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UWORLD Notes by Systems (Usmle Grassroots) PDF
UWORLD Notes by Systems (Usmle Grassroots) PDF
Check Table
Adminstration of Metyrapone will cause a decrease in cortisol
synthesis via inhibition of 11-beta-hydroxylase. In pts with an intact
Endocrine, Diabetes &
608 Pathophysiology hypothalamic pituitary axis, this will cause a reactive increase in
Metabolism
ACTH, 11-Deoxycortisol, and "urinary 17-hydroxycorticosteroid
levels"
Endocrine, Diabetes & 11-hydroxylase deficiency in congenitl adrenal hyperplasia causes
611 Pathophysiology
Metabolism high PB and Hirstutism (Big clit)
Pt with signs of Hyperthryroidism with eye involvement (bilateral
redness,proptosis(exopthalmos))wasgivenmedicationthat
Endocrine, Diabetes &
622 Pharmacology reduced her proptosis. The drug did that by affecting
Metabolism
*Inflammatory infiltration*
[Glucorticoids to treat exopthalmos in Grave disease pts]
Peritibial myxedema and exopthalmos are specific features of
Endocrine, Diabetes &
623 Pathophysiology hyperthyroidsim due to Grave's disease. Peritibial myxedema is
Metabolism
*Lower Leg Skin thickening and induration*
Endocrine, Diabetes & *TSH levels* should be monitored in pts receiving Amiodorone
625 Pharmacology
Metabolism therapy!
Endocrine, Diabetes & Methimazole inhibits *Coupling of iodotyrosines* in the thyroid
626 Pharmacology
Metabolism gland.
Endocrine, Diabetes & Oral conraceptives decrease hirsutism by suppressing LH
656 Pathophysiology
Metabolism secretion and thereby *Decreasing ovarian androgen production*
Pt with difficulty urinating and dribbling affecting quality of life
probably has BPH, treatment with Finasteride can cause releif but
Endocrine, Diabetes &
658 Pharmacology also cause increase hair growth over scalp. That's becuse
Metabolism
Finasteride is a *5-alpha-reductase inhibitor*. This is the enzyme
that converts testestrone into its active metaboloite DHT.
Pt with fatigue, bradycardia, weight gain, constipation, and
Endocrine, Diabetes &
764 Pathophysiology delayed relaxation of deep tendon reflexes has Hypothyroidism,
Metabolism
the most sensitive marker for Dx is *Serum TSH*
Signs of fatigue, weight gain and lumps rising from surface of
Endocrine, Diabetes & skeletal muscle following percussion with reflex hammer
765 Pathophysiology
Metabolism (MYOEDEMA) combined with Elevated CK level indicate
HYPOTHYROID MYOPATHY and *TSH levels* should be checked.
Pt being scheduled to be treated for hyperthryoidism usning
Endocrine, Diabetes & radioactive iodine therapy. Pretreatment with *Potassium
766 Pathophysiology
Metabolism perchlorate* would decrease the effects of radiotherapy thru
competitive inhibition of iodine transport.
Pt with signs hyperthyroid symptoms together with painful thyroid
enlargememt. Thyroid scan reveals decrease in radioactive iodine
Endocrine, Diabetes & uptake. ESR is elevated. Biopsy of thyroid will most likely reveal
768 Pathology
Metabolism *Mixed, cellular infiltration with occasional multinucelated giant
cells*
[Sabacutegranulomatousthyroiditis]
Thyroid peroxidase enzyme is involved in *Thyroglobin Iodination*
Endocrine, Diabetes &
770 Physiology also in oxidation of iodide, and coupling of 2 iodized tyrosine
Metabolism
residues.
An increase in estrogen activity leads to an increase in levels of
Endocrine, Diabetes &
772 Pathophysiology thyroxine-binding globulin. This leads to an *Increased Total T4
Metabolism
pool*
tan-Fat containing tissue found around the kidneys and adrenals of
Endocrine, Diabetes &
821 Physiology a newborn is Brown Fat that helps to prevent *Hypothermia* by
Metabolism
producig heat.
Cells that express more glucose transporters as insulin levels
increase are *skeletal muscle cells* and adipocytes.
