. Most patients with type 3 RPGN have ANCA (anti-neutrophil cytoplasmic antibodies) in their serum.Decreased serum C3 level = seen with poststreptococcal glomerulonephritis and with dense-deposit disease (type II MPGN). 2. This condition is often associated with Wegener’s granulomatosis. =abnormal decrease in myocardial contractility. http://www.usm. SLE.Rapidly progressive (crescentic) glomerulonephritis (RPGN) =Crescent formation on light microscopy = a syndrome of severe glomerular injury that rapidly progresses to renal failure within weeks to months of its onset.Type 3 RPGN is called “pauci immune” because there are no immunoglobulin or complement deposits on the basement membrane. Anti-GBM antibodies cross-react with pulmonary alveolar basement membranes. producing pulmonary hemorrhages (hemoptysis). the classical pathway is activated secondary to a lack of C1 esterase inhibitor. -Decreased serum C4 level=seen in hereditary angioedema. Here. or Henoch-Schonlein purpura.my/~pathology/KIDNEY. Type 2 RPGN can be a complication of poststreptococcal glomerulonephritis.jpg . There is a “lumpy bumpy” granular pattern of staining on immunofluorescence microscopy. The cause is activation of the alternative complement pathway so Cl and C4 levels are normal. 3. PRGN can be caused by a number of different diseases. It may be idiopathic or a consequence of viral myocarditis . -RPGN is divided into 3 types based on immunologic findings: 1. Type 1 RPGN is found in association with Goodpasture syndrome (anti-GBM disease). which permits unopposed breakdown of C4 by Cl esterase. IgA nephropathy. Linear GBM deposits of lgG and C3 are found on immunofluorescence. Congestive heart failure (CHF) .leeds.bmb. http://www.HTM DIFF .

socially inappropriate behavior. Renal cell carcinoma =most common renal neoplasm. Lesions of the prefrontal cortex cause inappropriate behavior impaired judgment and lost problem solving skills.neoucom. -subthalamic nucleus damage = hemiballism (involuntary flinging movements of extremities contralateral to the lesion). -typically affects patients who are 60 to 70 years old.On gross examination. accounting for about 70% of all kidney tumors.jp/npa. Incontinence and gait disturbances may be seen. The tumor cells are cuboidal to polygonal in shape.The important structures of the frontal lobe include the motor cortex. frontal eye fields and the prefrontal cortex. this tumor appears as a golden yellow mass.ftdrg. Broca’s speech area. aphasia.dysgraphia. and echolalia. The tumor cells show little polymorphism (the cells are similar in shape and size) and the nuclei are small (suggesting that the tumor is well-differentiated). the hippocampus is one of the first regions to suffer damage. -inferior parietal lobule of the dominant hemisphere damage = Gerstmann’s syndrome—right left confusion ..niigata-u. such as dysarthria.edu/chapter9/images9/9-9. . In Alzheimer disease.disinhibition. with clear abundant cytoplasm and eccentric nuclei.jpg DIFF -hippocampus damage = inability to form new memories (anterograde amnesia). Damage of the inferior parietal lobule of the non-dominant hemisphere causes apraxia and contralateral hemi neglect. Pick's disease: -pronounced atrophy of frontal and temporal lobes -neuronal loss in frontotemporal lobes. dyslexia.med. Risk factors include smoking and obesity.ages/Slides/RCC/1RCC_L. and dyscalculia.ac.In evaluating a patient Pick’s disease should be differentiated from the more common Alzheimer disease. It utilizes the neurotransmitter glutamate and sends axons to the globus pallidus. Pick bodies (cytoplasmic inclusions of microtubule-associated protein tau) -urinary incontinence -unknown genetic basis -most cases are sporadic -behavioral: apathy.org/wp-content/uploads/pick-bodies2. -originates from the epithelium of the proximal renal tubules. speech difficulties. http://www.jpg http://www.gif .Pick’s disease =rare cause of dementia that is characterized by the destruction of frontal lobes. . . .Prominent vascularity is evident. http://neuropathology.. These cells have this appearance because they are packed with glycogen and lipids. is a part of the basal ganglia system.

resulting in excessive pulmonary blood flow. 3. the ductus arteriosus closes during first 15 hours of life.healthofchildren.three groups: 1. http://wpcontent. After birth.ualberta. Pick disease. http://www. cyanosis and frequent respiratory infections may occur over time. In neonates prostaglandins (PGE1) can help to maintain a PDA and indomethacin and ibuprofen (NSAIDS) can help to close the PDA by inhibiting PGE synthesis.In diseases associated with cerebral atrophy (Alzheimer. CSF pressure is not increased.” Although the distended ventriculi produce a CT image similar to true hydrocephalus.jpg Hydrocephalus .. increased CSF production is a rare cause of hydrocephalus. heard best at the left upper sternal border..ages/Images-R/000p0115. well-differentiated neoplastic cells that contain numerous mitochondria.). -Delayed closure of the ductus arteriosus is associated with prematurity. perinatal distress.com/wikip..ca/resourc.jpg .jpg Patent ductus arteriosus (PDA) . allowing already-oxygenated blood from the mother to bypass the fetal lungs. however.answers. a PDA allows blood from the systemic circulation to flow to the pulmonary circulation (left-to-right shunt). 2. -In true hydrocephalus. Disorders of cerebrospinal fluid absorption are rare. Abnormal CSF circulation is the most common cause of hydrocephalus. Such compensatory ventricular expansion is called “hydrocephalus ex vacuo. ventricular enlargement occurs secondary to atrophy of the brain. Excessive CSF may be produced by choroid plexus papillomas.DIFF -Renal oncocytomas =very rare tumors that originate from collecting duct cells.. etc. congenital rubella and fetal alcohol syndrome.com/im. -The ductus arteriosus is a remnant of the 6th aortic arch that connects the aorta and left pulmonary artery. the increase in CSF volume and pressure cause ventricular enlargement.Normally. Cortical atrophy is a common sequelae of advanced HIV infection. ..lmp. Physical examination = continuous “machinery” murmur. the infant is asymptomatic.n/9/98/Schiavo_catscan. Oncocytes are large.ch_0001_0003_0_img0204. With a large shunt dyspnea. If the blood flow though the PDA is small. Obstruction is located in either the ventricles or arachnoid villi. http://www..

with dramatically elevated of LDL concentrations.jpg Lipoprotein lipase deficiency Dietary lipids are transported to the peripheral tissues as chylomicrons. eruptive skin xanthomas and hepatosplenomegaly.edu/classwar. . In patients with lipoprotein lipase deficiency. The body is unable to clear dietary lipid loads due to the defective hydrolysis of triglycerides in chylomicrons. This condition is accompanied by severe mental retardation. possible sequelae include optic nerve atrophy and blindness. encouraging the clearance of triglycerides from the circulation. pancreatitis (abdominal pain) lipemia retinalis. Defects in the LDL receptor lead to hypercholesterolemia. heparin-induced lipoprotein lipase activity is significantly reduced. at which point they are hydrolyzed by lipoprotein lipase.tulane. Defects in the LDL receptor . On both gross exam and imaging studies.. Those with the homozygous defect may present at a very young age. .ology/68_Lissencephaly. the brain surface has a smooth appearance.Individuals heterozygous for the defective LDL receptor gene have an LDL receptor density of about 50% normal. Lissencephaly (agyria) = a congenital absence of gyri.The risk of pancreatitis is significantly increased with serum triglyceride concentrations above 1000 mg/dL.mcl. Serum LDL in these individuals ranges from 200-400 mg/dL. Lipoprotein lipase deficiency is a rare disorder that results in increased concentrations of serum chylomicrons. (In contrast. -Patients with hypercholesterolemia are at high risk for accelerated coronary artery disease. obese women and manifests as headache and papilledema.LDL is composed predominantly of cholesterol.. -In normal individuals heparin releases endothelium-bound lipases.Pseudotumor cerebri (idiopathic intracranial hypertension) =elevated intracranial pressure with normal CSF content and normal neuroimaging. Individuals homozygous for the defect have LDL receptor activity that is less than 2% of normal. patients with lipoprotein lipase deficiency are not usually at . =in childhood:marked hyperlipidemia. The main mechanism by which LDL is cleared from the circulation is by “receptor-mediated uptake” by the liver. releasing triglycerides. http://www. This disorder classically occurs in young.

but this is less common. They occur due to formation of antibodies against blood cells and represent a form of type II hypersensitivity reaction. antibodies against platelets are formed causing destruction of platelets.jpg DIFF: -Burkitt lymphomas= translocations of the C-MYC gene on chromosome 8... and develops due to formation of warm lgG antibodies to RBCs. http://courseweb.The t(9. = chronic autoimmune disorder. It is characterized by spherocytosis.gs/follicular-lymphoma. thereby facilitating neoplastic growth. -Anemia in SLE is caused by autoimmune hemolysis.Overexpression of the N-MYC proto-oncogene is common in neuroblastoma and small cell carcinoma of the lung. affects mostly women of childbearing age.cytochemistry.22) BCR-ABL rearrangement is found in CML . http://medicineworld. Black women have a higher risk of developing SLE than Caucasian and Asian women. Tubular xanthomas are the hallmark of familial hypercholesterolemia. -Neutropenia due to antibody-mediated destruction of WBCs also occurs.increased risk for premature coronary artery disease making chest pain an unlikely presentation ).Clinically patients with defective LDL receptors have tubular xanthomas. -Hematologic abnormalities are common in patients with SLE.. Histologically.uottawa. -The pathogenesis of SLE-associated thrombocytopenia is identical to that of ITP. which are nodular lipid deposits in the tendons (most often seen in the Achilles and elbow tendons). http://www.org/images/ne. Burkitt lymphoma shows a diffuse population of medium-sized lymphocytes with a ‘starry sky appearance due to the high proliferation index and high rate of apoptosis. usually onto the Ig heavy chain region of chromosome 14 [t(8:14)]. -Juxtaposition of the bcl-2 gene with the lg heavy chain region results in overexpression of the Bcl-2 protein product..%20images/Burkitt%20lp. and extravascular hemolysis.jpg .jpg Systemic lupus erythematosus (SLE). Bcl-2 protein inhibits apoptosis of tumor cells. . B-cell neoplasm follicular lymphoma -The characteristic cytogenetic abnormality associated with follicular lymphoma is a translocation of the bcl-2 oncogene from chromosome 18 to the lg heavy chain locus on chromosome 14 [t(14:18)]. . a positive direct Coombs test.net/Cell-biology/medical/end4. Some patients also have xanthelasma and arcus cornea.edteched..

knees.With an adrenocortical adenoma. http://pathhsw5m54. Exogenous administration of supra physiological doses of glucocorticoid can produce clinical features indistinguishable from endogenous Cushing syndrome. resulting in atrophy of the contralateral adrenal gland. -The most common location of intestinal carcinoids is the appendix. where they secrete a number of hormone-like substances that play an important role in regulating organ function. ACTH and cortisol production. Suppression of CRH and ACTH causes atrophy of the bilateral adrenal cortices. APUD or enterochromaffin cells are found in many organs and tissues. upper back. and buttocks. and bullae that appear bilaterally and symmetrically on the extensor surfaces. elbows. DIFF . pruritic papules. -Carcinoid tumors are easily recognizable. Thus.ucsf. multiple dense-core granules are seen in the cytoplasm. as there is minimal to no variation in shape and size of tumor cells. these patients have low endogenous CRH. These cells are a part of the APUDsystem (Amine Precursor Uptake and Decarboxilation).e. and many others). -Intestinal carcinoids are malignant transformations of enterochromaffin (endocrine) cells of the intestinal mucosa. -Carcinoids can produce a number of hormone-like substances (such as insulin and gastrin) and vasoactive peptides (serotonin.Adrenal crisis -Cushing syndrome = glucocorticoid excess. or sheets may be formed. there is autonomous production of cortisol by the affected adrenal gland. vesicles. HPA axis suppression is more likely to occur with long-term use of exogenous glucocorticoids (i. Sudden cessation of glucocorticoids after prolonged use can cause adrenocortical insufficiency and adrenal crisis. Carcinoid tumor =uniformity in shape and size of the cells that comprise the nests and glands -Tumor cells have an eosinophilic cytoplasm and oval-to. This causes pituitary ACTH secretion to be suppressed.edu/case7/image76. with the . The term “herpetiformis” is applied because this distinctive vesicular grouping looks quite similar to the lesional clustering seen in herpesvirus infections. nests. more than three weeks duration). Cushing syndrome resulting from exogenous administration of glucocorticoids can lead to suppression of the entire hypothalamic-pituita-adrenal axis. rows. bradykinin. Glands. They also frequently occur in the ileum and rectum. Men are more frequently affected than women. These granules contain secretory products of the tumor cells.html Dermatitis herpetiformis = erythematous.round nuclei. -On electron microscopy.

involved segments of the intestine are thick and edematous. = strongly associated with celiac disease.com/sol/10190. Mucosal ulceration: long linear ulcers with spared intervening mucosa lead to a cobblestone appearance. will be present. pruritic. and legs.08/01/health/adam/2791. planar.jpg Crohn’s disease =non-caseating granuloma. Diseased and healthy areas of the mucosa are sharply demarcated (skip lesions formed by normal mucosa are characteristic of Crohn’s disease. trunk. -On macroscopic examination. These antibodies appear to cause clinical disease by cross-reacting with reticulin.jpg . a classical histologic finding = abdominal pain and bloody diarrhea.age of onset peaking in the third and fourth decades.nature. On contrast barium study. and blisters begin to form at the tips of involved papillae. Another complication is fistula formation between two adjacent loops of intestine or between the intestine and other organs such as the bladder or vagina. -pathogenesis =formation of IgA and IgG antibodies against gliadin (a protein unique to the gluten portion of wheat). hands. 3. -Histologically. http://www. and both the enteropathy and dermatitis tend to improve with a gluten-free diet. the “string sign” or narrowed segments of bowel.jpg Lichen planus = the “5 Ps”: polygonal.aafp.. Chronic inflammation involves the entire thickness of intestinal wall (transmural inflammation). = microabscesses containing fibrin and neutrophils at the dermal papillae tips. Older lesions may also demonstrate an eosinophilic infiltration.com/image..pathguy. http://www. Light microscopy findings in Crohn’s disease are characteristic: 1. a protein found in the anchoring fibrils of the epidermal basement membrane. purplish plaques on the wrists. 2.org/afp/20000601/3319_f2. A finely reticulated scale termed “Wickham’s striae” may be present on the plaque surface. http://graphics8. Strictures that commonly occur in Crohn’s disease may lead to symptoms of chronic intestinal obstruction. The overlying basal cells become vacuolated.nytimes.) Inflammation of the intestinal wall almost universally leads to the narrowing of that intestinal segment. Non-caseating granulomas may be present in all tissue layers.com/nri/journal/v3/n7/images/nri1132-i1.gif http://www.

. -On light microscopy. =Glomerular basement membrane (GBM) disruptions and fibrin deposition on electron microscopy .. On electron microscopy.jpg http://anatpat.bio.ac.idac.pathologypics. all glomeruli are enlarged and hypercellular due to leukocyte infiltration and proliferation of endothelial and mesangial cells.jpg http://www. hypoalbuminemia.pathologyatlas. This disease classically affects boys 2-10 years old.com/PictView.. -Symptoms of HSP generally develop a few weeks after the associated illness . with multiple surface punctuate hemorrhages.tohoku. Clinical manifestations of nephrotic syndrome include generalized edema. The GBM breaks are due to fibrinoid necrosis of the glomeruli.jpg Membranous glomerulopathy =Uniform.ive_glomerulonephritis.ro/patho. http://www.immunology/image/Exp-4. but crescents may not be detectable in early disease..br/erim. electron-dense deposits (“humps”) on the epithelial side of the basement membrane are seen. Renal involvement is often accompanied by pulmonary symptoms. The kidneys are enlarged and swollen. http://www. http://www.. There is crescent formation on light microscopy.jp/en/or.davidson.Poststreptococcal glomerulonephritis (PSGN) =inflammatory reaction involves all glomeruli in both kidneys..5 g/day). and is often preceded by viral or streptococcal upper respiratory infections. diffuse thickening of glomerular capillary walls on light microscopy = one of the most common causes of nephrotic syndrome in adults.edu/course.unicamp. An important contributor to crescent formation is fibrin escape into Bowman’s space. marked proteinuria (>3. hyperlipidemia and lipiduria.rter/restricted/Cresgn.html#micro Goodpasture syndrome (anti-GBM disease) = Linear lgG and C3 deposits on immunofluorescence microscopy -. There is typically crescent formation on light microscopy.aspx?ID=465 Henoch-Schonlein purpura (HSP) = the most common small vessel vasculitis in children. -Immunofluorescence reveals coarse granular deposits of lgG and C3 that have a characteristic “lumpy-bumpy” appearance.

Both diseases cause mesangial proliferation and crescent formation. Joints: Self-limited migratory arthralgias and arthritis are most commonly seen in the large joints of the lower extremities (ankle and knee joints) possibly because of their dependent nature. 3. women with inflammatory breast cancer present with breast tenderness skin discoloration (ranging from pale pink to deep red brown to purple). These lesions may begin as urticarial papules or plaques and subsequently evolve into purpura.technion. Patients with HSP also have an increased risk of intussusception.. Commonly.hdcn. It is commonly seen in the heart and liver of aging or cachectic. http://www. This yellow-brown. HSP is therefore an IgAmediated leukocytoclastic (hypersensitivity) vasculitis. Gastrointestinal tract: Intermittent severe abdominal pain is common in HSP.il/~mdcours. The effects of this vasculitis 1.org/images/lipofuscin.This malignancy causes lymphatic obstruction and tissue swelling when collections of neoplastic cells plug the dermal lymphatic channels. inducing an inflammatory reaction. finely granular perinuclear pigment is the product of free radical injury and lipid peroxidation. The cutaneous findings in HSP result from leuko cytoclasis of cutaneous vessels. and a rapidly progressive underlying mass. http://content. Skin: HSP classically causes “palpable purpura” on the buttocks and lower extremities. = a sign of “wear and tear” or aging.gif http://www. a condition characterized by IgA leukocytoclastic vasculitis limited to the kidney.jpg Lipofuscin =An insoluble pigment composed of lipid polymers and protein-complexed phospholipids. malnourished patients.resolves. Kidneys: Renal involvement in HSP is identical to that seen in IgA nephropathy (Berger disease).popup-ans7_breast_rash.jpg ..ac. respectively) as well as bowel wall edema.com/symp/lund/jtimg26..jpg Inflammatory breast cancer =Peau d’orange= the presence of pitting edema in subcutaneous breast tissue accompanied by skin thickening around exaggerated hair follicles. 4.jonbarron. Vasculitis within the GI tract may result in upper and lower GI bleeding (hematemesis and bloody diarrhea. 2. http://www.ac%20Muscle-Lipofuscin..revolutionhealth. . It is hypothesized that antigen from the infection stimulates production of IgA antibodies and that IgA-containing immune complexes then deposit on vessel walls.co.

On macroscopic examination. Clinically they present with hydrocephalus. It is typically located within the hemispheres (in the frontal or temporal lobe or near the basal ganglia). the neoplasm is cystic with a tumor nodule protruding from the wall. On imaging studies.rsna. The cerebellum is the most common location of pilocytic astrocytomas.html Childhood brain tumors: 1.bc. Pilocytic astrocytomas are the most common.bp..ca/NR/rdonl.157/pseudorosettesX100. This nodule is the active part of the tumor..250. http://neurosurgery.180/staticgalle.jpg Oligodendrogliomas =in patients of 40-50 years old....org/cgi/content-nw/full/27/2/525/F24C http://upload. a pilocytic astrocytoma appears as a mass with both solid and cystic components. http://1.seattlechildre. tumor cells form gland-like structures called “rosettes.logy/anthracosis20x04.wikimedia. This tumor is highly malignant and carries a bad prognosis. Clinical presentation is severe headache and cerebellar dysfunction. in the vermis).blogspot.jpg Glioblastoma multiforme (GBM) = tumor that arises from astrocytes and is the most common primary cerebral neoplasm in adults.” http://www.com/_oAQI4j4B.sagittal_with_contrast.bccancer.Anthracosis = coal dust that is taken up by macrophages within the lung parenchyma http://146.ts/images/tumors_large. Medulloblastomas are solid..jpg http://www....sort=0&s=20080802174937135 2. Medulloblastomas are the second most common brain tumors of childhood.I/s320/sag%2Bcontr%2B1. and are composed of sheets of small blue cells with hyperchromatic nuclei and scant cytoplasm. Their most common location is the white matter .. This tumor has a relatively good prognosis. Ependymomas are the third most common brain tumor in children.surgicalpathologyatlas.jpg 3. http://radiographics..201. On microscopic examination pilocytic astrocytes and Rosenthal fibers are seen.org/wikipe. They are located only in the cerebellum (most commonly. They arise from the ependymal lining of the ventricle and can obstruct the flow of CSE. On microscopic examination. They are low-grade neoplasms that arise from astrocytes...

and fibrotic.. By the time they reach adulthood. most patients with sickle cell anemia have undergone “autosplenectomy” as a result of these infarcts and are left with only a small. and desmoplastic small round cell tumors.symptoms of “acute chest syndrome” (ACS). -In patients with homozygous hemoglobin S disease vaso-occlusive crises can also cause splenic infarctions. which is vaso-occlusive crisis localized to the pulmonary vasculature that can occur in patients with sickle cell anemia. Degree of dysplasia. 2. The malignant potential of adenomatous polyps is determined by the following: 1.com/co. It is hypothesized that 10 years on average. The transformation of normal mucosal cells into malignant ones is caused by a series of gene mutations called the “adenoma-to-carcinoma sequence.molecular-cancer. Sickle cell anemia . Calcifications may be visible. Repeated infarctions overtime produce a spleen that is shrunken. areas of necrosis and hemorrhages are not common. mesotheliomas.7/1/41/figure/F7?highres=y Tumors that stain positive for keratin = carcinomas. >4cm —4O% risk of malignancy. . The initial appearance of small adenomatous polyps is attributed to mutation of the APC tumor suppressor gene. Early detection and excision of adenomatous polyps is therefore. Size of the polyp: <1cm — unlikely to undergo malignant transformation. ACS is commonly precipitated by pulmonary infection. an effective prophylaxis for colon adenocarcinoma. scarred splenic remnant. Histologic appearance: villous adenomas are more prone to be malignant than tubular adenomas. Progression from normal mucosa to a small polyp. 3.flickr. http://www. is required for malignant transformation of adenoma. The spleen may demonstrate brownish discoloration (hemosiderosis) due to extensive ingestion of sickled RBCs by splenic macrophages (extravascular hemolysis).of the frontal lobe.. discolored. trophoblastic tumors. thymomas. http://www. various sarcomas.” This sequence includes the following steps: 1.com/photos/14309782@N04/1607988490 Colon adenocarcinomas -most develop from preexisting adenomatous polyps (adenomas). -Colon adenomas usually occur in patients in 50-60 years old and are considered premalignant. On gross examination they oligodendrogliomas present as well-circumscribed gray masses.

2. Increase in the size of the polyps. Mutation of K-ras protooncogene is thought to facilitate this step by leading to uncontrolled cell proliferation. 3. Malignant transformation of adenoma into carcinoma requires mutation of two genes: p53 and DCC. Increase in the size of adenomatous polyps (and, therefore, increase in their malignant potential) is attributed to K-ras protooncogene mutation. This gene normally encodes for a protein that regulates cell cycle by stimulating and inhibiting it as necessary. Mutation of K-ras causes it to become the oncogene Kras, which encodes for a protein that has lost its ability to inhibit the cell cycle, but can still stimulate it. Thus, unregulated cell proliferation ensues. http://www.geocities.com/HotSpring.../7780/images/villaden.html http://www.ajronline.org/cgi/content-nw/full/189/1/35/FIG12

Rapidly progressive glomerulonephritis (RPGN). =a syndrome of severe renal injury that may be the result of a number of disease processes. RPGN usually leads to rapid (within weeks to months) and irreversible loss of renal function. -The crescents =proliferated glomerular parietal cells, monocytes and macrophages that have migrated into Bowman’s space, as well as abundant fibrin between the cellular layers of the crescents. Fibrin escape into Bowman’s space is an important contributor to crescent formation. As the disease progresses, crescents become sclerotic and obliterate Bowman’s space, thus impeding glomerular function. -C3 and lgG are deposited along the glomerular basement membrane in patients with type 1 RPGN (Goodpasture syndrome). In Goodpasture syndrome immunofluorescence microscopy shows linear deposits of these complexes. C4 deposition is usually not found. http://www.pathologyatlas.ro/patho..._glomerulonephritis_02.jpg

Pathogenesis of Crohn’s disease - Increased activity of TH-1 helper cells increases production of IL-2, interferony, and TNF causing subsequent intestinal injury. -Non-caseating granulomas= characteristic of Crohn’s disease. http://www.pathology.vcu.edu/education/gi/lab2.g.html DIFF: - TH-2 cells = involved in the pathogenesis of ulcerative colitis. They produce IL4, IL-5, IL-6, and IL-10, which might damage mucosal cells of the intestine.

Left recurrent laryngeal nerve impingement (Ortner syndrome)

-In rare instances, it may be compressed to the point of neurapraxia (failure of nerve conduction due to blunt injury) by enlargement of the left atrium and/or other structures in the vicinity of its course as it loops behind the ligamentum arteriosum, underneath and around the aortic arch, and back up alongside the trachea to the larynx. -Mitral stenosis can cause left atrial dilatation sufficient to impinge on the left recurrent laryngeal nerve -The recurrent laryngeal nerves innervate all of the intrinsic muscles of the larynx except the cricothyroid muscle. Paresis of vocal cord muscles innervated by left recurrent laryngeal nerve can cause hoarseness. http://www.drguide.mohp.gov.eg/New...-Learning/Cases/Case31.asp

Multiple sclerosis = optic neuritis( pain with ocular movements and decreased vision) + Intention tremor (sign of cerebellar dysfunction) =Waxing and waning neurological deficits in a 20-30 year old patient are suggestive of this disorder. -The etiology of multiple sclerosis remains unknown. Currently, it is considered an autoimmune disease, with viral and environmental factors also playing a role in its pathogenesis. The autoimmune character of this disorder is supported by the following features: 1. There is an elevated immunoglobulin G (lgG) level in the cerebrospinal fluid (CSF). It is seen as an oligoclonal band on electrophoresis and suggests an activation of B cells in multiple sclerosis. 2. The incidence of multiple sclerosis is increased in people with certain HLA types. 3. Immunomodulatory agents, such as interferon beta, have a positive impact on multiple sclerosis. Its mechanism is counteraction of the inflammatory action of immune cells. http://images.quickblogcast.com/80...tiple_sclerosis_MRI__2.gif

Goodpasture syndrome = anti-glomerular basement membrane (anti-GBM) disease =linear deposits of immunoglobulin along the glomerular basement membrane . -These deposits are composed of lgG and C3. Anti-GBM antibodies target the α3 chain of collagen type IV, a component of the glomerular basement membrane. The resultant renal injury is a type 1 RPGN. The presence of crescents in the damaged glomeruli on light microscopy is diagnostic of RPGN. Anti-GBM antibodies cross-react with the pulmonary alveolar basement membrane, causing pulmonary hemorrhages. The combination of renal failure with pulmonary hemorrhage (hemoptysis) is the typical clinical presentation of anti-GBM disease. http://www.pathguy.com/sol/16843.jpg http://www.pathologyatlas.ro/patho...tic_glomerulonephritis.jpg

http://www.dokkyomed.ac.jp/dep-k/c...litis/vas-html/vas-63.html DIFF: -Basement membrane splitting is seen on electron microscopy in Alport syndrome and membranoproliferative glomerulonephritis (MPGN) type 1. In Alport syndrome, symptoms of nephritis are accompanied by deafness and various ocular manifestations. In MPGN there are granular deposits on immunofluorescence. On light microscopy, the glomeruli of MPGN have a lobular appearance with proliferating mesangial cells and increased mesangial matrix. http://www.gamewood.net/rnet/renalpath/tut41.jpg http://www.uncnephropathology.org/jennette/mpgn_i/tut42.jpg -Uniform, diffuse capillary wall thickening on light microscopy is a sign of membranous glomerulopathy. The typical presentation is nephrotic syndrome: generalized edema, marked proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia and lipiduria. Immunofluorescence demonstrates granular deposits of lgG and C3 along the glomerular basement membrane. http://www.unckidneycenter.org/images/Membranous_capwalls.jpg - In focal segmental glomerulosclerosis (FSGS) IgM and C3 deposits are found in the sclerotic areas of the glomeruli on immunofluorescence. Linear deposition of immunoglobulins is not typically found. http://www.gamewood.net/rnet/renalpath/t9.jpg

Cholelithiasis -Estrogenic influence facilitates the biosynthesis of cholesterol by increasing hepatic HMG-CoA reductase activity. As the water-insoluble cholesterol is secreted in bile, it is rendered soluble in small amounts by detergent-like bile salts and phosphatidylcholine. Suppression of cholesterol 7α-hydroxylase activity (as accomplished through medications such as clofibrate) reduces the solubilization of cholesterol into bile acids, resulting in excess cholesterol secretion in bile. When the gallbladder is hypomotile or there is more cholesterol than bile salts, the cholesterol precipitates into insoluble crystals that eventually form to make gallstones. Cholesterol and mixed stones together comprise 80% of all gallstones in the Western population. -numerous risk factors for the formation of cholesterol gallstones: Caucasian race; obesity or rapid weight loss; female sex hormones or usage of oral contraceptive pills; glucose intolerance; hypomotility of the gall bladder (which is associated with pregnancy, advanced age, fasting hypertriglyceridemia, and prolonged total parenteral nutrition); malabsorption of bile acids as would occur secondary to ileal disease or resection; and pharmacotherapy with clofibrate, octreotide, or ceftriaxone. -Asymptomatic patients do not require intervention, but symptomatic cholelithiasis is usually treated with laparoscopic cholecystectomy. http://path.upmc.edu/cases/case23/images/gross1.jpg http://www.telepathology.com/cases/gall1a.htm

Infant of diabetic mother - Macrosomia is the classic “defect” this term describes a large infant (larger than 4.0 kg by conservative measures). If blood glucose is poorly controlled with diet and activity, insulin treatment is generally started. High glucose levels in the mother enter fetal circulation, causing high blood glucose levels to be present in the fetus. The fetus responds to this elevated blood glucose by increasing insulin. Obviously, the amount of insulin generated by these fetuses is more than normal, and beta cell hyperplasia results. Once free from the mother, the neonate continues to over-produce insulin (hyperinsulinemia), which can cause the neonate to experience severe hypoglycemia. High insulin levels are also responsible for the increased fat deposition and enhanced fetal growth that results in macrosomia. - Other birth defects in children whose mother’s had uncontrolled diabetes during pregnancy = caudal regression syndrome, neural tube defects, ventricular septal defect, transposition of blood vessels, rectal atresia, and renal agenesis. - Maternal insulin cannot be transferred to fetus because it is catabolized during transfer across the placenta

Superior vena cava syndrome =impaired venous return from the upper body. The superior vena cava provides the venous drainage of head, neck, upper trunk and upper extremities. -The superior vena cava is a 6-8 cm long vein that drains into the right atrium. It is located in the medial mediastinum and is surrounded by the sternum, trachea, right bronchus aorta, and pulmonary artery. It is located in close proximity to the perihilar and paratracheal lymph nodes. This vein has thin walls and is easily compressed by mediastinal masses. -Bronchogenic carcinoma is the most common cause of superior vena cava syndrome. -Non-Hodgkin lymphomas are the second most common cause. -Patients with SVC syndrome complain of dyspnea, cough, and swelling of the face, neck and upper extremities. Headaches, dizziness and visual disturbances may occur due to elevated intracranial pressure. Dilated collateral veins may be seen in the upper torso. http://img.medscape.com/pi/emed/ck...gy/1048885-1094030-708.jpg http://img.medscape.com/pi/emed/ck...y/1017692-1017949-3209.jpg

Superior sulcus tumor (or Pancoast tumor) = arises at the lung apex and may cause shoulder pain due compression of the brachial plexus. Involvement of the cervical sympathetic ganglia leads to Horner’s syndrome (ptosis, miosis and anhydrosis). http://www.mevis-research.de/~hhj/Lunge/imabc/BCWandTH_52.JPG

If it involves the muscular layer.ro/patho. flank/abdominal pain. http://hmg. -Patients are also at increased risk for renal cell carcinoma. http://www.WBC casts are also seen with acute interstitial nephritis. -Tumor stage is the most important criteria for determining prognosis.Patients develop neurofibromas.images/large/DDE08901.Colorectal tumor staging -The degree of tumor differentiation (from well. and café au lait spots (hyperpigmented cutaneous macules). WBC casts.cute_pyelonephritis_01. . Urine sediment microscopy reveals WBCs. and pancreas. http://www.gif Prognosis of colorectal adenocarcinoma is directly related to the stage of the tumor (not to the grade!).. vomiting.html http://www. -Sterile pyuria (WBCs. and bacteria. nausea. but no bacteria) is seen in a small number of patients with acute pyelonephritis. chills.ac.oxfordjournals. Lymph node involvement (stage C) and distant metastasis (stage D) have poor prognosis.differentiated to anaplastic) is referred to as the grade.jpeg Von Recklinghausen’s disease or neuro fibromatosis type (NF1) = inherited peripheral nervous system tumor syndrome. optic nerve gliomas. Pyelonephritis = fever. -WBC casts = pathognomonic -.in/path/seminars/Image5.. -If the tumor is confined to the mucosa (stage A).org/cont.osaka-u. but can also be seen with non-gonococcal urethritis caused by Chlamydia and Ureaplasma. liver. as well as congenital cysts and/or neoplasms in the kidney..jpg Von Hippel—Lindau disease =rare autosomal dominant condition characterized by the presence of capillary hemangioblastomas in the retina and/or cerebellum. but clinical presentation is different in that patients have only a low-grade fever and do not experience painful urination.pathologyatlas. 5-year survival rate is 7080%.. the patient has 90%+ chance of 5-year survival.med.sgpgi. .ac. Lisch nodules (pigmented nodules of the iris).jp/pub/hp-lab/www/atlas/EWBCCAST. and costovertebral angle (CVA) tenderness. which can be bilateral.

seizures are a major complication. Rupture of these telangiectasias may cause epistaxis. http://www.http://www. and skull radiopacities. seizures.uwo. http://www. liver..is also characterized by cutaneous angiofibromas (adenoma sebaceum).jpeg Sturge-Weber syndrome (encephalotrigeminal angiomatosis) = rare congenital neurocutaneous disorder characterized by the presence of cutaneous facial angiomas as well as leptomeningeal angiomas.ca/cns/resident/poc. http://img. and pancreatic cysts ..medscape. -This condition is associated with mental retardation.com/pi/emed/ck. Skin involvement typically overlies the ophthalmic (V1) and maxillary (V2) distributions of the trigeminal nerve. gastrointestinal bleeding.org/content/231/2/515.figures-only Tuberous sclerosis (TS) -may cause kidney.y/1048885-1086114-1749.uwo.mil/rad/home/cases/sw_dis.com/content/vol75/.bmj.central nervous system (CNS) involvement manifests as cortical and subependymal hamartomas.. or hematuria. http://rad.ages/large/np53603.usuhs.org/images/Resources/nf1bodyImage.jpg .jpg http://jnnp. hemiplegia.jpg Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia) = the autosomal dominant inheritance of congenital telangiectasias. visceral cysts.rsna.ca/cns/resident/piclib..org/uploads/images/NF2Body.. Clinically.tures/tuberousclinical. as well as renal angiomyolipomas and cardiac rhabdomyomas.nfmidatlantic. and a variety of other hamartomas.. Skull radiographs may show characteristic “tram-track” calcifications.f1.nfcalifornia.jpg Neurofibromatosis type 2 =autosomal dominant =bilateral cranial nerve VIII schwannomas and multiple meningiomas.html http://radiology. = autosomal dominant syndrome .html http://www.

thickening. http://missinglink.m/content/2/1/11/figure/F1 -The most common cause of transtentorial herniation is an ipsilateral mass lesion such as a brain tumor subdural or epidural hematoma..cerebrospinalfluidresea. as seen with rheumatoid arthritis.htm http://missinglink.registry.ucsf. This process is called herniation... Ipsilateral oculomotor nerve (CN III) compression leads to a fixed and dilated pupil on the side of compression. As a result portions of the brain may protrude through the openings in the falx cerebri tentorium cerebelli or through the foramen magnum. Compression of the contralateral cerebral peduncle against the tentorium may occur.jpg http://attra. Paralysis of oculomotor muscles occurs later. gluteal cleft... and scalp.In sub falcine herniation the cingulate gyrus herniates under the falx cerebri.The psoriatic arthritis ranges from mild to severe and has the potential to cause marked deformities in the joints. knees.edu/neuroslides/slide056.edu/lm/ids.html . -Transtentorial (uncal) herniation occurs when the medial temporal lobe (uncus) herniates through the gap between the crus cerebri and the tentorium.rochester. silvery scale. the following structures may become compressed: 1.ucsf.edu/lm/int.iation/UncalHerniation.htm http://www.jpg The cranial vault is limited by the rigid cranial bones and is divided into compartments by the dural folds (falx cerebri and tentorium cerebelli).htm -In tonsillar herniation..n/SubfalcineHerniation.com/medem/images/..edu/lm/int. 4.urmc. 2...edu/lm/ids. As a result. The most common areas of skin eruption include the elbows. the cerebellar tonsils displace through the foramen magnum and compress the medulla. The damage to the contralateral corticospinal tract leads to ipsilateral hemiparesis. and leads to ptosis and “down-and-out” gaze.com/images/medical/ortho/psoriatic_mod.ucsf. There is not room for brain expansion in an event of brain edema. Brainstem hemorrhages (Duret hemorrhages) may occur in the pons and . http://missinglink.rniation/PCAInfarction. glans penis.Psoriasis = a common chronic inflammatory skin disorder characterized by sharply demarcated salmon-colored plaques covered with a loosely adherent. Ipsilateral posterior cerebral artery (PCA) compression leads to contralateral homonymous hemianopsia...myfootshop. tumor or hemorrhage.jpg http://www. This mass causes an increase in supratentorial pressure on the side of the lesion and forces the ipsi lateral parahippocampal uncus through the tentorial incisure._Images/HerniationBlum./psoriaticka-artritida. http://www.. lumbosacral area..ucsf. -Nail changes occur in 30% of afflicted individuals and entail a yellow-brown discoloration with associated pitting. 3.cz/res/image.jpg Brain herniation http://missinglink. http://www. or crumbling.medem..lev20_psoriasis_jpp_01. .

This inflammatory focus maybe surrounded by some lymphocytes and occasional plasma cells. round to ovoid nuclei with central. http://www.nature.midbrain due to stretching and rupture of the basilar artery.biopsy =a circumscribed interstitial collection of mononuclear inflammatory cells.images/medium/coverfig. -There is disproportionate thickening of the ventricular septum compared to the free wall of the left ventricle and the septal muscle bulges into the left ventricular outflow tract. there is a progressive accumulation of cytoplasmic granules containing brownish lipofuscin pigment (the result of indigestible byproducts of subcellular membrane lipid peroxidation). These interstitial myocardial granulomas (Aschoff bodies) are typically found in acute rheumatic carditis. diffuse inflammation and Aschoff bodies may be found in any of the three layers of the heart..com/image/images/cns/CNS060. Aschoff bodies are later replaced by fibrous scar.jpg Normal aging of the heart .. This is usuallyfatal.cmu.com/nature/journ.html . there is extreme hypertrophy. slender chromatin ribbons are called Anitschkow cells (“caterpillar cells”).. Atrophy of cardiac myocytes results in increased interstitial connective tissue and. in some cases.68/fig_tab/415227a_F3. Finally. ARE is typically preceded by an episode of group A streptococcal pharyngitis 10 days to 6 weeks prior.ac.binglixue. This chamber length decrease causes the basal ventricular septum to bulge into the left ventricular outflow tract (sigmoid septum). as well as disarray and branching of myocytes. On histologic exam.med. including some large histiocytes and a prominent binuclear histiocyte (in the path of the black arrow). the deposition of amyloid.or. Hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis) =asymmetric septal hypertrophy. there is an associated thickening and biconvex shape of the interventricular septum. The plump macrophages with abundant cytoplasm and central. Although left ventricular cavity size is reduced. -During acute rheumatic fever (ARE).th/student/patho/Lertlakana/040.gif Acute rheumatic carditis .html http://eurheartj. When the larger macrophages become multinucleated they are referred to as Aschoff giant cells. http://www.Aging is associated with a decrease in left ventricular chamber size particularly in the apex to base dimension. http://www. None of the other cranial nerves become compressed due to uncal herniation.oxfordjournals..

