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Diseases of endocrine glands

Pitutary gland
HYPOPITUITARISM
 PATHOGENESIS: Many, diverse causes
 SHEEHAN SYNDROME:
 Ischemic necrosis or infarct of pituitary gland, secondary to
hypotension occurring in the late stage of pregnancy or post-
partum in women.
 PATHOGENESIS: Common cause of Sheehan Syndrome is post-
partum hemorrhage.
 The enlargement of the pituitary during late-stage pregnancy
renders it susceptible to ischemia with any reduced blood flow.
 SYMPTOMS: Amenorrhea, hypothyroidism, possible adrenal
atrophy.
 EMPTY SELLA SYNDROME:
 Radiologic term for an enlarged sella turcica, with an atrophied or 1
 Secondary Empty Sella Syndrome: Secondary to surgical
removal of the pituitary.
 Primary Empty Sella Syndrome: Downward bulge of
arachnoid membrane into the sella, compressing the pituitary
onto the sella floor.
 Condition is often associated with Pituitary Adenomas.
However, you still see hypopituitarism.
 PITUITARY TUMORS:
 Pituitary tumors usually result in hypofunction of the other
parts of the pituitary, due to compression by the tumor.
 CRANIOPHARYNGIOMA: Tumor of Rathke's Pouch can
compress the pituitary and result in hypofunction and atrophy.
 PITUITARY ADENOMAS

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 CLINICAL:
 SYMPTOMS: Atrophy of thyroid, adrenal, or gonads, depending on
which hormones are deficient.
 Deficient growth in children.
 HYPERPITUITARISM
 In most cases, excess production of anterior pituitary hormones is
caused by the presence of an adenoma arising in the anterior lobe
 PITUITARY ADENOMAS
 LACTOTROPE ADENOMA:
 The most common pituitary adenoma.
 Hyperprolactinemia results in amenorrhea, galactorrhea, and infertility in
women.
 It results in impotence and decreased libido in men.
 SYMPTOMS:
 Women: amenorrhea, galactorrhea.
 Men: Impotence, testicular atrophy. 3
 Somatotrope adenoma:
 Gigantism:
 Hypersecretion of gh before the growth-plates have closed.
 Now it is rare, because gonadotrope adenomas are usually diagnosed and
removed in childhood.
 ACROMEGALY:
 hypersecretion of GH after the growthplates have closed.
 Symptoms:
 Overgrowth of mandible and maxilla, thickened nose, space between
incisor teeth, enlarged hands and feet, larger hat-size.
 Hyperglycemia and diabetes, one fifth of patients.
 Hypercalcuria and renal stones, one fifth of patients.
 Variety of cv, cerebrovascular, and neurological problems, including
htn, chf, paresthesias, arthralgias.