Endocrine, Diabetes &
847 Biochemistry Cell that have constant glucose transporter expression even as
Metabolism
insulin level increases are *Renal tunular cells* also brain,
intestine, RBC, and Liver
Endocrine, Diabetes & Pt with Type 2 Diabetes. Most likely assoc with his condition is
848 Pathology
Metabolism *Pancreatic islet amyloid deposition*
A drug that activates peroxisome-proliferator activated receptor-y
Endocrine, Diabetes &
920 Pharmacology (a nuclear receptor and transcription factor) (such drugs are the
Metabolism
-glitazones) results in *Decreased Insulin Resistance*
Endocrine, Diabetes & To diagnose Type diabetes melitus use *Fasting blood glucose
921 Pathophysiology
Metabolism level*, random glucose, or HbA1c.
A fetus born to a mother who had gestational diabetes would have
hypoglycemia due to *Beta cell hyperplasia*
Endocrine, Diabetes &
922 Pathophysiology [Pancreas is used to a lot of glucose from mother. After delivery,
Metabolism
glucose suddenly stops but beta cells are still high in number and
secreting insulin, resulting in hypoglycemia]
Endocrine, Diabetes & Amenorhea in pt involved in strenous excersie and low body wieght
925 Pathophysiology
Metabolism is caused by *HYpothalamic Suppression*
Pt with history of SLE dies at home. At her last P.E, her BP was
150/90. Clinical records show progressive truncal obesity, facial
plethora, and proximal muscle weakness. Lab showed mild
Endocrine, Diabetes &
928 Pathophysiology hyperglycemia. Evaluation of her adrenal galnds will most likely
Metabolism
show *Bilateral cortical atrophy*
[Iatrogenic cushing syndrome due to prolonged glucucorticoid
use, leads to supression of of hypothalamic oituitary axis]
Pt with HTN at young age together with weakness and paresthesias
(electrolye or acid-base disturbance) and low Renin levels is
Endocrine, Diabetes &
929 Pathophysiology consisent with Primary Hyperaldostronism. His Serum level of *Na
Metabolism
is normal, K is low, HCO3 is High*
(Na is normal due to aldostrone escape)
An infant boy with recurrent vomitting (salt wasting) and poor
feeding and P.E shows dehydration (salt wasting) and hypotension
with labs showing low sodium (wasting) and hyperkalemia. Pt
Endocrine, Diabetes &
930 Pathophysiology probably has Congenital Adrenal Hyperplasia - 21-hyrdoxylase
Metabolism
deficiency. There would be low cortisol, low aldo, high ACTH, and
*High 17-hydroxyprogestrone* which is a precuror to cortisol
synthesis.
Symptoms of Headache, tachycardia, diaphoresis and severe
Endocrine, Diabetes & HTN. THese resolve before Tx is given. Same thing happened a
933 Pathophysiology
Metabolism month ago. This is pheochromocytoma and there is *Elevated
catecholamine release*
Endocrine, Diabetes & Sorbitol produced by aldolase reductase is normally metabolized to
934 Biochemistry
Metabolism *Fructose*
Pt with celiac disease will also develop vit D deficiency due to
defective mucosal absorption, presenting as bone pain and
Endocrine, Diabetes &
981 Pathophysiology weakness (Adult). Lab test would reveal *low Ca, Low PO4-, High
Metabolism
PTH*
[No vit D decreases absorption of Ca AND PO4- from GI tract]
Endocrine, Diabetes & In DKA there is *Increased (or normal) extracell K & Decreased
985 Pathophysiology
Metabolism Intracell K**
Pt with elevated serum gastrin levels. Multi organ disease is
Endocrine, Diabetes & suspected. Pt should be asked for a history of *MEN type 1*
986 Pathology
Metabolism (MEN Type 1 has primary hyperparathyroidism, pituitary tumors,
and pacnreatic tumors (esp "Gastrinomas"))
Aching bones and insdeous pain in back, pelvis and lower
extremities, combined with reduced sunlight exposure suggests Vit
D deficiency. UV light from the sun converts
*7-dehydrocholesterol* into *Cholecalciferol (Vit D3)*. Vit D3 is
Endocrine, Diabetes &
990 Physiology then converted into 25-hydroxycholecalciferol by 25-hydroxylase.
Metabolism
25-hydroxycholecalcifrol is then converted to
1,25-dihydroxycholecalciferol (active vitD) by 1-alpha-hydroxylase.