= due to rupture of saccular (berry) aneurysm or arteriovenous malformation. However.html Chagas disease -Recent travel to Latin America (particularly South America and Brazil) = caused by the intracellular protozoan parasite Trypanosoma cruzi.ac.daviddarling. Moreover. This vasospasm occurs in the vessels surrounding the ruptured aneurysm..SubarachnoidHemorrhage. in diphtheritic myocarditis.edu/N..http://www.cmu. so transcranial color Doppler is needed.jpg . a number of complications may occur.brown. CT scan without contrast reveals blood in the subarachnoid space (between the arachnoid and pia mater).” Confusion.info/images/aneurysms. this condition results from a circulating toxin produced by a primary focus of infection in the upper aerodigestive tract (tonsillopharyngitis).ocarditis-lymphocytic..cmu.jpg http://www.edu/Courses/Digit. which presents as new-onset confusion and/or focal neurological deficit 4-12 days after the initial insult.html Diphtheritic myocarditis .html Viral myocarditis http://www.Nimodipine..washington. and nuchal rigidity may also be present. Secondary vasospasm causes cerebral ischemia.dio/myocarditis-chaga. More than half of patients develop secondary arterial vasospasm.brown. The mechanism of vasospasm is related to impaired brain autoregulation.med. sometimes described as a ‘thunderclap headache.edu/Courses/Digit. http://uwmedicine.. Chagas disease can result in a myocarditis characterized histologically by distension of individual myofibers with intracellular trypanosomes. a selective calcium channel blocker.th/student/patho/Lertlakana/041.ac.A child who has not been immunized against diphtheria is susceptible to diphtheritic myocarditis.. http://www. CT scan may fail to show vasospasm.med. -If the patient survives initial subarachnoid hemorrhage. there is a pleomorphic interstitial infiltrate of macrophages.html http://www. Subarachnoid hemorrhage (SAH) =a life-threatening condition.th/student/patho/Lertlakana/042. fever. SAH manifests with the abrupt onset of severe headache. is often prescribed to prevent this vasospasm. .

resulting in an ostium primum atrial septal defect (ASD). causing regurgitation through the AV valves.. These endocardial cushion defects are commonly associated with Down syndrome. This disease is the result of mutations in frataxin.Endocardial cushion defects A congenital defect in the lower part of the interatrial septum is most likely the result of failure of the endocardial cushions of the atrioventricular canal to fuse completely during embryonic development. These patients usually also have a cleft in the anterior leaflet of the mitral valve as well as in the septal leaflet of the tricuspid valve. Down syndrome: endocardial cushion defects (ostium primum ASDI regurgitant AV valves) 2. DiGeorge syndrome: tetralogy of Fallot and aortic arch anomalies 3. There is initial loss of sensory (including proprioceptive) neurons in the dorsal root ganglia. Chromosome 22q11. http://www. -The dominant cardiac defects in this syndrome are tetralogy of Fallot and aortic arch anomalies. Tuberous sclerosis: valvular obstruction due to cardiac rhabdomyomas 6. Turner’s syndrome: coarctation of the aorta .ticles/images/asd-prim... Marfan syndrome: cystic medial necrosis of the aorta 5. a mitochondrial protein important in iron homeostasis and respiratory function.edu/Courses/Digit.interstitial-fibrosis. with accompanying gait ataxia.jpg DiGeorge syndrome = thymic aplasia and failure of parathyroid formation as a result of defective embryonic development of the third and fourth pharyngeal pouches. =hypocalcemic tetany and recurrent viral and fungal infections secondary to Tcell deficiency. http://www. This autosomal recessive condition may be associated with hypertrophic cardiomyopathy..2 deletion is found in 90% of cases..chelationtherapyonline.brown. Friedreich’s ataxia: hypertrophic cardiomyopathy 4.html Major associations: 1. Friedreich’s ataxia = spinocerebellar degeneration with predominantly spinal ataxia.

Anaplastic tumors: 1. however. perhaps secondary to a decrease in intracellular pH. When the mitochondria are injured irreversibly. Depletion of intracellular ATP is thought to promote the dissolution of polysomes into monosomes as well as the detachment of ribosomes from the rough endoplasmic reticulum. Loss of cell polarity and normal tissue architecture. Numerous often abnormal mitoses 6. Deep staining of nuclei (hyperchromatism) and significant variation in shape and size of nuclei (nuclear pleomorphism) 4. especially in hepatocytes. Larger nuclei than those found in normal cells of the same tissue (high nucleus-to-cytoplasm ratio) 5. -Disaggregation of polysomes= the dissociation of rRNA from mRNA in reversible ischemic/hypoxic injury. decreased production of lipid acceptor proteins prevents the normal incorporation of triglycerides into lipoproteins. -Glycogen loss=early and reversible cellular response to injury. . and implies a permanent inability to generate further ATP via oxidative phosphorylation. Since triglycerides cannot be rapidly exported from the cell in the form of lipoproteins.Cell injury -vacuoles and phospholipid-containing amorphous densities within mitochondria = signifies irreversible injury. ATP must be supplied to the cell via anaerobic glycolysis of glucose derived from the cell’s glycogen stores. Myocardial glycogen stores may be completely depleted within 30 minutes of the onset of severe ischemia. Myofibril relaxation corresponds with intracellular ATP depletion and lactate accumulation due to anaerobic glycolysis during this period. -Triglyceride droplet accumulation= characteristic of reversible cell injury. -Disaggregation of granular and fibrillar elements of the nucleus= reversible cell injury. the cell cannot recover. they accumulate intracellularly. Disaggregation of polysomes results in impaired protein synthesis. infiltrative fashion 2. In the hepatocyte. Significant variation in shape and size of cells (cellular pleomorphism) 3. Simple mitochondrial swelling may be associated with reversible cellular injury. As a result of lowered mitochondrial ATP production. This fatty change may result from the decreased synthesis of intracellular proteins that occurs with cell injury. -Myofibril relaxation=an early sign of reversible injury in cardiac myocytes. and also in striated muscle cells and renal cells. Giant multinucleated tumor cells The appearance of giant multinucleated cells in a muscle tumor would therefore suggest anaplasia. with cells coalescing into sheets or islands in a disorganized. Another common nuclear change associated with reversible cell injury is clumping of nuclear chromatin. which occurs within the first 30 minutes of severe ischemia.

Proposed mechanisms encompass autoimmune activity. involvement of other areas of the intestine is variable. and over hard bony surfaces (eg.JPG DIFF: -albinism=absent or defective tyrosinase. -granulomas are seen in the media of the arteries. type I diabetes mellitus.JPG Temporal arteritis = inflammatory condition that affects the walls of medium-sized and large arteries. http://www.can affect all races. 2. Addison disease. adenocarcinoma of the colon. Ulcerative colitis : 1. pernicious anemia.eregimens. Mucosal damage is continuous. knees). http://www. neurohumoral toxicity specific for melanocytes. Inflammation is limited to the mucosa and submucosa only.. genitalia. autoimmune hepatitis. but abdominal pain is virtually always present. -The pathogenesis of vitiligo remains unclear. -Postinflammatory hypopigmentation=redistribution of existing melanin within the skin.com/images/regimens/Vitiligo. The rectum is always involved. autoimmune thyroiditis). (In Crohn’s disease there may also be bloody diarrhea. There are no areas of normal mucosa between the affected segments.s/650_Ulcerative_Colon. Most of the available data supports an autoimmune causality for vitiligo. 4. umbilicus.) Complications: -toxic megacolon . -Histologic= loss of melanocytes and a complete absence of melanin pigment. is the hallmark of ulcerative colitis. 3. consisting of mononuclear infiltrates and multinucleated giant cells. Age of onset varies.virtualmedicalcentre. extremities. Not only have circulating melanocyte antibodies been identified in this population but there is a significant correlation between vitiligo and autoimmune disorders (eg.Vitiligo = partial or complete loss of epidermal melanocytes. Due to the characteristic histologic . Vitiligo typically erupts on the face. axillae. groin. varying in size from a few to several centimeters. the lesions are flat. .co.. well-circumscribed macules and patches of absent pigment. but most afflicted individuals will have developed lesions by the second or third decade of life. Graves disease. Bloody diarrhea with or without abdominal pain. but it is particularly striking in darkly pigmented individuals. Clinically. and melanocytic self-destruction secondary to toxic intermediate exposure during melanin synthesis. This finding may also be associated with reduced transfer of melanin to keratinocytes.

nature.pathology. Headache: Focal pain over the temple and tenderness on palpation . anti-cationic proteinase). 4. . and facial pain may occur. = hematuria. It may be transient or may result in permanent blindness.ry/jpgs575/spd/img0020. Polymyalgia rheumatica occurs in more then half of patients with temporal arteritis. C4 levels are usually normal. -On light microscopy. nodularity.washington. shoulder and pelvic girdle pain and morning stiffness. there are coarse granular deposits of lgG and C3 with the characteristic “starry sky” appearance. tongue claudication. -The changes in the arteries are segmental: abnormal areas are interspersed by segments of normal-appearing arterial wall. Electron microscopy typically shows electron-dense deposits (“humps”) on the epithelial side of the basement membrane. -Commonly reported symptoms include: 1. In some patients.html Rickets = Defective mineralization of the matrix occurs in growing bones causing weight- .jpg Poststreptococcal glomerulonephritis (PSGN). Affected segments cause narrowing of the vessel with a decrease in blood supply to the perfused areas. Sudden vision loss is a dreaded complication of temporal arteritis. http://www. Fatigue.com/lectures/temporal. 3. These deposits are composed of immune complexes. which involves all lobules of all glomeruli is the result of leukocyte infiltration and endothelial and mesangial cell proliferation..features. and low C3 concentration. this condition is also called giant cell vasculitis. The hypercellularity. -Cryoglobulins may be present in serum. and thickening found on palpation of the temporal area. On immunofluorescent microscopy. http://www.. Craniofacial pain syndromes: Jaw claudication. This tends to appear during mastication when the blood supply to the corresponding areas does not increase normally due to the narrowing of the arterial lumens. Sometimes patients have scalp tenderness with hair combing.com/ki/journal/v54/n67s/fig_tab/4490515f1.Whereas C3 levels are decreased in almost all patients with PSGN (suggesting activation of the alternative complement pathway).pathguy.ed. torso. 2. =enlarged hypercellular glomeruli . fever and weight loss may also occur. -The median age of onset of the temporal arteritis is 65 years.gif http://www. proteinuria and urine RBC casts are present in a patient with hypercellular glomeruli on light microscopy -Lab findings : elevated titers of anti streptococcal antibodies (anti-Streptolysin 0. anti-DNAse B. It is characterized by neck. pain. C4 levels are slightly low (suggesting the possibility of classical pathway activation as well). however.

jpg Hemosiderin -Golden yellow or brownish cytoplasmic granules may be either lipofuscin or hemosiderin. however the bone resorption in hyperparathyroidism mainly involves cortical bones. hypocalcemia.” http://www. colorless potassium ferrocyanide is converted by iron to blue-black ferric ferrocyanide. After leaking from congested capillaries.edu/diagradiology/TF/MS/MS05. In the Prussian blue histochemical reaction. hypophosphatemia.wellesley. New collagen is laid down in a haphazard manner compared to the linear manner found in normal bones. The Prussian blue stain.Histologically vitamin D deficiency is characterized by an increase in unmineralized osteoid and widening between osteoid seams. The latter can be measured by bone histomorphometry and by double tetracycline labeling. softening of the skull (craniotabes).jpg Paget’s disease = seen in elderly patients and involves only focal points of the skeleton.edu/stat. these iron-containing macromolecules are . which detects intracellular iron.000/902.ubperiostealResorption.rad.gif http://www.. hypertonia. bony prominence at the costochondral junction (rachitic rosary)..jpg Hyperparathyroidism . -Vitamin D deficiencies can be from poor sunlight exposure. indentations in the lower ribs (Harrison’s sulci). -The disease process starts as marked.net/Answers/pagets..wayne. -When there is increased intravascular pressures in the pulmonary capillary bed. Increased resorption of cortical bones results in subperiosteal thinning. an inadequate diet or defective absorption of vitamin D http://familydoctor.Par.0001. .increases osteoclastic activation resulting in increased bone resorption.bearing bones to bow laterally (genu varus).washington.mikety..Image.med. local osteoclastic activation followed by increased osteoblastic activity. a characteristic feature of hyperparathyroidism. and growth retardation.html http://www.org/online/etc.edu/Chemistry/chem227/lipids/ricketslegs. The net result is the focal formation of abnormal bone. irregular sections of lamellar bone are linked by areas of previous bone resorption known as “cement lines. can differentiate the two. iron-containing proteins and erythrocytes are extravasated into the alveoli. http://www. The end product is a mosaic of lamellar bone.

jpg Acanthosis = increase in thickness of the stratum spinosum (the prickle cell layer). especially if systemic antigen exposure (eg..ucsf.jpg http://www. encrusted lesions that may evolve into thickened.htm .rch. atopic dermatitis. -Allergic contact dermatitis arises when antigens at the epidermal surface are selected by Langerhans cells and carried into draining lymph nodes where they are presented by these Langerhans cells to naive CD4 T cells.phagocytosed by macrophages and converted to hemosiderin.com/1471-2407/6/87/figure/F3 Eczematous dermatitis = erythematous. papulovesicular. The intercellular bridges become more distinctive in an edematous background and the epidermis is often described as appearing “spongy.com/lectures/heart_failure_cells.biomedcentral. where they incite an inflammatory response within 24 hours of antigen re-exposure. acute eczematous dermatitis is characterized by an epidermal accumulation of edematous fluid in the intercellular spaces (spongiosis). then the inflammation is usually restricted to the superficial dermis. The T cells are activated and migrate to the skin.com/issue009/case09/diagnos3..edu/lm/Der.. http://missinglink. Psoriasis is commonly associated with acanthosis. -The conditions included under the heading of eczematous dermatitis can be separated into five distinct categories: allergic contact dermatitis. scaly plaques.s/spongiosis_mid_power.ucsf.jpg http://www. the edema can become so marked as to form intraepidermal vesicles by tearing the desmosomes apart.ages/Acanthosis_2x-201. or “heart failure cells”) indicate that episodes of pulmonary congestion and edema associated with chronic left-sided heart failure occurred previously.pathguy. While still “wet” these lesions are prone to bacterial superinfection and can develop a yellow crust.jpg http://www. This layer is situated between the granular cell layer and the basal layer of the epidermis.edu/lm/Der. photo-eczematous dermatitis. and primary irritant dermatitis. http://www. A superficial perivascular infiltrate of lymphocytes and eosinophils may also be seen. to drugs) has occurred.. When present this infiltrate typically extends to include the deeper vessels.thejcdp. http://missinglink.au/emplibrary/rchcpg/eczema_erythema2. Cutaneous delayed hypersensitivity in the form of spongiotic dermatitis is the end result. -Histologically. weeping. Hemosiderincontaining alveolar macrophages (also known as siderophages.” Eventually.org. drug-related eczematous dermatitis. Should the dermatitis be secondary to contact with a surface antigen.

Liquefactive necrosis usually occurs in the CNSI in sites of ischemic strokes. eventually lysis. It is characterized by relative preservation of cell outlines in the necrotic tissue. Organ ischemia (especially in myocardium or kidney) is the classic example of coagulative necrosis. are associated with coagulative necrosis.ic_keratosis_low_power. which signals incomplete keratinization. where individual cells die in isolation.jpg http://library.geocities. premature keratinization of individual keratinocytes.org/1502/case_presentations/darier/3. actinic keratosis) in other areas. The nucleus shrinks and there is chromatin clumping (pyknosis). necrosis is associated with the death of a large number of cells.jpg Tissue Necrosis = cell death that occurs in living tissue after exogenous injury. Fat necrosis is seen in acute pancreatitis. Most exogenous injuries..edu/lm/Der. Pancreatic enzymes. 3. -Tissue necrosis can occur in a number of distinct morphologic patterns: 1. Enzymes released from these cells injure the surrounding tissue leading to necrosis of cells not affected by the initial stimulus.Dyskeratosis = abnormal. Unlike apoptosis..jpg Hyper parakeratosis =retention of nuclei in the stratum corneum.com/sampurnaroy2001/lp1. 2. fragmentation (karyorrhexis) and. This finding is normal on mucous membranes.med.edu/kw/derm/mml/24830096. but suggests abnormality (eg. http://www. http://missinglink. Coagulative necrosis is the most common variant.utah. Cell cytoplasm becomes eosinophilic due to protein denaturation. The dyskeratotic cells are strongly eosinophilic and may have a small.cdlib. http://dermatology.jpg Hypergranulosis =excessive granulation in the stratum granulosum of the epidermis and is seen in conditions such as lichen planus. including a brown recluse spider bite .ucsf. including . Necrotic cells undergo fragmentation and are phagocytized by macrophages with the formation of a cystic cavity. basophilic nuclear remnant. Dyskeratosis can be found in diseases such as squamous cell carcinoma.

jpg DIFF: -Mutation of the Rb tumor suppressor gene =development of retinoblastomas and osteosarcomas. Normally. and adrenal cortex. which plays an essential role in maintaining the integrity of the human genome. Carcinoid syndrome -The vasoactive substances secreted by tumors in extra-intestinal locations are not filtered by the liver -If a carcinoid tumor is confined to the intestine. -The APO (adenomatous polyposis coli) gene mutation is found in patients with familial polyposis syndromes. such as the lung). Inheritance is autosomal dominant. digest the parenchyma with formation of fatty acids. 4. . Saponification (soap formation) occurs when fatty acids combine with calcium.lipases. as well as sarcomas and leukemias. the tumor metastasizes to the liver (or is present in an extra-intestinal site. -Mutation of NF2= risk for developing neurofibromatosis type 2. and are seen in the majority of sporadic human cancers. This gene is responsible for maintaining low levels of β-catenin (which is oncogenic) and for intercellular adhesion. Patients present with bilateral acoustic neuromas (schwannomas of the cerebellopontine angle).Mutation of the BRCA-1 tumor suppressor gene=risk for breast and ovarian cancers. so patients do not develop clinical manifestations. Caseous necrosis occurs in tuberculosis.fr/Database/p53_cancer/image_cancer/lfs1. the liver does not metabolize the vasoactive secretory products and carcinoid syndrome ensues. brain. Patients often have a family history of multiple cancers in individuals less than 45-years-old. Symptoms include bilateral hearing loss vertigo and tinnitus. Necrotic tissue has a “cheesy” appearance and consists of fragmented cells and acellular material. -The p53 gene codes for the p53 protein. http://p53. . somatic mutation of the second allele is needed for tumor development. These patients develop malignant tumors at a young age (<45 years old). Li-Fraumeni syndrome =genetically predisposed to the early development of cancer. its secretory products are metabolized by the liver. The syndrome is the result of a mutation in the p53 gene. Cells with irreversible DNA damage are not allowed to divide and proceed instead to apoptosis. . If however.Patients with Li-Fraumeni syndrome inherit one mutated allele of p53. Mutations of p53 can be acquired during one’s lifetime.free. sporadic colon cancer and melanomas. p53 causes cells with mutant DNA to arrest in the G1/S stage of the cell cycle until the damage is repaired. The most common malignancies in Li-Fraumeni syndrome are tumors of the breast.

edu/lumen/MedEd/orfpath/images/11-1-1. not Dubin-Johnson syndrome. Confirmation can be obtained by evaluating the urinary coproporphyrin for unusually high levels of coproporphyrin I. Pernicious anemia = immune-mediated destruction of gastric mucosa. Once the number of parietal cells has been sufficiently depleted and the stores of vitamin B12 are exhausted. pernicious anemia classically manifests with symptoms such as fatigue and paresthesias.luc.Dubin-Johnson syndrome = a defect in the hepatic excretion of bilirubin glucuronides across the canalicular membrane.mfi. Over time. though a dense pigment composed of epinephrine metabolites within the lysosomes can be seen. -Serum bilirubin levels usually range from 2-5 mg/dL but can also be normal or extremely elevated (20-25 mg/dL). or oral contraceptive usage. The icterus may be so mild as to only become evident in the context of a trigger such as illness. Histological features are normal. 3) megaloblastic changes in mucosal cells. no treatment is necessary and the prognosis is excellent. -Clinically icterus is evident.dk/ppaulev/chapter22/images/22-9. Most patients are asymptomatic. pregnancy. 2) marked lymphocytic and plasma cell infiltration. -Grossly. -For the diagnosis of Dubin-Johnson syndrome to be made. http://faculty. with some complaining of nonspecific issues (eg. including the complete blood count and liver function profile.jpg http://www. though the physical examination is typically otherwise normal. Because this condition is benign. Routine laboratory testing is unremarkable. conjugated hyperbilirubinemia with a direct bilirubin fraction of at least 50% and an otherwise normal liver function profile must be present. this damage results in chronic atrophic gastritis. round platelike cells in the periphery of upper-layer glands. the liver is strikingly black. Individuals with this rare. a condition characterized by: 1)loss of the intrinsic factor.jpg DIFF: Impaired bilirubin conjugation is seen in conditions such as Crigler-Najjar syndrome and Gilbert syndrome.jpg http://www.secreting parietal cells in the upper glandular layer.une.cytochemistry.htm -the parietal cells subject to pernicious anemia-induced atrophy are the oxyntic (pale pink). fatigue. benign condition have predominantly conjugated chronic hyperbilirubinemia that is not associated with hemolysis.meddean. http://www. weakness).net/microanatomy/digestive/stomach.ku.edu/com/abell/histo/fundiglandw. abdominal pain. These cells secrete hydrochloric acid and intrinsic factor .

.jpg M. the macrophages undergo epithelioid and Langhans giant cell transformation and fibroblasts are activated. This hypersensitivity reaction stems from the TH1 lymphocyte stimulation of both macrophages and CD8+ cytotoxic T lymphocytes.edu/chapter4/images4/4-2L. Caseous necrosis occurs through an incompletely understood mechanism. Reactive arthritis may be part of Reiter’s syndrome. Chlamydia.JPG http://www.neoucom. tuberculosis infection. It is often associated with temporal bone fracture. It most often occurs due to rupture of berry aneurysms or arteriovenous malformations of the posterior communicating.ah_coronal_berry_2_500. tuberculosis infection = granulomatous inflammation with caseous necrosis. this immune response is essential in containing the organism and preventing disseminated infection. but is believed to be largely due to a T lymphocyte-mediated delayed type hypersensitivity reaction elicited by M. followed by loss of consciousness.strokecenter. conjunctivitis and urethritis typically in the setting of Chlamydial infections. -Delayed-type hypersensitivity plays an important role in the host defense against M. an HLA-B27 spondyloarthropathy involving the triad of reactive arthritis.org/patien. . Clinical presentation is characterized by a “lucid interval”. tuberculosis.The tissue destruction caused by M. Reactive arthritis = a spondyloarthropathy that tends to affect HLA-B27 positive individuals following infections with Campylobacter. and is located between the bone and dura mater.. anterior communicating or middle cerebral arteries. Shigella. -Joint aspirates are always sterile (hence it is a reactive not infectious arthritis). Although the associated tissue damage is an unpleasant consequence. tuberculosis infection is the direct result of host immune activation and inflammation through a type IV delayed-type hypersensitivity reaction. Subdural hematoma=between the dura mater and arachnoid.Epidural hematoma=due to tear of the middle meningeal artery.edu/chapter4/images4/4-3L. The characteristic pathologic lesion consists of granulomatous inflammation and caseous necrosis. and is caused by tearing of the bridging cortical veins. or Bartonella.. Salmonella Yersinia.neoucom.JPG http://neuropathology. Subarachnoid hemorrhage=between the arachnoid and pia mater. Ultimately. It typically presents as an asymmetric arthritis of the large joints. http://neuropathology.

leading to refractory peptic ulceration and diarrhea (Zollinger-Ellison syndrome). Large pituitary tumors with suprasellar extensions are likely to cause visual disturbances (usually bitemporal hemianopsia). aureus settles on the valve leaflets because of the turbulence of the blood flow at these sites. diaphoresis. . About 70% of patients with MEN type I have endocrine pancreatic tumors that usually secrete gastrin. or vasoactive intestinal polypeptide. S. and it moves by hematogenous spread to the endocardium. thyroid nodule. In patients other than IV drug abusers. endocrine tumors of the pancreas in MEN type 1 secrete other hormones such as insulin. (Although pheochromocytomas are also a feature of MEN 2B. not all features have to be present to suggest a MEN syndrome. pituitary tumor. and send septic emboli to the lung (in the case of right heart endocarditis) and to the brain and systemic circulation (in the case of left heart endocarditis). aureus occurs from a primary disease process such as surgical I & D of an abscess or from infected IV catheters such as central lines. Pituitary tumors are present in 50% of patients with MEN type 1. which causes massive diarrhea. and Marfanoid habitus of this man indicate MEN type 2B. dissemination of S. which causes hypoglycemia.) Even without the mucosal neuromas. bovis is associated with colonic cancer in approximately 25% of cases. rupture the chordae tendineae. aureus has the ability to cause perforations in the heart valves. and headaches. Right-sided endocarditis = commonly occurs in IV drug users and is typically caused by S. aureus. All patients with medullary thyroid cancer should be screened for pheochromocytoma by clinical and biochemical assessment. S. Episodic secretion of catecholamines by pheochromocytomas causes episodic increases in blood pressure. and bacteremia or endocarditis caused by S. Streptococcus bovis = part of the normal flora of the colon. Hypercalcemia from hyperparathyroidism is the most common manifestation of MEN type 1 and is caused by parathyroid chief cell hyperplasia. DIFF: -The mucosal neuromas. flushing. one would suspect a MEN syndrome as about 20% of medullary thyroid cancers are familial. Rarely.MEN type 1 syndrome = hyperparathyroidism. and pancreatic tumor. The production of other pancreatic endocrine hormones is very rare.

g. focal neurological deficits are not present. Arteriovenous malformation also predisposes certain individuals to subarachnoid hemorrhage. -In SAH blood accumulates between the arachnoid and pia mater. with the anterior communicating artery being the most common site. Eikenella and Kingella). Histoplasma. Cerebral amyloid angiopathy = occurs in elderly patients. http://faculty.gif Acute pancreatitis -Gallstones and alcoholism are the most common causes of acute pancreatitis.it1Review/endocarditis. Coxiella.Culture-negative endocarditis -special serologies and cultures need to be sent for organisms that do not grow in standard blood culture. Bartonella. Lumbar puncture reveals gross blood or xanthochromia . These bleeds usually affect small areas of the cerebral hemisphere and present with headache and focal neurologic deficits (paresis. -Saccular (berry) aneurysms are the most common cause of SAH. http://wiki.” Fever and nuchal rigidity may also be present. Usually.org/wiki/images/a/a8/CAA1. It may be asymptomatic or may lead to recurrent intracerebral hemorrhage. Chlamydia and the HACEK organisms (Haemophilus.edu/mlj. but are not limited to.cns. Berry aneurysms are associated with Marfan syndrome Ehlers-Danlos syndrome.. sensory loss etc).. Mycoplasma. and adult polycystic kidney disease. l .jpg Subarachnoid hemorrhage (SAH) =abrupt onset of a severe headache often described by patients as “the worst headache of my life. Actinobacillus.matcmadison. -Gallstones typically affect middle-aged and older patients unless there is a predisposing condition (e. Cardiobacterium. These aneurysms usually occur at the circle of Willis. young patients with sickle cell disease are at increased risk for bilirubin gallstones). These organisms include. CT scan without contrast is diagnostic.

uptodate. Other serosal surfaces including the lung pleura may be involved. measles EBV. leukocytosis.g.htm Dressler’s syndrome =late-onset post-myocardial infarction pericarditis =typically begins one week to a few months after a myocardial infarction in fewer than 4% of patients. furosemide. NSAIDS.. Thus.geKey=card_pix/normal3. in other words. also after coronary artery bypass grafting) 7. which is adjacent to phrenic nerve afferents supplying the diaphragm. Typical features include fever. If serum triglyceride levels are higher than 1000 mg/dL. Hypercalcemia -High levels of triglycerides lead to increased production of free fatty acids.. and chest radiograph evidence of new pericardial or pleural effusions. A recent ERCP (endoscopic retrograde cholangiopancreatography) procedure is the third most common cause of acute pancreatitis 2. The inflammation affects the adjacent visceral and parietal pericardium. Mycoplasma pneumoniae.com/online/con. Pericarditis (post MI) =sharp and pleuritic nature of this patient’s new pain suggests pericardial involvement. pancreas divisum) or of the ampullary region (choledochal cyst stenosis of sphincter of Oddi) 6. . and Mycobacterium tuberculosis) 4.. Coxsackie virus. The exacerbation with swallowing indicates that the posterior pericardium may be involved.Lss common causes of acute pancreatitis 1. Dressler’s syndrome generally responds to aspirin. VZV.fibrinous_pericarditis. This type of early post-MI pericarditis is generally short-lived and disappears with 1 to 3 days of aspirin therapy.jpg http://www. Drugs (e. and/or glucocorticoids. Infections (mumps.. and the radiation into the neck suggests involvement of the inferior pericardium. the pericardium is usually diffusely inflamed. azathioprine. Normally fatty acids exist in serum bound to albumin. cancer. valproic acid) 3. hypertriglyceridemia causes acute pancreatitis via direct tissue toxicity. Surgery (particularly of the stomach and biliary tract. http://www. Thus. -Dressler’s syndrome is thought to be an autoimmune polyserositis provoked by antigens exposed or created by infarction of the cardiac muscle. pleuritis. the concentration of free fatty acids exceeds the binding capacity of albumin and leads to direct injury to acinar cells and pancreatic capillaries. sulfasalazine. pericardial friction rub. -A fibrinous or serofibrinous early-on set pericarditis develops in about 10-20% of patients between days 2 and 4 following a transmural myocardial infarction. the inflammation is usually localized to the region of the pericardium overlying the necrotic myocardial segment. Hypertriglyceridemia 5.ro/patho.pathologyatlas. This pericarditis is a reaction to the transmural necrosis. Structural abnormalities of the pancreatic duct (strictures.

Fourth-order neurons are found in the primary somatosensory cortex in the parietal lobe. Distended ventriculi distort the surrounding white matter that carries cortical afferent and efferent fibers (corona radiata). Additionally. http://webhome.htm Normal pressure hydrocephalus (NPH) =Gait abnormality and urinary incontinence are the first symptoms .drome/dresslerscorrect. are sometimes reversed by lowering the CSF volume.idirect. The areas commonly damaged in this condition are the ventral white commissure and the ventral horn..The order of symptoms are important in distinguishing NPH from Alzheimer and other dementing diseases.asap. cerebrospinal fluid-filled cavities (called “syrinx”) form.ts/webcontent/bqjpg141. -The ventral white commissure is the area of decussation of the fibers of the lateral spinothalamic tract. -LMN lesions of syringomyelia are characterized by areflexia. progressive dementia and emotional blunting will occur. This tract transmits pain and temperature sensation from receptors to the somatosensory cortex. http://www.com/~braino.org/images/abnormal_50.org/stellent/.html http://www..com/a.devpath_14_spinalcord.jpg Syringomyelia =classic presentation of disproportionate loss of pain and temperature sensation. Touch..http://www. flaccid paralysis. .order neurons decussate in the ventral white commissure and ascend in the contralateral lateral funiculus. These cavities enlarge over time and destroy adjacent portions of the spinal cord. usually in the cervical region of the spinal cord. Note that no permanent damage to the brain structures occurs. The axons of the second.. Its first-order neurons are located in the dorsal root ganglia and the second-order neurons are found in the dorsal horn. -Pathophysiology and etiology are debated. -occurs in elderly patients. including dementia. therefore symptoms of NPH. with slow accumulation of CSF.learningradiology. fasciculations and atrophy of the intrinsic muscles of the hands.jpg . CT scan will show symmetricallyenlarged ventriculi.. Third order neurons are located in the ventral posterolateral nucleus of the thalamus. Pressure remains normal in NPH because gradual ventricular distention accommodates the CSF increase. -Destruction of the ventral white commissure leads to loss of pain and temperature sensation in the arms and hands bilaterally. Ataxic gait and urinary incontinence occur due to traction of the sacral motor fibers that innervate the legs and the bladder.thebarrow.. In syringomyelia. but most agree that a gradual decline in the reabsorptive capacity of the arachnoid villi.left untreated. Distention of the periventricular limbic system leads to progressive dementia and emotional blunting. vibration and position senses are preserved in syringomyelia. is the root of the problem.

-Calcium channel blockers are used to treat and prevent attacks in patients with Prinzmetal’s angina. chest pain. -Bone marrow examination can distinguish a myeloproliferative disease with increased bone marrow cellularity from aplastic anemia. occurring during the nighttime hours and accompanied by temporary ST. -In aplastic anemia. RET proto-oncogene mutations are also commonly found in sporadic medullary thyroid cancers. aleukemic leukemia. very low reticulocyte count. and STsegment elevation. and can result in transient transmural ischemia with ST-segment elevations on ECG. and lack of splenomegaly. bone marrow hematopoietic elements are replaced by fat cells and fibrous stroma. where the bone marrow is markedly hypocellular. The RET proto-oncogene codes for a membrane-bound tyrosine kinase receptor involved in cell cycle regulation.segment elevations on Holter monitoring.med. -Nitrates are used to treat attacks in patients with Prinzmetal’s angina. -The ergonovine test is the most sensitive provocative diagnostic test for coronary vasospasm. Aplastic anemia. Ergonovine is an ergot alkaloid that constricts vascular smooth muscle by stimulating both alpha-adrenergic and serotonergic receptors. -The coronary artery vasospasm may occur near sites of atherosclerosis. and myelodysplastic syndrome. Medullary thyroid cancers = tumors of parafollicular calcitonin-secreting C-cells. -Germline mutations of the RET proto-oncogene are present in more than 95% of patients with familial medullary thyroid cancer. Bone marrow aspiration typically produces a “dry tap. 80% of medullary thyroid cancers are sporadic and 20% are familial (as in the MEN type 2 syndrome).html .Prinzmetal’s (variant) angina =Episodic and transient anginal chest pain. In patients with hypercontractile coronary artery segments (as in Prinzmetal’s angina).utah. low doses of ergonovine induce coronary spasm. a patient with pancytopenia and splenomegaly is very unlikely to have this condition.” The absence of splenomegaly is key in diagnosing aplastic anemia. generally occurs at rest. The differential diagnosis for pancytopenia without splenomegaly includes: severe vitamin B12 and folic acid deficiency anemia.edu/WebPath/ENDOHTML/ENDO028. -Inactivating mutations of p53 are fairly common in anaplastic thyroid cancer http://library. =pancytopenia.

ic. derived from macrophages and smooth muscle cells (SMC) that have engulfed lipoprotein (predominantly LDL) which has entered the intima through an injured leaky endothelium. shoulder and pelvic girdle.. Polymyalgia rheumatica .ma. Muscle pain and stiffness are more severe in the morning and are often exacerbated by exercise.uk/~ajm8/BioFl.ictures/70fatty_streak. Whereas some fatty streaks may be precursors of atheromatous plaques not all tally streaks progress to these more advanced atherosclerotic plaques. -Fibromyalgia affects women much more often than men. http://www. Atherosclerosis -fatty streaks = the earliest lesions in the progression to atherosclerosis. and commonly manifests between 20 and 50 years of age. -Fatty streaks are composed of intimal lipid-filled foam cells.. -A characteristic physical examination finding is the presence of multiple symmetrically distributed tender spots over the patients muscles joints and tendons such as over the spine of the scapula the lateral epicondyle and the medial fat pad of the knee . poor sleep and emotional disturbances. The foamy appearance is due to intracellular lipid-containing phagolysosomes. Because fatty streaks are not significantly raised they do not disturb normal blood flow.Fibromyalgia = chronic disorder characterized by widespread musculoskeletal pain in association with stiffness. They may contain a few lymphocytes.Tenderness in eleven of eighteen predetermined painful points is required for a diagnosis of fibromyalgia. The precise etiology of fibromyalgia is still unknown but it is presently postulated to be produced by a genetic predisposition to heightened pain sensitivity or pain misperception that results following a stressor such as an infection. They can be seen in the aortas of children less than 1 year old and are present in the aortas of all children over 10. Weight loss.jpg . -Fatty streaks begin as multiple yellow spots approximately 1 mm in diameter which join to form streaks approximately 1 cm long.ac. Polymyalgia rheumatica occurs in approximately half of patients with temporal arteritis.affects patients over 50 years old with morning stiffness of muscles of the neck. paresthesias. but foam cells are the predominant constituents. fever and an increased ESIR are characteristic.

Hereditary breast cancer =associated with mutation of BRCA-1 and BRCA-2. These are tumor suppressor genes that function in gene repair and regulation of the cell cycle. Mutation of these genes increases the risk of breast and ovarian cancer. -BRCA mutations are inherited as an autosomal dominant trait. The BRCA-1 gene is located on chromosome 17 and is a tumor suppressor gene. It codes the protein that acts to control the cell cycle and plays a role in gene repair and transcription. Women who carry BRCA-1 mutation have 70-80% lifetime risk for development the breast cancer. Their risk of ovarian cancer is also increased by 40% compared to the general population.

Adrenal crisis =The presence of shock in combination with hyponatremia, hyperkalemia, and hypoglycemia - fever, vomiting, nuchal rigidity and petechial rash = clinical signs strongly suggestive of meningococcal meningitis. The association of Neisseria meningitidis septicemia with adrenal hemorrhage is called Waterhouse-Friderichsen syndrome. Although Waterhouse-Friderichsen syndrome can occur at any age, it is more commonly seen in children.

Spherocytosis. =Hereditary spherocytosis is (usually) an autosomal dominant condition that results from red cell cytoskeleton abnormalities—most commonly, spectrin deficiency. The definitive test for spherocytosis is a positive osmotic fragility test. =anemia, an elevated LDH, and indirect bilirubinemia, suggesting hemolytic anemia. The lysing of blood cells when incubated in hypotonic saline describes a positive osmotic fragility test -Pigmented gallstones are a complication of any hemolytic anemia. In chronic hemolysis, the increased bilirubin from lysed red blood cells precipitates as calcium bilirubinate, forming pigmented stones in gallbladder. “Mature” pigmented gallstones are a mixture of calcium bilirubinate, bilirubin polymers, and calcium salts. http://www.unm.edu/~mpachman/Blood/spherocytosis.jpg

Multiple myeloma =when an elderly patient presents with the following combination of findings: 1. Easy fatigability (due to anemia) 2. Constipation (due to hypercalcemia) 3. Bone pain, most commonly in the back and ribs (due to production of osteoclast activating factor by myeloma cells and subsequent bone lysis) 4. Renal failure -A number of factors contribute to renal failure in multiple myeloma: hypercalcemia, hyperuricemia, infiltration of the kidney by myeloma cells, AL amyloidosis, and frequent infection. The role of these factors in MM-associated renal disease varies from patient to patient. Light chain deposition disease, however, is always present in multiple myeloma. - In small amounts, Bence Jones proteins (light chains) are filtered by the glomerulus, and then reabsorbed in tubules. When levels exceed the reabsorptive capacity of tubules however, these light chains precipitate with Tamm Horsfall protein and form casts. These casts compress tubular epithelium, obstruct tubular lumens, and thus impede renal function. Bence Jones proteins are also directly toxic to tubular epithelial cells, causing atrophy. On light microscopy, numerous, large, glassy, eosinophilic casts are seen in tubular lumens. http://library.med.utah.edu/WebPath/HEMEHTML/HEME070.html http://granuloma.homestead.com/myeloma_kidney_YR1432-01.jpg

Small cell carcinomas - show evidence of neuroendocrine differentiation. These tumors stain for neuroendocrine markers, such as neuron-specific enolase, chromogranin, and synaptophysin. Some small cell carcinomas express neurofilaments. -Neurosecretory granules can be identified in the cytoplasm of the tumor cells on electron microscopy. The fact that small cell carcinomas frequently synthesize hormone-like substances also suggests a neuroendocrine derivation. -Small cell carcinoma of the lung (also called oat cell carcinoma) is the most aggressive type of lung cancer. It is characterized by rapid local invasion and distant spread. Most patients have distant metastases at the time of diagnosis. Although small cell carcinoma is sensitive to chemotherapy and radiation, the 5year survival rate of these patients is very low. http://library.med.utah.edu/WebPath/LUNGHTML/LUNG074.html http://library.med.utah.edu/WebPath/LUNGHTML/LUNG075.html DIFF: -Expression of ECE-receptors, mucin and surfactant-associated proteins is seen in non-small cell carcinomas. -Vimentin is an intermediate filament found within cells of mesenchymal origin. It is used in diagnosing sarcomas. -Leukocyte common antigen (LCA or CD 45) = for differentiating malignant lymphomas from poorly differentiated neoplasms of other types.