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 CORTICOTROPE ADENOMA:
 Has a higher chance of becoming malignant than the other adenomas.
 Associated syndromes
 Cushing's Disease
 is defined as hypercorticism caused by an overproduction of ACTH.
 This can be caused by
 Pituitary Corticotrope Adenoma, or
 Ectopic production of ACTH by another tumor,
 such as carcinoid tumor or small-cell carcinoma of the lung.
Diseases of thyroid gland
 Nontoxic (colloid) goiter:
 Euthyroid goiter, either diffuse or multinodular.
 Pathogenesis:
 a deficiency of thyroid production
 leads to increased secretion of tsh,
 which causes the thyroid to become goiterous. 5
 Deficiency of iodine, turnips,
 rutabaga, cabbage, rape seeds, rale can cause it
 subtypes:
 diffuse non-toxic goiter:
 early stages of disease,
 gland is diffusely enlarged.
 amount of colloid is decreased.
 multinodular non-toxic goiter:
 chronic disease.
 soft, glistening, reddish nodules containing large amounts of colloid.
 pathology:
 colloid cysts may be formed by the coalescence of multiple nodules of
excess colloid.
 clinical:
 related to anatomical enlargement of thyroid gland.
 dysphagia, inspiratory stridor, hoarseness of voice, venous congestion of head and6 neck.
 HYPOTHYROIDISM
 CRETINISM:
 Congenital hypothyroidism, leading to retardation and deficient growth.
 CLINICAL:
 Baby born with puffy eyelids, narrow palpebral fissures, protruded tongue.
 Infants are apathetic and sluggish, poor growth and failure to thrive.
 SUBTYPES:
 Sporadic Cretinism:
 Congenital malformation of thyroid.
 There is no goiter and the thyroid is small.
 Endemic Cretinism:
 Thyroid due to maternal dietary deficiency of iodine.
 The thyroid is goiterous at birth.
 MYXEDEMA:
 Adult hypothyroidism
 Symptoms: 7
 Cold Intolerance
 Skin:
 Non-pitting edema of extremities
 Puffy eyelids ,enlarged tongue
 Coarse, frowsy hair.
 Pale, cool skin, and scaly dermatitis.
 CV:
 Decreased cardiac output
 CNS:
 Lethargy, somnolence, memory loss, depression, cerebellar
ataxia, dulled reflexes.
 Deafness and/or night-blindness may be seen.
 GI:
 Constipation,
 fecal impaction
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 HYPERTHYROIDISM (THYROTOXICOSIS)
 Symptoms
 Palpitations, tachycardia, high cardiac output.
 Heat Intolerance
 Nervousness, fatigue, excessive perspiration, difficulty sleeping.
 Very fine-amplitude tremor of the hands.
 Thyroid Storm:
 Acute attack of severe hyperthyroidism.
 Hyperpyrexia, dehydration (due to hyperperistalsis), hypertension,
tachycardia, arrhythmias.
 Cuase
 Grave's disease
 Toxic multinodular goiter
 Toxic adenoma
 Hypersecretion of TSH
 Iodine-induced hyperthyroidism 9
 THYROID CARCINOMA
 Pathogenesis:
 Two things have been shown to generally cause thyroid cancer.