This is the enzyme in the kidney acted on by PTH (+) and Ca2+
(-).
Pt with mild hypercalcemia, borderline high PTH levels and urinary
Endocrine, Diabetes &
992 Physiology Ca that is very low and normal 25-hydroxyvit D pobably has a
Metabolism
mutation in *Membrane-bound receptor coupled with a G-protein*
Oxaloacetate-----> Phosphoenolpyruvate (catalyzed byPEP
Endocrine, Diabetes &
997 Biochemistry carboxykinase) is the 2nd commited step in gluconeogenesis
Metabolism
which predominates in starvation states.
Pts with pyruvate dehydrogenase deficiency should be on a
Endocrine, Diabetes &
998 Biochemistry ketogenic diet. Soley Ketogenic aminoacids include *lysine* and
Metabolism
leucine.
Insuline resistance by the pancreatic cells i sstimulated by
increased ATP production. *Glucokinase* functions as a glucose
Endocrine, Diabetes &
1010 Biochemistry sensor in pancreatic beta cells by controlling the rate of glucose
Metabolism
entry into the glycolytic pathway. Mutations in the *glucokinase*
gene are a cause of maturity-onset diabetes of the young.
Pt has absent lactate dehydrogenase activity in muscles. In this pt,
Endocrine, Diabetes &
1019 Biochemistry strenuous exercise leads to inhibition of glycolysis in skeletal
Metabolism
muscles due to intracellular depletion of *NAD+*
Homeless pt with signs of wernicke encephalopathy after admin of
glucose without thiamine supplemenation would have an impaired
Endocrine, Diabetes &
1021 Biochemistry *Alpha ketoglutarate to Succinly CoA reaction*
Metabolism
[Thiamine is needed for alpha ketogluyerate dehydrogenase][Also
needed for other dehydrogenases and transketolase]
Endocrine, Diabetes & A direct source of energy in the TCA cycle is in the conversion of
1022 Biochemistry
Metabolism succinylcoA into Succinate thus yeilding GTP.
Increasing fructose-2,6-bisphosphate promotes glycoloysis (insulin
Endocrine, Diabetes & like effect) and inhibits Gluconeogensis. Inhibiting
1031 Biochemistry
Metabolism Gluconeogenesis means less alanine and other glucuneogenic
substrates are converted to glucos.
During fasting, maintenance of pt blood glucise is facilitated by
hepatic conversion of pyruvate into glucose. The substance that is
Endocrine, Diabetes &
1034 Biochemistry an allosteric activator of the first step of this process is
Metabolism
*Acetyl-CoA*
[Gluconeogenesis]
Pt presents with myalgias, anorexia, and skin rash. He has been
consuming raw white eggs for several months. P.E shows macular
Endocrine, Diabetes & dermatitis of extremities. A water soluble vit def is suspected. The
1063 Biochemistry
Metabolism biochemical conversions that most likely uses the def vit as a
cofactor are *Pyruvate to Oxaloacetate*
[Vit B7 (Biotin) needed as a cofactor for Carboxylases]
Pt presents with progressve lethargy. For past 3 weeks she had
loss of appetite, constipation, muscle weakness, polyuria and
Endocrine, Diabetes & polydipsia. She has been taking large doses of vitamins. Exam
1065 Physiology
Metabolism shows she is stuporous and has dry mucus membranes. The
metabolic abnormality in this pt can also be found in *Sarcoidosis*
[Hypercalcemia]
Pt with hereditary defect in fructose metabolism. He is
Endocrine, Diabetes & asymtomatic however. This pt is still able to metabolize fructose
1070 Biochemistry
Metabolism due to compensatory activity of *Hexokinase*
[Essential fructose uea]
Endocrine, Diabetes &
1073 Biochemistry In Aldolase deficiency, remove *Sucrose* from Diet.
Metabolism
Reactions of the pentos phosphate pathway (HMP shunt) occur in
Endocrine, Diabetes &
1119 Biochemistry the cytoplasm. Therefore this includes activity of enzyme
Metabolism
*Transketolase*
Insulin increases intracellular glycogen stores and decreases
Endocrine, Diabetes &
1121 Biochemistry hepatic glucose release into blood (gluconeogenesis), it does so
Metabolism
by activating *Protein Phosphatase-1*
Endocrine, Diabetes & Upregulation of *Serine Phosphorylation* decreases
1326 Pathophysiology
Metabolism insulin-mediated glucose uptake.