Glucagonomas =rare pancreatic tumors that characteristically present with necrolytic migratory erythema, an elevated erythematous rash typically affecting the groin area. -Other clinical features of glucagonomas include: hyperglycemia, stomatitis, cheilosis, and abdominal pain. Diagnosis is made by the measurement of serum glucagon levels. -Glucagon is a hormone secreted by the alpha-cells of the pancreatic islets of Langerhans. The three other types of pancreatic endocrine cells in the islets include: insulin-secreting beta-cells, somatostatin-secreting delta-cells, and pancreatic polypeptide-secreting PP-cells. http://imaging.cmpmedica.com/consu...2007/0711ConPEGlucagoA.jpg http://www.scielo.br/img/revistas/clin/v63n2/a16fig06.jpg

Pancreatic VIPoma = intractable diarrhea, metabolic acidosis, and hypokalemia. Additionally, these patients are usually hypotensive secondary to both dehydration as well as the vasodilatory effects of VIP. http://www.surgicalroundsonline.co.../2007-09/2007-09_01-04.jpg

Somatostatinoma =a rare tumor of the pancreatic delta-cells = abdominal pain, gallbladder stones, constipation, and steatorrhea. These manifestations are due to somatostatins inhibition of the secretion of insulin, glucagon, gastrin, cholecystokinin, and secretin, as well as its inhibition of gastrointestinal motility.

Ectopic ACTH production = present with rapid-onset hyperpigmentation, proximal muscle weakness, hypokalemia, hyperglycemia, and markedly elevated levels of serum ACTH.

Juvenile pilocytic astrocytomas = usually arise in the cerebellum, brainstem, hypothalamic region, or optic pathways. Microscopically pilocytic astrocytomas are well-differentiated neoplasms comprised of spindle cells with hair-like glial processes that are associated with microcysts. These cells are mixed with Rosenthal fibers and

granular eosinophilic bodies. http://www.uhrad.com/mriarc/mri052.htm http://www.pedsoncologyeducation.com/images/jpabiphasicx50.jpg

Medulloblastoma (primitive neuroectodermal tumor, or PNET) = the second most common posterior fossa tumor in children. On microscopic examination, cells are small and poorly differentiated, with scant cytoplasm and little stroma. A high mitotic index is common. Classic Homer-Wright rosettes can be seen in one fifth of cases. http://moon.ouhsc.edu/kfung/IACP-O...Q-Text/N1-TU-01-17-Ans.htm

Ependymomas = account for 10% of posterior fossa tumors in children. - Intracranial lesions usually occur infratentorial, arising from the roof of the fourth ventricle in children, while spinal ependymomas typically occur in adults. -Histologically, ependymal pseudorosettes with glial fibrillary acidic protein (GFAP)—positive processes tapering toward blood vessels characterize ependymomas. http://library.med.utah.edu/WebPath/CNSHTML/CNS122.html http://library.med.utah.edu/WebPath/CNSHTML/CNS121.html

Glioblastoma multiforme =occur most often in the subcortical white matter of the cerebral hemispheres. When a tumor in the frontal cortex spreads across the corpus callosum into the contralateral hemisphere, it creates the appearance of a bilateral symmetrical lesion, hence the term “butterfly glioma.” GBMs are composed of poorlydifferentiated often pleomorphic astrocytic cells with marked nuclear atypia and brisk mitotic activity. Necrosis is an essential diagnostic feature, and prominent microvascular proliferation is common. http://library.med.utah.edu/WebPath/CNSHTML/CNS139.html

Neuroblastomas = the most common extracranial solid tumors occurring in children. -Undifferentiated neuroblastomas are small, round, blue-cell tumors. A neuritic process, also called neuropil, is a pathognomonic feature of neuroblastoma cells.

dementia. The most important biologic marker is MYCN (N-MYC) of chromosome 2. Other precipitating factors include coughing. Mallory-Weiss syndrome is very commonly associated with alcoholism. The intensity of hemorrhage and amount of blood loss varies widely according to the length and depth of the tears..edu/lectures/gi/esoph-a/10.Tremors. depression or a loss of interest..NSEI chromogranin. Slow movements. About 10% of all upper gastrointestinal bleeds are from Mallory-Weiss syndrome. as when happens during retching and vomiting. learning new information. anger.Loss of neurons in the caudate nucleus and putamen is characteristic.med. hiccupping. .stanford. Decreased cognitive abilities. answering questions and remembering important information._images/neuroblastoma1. and abdominal trauma. -Mallory-Weiss tears can be asymptomatic or can lead to gastrointestinal hemorrhage that manifests as hematemesis.pathology. http://www. other repeated abdominal straining. History of the disease in a first-degree relative is important for diagnosis. Mild balance problems .htm .folding/pics/HD_effect. http://surgery. .Early signs and symptoms of Huntington's disease often include: Personality changes.pitt.Young people who develop Huntington's disease may have signs and symptoms that mimic Parkinson's disease: Muscle rigidity.edu/pedia. and S-100 immunohistochemical stains are usually positive.. such as difficulty making decisions. More than 90% of patients have elevated urinary levels of homovanillic acid (HVA) and/or vanillylmandelic acid (VMA). but is almost never life-threatening.edu/group/pand. such as irritability. Acetylcholine and substance P in the striatum (caudate nucleus and putamen) -molecular = NMDA (N-Methyl-D-aspartate) receptors bind glutamate and cause neuronal death (NMDA-associated toxicity) -Huntington disease is inherited as an autosomal dominant trait with 100% penetrance. -loss of GABA.jpg Huntington disease =Involuntary choreiform movements.gif Mallory-Weiss syndrome =Longitudinal mucosal tears at the esophagogastric-squamocolumnar junction -Most commonly these tears occur secondary to rapid increase of intraabdominal and intraluminal gastric pressure. and behavioral abnormalities = a progressive neurodegenerative disorder with symptom onset usually at 3545 years old: average lifespan after diagnosis is about 15-20 years.. synaptophysin. Additionally hiatal hernias are found in about half of patients with Mallory-Weiss syndrome and are considered a strong predisposing factor.umich. Clumsiness http://www.

DM -Myocardial infarction is the most common cause of death in patients with diabetes. -diabetes is the strongest risk factor for coronary heart disease. Approximately 40-50% of patients with diabetes mellitus die secondary to coronary artery disease. For a person with diabetes the risk of dying from ischemic heart disease exceeds the risk of dying from any of the other causes listed. Even in the absence of other major risk factors for ischemic heart disease—hypertension hypercholesterolemia, and smoking—the relative risk of ischemic heart disease in diabetes is elevated. Lung abscesses Patients experiencing decreased consciousness (e.g. patients with a seizure disorder) may aspirate oropharyngeal contents, causing a lung abscess. On chest x-ray, a lung abscess appears as a cavitary lesion with an air-fluid level. -Peptostreptococcus and Fusobacterium species are components of the normal mouth flora. - Lung abscesses arising as a complication of aspiration typically contain mixed flora, often including these two species. Lung abscesses cause fever, weight loss, cough and foul-smelling sputum. There may also be anorexia, malaise, chest pain and clubbing. -Lung abscesses may develop by the following mechanisms: 1. Aspiration of oropharyngeal contents is the most common cause. These abscesses often contain Fusobacterium, Peptostreptococcus and Bacteroides species. Risk factors include all conditions associated with loss of consciousness, such as alcoholism, seizure disorders, prolonged anesthesia, and severe neurologic diseases. Aspiration-associated abscesses are found in the dependent parts of the right lung. 2. Lung abscesses may also occur as a complication of bacterial pneumonia. Predisposing factors include immunosuppression, old age and underlying chronic disease. Necrotizing pneumonias are usually nosocomial, caused by S. aureus, E. coli, K. pneumoniae or S. pneumoniae type 3. 3. In patients with septicemia or infectious endocarditis, there may be hematogenous spread of infection to the lung. Lung abscesses that develop in this manner are oftentimes multiple. The most common causative agents are Staphylococcus and Streptococcus species. E. coli and fungi may also be implicated. http://www.cvmbs.colostate.edu/ilm...pulmonary%20abscesses2.JPG http://www.szote.u-szeged.hu/radio/mellk1/amelk5a.htm

Brain tumors in adults -In adults, brain tumors are most commonly metastases from other cancers

especially those of the lung, breast, kidney, and skin (melanoma). On macroscopic examination, brain metastases appear as multiple wellcircumscribed masses at the junction of gray and white matter. Brain metastases are usually multiple. - The following types of primary brain tumors listed in order of frequency, are the most common in adults: 1. Glioblastoma multiforme (GBM) is a tumor that arises from astrocytes and is the most common primary cerebral neoplasm in adults. It is typically located within the hemispheres (in the frontal or temporal lobe or near the basal ganglia). GBMs may become significantly large and may cross the midline. On macroscopic examination GBMs are soft and poorly defined with areas of necrosis and hemorrhage. GBMs are highly- malignant tumors with a very poor prognosis: most patients die less than a year after diagnosis. http://library.med.utah.edu/WebPath/CNSHTML/CNS136.html 2. Meningiomas are derived from arachnoid cells and are the second most common brain neoplasm in adults. Meningiomas are benign and well circumscribed. They are located on the brain surface, where they are attached to dura. Meningiomas can be found over the lateral and parasagittal brain convexities falx cerebri, sphenoidal ridge and olfactory groove. http://library.med.utah.edu/WebPath/CNSHTML/CNS114.html 3. Acoustic neuromas are a special type of schwannoma that arise from Schwann cells of CN VIII; acoustic neuromas are found at the cerebropontine angle. http://www.ent.uci.edu/images/acoustic_neuroma_copy.jpg -oligodendrogliomas present as well-circumscribed gray masses. Calcifications may be visible; areas of necrosis and hemorrhages are not common. http://www.medi-fax.com/atlas/brai...igodendroglioma/case2.html

Metalloproteinases - are Zn-containing enzymes that degrade extracelluar matrix. They participate in the normal tissue remodeling and in tumor invasion through the basement membrane and connective tissue. - Penetration of the basement membrane distinguishes an invasive tumor from carcinoma in situ. This process includes the following steps: 1. Detachment of tumor cells from surrounding ceils occurs due to decreased expression of cell adhesion molecules in most tumors itis determined by downregulation of the adhesion molecules E-cadherins. 2. Detached tumor cells have the ability to adhere to basement membranes. Neoplastic cells may acquire this ability due to increased expression of laminin and other adhesion molecules. 3. Invasion of the basement membrane occurs due to secretion of proteolytic enzymes by the tumor ceils. A number of enzyme metalloproteinases play an active role in this process. Another important enzyme is the cathepsin D protease. -Metalloproteinases degrade components of the extracelluar matrix and basement membrane, composed primarily of laminin and collagens IV and VII. These enzymes participate in a number of physiologic processes, such as tissue

remodeling and embryogenesis. http://php.med.unsw.edu.au/cellbiology/images/4/4a/Cadherin2.gif

Retinopathy of prematurity -Respiratory distress in a premature neonate is most commonly due to pulmonary surfactant deficiency resulting in hyaline membrane disease. -Treatment involves administration of supplemental oxygen at high concentrations, nasal continuous positive airway pressure, and/or mechanical ventilation with intratracheal surfactant. One potential adverse effect of oxygen therapy is retinal damage. -Temporary local hyperoxia in the retina is thought to induce changes that cause up-regulation of proangiogenic factors such as vascular endothelial growth factor (VEGE) upon return to room air ventilation. Retinal vessel proliferation (neovascularization) and possible retinal detachment with blindness may result. This complication of neonatal respiratory distress syndrome is referred to as retinopathy of prematurity or retrolental fibroplasia. http://www.sciencedaily.com/images/2007/06/070624141851-large.jpg

Cystic medial degeneration =Myxomatous changes in the media of large arteries - Medial degeneration is characterized by the fragmentation of elastic tissue and by separation of the elastic and fibromuscular components of the tunica media by small, cleft-like spaces. These spaces become filled with amorphous extracellular matrix, and the normal elastic tissue is lost. Such medial degeneration is the frequent histopathological abnormality found in association with aortic dissections (dissecting hematomas) in humans. Aortic dissection can occur in inherited connective tissue disorders, especially in Marfan syndrome. Marfan syndrome is an autosomal-dominant defect in an extracellular glycoprotein called fibrillin-1 that causes a specific body habitus (tall and thin with spidery fingers) and an increased risk of aortic dissection. Fibrillin-1 is a major component of extracellular matrix microfibrils, which form scaffolding for elastic fibers. The weakness of the aortic media in Martan’s patients maybe mimicked by anti nutritional feeding of experimental animals. Ingestion of βaminopropionitrile, a chemical found in certain kinds of sweet peas, causes “angio lathyrism,” a change in the elasticity of the aorta. Note that aortic dissection in humans can occur without any identifiable histopathological abnormality of the aortic wall especially when hypertension is present. http://pathologyoutlines.com/images/softtissue/02_08L.jpg

Pseudoaneurysm = the entire wall of a blood vessel (usually arterial) ruptures. There is a breach in the original continuity of the adventitia (or epicardium). The resulting hematoma is then contained within a sac of the connective tissue surrounding the original point of arterial wall rupture. Examples are leaks at the anastomosis sites of vascular grafts and postinfarction myocardial ruptures that have been contained by pericardial adhesions. http://applications.spectrum-healt...types%20of%20aneurysms.gif

Giant cell arteritis (GCA) involves granulomatous inflammation of the media and fragmentation of the internal elastic lamina, perhaps due to autoimmunity to elastin. http://www.djo.harvard.edu/files/5077_728.jpg

Primary spontaneous pneumothorax = a pneumothorax in someone without pre-existing pulmonary disease and not caused by trauma or barotrauma. Though the exact pathogenesis of this condition is uncertain it is thought to result from rupture of apical subpleural blebs. Blebs are continuous, distended airspaces that range in diameter from <0.5 cm to more than 2.0 cm and sometimes form cyst- like sacs. Blebs may spontaneously rupture usually while the patient is at rest causing a pneumothorax. Tall thin males around the age of 20 are the most commonly affected. There is also an association with smoking.

Panacinar emphysema = occurs more commonly in the lower zones and anterior margins of the lung. This condition is associated with a1-antitrypsin deficiency. Centriacinar emphysema -The emphysematous dilatation has a predominantly upper lung lobe distribution but initially affects the respiratory bronchioles rather than the peripheral alveoli and alveolar ducts. This type of emphysema is strongly linked to smoking. http://www.geocities.com/drroy5/Emphysema1.JPG

the stroke volume decreases. tachycardia.com/fi. -IL-10 is an anti-inflammatory cytokine produced by macrophages and Th2 Thelper cells. and decreased urine output are observed. an acute phase cytokine produced by activated macrophages. When sepsis progresses. -IL-4 is a cytokine produced by Th2 T-helper cells. and distal hypoperfusion becomes evident. delayed capillary refill. Embolism is the most common cause of central retinal artery occlusion. It stimulates the growth of B cells and increases the number of Th2 T-helper cells at the site of inflammation.medschl. -Gamma interferon (INF-y) is produced by activated T cells and serves to recruit leukocytes and activate phagocytosis. -The most important mediator of sepsis is tumor necrosis factor alpha (TNF-a).s/2004RSPMay19_Figure1.topnews.gif DIFF -Amaurosis fugax http://www. Other cytokines responsible for inducing the systemic inflammatory response include IL-i and IL6.Early sepsis is characterized by increased cardiac output. and markedly elevated or decreased body temperature . peripheral vasodilation.. Central retinal artery occlusion =Acute and painless monocular vision loss .jpg -hypertensive retinopathy http://www-clinpharm.a.jpg . These findings develop within an hour of the event. which arises from the internal carotid artery...eyesite. These findings are explained by the fact that the macula has a separate blood supply from the choroid artery. while the rest of retina is supplied by the central retinal artery.mages/HT_retinopathy_4. cardiac output decreases. -The central retinal artery is a branch of the ophthalmic artery. and warm extremities . TNF-a). It stimulates the growth and differentiation of stem cells in the bone marrow. tachypnea.ca/7modules/Module7/jpg/Mod7_08.jpg -diabetic retinopathy http://www. IL-10 limits the production of pro-inflammatory cytokines (eg.red macula. -IL-3 is a cytokine produced by activated I cells. altered mental status. Specific funduscopic findings include a pale retina and a cherry.The vision loss includes the entire visual field and is often permanent.residentandstaff. Its main function is to stimulate neutrophil migration to the site of inflammation.in/health/files/diabetic-retinopathy. http://www. IL-3.cam. cool and clammy extremities.. Predisposing conditions include atrial fibrillation and carotid artery stenosis. gamma interferon IL-2. DIFF: -Leukotriene B4 is a metabolite of arachidonic acid. In advanced septic shock.Septic shock =infection + the tetrad of hypotension.

ver_iron_prussian_blue.com/lectures/iron_overload. however. hypogonadism). -Urinary retention results in increased pressure in the urinary tract and resultant reflux nephropathy. The disease is typically silent in early adulthood.kumc.leads to intermittent bladder outlet obstruction and overflow incontinence. men can present with signs and symptoms typical of hemochromatosis (eg. hesitancy. hepatomegaly. a rare malignant neoplasm of the endothelial lining of lymphatic channels. skin pigmentation. After entering menopause. Overflow incontinence is the next clinical stage. urgency nocturia. deranged glucose homeostasis.After the age of 40.0 grams of iron (primarily in the parenchymal organs) each year.. This usually signifies urinary retention.. The condition should be promptly treated as prolonged obstruction can cause permanent damage and chronic renal failure.-“pie in the sky” visual defect http://www2.gy/images/TemporalLobe. Ultimately. . she would not have accumulated significant quantities of iron until after menopause. manifesting only once at least 20 grams of iron have been accumulated.. As the prostate enlarges further and the bladder outlet obstruction worsens. atypical arthritis. -Women tend to present significantly later secondary to the protective effects of blood (iron) loss during menses or pregnancy.pathguy.jpg Lymphangiosarcoma -Persistent lymphedema (with chronic dilatation of lymphatic channels) predisposes patients to the development of lymphangiosarcoma. . abdominal pain. cardiac dysfunction.Early symptoms of BPH include frequency.5-1.. and weak urinary stream.gif Benign prostatic hyperplasia . A typical . patients experience a sensation of incomplete bladder emptying.edu/coa/Education. http://www. hydronephrosis and renal interstitial atrophy and scarring ensue. Hereditary Hemochromatosis = there is a defect in the intestinal absorption of dietary iron that results in the storage of 0. if a woman had a particularly heavy menstrual flow.org/wikipe. women begin to accumulate iron at a faster rate and may become symptomatic.jpg http://upload.wikimedia. Therefore.

enicGranuloma_35737_lg. Histologically.skinsight.com/learning/olig/olig_fig9.pathology.jpg Cystic hygroma =cavernous lymphangioma consisting of a network of endothelium-lined lymph spaces beneath the epidermis. Cystic hygromas typically occur in children. these lesions resemble hypertrophic granulation tissue. these lesions present as dark red or purple patches...dermis. as exophytic red nodules attached by a stalk to the gingival or oral mucosa or skin. http://www.jpg Cavernous hemangiomas =benign neoplasms of small blood vessel endothelial cells. http://www.clinical scenario would be the appearance of lymphangiosarcoma approximately 10 years following radical mastectomy for breast cancer. Onethird of these lesions develop following local trauma.. dilated blood vessels in the superficial dermis.cmpmedica..html Port-wine stain (nevus flammeus) = a birthmark consisting of malformed.microscopyu. Clinically.. http://www..net/bilder/CD036/550px/img0076.jpg . http://imaging.rnoushemangioma10x01_b. http://www..ed.washington. Pyogenic granulomas often grow rapidly. Cystic hygromas are associated with Turner’s syndrome.com/galleri. and may be ulcerated.iame. Pyogenic granulomas bleed easily.jpg http://www. Port-wine stains are permanent lesions present from birth.jpg Pyogenic granuloma =a polypoid form of capillary hemangioma. typically involving the face or limbs. Cystic hygromas differ from cavernous hemangiomas only by the absence of luminal blood cells.ry/jpgs575/spd/img0041.com/images/dx.com/consu.3/2004/w_0406conpcport. and tend to affect the neck or axilla..

pathguy. a non-focal neurologic disturbance. thrombocytopenia. and polyvinyl chloride (a plastic widely used in industry). and spinal cord causes the neurologic manifestations. and is characterized by pulmonary insufficiency. It is associated with HIV infection and other immunocompromised states http://depts. The pulmonary and CNS microvascular and parenchymal dysfunction may be promoted by: 1. diffuse neurological impairment. impairing gas exchange. . =respiratory distress.Kaposi’s sarcoma = a hyperplasia or neoplasm of spindle-shaped cells with markers of both smooth muscle and vascular endothelial lineage. Fat globules dislodged from bone marrow enter the marrow vascular sinusoids and then occlude pulmonary microvessels. and chest lesions consistent with thrombocytopenia after suffering multiple long bone fractures . as well as possible pulmonary hemorrhage.The fat embolism syndrome is a condition affecting less than 10% of patients with severe skeletal injuries. thorotrast (a former radioactive contrast medium).washington. brain stem. Microvascular occlusion in the cerebral white matter.jpg Liver hemangiosarcoma = rare malignant vascular endothelial cell neoplasm associated with such carcinogens as arsenic (exposure to pesticides).edu/hivaids/images/derm/derm_c3_q01. http://www. and anemia.jpg Fat embolism syndrome. release of mediators from platelets which adhere to and coat the fat emboli (a phenomenon also resulting in thrombocytopenia). systemic activation of lipoprotein lipase and intravascular release of toxic levels of oleic acid -The anemia is thought to be due to increased RBC aggregation and destruction. and 2.com/sol/10863.

Subarachnoid hemorrhage is the result. and intracranial hemorrhage.Squatting. http://www. overtime the resultant pulmonary hypertension can cause pulmonary vascular sclerosis. ruptured dissecting aortic aneurysm. and reversal of shunt flow across the ductus. -Sustained (isometric) handgrip increases the systemic vascular resistance and thus reduces the gradient across the LV outflow tract. .Spontaneous intracranial hemorrhage (SICH) -The most common causes of SICH in young adults are arteriovenous malformations. or abuse of sympathomimetic drugs such as cocaine. causing cyanosis restricted to the lower body. The most likely cause is right-to-left shunting of blood flow through a patent ductus arteriosus (PDA) into the junction between the aortic arch and the descending aorta. However these .-aneurysm-common-sites.neurosurgery. Differential cyanosis = cyanosis of the lower extremities but not of the upper body. or lying supine increase venous return thereby increasing right and left ventricular preload. sitting. increased pulmonary vascular resistance.ufl. ruptured cerebral aneurysms. Although PDAs initially involve left-to-right shunting. .. ..edu/pa. -Phenylephrine (a selective al agonist) increases systemic vascular resistance and thus reduces the gradient across the LV out flow tract. -Passive leg raising augments venous return thereby increasing right and left ventricular preload. The PDA causes shunting to the aorta distal to the point of aortic constriction. because of hypertension in branches of the aortic arch proximal to the coarct.The infantile. . including left ventricular failure. preductal form of coarctation of the aorta is generally associated with a PDA.Patients with adult-type coarctation of the aorta commonly die of hypertensionassociated complications.jpg Hypertrophic cardiomyopathy (HCM) = asymmetric ventricular septal hypertrophy and variable dynamic left ventricular outflow tract obstruction which may produce a systolic ejection murmur. Differential cyanosis is the result of reduced arterial oxygen saturation in the distal aorta compared to that in the aorta proximal to the takeoff of the left subclavian artery.Berry aneurysms are particularly prone to rupture when associated with coarctation. . Actions like standing suddenly from the supine position and the Valsalva maneuver decrease venous return and thus accentuate the murmur.Decreases in the LV end diastolic volume increase the obstruction causing the murmur of HCM to be enhanced.

elbows.mfi.jpg Whipple disease The periodic acid.. Adult-type COA can limit lower extremity exercise tolerance but does not commonly cause cyanosis. two sugars that are easily washed from sections during processing (therefore giving a negative reaction). since the PDA is closed. which is found in skin. and basement membranes. -Dermatitis herpetiformis is an autoimmune disorder associated with celiac disease (gluten-sensitive enteropathy). liver.AS%20positive%20macrophage Dermatitis herpetiformis = groups of small vesicles that occur on extensor surfaces. forming aldehydes that produce a brilliant magenta color upon reacting with the fuchsin-sulfurous acid. -Immunofluorescence reveals IgA deposits also present in the tips of dermal papillae. The eruptions are symmetrically distributed and extremely pruritic. -The glycoprotein present in the cell walls of the gram-positive actinomycete Tropheryma whippelii appears magenta with PAS and is diastase-resistant. parathyroid. steatorrhea. http://www.patients generally develop congestive heart failure and are unlikely to survive beyond infancy without surgical correction. -The adult form of COA represents a lesser degree of aortic constriction and is not associated with a right-to-left shunt.Schiff (PAS) reaction is used in histochemical staining because the periodic acid oxidizes carbon. DIFF: -Atrial and ventricular septal defects initially present with left-to-right intracardiac shunting and are therefore not associated with cyanosis at birth. On endoscopy. and skeletal/cardiac muscle. .. forming.uptodate.com/online/con. If arterial oxygen desaturation develops later in life because of shunt reversal (Eisenmenger syndrome). As a result the PAS stain is particularly effective at highlighting polysaccharides of the fungal cell wall mucosubstance secreted by epithelia.carbon bonds. Skin biopsy will show neutrophils and fibrin at the tips of dermal papilla. The diastase works by digesting glycogen to form maltose and glucose. which makes this stain an excellent choice when microscopically evaluating small bowel mucosa for Whipple disease. or other symptoms of malabsorption. buttocks. Knees. http://www. and microabscesses. and back are the most typical locations for the rash.dk/ppaulev/chapter12/images/12-7. -Twenty to thirty percent of patients with dermatitis herpetiformis also have diarrhea. the resulting cyanosis affects the upper and lower body equally. Diastase can be used in conjunction with PAS to demonstrate glycogen.ku.

failure to thrive.jpg Squamous cell carcinoma of the esophagus = solid nests of neoplastic squamous cells with abundant eosinophilic cytoplasm and distinct borders.pathguy. cells vary in size and shape.. which improves after dialysis.edu/cou. http://www. Bleeding time however.edu/education/gi/lab2. Symptoms of both dermatitis herpetiformis and celiac sprue diminish or resolve completely on a gluten-free diet. A number of dialyzable platelet-inhibitory factors have been shown to inhibit platelet function. while oats and rice do not.almost all patients with dermatitis herpetiformis have villous atrophy.med-ed.pathology. rye. Areas of keratinization (keratin pearls) are easily noticed. progressive ataxia.jpg Abnormal bleeding in uremia =is due to a qualitative platelet disorder with normal platelet count.com/galleri.html Abetalipoproteinemia =an inherited inability to form chylomicrons. which is typical for celiac disease. This disease manifests during the first year of life with malabsorption. and cells have large darkly-staining nuclei.c. Wheat.. there is usually no keratinization.virginia.vcu.com/sol/13871. PT and PTT. http://www. .. is generally very prolonged in patients with uremia.es/burrcelluremia40x04. and barley do contain gluten.microscopyu. -In poorlydifferentiated squamous cell carcinoma. http://www. Keratin pearls are a sign that the tumor hasn’t yet lost the properties of an original tissue—in other words. signifying a major defect in platelet function.. such as erythema nodosum (tender subcutaneous nodules) and pyoderma gangrenosum (deep ulcers with violaceous borders) http://www. and abnormal red blood cells (acanthocytes). Numerous mitotic figures might be seen.jpg Crohn’s disease =associated with skin manifestations./images/medium/fm00060. it is a well-differentiated tumor.

jpg . 2.. then for both solids and liquids.com/sol/26249. This membrane protein is normally responsible for transporting chloride ions across mucosal epithelial cell membranes. Pancreatic insufficiency causes the symptoms of malabsorption (steatorrhea and poor weight gain).med. Repeated pulmonary infections particularly with Pseudonomas aeruginosa. Viscous pancreatic secretions are not transported to the intestinal lumen and instead accumulate in pancreatic ducts. Decreased secretion of water by the intestinal epithelium may cause intestinal obstruction.html Benign tumors of esophagus = quite rare and slow growing.gastrointestinalatlas. -Characteristic findings include: 1. -The most pronounced changes in cystic fibrosis are seen in the respiratory tract and pancreas. Cystic fibrosis =Recurrent pulmonary infections and malabsorption in a Caucasian child =autosomal recessive disorder of exocrine secretion..c. first for solids. leading to fibrosis of pancreatic tissue. http://www.html http://library. and salivary gland ducts. There is stasis and accumulation of these viscous secretions in tissues. The most common of them is leiomyoma.edu/WebPath/GIHTML/GI014. The male reproductive system. Presentation includes progressive dysphagia. 3.pathguy. Pancreatic secretions form mucous plugs that with time totally obstruct the ductal lumina. -Mucous plugging can also be seen in biliary ducts (with development of biliary cirrhosis) vas deferens (causing male infertility). Mucus plugging of bronchi causes dilatation and bronchiectasis. the cystic fibrosis transmembrane conductance regulator (CFTR) is non-functional. Neonates with cystic fibrosis may develop meconium ileus. Upper respiratory tract symptoms include bilateral sinusitis and nasal polyps.ncer/esophagus_cancer.utah. When the CFTR gene is mutated transport of chloride and water from the cells is suppressed. On light microscopy leiomyomas consists of fascicles of spindled cells with variable amount of fibrosis. Increased viscosity of bronchial secretions leads to impaired mucociliary clearance of bacteria. are characteristic. achalasia and corrosive strictures of esophagus are other risk factors -Most squamous cell carcinomas of the esophagus occur in male patients older than 50 years old. Significant weight loss is common. liver and salivary glands may also be involved. http://www. Plummer-Vinson syndrome.The most important risk factors are alcohol and tobacco use. leading to the secretion of viscous mucus.. In CE.

http://www. spinal cord (posterior and lateral columns). However. nausea and cola-colored urine 2-3 weeks after recovering from a streptococcal skin or throat infection. . -Age is the most important prognostic factor in patients with poststreptococcal glomerulonephritis. hypersegmented neutrophils. and the cerebrum. Importantly.gif Poststreptococcal glomerulonephritis The classic presentation = a 6 to 10-year-old child developing malaise. neurologic abnormalities can occur in vitamin B12 deficiency in the absence of frank anemia. This is because B12 deficiency also causes axonal demyelination and degeneration. Decreased vibratory and position sense are early signs of vitamin B12 deficiency. -Therapy includes loop diuretics and vasodilators to relieve the edema and hypertension. However RBC macrocytosis can also occur in liver disease. 1-2% develops chronic glomerulonephritis. -MCVs greater than 110 fL are typically seen only with vitamin B12 and folic acid anemias.com/UserF.B12 deficiency -Vitamin B12 and folic acid deficiencies cause similar hematological pictures.vitaminsdiary. and large bizarrely shaped platelets. RBC casts.. -The main sites of neurological involvement include the peripheral nerves.e/megaloblastic-anemia. In late disease. Only 60% of sporadic cases in adults will resolve completely. fever. 95% of children recover completely with conservative therapy. and alcoholic liver disease. and mild proteinuria (<1 g/day) are present in urine. -The prognosis in adults is not as good. On peripheral blood smear there is macrocytosis . Treating megaloblastic anemia due to vitamin B12 deficiency with folate alone could worsen the neurological dysfunction. Periorbital and facial edema and hypertension are also usually detected. the rest will develop chronic glomerulonephritis or RPGN. and less than 1% progress to RPGN. The presence of even a single neutrophil with more than 6 lobes should raise the suspicion of megaloblastic anemia. Dysmorphic red cells.. the neurological dysfunction may be irreversible. hypothyroidism. The medications listed in the other answer choices are not used for the treatment of megaloblastic anemia. Patients experience ataxia and recurrent falls because of compromised proprioception. -An RBC mean corpuscular volume (MCV) of more than 100 fL is suggestive of megaloblastic anemia. neurological dysfunction is only seen in patients with vitamin B12 deficiency.

Patients generally do not develop intestinal obstruction because the right-sided colon has a larger caliber than the left. -The amenorrhea results from loss of pulsatile GnRH release from the hypothalamus. However. Non-specific symptoms such as anorexia. and amenorrhea. Anorexia nervosa = is an eating disorder characterized by an intense fear of eating significant loss of bodyweight(to less than 85% of expected weight or BMI less than 17. malaise and weight loss also occur. the low estrogen levels in these amenorrheic individuals could lead to osteoporosis. Aortic dissections give rise to these hematomas as more and more blood creeps behind the medial wall. which in turn causes circulating estrogen levels to be low. long distance runners.Colon adenocarcinomas . . An intimal tear is thought to be the primary event in the process that leads to aortic dissection. hence they present with symptoms of partial intestinal obstruction.Patients with anorexia nervosa can develop the abnormality of thyroid functioning termed “sick euthyroid syndrome” orl owT3 syndrome. via the same mechanism. Right-sided colon cancers usually present with manifestations of iron deficiency anemia (fatigue and pallor) due to the ongoing blood loss. -Amenorrhea also often occurs in serious athletes with very low body fat (e.” An apparent tissue septum divides the lumen of the aorta. inaccurate perception of ones own body shape and size. abdominal distention. The “septum” is actually the normal wall of the descending aorta.g. and vomiting occur. . both T3 and T4 levels are low. Aortic dissection = widened descending thoracic aorta with a “double barrel. Administration of pulsatile GnRH in individuals with anorexia nervosa allows for the normalization of estrogen levels and subsequent ovulation. Loss of this cyclic gonadotropin release leads to a decrease in LH and ESH secretion from the pituitary. If left untreated. Early in the course of anorexia T3 levels are low and T4 and TSH levels are normal. ballet dancers) as well as in individuals with prolonged cachectic illnesses. which is now medially flanked by a second cavity. constipation. nausea.5 kg/m2). -Right-sided colon cancers usually grow as exophytic masses. in prolonged severe disease. cramping abdominal pain. This apparent second cavity is really an intramural hematoma. Change in the stool caliber.Left-sided colon cancers tend to infiltrate the intestinal wall and encircle the lumen. which occurs when the level of body fat falls below a certain critical level.

.edu/WebPath/RENAHTML/RENAL089.IgA/IgA.utah..ispub. dense deposits laid between the basement membrane and the epithelial cells.) Up to 85% of cases are idiopathic. penicillamine. (The most common cause is focal segmental glomerulosclerosis. hepatitis C.hepatitis B. Immunofluorescence microscopy reveals that these granular deposits contain immunoglobulins (IgG) and C3.diabetes mellitus. The remainder occur secondary to the following: *Systemic diseases . solid tumors (lung and colon). malaria.utah.The microscopic findings : uniform.html Berger disease = painless hematuria in children and young adults a few days after upper respiratory infection. http://library.com/Im%.l_features/aortic-fig1. http://www.edu/WebPath/RENAHTML/RENAL088.IFw. and immunologic disorders (such as SLE) *Certain drugs . IgA deposits in the mesangium are found on immunofluorescence.med.. Cystic medial degeneration (which may be seen in Marfan syndrome) also predisposes patients to aortic dissections. Electron microscopy reveals that this thickening is caused by irregular. but is relatively infrequent.-The dissection can extend both proximally toward the heart and distally—sometimes it runs all the way to the iliac and femoral arteries! -Hypertension is the single most important risk factor for the development of intimal tears leading to aortic dissections. effacement of the foot processes of podocytes are seen.jpg Minimal change disease =the most common cause of nephrotic syndrome in children.. and NSAIDs *Infections . http://www.htm .edu/PathDemo/kid1/kid170.gold.mesangial..com/ispub/ijem/vo.med. On electron microscopy.html http://library.kidneypathology. No abnormalities are found on light or immunofluorescent microscopy. and syphilis .jpg Membranous glomerulopathy= “spike and dome” appearance = the second most common cause of nephrotic syndrome in adults. diffuse thickening of the glomerular capillary wall on light microscopy. These protrusions resemble “spikes” when stained with silver. http://pathcuric1.swmed.

-The following sites of involvement are characteristic: 1. http://www. Degeneration of the dorsal columns and dorsal root ganglia causes loss of position and vibration sensation. An increased number of trinucleotide repeats is present in the mutated gene. 5. Gastric emptying occurs usually 2-3 hours after a meal.com/nrn/journal/v5/n8/fig_tab/nrn1474_F1. 3. Heart involvement includes hypertrophic cardiomyopathy and congestive heart failure. the pain associated with a duodenal ulcer typically happens 2-4 hours after a meal or with an empty stomach.htm Friedreich ataxia =autosomal recessive disorder. Symptoms of a duodenal ulcer occur when acid is secreted without a food buffer. This area is called the duodenal bulb and is exposed to the most gastric acid.html . 2. Thus. Gastric ulcers tend to occur later in life (average age of patients is 50-60 years old). It is caused by the mutation of a gene on chromosome 9 that codes for the protein “frataxin" which is essential for normal mitochondrial function. 4.nature.Peptic ulcer disease (PUD) = most commonly occurs due to infection with Helicobacter pylori.u-szeged. -On the other hand.szote.hu/radio/nyelocs/anyel11c. pain associated with gastric ulcers occur immediately after meals and responds poorly to antacids. Most patients also complain of pain between 11 PM and 2 AM because maximal circadian acid secretion occurs then. http://www. -Friedreich ataxia causes degeneration of neural tracts and peripheral nerves. -The most common site for duodenal ulcers is the first portion of the duodenum (within 3 cm of the pylorus). and manifest in young and middle-aged people. Ascending and descending spinocerebellar tract degeneration causes gait ataxia. -symptoms of a duodenal ulcer—pain a few hours after eating that resolves with antacid. but foodstimulated acid secretion continues for 3-5 hours. -Duodenal ulcers affect 10-15% of the population. Kyphoscoliosis and foot abnormalities (pes cavus) are characteristic skeletal deformities. causing diminished levels of frataxin in patients with Friedreich ataxia. Gastric ulcers are usually located within the body of the stomach at the lesser curvature and affect about 1% of the population. Diabetes mellitus develops in about 10% of patients with Friedreich ataxia. Peptic ulcer disease encompasses both gastric and duodenal ulcers. The disease occurs only if the both alleles of the gene are abnormal.

red. -Acute necrotizing pancreatitis is a major risk factor for progression to adult respiratory distress syndrome http://www. inflammation.. decreasing lung compliance. although immunologic hyperreactivity is suspected. Excessive tissue fibrosis ensues and is the hallmark of systemic sclerosis.JPG Frank intraalveolar hemorrhage = could impair gas exchange and cause dyspnea if widespread but would also tend to produce hemoptysis as a clinical sign. and lupus erythematosus. -In ARDS. the lungs are heavy. Wegener granulomatosis. regurgitation.net/ARDS1.html CREST syndrome =Calcinosis.8/Lung_Review/Lung-51. http://www. The esophageal body and the LES become atonic and dilated. These membranes consist of fibrin exudate and plasma protein-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells.Adult respiratory distress syndrome (ARDS) =progressive hypoxemia refractory to oxygen therapy.histopathology-india. The interstitial and intra-alveolar edema. These patients are at risk of development of Barrett esophagus and subsequent esophageal adenocarcinoma. These membranes are morphologically similar to those seen in hyaline membrane disease of newborns. -Esophageal dysmotility is a result of atrophy and fibrous replacement of esophageal muscles. Barium esophagram shows a dilated esophagus and absent peristalsis. Widespread intraalveolar hemorrhage may occur in pulmonary hemorrhage syndromes. An unknown antigen is thought to stimulate accumulation of CD4 lymphocytes in skin and other tissues.som. and absence of cardiogenic pulmonary edema (normal pulmonary capillary wedge pressure) in most cases. CD4 lymphocytes secrete biologically-active substances and stimulate fibroblasts to produce collagen. In the acute stage. -The main symptoms of esophageal dysmotility in CREST syndrome are heartburn. -The pathogenesis of systemic sclerosis is unknown. diffuse injury to the pulmonary microvascular endothelium and/or the alveolar epithelium results in a leaky alveolocapillary membrane. resulting in severe reflux..tulane. Raynaud syndrome. and dysphagia. including Goodpasture syndrome. interstitial edema progressing to diffuse alveolar infiltrates. Sclerodactyly. esophageal dysmotility. . and boggy.edu/classwar. It is a systemic sclerosis variant that mostly involves skin of the face and fingers. and Telangiectasia . and fibrin deposition cause the alveoli to become lined with waxy hyaline membranes.