 Goiter: Thyroid carcinoma has higher incidence in regions of endemic
goiter.
 Radiation Treatment: Any radiation treatment of thyroid (such as
Hiroshima) has been shown to cause cancer.
 PAPILLARY CARCINOMA:
 CLINICAL:
 Occurs in younger population,
 slight predilection for females.
 Good prognosis -- even if there is metastases to regional nodes.
 Can present as cold nodule on a thyroid scintiscan.
 Typically metastasizes via lymphatics to regional nodes.
 PATHOLOGY:
 Papillae with central fibrovascular core. 10
 No capsule -- the capsule has been penetrated.
 Psammoma Bodies can be found.
 FOLLICULAR CARCINOMA:
 PATHOLOGY:
 Whitish, indistinct borders, and no capsule.
 Diagnosis of carcinoma is made (rather than adenoma) when the capsule is
penetrated.
 Two subtypes: Minimally Invasive and Widely Invasive Carcinomas.
 CLINICAL:
 Tends to metastasize hematogenously, to bones of shoulder, pelvis,
sternum, skull.
 Also has a good prognosis.
 MEDULLARY CARCINOMA:
 PATHOGENESIS:
 C-Cell Hyperplasia is the precursor lesion to medullary carcinoma.
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 PATHOLOGY:
 Tumor of Parafollicular or C-Cells.
 Firm thyroid nodule with cervical lymphadenopathy.
 Will see bands of epithelial cells, with histologically variably appearance:
trabecular, tubular, carcinoid-like, pseudo-papillary patterns.
 DIAGNOSIS:
 Familial form associated with Multiple Endocrine Neoplasia (MEN Type II)
 Calcitonin is markedly elevated, up to tenfold.
 Carcino-Embryonic Antigen (CEA) Positive: This tumor marker is useful
for diagnosis and tracking of the tumor.
 Chromogranin is another tumor marker that is sometimes monitored.
 SYMPTOMS:
 Related to endocrine secretion.
 Carcinoid Syndrome: Watery diarrhea, due to release of VIP, serotonin.
Cushing Syndrome
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 ANAPLASTIC CARCINOMA:
 Highly aggressive, rapidly fatal tumor.
 Can compress the trachea and cause suffocation.
 CLINICAL:
 Dysphagia, dyspnea, from physical compression.
 Also highly metastatic.
Diseases of adrenal gland
 ADRENAL INSUFFICIENCY
 Chronic adrenal insufficiency (addison disease):
 PATHOGENESIS:
 Most cases are idiopathic.
 Autoimmune Adrenalitis:
 75% of cases.
 Granulomatous, lymphocytic inflammation of adrenal glands, of auto-
immune origin.
 Genetic Predisposition: HLA-B8, HLA-DR3, HLA-DR4 13
 Other Causes: Metastatic carcinoma, amyloidosis, sarcoidosis, fungal
infections.
 PATHOLOGY:
 Atrophic, shrunken adrenal cortex, overlying a normal medulla.
 SYMPTOMS:
 Progressive weakness, cachexia
 Hyperpigmentation:
 Results from increased secretion melanocyte-stimulating hormone
(MSH)
 Hyponatremia, Hyperkalemia:
 result from deficient mineralocorticoids.
 Hypotension, Hypoglycemia.