Insulin Resistance correlates strongly with Ecxess Visceral Fat
Endocrine, Diabetes &
1327 Pathophysiology which can be assessed using *Wasit Circumference* or waist-to
Metabolism
hip-ratio.
*Orinithine Transcarbamoylase* deficiency is the mcc urea cycle
disorder. The high NH3 causes neurologic abnormalities. Typical
Endocrine, Diabetes &
1370 Biochemistry tell tale sign is high urine OROTIC ACID. becasue with no OTC,
Metabolism
carbamoyl phosphate is converted to orotic acid in pyrmidine
synthesis.
Pt with Phenylalanemia who is place on dietary requirements and
supplemented with tyrosine and presents with normal
Endocrine, Diabetes & phenylalanine levels but with axial hypotonia and microcephaly.
1501 Biochemistry
Metabolism Also, prolactin is elevated. The enzyme missing in this pt
*Dihydrobiopterin reductase*
(Involved in converting tyrosine to DOPA, hence high prolacin)
Endocrine, Diabetes & High T3 would have negative feedback effects reducing TSH, T4
1615 Physiology
Metabolism and rT3.
Pt with type 2 diabetes. Tx that would increase serum C-peptide
Endocrine, Diabetes & level include *Glyburide*
1655 Pharmacology
Metabolism {Sulfonylureases like glyburide and Meglitinide increase
endogenous insulin producttion and henc c-peptide]
Medullary thyroid carcinoma would show *Nests of polygonal cells
Endocrine, Diabetes &
1659 Pathology with Congo-ed positive deposits*
Metabolism
[Amyloid stains with Congo red]
Endocrine, Diabetes & In Medullary Thyroid Cancer, the gene changes responsible is
1660 Pathology
Metabolism *Activating mutation of RET proto-oncogene*
Pt with redistribution of fat from the extremities to the trunk. This is
Endocrine, Diabetes &
1673 Pharmacology a common adverse effect of *highly-active antiretroviral therapy
Metabolism
(HAART)*
A nerby nerve injury while ligating an artery entering the superior
Endocrine, Diabetes & pole of the thyroid lobe(superior thyroid artery) would most likely
1747 Anatomy
Metabolism deninnervate the *Cricothyroid Muscle* which is innevated by the
external branch of the superior laryngeal neerve.
Endocrine, Diabetes & Proinsuline is cleaved by beta peptidases into Insulin and
1768 Physiology
Metabolism C-peptide, both of which are then *Packed in Secretory Granules*
Pt with history of thyroidectomy (Medullary thyroid Cancer), flesh
Endocrine, Diabetes &
1844 Pathology color nodule on lips and tongue (Mucosal Neuromas), & Marfinoid
Metabolism
Habitus (tall, long fingers etc) probably has *MEN 2B*
Endocrine, Diabetes & In a non medical setting, severe hypoglycemia is treated wih *IM
1984 Pharmacology
Metabolism Glucagon*
An autosomal recessive diroder of Sphingomyelinase deficiency.
Most consistent with this condition is *Neurodegenration and
Endocrine, Diabetes &
1990 Biochemistry Hepatosplenomegaly*
Metabolism
[Neiman-Pick disease. aslo foamy macrophages and cherry-red
macular spot]
Pt with orotic acid urea and normal ammonia levels could have a
Endocrine, Diabetes &
2066 Biochemistry defect of UMP synthase (hereditary orotic aciduria)
Metabolism
Supplementation with *URIDINE* helps this pt.