. This neurological finding is consistent with a tumor of the pineal region.. -Paralysis of upward gaze is called Parinaud syndrome (or dorsal midbrain syndrome).lsbu. https://www.ac.jpg Hiatal hernia -An abnormal location of the gastroesophageal junction describes a sliding hiatal hernia.” http://myweb. These germ cell neoplasms have identical counterparts that occur in the .. In this condition.rticles/Images/1324-74.. and ovarian and adrenal tumors. -A number of diseases can cause precocious puberty including congenital adrenal hyperplasia.uk/dirt/museum/margaret/718-741-1641420.learningradiology.htm Diffuse esophageal spasm (DES) =Periodic non-peristaltic esophageal muscle contractions .Clinical manifestations are dysphagia and chest pain.co.For girls = an appearance of secondary sexual characteristics before age 7. Germinomas are the most common tumor of the pineal gland. Germinomas are malignant tumors thought to originate from embryonic germ cells.radiology.htm Achalasia = increase in resting lower esophageal sphincter tone and diminished LES relaxation during meals.ch/OESO/books/Vol_. http://www. Barium swallow reveals a distended esophageal body and narrowed LES (“bird’s beak”).http://www.hon. Such neurologic abnormalities are caused by mass effect. The association of precocious puberty with a neurologic abnormality (such as paralysis of upward gaze) suggests a hormone-secreting brain tumor.jpg Precocious puberty =Growth of facial and pubic hair along with enlarged genitalia in a boy younger than 9 years old .tzkis%20Ring/hhcorrect.uk/srs-x/cases/081/d.com/a. Barium esophagogram will reveal the characteristic “corkscrew esophagus. the gastroesophageal junction along with a portion of the stomach moves up through the esophageal hiatus. These patients are prone to GERD.

http://radiopaedia. from middle to end. This growth is regulated by a number of factors including hormones and cytokines. and epiphysis. Precocious puberty may occur in males and is caused by beta-hCG production. and show a strong male predominance. Young bone has several layers.dote. they are diaphysis metaphysis epiphyseal cartilage. The major factors are growth hormone IGF-1. thick tubular long bones in .jpg Achnodroplastic dwarfism =disproportionately short stature (short upper and lower extremities compared to the axial skeleton) and some cranial abnormalities.gonads and mediastinum. -The following combination of symptoms are associated with pineal germinomas: 1. growth is inhibited at the epiphyseal growth plate ultimately resulting in short. Aqueductal compression by the tumor may lead to obstructive hydrocephalus.usuhs.The most common defect in achondroplasia is the mutation of the “fibroblast growth factor receptor-3” at the epiphyseal growth plate. 3.hu/wallenb/wallenb. -Expansion of the epiphyseal cartilage. sex steroids and fibroblast growth factor. tubular diaphysis in the middle.. thyroid hormone. . 2. insulin. Parinaud syndrome includes paralysis of upward gaze and of convergence—these symptoms occur due to compression of the tectal area of the midbrain.org/cases/pineal-germinoma "Locked-in” syndrome =Pontine hemorrhage or tumor (spastic quadriplegia and paralysis of most cranial nerves). Germinomas are found in children and adolescents. -Lateral medullary syndrome (Wallenberg) leads to contralateral loss of pain and temperature sensation along with ipsilateral paralysis of CN V.r&imageid=30646&pt_id=9764 Lesions of the medulla =can cause lateral and medial medullary syndromes.ufl. X. http://www. also called the “growth plate” is responsible for linear growth.. in order.neuropat. and Xl.edu/year2/neuro/review/images/fig09. If fibroblast growth factor receptor-3 has an activating mutation. IX. http://rad. -Long bones have a wide epiphysis at each end and narrower.edu/medpix/parent. http://medinfo.htm -Medial medullary syndrome causes contralateral spastic paralysis and ipsilateral flaccid paralysis of the tongue (CN XII).

jpg 2.jpg Metaplasia = adaptive change that occurs in response to chronic epithelial irritation. The following criteria determine the malignant potential of adenomatous polyps: 1. Size: adenomas >4 cm have 40% risk of becoming malignant.ch/polyp/bilder/gross/p011-01./n4/fig_tab/3880773f4.. adenomatous polyps contain dysplastic mucosal cells and can transform into adenocarcinoma...ispub. Both these conditions increase the risk of malignancy and are therefore referred to as premalignant. Degree of dysplasia._report/polyposis-fig1.jpg DIFF: -Hypothalamic and pituitary lesions cause short stature by decreasing the growth hormone / insulin like growth factor-1 (IGF-1) pathway. Axial (spine) length is usually normal. Hyperplastic polyps are composed of well-differentiated mucosal cells that form glands and crypts. The squamous epithelium. smooth muscle and connective tissue.types of non-neoplastic polyps: 1.html 3.. that is the axial and appendicular skeleton are proportionate. Hamartomatous polyps consist of mucosal glands. however. They consist of intestinal mucosa infiltrated with lymphocytes.org/obgyn/gr. http://www.nature. does not have cilia and goblet cells. while long-standing reflux results in columnar metaplasia of the distal esophagus (Barrett’s esophagus).hondroplasiacomparison. http://kathrin. Metaplastic epithelia can progress to dysplasia (low-grade atypical cells confined to the epithelium) and is therefore a . This change of cell types is called metaplasia and is initially adaptive. They are composed of regenerating intestinal mucosa.. -Smoking induces squamous bronchial metaplasia.ro/patho.com/ispub/ijpa/vo.com/modpathol/jo.jpg -Unlike non-neoplastic polyps... . those <1 cm are most likely benign. Inflammatory polyps are seen in ulcerative colitis and Crohn disease.moondragon. 3. http://www.pathologyatlas.. http://www.. 4. They may occur sporadically or in Peutz-Jeghers syndrome or juvenile polyposis. Histologic pattern: villous adenomas are more likely to undergo malignant transformation than tubular adenomas.unibas. Short stature in growth hormone / IGF-1 deficiency is proportional. Colonic polyps . and is unable to provide mucociliary clearance.dunculated_polyp_colon. 2. http://www. Squamous epithelial cells are more resistant to irritation than columnar cells and are more likely to survive in the bronchial lining of a chronic smoker.the appendicular (limb) skeleton. Lymphoid polyps are found in children.

is induced by the tumor necrosis factor (TNF) when bound to tumor necrosis factor receptor (TNFR1) or the Fas ligand when bound to cell surface receptor Fas.-cellcycle-10-14-10_29. These changes are responsible for the formation of the mitochondrial permeability transition (MPT) and the release of cytochrome c and other pro-apoptotic proteins into the cytoplasm.new-science-press. Initiator caspases activate the effector caspases. Cells damaged by ultraviolet light. Initiation: Apoptosis is triggered by different stimuli and can occur through either the intrinsic mitochondria mediated pathway or the extrinsic.gif Shaken baby syndrome =the combination of subdural hematoma with bilateral retinal hemorrhages in an . Destruction: Both the intrinsic and extrinsic pathways converge at this step resulting in caspase activation. Caspases are proteolytic enzymes that destroy cell components. Bak. the binding of the death ligand and the death receptor allows for pro-caspase molecules to be brought into close proximity...gif Protein kinase A = a component of the cAMP-associated signaling system.com/i.. Control: Intrinsic apoptosis is mediated by a group of bcl-2 proteins. http://www.edu/Course.ca/resourc..jpg Apoptosis involves the following steps: 1. Squamous bronchial metaplasia is reversible and may resolve upon discontinuation of smoking. and Bim proteins) while others are anti-apoptotic (eg.risk factor for carcinoma (high-grade atypia with or without invasion beyond the epithelial space). receptorinitiated pathway. Bcl-x and Bcl-2 proteins). 2. The eleven caspases that have been identified are classified as either initiator or effector caspases..ualberta.ages/Images-S/000p027y. hypoxia. The binding of a ligand to S-protein-linked receptor results in adenylyl cyclase activation and the release of cAMP. phosphatidylserine or thrombospondin) on their plasma membranes. toxins. Some of the components of this system are pro-apoptotic (eg.edu/hjakub.1/signaltrans/sigtrans.. Bax. Apoptotic signals tip the balance between these two forces resulting in changes of the inner mitochondrial membrane.wails/apoptoticpathway.lmp..davidson.bio. Elevated levels of cAMP activate protein kinase A. heat. in contrast.csbsju. which then cleave the cellular proteins. In extrinsic apoptosis. 3.jpg http://www. http://employees. Extrinsic apoptosis.. They contain cysteine and are able to cleave aspartic acid residues (cysteine-aspartic-acid-proteases). http://www. or radiation display intrinsic apoptotic signals (eg. which then activate caspases.

Retinal hemorrhages occur due to rupture of congested retinal veins. as it derives its blood supply from the renal capsule. as well as multiple fractures in different stages of healing. resulting in a subdural hematoma.. and infective endocarditis.utah.ualberta. larger subarachnoid spaces. This “end-organ” blood supply means that interruptions of blood flow lead to the formation of coagulative infarcts. apex pointing to medulla). oliguria. Macroscopically.med.med.The injuries produced by severe shaking are due in part to the unique anatomic features of the head of a young child.jpg Sistemic embolism -Because of his high blood supply the kidneys are more likely than other organs to suffer embolic infarctions. Emboli can form adjacent to a necrotic ventricular wall following an acute Ml or in the resultant ventricular aneurysm weeks later. Other common causes of systemic embolism include atrial fibrillation.rier/Vol1/Fig.medscape. are also typical. http://library.html Acute interstitial nephritis = a hyper sensitivity reaction that occurs 1-2 weeks after starting a new medication.fig2. . Any suspicion of child abuse should be reported to state protective agencies. http://cnserver0.. Bruises and lacerations in the different stages of healing may indicate repeated abuse. Fever. or perineum may be indicative of forced immersion burns.infant.%209-17a. Most often.edu/WebPath/RENAHTML/RENAL011.53/art-adnc478153.nkf. Burns to the genitals buttocks.. Other types of trauma suggestive of child abuse include bruises.. burns and fractures. these emboli arise from the left atrium or left ventricle. eosinophilia and eosinophiluria are common manifestations. A thin rim of subcortical tissue maybe preserved. -Another distinctive feature of the renal circulation is the small number of collaterals between the segmental renal arteries. and subsequent tearing of the bridging veins.jpg . these appear as pale wedges (base facing cortex. http://www.com/content/20. Spiral fractures. and decreased cervical muscle tone compared to adults. aortic aneurysm. Shaking leads to movement of the immature brain in relation to the skull. rash. higher brain water content. Infants have larger heads.. -a stroke and renal infarction suffered simultaneously most likely resulted from systemic emboli.

http://www.The pericardial knock occurs earlier in diastole than an S3 gallop. -The risk of metastasis is based on the growth phase of the tumor. although it has also been identified in the eye.. is evident. In patients with chronic constrictive pericarditis. The borders are frequently irregular and notched. immunization.edu/classwar.cPath/GR_Heart/Heart3.Chronic constrictive pericarditis results in replacement of the normal pericardial space by a thick fibrous shell which can cause heart failure by restricting ventricular filling .Histologically the melanoma cells congregate in poorly formed nests and are large with irregular nuclei.howtogetridofmoles.net/Malignant_Melanoma. immature cells that travel downward into the deeper dermal layers increasing the risk of metastasis. In normal individuals the jugular venous pressure decreases with inspiration. or with .html Nephrotic syndrome = clinically characterized by facial edema combined with massive proteinuria. In contrast melanomas in the vertical growth phase contain atypical. Those melanomas in the radial growth phase remain superficial and extend horizontally within the epidermis and superficial dermis with no risk of metastasis. as are hereditary factors and a history of pre-existent dysplastic nevus in the same location. .. or shape. esophagus.jpg Chronic Constrictive pericarditis . Sunlight exposure appears to be an important factor in the pathogenesis of skin malignant melanoma.som. Marked variability of pigmentation may occur. with shades of black brown red navy blue and/or gray present. also called as lipoid nephrosis. Kussmaul’s sign. . -Clinically these lesions are either asymptomatic or pruritic. -The most common cause of nephrotic syndrome in children between 2 and 8 years old is minimal change disease (MCD). clumped chromatin and prominent nucleoli. -Light-skinned individuals are more likely than dark-skinned individuals to develop malignant melanoma.Malignant melanoma = an increasingly common neoplasm that typically arises in the skin. however.tulane.Tuberculous caseous pericarditis is the common cause. This disease may be associated with respiratory infections. Measurement of the depth of invasion (Breslow thickness) is the most important prognostic indicator for patients with malignant melanoma. http://www. meninges and on mucosal surfaces. Most melanomas are greater than 1 cm in diameter and have demonstrated change in color size. a paradoxical rise in the height of the jugular venous pressure during inspiration. This occurs because of the increase in venous return that occurs with inspiration and the restriction of right heart filling that occurs in chronic constrictive pericarditis.

the transferrin saturation drops.pathology. it usually resolves before puberty.pathguy. when the supply of iron is increased. The “fusion” of foot processes is the only pathological finding in MCD: renal function.An important feature of this condition is its rapid response to corticosteroid therapy. hypochromic red blood cells -Ferritin is the cellular iron storage protein. and no hypersegmented neutrophils. however. approximately one-third of the circulating transferrin is saturated with iron. http://www. Decreased blood hemoglobin 6. In patients with .html Iron deficiency anemia -the following sequence of changes can be tracked with laboratory testing: 1. Hepatic synthesis of transferrin is markedly increased in states of iron deficiency.com/lectures/low_iron. Immunofluorescence microscopy doesn’t reveal any immunoglobulin or complement deposits. Although nephrotic syndrome may recur.vcu. and light microscopy remain unchanged. low (microcytic) MCV. The pathology of MCD is completely reversible after steroid therapy. Likewise. -Electron microscopy. -Transferrin transports iron through the plasma. . Appearance of microcytic. normal folate levels. -The long-term prognosis for these patients is excellent: renal function remains good. shows diffuse effacement of the foot processes of podocytes with a morphologically-normal glomerular basement membrane. high circulating transferrin. Decreased bone marrow iron stores (ferritin and hemosiderin) 2. reflecting increased serum transferrin 4. Increased serum total iron binding capacity (TIBC). In individuals with normal iron levels. When the supply of iron is decreased.edu/education/em/case11.atopic disorders. -This patient would be expected to have low serum ferritin. Serum ferritin is decreased in cases of iron deficiency and elevated in cases of iron overload.jpg Hereditary non-polyposis colon cancer (HNPCC) or Lynch syndrome = autosomally-dominant genetic predisposition to colon cancer. Decreased serum iron concentration 5. . and serum ferritin is an excellent marker of iron stores.Anemia in a woman of childbearing age is most commonly caused by iron deficiency secondary to menstrual blood loss http://www. Decreased serum ferritin 3. -Light microscopy in MCD shows normal glomeruli. the transferrin saturation rises.

malignancies develop readily.degree relatives. colon cancer occurs at a young age (<50 years old). cancers of the stomach. Germline mutations in MLH1 and MSH2 account for 90% of Lynch syndrome. Amyotrophic lateral sclerosis (ALS) = Lou Gehrig's disease = the most common motor neuron disease. and fleeting twitches of muscles that can be seen under the skin (fasciculations). . Respiratory complications (such as aspiration pneumonia) are the most common cause of death. Lynch I is characterized by a family predisposition to colon adenocarcinoma.Symptoms of lower motor neuron degeneration include muscle weakness and atrophy. Family history reveals high incidence of colon and other cancers in first. -Unlike sporadic colon cancer. . About 20 % of all familial cases result from a specific genetic defect that leads to mutation of the enzyme superoxide dismutase 1 (SOD1). Combined upper motor neuron (UMN) and lower motor neuron (LMN) lesions are characteristic: damage to motor neurons of the anterior horns (LMN lesion) and demyelination of the corticospinal tracts (UNM lesion) are present. .Patients with HNPCC inherit a mutation in one allele of the gene: and mutation of the second allele occurs during adult life. HNPCC does not involve mutations of protooncogenes or anti-oncogenes. MSH2.Symptoms of upper motor neuron involvement include tight and stiff muscles (spasticity) and exaggerated reflexes (hyperreflexia) including an overactive gag reflex .About 5 to 10 percent of all ALS cases are inherited. muscle cramps. -genetic basis = mutations of DNA mismatch repair genes: MLH1. Instead there is an inherited mutation in one of the four genes responsible for DNA mismatch repair. The products of these genes “proofread” DNA during replication.this syndrome. Endometrial and ovarian carcinoma. The result is denervation atrophy of the muscles (amyotrophy). .Riluzole is believed to reduce damage to motor neurons by decreasing the release of glutamate. MSH6 and PMS2. . . pancreas. Most patients die within 5 years of diagnosis. -The disease manifests in middle-aged people and has a progressive course.Two-thirds of colon cancers in those with HNPCC occur in the right side of the colon. When two dysfunctional copies are present. . and urothelial tract (among many others) may occur. while mutations in MSH6 and PMS2 are responsible for approximately 10%. Clinical trials with ALS patients showed that riluzole prolongs survival by several months. Lynch syndrome type II causes predisposition to colon cancer (with features common to Lynch I) and increased incidence of extraintestinal cancers. whereas in the general population colon cancer occurs more frequently on the left side of the colon. mainly in those with difficulty swallowing.There are two types of Lynch syndrome.

ataxia. therefore hematological manifestations of B12 deficiency are megaloblastic anemia and pancytopenia.JPG Transketolase = an enzyme of the hexose monophosphate pathway.nih. Accommodation and the pupil’s response to light remain intact. Loss of position and vibration sensation.mercola. -In diabetes oculomotor nerve (CN III) neuropathy is ischemic. . dilated pupil and no accommodation reflex. Its somatic component innervates the inferior superior.niaaa. Axonal degeneration of peripheral nerves is also seen. Somatic and parasympathetic fibers of CN IIIhave separate blood supplies.) -CNIII (oculomotor nerve) has the following functions: 1.Vitamin B12 is important in DNA synthesis. .DM causes a number of complications. Diabetics most commonly have (symmetric) peripheral neuropathy mononeuropathy and autonomic neuropathy.. Ptosis occurs due to paralysis of the levator palpebrae. Symptoms are ptosis and a “down and out” gaze. Levels of RBC transketolase are decreased in thiamine deficiency.. http://products.Vitamin B12 deficiency .Neurological damage associated with B12 deficiency includes subacute. Deficiency of B12 leads to an accumulation of methylmalonic acid) -Elevated levels of methylmalonic acid result in myelin synthesis abnormalities. with neuropathy being very common.. Succinyl CoA is the final product of fatty acid oxidation that enters citric acid cycle. (Alternatively if nerve compression causes CN Ill neuropathy both somatic and parasympathetic fibers will be affected. whereas the unopposed action of the lateral rectus (CN VI) and superior oblique (CN IV) muscles lead to a “down and out” gaze. Mononeuropathies are divided into cranial and somatic—among cranial nerves CN III is affected the most often. Increased serum levels of methylmalonic acid are diagnostic of vitamin B12 deficiency. Patients will have ptosis a “down and out” gaze a fixed.gif Diabetes mononeuropathy . and medial rectus interior oblique and levator palpebrae muscles.rh27-2/IMAGES/Page137b.. It utilizes thiamine (vitamin B1) as a coenzyme. diabetic CN III neuropathy affects only somatic fibers leaving parasympathetic fibers intact. http://pubs. -Vitamin B12 (deoxyadenosyl cobalamin) also serves as a cofactor for methylmalonyl CoA mutase. and spastic paresis result. (This enzyme catalyzes the conversion of methylmalonyl CoA into succinyl CoA.com/Images. For this reason. combined degeneration of the posterior and lateral spinal columns. they increase after thiamin supplementation.in-b12-spray/chart-b12.gov/publicat.

jpg Pulmonary hypertension -Primary pulmonary hypertension is often familial. -Pulmonary hypertension leads to right ventricular hypertrophy. Hypoxemia induces a number of changes in the endothelium of the pulmonary artery that lead to increased vascular resistance. Gallstone ileus = rare type of mechanical bowel obstruction caused when a large gallstone (usually greater than 2. Idiopathic dysfunction of the endothelium causes primary pulmonary hypertension (PPH). causing waxing and waning of symptoms. As the gallstone travels down the intestinal passage. Both somatic and parasympathetic fibers of CN III are equally affected in this condition. Any decompensated cardiac disorder produces volume overload. The following mechanisms can lead to the development of pulmonary hypertension: 1. Because the compensatory capability of the right ventricular wall is low. right ventricular failure (cor pulmonale) develops. Parasympathetic fibers of CN III innervate the sphincter of the iris and the ciliary muscle. hepatomegaly.. Paralysis of parasympathetic fibers causes a fixed dilated pupil and loss of accommodation DIFF: . inherited as an autosomal dominant trait.. Eventually. Any pulmonary disease that causes hypoxemia can cause pulmonary hypertension.CN III neuropathy due to nerve compression: Causes include transtentorial (uncal) herniation or aneurysm of the posterior communicating artery. COPD is the most common cause of this hypoxic vasoconstriction of the pulmonary artery. http://ww2. which has the smallest lumen of the intestinal tract. Increased pulmonary artery pressure causes an accentuated pulmonary component of the second heart sound (P2) as well as paradoxical splitting of S2.lafayette. Increased thickness of the vascular wall (due to impaired apoptosis) and decreased production of prostacyclin and NO are considered the main pathogenetic factors of this disease. and peripheral edema. the gallstone may come to rest in the ileum. An increased volume of blood in the left atrium causes a compensatory increase in pulmonary artery pressure. . it intermittently obstructs the lumen.5 cm in diameter) erodes into the intestinal lumen through a cholecystenteric fistula.ages/humanCranialNerve. chest pain and distended neck veins. Additional physical examination findings may include a holosystolic tricuspid insufficiency murmur that is accentuated with inspiration. 2.edu/~dearworj. producing dyspnea on exertion. Disorders of the left ventricle (MI) valvular heart disease. and CHF can produce pulmonary artery hypertension.2. 3.

or duodenum in patients with high intracranial pressure are particularly prone to perforation and are called Cushing ulcers.org/radiology/. -Removing the stone can be accomplished through a small enterotomy.h:+Radiology&type1=2Select Left pleural effusion = suggestive of a wide range of conditions. -Ultrasound is used to confirm cholelithiasis and can occasionally identify the fistula..Ulcers arising in the esophagus. and abdominal distention.-Most patients with gallstone ileus are female and over 70 years old. The classic clinical presentation includes crampy abdominal pain. stomach. severe trauma. with pancreatitis and esophageal rupture two of the more likely gastrointestinal causes in the differential. healing with full re-epithelization of the gastric mucosa occurs within days to weeks. Once the causative stressors are resolved. -Abdominal radiographs tend to demonstrate an intestinal gas pattern that is consistent with intestinal obstruction. extensive burns. Chronic antral-predominant gastritis = suggestive of Helicobacter pylori infection. vomiting. http://nypemergency. Cushing ulcers are likely induced by direct stimulation of the vagus nerve by increased intracranial pressure. thereby resulting in hypersecretion of gastric acid. . . and pneumobilia (air in the biliary tree) is evident in roughly half of these patients.. Granulomatous gastritis = idiopathic. Curling ulcers =Ulcers arising in the proximal duodenum in association with severe trauma or burns . benign condition characterized by intramucosal epithelioid granulomas that cause narrowing of the antrum secondary to transmural inflammation.Events that trigger such stress include shock. and intracranial injury or surgery. with bowel resection typically unnecessary. This form of gastritis is associated with increased acid production and an elevated risk of duodenal ulcer formation. sepsis.

. or diffuse hyperplasia. -When malignant transformation occurs (as in lymphomas). http://medsci. frequent nitrate consumption. and cigarette smoking are some of the risk factors for developing this neoplasm. with the former arising from precursor lesions. http://www.JPG Gastric adenocarcinoma . is monoclonal in that it results from the proliferation of one cell line. This effacement of nodal architecture may be follicular or diffuse. whereas sinus hyperplasia occurs when the sinuses enlarge and fill with histiocytes..jpg Lymphadenopathy . reversible enlargement of the lymphoid tissue secondary to antigenic stimulus. Follicular hyperplasia occurs when the follicles increase in size and number. the normal lymph node architecture is distorted or effaced by the proliferation of malignant lymphoid cells.com/drroy2005/gragas3. diet lacking in fresh fruit and vegetables. Diffuse hyperplasia is observed when the nodal architecture is diffusely effaced by sheets of lymphocytes. Clonal rearrangement of the genes for immunoglobulin heavy chains is suggestive of a B cell lymphoma. Malignant transformation in contrast. If a single allele for the V region of the T-cell receptor predominates in a lymphocytic population. The clonality of a T cell population is assessed by molecular methods that examine the rearrangement of T-cell receptor (TCR) genes.arcinomaofstomach20x03. monoclonal proliferation is suspected..Reactive hyperplasia is a broad term that encompasses all benign. -The diffuse sub-type is classically characterized by signet-ring cells.microscopyu. -Chronic gastritis. -Reactive lymphoid hyperplasia is polyclonal in that it consists of a proliferation of many different cell types within the lymph node. immunoblasts. The same principle applies when assessing B-cell clonality.geocities.edu/c602web/602/C602web/lymphnd/slide84.com/galleri.occurs in two forms: the intestinal and diffuse sub-types. Helicobacter pylori infection.http://www. -The intestinal sub-type is characterized by intestinal glands that are similar in appearance to those of colonic adenocarcinoma. The nodal response to antigenic stimuli is highly variable and can be classified as follicular hyperplasia.indiana.htm . and macrophages.can represent inflammatory changes within the lymph node (reactive hyperplasia) or malignant transformation. sinus hyperplasia. -Evaluation for monoclonality of the lymphocyte population is important when lymphoma is suspected. Barrett esophagus.

” Histological examination reveals areas of mature hyaline cartilage mixed with connective tissue.edu/Courses/Digit. some may present with right upper quadrant pain or with a firm. The pathogenesis of the condition remains unclear. nontender mass in the right upper quadrant. calcium-laden gallbladder wall that can develop in some patients with chronic cholecystitis. http://lh6. -is uncommon. sometimes incidentally. The bacterial organisms responsible for hepatic abscess typically reach the liver through one of five routes: portal vein.html . ascending biliary tract infection. http://www. http://library..org.utah..nary/badenocarcinoma1. Cholecystectomy is recommended for those with porcelain gallbladders because 11-33% of this patient population will eventually develop gallbladder carcinoma.nz/journal/119-1231/1906/content01. and right upper abdominal pain .ggpht.html Pulmonary Hamartomas (=pulmonary chondroma) = the most common benign lung tumors. The tumor arises from the alveolar epithelium and is located at the periphery of the lung. composed of tall columnar cells that line the alveolar septa without evidence of vascular or stromal invasion. Hamartomas are usually asymptomatic and detected incidentally on chest x-ray as a peripheral “coin lesion" with “popcorn calcifications. Imaging shows a pneumonia-like consolidation. amebic or echinococcal). but it is thought that calcium salts are deposited intramurally secondary to either chronic irritation from gallstones or as a component of the natural progression of chronic inflammation. On microscopic examination.In developed countries. hepatic abscesses are relatively uncommon and are usually secondary to bacterial infection. developing countries have a relatively high incidence of hepatic abscesses secondary to parasitic infections (eq.nzma.edu/WebPath/LUNGHTML/LUNG076.. Enteric bacteria can cause hepatic abscess by ascending the biliary tract or directly invading from an adjacent area.com/_dcyYRih3ez8/. or a penetrating injury. -Although patients are often asymptomatic. by a rim of calcium deposits that outline the gallbladder. .med. -In contrast.jpg Bronchioloalveolar carcinoma =a subtype of lung adenocarcinoma (sometimes regarded as a separate entity).njuRS9Ar0/Porcelain+GB. arterial supply.Hepatic abscess =The presence of a fluid-filled cavity in the liver in conjunction with fevers. http://www. brittle. -The porcelain gallbladder is typically diagnosed on radiograph..brown. smooth muscle and fat.jpg Porcelain gallbladder = a term used to describe the bluish. chills. direct invasion from an adjacent source. representing less than 10% of all lung cancers. the tumor is usually well-differentiated.Staphylococcus aureus can cause hepatic abscess through hematogenous seeding of the liver.

These granulomas sometimes coalesce into nodules or undergo cavitation. low urinary volume. Involvement of the upper respiratory tract (ear. This situation also occurs in Crohn’s disease and other syndromes of intestinal malabsorption. such as cough and/or hemoptysis.jpg . high purine diets and high alcohol intake can also be associated with increases in serum uric acid concentration. This condition is characterized by normal serum calcium levels with high levels of calcium excreted in the urine. Wegener granulomatosis = “necrotizing granulomatous vasculitis” with a characteristic triad of findings.Hyperuricemia and hyperuricosuria typically affect patients with myeloproliferative disorders or who are undergoing chemotherapy for malignancies (tumor lysis syndrome). hyperuricosuria. nuts. -The RPGN that is associated with Wegener granulomatosis is classified as type 3. . Symptoms of chronic sinusitis and mucosal ulceration of the nasopharynx result from the development of mucosal granulomas that later ulcerate. Low calcium diets can also cause hyperoxaluria.com/sol/24847. Pulmonary symptoms.asp http://www. there are no immunoglobulins or complement deposits found by immunofluorescent studies as in other types of RPGN such as RPGN type 1 (antiGBM disease or Goodpasture syndrome) and RPGN type 2 (immune complexmediated disease). because when there is less calcium available to bind oxalate in the gut.org/ferrarioanca.pathguy. 3. Lesch-Nyhan syndrome. and hypocitraturia. 2. Uric acid stones can be formed as well.Kidney stones . and spinach).ndt-educational. Although crescent formation is obvious on light microscopy. are caused by focal necrotizing granulomas in the lungs. Renal disease is most often in the form of rapidly progressive (crescentic) glomerulonephritis (RPGN).Idiopathic hypercalciuria is the most common cause of calcium kidney stone disease. there is more oxalate available for absorption and subsequent renal excretion. and there are specific microscopic findings. . Hyperuricosuria stimulates calcium oxalate stone formation. http://www. Other causes of calcium nephrolithiasis include hyperoxaluria.Hyperoxaluria can result from a diet high in oxalate (found in foods like chocolate. 1. nose. or pauci-immune. A high serum level of c-ANCA is diagnostic. sinuses throat). Gout.

Pyridoxine deficiency manifests with seborrheic dermatitis. Hydroxyproline and hydroxylysine are essential for cross-linking collagen molecules. and peripheral neuropathy. -Vitamin B12 is necessary for the synthesis of methionine as well as for the synthesis of succinyl CoA from methylmalonyl CoA. In scurvy. glossitis. Bladder carcinomas . with vitamin C serving as a reducing agent. collagen cross. Vitamin B1 deficiency can cause peripheral neuropathy (dry beriberi) and high-output heart failure (wet beriberi).Thiamine (vitamin B1) serves as a coenzyme in decarboxylation reactions. DIFF: .In the United States. Less often. The tumor stage is the most important factor determining prognosis. These patients also suffer gum disease (gum swelling. Vitamin C is necessary for the hydroxylation of the proline and lysine residues of procollagen. Staging of this type of tumor depends on the degree of its invasion into the bladder wall and adjacent tissues. These tumors are called urothelial (or transitional cell) carcinomas. -Vitamin B6 (pyridoxine) serves as a cofactor in many reactions that involve amino acids (such as transamination. It is necessary for the conversions of pyruvate to acetyl CoA and of alphaketoglutarate to succinyl CoA in the citric acid cycle.linking is compromised. decarboxylation and deamination). Here. causing easy bruising and a propensity to bleed. Carcinoma in situ is confined to the epithelium. -The symptoms of vitamin C deficiency are the result of decreased connective tissue strength.The size of the bladder carcinoma is not reflected in its stage. alcoholics. loosening of the teeth and periodontal infection) and poor wound healing. hemorrhages may cause subperiosteal and joint hematomas. This reaction is executed by prolyl and lysyl hydroxylases. thus greatly reducing its strength. the neoplastic cells resemble those of normal bladder epithelium. -Vitamin C deficiency is even more severe in children. vitamin C deficiency (scurvy) is most often seen in severely malnourished individuals (the homeless. A bigger tumor . -The classic presentation of bladder carcinoma is painless gross hematuria. Deficiency of vitamin B12 causes megaloblastic anemia and subacute combined degeneration of spinal cord. . Perifollicular petechial hemorrhages and ecchymoses of the skin and mucosa also occur. the growth pattern may be flat or nodular. Squamous cell carcinomas and adenocarcinomas of the bladder are rare. The tumor most often grows as a papillary or sessile mass and is easily diagnosed on cystoscopy. drug users). Urothelial carcinomas compose 90% of malignant bladder neoplasms. whereas tumor penetration through the mucosa and into the lamina propria and deeper layers signifies invasiveness.Scurvy .arise from the transitional epithelium lining the bladder. In most cases. The capillary walls are especially fragile.

It is not a pathologic process. contraction of the ciliary muscle causes relaxation of the zonular fibers allowing the lens to relax and assume a more convex shape.confined to the epithelium has a better prognosis than a smaller tumor that involves deeper layers of the bladder wall. When the eye focuses on a near object. This factor. -With age the stroma of the lens undergoes sclerosis leading to decreased lens elasticity. along with changes in lens curvature and diminished strength of the ciliary muscle leads to presbyopia (inability of lens to focus on near objects). -One of the minor diagnostic criteria for ARDS is absence of cardiogenic pulmonary edema which means that the pulmonary capillary wedge pressure is usually normal. In myopic (near-sighted) individuals. inflammation. and abnormal organization of collagen and elastin fibers. and hyaline membrane formation cause lung compliance to decrease. and the need to hold objects further from the eye in order to see them clearly. eye stain after reading.both chronological aging and photoaging resulting from the harmful effects of UV light contribute to their development. aging skin is characterized by a decreased number of fibroblasts. the work of breathing to increase. Age-related changes -Accommodation (near reflex)= a change in the optical power of the eye in order to maintain an image focused on the retina. An elevated wedge pressure would be more suggestive of a cardiogenic (hemodynamic) cause of pulmonary edema. increased collagen and elastin breakdown. The interstitial and intra-alveolar edema. it is an age-related condition that occurs in most people beginning at approximately 40-50 years of age. such as pulmonary venous hypertension. . the ciliary muscle relaxes and the lens flattens due to outward radial tension exerted by zonular fibers. http://atlasgeneticsoncology. Morphologically. and the oxygen diffusion capacity of the lung to decrease. -ARDS is characterized by diffuse injury to the pulmonary microvascular endothelium and/or alveolar epithelium.org/Tumors/blad5001. -Presbyopia manifests with difficulty reading fine print. More severe involvement and/or atelectasis of regional alveoli can cause V/Q mismatch (decreased ventilation with maintained perfusion).html Adult respiratory distress syndrome (ARDS) -sepsis is a major risk factor. resulting in increased pulmonary capillary permeability and a leaky alveolocapillary membrane. age-related presbyopia may lead to improvement in distant vision -skin rhytids (wrinkles) are clearly age-related . however. decreased collagen and elastin synthesis. When looking at the distant object. for example while reading.

Although syphilis is not common in the United States any more. Involvement of the dorsal sensory roots leads to the loss of pain sensation and areflexia. and their number often increases with age which is why they are also referred to as senile hemangiomas. bright-red papular lesions = the most common benign vascular tumors in adults. 3. vascular.nei.med. Older texts may refer to this phenomenon (albeit pejoratively) as “whore’s pupils” because both Argyll Robertson pupils and sex-workers can be said to accommodate.jpg http://pathmicro.jpg DIFF: . Progressive multifocal leukoencephalopathy (PML).nih. but not react. are always cutaneous and are not found on the mucosa or deep tissues.http://www. Patients display ataxia and a wide-based gait. -The pathophysiology of tabes dorsalis : 1. = Infection with JC virus (polyomavirus) . The pupil fails to constrict in response to light but constricts normally in response to accommodation..com/wp-content/u. Argyll Robertson pupil occurs due to the involvement of periaqueductal gray matter of the midbrain. but cannot maintain balance with their eyes closed (positive Romberg sign). lymphoma. such as those who suffer from AIDS. 2..edu/mhunt/pml. They do not regress spontaneously. or leukemia.sc. Involvement of the dorsal column causes loss of positional and vibratory sensation. Cherry hemangiomas. this infection may still be found in immigrants and in HI V-positive patients.gov/healthyeyes/eye_images/Presbyopia.This infection usually occurs in severely immunocompromised patients.edu/mhunt/pml2. also referred to as cherry angiomas.ell-de-morgan-angiomas.med. http://pathmicro. Cherry hemangiomas appear during the third or forth decade of life. PML causes progressive dementia and various neurologic deficits. Histologically they appear as sharply circumscribed areas of congested capillaries and post-capillary venules in the papillary dermis http://medsapiens. Affected patients may compensate for poor balance with visual clues.gif Tabes dorsalis =a form of neurosyphilis that involves the dorsal columns and dorsal roots of the spinal cord.jpg Cherry hemangiomas =small.sc.

http://www.-Strawberry (infantile) hemangiomas appear during the first weeks of life. http://www.pathology. initially grow rapidly. -Pancreatic exocrine insufficiency (failure to secrete adequate amylases.. Cavernous hemangiomas of the brain and viscera are associated with von Hippel-Lindau disease.jpg . They present as soft blue compressible masses up to a few centimeters in size.gif Primary biliary cirrhosis (PBC) .com/images/dx. Weight loss and bulky.b. They may appear on the skin mucosa. it is thought that alcohol-related chronic pancreatitis may develop secondary to alcohol-induced protein precipitation within the pancreatic ducts.edu/education/gi/images/2. Ductal obstruction by such concretions may cause exocrine insufficiency due to atrophy of the pancreatic acinar cells and pancreatic fibrosis.dependent.Although the pathophysiologic mechanism is not well-defined.br/img/fbpe/rhc/v54n1/a07f01.jpg Short bowel syndrome = can result from extensive surgical small bowel resection. . Alcoholic pancreatitis = epigastric calcifications and history of alcoholism . forming calculi consisting in part of calcium carbonate. when they appear on the skin they are most frequently based in the dermis.1a. The excessive delivery of intestinal fluid and osmotically active solutes to the colon can produce diarrhea. They occur due to dilatation of a central arteriole and its superficial capillary network and are estrogen.skinsight. They are bright red when near the epidermis and more violaceous when deeper http://www. These proteins form ductal plugs which may calcify.Cavernous hemangiomas consist of dilated vascular spaces with thin-walled endothelial cells..Spider angiomas consist of a bright red central papule surrounded by several outwardly radiating vessels. deep tissues and viscera. They are less likely to regress spontaneously than capillary hemangiomas.vcu. proteases and lipases) leads to malabsorption with consequent diarrhea/steatorrhea. The decreased small intestinal surface area available for absorption causes impaired reabsorption of fluid and electrolytes. frothy stools are typical clinical findings.scielo. and then frequently regress spontaneously by 5-8 years of age.ileHemangioma_3670_med.

= chronic liver disease characterized by autoimmune destruction of the intrahepatic bile ducts and cholestasis. The condition presents most commonly in middle-aged women and is insidious in onset. Pruritus is usually the first symptom and may be very severe especially at night. Fatigue is also often reported. Physical findings typically include hepatosplenomegaly and evidence of cholestasis (eg, xanthelasma, pale stool). As the disease progresses jaundice, steatorrhea, portal hypertension, and osteopenia may develop. -Histologic findings of PBC include the destruction of interlobular bile ducts by granulomatous inflammation (“florid duct lesion”) and a heavy portal tract infiltrate of macrophages, lymphocytes, plasma cells, and eosinophils. http://granuloma.homestead.com/biliary_cirrhosis4_S91-11804.jpg

Crohn’s disease - Normally, the mucosa of the terminal ileum plays an important role in “recycling” bile acids that are necessary for the absorption of fat. Bile acids are produced in the liver, excreted with bile, and then reach the terminal ileum. There they form micelles with fat droplets, are reabsorbed, and return to the liver to start a new cycle. When the mucosa of terminal ileum is inflamed (as in Crohn’s disease), bile acids are not reabsorbed, becoming lost with feces. As a result, a lesser amount of bile acid is present in bile, and the ratio of cholesterol/bile acids increases. Cholesterol precipitates in bile of the gallbladder and forms gallstones.