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 CUSHING SYNDROME:
 Hypersecretion of Cortisol from any cause.
 PATHOGENESIS:
 CUSHING DISEASE:
 Hypersecretion of Cortisol resulting from hypersecretion of ACTH.
 With the exception of corticosteroid administration, Cushing Disease
accounts for the majority of cases of Cushing Syndrome.
 The excessive ACTH can result from several different places:
 Pituitary Hypersecretion of ACTH. This can result from a corticotrope
microadenoma, or diffuse corticotrope hyperplasia.
 Ectopic ACTH production from some other tumor.
 Small-Cell Carcinoma of Lung is responsible for majority.
 Carcinoids, neural-crest tumors, thymoma
 Ectopic CRH production from some other tumor.
 Medullary carcinoma of the thyroid, prostate adenocarcinoma, bronchial
carcinoid.
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 ADRENAL ADENOMA: Rare.
 PATHOLOGY:
 Thin rim of normal tissue surrounds the tumor.
 Lipofuscin is found in the tumor.
 The rest of the adrenal cortical tissue, and the contralateral gland, is usually
atrophic.
 ADRENAL CORTICAL CARCINOMA:
 Most adrenal carcinomas are functional tumors.
 SYMPTOMS: Grim prognosis, survival only 2-3 years, even with surgical
resection.
 The tumor is very difficult to resect completely, and it comes back.
 Non-functional carcinomas (minority) are especially malignant.
 CHRONIC CORTICOSTEROID ADMINISTRATION:
 By far the most common cause of Cushing Syndrome.

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 PATHOLOGY:
 Diffuse Adrenal Hyperplasia: 75% of cases
 Nodular Adrenal Hyperplasia: 25% of cases, grossly visible nodules.
 SYMPTOMS / CLINICAL
 OBESITY:
 Moon Facies: Fat accumulation in face, characteristic appearance.
 Flush Face: Hyperemia and excess accumulation of RBC's in the face give
it a flush appearance.
 Truncal Obesity: Obesity in the thorax and abdomen, with relatively thin
extremities.
 Buffalo Hump: Characteristic fat-collection over the skin covering thoracic
spinal column.
 SKIN / MUSCLE:
 Muscle Atrophy
 Thin Skin: Purple striae result from the stretching of thin skin.
 Acanthosis Nigricans: Darkening of skin around neck, as occurs with17
 METABOLIC:
 Cortisol Diabetes: Hyperglycemia and Glucose Intolerance.
 Hypokalemia and hypertension (due to Aldosterone-induced renal excretion
of potassium)
 BONE:
 Osteoporosis due to negative Ca+2 -balance.
 Back pain, and wasting of proximal muscles.
 Glucocorticoids inhibit Ca+2 absorption in gut ---> negative Ca+2 -Balance
---> PTH is stimulated to restore Ca+2 in the blood ---> Ca+2 is taken
from bone.
 Glucocorticoids inhibit the gonadotropins ---> inhibit estrogen ---> more
Ca+2 resorption.
 This effect also holds for men. Testosterone levels are down-regulated,
and Ca+2 resorption increases as a result.
Glucocorticoids inhibit collagen synthesis in osteoblasts.
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 BLOOD:
 Immune suppression, lymphopenia, eosinopenia.
 Hyperglobulia: Elevated RBC count.
 ENDOCRINE:
 Acne. Virilization,
 amenorrhea in females,
 impotence in males