The adrenam medulla is demaracted from the cortex and is
Endocrine, Diabetes &
8424 Histology composed of Chromaffin cells with a deeply basophilic (blue)
Metabolism
cytoplasm. The medulla is stimulated by Acetycholine.
A diabetic drug that can cause hypoglycemia is *Glyburide*
Endocrine, Diabetes & [Sulfonlureas increase insulin secretion from pancrease. Glipizide
11565 Pharmacology
Metabolism is also a sulfonylurea but it is short acting (unlike Glyburide) and
hence its risk of hypoglycemia is reduced]
Endocrine, Diabetes & An anti-hyperlipidemia drugs that inhibits cholestrol absorption at
11634 Pharmacology
Metabolism the brush border of the small intestine is *Ezetimibe*
Postoperative HypoParaThyroidism is common after
Endocrine, Diabetes & thyroidectomy. Symptoms include Tingling, Numbness, Muscle
11660 Physiology
Metabolism Spasms, Seizure, Trousseau and Chvostek signs ( twitching of
lower face muscle on percusiion below zygomatic arch)
*Hormone Sensitive Lipase* is found in adipose tissue, it catalyzes
the mobilization of stored triglycerides into free fatty acids and
Endocrine, Diabetes &
11917 Biochemistry glycerol. The liver can further oxidize FFA to acetyl-coA and then
Metabolism
further metabolized into Ketoen Bodies.
This can be seen during Starvation.
In an animal that well fed with CHD's. beta-oxidation of fatty acids
Endocrine, Diabetes &
11918 Biochemistry is inhibited via *Malonyl-coA* which inhibits carnitine
Metabolism
acyltransferase from shuttling acyl groups into the mitochondria.
Zinc finger mtoif are composed of chains of aminoacids bound
together around a zinc atom via linkage with cystein and histidine
Endocrine, Diabetes &
11950 Biochemistry residues. Intracellular receptors that bind steroids, *Thyroid
Metabolism
Hormones*, and fat-soluble vitamins act directly as transcription
factors and conatin zinc biding domains.
Tumor of cells heavely loaded with mucus that has metastasized to
FemaleReproductive the ovaries suggests adenocarcinoma of the *Stomach* Classicly
127 Histology
System & Breast they are mucin-producing signet-ring neoplastic cells in ovarian
stroma. (Krukenberg tumor)
FemaleReproductive Pulsatile (every 90 mins 4e.g) adminstration of GnRh is indicated
208 Physiology
System & Breast in Infertility (e.g Anovulation)
FemaleReproductive Pt with signs of Turner Syndrome is likey to have *Bicuspid Aortic
256 Genetics
System & Breast Valve*
FemaleReproductive Progestron withdrawal leads to menses (i.e bleeding) which is a
299 Physiology
System & Breast result of *Apoptosis*
Woman comes for infertility evaluation. She complains of
dyspareunia. Menstrual cycles are accompanied by moderate to
sevee lower abdominal pain. Pelvic exam shows a normal-sized,
retroverted uterus. The post vaginal fornix is very tender to
FemaleReproductive
333 Pathology palpitation. Pt's condition most likely involves *Ectopic Endometrial
System & Breast
Tissue*
[Endometriosis][Adhesions interfere with
ovulation=infetolity][imaplantsandadhesionsinvolvinguterosacral
ligament result in retroverted uterus, ligament]
Cervical Intraepithelial neoplasia can be caused by HPV infection
FemaleReproductive
869 Pathophysiology which can result from sexual infection due to *Lack of barrier
System & Breast
contraception*.