Wilson’s disease = an autosomal recessive disorder characterized by toxic accumulation of copper within organ tissues (especially the liver, brain, and eye). -Normally, approximately 60% of ingested copper (0.6-3.0 mg/day) is absorbed in the stomach and duodenum, loosely bound to circulating albumin and then transported to the liver. Within the liver, copper is incorporated into an α2globulin to form ceruloplasmin. The ceruloplasmin is then resecreted into plasma, where it accounts for 90-95% of circulating copper. Normal total body copper is estimated at 50-150 mg. -Senescent ceruloplasmin and the remainder of ingested, unabsorbed copper are secreted into bile and excreted in stool, which is the primary route for copper elimination. Renal losses represent only 5-15% of daily copper excretion. http://www.kellogg.umich.edu/theey...nital/wilsons-disease.html

Varicose veins

= dilated superficial veins = associated skin changes consistent with stasis dermatitis. Normally, venous blood flows from superficial veins through perforating veins into the deep veins of the extremities. Blood from the deep veins travels upward and eventually drains into the inferior vena cava. Valves are located in the superficial perforating and deep veins to prevent backward flow from deep to superficial veins. When these valves are incompetent, retrograde flow into the superficial veins occurs. Increased pressure in the superficial veins causes them to dilate and normal venous out flow from the tissues becomes restricted. -Incompetence of venous valves is the main mechanism for development of varicose veins. It may occur after deep venous thrombosis (DVT), in pregnancy, or by genetic predisposition. http://wirawanady.files.wordpress.com/2007/11/varicose.jpg

Acute dissecting aortic aneurysm - Such dissections are likely initiated by an intimal tear. -The origins of these tears are usually 10 cm or less downstream from the aortic valve (type A dissection). The tears are usually oblique or transverse and about 1 to 5 cm in length. The dissection can extend through the media both proximally and distally. It is not unheard of for a tear to extend all of the way to the iliac and femoral arteries. -Major arterial branches from the aorta can be compressed by the dissecting intramural hematoma. This arterial branch blockade accounts for the differing blood pressures in the right versus the left arm of this patient. The reduced right-arm blood pressure suggests compromise of the proximal brachiocephalic trunk. - Severe retrosternal pain radiating to the mid—upper back is characteristic of an aortic dissection. Back pain may indicate extension of a type A dissection into the descending thoracic aorta, or a type B dissection. The level of back pain may descend as the dissection progresses distally. Hypertension often primarily promotes aortic dissections. http://heart.chungbuk.ac.kr/slide/lecimage/aortic_ds_ytjin_02.gif http://www.health-res.com/EX/07-28...rtic%2520dissection_lg.gif http://home.earthlink.net/~radiologist/tf/060302.htm

Medial calcification (Monckeberg’s medial calcific sclerosis, medial calcinosis) = a form of arteriosclerosis characterized by calcific deposits in muscular arteries. These lesions generally occur in people older than 50 and are not clinically significant. The etiology of these calcifications is not well understood. http://www.pathology.vcu.edu/education/cardio/lab1.d.html

Pseudogout (or calcium pyrophosphate deposition disease CPPD) = results from the accumulation of calcium pyrophosphate crystals in the synovial fluid. Patients present with an acute mono- or oligoarticular arthritis characterized by pain joint swelling erythema and warmth. Pseudogout and gout can be difficult to distinguish clinically. The knee joint is involved in more than 50% of cases of pseudogout, whereas the first metatarsophalangeal joint is more frequently involved in gout. -In pseudogout, synovial fluid analysis reveals increased white blood cells with a neutrophilic predominance. The presence of rhomboid-shaped calcium pyrophosphate crystals is diagnostic. These crystals are positively birefringent under polarized light meaning that the color pattern is the opposite of that seen in gout. Pseudogout crystals are blue when aligned parallel to the slow ray of the compensator and yellow when aligned perpendicularly. http://img.medscape.com/pi/emed/ck...logy/336139-388348-510.jpg http://www.e-radiography.net/radiology/djd/CPPD3.jpg http://img.medscape.com/pi/emed/ck...ogy/329097-330936-4264.jpg

Calcific tendonitis - results from the deposition of calcium hydroxyapatite crystals in periarticular soft tissues (especially tendons). The rotator cuff tendons are most commonly affected. http://www.shoulderdoc.co.uk/img/s.../calcific_deposit_xray.jpg

Hepatitis B virus infection Can produce one of three syndromes: -acute hepatitis with complete resolution -chronic hepatitis (with or without cirrhosis and the attendant increased risk of hepatocellular carcinoma); -or fulminant hepatitis with massive liver necrosis. By far the most common outcome in HBV-infected adults (>95%) is acute hepatitis with mild or subclinical symptoms that eventually completely resolve. Fulminant hepatitis occurs in< 1% of patients who develop acute hepatitis. Only 4-5% of patients with hepatitis B virus infection will go onto develop chronic hepatitis. Of those 50- 80% will remain stable with no evidence of cirrhosis. Approximately 20-50% of patients with chronic hepatitis B infection will also eventually develop cirrhosis. Hepatocellular carcinoma arises in 10% of patients with chronic hepatitis and cirrhosis.

Iron-deficient individuals - on replacement therapy should experience hemoglobin level increases of approximately 2 g/dL per week for the first three weeks. This increase in hemoglobin results from enhanced erythropoiesis and the accelerated release of both mature red blood cells and reticulocytes into the blood stream. -The reticulocyte is an immature RBC that is slightly larger and bluer than a mature RBC. It lacks a cell nucleus but retains a basophilic, reticular (mesh-like) network of residual ribosomal RNA. The ribosomal RNA appears blue microscopically after the application of the Wright-Giemsa stain. After spending a day or so in the bloodstream, the reticulocytes are transformed into mature red blood cells that have a lifespan of approximately 120 days. http://www.healthsystem.virginia.e...tic-cells/Reticulocyte.cfm

Traumatic hemolysis = Red blood cell fragments, burr cells and helmet cells =can result from either microangiopathic hemolytic anemia or mechanical damage (e.g. prosthetic valve). -Prosthetic valves produce excessive shear and turbulence in the cardiac circulation, causing mechanical trauma to the RBCs. -Burr cells are erythrocytes with short, evenly-spaced projections. They can occur as an artifact or in association with uremia, pyruvate kinase deficiency, microangiopathic hemolytic anemia, or mechanical damage. http://www.brown.edu/Courses/Digit...emic_path/heme/helmet.html

Viral meningitis -The typical “viral pattern” of CSF includes lymphocytic pleocytosis, normal glucose, and elevated protein. A few RBCs may also be present in the CSF due to hemorrhagic destruction of the temporal lobes. http://www.healthhype.com/wp-conte...ges/ViralMeningitis450.jpg

Atheroembolic renal disease =A patient with signs of renal failure and toe gangrene or livedo reticularis following an invasive vascular procedure

multi genic disorder rather than in the standard Mendelian manner. -Most of the patients that sustain atherosclerotic damage to the renal arteries are elderly. HLADR1//DQw5 in Crohn’s disease or HLA-DR2 in ulcerative colitis) and a gene termed NOD2 which stands for nucleotide-binding oligomerization domain.html Inflammatory bowel disease = appears to be inherited as a complex. The kidneys are frequently involved. There may also be evidence of extra-renal embolization..edu/WebPath/RENAHTML/RENAL049.The classic presentation is a patient in his 40s or 50s with a family history of renal disease who presents with flank pain. -Renal biopsy shows needle-shaped cholesterol crystals that partially or completely obstruct renal arterioles. Many never recover normal renal function.utah.com/20. causing ischemia of the corresponding organs and tissues. In sarcoidosis. Candidate genes include HLA associations (eg. cholesterol-containing debris gets pushed from larger arteries and lodges in smaller vessels.. -During the procedure.med. NF-KB is a transcription factor responsible for cytokine production in the immune response to infectious pathogens. the NOD2 protein appears to act as an intracellular microbial receptor that triggers the NF-KB pathway.blogspot. including livedo reticularis. Oliguria. = Cystic dilatation of the collecting ducts http://library. http://renalfellow. Sarcoidosis = inflammatory disease of unknown etiology that leads to development of noncaseating granulomas in many organs and tissues. with multiple atherosclerosis-related comorbidities. It has been proposed that the NOD2 mutation linked with Crohn’s disease reduces the activity of the NF-KB protein thereby allowing the inflammation-inducing intracellular microbes to persist.html ADPKD (autosomal dominant polycystic kidney disease) .Light microscopy shows cholesterol emboli obstructing renal arterioles. azotemia and other features of renal failure develop a few days to weeks after the procedure.. . and skin infarcts. cholesterol emboli on retinal examination.embolic-renal-disease. -Expressed in both epithelial cells and leukocytes. hematuria and hypertension. noncaseating granulomas consist of aggregates of epithelioid cells (activated macrophages) and multinucleated giant cells consistent with chronic granulomatous inflammation.

cholesterol. violaceous. -Chest X-ray is essential for diagnosis. and a raised. The presence of this enzyme contributes to the hydrolysis of bilirubin glucuronides and increases the amount of unconjugated bilirubin in bile. Progression of the disease leads to disappearance of hilar lymphadenopathy.com/sol/14338.org/1502/reviews/photoessay/16.edu/Courses/Digit.net/vermi/diplostomatidae/sinensis. and manifests clinically with cough.. or mixed stones. .d/gallbladder/07bb0440. and greasy.pathguy. -Brown pigment stones typically arise secondary to infection of the biliary tract.jpg http://dermatology.ath/lymph/sarcoidosis.brown. http://radiopaedia. and mucin glycoprotein.Pigment stones are most common in rural Asian populations (accounting for only 10-25% of gallstones in the United States).html Dermatomyositis = autoimmune disorder that presents with proximal muscle weakness and skin involvement including a violaceous discoloration of the upper eyelids (heliotrope rash).cdlib. In stage I of sarcoidosis. or the liver fluke Opisthorchis sinensis significantly elevates the risk of developing brown pigment stones. dyspnea and chest pain..-The typical patient with sarcoidosis is a young black woman with non-specific complaints of fever malaise and weight loss.jpg .org/cases/sarcoidosis-2 http://www. biliary infection with Escherichia coil.fortunecity. and the chest X-ray in stage Ill disease shows lung infiltrates only. Lung involvement is present in the majority of patients. Ascaris lumbricoides.. with an increased incidence in women and the elderly.jpg Gallstones = cholesterol stones. http://members. which results in the release of β. Because these stones contain large amounts of calcium soaps. Stage II is characterized by bilateral hilar lymphadenopathy along with pulmonary infiltrates commonly in the upper lobes. Skin involvement is varied in presentation ranging from macules to plaques to erythema nodosum (painful shin nodules). http://www. they are radiolucent and do not appear on x-ray. CPK levels are typically elevated.gif http://millenniumdogs.. pigment stones. Therefore. while stage IV is characterized by lung fibrosis. -Grossly.com/dan. it classically reveals bilateral hilar lymphadenopathy.glucuronidase by injured hepatocytes and bacteria. brown pigment stones are soft laminated. scaling eruption on the knuckles (Gottron’s sign).

The autopsy finding of asymmetric hypertrophy of the interventricular septum confirms the diagnosis...Almost all cases of HCM are thought to be due to mutations in cardiac sarcomere proteins.221. .uk/wp-co. Inactivation of the Rb protein permits cell division. When the cell is stimulated by a growth factor the Rb protein is phosphorylated and converted into the inactive state. -Familial retinoblastoma occurs due to a germline mutation that affects the Rb tumor suppressor gene on chromosome 13. http://www. It usually presents with a white pupillary reflex (leukocoria) in children less than 5 years old.Children with sporadic retinoblastoma are not at risk for other malignancies. these are predominantly single point missense mutations in the genes for beta-myosin heavy chain [MHC] (35-50%).ploads/retinoblastoma2. cardiac troponin T (15-20%).jpg http://219. . the malignancy does not occur while the second allele is functional. A somatic (occurs in the retinal cells only) second mutation acquired early in life is the “second hit” that leads to malignancy.co.ukoptometry. Sporadic retinoblastomas occur due to two acquired somatic mutations that affect retinal cells only.L2060/BIOL2060-19/1938. http://pawpeds.. As there are two alleles of Rb gene (one from each parent). or tropomyosin (<5%).200. All cells in the body of an affected individual carry this mutation. later in life.jpg http://www. The majority of these cases are due to . while patients with familial retinoblastoma often develop other tumors usually sarcomas. These mutations cause myofibril and myocyte structural abnormalities and possible deficiencies in force generation.ca/biology/desmid/b.com/pawacademy/health/mybpc3/figure1. The cell with two inactivated Rb genes becomes the source of the malignant tumor. myosinbinding protein C (15-25%).jpg Hypertrophic cardiomyopathy (HCM) .61/ywwy/zbsw(E)/pic/ech12-21. Among these secondary malignancies osteosarcoma occurs most often. while 4O% are familial (bilateral).Approximately 1/3 of case are genetic. Specifically. Cells with two inactive Rb genes divide uncontrollably and give rise to malignancy. About 6O% of retinoblastomas are sporadic (usually unilateral).mun. The Rb gene is a tumor suppressor. Most cases of HCM are familial. The active (dephosphorylated) Rb protein does not allow the cell to proceed from G1 to the S stage of the cell cycle..Retinoblastoma =the most common ocular tumor of childhood. The transmission is autosomal dominant with variable expression.jpg Dilated cardiomyopathy . the corresponding protein exists in an active and inactive state.

mfi.autosomal dominant mutations of cardiac myocyte cytoskeletal proteins (dystrophin) or mitochondrial enzymes. . patients have difficulty climbing stairs.. and an overriding aorta (which straddles the VSD).jpg .Gottron papules= red or violaceous flat-topped papules with a light scale that appear over bony prominences. AntiJo1 antibodies are specific. Positive ANA (antinuclear antibodies) is typical for dermatomyositis but nonspecific.ku. Both Gottron papules and the heliotrope rash are specific for dermatomyositis. Their most common locations are metacarpophalangeal. .org/1502/reviews/photoessay/2.jpg Dermatomyositis =autoimmune disorder that combines inflammatory myopathy and cutaneous involvement. -Cutaneous manifestations of dermatomyositis include Gottron papules and a heliotrope rash.dk/ppaulev/chapter12/images/12-7.com/DMD/physiology5. Any decrease in the ratio of total pulmonary vascular resistance to SVR decreases right-to-left shunting. http://jennyndesign.cdlib.gov/medlineplus. Squatting increases total systemic vascular resistance (SVR) thereby raising mean arterial pressure. . The CK level is characteristically elevated in myositis.nlm. proximal and distal interphalangeal joints.The major physiological problem in cyanotic TOF is stenosis of the pulmonary out flow tract due to asymmetric division of the embryonic truncus arteriosus. rising from the sitting position and combing their hair. a ventricular septal defect (VSD). It is characterized by pulmonic stenosis. The result is right-to-left intracardiac shunting.jpg http://dermatology. -The myopathy of dermatomyositis manifests with proximal muscle weakness.nih. this increases pulmonary blood flow via the ductus (compensatory leftto-right shunt). -Cyanotic spells occur when there are episodic decreases in lung blood flow due to increased right-to-left shunting. If the ductus arteriosus is patent. right ventricular hypertrophy (RVH). -The heliotrope rash presents as an erythematous or violaceous edematous eruption on the upper eyelids and periorbital skin.html Tetralogy of Fallot =recurrent cyanotic spells that he counteracts by squatting. http://www. http://www.TOF accounts for approximately 10% of congenital heart disease and is the most common cyanotic heart disease seen in children after infancy.. -Patients that develop dermatomyositis after 50 years old have increased risk of an underlying malignancy as the occult cause.ges/ency/fullsize/2402.

If large quantities of estrogen are released. CA-125 is not an appropriate screening tool for ovarian cancer because it is highly nonspecific.Cancer antigen 125 (CA-125) is found in elevated amounts on the surface of malignant ovarian epithelial cells in serous.Granulosa-theca cell tumors = comprise approximately 5% of all ovarian tumors. with the lipid content (and therefore the hormonal activity) indicated by the yellow cut surface. -Derived from the ovarian stroma. nonseminomatous testicular carcinomas. these tumors fall under the broad category of sex cord stromal tumors. http://www. and are suggestive of immature follicles. not palpable. Small. and ovarian carcinomas. Tumors that primarily consist of thecoma cells are almost always benign.jpg?v=0 DIFF: . endometrioid.. -Petechiae are cutaneous or subcutaneous collections of extravasated blood measuring less than 5 mm in diameter (ranging from pinpoint to pinhead size).Telangiectasias= small focal permanent dilatations of superficial capillaries and venules. This glycoprotein is best used in monitoring therapeutic response.JPG http://farm3.Lentigos are small tan or brown macules most often seen on the sun-exposed skin of a middle-aged or elderly person (eg. Thecoma cells present as clusters or sheets of cuboidal cells. Typically granulosa-theca cell tumors are unilateral and variable in size. Petechiae are asymptomatic. Older women may develop fibrocystic change of the breast. This is not typical. and clear cell carcinomas of the ovary. and are primarily identified in postmenopausal women. precocious sexual development can occur in prepubertal girls.Alpha-fetoprotein is normally produced by the fetal liver and yolk sac. . endometrial hyperplasia.com/2400/1608008262_2963806ce3. Granulosa-theca cell tumors tend to contain a predominance of granulosa cells and a scattering of theca cells.. -Histologically granulosa cells are small cuboidal cells that grow in cords or sheets. Frequently ecchymoses arise superficially without a history of noticeable trauma. .Purpurae=cutaneous or subcutaneous collections of extravasated blood measuring approximately 5 mm to 1 cm in diameter. gland-like structures that contain an acidophilic material may be present. these tumors have a feminizing effect.med. these are termed Call-Exner bodies. or endometrial carcinoma. . Ecchymosis =cutaneous or subcutaneous collection of extravasated blood measuring at least 1 cm in diameter. arms).Rarely granulosa cell tumors will produce androgens and have a masculinizing effect.pathology. face hands. . Telangiectasias are usually found in the skin or mucous membranes and . Because the granulosa and theca cells secrete estrogen variants. such as the feet and ankles.ohio-stat. and tend to appear in areas of increased venous pressure.static.flickr. . however. but can also be used as a tumor marker in patients with hepatocellular carcinoma./Images/10532/PAXIT009.

it can seed organs throughout the body. Laboratory findings include mildly elevated liver function tests. The triad of skin hyperpigmentation. Eventually. M. tuberculosis = passed from person to person through the transmission of aerosolized airway secretions. tuberculosis allows for intracellular bacterial proliferation. tuberculosis. ascites. M. elevated plasma iron with more than 50% saturation of transferrin. DIFF: . hepatomegaly. The mycobacteria are phagocytosed by alveolar macrophages. and cardiac dysfunction and enlargement. while smaller droplets are carried to the alveoli and can establish infection. primarily in parenchymal organs such as the heart. diabetes mellitus secondary to pancreatic islet destruction. organism-laden droplets into the lower lung fields. Budd-Chiari syndrome = secondary to thrombotic occlusion of the hepatic veins and/or the intra. Hemochromatosis =autosomal recessive disease characterized by abnormally high iron gastrointestinal absorption that causes an iron overload. Most droplets of infectious size carry approximately five organisms. The venous occlusion causes the sinusoidal pressure to increase. arthropathy. diabetes mellitus. and liver. ultimately leading to portal hypertension. Pulmonary tuberculosis infection is first established after the gravity assisted entry of small. While nestled within these macrophages. and elevated serum ferritin. . pancreas. larger droplets make contact with the tracheal and bronchial epithelium and are typically removed by mucociliary motion. impotence. and splenomegaly. and the sulfatide virulence factor expressed by M. tuberculosis enters the lymphatic circulation. Common clinical manifestations of hemochromatosis include liver disease with hepatomegaly.Epithelioid transformation of macrophages can occur in a chronic granuloma caused by infection with fungi or M. abdominal pain.will blanch under pressure because the red blood cells present are confined to the vasculature.or suprahepatic inferior vena cava. and pigment cirrhosis with hepatomegaly is described as “bronze diabetes” and may not arise until late in the disease course. skin hyperpigmentation (particularly in sun-exposed areas). These droplets are of varying sizes.

The activated macrophages and T-lymphocytes release chemotactic cytokines to attract other leukocytes. The killing of M. The T-cells then release cytokines. leaving the epithelium exposed to the detergent action of the bile salts.Mounting response by B lymphocytes occurs after the antigen-presenting cells stimulate specific T cells against M.Scattered caseous necrosis is a secondary immune response that occurs because of TH1 T-lymphocyte activation of macrophages. The stones disrupt the protective mucus layer. IFN-y driven) and B-cells (TH2 response IL-4 driven)..absoluteastronomy. http://images.The ovaries are the site most commonly affected. With time. leading to the activation of both macrophages (TH1 response. tuberculosis is therefore dependent on the cell-mediated TH1 response. tuberculosis. and gallbladder hypomotility ensues. Such a “walled off” area (Ghon focus) is a potential source of reactivated should the patient later become immunosuppressed. as it is a facultative intracellular organism. The increasing distention and internal pressure within the gallbladder eventually result in ischemia. initiated 90% of the time by obstruction of the gallbladder neck or cystic duct. while the larger necrotic areas are simply “walled oft” and calcified. Prostaglandins released in the gall bladder wall further incite inflammation of the mucosa and deeper tissues.gif . Local inflammation is followed by the formation of . which leads to an enhanced inflammatory response against the foci of M. tuberculosis. bacteria invade the injured and necrotic tissue. immunoglobulins are rarely effective against M.images/g/gh/ghon_focus. Unfortunately. As the most common complication of cholelithiasis. Ectopic endometrium responds to hormonal influences in the same way as uterine endometrium. giant cells. the blood undergoes hemolysis and induces an inflammatory response around the ectopic endometrium. Small foci of bacteria are destroyed by this process. The end result is local tissue necrosis and a collection of macrophages. acute calculous cholecystitis typically results from chemical irritation and inflammation caused by the presence of stones in the gallbladder. during the woman’s menstrual period. tuberculosis. causing an infection. bleeding and shedding of tissue outside the uterus lead to the formation of blood collections. Thus. Acute calculous cholecystitis =acute inflammation of the gallbladder.secreting fibroblasts produced secondary to local cytokine secretion) that combine to form caseating granulomas. Finally..co. Endometriosis . Activated B-lymphocytes undergo class switching of their immunoglobulins from IgM to IgG and other subsets. and lymphocytes (as well as collagen.. because immunoglobulins are unable to reach the organism while it resides within macrophages.

capillary hemangiomas consist of thin-walled blood vessels with narrow lumens filled with blood and separated by connective tissue.. Vertigo is commonly associated with lightheadedness. vertigo and sensorineural hearing loss. 2. Dizziness is the sensation of .jpg Strawberry (infantile) hemangioma =a variant of a capillary hemangioma that is the most common benign vascular tumor in children. Tinnitus refers to ringing in the affected ear.. Capillary hemangiomas can be also found in deep tissues and the viscera. Vertigo is the subjective sensation of motion in the absence of actual motion. especially the liver. Many patients are diagnosed with endometriosis while being evaluated for infertility. -Strawberry hemangiomas appear during the first days or weeks after birth and grow rapidly during the first one to two years of life. Ectopic endometrial tissue also secretes prostaglandins that interfere with ovulation and tubal function. On microscopic examination. In the ovaries the collections of old blood may form endometriomas (chocolate cysts). Individual lesions can have superficial and deep components.medscape. Superficial infantile hemangiomas are bright-red compressible plaques with sharply demarcated borders and are referred to as strawberry hemangiomas. often accompanied by a feeling of fullness.au/images/endometriosis_over_bladder. Painful defecation (dyschezia) can also occur due to pelvic adhesions. 1. These vessels are lined by endothelium that rapidly proliferates during the growth phase of the tumor.adhesions and distortion of organ structure. The majority of these tumors regress by five to eight years of age. nausea and sometimes vomiting. Ménière’s disease is characterized by the triad of tinnitus.com. Deeper infantile hemangiomas have a duskier blue appearance. http://www. thought due to defective resorption of endolymph. Patients may have difficulty conceiving because of adhesions involving the ovaries and fallopian tubes.com/pi/emed/ck.jpg Ménière’s disease = a disorder of the inner ear characterized by an increased volume of endolymph. Painful intercourse (dyspareunia) is related to retroversion of the uterus and endometrial implants on the uterosacral ligaments. The resultant distention of the endolymphatic system causes damage to both the vestibular and cochlear components of the inner ear.swec. Nodularity of the uterosacral ligaments and fixed retroversion of the uterus are commonly found in patients with endometriosis on vaginal examination. they are not synonyms. http://img.gy/1048885-1083849-980. -Shedding of the ectopic tissue causes pain during the menstrual period (dysmenorrhea). Note that although dizziness and vertigo are often used interchangeably.

http://odlarmed. DIFF: . . nausea and vomiting. Hearing loss is sensorineural in Ménière’s disease. Moreover.lightheadedness. breast. while its specificity ranges from 80-94%. cirrhosis.Carcinoembryonic antigen (CEA) is a serum marker associated with colorectal cancer . However. an elevated serum AFP is associated with numerous other conditions. AFP is a useful marker in the evaluation of cirrhotic patients who are at increased risk for developing HCC. A rise in serum AFP to levels exceeding 500 mcg/L (with the normal range typically 10-20 mcg/L) in a high-risk patient is considered diagnostic of HCC. lung. -Despite these limitations. viral hepatitis). Hepatocellular carcinoma (HCC) -Normally produced by the fetal liver and yolk sac during gestation.Labyrinthitis = inflammation of the vestibular labyrinth that causes acute-onset vertigo. including pregnancy. as serum AFP levels do not correlate well with the size. .com/wp-content/uploads/2009/01/s-212a. 3. or pelvic inflammatory disease). tumors of gonadal origin.Otosclerosis is an inherited condition with onset in middle-age. A history of recurrent episodes would be unusual. The sensitivity of AFP in detecting HCC ranges from 41-65%. or prognosis of HCC. Vertigo does not occur. CA-125 is not an effective screening tool for ovarian cancer.Acid phosphatase is a secondary prostate tumor marker antigen that is also elevated in patients undergoing active osteoclast-initiated bone resorption.jpg DIFF: . and pancreatic cancer) and in patients with various benign conditions (such as endometriosis. and chronic liver disease (eg. . Patients often describe feeling like the room is spinning. the Rinne test will show air conduction superior to bone conduction in the affected ear (normal pattern). On physical examination. This neoplasm can also be diagnosed in regularly monitored cirrhotic patients who experience a sudden surge in AFP above their baselines. whereas vertigo is the subjective sensation of movement of one’s body or environment. alphafetoprotein (AFP) is a glycoprotein that is often elevated in patients with hepatocellular carcinoma (HCC). as its positive predictive value is only 3%.CA-125 is a serum marker elevated in more than 80% of those women with ovarian cancer. This serum marker is not without clinical limitations. it is also elevated in patients with other malignancies (endometrial. The Weber test will reveal lateralization to the healthy side. stage. Patients present with conductive hearing loss that occurs due to bony overgrowth of the footplate of the stapes.

sarcoidosis.Histologically. -NBTE associated with disseminated cancer is termed “marantic” (or “marasmic”) endocarditis. and bronchogenic carcinoma. although they may also be caused by endothelial injury. Sarcoidosis -Dry cough. When caused by hypercoagulability. assuming normal bone marrow function. silicosis. including tuberculosis. Lambert-Eaton syndrome is associated in most cases with oat cell carcinoma of the lung. NBTE is most often related to some underlying disease. Lambert-Eaton syndrome =autoimmune paraneoplastic myasthenic syndrome that affects the presynaptic calcium channels. sterile. tumorassociated release of procoagulants is thought responsible for the migratory thrombophlebitis (Trousseau syndrome) sometimes seen in patients with disseminated cancers. which may relate to procoagulant effects of circulating mucin. coccidioidomycosis).Non-bacterial thrombotic endocarditis (NBTE) =Small (1-5 mm). these vegetations consist of bland thrombus without accompanying inflammation or valvular damage.A compensatory increase in circulating erythropoietin levels would be expected in individuals with aplastic anemia and normal renal function.An increased reticulocyte index would be expected in a hemolytic or hemorrhagic anemia. The biopsy specimen shows a central collection of tightly clustered epithelioid macrophages surrounded by a rim of mononuclear . There is a particularly strong association of NBTE with mucinous adenocarcinomas of the pancreas and adenocarcinomas of the lung. such as a cancer. resulting in decreased presynaptic acetylcholine release. non-destructive fibrinous vegetations along the lines of closure of cardiac valve cusps . Reticulocyte count is low in aplastic anemia because there are few progenitor cells in the marrow. lymphoma. pulmonary infiltrates and hilar adenopathy can be found in a number of lung diseases. Transbronchial biopsy may be required to establish and/or confirm the diagnosis. endemic mycoses (histoplasmosis. derived from the term for cancer-related wasting of body tissues (“marasmus”). Aplastic anemia =The triad of low hemoglobin. . and berylliosis. By a similar mechanism. They are typically the result of a hypercoagulable state. and absent hematopoietic cells in the bone marrow . thrombocytopenia.

the pulmonary capillary wedge pressure remains within normal limits. Those affected are usually miners or industrial workers (especially those who work in battery manufacturing) who inhale particulate lead while working. The classic diagnostic finding on peripheral blood smear is coarse basophilic stippling on a background of hypochromic microcytic anemia. The hypochromic microcytic anemia results from inhibition of 6-ALA dehydratase and the resultant reduced incorporation of iron into heme. http://www.D/Basophilic-stippling.In 75% of cases ARDS arises within 24 hours of the precipitating cause. Adults with lead poisoning present with weakness. -However. -The combination of hilar adenopathy.cfm Adult respiratory distress syndrome (ARDS) . lead poisoning can occur in adults as well. In noncardiogenic pulmonary edema. 95% of cases arise within 72 hours. the pulmonary capillary endothelial injury results from endotoxin-induced release of injurious products from adherent leukocytes and/or ischemia-induced release of injurious cytokines. and alveolar hyaline membrane formation.virginia. In severe cases there may be neurologic signs. Matrix metalloproteinases Secreted by several different cell types (eg. macrophages. inflammation..Sepsis and shock are two major risk factors for ARDS .e. and noncaseating granulomas in an African American female suggest a diagnosis of sarcoidosis. On physical exam.cells — a non-caseating granuloma. lead poisoning (plumbism) is typically thought of as a pediatric condition (usually the result of children ingesting lead-containing paint chips). In sepsis and/or shock. In ARDS. .healthsystem. fibroblasts. The net effect of these defects is decreased hemoglobin synthesis. abdominal pain and constipation. Basophilic stippling results from the abnormal aggregation of ribosomes. Lead poisoning -In the United States. patients may have blue “lead lines” at the junction of the teeth and gingivae. widespread injury to the pulmonary microvascular endothelium and/or the alveolar epithelium causes the alveolocapillary membrane to be leaky. This endothelial injury causes pulmonary interstitial and intra-alveolar edema. pulmonary infiltrates..

a rich lipid core.htm . distinct intracellular features are lost (pyknotic nuclei.3-5 day: macrophage infiltration and phagocytosis . -Several months or years after an infarct. some epithelial cells). A thin fibrous cap.By 2-3 weeks. matrix metalloproteinases primarily function in the degradation of collagen and other proteins in the extracellular matrix.. macrophages phagocytize the products of neuron and myelin breakdown. Nissl substance disappears. The amassed myofibroblasts initiate wound contraction during healing by second intention. Contractures may occur when unusually pronounced MMP activity results in excessive wound contraction. as it encourages both myofibroblast accumulation at the wound edges and scar tissue remodeling.com/media/image/AJMC_07decDavidson_Fig_S260. http://www. the process of tissue destruction and .ajmc.The major determinant of whether or not a coronary artery plaque will cause ischemic myocardial injury is the rate at which it occludes the involved artery. -A thin fibrous cap. Astrocytes proliferate around the area of necrosis (reactive astrocytosis. A slowly developing occlusion would allow for formation of collaterals that could prevent myocardial necrosis.4-12 hours after the ischemic event: the earliest definitive microscopic signs of irreversible ischemic injury in the infract are eosinophilic (red) neurons.ucsf.1-2 weeks: reactive gliosis and vascular proliferation around the necrotic area (macroscopic = liquefactive necrosis) . loss of Nissl substance) . MMP activity is important in wound healing. .24-72 h: necrosis and neutrophilic infiltration .. http://missinglink. Keloids are not known to be specifically related to excessive matrix metalloproteinase or myofibroblast activity. synovial cells.Keloids are hypertrophic scars in which excessive collagenous scar tissue deposited by fibroblasts permanently extends beyond the margins of the original wound. . or gliosis).These “red neurons” are a sign of irreversible neuronal injury.edu/lm/int. and the nucleus becomes pyknotic (small and deeply basophilic). These damaged neurons subsequently undergo fragmentation and will ultimately be phagocytized by macrophages.to_Injury/InfarctIntro. Coronary artery plaque -A slowly developing occlusion would allow for formation of collaterals that could prevent myocardial necrosis. New vessel formation peripheral to the necrotic area may begin at this time.gif Eosinophilic neurons .> 2 weeks: glial scar (macroscopic = cystic area surrounded by gliosis) .neutrophils. and active inflammation in the atheroma would all decrease plaque stability and thus potentially promote rapid coronary occlusion via superimposed thrombosis if the plaque were to rupture. and active inflammation in the atheroma would all decrease plaque stability and thus potentially promote rapid coronary occlusion via superimposed thrombosis if the plaque were to rupture. a rich lipid core.

. . http://www..dizziness-and-balance. -Pseudobulbar palsy is characterized by head and neck muscle weakness. to the contrary.. The severity of chronic bronchitis is largely dependent upon the extent to which the luminal diameter of the bronchi and bronchioles is decreased.tulane. The major contributor to this wall thickening is submucosal mucous gland enlargement which can be quantified by the ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage (Reid index). is caused by a pathologic process in the nuclei of these nerves. Bulbar palsy.som. This palsy is called “pseudobulbar” because the nuclei of corresponding cranial nerves remain intact.edu/classwar. This cavity is surrounded by a wall formed by astrocyte processes (glial scar) and new capillaries. .ontine%20myelinolysis. Involvement of teeth leads to . A cystic cavity replaces brain tissue in the ischemic area.The typical clinical features include quadriplegia due to demyelination of the corticospinal tracts and pseudobulbar palsy due to demyelination of the corticobulbar tracts of CN IX.4.c.edu/classwar.there is progressive thickening of the walls of the bronchi and bronchioles.html http://www.8/Lung_Review/Lung-20.tulane. As chronic bronchitis progresses both the total bronchial wall thickness and the Reid index increase. skin and sclera.html Central pontine myelinolysis =Rapid correction of chronic hyponatremia= may lead to osmotic demyelination of the axons in the central part of the pons.html “Blue sclera” = presumes “osteogenesis imperfecta” until ruled out.organization is complete.. Type I collagen is the predominant collagen in the bones but it is also present in teeth ligaments... . The Reid index is normally = 0.8/Lung_Review/Lung-21. and dysarthria. Chronic bronchitis = caused by smoking and exacerbated periodically by superimposed bacterial bronchitis. Thus the degree of elevation of the Reid index correlates with the duration and severity of the chronic bronchitis.Osteogenesis imperfecta is the heritable disorder resulting from quantitative or qualitative abnormalities in type I collagen which results in abnormally weak bones.som. dysphagia. http://www. X and XI.

thachers. Some patients are also susceptible to bruises and hearing loss. A prolactin-secreting pituitary adenoma is the most likely cause of both amenorrhea and visual defects. .. The most common cause of bitemporal hemianopia is a pituitary tumor. -The Erb-B2 protein is a transmembrane glycoprotein with tyrosine kinase activity. is often associated with aggressive tumors. and can be used to predict therapeutic response to anti-HER-2 monoclonal antibody (trastuzumab).eyecancer. lung. These tumors occur in children and cause obstructive hydrocephalus. http://www.imperfecta_blue_sclera. and joints can have excessive laxity.org/images/Osteogenesis_imperfecta. In most subjects.JPG Bitemporal hemianopsia =Loss of peripheral vision =caused by pressure on the central part of the optic chiasm. “Pinealoma” = a generic term for a tumor of the pineal region. Their presence in tumor cells positively correlates with response to anti-estrogen treatment (tamoxifen) or chemotherapy..a+bilateral+retinoblastoma The ERB-B2gene (also called HER-2Neu) = a member of the epidermal growth factor receptor family that is overexpressed in 25-30% of breast cancers as well as in adenocarcinomas of the ovary.org/images/Ost. Most often they are germinomas. causing endocrine disorders. and salivary glands.thachers. . The overexpression of this protein.” The sclera are often blue.. stomach. Pituitary tumors can also secrete hormones. osteogenesis imperfecta is transmitted by autosomal dominant inheritance.. Parinaud syndrome.com/ViewImage. -The other markers used to predict tumor response to treatment are the estrogen and progesterone receptors (ER/PR). The clinical phenotype of osteogenesis imperfecta can vary from a mild asymptomatic defect to the lethal form. is only weakly associated with a poor prognosis and is not helpful in forecasting tumor response to broader chemotherapy. http://www. and is present in minute amounts in normal breast and ovarian cells. however.JPG http://www.malformed small teeth a condition called “dentinogenesis imperfecta.Most patients with osteogenesis imperfecta have a mutation in the gene that encodes type I bone collagen. and precocious puberty.

ca/TROP.N-myc is a proto-oncogene located on chromosome 2 that is associated with neuroblastomas and small cell carcinoma of the lung. gelatinous sheets surrounded by a thick fibrous capsule. the echinococcal larvae implant within the capillaries.. http://www.bio.19. with subsequent signs and symptoms dependent upon the site of the cysts and their size. granulosus hydatid cysts. multilocularis infection. though other organs can be involved.htm . Mutated ras results in an increased cell response to growth factor stimulation. -The sis proto-oncogene encodes the platelet-derived growth factor. Most cases occur either in individuals from endemic regions (eg...Ras. Ultimately.org/2007/06/14/pulmonary-hydatid-cyst/ http://workforce.medicine. or MRI) and serology testing can be used to establish the diagnosis. Overexpression of this gene is seen in astrocytomas and osteosarcomas. muscle.DIFF: .12a. triggering an inflammatory reaction composed of monocytes and eosinophils. The liver is affected in most patients. patients may experience hepatomegaly. nausea.jpg Echinococcus granulosus =the most common cause of hydatid cysts in humans. http://www. New Zealand. The outer cyst wall is composed of many layers of delicate.jpg http://www.com/nature/journ. CT..hapter3/large3/03-119A.gif http://www.. granulosus.hology_platyhelminths3. Unilocular lesions are typical of E.laris%20hydatid%20cyst. Middle East.org/tropica. Surgery and adjunctive chemotherapy with mebendazole or albendazole is considered the treatment of choice for those symptomatic patients with E.jpg http://www.radpod. -Microscopic examination of hydatid cyst tissue demonstrates a characteristic encapsulated and calcified cyst (“eggshell calcification”) that contains fluid and budding cells that will eventually become daughter cysts. including the lung. Aspiration is generally inadvisable. -The ras protein is a component of the MAP kinase-associated signaling pathway. Iceland. or bone. Austria.miami..cup. -Bcl-2 encodes the group of proteins that inhibit apoptosis. Mediterranean countries. right upper quadrant pain.mcgill.. and vomiting./images/387773ab. and multilocular lesions are typical of E.isradiology.edu/buckelew/. -When infection first occurs. This molecular abnormality has no bearing on breast cancer response to therapy. -Both imaging (ultrasound. Overexpression of the Bcl-2 protein is observed in follicular lymphomas and facilitates neoplastic cell survival. -The initial infection is always asymptomatic. as the spilling of cyst contents within the peritoneum can cause anaphylactic shock.nature. but others encyst.eps.2. and southern Africa) or in those people residing in the Southwest region of the United States with sheep and dog exposure (two animals that participate in the tapeworm life cycle). Some larvae are destroyed by the host. southern South America.edu/~cmallery/150/gene/c7..