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Diseases of pancrease
Diabetes Mellitus
 is a chronic disorder of carbohydrate, fat, and protein metabolism.
 Characteri zed by
 A relative or absolute deficiency in insulin secretory response
 impaired carbohydrate (glucose) use
 Hyperglycemia
 CLASSIFICATION
 primary
 the most common form
 arising from a defect in insulin production and/or action
 Secondary
 arising from any disease causing extensive destruction of pancreatic
islets
 such as pancreatitis, tumors, certain drugs surgical removal of
pancreatic substance, etc. 20
 The two major variants of diabetes are
 Type 1 diabetes,
 accounts for 5% to 10% of all cases of diabetes.
 there are two subgroups of type 1 diabetes.
 type 1A
 By far the most common form
 caused by autoimmune destruction of beta cells;
 type 1B
 is also associated with severe insulin deficiency,
 but there is no evidence of autoimmunity.
 type 2 diabetes
 Approximately accounts 80% of
 caused by Insulin resistance

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TYPE 1 VERSUS TYPE 2 DIABETES MELLITUS

  Type 1 Type 2

Clinical Children > adults Adults > children

  Normal weight Obese

  Decreased blood insulin Normal or increased blood insulin

  Anti-islet cell antibodies No anti-islet cell antibodies

  Ketoacidosis common Ketoacidosis rare

Genetics 40% concordance in twins 60% to 80% concordance in twins

  HLA-D linked No HLA association

Pathogenesis Autoimmunity, immunopathologic Insulin resistance


mechanisms

  Severe insulin deficiency Relative insulin deficiency

Islet Cells Insulitis early No insulitis

  Marked atrophy and fibrosis Focal atrophy and amyloid


deposits
  Severe beta-cell depletion Mild beta-cell depletion

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 Currently, the following criteria are used for the laboratory diagnosis DM
 Fasting (overnight) venous plasma glucose concentrations of 126 mg/dL or
greater on more than one occasion
 Clinical symptoms of diabetes and a random glucose level of 200 mg/dL or
greater
 After ingestion of 75 g of glucose, a 2-hour venous plasma glucose
concentration of 200 mg/dL or greater
 Complications:
 Acute attacks of hyper or hypoglycaemia and acidosis due to metabolic
derangements, may rarely cause coma or death.
 Chronic complications are mainly due to glyucosylation (combination of
glucose) of blood vessel wall proteins resulting in thickening of walls of small
blood vessels known as "Hyaline arterolosclerosis" leading to ischemic
damage to vital organs.
 Acute metabolic complications - Hypoglycemic coma, Ketoacidosis
 Chronic Vascular complications - Thickening of small blood vessels 23
Diseases of the kideny
POLYCYSTIC KIDNEY DISEASE (PKD):
 AUTOSOMAL DOMINANT PKD (ADPKD):
 A very common form of PKD that does not manifest until mid-adulthood.
 PATHOLOGY:
 Formation of very large, disparate cysts.
 Process can involve any part of the nephron.
 CLINICAL:
 Renal failure occurs late-onset (adult) when it occurs,
 t it only occurs in about 50% of cases.
 The kidneys can withstand an incredible number of cysts before
function is compromised.
 SYMPTOMS:
 Nocturia is a common early symptom, from Non-Oliguric failure.
 Pain, due to bleeding infection, or rapid cyst growth.
 PATHOGENESIS:
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 Autosomal dominant. Penetrance of the disease is 100%. If you have the gene, you're sick
 AUTOSOMAL RECESSIVE PKD (ARPKD):
 PATHOLOGY:
 The cysts uniformly arise in the collecting ducts, rather than the whole
nephron.
 As compared to ADPKD, the cysts are diffuse and evenly distributed.
 CLINICAL:
 Renal failure is virtually inevitable,
 usually occurring in childhood, but it can occur in adulthood.
 ACQUIRED PKD:
 PATHOGENESIS:
 Happens with renal failure patients on dialysis.
 The other kidney hypertrophies in response to unilateral kidney failure
---> healthy kidney hypertrophies ---> cysts form.
 COMPLICATIONS
 Renal Cell Carcinoma is the most common complication.
 Renal tumors do not occur in the other forms of PKD. 25
 RENAL FAILURE:
 GENERAL PROPERTIES:
 High serum creatinine:
 Creatinine >> 1.0, indicating no glomerular filtration.
 Azotemia: High BUN
 Uremia: High frank urea in the blood, which can lead to encephalopathy in
late stage.
 Anemia: Anemia can occur due to no secretion of erythropoietin in
damaged renal cells.
 EPIDEMIOLOGY:
 Statistically, the most important causes of renal failure:
 Autosomal Dominant PKD (high incidence)
 Diabetes: due to both glomerulosclerosis and pyelonephritis.
 Glomerulosclerosis is from Diabetic nephropathy
 Chronic pyelonephritis results from recurrent UTI's (due to sweet urine,
lost bladder motility) 26
 Analgesic Nepropathy (interstitial nephritis due to phenacetin analgesics);