Pt presents to fertility clinic. Attempting to concieve for past year,
no success. She used OCP for 15 years. 7 years ago she got
ceftriaxone for fever, abdominal pain, and vaginal discharge. Major
FemaleReproductive contributing factor to her inability to conceive is *Insufficient
1027 Microbiology
System & Breast antibiotic use*
[PID was treated only for gonorhea, azithro was not used for
coverage of chlamidya, this led to subclinical continous infection
that led to scaring of fallopian tubes and subsequent infertility]
Asymptomatic pt's mamogram reveals microcalcifications. Biopsy
FemaleReproductive shows ducts distended by pleomorphic cells with prominent central
1057 Pathology
System & Breast necrosis. Origin of this lesion is the *Breast Duct*
[Ductal Ca in Situ]
Symptoms of primary herpes infections include inguinal
lymphadenopathy, tender vesicular lesions covering both labia
FemaleReproductive
1549 Pathophysiology majora and pernium with dysuria and itching. The infection
System & Breast
(probably hsv-2) can lead to *Recurrent Genital Ulcers* (less
sever) (HSV lies dormant in sacral dorsal root ganglia)
LH stimulates the theca interna cells of the ovarian follicle to
produce androgens. Aromatase within the follicle's *Granulosa*
FemaleReproductive
1560 Physiology cells subsequently converts these androgens to estradiol under
System & Breast
FSH stumulation. The theca externa cells serve as connective
tissue support structure for the follicle.
*The suspensory ligament of ovary* must be ligated during removal
of ovaries to prevent bleeding. It carries the ovarian artery. It also
FemaleReproductive
1632 Anatomy known as the infundibulopelvic ligament. Note that the Cardinal
System & Breast
Ligament (transverse cervical ligament) holds the uterine artery
and needs to be ligated in a hysterectomy.
A *pudendal nerve* block is performed by injecting an anesthetic
FemaleReproductive
1739 Anatomy intravaginally, medial to the ischial spine, through the sacrospinous
System & Breast
ligament. This provides anesthesia to most of the perineum.
*Vaginal Agenesis* is characterized by short vagina and
rudimentary uterus and Amenorrhea with normal 2ndry sex
FemaleReproductive
1809 Embryology characteristics and normal wieght and stature. It is a.k.a Mullerian
System & Breast
Aplasia or MRKH syndrome. It often presents with urologic issues
as as unilateral renal agensis.
Pt's P.E reveals a large adnexal mass. Ultrasonography reveals a
FemaleReproductive
1928 Pathology large ovarian cyst. She has signs of virlization togther with
System & Breast
clitoromegaly. Most likely Dx is *Sertoli-Leydig tumor*
Pt with gray white fishy vaginal discharge with no inflammation that
FemaleReproductive
1929 Microbiology shows clue cells is characteristic of bacteril vaginosis caused by
System & Breast
Gardnerella vaginitis which an *Anaerobic gram variable organism*
Pt with abdominal pain, bloody vaginal discharge, orthostatic HTN
and a positive preganancy test. Prior infection with
FemaleReproductive *N.Gonorrhoeae* is likely responsible for her current condition.
1932 Microbiology
System & Breast [Pt has a ruptured ectopic preganncy. Primary resik factor for
Ectopic preg is tubal scaring and prior infection with Chlamidya
and N. gonorrhea are major predisposing factors.]
Pt with heavy and painful menstrual bleeding with uniformly
FemaleReproductive
1957 Histology enlarged uterus has Adenomyosis, which is *Endometrial tissue in
System & Breast
theMyometrium*
Pt with HIV whose PAP semar shows high grae cervical dysplasia.
FemaleReproductive The strongest risk factor for cervical dysplasia in this pt is
1992 Pathology
System & Breast *Immunosupression*
[Risk factors for cervical cancer]
FemaleReproductive The female reproductive structure that contains simple cuboidal
2056 Pathology
System & Breast epithelial cells is *Ovary*
Pt with menstrual irregularities, who is obese and has acne and
FemaleReproductive
2094 Pathophysiology hirsutism probably has Polycystic Ovarian Syndrome, and
System & Breast
therefore has *Enlarged Ovaries*
FemaleReproductive Pts with PCOD who desire fertility are treated with Clomiphene,
2095 Pathophysiology
System & Breast *An estrogen receptor Modulator*
16 year old female with pelvic pain every 28 days and resolves in a
FemaleReproductive day or two with fully developed 2ndry sexual characteristic. She
8390 Anatomy
System & Breast has a palpable mass anterior to the rectum. Serum Beta-hCG is
negative. Most likely Dx is *Imperforate hymen*
FemaleReproductive Turner syndrome pt can become pregnant but with oocyte
8556 Genetics
System & Breast donation.