-Patients with Barrett esophagus have a 30-40 times increased risk of developing esophageal adenocarcinoma. uterus.f1. they irritate the mucosa. When acidic gastric contents enter the esophagus.Some of the paraneoplastic syndromes do occur because of the production of hormone-like substances from tumor cells. lack of coordination. At this point. This malignant cancer typically develops from the metaplastic intestinal epithelium in the distal part of esophagus: it is clinically silent until it obstructs the esophageal lumen. Paraneoplastic cerebellar degeneration occurs predominantly in patients with cancer of the ovary. This metaplasia is hypothesized to be adaptive at first. Sustained epithelial damage promotes the replacement of normal.http://www. Regular biopsies of the area should be performed to monitor for cellular dysplasia. Examples of paraneoplastic syndromes with an endocrine etiology are Cushing syndrome (due to secretion of ACTH) and hypercalcemia (due to production of PTHrP).bmjjournals.ages/large/cp35337.jpg Paraneoplastic syndromes = non-metastatic systemic effects that accompany malignant disease.jpg http://jcp. it is very important to diagnose Barrett esophagus early. stratified squamous epithelium with intestinal—type columnar cells..edu/beWeb/images/newesphcan2.jpeg Hepatic adenomas = found predominantly in young and middle-aged women who have a lengthy history of oral contraceptive usage. http://pathology2. Barrett esophagus .jhu.com/content. Hepatic adenomas are typically identified .pathconsultddx.. Antibodies produced against tumor cells cross-react with neurons and cause their degeneration.com/imag.59867506708294/gr1-sml. the cancer is usually large: thus. Other neurologic paraneoplastic disorders are limbic encephalitis and sensors neuropathy. and nystagmus. . breast. the rarely-occurring neurologic paraneoplastic syndromes have an autoimmune etiology. Patients present with limb and truncal ataxia..People with a history of severe and longstanding reflux disease are most prone to Barrett esophagus. They are often caused by substances produced from tumor cells -For example.. as intestinal-type epithelium is more resistant to acidic environment: however itis also a major risk factor for esophageal adenocarcinoma. causing inflammation and subsequent epithelial necrosis. and small-cell carcinoma of the lung. dysarthria.

usapowerlifting..medscape. which together form the striatum. Serum AFP levels are not elevated. Loss of GABA-containing neurons leads to decreased GABA in the brain: this is the most characteristic biochemical feature of Huntington disease. flat affect. Caudate atrophy leads to the typical dilation of the frontal horns of the lateral ventricles and microscopy of the atrophic areas reveals gliosis and neuronal loss.org/docrep/v4700e/V4700E0O.gy/336139-416016-10513. or when an individual suddenly collapses because of rupture and intraabdominal bleeding. The disease classically presents between 30 and 40 years of age with an insidious onset of personality changes followed by physical symptoms.com/newsletter/07/photos/fig8. when imaging is obtained for unrelated issues.when patients complain of abdominal pain in the epigastrium or right upper quadrant. The patients may demonstrate aggressiveness.. decreased memory and concentration. -The characteristic abnormality seen in patients with Huntington disease is bilateral atrophy of the caudate nucleus and putamen. Huntington disease =neurodegenerative disorder inherited as an autosomal dominant trait. depression or anxiety.gif .fao.com/imag1/noeffect. cerebellum and olfactory system and is thought to participate in formation of new memories.GIF The most potent chemotactic eicosanoid is leukotriene B4 Other significant chemotactic agents include 5-HETE (the leukotriene precursor) and complement component C5a. http://www. It is a unique neurotransmitter in that it freely diffuses across cell membranes and does not need to interact with other neurons via a synapse. hippocampus. less commonly bradykinesia. and psychosis. http://img.com/pi/emed/ck. http://cgmp.jpg Nitric oxide =found in the cortex.jpg Arachidonic acid http://www. The movement disorder presents with purposeless choreiform movements of the extremities or. hypothalamus.blauplanet.

Colon cancer .Serum carcinoembryonic antigen (CEA) levels are increased in 60-90% of patients with colon cancer. -Although not useful for diagnosis. weight loss. .Celiac disease is diagnosed when flattening of the mucosa with loss of villi and chronic inflammatory infiltration of the lamina propria is seen on small intestine biopsy. It is produced in the embryonic pancreas. etc. Abnormal response to tissue transglutaminase.c. These cells may resemble lymphocytes.vcu. . such as inflammatory bowel disease. a patient’s CEA level is a sensitive indicator of colorectal cancer recurrence. is found. Other antibodies frequently found in patients with celiac disease are anti-endomysial and antireticulin. and deficiencies of vitamins and minerals occur. CEA is a glycoprotein involved in cell adhesion. gastric and breast malignancies. It comprises 10-20% of all malignant lung tumors. On light microscopy itis composed of round or oval cells with scant cytoplasm and large hyperchromatic nuclei. A rising CEA level in such a patient is an indication to search for cancer recurrence/metastases (with chest x-ray. This disorder may manifest at an early age or later in life and is caused by hypersensitivity to gluten. The most pronounced changes are seen in the duodenum and proximal ileum because the concentration of gluten is higher there.pathology. This tumor arises from the primitive cells of the basal layer of the bronchial epithelium. -Small cell lung carcinoma is strongly associated with smoking and is usually centrally located. http://www. but are smaller in size. an enzyme that participates in metabolism of gluten. Tumor cells can form sheets or clusters.). liver and intestine. cirrhosis and pancreatitis. Immunoglobulin A (IgA) antibodies to gliadin (a mixture of polypeptides extracted from gluten) is a typical finding in these patients. It should be measured in colon cancer patients perioperatively and in regular intervals after surgery. -Celiac sprue is thought to occur by an immune-mediated mechanism in genetically-susceptible individuals. as well as in a number of benign diseases. Smokers have higher CEA levels than non-smokers. and is also detected in minute amounts in the serum of healthy adults. a component of wheat and some other related grains. The CEA level cannot be used to diagnose colon cancer because it is also increased in pancreatic. Celiac disease (gluten-sensitive enteropathy) = symptoms of malabsorption. abdominal CT scan colonoscopy.html Small cell lung carcinoma =also called undifferentiated or oat cell carcinoma.edu/education/gi/lab2. Diarrhea steatorrhea.

http://www.cute_pyelonephritis_02. Acute pyelonephritis. -Acute pyelonephritis is usually caused by gram-negative rods that ascend from the bladder.pathologyatlas.ro/patho. shaking chills. VwBC casts bacteriuria. without reflux. . . Normally. -Clinically.jpg Hirschsprung disease Submucosal (Meissner) and myenteric (Auerbach) autonomic plexi are absent in the affected segment of the bowel in Hirschsprung disease. If only a short area is affected.In addition. =massive infiltration of the interstitium by polymorphonuclear leukocytes (neutrophils). In this case persistent constipation. Rectal biopsy is necessary for the diagnosis of Hirschsprung disease a condition that results from the failure of neural crest cells to migrate to the intestinal wall. such as neuron specific enolase.Abundant mitoses are usually seen. along with microabscesses in the interstitium.. tubular epithelial disruption may be seen. Since those cells migrate caudally. .. acute pyelonephritis manifests with flank and abdominal pain. chromogranin and synaptophysin. abdominal distention and failure to thrive are typical. Barium enema in such patients shows narrowing in the rectosigmoid area. and often hematuria. Proximal to the obstruction the bowel is dilated and filled with feces. Urinalysis reveals pyuria (WBCs). -Costovertebral angle (CVA) tenderness is commonly found on physical examination. and vomiting. the rectum is always involved. as well as a large number of neutrophils in the tubular lumina. The submucosa of rectum (the narrowed segment) should be biopsied to demonstrate the absence of ganglionic cells. fever.If a large area of the bowel is involved the disease will manifest during the first few days of life with obstructive symptoms (failure to pass meconium. nausea. On electron microscopy some of the cells are found to have secretory granules in the cytoplasm. the disease may go undetected for months or years. -Small cell carcinomas can display varying degrees of neuroendocrine differentiation. Immunohistochemical stains are frequently positive for neuroendocrine markers. The submucosa of the narrowed area is the most superficial layer where the absence of ganglion cells can be seen. bilious vomiting and abdominal distention). these cells develop into ganglion cells of the submucosal (Meissner) and myenteric (Auerbach) plexi of the bowel wall. bacteria remain localized in the bladder and do not reach ureters or renal tissue. Ureterovesical reflux is necessary in the pathogenesis of acute pyelonephritis.

html http://orthoinfo. Production of monoclonal immunoglobulin by abnormal plasma cells impairs the secretion of normal immunoglobulins. The presence of M protein (monoclonal immunoglobulin) in the serum and monoclonal light chains (Bence-Jones protein) in the urine is characteristic for multiple myeloma. deposition of amyloid.utah. 4. It is seen as an eosinophilic extracellular deposit on H&E stain.t/amyloid/kidneyLargeA. in order to determine the type of this patient’s lipid disorder and to rule out underlying diabetes. and shows “apple-green” birefringence with Congo red stain viewed under polarized light. 5. Xanthelasmas are dermal accumulations of benign-appearing macrophages with abundant finely vacuolated (foamy) cytoplasm.jpg http://stanfordhospital. tongue and other muscles. hypercalcemia leading to metastatic calcification and inflammation by macrophages and giant cells.jpg . It manifests with fatigue.org/ImageG. http://library. and constipation. diabetics may develop a secondary Type IV or V hyperlipidemia (increased VLDL chylomicrons) and/or a secondary diabetic dyslipidemia with elevated LDL cholesterol and low HDL cholesterol. The following symptoms are characteristic for this disease: 1. and leads to increased susceptibility to infection..med. Hyperimmunoglobulinemia also causes roleaux formation on peripheral blood smear and an increased ESR.aaos. Due in part to insulin resistance promoting increased VLDL production.Hyperlipidemia and/or dyslipidemia can result in xanthomas (including xanthelasmas). confusion. 2. Multiple myeloma =plasma cell neoplasm that occurs in patients 40 to 60 years of age. phospholipids. AL amyloidosis contributes into the development of renal failure in multiple myeloma. Patients present with bone pain pathologic fractures. and “punched-out” lytic lesions on X-ray. 3. AL amyloid forms due to accumulation of monoclonal immunoglobulin light chains.. her serum lipids and blood glucose should be measured. 6. Thus.org/figures/A00086F01. containing cholesterol (free and esterified). amyloid id also characteristically deposited in the heart. and triglycerides. Normocytic and normochromic anemia develops due to bone marrow infiltration and replacement by malignant plasma cells with resultant suppression of normal hematopoiesis. Hypercalcemia occurs due to increased bone destruction. Bence-Jones casts in the tubules. Renal failure develops due to infiltration of kidney by plasma cells. Secretion of IL-6 (osteoclast activating factor) by neoplastic cells activates osteoclasts and leads to bone resorption with resultant osteopenia.Xanthoma .edu/WebPath/HEMEHTML/HEME070.

IgM..utah. alcoholic cirrhosis.html http://library. Urine contains dysmorphic red cells RBC casts and some protein (usually < 1 g/day). and is often preceded by HBV-induced cirrhosis. the integration of viral DNA into the cellular genome of the host is considered a trigger of neoplastic changes. . -On light microscopy. the glomeruli are enlarged and hypercellular. fever. cola-colored urine and facial edema 2-4 weeks following a streptococcal infection of either the pharynx or skin in a 6 to 10-yearold child . Elevations of creatinine and BUN may also be present. If there is damaged DNA. . On electron microscopy.Other risk factors for hepatocellular carcinoma include HCV. aflatoxins and hemochromatosis.jpg http://library. and C3 along the basement membrane and in the mesangium of glomeruli (“lumpybumpy” appearance).Physical examination reveals facial and periorbital edema and mild to moderate hypertension.utah. p53 regulates cell proliferation. http://www. but if the damage is so severe that repair is impossible the cell will proceed instead to apoptosis. The viral protein HBV activates the synthesis of insulin-like growth factor II and receptors for insulin-like growth factor I. thereby stimulating cell proliferation. p53 will prevent the cell from progressing to mitosis. there are electron-dense deposits on the epithelial side on the basement membrane.edu/WebPath/RENAHTML/RENAL086. It acts during phase 01 of the cell cycle to detect abnormalities of the cellular genome. the cell will subsequently be allowed to divide. It is inactivated in many tumors.Hepatocellular carcinoma =A liver mass associated with an increased alpha-fetoprotein level . Immunofluorescence studies reveal granular deposits of IgG.edu/WebPath/RENAHTML/RENAL087.Development of hepatocellular carcinoma is strongly associated with HBV infection. causing the cell to be arrested in the G1 phase.html p53 = a tumor suppressor gene that controls cell division and apoptosis. All these events result from integration of the viral genome into host cells. Although the pathogenesis of HBV-induced hepatocellular carcinoma is still unclear.. These “humps” are composed of immune complexes. If the DNA can be repaired. p53 is nicknamed ‘the molecular policeman” because of its important role in guarding the integrity of . It is also believed that chronic inflammation and regeneration induced by HBV infection facilitates accumulation of mutations in hepatocytes leading to carcinogenesis._glomerulonephritis_02. Poststreptococcal glomerulonephritis (PSGN) = Abrupt onset of malaise.pathologyatlas. Another effect of HBV gene products is suppression of the p53 tumor suppressor / cell cycle regulatory gene in host cells.med.ro/patho.In normal individuals.med.

V. IAPP) is one factor thought to be responsible for this beta cell dysfunction. The partial thromboplastin time (PTT) assesses the activity of factors II. Hemophilia =X-linked recessive bleeding disorder that develops due to a decreased level of factor VIII (hemophilia A) or factor IX (hemophilia B) in serum. It is a physiologic anticoagulant that degrades factors Va and Vllla.. VII. V.Coagulation studies in both types of hemophilia reveal a normal bleeding time and platelet count. a normal PT and a prolonged PTT. The prothrombin time (PT) tests the extrinsic clotting pathway and reflects the function of factors II.adindoc_files/image002. A number of genetic and acquired factors are implicated in the beta-cell dysregulation of type 2 diabetes. Administration of thrombin however will make up for the deficiency and result in blood clotting. Islet associated polypeptide (amylin. Xl and XII the intrinsic clotting pathway . Although still very controversial. causing poor glucose tolerance. . It triggers the intrinsic coagulation pathway by activating factor Xl. Type 2 diabetes mellitus . Factors VIII and IX are components of the intrinsic coagulation pathway. Diagnosis of hemophilia A and B is made by measuring plasma levels of factors VIII and IX respectively. IAPP is co-secreted with insulin from beta cells: IAPP is then deposited in islet cells.jpg http://intmedweb. many researchers believe that insulin resistance is the primary abnormality in type 2 diabetes mellitus. http://www.edu/grand_. These factors are necessary for activation of factor X: activated factor X (Xa).Two cardinal defects involved in pathophysiology of type 2 diabetes mellitus are insulin resistance and defective insulin secretion.Factor Xll (Hageman) is synthesized by the liver and is activated by endothelial injury. in turn catalyzes the conversion of prothrombin (factor II) into thrombin. Deposits of islet amyloid polypeptide are universally seen . . X.Early in the pathogenesis of type 2 diabetes glucose tolerance remains normal because of a compensatory increase in insulin secretion from beta cells.jpg Protein C = vitamin K dependent factor synthesized in the liver.org/images2/mildhemophilia. This compensatory insulin response from beta cell insulin ultimately fails. IX.genetic material.moondragon. and X.wfubmc.. VIII. . activation of factor X and subsequent conversion of prothrombin into thrombin does not occur. In the absence of factors VIII or IX.

In the general population HLA-DR3 and DR4 are seen in approximately 40% of subjects: however in patients with type 1 diabetes mellitus HLA-DR3 and DR4 haplotypes are seen in more than 9O% of subjects. -Type 1 diabetes has a very strong genetic component.Because pancreatic enzymes are necessary for the proper absorption of nutrients in the gut. . These patients need insulin for survival. . . Type 1 diabetes = occurs when autoimmune response is triggered by an environmental insult in genetically-susceptible individuals. The cells that are most susceptible to increased oxidation in vitamin E deficiency are neurons with long axons (and therefore increased surface area) and erythrocytes. In Caucasians there is a strong association of DR3 and DR4 haplotypes with diabetes mellitus. vitamin E deficiency predisposes those cell membranes with high fatty acid content to oxidative injury. Vitamin E =primarily serves to protect fatty acids from oxidation. skeletal myopathy. The most common clinical manifestations of vitamin E deficiency are neuromuscular disease (eg. However this theory has been seriously questioned by the normal glucose tolerance and normal insulin response of transgenic mice that over-express human IAPP. Most researchers believe that these antibodies do not cause beta cell destruction but are instead generated as a result of beta-cell destruction by cellular immunity by T lymphocytes in particular. Gene polymorphism within the major histocompatibility complex contributes to disease in humans. Involvement of the dorsal column in the spinal cord is associated with the loss of proprioception and vibratory sense. Twin studies have shown a concordance rate of 50% in identical twins.in pancreatic islets of patients with type 2 diabetes mellitus. E and K frequently occur in patients afflicted with cystic fibrosis. HLA-DQ and DR are the most important determinants of type 1 diabetes mellitus. pigmented retinopathy) and hemolytic anemia. Blood glucose starts to increase when lO% of beta cells remain. Antibodies against islet antigens can be detected in serum of a large number of patients with type 1 diabetes mellitus. As a result.Patients with type 2 diabetes retain at least some beta cell function but patients with type 1 diabetes mellitus develop absolute deficiency of insulin secondary to immune destruction of pancreatic beta cells. Infiltration of islets by inflammatory cells is called insulitis. spinocerebellar ataxia. Spinocerebellar tract involvement causes ataxia. D. Islet associated polypeptide was originally thought to be the causative agent in beta cell apoptosis and defective insulin secretion. deficiencies of the fat-soluble vitamins A.

g. aorta. and the circle of Willis. This tumor is extremely aggressive and associated with a poor prognosis. the region most prone to atherosclerosis is likely the carotid sinus at the origin of the internal carotid artery.g. The upper limb arteries are usually spared. Hepatic angiosarcomas =associated with recent or remote exposure to vinyl chloride. After the abdominal aorta. with marked hepatomegaly a common result. In humans. dual blood supply. patients tend to present with jaundice or abnormal hepatic enzymes. the abdominal aorta is the vessel most heavily involved with lesions most prominent around the ostia of major arterial branches. the next most heavily involved vessels are (in decreasing order): the coronary arteries. The mesenteric and renal arteries tend to be spared except at their ostia (openings from the aorta). The liver is the second most common site of metastatic spread (after the lymph nodes) because of its large size. the nodules outgrow their vascular supply and become centrally necrotic and umbilicated. Even with significant metastatic involvement. . or Thorotrast. coronary and popliteal arteries). -Patients with liver metastases typically have multiple nodules throughout the liver that may replace more than 80% of hepatic parenchyma. In the carotid system. as most patients die within one year. -Although the common carotid artery may be affected by atherosclerosis it is less commonly involved than the abdominal aorta and other arteries. carotid. patients may have no clinical or laboratory signs suggestive of hepatic insufficiency. Grossly it appears as a treelike mass that grows along the intrahepatic portal tract system. and the filtration function of Kupffer cells..Atherosclerotic plaques = develop predominantly in large elastic arteries (e. and in large or medium-sized muscular arteries (e. the popliteal arteries the internal carotids. typically resulting in extensive .Intrahepatic cholangiocarcinoma= a rare malignancy that arises from the intraand extrahepatic bile ducts. and iliac arteries). high perfusion rate. Once the majority of the liver parenchyma is destroyed or the major bile ducts become obstructed with tumor however. Liver Metastases =the most common malignant neoplasms of the adult liver and are twenty times more common than hepatocellular carcinoma. arsenic. Frequently.

http://www..med. hyperchromatic cells with bizarre nuclei and atypical mitoses are commonly observed. The prognosis is very poor. esophageal adenocarcinoma. Axonal degeneration of peripheral nerves can cause numbness or paresthesias. combined degeneration -B12 deficiency occurs due to abnormal myelin synthesis./Images/10533/PAXIT038. and pathologic reflexes (Babinski sign)..ohio-stat. In Asia.edu/neuroslides/slide164.html Esophageal squamous cell carcinoma (SCC) =demonstrates flattened polyhedral or ovoid epithelial cells with eosinophilic cytoplasm keratin nests or “pearls” within or between cells. especially when the patients eyes are closed (sensory ataxia).urmc.brown.pathology. Caroli disease and choledochal cysts).html . -The incidence of esophageal SCC is decreasing in the United States. combined degeneration.med. congenital fibropolycystic diseases of the biliary system (eg.. eventually.iary/cholangiosarcoma. The most significant risk factors for the development of SCC in the United States include cigarette smoking and alcohol intake. Gait abnormalities are typical. Large.intrahepatic metastasis. http://www. and a history of Thorotrast exposure. Upper motor neuron signs: spastic paresis. and intercellular bridging. Lateral corticospinal tracts.rochester.pathology. Subacute. 2. the chewing of betel nuts and the consumption of foods containing N-nitroso compounds are commonly associated with the development of SCC. -Esophageal squamous cell carcinoma typically presents with progressive solid food dysphagia that may be accompanied by weight loss. The myelopathy associated with vitamin B12 deficiency is called subacute. “Combined” refers to the degeneration of both ascending (dorsal columns) and descending (corticospinal tract) pathways./Images/10533/PAXIT002.. Risk factors include primary sclerosing cholangitis.. hyperreflexia. Damage to these tracts leads to bilateral loss of position and vibration sensation.edu/Courses/Digit. It leads to degeneration of the following: 1. with middle-aged and older individuals of African or Asian heritage at greatest risk for developing the disease.JPG http://www.. 3. Dorsal columns of the spinal cord.ohio-stat. Chronic gastrointestinal blood loss is a frequent finding in this patient population and may result in iron deficiency anemia. http://www.JPG DIFF: -Heartburn and reflux esophagitis are associated with the development of Barrett’s metaplasia and.

edu/courses/Biol566/Images/Adherontypes.le. fibronectin.png . Compression may be from bone fragments or disc herniation. Because integrins bind ligands with relatively low affinity. S phase .aan. A high proliferation rate suggests a high tumor grade and. -Fibronectins are large glycoproteins produced by fibroblasts and some epithelial cells.wku. http://www. http://www. -Patients with anterior spinal cord syndrome usually have complete loss of strength below the level of injury with loss of pain and temperature sensation but preserved vibratory senses.jpg http://www.anaesthesiauk. serving as a mediator of normal cell adhesion and migration. Fibronectin binds to integrins.ac. matrix collagen. The integrins are a family of transmembrane protein receptors that interact with the extracellular matrix by binding to collagen.The avid uptake of bromodeoxyuridine by the tumor reflects the high number of tumor cells in S phase (preparing to divide) .com/images/spinal-cord4.cadherins . and laminin. and glycosaminoglycans. cells are allowed some flexibility to explore the surrounding environment without becoming affixed to one location or losing an attachment altogether.Anterior spinal artery syndrome = a result of compression/occlusion of the artery that runs along the front of the spinal cord.gif Adhesion molecules = integrins. selectins. http://bioweb. It contributes to vascular endothelial cell attachment to the basement membrane .com/globals/axon/assets/4817.Keratan sulfate is a galactose-containing glycosaminoglycan that may play a role in maintaining type I collagen fibril organization in the cornea.JPG Heparan sulfate = a proteoglycan component of the extra cellular matrix that is primarily associated with reticular fibers and basal laminae. and lg superfamily members. therefore a poor prognosis.uk/ge/genie/vgec/images/cellcycle.

kmu. -Histologically urticaria presents with subtle features. Excessive hCG also stimulates ovarian growth and can cause the formation of theca-lutein cysts.Hydatidiform moles . Epidermal changes are not identified. -In the majority of patients with a complete mole. Invasive moles and choriocarcinomas can be detected by serial measurements of hCG levels and are treated with chemotherapy. an IgE-independent urticaria can also develop after exposure to substances that directly stimulate mast cell degranulation (eg. Some patients have severe nausea and vomiting as the result of increased hCG secretion by the proliferating trophoblast. -A complete mole will cause vaginal bleeding during the first trimester of pregnancy. antibiotics and radiographic contrast media). A mild superficial infiltrate composed of mononuclear cells and occasional eosinophils is observed immediately around dermal venules. Microscopic examination of a complete mole would reveal large villi with decreased villous blood vessels and proliferation of the villous trophoblastic lining. opiates.tw/ch09/Slide77.class. An invasive mole would consist of hydropic villi and proliferated trophoblast.jpg Hemochromatosis . http://strawberriesweb. or “hives” = common transient dermatologic disorder that arises secondary to the antigeninduced degranulation of focal mast cells through IgE antibody sensitization.jpg http://pathology.gov. The lesions may coalesce into larger lesions that assume annular linear or acriform shapes. Superficially.characteristically have the macroscopic appearance of a “bunch of grapes. hemochromatosis is an autosomal recessive disease characterized by abnormally high iron . The size of uterus may be out of proportion to the gestational age.nsw. http://www. evacuation leads to recovery.sswahs. while choriocarcinoma would contain atypical cytotrophoblastic and synticyotrophoblastic cells with foci of hemorrhage and necrosis. -Both degranulation pathways cause microvasculature hyperpermeability and the formation of wheals that typically surface and resolve within hours with some episodes persisting for days to months. In some.htm Urticaria.com/urticaria. Alternatively.” -Hydatidiform moles are the result of trophoblast proliferation.au/sswahs/sgog/assets/Mole. an invasive mole (penetrates the uterine wall) or choriocarcinoma (malignancy of trophoblastic cells) may develop. Fetal tissue is absent.Caused by a mutation of the HFE gene on chromosome 6. however. the collagen bundles are parted by dermal edema and the lymphatic channels are dilated with excess transudate.edu.

Schwannomas. -Schwannomas are biphasic: highly cellular areas (Antoni A pattern) are intermixed with myxoid areas of low cellularity (Antoni B pattern). oval nuclei.fig. a characteristic “foamy” appearance to cytoplasm. Liver cirrhosis and hepatocellular carcinoma are two of the more ominous potential complications of this disease.figures/723539. pancreas. and are peripheral: thus .. The cells in the Antoni A areas may form “palisading” patterns (like a picket fence).com/journals/cd. and retinitis pigmentosa.asp?IDNUM=301210 http://www. These changes occur due to accumulation of lipids in the cells of intestinal absorptive epithelium. Impaired synthesis of apoB is present in abetalipoproteinemia. Microscopically they are composed of spindle cells.gif Abetalipoproteinemia = normal intestinal mucosal structure and epithelial cells with clear (or foamy) cytoplasm. which is more prominent on the tips of the villi. primarily in parenchymal organs such as the heart. By middle adulthood. there is unregulated expression of the iron uptake proteins and an excessive amount of iron is absorbed gastrointestinally. -Apolipoprotein B (apoB) is a lipid transport protein that coats chylomicrons. Another important S100-positive tumor is the melanoma (both melanocytes and Schwann cells are derived from neural crest cells).gastrointestinal absorption.. as oligodendrocytes are to the CNS. http://www.. -Schwannomas are universally S100 positive.nl/im. Excessive lipids are stored in the intestinal epithelium cells. and both synthesize myelin. -Schwann cells are to the peripheral nervous system. The crucial site for HFE expression is the basolateral surface of epithelial cells of the small intestine crypts. which determines the intensity of apical iron uptake expression. may arise within the cranial vault and spinal canal.jpg Schwannomas =tumors of the peripheral nervous system that arise from Schwann cells. http://www.pathologieutrecht. despite belonging to the PNS. neurologic deficiencies (progressive ataxia). The transition from oligodendrocytes to Schwann cells occurs within a few mm from the surface of the brain and spinal cord.hindawi.r_with_hemochromatosis. therefore. where it complexes with 2microglobulin and then binds to the transferrin receptor to facilitate endocytosis of the transferrin/iron complex into cells.eyepathologist. hemochromatosis causes an iron overload.com/disease. The crypt cells in individuals with hemochromatosis have mutant HFE that is unable to detect circulating iron levels. and liver.003. It manifests during the first year of life with symptoms of malabsorption (abdominal distention. Serum levels of all lipids are decreased. -Abetalipoproteinemia is an inborn metabolic error transmitted as autosomal recessive trait. resulting in an inability to transport lipids from the intestine.. Both protect and insulate axons. As a result. which are the elongated cells with regular. foul-smelling stool). The iron is released once inside the cell and added to the iron regulatory pool. -Cranial nerves are covered with Schwann cells.

Schwannomas in this particular location are also called acoustic neuromas.htm Acute MI Ten days following acute myocardial infarction.neurobio.Edema and punctate hemorrhages maybe detected in infarcted myocardium by light microscopy from about 4 hours to 12 hours following myocardial infarction. before receding around day5 to 7.ch/researchgr.yte_Function/mat_Fig_1. http://ocw.images/2_adipose_cells... and heart muscle. however.imsb. -Increased collagen deposition and decreased cellularity in the zone of infarcted myocardium generally becomes evident beginning at 2 weeks post-infarction. -Approximately 24 hours after acute myocardial infarction neutrophilic infiltration of the zone of dead myocardium begins. light microscopic signs of early coagulative necrosis appear. The optic nerve (CN II) is an important exception—it is covered by oligodendrocytes and cannot develop a schwannoma.ed. This granulation tissue is most prominent on light microscopy at days 10-14 postinfarction.ethz.jpg . This enzyme is synthesized by cells of adipose tissue (Uni loculated adipocytes). when the accumulated macrophages begin to be replaced by granulation tissue.edu/data/51/551163/551231_xlarge.schwannomas can arise from any cranial nerve. This acute inflammatory infiltrate then becomes increasingly prominent. resulting in a dense collagenous scar at around two months post-infarction. granulation tissue with neovascularization begins to replace the zone of dead cardiac muscle. -Macrophage phagocytosis of infarcted myocardium begins at around 5 days post-infarction. Fibrosis continues during weeks 2 to 8..causes impaired triglyceride clearance from the bloodstream. skeletal muscle. most of the dead myocytes have been phagocytosed by macrophages. and is usually complete by day 10. They can cause tinnitus. vertigo. After this period. -Infarcted myocardium may appear normal under light microscopy until about 4 hours after the onset of lethal ischemia.jpg Lipoprotein lipase deficiency . Recurrent bouts of acute pancreatitis. -Cytoplasmic hypereosinophilia is one of the earliest light microscopic signs of coagulative necrosis of cardiac myocytes. lipemia retinalis and eruptive xanthomas are seen in these patients. It begins approximately 4 hours after the onset of lethal ischemia. By post-infarction day 14. .gif http://www. The most common site of intracranial schwannomas is the cerebellopontine angle at CN VIII.ucla.. and sensorineural hearing loss. http://www.tufts.otopathology.com/acoustic. http://neuromedia.

. This damage manifests itself histologically as ballooning and vacuolar degeneration. Although glomeruli appear normal signs of tubular epithelial damage are clearly visible on light microscopy.000107f1. has caused cor pulmonale and symptoms of right-sided heart failure such as dyspnea on exertion. Diagnosis is made by peripheral smear and osmotic fragility testing.html#figure-title Hereditary spherocytosis 1. . It is thought to be triggered by increased proliferation and accumulation of monoclonal T-cells in the affected .nature.ezhemeonc.Ethylene glycol =is a widely-available substance found in automobile antifreeze...com/ki/journal/v.Spherocytosis also increases the risk of pigmented gallstones and aplastic crisis (parvovirus B 19 infection). jaundice and splenomegaly are classic clinical manifestations. predominantly in the proximal convoluted tubules is seen on light microscopy. which is toxic to renal tubules.. http://www. Ethylene glycol is rapidly absorbed from the GI tract and metabolized to glycolic acid. which precipitates as calcium oxalate crystals in the renal tubules. anorexia.yte-100x-website-arrow. 3. and to oxalic acid. in turn. -An accentuated pulmonary component of the second heart sound suggests an increase in pulmonary artery pressure. -Symptoms of acute renal failure (oliguria. Spherocytes also stain a deeper red than normal RBCs when viewed on Wright’s stain.com/ki/journal/v. lower extremity edema and hepatomegaly. Calcium oxalate crystals are detected by microscopy of the urine and are shaped like folded envelopes. http://www. -Normal pulmonary function tests exclude chronic lung disease as the cause of pulmonary hypertension.html#figure-title http://www. A high anion-gap metabolic acidosis and osmolar gap are typical.jpg CREST syndrome = a localized variant of scleroderma.nature. engine coolants and hydraulic brake fluids.. -Both variants of scleroderma (systemic sclerosis and CREST syndrome) develop due to increased deposition of collagen in tissues. Hemolytic anemia.com/wp-conten. and pulmonary hypertension. 2...5000107a.Spherocytes can be identified by the following criteria: they are approximately two-thirds the diameter of normal RBCs. they are more densely hemoglobinated at the periphery and they often lack a zone of central pallor. Hereditary spherocytosis results from red cell cytoskeleton abnormalities—the most common is a spectrin deficiency. and the absence of a heart murmur on physical examination makes valvular heart disease less likely. flank pain) are characteristic of ethylene glycol poisoning and occur in 24-72 hours after the ingestion.

. Because the tumor is located on the periphery of the prostate. . These adenocarcinomas arise from the peripheral zone of the gland. -Microvascular injury of pulmonary arterioles leads to narrowing of the lumen and increased pressure in pulmonary circulation . -Prostate cancer is the most common type of malignancy in men.jpg Metastatic prostate cancer . and hesitancy with constant back pain in an elderly man together suggest prostate cancer. which can occur in any area of white matter.CSF of these patients demonstrates increased concentration of gamma globulin (lgG). All tissues can be affected. It is found as an “oligoclonal band” on protein electrophoresis. especially TGF-beta. . -MRI of the brain is diagnostic in most cases and typically shows demyelinating plaques. which slows in MS due to demyelination of nerve fibers.tissues that secrete a variety of cytokines. .saintlukeshealthsy. but the earliest damage is seen in small arterioles and capillaries. detected by radionuclide bone scanning. Multiple sclerosis (MS) =neurological deficits that cannot be explained by a single lesion. It leads to hypertrophy of the right ventricle.The hallmark of MS is demyelination of the axons. that increase the production of collagen and extracellular matrix proteins by fibroblasts.Oligodendrocyte depletion is also seen in progressive multifocal leukoencephalopathy. The combination of symptoms of urinary urgency nocturia.Back pain not relieved by rest or position change is a typical presentation for neoplastic bone disease.. Prostate cancer is associated with increased level of prostate-specific antigen (PSA). frequency. Lipid laden macrophages containing the products of myelin breakdown are also seen within plaques. Bone metastases in prostate cancer are blastic (sclerotic).Metastatic prostate cancer has a strong predilection for bones (especially the axial skeleton). with subsequent development of right-sided CHF. Loss of myelin sheaths and depletion of oligodendrocytes is seen within the plaques. nocturia and hematuria. https://hvelink.ia/medical/hw/h9991221. there may be increased prostatic acid phosphatase (when the tumor penetrates the capsule of prostate) and increased alkaline phosphatase (due to bone . -Visual evoked potentials are used to assess conduction velocity. . The most common presenting symptoms of prostate cancer are urinary frequency. hesitancy. it is easily detected on digital rectal examination as an asymmetric nodular enlargement of the prostate. Pulmonary hypertension is a common complication of CREST syndrome. In advanced disease.

This force is sufficient to cause collapse of the atria. . Symptomatic cardiac tamponade typically occurs when the pericardial pressure exceeds 10 mmHg. viral HBsAg and HBcAg are expressed in conjunction with the major histocompatibility complex (MHC) class I molecules. reduced ventricular preload. and eventually decreased cardiac output.html http://library. http://library. . Pulsus paradoxus can be grossly diagnosed by palpating the radial pulse and noting that it disappears during inspiration. Note that . one during systole and the other during diastole. A more accurate means of diagnosis is done by blood pressure measurement with a sphygmomanometer noting a decrease in arterial pressure greater than 10 mmHg during inspiration. This can occur during fever or exercise in normal subjects. when cardiac output becomes insufficient to provide the necessary oxygen to the patient’s tissues. It can be best palpated in the carotid arteries. -In the proliferative phase the entire virion and all related antigens of the episomal HBV DNA are present.edu/WebPath/MALEHTML/MALE114.large.med.A hyperkinetic pulse refers to the rapid ejection of a large stroke volume against a decreased afterload. . Pulsus paradoxus is an exaggeration of the normal physiologic decrease in blood pressure that occurs during inspiration.utah.utah.Pulsus alternans occurs in patients with left ventricular dysfunction. This expression serves to activate the cytotoxic CD8+ T lymphocytes.rsna. http://radiographics. On the hepatocyte cell surface. -Pulsus paradoxus is an important clue to cardiac tamponade.dicrotic pulse refers to a pulse with two distinct peaks.utah. This pulse alteration literally refers to a pulse of low magnitude with a delayed peak.jpg DIFF: .Pulsus parvus et tardus refers to the pulse palpated in patients with aortic stenosis. -Death from cardiac tamponade occurs from cardiogenic shock.html http://library.med.edu/WebPath/MALEHTML/MALE074.html Cardiac tamponade -Clinically significant cardiac tamponade is associated with hemodynamic findings such as pulsus paradoxus and arterial hypotension. It is defined as a beat to beat variation in the magnitude of the pulse pressure in the presence of a regular cardiac rhythm.metastases).two phases: the proliferative phase and the integrative phase. which respond by destroying the infected hepatocytes. This finding typically occurs in patients with severe systolic dysfunction.med. or in patients with high-output conditions such as a PDA or an A-V fistula Hepatitis B virus infection .org/content/27/6/1595/F5. which results in an increase in systemic venous pressure.edu/WebPath/MALEHTML/MALE113. It is defined as a drop in arterial blood pressure during inspiration of over 10 mmHg (a decrease of less than 10 mmHg during inspiration is physiologic).

spleen.the virion itself does not have a cytopathic effect.Infarcts in a normal liver are rare because it has a dual blood supply: the portal vein and hepatic artery. myocardium. arthritis. Liver infarction . Oral contraceptives reduce the risk of nonhereditary ovarian cancer by decreasing the total number times a woman . and urticaria) as well as some of the chronic complications (eg. .edu/hepstudy/images/hepB/hbvdx1_d05. and use of clomiphene citrate to induce ovulation. . In this case the liver can develop biliary tree infarction and organ failure because the collateral blood supply is severed during transplantation. Should the hepatic artery be occluded the portal venous supply and retrograde arterial flow through accessory vessels is typically sufficient to sustain the liver parenchyma.Host antibody HBsAb neutralizes HBV infectivity by binding to the viral surface antigen HBsAg and preventing the antigen from interacting with hepatocyte receptors. Itis postulated that the risk of ovarian cancer is increased in these conditions due to irregularities of reparative processes on the ovarian surface (repeated aberrant repair is thought to induce cellular dysplasia and neoplasia).philadelphia-reflections.jsp? http://www. -The pathogenesis of autoimmune hepatitis (not hepatitis B infection) involves antigen mimicry with generation of self-antigen recognizing CD4 + T lymphocytes that damage hepatocytes.Antigen-antibody complexes cause some of the early symptoms of hepatitis B virus infection (eg.. nulliparity.washington.jpg .. arthralgias. the HBV DNA is incorporated into the host genome of those hepatocytes that survived the immune response. cryoglobulinemia. immune complex glomerulonephritis.upmc. These complexes are not responsible for hepatocellular damage however.com/TPIShome/chan. -In the integrative phase. Ovarian cancer -Epidemiological studies have linked ovarian cancer to conditions associated with ovarian dysfunction such as infertility.com/images/hepB. The notable exception is when a transplanted liver undergoes hepatic artery thrombosis.Organ susceptibility to infarction after occlusion of a feeding artery is ranked from greatest to least as follows: central nervous system. Infectivity ceases and liver damage tapers of when the antiviral antibodies appear and viral replication stops. and liver. The risk of hepatocellular carcinoma however remains elevated because of the HBV DNA that has been integrated into the host genome. and vasculitis).gif http://tpis. miscarriages.?url=/tpis/HB/H00030x. The presence of a dual or collateral blood supply (as seen in the liver which is supplied by the hepatic artery and portal vein) enables organs to tolerate arterial occlusion. http://depts. kidney.

. cervix. cancers of the endometrium. PRCA can also result from parvovirus B19 infection. http://wpcontent. patients with metastatic ovarian cancer have elevated circulating levels of CA-125. there is less need for repair at the ovarian surface.learningradiology.. lung and colon) as well as non-malignant conditions making it a poor screening marker for ovarian cancer.answers. There may also be some commissural fusion at the leaflet edges and the mitral valve orifice maybe somewhat stenotic...edu/classwar.cancersafe. patients often present with advanced disease.jpg Pure red cell aplasia (PRCA) =a rare form of marrow failure characterized by marked hypoplasia of marrow erythroid elements in the selling of normal granulopoiesis and thrombopoiesis. CA-125 can also be elevated in number of other malignant conditions (e. Thus.tulane.. This virus .html http://www.ovulates in her lifetime.asp Rheumatic mitral valvular disease =diffuse fibrous thickening.. fallopian tube. All of these findings are characteristic of rheumatic mitral valvular disease. Mitral stenosis can cause atrial enlargement. -Mortality rates are higher for ovarian cancer than for endometrial or cervical cancer.som. With fewer ovulatory cycles.cPath/GR_Heart/Heart9. .) Multiparity and breast-feeding also decrease the risk of ovarian cancer..html Degenerative calcific deposits -most commonly develop in the mitral valve annulus in women over age 60 and in individuals with a myxomatous floppy mitral valve or an elevated left ventricular pressure. The relatively large surface area of the walls of the left atrium is consistent with atrial dilatation.edu/classwar. accounting for up to 99% of cases. http://www. distortion of the mitral valve leaflets.cPath/GR_Heart/Heart7. However. (It is unclear whether oral contraceptive pills reduce the risk of hereditary ovarian cancer associated with the BRCA gene mutation. Because there is no effective screening method for ovarian cancer.som.com/wikip. -Fibrosis of the valve leaflets in chronic rheumatic heart disease following acute rheumatic fever is the most common cause of mitral stenosis. which may lead to atrial mural thromboses. http://www. as likely occurred in this patient. The association between thymomas and PRCA is well-documented.jpg http://www..eekpix2007-1/cow247arr. Thrombi dislodged from the wall of the left atrium may later cause an embolic stroke. -PRCA can be idiopathic or due to a secondary process like a thymoma.mitral annular calcification generally does not impair valve function. Removal of the thymoma can cure the PRCA.athology_20G0013_lores.g. all patients with PRCA should undergo a chest CT scan. Oftentimes.com/cancers/ovarian.com/c.tulane.