very common.
 ACUTE RENAL FAILURE:
 Most often occurs due to trauma, shock, or acute ischemia.
 CHRONIC RENAL FAILURE:
 End-stage renal disease
 NEPHROTIC SYNDROMES:
 Non-inflammatory nephropathies.
 NEPHROSIS: Clinically characterized by
 proteinuria, loss of protein in the urine, usually due to loss of negative
charge, or holes, in the glomerular basement membrane.
 Complications:
 Hypoalbuminemia
 Edema, resulting from hypoalbuminemia
 Hyperlipidemia, resulting from compensatory synthesis of lipoproteins in liver.
 No hypertension. 27
 MINIMAL CHANGE DISEASE (Epithelial Cell Disease):
 Loss of negative charge on glomerular basement membrane, leading to
idiopathic proteinuria.
 PATHOGENESIS:
 Loss of negative charge on glomerular basement membrane
 leads to loss of epithelial foot-processes,
 which is only visible at the EM microscopic level.
 PATHOLOGY:
 The glomerulus appears histologically normal,
 but GBM appears flattened on EM.
 Size normally is not a barrier to the passage of albumin through the GBM.
 Normally negative charge is the only barrier.
 CLINICAL:
 The condition is not diagnosed until severe proteinuria (edema) occurs.
 TREATMENT:
 Treatment with corticosteroids is always quite successful 28
 FOCAL SEGMENTAL GLOMERULOSCLEROSIS:
 An extension of Minimal Change Disease, with same basic pathology.
 PATHOGENESIS:
 Usually idiopathic, simply an extension of Minimal Change Disease with a
worse prognosis.
 But, it can be caused by HIV or heroin.
 PATHOLOGY:
 In addition to loss of negative charge and flattening of epithelial foot-
processes, we have:
 Glomerular Sclerosis: Some Glomeruli are fibrotic, sclerosed, or totally
obliterated. But, the damage is sparse:
 "FOCAL": Only some nephrons are affected, whereas others are spared.
 "SEGMENTAL": Only part of the glomerulus is affected. Half of the
glomerulus may appear normal.
 Hyalinosis: PAS-Positive material will appear in the affected glomeruli
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 DIABETIC GLOMERULOSCLEROSIS (Kimmelstiel-Wilson Disease):
 Negative charge on GBM can be lost in Diabetes, too.
 PATHOGENESIS:
 Proteinuria: Glycosylation of GBM proteins causes loss of charge on
GBM ---> proteinuria.
 Progressive Renal Failure (lost filtration):
 Mesangial Matrix (kidney macrophages) builds up, and mesangial cells do
not turnover.
 Microangiopathy: Capillary lumen become compromised as a result of
mesangial cell buildup
 Hyaline Arteriosclerosis: Uniquely, both the afferent and efferent
arterioles can become atherosclerotic in Diabetes.
 PATHOLOGY:
 Thickened basement membrane.
 CLINICAL:
 Proteinuria occurs before renal failure. Hematuria is rarely or never seen.
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 NEPHRITIC SYNDROMES:
 NEPHRITIS:
 Inflammatory disease of the glomerulus.
 General symptoms:
 Hematuria
 Oliguria. Inflammation and edema lead to impaired filtration.
 Proteinuria
 Hypertension results from impaired filtration.
 DIFFUSE GLOMERULONEPHRITIS:
 Glomerulonephritis caused by general immune-mediated mechanisms (cell-
mediated immunity and inflammation).
 ACUTE (POST-INFECTIOUS) GLOMERULONEPHRITIS:
 PATHOGENESIS:
 The glomerulonephritis is not caused by immune complexes
themselves, although immune complexes are present.
 The disease-process is cell-mediated, caused by inflammatory cells.
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 Streptococcus Pyogenes is the classical organism that results in
post-infectious glomerulonephritis.
 Hepatitis-C (HCV) can also cause it.
 PATHOLOGY:
 Sub-epithelial, sub-endothelial, and mesangial deposits of immune
complexes.
 Inflammatory cells found within the glomeruli will release hydrolytic
enzymes leading to rupture of capillaries and hematuria.
 Variable deposition of immune complexes in GBM
 CLINICAL:
 Hematuria is presenting symptom, along with flank pain.
 DIAGNOSIS:
 Glomerulonephritis can be distinguished by other hematuria-presenting
disease (prostatitis, cystitis, UTI), by the presence of red-cell casts in
the urine.
 By definition, the acute disease regresses by itself, leaving no permanent damage
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 PYELONEPHRITIS:
 PATHOGENESIS:
 Several factors predispose to an ascending infection of urinary tract.
 Increased Residual Urine:
 BPH, urinary obstruction, lost urinary motility due to Diabetes,
 all make it so that the bladder doesn't completely empty on micturition.
 The remaining urine collect bacteria and can seed infection.
 Bladder Reflux:
 Abnormally short, perpendicular entrance of the ureter into the bladder
wall.
 NORMAL: Ureter enters at an elongated, oblique angle.
 Pressure of micturition closes off the ureteral entrance, preventing
backflow of urine.
 SHORT INTRAVESICAL URETER: Ureter entrance is perpendicular.