Pt with right sided back pain and voiding is normal after a
FemaleReproductive
11781 Anatomy hysterectomy probably has an injured *Ureter* during the surgery.
System & Breast
Voiding is normal becuase other ureter is functionl.
FemaleReproductive
11820 Anatomy Exercise to strengthen pelvic floor targets *Levantor Ani Muscle*
System & Breast
To help with delivery, a vertica; midline incision is made at the post
FemaleReproductive
11823 Anatomy vaginal opening through the vaginal and subvaginal mucosa. The
System & Breast
structure most likely involved in this incision is the *Perineal Body*
Histopathology of High-grade cervical intraepithelial neoplasia
FemaleReproductive
11858 Pathology (CIN) would show *Expansion of immature basal cells to the
System & Breast
epithelial surface*
FemaleReproductive
11890 Histology Revisebreastneoplasia!
System & Breast
Woman who delivers twins and has postpartum hemorrhage and
surgery is started. To control her bleeding, bilateral ligation of
FemaleReproductive
11908 Anatomy *Internal Iliac* arteries is preformed and this would preserve her
System & Breast
fertility due to the dual supply of the uterus from the ovarian
arteries.
Septic Abortiontypically prsents with fever, abodominal pain,
uterine tenderness, and/or foul-semlling discharge after
FemaleReproductive
11961 Microbiology preganancy termination. Common offending pathogens inculude
System & Breast
*Staph Aureus* and E. coil due to seeding of the uterine cavity
duringinstrumentation.
A cavernous Hemangioma is the MC benign liver tumor. Typically
54 Pathology Gastrointestinal & Nutrition
in adults 30-50 years.
Pt with chronic hepatitis C, a large hepatic mass and multiple
56 Pathology Gastrointestinal & Nutrition satelite lesions has hepatocellular carcinoma. The marker for
recurrenc is *ALPHA FETOPROTEIN*
Moldy grains from asia that cause specific G-to-T mutation in gene
57 Pathology Gastrointestinal & Nutrition p53. This is aflatoxin exposure, the mutation of which can increase
risk for developing *Hepatocellular Carcinoma*
The prsence of a fluid-filled cavity in liver in conjuction with fever,
chills and RUQ pain. Microorganism/route combinations that is
62 Microbiology Gastrointestinal & Nutrition
most likely cause is *Staph Aureus via Hematogenous route*
[Hepatic Abscess caused by staph]
Gallstones caused by the use of fibrates for dyslipidemia are
67 Biochemistry Gastrointestinal & Nutrition
caasued by decreased activity of 7-lpha-hydroxylase.
Pt with slow and incomplete gallbladder emptying (gallbladder
71 Pathology Gastrointestinal & Nutrition
hypomotility) is at risk of developing a *Billiary Sludge*
Pt with cholestrol gall stones would have *High cholestrol, low bile
78 PathophysiologyGastrointestinal & Nutrition
salts and low Poshatidylcholine* in the gallbladder.
Pt with severe right upper quadrant tenderness and laprascopic
surgery that reveals an erythematous, distended gallbladder with
79 Pathology Gastrointestinal & Nutrition patchy necrosis probably has acute calculous cholecystitis which
usuallu results from a *Gallbladder outflow obstruction* due to
gallstone obstruction of cystic duct.
The diagnostic test most specific fro acute cholecystitis is *Failed
80 PathophysiologyGastrointestinal & Nutrition
gallbladder visualization on radionuclide billary scan*
Pt with a mass obstructing the iliocecal valve with a high cholestrol
content. A radiographic finding conistent with this presentation
88 Pathology Gastrointestinal & Nutrition
would be *Air in the billary tree*
(Gallstone ileus, gallstone penetrated intestine and lodged)
Pt who is in shock and Hb level drops from 14 to 12. Nasogastric
125 Pathology Gastrointestinal & Nutrition suctioning reveals bright red blood. Pt's bleeding is most likely a
result of *Physiologic strss*
*Intestinal Influences* help Down-Regulate gastric secretions after
126 Physiology Gastrointestinal & Nutrition
a meal.
submucosal glands that have alkaline secretions in Gi endoscopy
probably are the Submucosal (Brunner) glands which can be
129 Anatomy Gastrointestinal & Nutrition
found at the *First part Duodenum* (ampulla of vater) and the
Pylorus.