It manifests with a severe headache that may be described as “the worst headache of my life”. Fever and nuchal rigidity are commonly present. On CT scan.JPG Posterior communicating artery rupture = the second most common site of rupture of berry aneurisms in the circle of Willis (anterior communicating artery is the most common site). This increased incidence is explained by age-related brain atrophy.jpg Subdural hematoma = an accumulation of blood between the dura mater and arachnoid. confusion and memory loss.wz16.org/wiki/. The classic clinical presentation is colicky flank pain and ..edu/atlas/n3a8p2.preferentially attacks and destroys proerythroblasts. In elderly patients. and often rupture in hypertensive strokes.umich. They can rupture as a result of acceleration-deceleration injury. http://www. subdural bleeding is called a “great imitatorâ€ン due to its subtle and variable presentation. -Venous bleeding is relatively slow which explains the gradual onset of symptoms in subdural hematoma. somnolence. As the hematoma expands. -Subdural hematoma often occurs in elderly individuals after a minor trauma. It may present as gait abnormalities.net/Upload/Update/Info/2006330111442727. http://www.. The only clinical manifestation of this disorder is lifelong recurrent urolithiasis.ittal_view_description. http://anatomy.med. This results in subarachnoid bleeding. Patients complain of gradually worsening headache and display a slow decline in mental function. These vessels supply the internal capsule and the basal ganglia. http://commons. These patients may go undiagnosed for weeks.. seizures.The lateral striate arteries arise from the middle cerebral arteries. They are also called the penetrating branches.com../neurotrauma/LtSDHpre2.wikimedia.neurosurgery. subdural hematoma is seen as a crescent-shaped mass.sg/ima. Recent parvovirus infection can be confirmed via the detection of anti-B19 1gM antibodies in the serum. The blood comes from the bridging cortical veins which carry blood from the cortex to the venous sinuses. it raises the intracranial pressure and compresses the brain.jpg Rupture of lateral striate arteries . As the distance from the skull to the brain surface increases cortical bridging veins are under more tension and rupture more easily.html Cystinuria =resulting from a defective transporter of dibasic amino acids is an autosomal recessive disorder.

Asbestosis =Localized pleural thickening with calcification particularly of the parietal pleura of the posterolateral mid-lung zones and diaphragm.us/vpap/asbestosis. Mental retardation is not seen in cystinuria. and urine supersaturation.. http://www.3).Cystine.jpg DIFF: .edu/cme/clia/images/testID20/UA067.Unlike asbestosis.jpg .. These calcified lesions are referred to as pleural plaques. http://www.gov/asbestos/. Thus as the urine pH increases so does cystine’s solubility.com/pi/emed/ck. In the gut these amino acids are reabsorbed via a high affinity transporter on jejunal cells.medscape. and arginine are soluble in urine. -Ornithine. cystine however is relatively insoluble at the physiologic urine pH of 5-7 (pKa = 8.hematuria.4mm).medicine. Pleural plaques or effusions are not typical.iseases/environmental4.uiowa. pulmonary silicosis is not strongly associated with pleural plaques or effusions. lysine and arginine are dibasic amino acids that share a common transport mechanism in the kidney and intestinal lumen.medscape.jpg http://familyrights.luc.com/pi/emed/ck.luc. In the kidneys these substances are filtered at the glomerulus and reabsorbed by a similar transmembrane channel on proximal tubular cells.logy/295571-296759-206. most prominent in the upper lung zones.. lysine.htm -Pulmonary berylliosis closely resembles sarcoidosis (nodular infiltrates. Nodular densities and eggshell calcifications of the hilar nodes are seen.jpg -The coal macules of coal worker’s pneumoconiosis are seen radiologically as multiple discrete nodules (1. the presence of already formed cystine crystals..jpg http://img.meddean. homocystinuria and in some patients with maple syrup urine disease. enlarged lymph nodes.net_3q4959_Asbestosis.NAR/images/path3/sld19. Inherited defects of this transport channel lead to defects in renal and intestinal reabsorption thus causing these amino acids to be excreted in urine and feces....edu/lumen/m. noncaseating granulomas) but is not strongly associated with pleural plaques or effusions.edu/lumen/M. Small pleural effusions which are exudative and possibly blood stained may occasionally be noted... Risk factors for cystine precipitation include: low urine pH.atsdr. ornithine. http://img.meddean. http://www. -Lung injury due to asbestos inhalation predominantly affects the lower pulmonary zones and manifests radiographically as linear interstitial densities in the lower lobes.cdc.Hypersensitivity pneumonitis due to inhalation of organic dusts tends to result in diffuse nodular interstitial infiltrates on chest x-ray. . Pleural plaques or effusions are not typical..Mental retardation occurs in several inborn errors of amino acid metabolism including phenylketonuria. followed by the eventual passage of a stone.5-435576-435678-435819. http://www..jpg . .

healthsystem.htm http://www. monomorphic B-lymphocytes in the peripheral blood.ALL is primarily a disease of children (75% occurs in children under six years of age). round.jpg http://www.ocytic-T-cell-leukemia. . -The differential diagnosis of this acute lymphoblastic leukemia (ALL) includes precursor B-cell leukemia (precursor B-ALL) and precursor T-cell leukemia (precursor T-ALL)..org/chemheme/heme/microscope/aml. The leukocyte count may be normal.ssIDB/Cell-Comparisons. Findings would include more mature lymphocytes (not blasts) expressing T-cell markers. CD3. and almost always for CD19.wadsworth. CD4.Mature T-cell leukemia is a group of uncommon neoplasms that are derived from mature or post-thymic T cells.bone marrow smear shows several lymphoblasts with a high nuclear-tocytoplasmic ratio.virginia.meb. Patients typically present with a high leukocyte count and often a large mediastinal mass.healthsystem. CDT and CD8.gov/Media/CDR0000526538. CD4. (Choice B) Precursor T-ALL accounts for about 15% of all childhood ALL and is more common in adolescents than younger children..cfm http://www. influenza. but it is hypothesized that . varicella or another viral disease.de/cancer. lymphoblasts in precursor T-ALL are TdT positive and variably express CD1a and the T cell markers CD2.htm http://www.. The lymphoblasts in precursor T-ALL variably express CD1a and T-cell markers like CD3. These neoplastic lymphocytes express CD19 (B-cell marker) and coexpress CD5 (T-cell marker) on their surface. -The pathogenesis of this condition is still unclear. DIFF: . CD5. Lymphoblasts in precursor B-ALL are positive for TdT..healthsystem.cfm http://www.cfm Reye syndrome = hepatic failure and acute encephalopathy.virginia. CD1O.ALL present with evidence of bone marrow failure: thrombocytopenia and/or anemia and/or neutropenia.htm http://www.wadsworth.uni-bonn. and CD8.wadsworth. and is most commonly associated with the use of aspirin in patients 5-14 years old.org/chemheme/heme/microscope/cll.. and prominent nucleoli.htm http://www. decreased or increased.wadsworth.e. http://www.org/chemheme/heme/microscope/all.e. bone marrow and lymph nodes. . Precursor B-ALL and precursor T-ALL can be distinguished from each other only by immunophenotyping.virginia. Most patients with precursor B.e.. In contrast.rders/Leukemias/ALL-L1.org/chemheme/heme/microscope/cgl. The febrile illness that proceed Reye’s syndrome is frequently an upper respiratory infection. CLL/SLL) is a neoplasm of small. variably condensed nuclear chromatin. measles.Mature B-cell leukemia (or chronic lymphocytic leukemia/small lymphocytic lymphoma.ALL .

-On macroscopic examination gestational choriocarcinoma is seen as a bulky intrauterine mass that is usually soft and yellow-white. It is most commonly preceded by an evacuated hydatidiform mole. Electron microscopy findings include swelling.Carcinosarcomas (malignant mixed mullerian tumors) of the uterus are composed of epithelial (endometrial-type glands) and mesenchymal (sarcomatous) elements.com/imag. http://www. a decreased number of mitochondria and glycogen depletion.pathguy. No villi are present.59867506701565/gr2-sml. uterine enlargement.jpg . normal pregnancy. but jaundice is rare. http://en. Endometrial adenocarcinoma is not related to pregnancy and patients do not have elevated b-hCG levels.htm . and significantly increased chorionic gonadotropin levels.. These tumors can occur in the ovaries.pathguy. However this neoplasm can also occur following abortion. Encephalopathy of Reye syndrome is attributed to hepatic dysfunction and the toxic effect of hyperammonemia on the CNS leading to cerebral edema. http://www. 2.. Patients present with abdominal pain and an ovarian mass. This tumor is highly sensitive to chemotherapy. These tumors are not associated with pregnancy and do not cause b-hCG elevations. or ectopic pregnancy. http://www.jpg Gestational choriocarcinoma = malignant tumor that arises from the trophoblast.com/wp-content/uploads/hydatidiformmole. ammonia. Hepatic dysfunction manifests with vomiting and hepatomegaly. and bilirubin. Choriocarcinoma is an aggressive tumor that rapidly invades the uterine wall and metastasizes hematogenously.org/wiki/File:Uterine_carcinosarcoma. it is composed of abnormal proliferations of both cyto trophoblasts and syncytiotrophoblasts. the tumor causes abnormal vaginal bleeding. the presence of small fat vacuoles in the cytoplasm of hepatocytes . -Clinically.pathconsultddx. but not in the uterus. To avoid the possibility of inducing Reye syndrome. and a prolonged PT and PTT.wikipedia.Endometrial adenocarcinoma consists of disorganized glands composed of neoplastic columnar cells. AST. It is especially pronounced in viral-infected cells and causes mitochondrial dysfunction. -Histologically. An ovarian teratoma would . The two components of Reye’s syndrome include: 1. with extensive areas of necrosis and hemorrhage. No necrosis or inflammation is present in the liver. This malignancy occurs in postmenopausal women and presents with vaginal bleeding.com/sol/40040. aspirin should not be administered to children under the age of sixteen except for very specific circumstances where it is indicated for the treatment of a serious illness such as in Kawasaki disease where salicylates are a mainstay of treatment. Light microscopy of a liver biopsy shows microvesicular steatosis. Liver function tests reveal increased levels of ALT.jpg DIFF: .jpg http://nursingcrib.affected children have some inborn metabolic error that renders them sensitive to the toxic effects of salicylates.Malignant teratomas can contain tissue elements resembling immature cartilage. -The lungs are the most common site of distal spread.com/~dlaporte/endo_ca.

These anti-GBM antibodies cross-react with other basement membranes.com.pathguy.ro/patho. Cystic medial aortic degeneration may lead to aortic dilatation and dissection. http://path.jpg http://www.pathologyatlas. followed by cardiac failure (which maybe secondary to mitral and/or aortic regurgitation).edu/cases/case52/images/gross4. The two most common cardiac abnormalities are mitral valve prolapse and cystic medial degeneration of the aorta.scoliosisassociates. and the patient may become hypertensive. 2. as occurs in sickle cell disease with salmonella. Since this is a nephritic picture. The cardiovascular lesions are the most potentially life-threatening. -Osteomyelitis is an infection of bone and bone marrow that occurs by: 1. and long tapering fingers -Marfan syndrome is an autosomal dominant defect in the connective tissue glycoprotein fibrillin-1 which causes abnormalities in the skeleton.com/sol/00049. This is also the mode by which M. -spinal scoliosis and kyphosis (posterior convex angulation of the spine). http://www..upmc. tuberculosis gains access to the bone and causes chronic osteomyelitis (Pott .jpg Marfan syndrome -upper body (head to pubis) is disproportionately short compared to leg length. aureus. especially those in the lung alveoli causing pulmonary hemorrhage (hemoptysis).jpg Goodpasture syndrome = caused by anti-glomerular basement membrane antibodies (anti-GBM antibodies) that target the a3-chain of collagen type IV. The average age at death in Marfan syndrome is between 30 and 40 years.com. there are red blood cell casts and mild proteinuria (<1 g/day) on urinalysis. http://www.jpg http://www.. as occurs in children with S.tic_glomerulonephritis.medstudents. long extremities. S. Crescents will have fibrin deposition. eyes (lens dislocation).br/original/revisao/marfan/marfan2. (It is important to remember that the GBM is composed of collagen type IV..jpg Osteomyelitis -The metaphyses of long bones are typically affected by hematogenous osteomyelitis due to their rich vascularization and capillary fenestrae.not cause vaginal bleeding.. and cardiovascular system. Seeding of ischemic or infarcted bone. Aortic dissection is the cause of death in 30% to 45% of patients with Marfan syndrome. pyogenes and E.) These patients develop rapidly progressive glomerulonephritis (RPGN) that results in acute renal failure with crescent formation on light microscopy. Fluorescence microscopy shows “linear” lgG and C3 deposition. coil./our_unusualscoliosis7. Hematogenous seeding of infection in normal bone.

Avascular necrosis of the femoral head is strongly associated with the following conditions: 1. and if infection gains access to this area of the bone there will be resultant necrosis of a large portion of bone as well as a risk of sepsis. http://medical-dictionary. 4. the proximal tibia. MRI is the most sensitive modality for diagnosing avascular necrosis.Staphylococcus aureus and Streptococcus pyogenes (Group A Strep) are the first and second most common causes of this disease.xray2. 3. In the case of hematogenous osteomyelitis. -Hematogenous osteomyelitis is predominantly a disease of male children. Sickle cell disease leads to avascular necrosis due to thrombotic occlusion of arteries. This is also the location of Pott Disease.html . Physical examination reveals painful and restricted passive and active movement in the affected joint. Direct infection of bone. http://www. Spread from a contiguous focus of infection. 3. respectively.Disease in the vertebrae).orland&name=sequestrum. Proper treatment includes antibiotic therapy and debridement of necrotic bone.com/custom2. -Pseudomonas aeruginosa frequently plays a role in osteomyelitis resulting from chronic wounds such as in diabetics. Injury to the vessel wall (vasculitis) causes impaired blood supply to the femoral head in systemic lupus erythematosus (SLE). Embolic occlusion (fat emboli. There is no swelling.occurs due to impaired blood supply to a segment of bone. . It is initially an acute process. distal femur and proximal humerus are the most common bones involved. but without proper treatment it progresses to chronic suppurative osteomyelitis where necrotic bone (sequestrum) serves as a reservoir for infection and becomes covered by a poorly constructed shell of new bone called the involucrum.. -The diaphysis can be involved in hematogenous osteomyelitis if the acute event is not recognized and treated due to local bacterial invasion. -The long bone epiphysis is usually spared in osteomyelitis unless the acute infection is not treated at which point the infection could spread into the joint resulting in a pyogenic arthritis. and hematogenous osteomyelitis most frequently affects children and young adults. 2.20m.. Avascular necrosis (osteonecrosis) . air emboli) can also cause avascular necrosis. The femoral head is the most common location. as occurs in a compound fracture. The diaphysis is the location of the bone marrow. High-dose steroid therapy and alcoholism are also associated with avascular necrosis of the femoral head -Avascular necrosis of the femoral head presents with groin pain that is exacerbated by weight bearing. osteomyelitis of the vertebral body caused by Mycobacterium tuberculosis. erythema or temperature change to the affected area.jpg -The vertebral body is the most common location for hematogenous osteomyelitis in the adult. as occurs in Pseudomonas aeruginosa osteomyelitis from an infected diabetic foot wound.thefreed.

The chromosome that carries the fusion gene BCR-¼BL is called the Philadelphia chromosome.. Light microscopy would reveal interstitial fibrosis with patches of mononuclear infiltration and tubular atrophy.com/leu/journal/. tumor. When urinary pressure reaches a critical level.act. The new gene BCR-ABL codes for a protein with tyrosine kinase activity. http://health.On cut surface. -Hydronephrosis is caused by prolonged urinary tract obstruction. The ABL oncogene is transported from chromosome 9 to chromosome 22 where it is placed adjacent to the BCR proto-oncogene. and cortical atrophy follow. pregnancy. http://www. -Since Sydenham chorea is a manifestation of acute rheumatic fever.jpg Chronic myelogenous leukemia (CML) -is associated with a specific cytogenetic abnormality.Hydronephrosis -significantly enlarged kidney. Imatinib (Gleevec) is a tyrosine kinase inhibitor specific for the BCR-ABL fusion protein of CML. The obstruction causes urinary stasis proximal to the blockage. with dilatation and deformation of the calices and renal pelvis. and is the sole neurologic manifestation of acute rheumatic fever. In older males. In this condition. with gradually increasing urinary pressure and subsequent dilatation of ureters.com/watch?v=VoHWsQWHbWQ&feature=related . Sydenham chorea is thought to be a CNS autoimmune reaction precipitated by a group A 3-hemolytic streptococcal sore throat after a latency of 2-3 months. the classic and most common cause of disease is a translocation between chromosome 9 and 22 in an immature myeloid precursor cell.nature. including mitral and aortic valve involvement. or functional disorders (such as neurogenic bladder) are common causes.youtube. this kidney would show marked atrophy and scarring of the renal parenchyma and distortion of renal architecture. a patient with this disorder would be at risk for chronic rheumatic heart disease. . Ischemia. benign prostatic hyperplasia is the most common cause of urinary obstruction. it overcomes renal blood flow and disables glomerular filtration. urinary pelvis and calices..au/gfx/pubs/-554515641_r0./fig_tab/leu2008119f1. This protein stimulates proliferation of granulocytic precursors and leads to development of CML. Anti-neuronal antibodies binding to the caudate and subthalamic nuclei may be involved. http://www.gov. -Nephrolithiasis. It competitively binds the ATP binding site of the ABL portion of this protein thereby decreasing its activity. anatomic abnormality.html Sydenham chorea( hyperkinetic extrapyramidal movement disorder) =purposeless extremity movements and restlessness = the most common acquired chorea of childhood. nephron loss.

tumor or inflammatory bowel disease) is characterized by the presence of a defect in the intestinal wall along with signs of peritonitis. On light microscopy. prolonged PR-interval -Supporting evidence of an antecedent group A streptococcal infection may be a positive throat culture or rapid antigen test or an elevated or rising streptococcal antibody titer. mesenteric ischemia.yellow suppurative exudate. This results in formation of fatty acids that bind calcium ions and precipitate as insoluble calcium salts. Acute pancreatitis . Ischemia damages the acinar cells and causes abnormal intracellular activation of trypsin.It occurs due to damage of the contralateral subthalamic nucleus—most commonly from a lacunar stroke.Intestinal perforation (due to ulcer. Patients suffering lacunar strokes usually have . benign acute interstitial pancreatitis develops. erythema marginatum.a. arthralgia. Black areas of hemorrhage are also seen on gross examination. The Jones criteria are: Major Criteria: carditis.Bacterial peritonitis is characterized by a dull-appearing peritoneal surface with areas of viscous white. Macroscopically.html . Acute necrotic pancreatitis develops.Diagnosis of acute rheumatic fever requires either two major Jones criteria or one major and two minor Jones criteria.vcu. Hemiballism =Wild flinging movements of the extremities on one side of the body (arm and/or leg) . areas of white chalky fat necrosis are visible in the pancreatic tissue.uk/foto/Acute%20Pancreatitis. Trypsin then activates other proteolytic enzymes. If the pathologic process stops at this stage. renal failure is not part of the acute rheumatic fever clinical syndrome. http://www. the pancreas looks edematous on macroscopic examination.edu/education/cardio/lab2. thus initiating autodigestion (autolysis) of pancreatic tissue. interstitial edema. In this subtype of acute pancreatitis.jpg DIFF: .pathology. polyarthritis. omentum and other parts of abdominal cavity. with supporting evidence of an antecedent group A streptococcal infection. . Destruction of blood vessel walls can cause hemorrhage into the necrotic areas. subcutaneous nodules Minor Criteria: fever. They can spread onto the mesentery. chorea. blood flow to the pancreatic acini is compromised as a result of the edema. If the inflammatory process continues.org.duct obstruction leads to stasis of pancreatic secretions and digestion of adipose cells by lipase.http://www. As is evident from these criteria. elevated acute-phase reactants (erythrocyte sedimentation rate or C-reactive protein).wses. The areas of focal necrosis and calcium precipitation induce an inflammatory reaction. focal fat necrosis and calcium deposits are seen.

urine output decreases.0 mEq/L. The subthalamic nucleus is a component of the basal ganglia. It manifests by vigorous diuresis (sometimes >3 L/day).neoucom. and urate) will lead to high anion gap metabolic acidosis. 4.. Hyperkalemia is usually asymptomatic when serum K concentration is <6. http://www. and pulmonary vascular congestion. Increased extracellular fluid volume can cause weight gain. 5.jpg ATN -Decreased renal blood flow triggers a chain of pathophysiologic changes in the nephron that cause tubular epithelial necrosis and acute renal failure. Because renal tubules cannot yet function fully .Involvement of lentiform nucleus (globus pallidus and putamen) is characteristic of Wilson disease (hepatolenticular degeneration).html#lacunar . and metabolic changes of acute renal failure manifest. and high urinary fractional sodium excretion (Fe Na >1). -In spite of the seemingly-profound damage that occurs to nephrons in ATN tubular epithelial cells have an excellent regenerative capacity.If significant tubular damage occurs the oliguric stage (maintenance stage) follows in 24-36 hours.uk/anar. If the patient survives the oliguric stage (by conservative management or dialysis) the recovery stage will follow in 1-2 weeks. high urinary sodium (>30). During this stage. psychosis and cirrhosis.jpg .inf. It is ventral to the thalamus and superior to the internal capsule..Atrophy of the caudate nucleus occurs in Huntington disease.hallym. low urinary osmolarity (<350). Retention of both hydrogen and anions (sulfate. Urinalysis reveals pathognomonic muddy brown casts. 3.com/uploads/Forebrain/thalamus. and potentiallyfatal ventricular arrhythmias are possible.html DIFF: . Other electrolyte changes include a decreased concentration of sodium and calcium and an increased level of phosphate and magnesium.kr/d/kns/tutor/medical/ns10. and behavioral abnormalities are typical.Damage to the internal capsule occurs when perforating arteries are obstructed (lacunar infarcts) and results in pure motor or pure sensory deficits. . This syndrome of poststroke pain occurs in about 2% of stroke victims and is often described as a burning or stabbing sensation of one half of the body (contralateral to the lesion).ac. phosphate. The most significant of these changes are detailed below: 1.ed.ac. The initiating stage of ischemic ATN is usually unnoticed by clinicians as the symptoms of the main disorder (hemorrhage. peaked T waves are apparent on ERG.Damage to the substantia nigra occurs in Parkinson disease .Lesions of the thalamus can cause thalamic syndrome.ebralinfarcts. Kayser Fleischer rings are seen in the cornea. . acute MI. Manifestations include wing-beating tremor. http://aids.thebrainwiki..edu/.a long history of hypertension. Chorea. Above this level. edema. http://neuropathology.arch/anatomy/anatomy1. 2. sepsis etc) prevail. dementia.. http://homepages.

denervation. 3. Flattening of the nail folds and shininess of the nail and distal portion of the finger will also be evident. Clubbing =Thickening of the distal portion of the distal phalanges -This deformity of the fingers and fingernails is associated with a number of chronic diseases causing hypoxia. or interruption of lymphatic outflow. the fingers will have a “drumstick” appearance due to thickening of the distal phalanges. Hypokalemia is one of the most serous complications of the recovery phase of ATN. A number of circulating vasodilators have also been implicated in the development of clubbing.jpg Lung transplantation . however. is a major cause of morbidity and mortality among transplant patients. Scarring leads to progressive obliteration of small airway lumens.may be complicated by both acute and chronic rejection. malabsorption. Reperfusion edema . 2.During the recovery phase (polyuric phase) of ATN patients can become dehydrated and can develop severe hypokalemia due to high-volume hypotonic urine. Early on. The following conditions commonly cause digital clubbing: 1. Mg. Lung diseases: lung cancer (especially large-cell carcinoma). Heart diseases: cyanotic congenital heart diseases (five T’s.com/files/images/finger%20clubbing2. pulmonary hypertension empyema and many other chronic lung diseases associated with hypoxia. On physical exam. . especially tetralogy of Fallot). http://inventorspot. Chronic rejection affects the small bronchioli producing the obstructive lung disease known as bronchiolitis obliterans. Pressing on the nails reveals a spongy fluctuant sensation of the nailbeds. High-volume hypotonic urine causes sodium retention and decreased concentrations of K. interstitial edema and increased growth of fibrovascular tissue. The pathophysiology of digital clubbing has yet to be completely elucidated but it is thought to be caused by vasodilatation of the capillaries in the distal phalangeal region leading to increased blood flow to the distal portion of the finger.electrolyte balance is still altered. cystic fibrosis bronchiectasis . . tuberculosis. organ ischemia. Acute rejection can be effectively treated with immunosuppressants. and Ca. -The pathologic basis of this condition is lymphocytic inflammation and necrosis of the bronchiolar walls. Other: Inflammatory bowel diseases (Crohn. -Clubbing develops insidiously and is a sign of chronic hypoxic disease most commonly. fibrinopurulent exudate and granulation tissue are found in the lumen of the bronchioli. They are later replaced by connective tissue. ulcerative colitis) hyperthyroidism. Chronic rejection. P04.Ischemia-reperfusion injury (or reperfusion edema) is a form of noncardiogenic pulmonary edema that can occur in the allograft due to surgical trauma.

.. . Arnold-Chiari malformation = congenital disease due to underdevelopment of the posterior fossa. There are perivascular mononuclear infiltrates on histologic examination. and fever.gif http://www.is seen during the first few days following transplantation .brown. The symptoms of acute rejection include dry cough.edu/pedisurg/imag. hydrocephalus can cause mental impairment. Parenchymal infiltrates are seen on chest x-ray.rochester. -Arnold-Chiari type II causes symptoms of compression of the medulla such as difficulty swallowing. dysphonia.com/i.html . The narrowing of the pyloric channel is thought to be exacerbated by localized edema and inflammation. Infected cells have a characteristic intranuclear inclusion surrounded by a clear halo (owl’s eye inclusion). -Arnold-Chiari malformation type II is more severe and becomes symptomatic in the neonatal period. Congenital pyloric stenosis =a relatively common disorder that is encountered primarily in male infants (at a 3:1 ratio) and characterized by a multifactorial pattern of inheritance.icStenosisUmbrellaSign.medscape. or a neoplastic process (eg.com/content/20. It is characterized by an abnormally formed cerebellum and medulla.. stridor. and apnea.14/art-jphc458614. dyspnea. The mass is thought to develop secondary to hypertrophy of the pyloric muscularis mucosae. The small size of the fossa causes parts of the cerebellum and medulla to herniate through the foramen magnum. Lumbar myelomeningocele usually leads to leg paralysis. Both the cerebellar vermis and medulla extend downward through the foramen magnum.fig2.jpg DIFF: . Neoplasm in this area would not be expected in an infant. and physical examination demonstrates visible peristalsis and the presence of an olive-sized mass in the distal stomach or pyloric region. It may be asymptomatic in infants. peptic ulcers in the pylorus. http://www. but in adults manifests with headaches and cerebellar symptoms (such as ataxia).Infants typically present with recurrent projectile nonbilious vomiting. -There are two types of Arnold-Chiari malformations.spinabifidainfo.Infection is the leading cause of death in lung transplant recipients.gif http://www.nl/CsfHead2.urmc. CMV is the most significant opportunistic infection in lung transplant recipients.. low-lying cerebellar tonsils extend below the foramen magnum into the vertebral canal. however. The stenosis is relieved by surgical splitting of the muscle...Acute rejection occurs within days to weeks of transplantation. In Arnold-Chiari malformation type I. carcinoma of the pyloric region or lymphoma).. Lumbar myelomeningocele and hydrocephalus (due to aqueductal stenosis) are almost always present in these patients.ultrasound-images.Acquired pyloric stenosis occurs in adults and is associated with gastritis. http://www. If untreated.jpg http://bms.edu/neuroslides/slide169.ic-pyloric-stenosis-1a.

In patients with persistent truncus arteriosus. combined with a continuous lower atrial and upper ventricular septal defect.. results in death due to congestive heart failure within the first year of life. there is always an associated ventricular septal defect. Endocardial cushion defects are commonly associated with Down syndrome.html http://www.jpg Persistent truncus arteriosus -accounts for less than 1% of congenital heart defects.es/ency/fullsize/22696. http://www. -The result is usually a persistent atrioventricular (AV) canal. .Hypoxemia and paradoxical embolization may result. http://www.com/FetalEcho/04%20Standard.fetal.. the atrial and ventricular components of the septal defect are separated by abnormal AV valves.gif Endocardial cushion defect =the result of failure of complete fusion of the endocardial cushions in the atrioventricular canal during embryonic development.rush.. http://www.nih.l_fixed/images/ei_0350.gov/medlineplus. even though individuals with a patent ductus arteriosus may survive to middle age.is patent in 20-30% of normal adults.guidetobelize. then. this condition would not normally be found in an adult.Foramen ovale . resulting a single great vessel leaving the heart.edu/rumc/images/ei_0427.nlm. This defect causes cyanosis and.. Obviously. Patency beyond one year of age is abnormal. if not corrected.schneiderchildrenshospi.gif .The ductus arteriosus normally closes by the third month of life in response to the high Pa02 of blood shunting from left to right through the ductus afterbirth. any abnormality increasing right atrial pressure above left atrial pressure can produce a right-to-left shunt across a patent foramen ovale.gif DIFF: . The aorta pulmonary artery. and coronary vessels originate from an ascending portion of this solitary vessel.. Moreover. http://www.gtb-dive-foramen-ovale. A patent foramen ovale should be suspected in any patient who has evidence of deep venous thrombosis of the extremities and has developed a stroke. Although it usually remains functionally closed. It results from incomplete embryonic development of the aorticopulmonary septum..info/en/d.

Primary syphilis = painless ulceration with raised. hCG levels are increased in a small percentage of patients with seminomas. Very high circulating levels of hCG then can stimulate the thyroid gland. Gummas are white-gray granulomatous rubbery lesions that may ulcerate.sc. Placenta-like alkaline phosphatase (PLAP) can be increased in testicular germ cell tumors. http://pathmicro. which may be asymptomatic or cause subacute meningoencephalitis. but also produced by tumors such as teratomas. Because of the structural similarities hCG can bind to the TSH receptor. and FSH. producing hyperthyroidism. LH. The chancre develops at the site of inoculation of Treponema pallidum. it’s the beta-subunit of hCG that is a tumor marker.) The structure of hCG is similar to TSH. Circulating alkaline phosphatase . gastrointestinal tract. -Tertiary syphilis develops many years after infection in untreated individuals and includes neurosyphilis. PLAP can be increased in other malignancies. although with a much lower affinity than TSH. lung and colon cancer. LDH . which are tumors often found in testes and ovaries (Actually. liver and other organs. It presents with a diffuse macular rash that include the palms and soles. Tertiary syphilis also causes ascending aortic aneurism and resultant aortic valve insufficiency.edu/fox/syph1. indurated borders known as a chancre. -Latent syphilis is an asymptomatic period divided into early latent (within a year after resolution of symptoms of secondary syphilis) and late latent (more than a year of asymptomatic state). Condylomata lata are large grey wart-like growths that occur typically in the genital and perineal region. They are most commonly cutaneous but also appear in the subcutaneous tissue. one to three weeks after contact and resolves in three to six weeks. these are another typical manifestation of secondary syphilis.jpg Human chorionic gonadotropin (hCG) = a peptide hormone normally produced by the placenta. most commonly on the penis or vulva. bones.med. The organism commonly disseminates systemically during this primary stage. liver. as well. Gummas are also characteristic of tertiary syphilis. tabes dorsalis or other neurologic sequelae.comes from bone. including pancreatic. and the placenta in gravid women. but it is a nonspecific marker for testicular malignancies. -Secondary syphilis represents a bacteremic stage of infection and develops five to ten weeks following resolution of the chancre.

Immunoreactivity for GFAP is characteristic for astrocytomas including glioblastoma multiforme. . Immunoreactivity of a CNS tumor for synaptophysin indicates a neuronal origin . Neoplasms of glial origin (astrocytomas. gliomas are stain positively for glial fibrillary acidic protein (GFAP). swelling and irregularity are noted in the distal segment of the axon.= an enzyme involved in anaerobic glycolysis. The cell body shows signs of cellular edema. Such neoplasms are rare and compose less than 1% of CNS tumors. and oligodendrogliomas) stain for GFAP. most of which are benign. Similar degenerative changes occur in the segment of axon that lies proximal to the injury. Wallerian degeneration -occurs in the segment of axon that has lost connection with the cell body. Nissl substance becomes fine granular and dispersed through out the cytoplasm (central chromatolysis).Primary tumors in adults tend to be supratentorial while those in children tend to lie below the tentorium. meningiomas and pituitary adenomas are the next most common. ependymomas and peripheral neural sheath tumors. with the nucleus displaced to the periphery. The majority of primary CNS tumors in adults are of glial origin.Cells of the arachnoid villi give rise to meningiomas. oligodendrogliomas. It becomes swollen and rounded. Maximal changes in the neuronal body occur approximately 12 days after the injury.. LDH increase can occur in both seminomatous and non-seminomatous tumors of the testes. neuroectodermal and neuroendocrine cells. These changes reflect an increased synthesis of protein by the cells in order to regenerate the severed axon. -The changes seen in the neuronal body after the axon is severed are called axonal reaction.CNS tumors of neuronal origin frequently stain positively for synaptophysin on immunohistology.edu/lm/ids.ucsf. First. Axonal reaction becomes visible in 24-48 hours after the injury.. These tumors are diagnosed by imaging. ependymomas. It represents the degeneration of axon and myelin distal to a point of injury. http://missinglink. DIFF: . Degeneration of the proximal segment extends to the closest node of Ranvier. -Unlike tumors of neuronal origin. . Within a week the axon is destroyed and its fragments are digested by Schwann cells and macrophages. Metastatic disease to the CNS occurs more commonly than primary CNS tumors. Synaptophysin =a transmembrane glycoprotein found in the presynaptic vesicles of neurons.jpg . they do not stain for GEAP or synaptophysin.nation/Figures/MS_GFAP.

ischemia or toxic injury may lead to the loss of neurons. When renal vein thrombosis occurs on the left side in male patients.. . is responsible for the thrombotic and thromboembolic complications of nephrotic syndrome. Irreversible neuronal injury manifests with shrinkage of the neuronal body. Loss of anticoagulant factors. and from there enters the inferior vena cava. a condition that often indicates an occlusion of the left renal vein by a malignant tumor or thrombus. This difference in venous drainage gives diagnostic significance to left-sided varicocele.secreting columnar epithelium. the obstruction impedes venous flow from the left testis. Renal vein thrombosis can be a manifestation of this hypercoagulable state. respiratory and urinary tracts.Vitamin A maintains orderly differentiation of specialized epithelia. -Membranous glomerulopathy is a common cause of nephrotic syndrome in adults. causing a number of varied complications. and pancreatic and other exocrine ducts. Avitaminosis A in particular may contribute to squamous metaplasia of the epithelial lining of pancreatic exocrine ducts. Avitaminosis A . including the mucus-secreting columnar epithelia of the ocular conjunctiva.Recurrent sinopulmonary infections and exocrine gland fibrotic atrophy in a young Caucasian are suggestive of cystic fibrosis (CF). . the epithelium undergoes squamous metaplasia to a keratinizing epithelium.Transient but profound hypoxia. which are already injured and predisposed to squamous metaplasia by inspissated mucus. deep eosinophilia of the cytoplasm. The resulting pancreatic insufficiency can cause a deficiency of fat soluble vitamins. Due to the increased permeability of the glomerular capillary wall in nephrotic syndrome. and left-sided varicocele appears. retinoic acid. . are required to maintain orderly differentiation of specialized epithelia. Patients present with sudden onset abdominal or flank pain and gross hematuria. In contrast the right testicular vein empties directly into the inferior vena cava. including mucus.A decrease in the size and number of neurons is characteristic of compression atrophy Renal vein thrombosis . pyknosis of the nucleus and loss of Nissl substance. many important substances are lost in the urine.Venous drainage from the left testis travels through the left testicular vein into the left renal vein. severe CF may cause total obstruction followed by complete fibrotic atrophy of the exocrine glands. Normal levels of vitamin A and its metabolite. In the pancreas. Avitaminosis A can cause squamous metaplasia of such epithelia to a keratinizing epithelium. especially antithrombin Ill. When a deficiency state exists.

trunk. The lesion has a velvety to granular texture and is classically described as having a “stuck on” appearance. greasy. Diffuse large B-cell lymphoma is the most common subtype.htm Acute pyelonephritis . Appearing most often on the trunk.edu/lm/Der. seizures. http://missinglink.Seborrheic keratosis =benign epidermal tumor that is commonly identified on the skin of middle-aged or elderly individuals. http://img. purplish plaques on the wrists hands. -Primary CNS lymphomas are universally associated with the Epstein-Barr virus (EBV). A finely reticulated scale termed “Wickham’s striae” may be present on the plaque surface.com/pathCon/diagnosis?pii=S1559-8675(06)704764 http://www.jpg Lichen planus =characterized by the “5 Ps”: polygonal. extremities. and legs. The cells of CNS lymphomas are commonly positive for the B-cell markers CD2O and CD79a. round.medscape. pruritic. The clinical presentation is non-specific. seborrheic keratosis presents as a tan to brown. atypical lymphoid cells.ucsf. planar.122151-1123213-1123299. or progressive focal neurologic deficits may occur..atsjournals.eborrheic_Keratosis-KK.. or neck.uhrad.. pulmonary function tests showing a restrictive profile and surgical biopsy showing extensive interstitial fibrosis together with paraseptal and subpleural cystic airspace enlargement (honeycomb lung) http://ajrccm. cellular aggregates of uniform. http://www. Mental status changes.jpg Idiopathic pulmonary fibrosis =Insidious-onset progressive exertional dyspnea.org/cgi/content-nw/full/165/2/277/F3 Primary CNS lymphoma =The most frequent CNS tumor in immunosuppressed patients .com/pi/emed/ck. head. flat. The majority of primary CNS lymphomas arise from B-cells.pathconsultddx.com/mriarc/mri001.is commonly associated with AIDS.. Most of CNS lymphomas are high-grade and respond poorly to chemotherapy. -Primary CNS lymphomas appear microscopically as dense. coin like lesion ranging in size from a few millimeters to several centimeters.

the introitus. the ascent of pathogens to the kidneys is impossible. Leukemic spread can cause lymphadenopathy. The most common pediatric malignancy in children is acute lymphoblastic leukemia (ALL). pallor. Proteus. -Frequent bladder infections. The bladder mucosa normally does not allow bacterial attachment. accompanying these chronic symptoms will be an acute presentation. cystitis occurs. and the vagina of healthy females are populated by non pathogenic flora (lactobacilli. coli . may weaken the vesicoureteral junction and facilitate reflux. Pituitary apoplexy = acute bleeding in to a preexisting pituitary adenoma. The distal urethra. present only in the latter. and bleeding. non-pathogenic staph and strep) that prevent colonization by pathogenic strains. T-cell ALL is more likely to present with a large anterior . fatigue. some urine returns to the ureter.). acute and chronic. The neoplastic cells of ALL arise from lymphocytic precursors that are of either pre-B or pre-T lineage. and pyelonephritis does not occur. and Enterococci are the pathogenic bacteria that usually cause acute pyelonephritis. mimicking a subarachnoid hemorrhage. A careful physical exam can differentiate a subarachnoid hemorrhage from a sellar mass with suprasellar extension (pituitary tumor) by the presence of bitemporal hemianopsia. When these mechanisms are disrupted. hepatosplenomegaly and bone pain. antibiotic use. without treatment. If there is an anatomic abnormality of this area. ALL . petechiae. the distal urethra is colonized by pathogenic gram-negative rods more easily.Blast cells in the peripheral blood are strongly suggestive of leukemia. If this endogenous flora is suppressed (due to systemic illness. which has several defenses against bacteria. as with the severe headache and visual disturbances in this patient. bringing along any pathogens present in the bladder (vesicoureteral reflux). An urgent neurosurgical consultation and treatment with glucocorticoids are required. pregnancy. normal urine is bactericidal due to high urea content and high osmolarity. Without vesicoureteral reflux. or are overcome by bacterial virulence factors. The long-standing symptoms of a pituitary tumor will be present for months as with this man’s headache and decreased libido. -Clinical manifestations of ALL include fever.Klebsiella. -Signs of meningeal irritation can also be seen in pituitary apoplexy. Patients suffering from pituitary apoplexy develop cardiovascular collapse because ACTH deficiency leads to adrenocortical insufficiency. or an increase in bladder pressure. prognosis is poor.-Gram-negative rods such as E. Symptoms will be bimodal. and urine flow washes the bacteria downstream. Pituitary apoplexy is a medical emergency. -The normal vesicoureteral junction does not allow retrograde flow of urine. Pathogens present in the urethra next encounter the bladder. etc.