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 Interstitial Infection:
 Bacteria tend to infect the upper and lower poles of the kidney,
 because that is where the renal papillae are compound, flattened, and
therefore receptive to infection by bacteria.
 Renal Papillae in the center of the kidney tend to resist infection, due to
shape of papillae.
 PATHOLOGY:
 Acute, pyogenic (PMN) inflammation of renal pelvis and tubules.
 CLINICAL: SYMPTOMS
 Polyuria, due to inability to concentrate urine.
 Flank pain, costovertebral angle tenderness
 Hematuria
 Leukocyte Casts in urine indicates that the infection has ascended to the
tubules, rather than just remaining in the lower urinary tract.
 CHRONIC PYELONEPHRITIS:
 Longstanding pyelonephritis leads to end-stage kidney, a shrunken, fibrotic kidney that cannot
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maintain renal function.
 ACUTE TUBULAR NECROSIS (ATN):
 Acute damage to the tubules, from drugs (hypersensitivity), chemical toxicity, or
ischemia.
 PATHOGENESIS:
 ATN is not an inflammatory process, but is rather due to ischemia.
 Prerenal: Fall in renal blood flow, from hypotension or shock.
 Intrarenal: Toxic injury to any part of the kidney nephrons, from glomerulus
to collecting ducts.
 Postrenal: Due to urinary obstruction. To cause ATN, it must be a complete
obstruction, i.e. involving both ureters or common urinary outflow.
 ISCHEMIC ATN: Coagulation necrosis of renal tubules due to impaired blood
flow or impaired filtration.
 TOXIC ATN:
 Cisplatin = Chemotherapeutic drug is directly nephrotoxic.
 Heavy metals, such as Mercury or Lead
 Organic solvents 35
 UROLITHIASIS (RENAL STONES):
 PATHOGENESIS:
 More common in men than in women.
 Multiple causes:
 Calcium Stones:
 most common.
 Can occur from hypercalcemia which leads to hypercalcuria.
 There is also idiopathic hypercalcuria in which high urine calcium
occurs without hypercalcemia.
 Magnesium-Ammonium Phosphate:
 Can result from infection with urease(+) bacteria ------> alkaline urine
------> renal stones.
 Urate Stones:
 Hyperuricemia ------> renal stones. Occur in 25% of patients with Gout.
 CLINICAL:
 Stones may be asymptomatic, or can lead to severe hydronephrosis and
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 Renal Colic:
 Colicky (waxing and waning), excruciating flank pain of renal stones.
 HYDRONEPHROSIS
 is the result of renal stones.
 Dilation of renal pelvis and calyces, and flattening of renal papillae.
 RENAL CELL CARCINOMA:
 Malignant tumor of renal tubular epithelial cells.
 RISK FACTORS
 Cigarette smoking
 Obesity, particularly in women.
 PATHOLOGY:
 Uniform renal cells displaying clear cytoplasm.
 Yellow fleshy tumor.
 CLINICAL:
 Metastases is common.
 Tumor cells may become secretory. 37
 SYMPTOMS:
 Hematuria, flank pain, palpable mass
 Excessive erythropoietin ------> Polycythemia
 Paraneoplastic Syndromes are common
Diseases of the lower urinary tract
OBSTRUCTION:
 Urinary obstruction can occur at the level of
 renal pelvis,
 ureter,
 ureterovesical junction,
 urinary bladder or the urethra.
 Such an obstruction may cause
 hydronephrosis,
 hydroureter and
 predispose to urinary infections.
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 PATHOGENESIS:
 Obstructions can be congenital, due to developmental anomalies or
acquired;
 bilateral or unilateral.
 EXTRINSIC: The ureter is compressed from outside
 Pelvic tumors
 Pregnancy
 Retroperitoneal fibrosis
 BPH: common.
 INTRINSIC:
 Ureteric tumors
 Urinary stones: common
 Blood clots
 Urethral strictures secondary to urethritis.

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 CYSTITIS:
 Occurs in women because of short urethra.
 PATHOGENESIS: Various causes
 Urinary stones denude epithelium and expose the basement membrane,
allowing bacteria to attach and predisposing to cystitis.
 Bladder outlet obstruction, as in BPH.
 Chemotherapy
 Indwelling catheters
 Gram-negatives: E. Coli, Proteus, Pseudomonas, Klebsiella
 Gram-positives: Staph Saprophyticus, Enterococci
 URETHRITIS:
 ACUTE URETHRITIS:
 Dysuria with urethral discharge.
 PATHOGENESIS:
 Sexually transmitted, in males.
 Neisseria gonorrhoeae = yellow discharge 40
 Chlamydia Trachomatis, Ureaplasma urealyticum = white
discharge.
 EPIDEMIOLOGY:
 Transmission risk of 17-20% for the male, with unprotected sex.

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