Pt presents with abdominal discomfort, greasy stool, and weight
loss. He has been treated for joint pain with Ibupropfen. Intestinal
biopsy shows multiple macrophages loaded with PAS-positive
131 Pathology Gastrointestinal & Nutrition
granules in the lamina propria. This pt shud be Tx with *Antibiotics*
[Wipple disease caused by g+ve actinomycete Tropheryma
whippelii]
The *Glycoprotein* in cell walls of actinomycete Tropheryma
whippeli colors magenta with PAS and is diastase-resistant,
132 Pathology Gastrointestinal & Nutrition
making this stain an excellent choice for evaluating tissue for
whippledisease.
Lactase deficeiency causes osmotic diarhea and *Acidification of
133 PathophysiologyGastrointestinal & Nutrition
stool*
135 Pathology Gastrointestinal & Nutrition The NF-kB factor pathway stimulates *Cytokine Production*
Pt with sharp pain and bright red rectal bleeding on defecation
255 Pathology Gastrointestinal & Nutrition suggest an Anal Fissure. Which is at the *Posterior midline Distal
to the Dentate line*
65 yr old man with iron def anemia. He has weight loss and
anorexia. He has no change in bower habits. Rectal exam shows
guaiac-positive brown stool. A 3cm mass is found on colonoscopy.
Biopsy shows pleomorphic cells with large, dark nuclei forming
257 Pathology Gastrointestinal & Nutrition
irregular, crowded glands, some of which contain mucus. Studis
show multiple mass lesions in the liver and lungs. Pt's neoplasm
most likely originated from *Ascending colon*
[Right sided colon Cancer]
Dysphagia for liquids and difficulty belching in association with a
diated esophagus and absent peristalsis in the smooth portion is
278 Microbiology Gastrointestinal & Nutrition
diagnostic of Achalasia. If pt is from south america or central
america suspect *T. Cruzi*
279 PathophysiologyGastrointestinal & Nutrition Zenker Diverticulum is due to *Cricopharyngeal motor dysfunction*
Alcoholic male presents with hematemesis. Endoscopy shows
longitudinal mucosal tears at the gastroesophageal junction. This pt
281 Pathology Gastrointestinal & Nutrition
condition is most likely related to *Intraabdominal pressure*
[Mallory-Weiss syndrome]
Pt presents with anatcid resistant severe Heart Burn. P.E shows
scattered Telangiectasias on face, several ulcers at tip of fingers,
and small Ca deposits on hands and elbows. Most likely cause of
pt heart burn is *Fibrous Replacement of the muscularis in the
284 Pathology Gastrointestinal & Nutrition loweresophagus*
[CREST syndrome, Calcinossi, Raynaud Phenomenon,
Esophagealdysmotility,Sclerodactly,Telangiectasia]
[Esophageal dysmoti is result of atrophy and "Fibrous
replacement" of muscularis in lower esoph]
Erosions are defined as mucosal defects that do not fully extend
290 Pathology Gastrointestinal & Nutrition
thru the *Muscularis Mucosa*
A peptic ulcer localized PROXimally on the lesser curvature
292 Anatomy Gastrointestinal & Nutrition probably penetrated the *Left gastric Artery* which is a branch of
the celiac trunk.
Laparotomy shows decreased angle between superior mesenteric
artery and aorta. The structure most likley obstructed is
303 Anatomy Gastrointestinal & Nutrition
*Transverse portion of duodenum*
[Superior mesenteric artery syndrome]
Pt with paraital cell hyperplasia (Zollinger-Ellison) causing visible
304 Pathology Gastrointestinal & Nutrition enlargement of gastric folds. The stimuli that caused this probably
*Gastrin*
A pt with distal ulcer and high-normal gastrin levels that rise in
response to secretin adminstration are suggestive of
Zollinger-Ellison Syndrome. The is caused by gastrin-secreting
305 Pathology Gastrointestinal & Nutrition
tumors (Gastrinomas) which is a *Neoplasia*