but is often not performed because of cost and delay of treatment. and CD2O+. tachypnea.jpg Mitral valve thickening with vegetations . Ventilation/perfusion scanning is usually the next step in evaluating these patients.) -Deep venous thrombosis (DVI) is the number one cause of PE.mediastinal mass that can compress the great vessels. sharp-edged aggregates. resulting in acute symptoms like chest pain shortness of breath tachycardia.html Pulmonary embolus (PE) -Lung scans display both the blood perfusion and the ventilation of each area of the lung. Grossly. lung collapse or condensation is indicated. Angiography remains the gold standard in establishing the diagnosis of a PE.hic_calcification. http://rebeccanelson. while pre-T lymphoblasts are CD2+. CD5+. CD4+. CD 7+ and CD8+.org/2006/12/07/saddle-pulmonary-embolus/ Dystrophic calcification =hallmark of cell injury and death. http://www. -The most common sites of dystrophic calcification include aged or damaged cardiac valves and atheromatous plaques. CD3+. CD 19+. http://www. A perfusion defect that is not anatomically matched by a ventilation defect indicates that blood flow has been occluded to that segment of the lung.” Many patients do not realize they have a DVT until the clot migrates to the pulmonary vasculature.org/wikipe.medskool. Both lineages express TdT (an antigen of lymphocyte precursors) on their cell surfaces. and in such cases are better termed “pulmonary thromboembolism.. Chest radiographs are often within normal limits. it is described as a psammoma body. Because pre-B and pre-T lymphoblasts can look identical in peripheral blood -smear. Mediastinal mass compression of the esophagus causes dysphagia. although lung scans can be negative despite the presence of a PE. occurring in all types of necrotic tissue — including areas with fat necrosis.net/images/circulatory/heart%20valve. If the deposit develops lamellated outer layers. (If there is a ventilation defect with the perfusion defect. causing superior vena cava syndrome.com/leukemia/all. Pre-B lymphoblasts are CD1O+. while mass compression of the trachea leads to dyspnea and stridor.jpg http://upload. and hypotension.wikimedia. On hematoxylin and eosin staining.radpod. immunohistochemical staining is used to differentiate the two cell lineages. dystrophic calcium deposits are fine gritty white granules or clumps. these deposits typically appear as dark purple.. -The process of calcification is defined in two stages: initiation (which transpires within the mitochondria of dead or dying cells) and propagation (which can eventually perforate the cell membrane from within)._H&E.

http://radiographics.html DIFF: . -Of these SLE is most likely to also affect the coronary arteries via arteritis and/or thrombosis.. -In interstitial pneumonia.com/sol/06962.org/content/20/3/795/F8.pathology.jpg -Intrahepatic hydatid cysts with surrounding fibrous reaction can be seen in patients with an Echinococcus infection. http://www. the inflammatory infiltrate is confined to the alveolar walls..jpg .jpg -Granulomatous destruction of bile ducts is seen in patients with primary biliary cirrhosis. The condition may progress to valve fibrosis resulting in regurgitation or possibly stenosis.pathguy.can be classified as one of three morphologic variants. -Cirrhosis is considered micronodular if most nodules are 3 mm in diameter and macronodular if most nodules are > 3 mm in diameter.. In SLE thrombosis occurs due to the hypercoagulable antiphospholipid antibody syndrome -The verrucous endocarditis that occurs in up to 25% of patients with SLE (Libman-Sacks endocarditis) produces small (1-4 mm in diameter) cardiac valvular vegetations on either side of the valve consisting of sterile finely granular fibrinous eosinophilic material. http://www. http://img.rsna.Dilation of sinusoids and perivenular hemorrhage is associated with acute venous outflow obstruction within the liver.includes infectious endocarditis. . Libman-Sacks endocarditis associated with systemic lupus erythematosus (SLE) and nonbacterial thrombotic endocarditis. **Congestion (first 24 hr)is the first stage of lobar pneumonia. Pneumonias .large. in which the hepatocellular accumulation of coarse pigmented granules causes the liver to appear black.ogy/169972-173517-3384. These vegetations may result from immune complex deposition. -When the inflammatory process involves an entire lung lobe.vcu. it is a lobar pneumonia.medscape.SLE may cause an acute coronary syndrome at a young age even with angiographically normal coronary arteries. It is . Cirrhosis = diffuse hepatic fibrosis with replacement of the normal lobular architecture by fibrous-lined parenchymal nodules (“nodular parenchymal regeneration”).com/pi/emed/ck.h.edu/education/gi/lab3.Substance accumulation within hepatocytes occurs in conditions such as DubinJohnson syndrome. -Patchy inflammation of a number of lobules is characteristic of bronchopneumonia. rheumatic valvulitis.

ipsilateral deficits of CN V. occurs due to the occlusion of the middle cerebral artery (MCA).org/wiki/. grasp tonic neck reflexes) may also be present. ** Resolution is the last stage of lobar pneumonia. and the frontal eye field. PICA occlusion is characterized by contralateral loss of pain and temperature sensation.characterized by pronounced dilatation of the alveolar capillaries. Urinary incontinence and primitive reflexes (i. When these lesions resolve and become cystic. Hemispheric stroke .. they form small cavitary spaces called “lacunas” .. with more involvement of the arm than the leg. and by Horner’s syndrome. Lacunar infarcts occur because of hypertensive changes in the arterioles.Hemiparesis. . Broca’s and Wernicke’s speech areas. firm and airless. **In the red hepatization stage (days 2-3) the intra-alveolar exudate consists of RBCs. Broca’s area is located in the inferior frontal gyrus in the dominant (left) hemisphere and is supplied by the left middle cerebral artery.wikimedia. fibrin and fragmented RBCs.com/pi/emed/ck. This artery supplies the face and arm areas of the motor and sensory cortex. http://commons.e. Microscopic examination of the exudates would show neutrophils.. penetrating branches that perfuse the internal capsule and basal ganglia. neutrophils and fibrin. -Occlusion of the anterior inferior cerebellar artery causes lateral inferior pontine syndrome.An infarct in the area of distribution of the left anterior cerebral artery leads to right hemiplegia with lower extremities affected more than upper extremities. Contrary to popular belief the left hemisphere of the brain is most often dominant in both right-handed and left-handed people.jpg DIFF: . & Xl. Contralateral loss of pain and temperature sensation is accompanied by ipsilateral deficits of cranial nerves V and VIII. . and cerebellar symptoms. It is characterized by resorption of the exudate and restoration of the pulmonary architecture. usually less than 15 mm. X. penetrating arterioles causes infarcts of only a few mm in diameter. ** A lung lobe that is pale and firm macroscopically suggests the gray hepatization phase (days 4-6).com/?page=oll&topic=24&qid=1492 Lacunar infarcts -The occlusion of distal. Horner’s syndrome. Along with hemiparesis. VIII.cine/756148-810904-783. Moro.medscape.A-Stroke-Brain-Humn-2A.Occlusion of the posterior inferior cerebellar artery (PICA) leads to lateral medullary (Wallenberg) syndrome. The affected lobe is red. Some exudate containing mostly bacteria may be present in the alveolar spaces. this patient has Broca’s (expressive) aphasia which manifests with an inability to speak or write but preserved comprehension of the spoken and written word. http://frontalcortex.. The MCA also gives rise to the small. These small.jpg http://img. IX.

tortuous veins resulting from prolonged increases in intraluminal pressure and from loss of vessel-wall tensile strength.edu/anatomyhtml/atlas_html/n1a5p7. stasis dermatitis. Varicose dilation of veins leads to incompetent venous valves. Although deep venous thromboses (DVTs) are the number one cause of pulmonary emboli varicose vein thromboses are restricted to the superficial venous system. skin ulcerations. and multiple pregnancies.. Pure sensory stroke -.These patients are likely to have an underlying chronic thiamine deficiency—and because thiamine (B1) is used in the metabolism of simple sugars. Watershed infarcts occur at the border of perfusion zones between the anterior and middle cerebral arteries. Below.uk/images/varicose%20veins%2018. -Complications result from the poor blood flow—painful thromboses. -The predominant location of varicosities are in superficial veins of the leg. depending on exactly which portion of the brain is infarcted. Thiamine is essential for glucose utilization in the brain cells.jpg Varicose veins =dilated.medscape. ataxia-hemiplegia syndrome-.penetrating branches supply the basal ganglia and deep white matter. 1.edu/kfung/IACP-OLP/APAQ-Images/N1-MS-01-16.com/pi/emed/ck.the base of the pons or the genu of the internal capsule http://anatomy. these specific syndromes are listed with their anatomical counterparts. http://moon.y/336139-341971-2971tn. glucose infusion seriously exacerbates this pre-existing B1 deficiency.base of the pons 4. ataxia.lonclin. Defective venous wall development may account for a familial tendency. and an increased incidence of thrombosis. as from cardiac arrest or shock. therefore thromboembolism is very infrequent with varicose veins. The end process is called hyaline arteriolosclerosis.ventrolateral thalamus 3. -Lacunar infarction leads to characteristic clinical syndromes. poorly healing wounds. and ocular abnormalities .ouhsc. Risk factors are all related to a chronic increase in lower extremity venous pressure and include long periods of standing age greater than 50. http://www.gif http://img. Pure motor hemiparesis-..uams. dysarthria-clumsy hand syndrome -. which causes narrowing of the vessel lumen and possible occlusion. -Thiamine should be administered immediately when symptoms of Wernicke .Hypoxic encephalopathy occurs due to abrupt cessation of cerebral blood flow.co. The leakage of plasma components through the endothelium and increased production of extracellular matrix cause changes in the arteriolar wall. venous stasis/congestion. edema. and superficial infections that may promote chronic varicose ulcers.posterior limb of the internal capsule 2. obesity. Pyramidal cells of hippocampus and Purkinje cells of the cerebellum sustain ischemic damage first.jpg Wernicke syndrome =Confusion.html .

IV and VI. Mental status changes (confusion) usually respond to treatment well. Bone resorption in hyperparathyroidism primarily involves . Trabecular bones are also called spongy or cancellous bones. The most prominent changes in osteoporosis occur in dorsolumbar vertebral bodies as vertebrae are predominantly trabecular. white females.gif DIFF: . Unlike ophthalmopathy.cdc.In Wernicke syndrome ataxia is caused by damage to the cerebellar cortex and vestibular nuclei.Hyperparathyroidism increases osteoclastic activity. Osteoporotic fractures are most common at vertebral bodies and second most common at the neck of the femur. Memory and learning impairment is usually permanent. . which results in increased bone resorption. -Ophthalmopathy in Wernicke syndrome occurs due to damage to the nuclei of CN Ill.jpg Osteoporosis =predominantly a disease of postmenopausal. Vitamin D is important for the absorption of calcium and phosphorus from the gastrointestinal tract and for bone mineralization. These symptoms are rapidly reversible. http://www. Trabecular bone composes only 15% of the total skeleton. ataxia takes longer to resolve. Cortical bones (long bones) contribute by serving as mechanical support and sites of muscle attachment. Damage to this nucleus causes memory loss and a fascinating psychological phenomenon called “confabulation. http://www.org/health/graphics/beriberi1. -Drowsiness and apathy are the early symptoms of Wernicke encephalopathy. Korsakoff syndrome also causes an inability to form new memories (anterograde amnesia). and permanent gait abnormalities may persist. a condition known as Korsakoff syndrome.moondragon. White females have lower bone mass compared to black females.gov/nutrition/images/badbone. The neck of the femur consists of 50% of trabecular and 50% of cortical bone. Most of the appendicular skeleton (the limbs) is cortical bone.Increased deposition of unmineralized osteoid is very characteristic of vitamin D deficiency. Ataxia takes longer to resolve.” When patients with Korsakoff syndrome unsure of a fact they fill in the memory gap with a fabricated to that they themselves believe to be true. Ocular motor signs (horizontal nystagmus. Osteoporosis primarily involves trabecular. -Korsakoff syndrome is associated with the damage of the medial dorsal nucleus of the thalamus.encephalopathy manifest. Some patients may have permanent symptoms. They resolve rapidly after thiamine administration. In a small number of patients the improvement of mental status is followed by memory abnormalities. -The two major types of bone present in an adult skeleton are trabecular and cortical. . or spongy bone. by weight but trabecular bone is metabolically more active because of its large surface area. After menopause declining estrogen levels accelerate the loss of bone mass mainly through a decrease in osteoblastic activity and an increase in osteoclastic activity. bilateral abducens palsy) usually resolve completely within hours of thiamine supplementation.

unmineralized spongiosa in the medullary canals.cortical bones (bone loss in postmenopausal osteoporosis is trabecular). Previous MIs may be protective because fibrosis tends to decrease the probability of myocardial tearing. a very characteristic feature of hyperparathyroidism.The risk factors for ventricular free-wall rupture following an Ml include: age greater than 60. . these patients present with profound hypotension and shortness of breath. The net result is a focal formation of abnormal bone. and absence of left ventricular hypertrophy. venous return to the heart is reduced. especially in patients receiving invasive procedures. and enzymatic lysis of connective tissue have substantially weakened the infarcted myocardium (mean 4-5 days. -Histologically osteopetrosis is characterized by the persistence of primary. It is not clear whether this early increased risk includes an increased risk of myocardial rupture. The disease process starts as marked osteoclastic activation in particular locations followed by increased osteoblastic activity. In normal individuals the primary spongiosa is replaced by bone marrow. Failure to relieve the obstruction results in death. -Clinically. Additionally. Cement lines represent previous areas of bone resorption. The new collagen is laid down in a haphazard manner in lieu of the linear deposition in normal bones. though there is a survival benefit overall. . also called analgesic nephropathy -pathogenesis is multifactorial. NSAIDs concentrate in the renal medulla. As the pressure increases in the pericardial cavity. rupture is more likely to occur if this is the patient’s first MI. . -Free wall rupture causes cardiac tamponade. . The end product is a mosaic pattern of lamellar bone where irregular sections of lamellar bone are linked by cement lines. The frequency of early death (within the first 24 hours of an Ml) is actually increased by myocardial reperfusion via fibrinolytic therapy. when coagulative necrosis neutrophil infiltration. Ruptured left ventricular (LV) free wall = a complication of transmural (ST elevation) myocardial infarction (Ml) that generally occurs 3 to 7 days after the onset of total ischemia.the most common cause of death in a patient hospitalized for a Ml is ventricular failure (cardiogenic shock). On physical examination. female gender. -Paget’s disease of the bone involves only focal areas of the skeleton. This leads to profound systemic hypotension and pulseless electrical activity. Intracranial hemorrhage is a serious bleeding complication. which greatly limits ventricular filling during diastole. which accounts for 2/3 of in-hospital Ml deaths. NSAID-induced nephropathy. the heart sounds are muffled and the jugular venous pressure is elevated.The most frequent complication of fibrinolytic therapy for Ml is bleeding. pre-existing hypertension. range 1-10 days). Increased resorption of cortical bones results in subperiosteal thinning.

com/pi/emed/ck. Atrial flutter and atrial fibrillation are arrhythmias that do not usually result in sudden cardiac death. nocturia). -Ventricular tachycardia and ventricular fibrillation are the most lethal arrhythmias in patients with acute Ml. Ischemia produces electrical instability in the heart and can generate a potentially lethal arrhythmia. prior to arrival in the emergency room).. Morphologic abnormalities in glomeruli and vascular channels are often mild.Following a myocardial infarction (MI) there may be ventricular mural thrombosis and cerebral thromboembolism.Extensive myocardial infarction (Ml) may result in terminal ventricular failure. Ventricular fibrillation is also the most common cause of death from myocardial infarction in the pre-hospital phase (i. thus causing direct cell damage. Ventricular failure is the most common cause of death due to Ml during the in-hospital phase. gross hematuria.allowing higher levels in the papillae than in the renal cortex.y/336139-379762-6072tn. -With prolonged NSAID use. While the previous factors predispose to papillary necrosis. . distortion of caliceal architecture and tubular atrophy are seen on light microscopy. However it is unusual to have significant mural thrombosis prior to 48 hours after the Ml. the major pathophysiologic abnormality is chronic interstitial nephritis. Proteinuria is usually mild often less than 1 gm/day. Approximately 80% of SCDs are due to coronary artery disease (CAD). and is the most common cause of lethal cardiac arrest in CAD-related SCD. http://img. . In the majority of CAD-related SCDI the pathogenesis is acute plaque change producing acute myocardial ischemia. or Fanconi syndrome (aminoaciduria. glycosuria. evidence of tubular dysfunction (polyuria. Patchy interstitial inflammation with subsequent fibrosis. hypouricemia). NSAIDs also uncouple the oxidative phosphorylation in renal mitochondria. and the passage of tissue fragments in urine. death may result due to ventricular septal rupture but this also does not occur until 3-7 days after the onset of infarction. necrosis and scarring of papillae. death due to heart failure caused by an Ml usually does not occur suddenly. However.medscape.e.LV rupture generally does not occur until 3 to 7 days after the onset of infarction.. patients with chronic interstitial nephritis may show modest elevation in serum creatinine. Papillary necrosis may manifest with colicky flank pain. Ventricular fibrillation is usually the first arrhythmia to appear as a result of acute myocardial ischemia.jpg Sudden cardiac death (SCD) . -Clinically.SCD is defined as cardiac arrest that begins within one hour of the precipitating event and ultimately proves fatal. . hypophosphatemia. Decreased prostaglandin synthesis also facilitates the constriction of medullar vasa recta promoting ischemia. Similarly. .

-The presence of numerous neutrophils in the alveolar fluid would be consistent with an exudate. with food faddists or those who are taking vitamin D replacement therapy the most commonly affected. -Excessive vitamin D supplementation may result in hypercalcemia. polydipsia. 2) the vitamin D is bound to a plasma D-binding protein and transported to the liver. 4) the 25(OH) D is converted to 25(OH)2D (calcitriol) by al-hydroxylase in the kidney.Hodgkin’s lymphoma) frequently develop hypercalcemia and hypercalciuria. sarcoidosis. siderophages. Additionally.Hemosiderin-containing macrophages in the alveoli (ie. conversion to 25-hydroxy vitamin D. When erythrocytes extravasate into the alveoli due to the increased intravascular pressures in the pulmonary capillary bed hemosiderin accumulates in alveolar macrophages.Cardiogenic acute pulmonary edema = increased filtration of plasma water and electrolytes into the lung interstitium and alveoli. The metabolism of vitamin D is summarized as follows: 1) vitamin D is absorbed in the gastrointestinal tract or synthesized from precursors in skin after sunlight exposure. It is also readily available via dietary consumption. being found in fortified milk fatty fish. 3) once in the liver. . anorexia. or “heart failure cells”) are suggestive of prior episodes of pulmonary congestion and edema that arose due to chronic left heart failure. cod-liver oil. vomiting. polyuria. . Vitamin D intoxication usually occurs in adults taking in excess of 60000 IU/day. The fluid that accumulates is a transudate (an ultrafiltrate of plasma caused by hemodynamic changes) rather than an exudate (an extravasation not only of plasma water and small ions but also plasma protein components and circulating leukocytes. and non. muscle weakness.Focal necrosis of alveolar walls and intra-alveolar hemorrhages are more typical of pulmonary hemorrhage syndromes such as Goodpasture syndrome and vasculitis-associated hemorrhage (as seen in hypersensitivity angiitis Wegener granulomatosis. confusion. Calcitriol is the most active form of vitamin D. as seen in inflammatory states). Hodgkin’s disease.hydroxylase takes place. It is thought that patients with sarcoidosis experience increased intestinal calcium absorption and bone resorption secondary to high serum calcitriol concentrations. tuberculosis. and lupus erythematosus). -Fat-globule occlusion of pulmonary vasculature is an early histologic manifestation of fat embolism syndrome which is not associated with myocardial infarction but multiple fractures of the long bones pelvis or ribs. and painful bone demineralization. hypercalciuria. Vitamin D = normally produced endogenously via photoisomerization with casual exposure to sunlight. patients with granulomatous disorders (eg.Mononuclear interstitial pulmonary infiltrates are found in the early stages of various interstitial lung diseases. . DIFF: . 25(OH)D (calcidiol) by 25. which occurs in the setting of an acute bacterial or aspiration pneumonia. and eggs.

but also to the degree of any concomitant hypertension.like. and seizures may follow.Malignant hypertension produces hyperplastic arteriolosclerosis.. -EEG can reveal focal temporal abnormalities. http://lh5. and elevated protein levels. http://doctorxdrive2. CT or MRI detect edema and hemorrhage in the temporal lobe. olfactory hallucinations (olfactory cortex involvement).HSV-1 mostly affects teenagers and young adults and is the most common cause of sporadic encephalitis. which consists of homogeneous onion. confusion).radpod. anemia. concentric thickening of the walls of arterioles.Herpetic encephalitis .com/_czdfK6r5I8o/. -The most common early symptoms of acute encephalitis are headache and fever.tic+arteriolosclerosis. Eosinophilic intranuclear inclusions (Cowdry type A) are present in glial cells and neurons. Mental status changes (lethargy. and from excessive extracellular matrix production by smooth muscle cells (3MG). http://pathology.ggpht. The hyaline material is thought to result from leakage of plasma constituents across the vascular endothelium.com/images/0016. Macroscopic brain examination reveals edema and hemorrhagic necrosis of the temporal lobes. which may result from nonmalignant hypertension or diabetes. Multinucleated giant cells may also be found. and personality changes (amygdala damage).jpg http://www. Temporal lobe involvement is characteristic of HSV-1 encephalitis. The underlying structure of the vessel wall is maintained but the intima is thickened and the arterial lumen is narrowed.edu/neuropath/CNSlecture2/hsv.mc. malaise. Specific symptoms of herpetic encephalitis are related to HSV-1’s predilection for the temporal lobe including aphasia (damage of speech areas).jeeran. In diabetics. Encephalitis results from the reactivation of latent virus “living” in the trigeminal ganglion and the virus spread along this nerve into the cerebral vault. The 3MG may be stimulated by chronic/repetitive endothelial injury caused by the hemodynamic stress of longstanding hypertension or by the metabolic derangements of diabetes.jpg DIFF: . weight loss and .. cranial nerve deficits. normal glucose.duke.org/2007/03/24/herpes-simplex-encephalitis/ Hyaline arteriolosclerosis =Homogeneous deposition of eosinophilic hyaline material in the intima and media of small arteries and arterioles characterizes . CSE has a typical “viral pattern" with lymphocytic pleocytosis. This morphologic pattern results from laminated SMC and reduplicated basement membranes. development of hyaline arteriolosclerosis is related not only to the duration of the disease.jpg Cachexia = a syndrome that encompasses anorexia.

Cachexia in the patient described above is a manifestation of the lung neoplasm revealed on his chest Xray.html . The use of NSAIDs. a condition that results from short-term.along with IL-1 mediates many of the symptoms of septic shock and causes hepatic release of acute-phase reactants such as C-reactive protein and fibrinogen. The likelihood of an adult-type 1 postductal coarctation is greatly increased by the finding of enlarged. In experimental animals it also produces symptoms of cachexia. http://www. For this reason TNF-α is also called cachectin and is considered a main mediator of paraneoplastic cachexia. Acute erosive gastritis can cause upper GI hemorrhage. burns (Curling ulcers). . Its role in cachexia is explained by its influence on hypothalamus that leads to appetite suppression. and alcohol consumption are the most common causes. the stenosis is post-ductal (in contrast to the infantile form where the coarctation is generally preductal and fatal soon after birth without surgical repair). Erosions are defined as mucosal defects that do not penetrate the muscularis mucosa. severe mucosal injury that leads to inflammation and superficial mucosal destruction. -In bacterial infections.. head trauma (Cushing ulcers). palpable intercostal vessels which indicate the development of a collateral arterial circulation to the region of the aorta distal to the coarctation.. ascites and varicosities in portocaval anastomoses. -TNF-α is produced by macrophages in response to infection as well as by some neoplastic cells. patients with adult-type aortic coarctation often have notching of the ribs as a result of the enlarged tortuous intercostal arteries. smoking alcohol acute stress or bacterial infection. splenomegaly. having surgery. -On radiographic exam. TNF-α produces fever .generalized wasting due to underlying systemic disease. It does not cause histologic changes to the hepatic parenchyma. A number of causative agents can cause acute erosive gastritis.heartpearls.rctation-of-the-aorta. Acute erosive gastritis .In adult-type aortic coarctation.can be caused by a number of factors such as NSAID use. . Erosions usually occur in the setting of acute erosive gastritis.can produce hypertension in the upper aortic circulation and simultaneously low perfusion in the distal aorta supplying the legs.A gastric erosion is defined as a mucosal defect that does not penetrate the muscularis mucosa. Adult-type aortic coarctation . Portal vein thrombosis -causes portal hypertension.com/2009/05. Tumor necrosis factor-alpha is a cytokine that causes necrosis of some tumors in vitro. smoking.

-Salmonella is the most common cause of osteomyelitis in children with sickle cell disease: staphylococcus aureus is the second most common cause in these patients. and then migrate to the scrotal sac via the inguinal canal. circulating .Embryologically. Undescended testes. If undescended testes are not surgically moved to the scrotal sac the seminiferous tubules become atrophic and hyalinized overtime. The undescended testes can lie anywhere along the path from the abdomen to the scrotal sac. The failure to completely descend may be unilateral or bilateral. Monitoring of fibrinogen and platelet count is helpful in early identification of the onset of DIC in high-risk patients. resulting in a low sperm count. cryptorchidism .45% (or 1 in 220). creating an ideal environment for the seminiferous tubules. Know the findings of DIC: Prolonged PTT and PT Thrombocytopenia and microangiopathic hemolytic anemia Low fibrinogen Elevated fibrin split products (D-dimer) Low factor V and VIII levels -Sickle cell patients become functionally asplenic and thus are at an especially increased risk for infection by encapsulated organisms (Hemophilus influenza and pneumococcus). with the most common being a missense mutation that results in cysteine-to-tyrosine substitution at amino acid 282 (mutation C282Y). In white populations of northern European descent. The hemochromatosis gene (HLA-H) . -The temperature inside the scrotal sac is lower than body temperature.On the short arm of chromosome 6 the hemochromatosis gene (called HFE) encodes an HLA class I-like molecule that appears to affect iron absorption from the gastrointestinal tract. which are very temperaturesensitive and prone to heat-induced damage. because the seminiferous tubules are responsible for the secretion of inhibin. Multiple mutations have been identified.A retained dead fetus in the uterus = associated with disseminated intravascular coagulation (DIC) and progressive hypofibrinogenemia. Additionally. Hemochromatosis is therefore one of the most common inherited diseases. the testes originate within the abdomen. the frequency of HFE is approximately 6% and the homozygous frequency is approximately 0. as well as one of the most common inborn defects in metabolism. The exact cause of cryptorchidism is poorly understood in most cases.

.levels of inhibin decrease as the seminiferous tubules degenerate. Diabetes mellitus: diabetic metabolic abnormalities. Renal papillary necrosis -The abrupt onset of gross hematuria in a patient with family histor of sickle cell disease suggests renal papillary necrosis. Patients with chronic papillary necrosis may remain asymptomatic until gross hematuria or the passage of tissue fragments in urine occurs. and acute renal failure. After the acute phase. rust-colored or bloody urine and acute. leading to compromised renal vasculature.. Congenital bicuspid aortic valves . especially when orchiopexy is not performed by age 2. with preserved tubule outlines. scars can be seen on the cortical surface as fibrous depressions replace the inflammatory foci. -Patients with cryptorchidism are at increased risk for testicular cancer. Sickle cell disease or trait: sickling causes obstruction of small kidney vessels and predisposes to ischemia. Unlike the seminiferous tubules. The following conditions are most strongly associated with papilla necrosis: 1. Microscopically.occur in approximately 1 .S. certain analgesics can cause ischemia. including non-enzymatic glycosylation. has been withdrawn from the U. 4. severely ill patients. -Dark.edu/classwar. Acute pyelonephritis and urinary tract obstruction :the edematous interstitium of the pyelonephritic kidney compresses the medullary vasculature.4% of live births. which can be caused by a number of systemic conditions associated with ischemia.tulane. thus predisposing the patient to ischemia. Many of the other NSAIDs. market. cause changes in vascular walls. The congenital bicuspid valve accelerates the normal aging process. Patients whose testes are located intra-abdominally have a higher risk of malignancy compared with those whose testes are located in the inguinal region. -Hemolytic uremic syndrome (HUS) consists of the triad of microangiopathic hemolytic anemia. however. the most nephrotoxic analgesic drug. 2.som. Macroscopic pathological findings include gray-white or yellow necrosis of the tips or distal two-thirds of renal pyramids. colicky flank pain are common symptoms and are due to acute ureteral obstruction from sloughed papillae. leading to premature calcific aortic . Analgesic nephropathy: phenacetin. Thus. testosterone and LH levels are usually normal. 3. This occurs most commonly in children and young adults.html DIFF: -Ischemic tubular necrosis presents with oliguria in hospitalized. the tissue shows coagulative infarct necrosis.Path/GR_Renal/Renal23. FSH levels are elevated due to loss of negative inhibition by inhibin. http://www. inhibit renal blood flow by decreasing prostaglandins synthesis. Muddy-brown granular casts are pathognomonic. the testosterone-producing Leydig cells are not very sensitive to temperature. In patients predisposed to renal hypoperfusion. thrombocytopenia.

neuropathologyweb. In patients without the defect. they can be differentiated by histology.org/Publ. http://www.m04Image/Com401-2-FR4b. and lethargy).d_aortic_valve_disease. round.Pilocytic astrocytoma is the most common brain neoplasm of childhood.. and central nervous system. They arise in the walls of the ventriculi and can hamper CSF flow and cause hydrocephalus. blue cells). This is in contrast to congenital aortic stenosis. -Classic histologic findings include small intestine mucosa containing enlarged.jpg DIFF: . On microscopic examination.org/chapter7/images7/7-16b. without any hemodynamically significant degree of aortic out flow tract obstruction or audible murmurs.” http://www. an isolated congenital bicuspid aortic valve usually remains asymptomatic.edu/kfung/jty1/C.In early life. which occurs in approximately 0. PNETs are composed of sheets of small cells with deeply basophilic nuclei and scant cytoplasm (small. Symptoms include signs of increased intracranial pressure (morning headaches.ents/image/090medblast. Abundant mitoses are also seen. Medulloblastomas = part of a group called “primitive neuroectodermal tumors” (PNETs).. On microscopic examination of a pilocytic astrocytoma.clevelandclinic. pilocytic astrocytes and Rosenthal fibers are seen. provoking no inflammatory response as a consequence. . and usually produces a systolic murmur at birth. vomiting..org/images/ependymomas-bdy.vcu.php/Pilocytic_Astrocytoma http://moon.org/wiki/index. Cerebellar dysfunction occurs as the tumor compresses adjacent structures.jpg http://www.jpg Whipple disease =Caused by the gram-positive actinomycete Tropheryma whippelii.gif -Ependymomas are the third most common brain neoplasm found in children. joints. ependymal cells form gland-like structures called “rosettes. is a rare systemic illness that involves the small intestine.jpg . The cerebellar vermis is the most common location of a medulloblastoma.stenosis in the sixth and seventh decades. and results from more severe subvalvular.edu/WirSe. http://my. Pilocytic astrocytomas are low-grade tumors and have a better prognosis than medulloblastomas.. The actinomycete proliferates only within the macrophages of these tissues..ouhsc. valvular.cns. Although both pilocytic astrocytomas and medulloblastomas are often located in the cerebellum.04% of live births. http://wiki.mayoclinic. or supravalvular anatomic defects. -Medulloblastomas are undifferentiated and aggressive tumors. senile calcific aortic stenosis typically comes to clinical attention in the eighth or ninth decades.pathology..

pylory do not appear to invade these tissues and are susceptible to gastric acidity. exercise regimen. pylori leads to malignancy remains unclear. H. . The mechanism by which H.pathconsultddx. pylori associated . Somatostatin is a hormone that inhibits gastrin release. though it has been hypothesized that immune activation or local inflammation may play a role. long distance runners) who are not anorexic also sometimes develop amenorrhea. diastase-resistant granules (which consist of lysosomes and partially digested bacteria).com/pathCon/diagnosis?pii=S1559-8675(06)709214 Anorexia nervosa =distorted body image.Gastric adenocarcinoma and gastric lymphoma are associated with H. pylory live in the mucus layer overlying the epithelium of the gastric antrum and fundus. . The organisms are protected by the mucus layer and their urease production. Intense exercise regimens may contribute to inadequate hypothalamic-pituitary gonadotropin secretion. pylory cause local inflammation of the gastric mucosa which decreases the number of somatostatin-producing antral cells by an unclear mechanism. -H. H. pale.foamy macrophages packed with both rod-shaped bacilli and PAS-positive. patients with anorexia nervosa can resume menses within 6 months of returning to 90% of their ideal bodyweight.Physical examination findings in patients with anorexia often include dry skin. Arthropathy... downy hair). and if not adequately neutralized by local bicarbonate production. H. and estrone. estradiol. restricted diet.astro_non_neo_smbowel. In its absence. FSH. and physical exam findings . The resulting very low pH gastric fluid enters the duodenum. polyarthritis.ctisus. causes duodenal ulceration. With successful treatment. -Anorexic females commonly have low levels of LH. as well as in any ectopic gastric tissue in the duodenum or esophagus. high gastrin levels cause increased local release of histamine which stimulates the gastric parietal cells to secrete increased levels of acid. and psychiatric and cardiac abnormalities may also be observed.html http://www. presenting as malabsorption with diarrhea and weight loss. Helicobacter pylori-associated antral gastritis -leads to a decrease in the number of somatostatin-producing antral cells. Antibiotic therapy is usually successful in quickly resolving the illness. http://www. As patients percentage of body fat decreases to abnormally low levels. and hypotension. the normal cyclic LH surge is lost and hypogonadotropic amenorrhea develops.H. -Clinically Whipple disease is most commonly seen in middle-aged Caucasian males. pylori is associated with gastric as well as duodenal ulceration.g. pylori infection. lanugo (fine.org/organsys/sma. which is why thin female athletes (e. but gastric ulceration does not require increased acid secretion to occur.

patients with AIN present with fever. the free cholesterol is converted into cholic and chenodeoxycholic acids (bile acids) through a series of chemical reactions. Plasma cells and eosinophils are also commonly seen. Therefore. Interstitial edema and infiltration with mononuclear cells (lymphocytes and macrophages) are typical. granuloma formation may be observed. When the gallbladder is hypomotile or there is more cholesterol than bile salts. and diuretics are also cited often. -Once in the liver. which may cause tubulorrhexis and spillage of tubular content into the interstitium. Sometimes. cholesterol quantities should be kept low and bile salt quantities kept high. Normal levels of gastric acidity are sufficient to cause gastric ulceration when the mucosal layer is degraded. If the latter occurs. and 2) hepatic synthesis. -Clinically. foreign-body granulomas may be formed in the interstitium. and oliguria one to three weeks after the initiation of treatment a b-lactam antibiotic is highly suggestive of drug-induced acute interstitial nephritis (AIN). rash. damage primarily involves the interstitium. rifampin. Many patients have increased levels of eosinophils and IgE in serum: also. NSAIDs. These bile acids are then conjugated to either glycine or taurine to create the bile salts that are secreted into bile canaliculi. maculopapular rash. and acute renal failure. Symptoms almost always resolve completely after cessation of the offending medication. As more water-insoluble cholesterol is secreted in bile. the inflammatory cells may infiltrate the tubular epithelium. -As the name of the condition implies. IgE-mediated hypersensitivity combined with cell-mediated reactions are thought to be involved in the pathogenesis of AIN. the cholesterol precipitates into insoluble crystals that eventually form to make gallstones. Peripheral eosinophilia and eosinophiluria (detected by Hansel or Wright stain) are the most important clues. sulfonamides. Acute interstitial nephritis -Fever. -Drug-induced hypersensitivity reactions are thought to be the cause of AIN. which is controlled by HMG-CoA reductase. -To reduce the likelihood of cholesterol precipitation (and gallstone formation). it is rendered soluble in small amounts by the detergent action of the amphipathic (both hydrophobic and hydrophilic) bile salts and the phospholipid phosphatidylcholine. Cholesterol precipitation -The two primary means by which we obtain cholesterol are: 1) dietary ingestion of animal fat. leaving the glomeruli intact. .gastric ulceration results from its destruction of the local mucous layer as well as from the local inflammatory response to these bacteria.

and is characterized by apical cavitary lesions and hemoptysis. . It is strongly associated with Campylobacter jejuni infection. -Guillain-Barre syndrome manifests with ascending muscle weakness that starts after recovery of respiratory or gastrointestinal infection. Involvement of the distal lower limb is characteristic.Eaton-Lambert syndrome clinically resembles myasthenia gravis. some infectious agents contain ganglioside-like substance in their lipopolysaccharide layer. Secondary (reactivation) tuberculosis -occurs in patients who have been previously infected with tuberculosis. spastic paresis. -It is hypothesized that in Guillain-Barre syndrome. immunization. Primary tuberculosis causes the formation of Ghon foci in the lower lung fields. associated with pain and paresthesia. Paralysis of respiratory muscles is fatal without supportive care. Muscle weakness is accompanied by the disappearance of deep tendon reflexes (areflexia). Unlike Guillain-Barre syndrome. Antibodies formed against this substance cross-react with the ganglioside components of myelin. Paralysis may ascend to the cranial nerves (especially CN VII ” Bell's" palsy).Beriberi (thiamine deficiency) can cause demyelination of peripheral nerves. Segmental demyelination and endoneural inflammatory infiltrate are seen on light microscopy of the peripheral nerves.Werdnig-Hoffman syndrome results from anterior horn cell damage. areflexia. DIFF: . It is caused by a frame shift mutation of the dystrophin gene. or allergic reaction. Loss of position and vibration sensation. no perineural inflammation is present. -Duchenne muscular dystrophy is an X-linked muscular dystrophy that affects male children. This deficiency leads to degeneration of dorsal columns and lateral cerebrospinal tracts. Its pathogenesis is explained by autoantibodies that react with presynaptic calcium channels and hamper the release of acetylcholine -Subacute. Symptoms include muscle weakness and areflexia. Reactivation tuberculosis occurs in immunosuppressed patients. Is nota neurologic disease.Guillain-Barre syndrome =acute demyelinating disease occurs after infection. pathology is at the level of the muscle. Lower motor neuron lesion signs are present: flaccid weakness. and ataxia are typical. combined myelopathy occurs due to vitamin B12 deficiency. . . It is a paraneoplastic syndrome associated with small cell carcinoma of the lung. and fasciculation ('floppy child' syndrome). muscle atrophy.

and are usually associated with urinary tract infections due to urease-forming organisms (such as Proteus). Glioblastoma multiforme (GBM) =the most common primary brain neoplasm in adults. These are the most common type of stone accounting for 70-80% of all cases of nephrolithiasis. or triple phosphate) calculi are radiopaque. high protein diets low fluid intake. When these stones assume the shape of the renal pelvis they are called staghorn calculi. 'pseudopalisading' tumor cells around areas of necrosis are diagnostic. Lesch-Nyhan syndrome). Struvite stones can grow to be quite large filling the renal pelvis. They form in alkaline environments (pH >7. -Cystine stones are relatively radiopaque because they are composed of sulfurcontaining compounds. They can be visualized instead by abdominal ultrasound or CT scan.Only uric acid stones are radiolucent (not seen on plain abdominal films).Urinary calculi . On light microscopy.4). Cystine stones are found in cystinuria. They are radiopaque. http://frontalcortex. An acidic pH is needed for the formation of these calculi. . -Magnesium ammonium phosphate (struvite. Uric acid stones occur in patients with gout myeloproliferative disorders.g.containing calculi.com/?page=oll&topic=24&qid=1113 . -Calcium oxalate and calcium phosphate stones are commonly grouped together as calcium. Calcium stones can form in acidic urine (pH = 6) or neutral urine (pH = 7). or certain inborn errors of metabolism (e. an autosomal recessive disorder characterized by a defect in the proximal tubule reabsorption of cystine.Areas of necrosis and hemorrhage are seen on gross examination.

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