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1
Q

Omphalocele, gastroschesis due to failure of

A

Lateral fold closure

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2
Q

Bladder exstrophy due to failure of

A

Caudal fold closure

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3
Q

Sternal defects due to failure of

A

Rostral fold closure

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4
Q

Embryology of spleen

A

Arises in mesentery of stomach (hence is mesodermal) but is supplied by foregut (celiac artery)

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5
Q

What is the portal triad contained within?

A

Hepatoduodenal ligament

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6
Q

What is the Pringle maneuver?

A

Compressing the hepatoduodenal ligament (and therefore the portal triad to control bleeding) between the thumb and index finger in mental foramen

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7
Q

What is contained in the gastrohepatic ligament?

A

Gastric arteries

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8
Q

What is contained in the gastrocolic ligament?

A

Gastroepiploic arteries

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9
Q

What is contained in the gastrosplenic ligament?

A

Short gastric, left gastroepiploic vessels

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10
Q

What is contained in the splenorenal ligament?

A

Splenic artery and vein, tail of pancreas

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11
Q

What are the three zones of the liver anatomy?

A

Zone 1- periportal (branch of portal vein and hepatic artery- bringing blood IN); zone 2- intermediate zone; zone 3- pericentral vein (centrilobular) zone (branch of hepatic vein- taking blood OUT)

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12
Q

Which way do blood and bile flow in the liver?

A

Blood flows from zone 1-> zone 3; bile flows from zone 3-> zone 1

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13
Q

Which zone is affected first by viral hepatitis?

A

Zone 1

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14
Q

Which zone is affected first by ingested toxins?

A

Zone 1

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15
Q

Which zone is affected by yellow fever?

A

Zone 2

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16
Q

Which zone is affected first by ischemia?

A

Zone III

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17
Q

Which zone contains the cytochrome P450 system?

A

Zone III

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18
Q

Which zone is most sensitive to metabolic toxins?

A

Zone III

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19
Q

Which zone is the site of alcoholic hepatitis?

A

Zone III

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20
Q

What produces gastrin and where are they located?

A

G cells (antrum of stomach, duodenum)

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21
Q

Action of gastrin

A

Increased gastric secretion, increase growth of gastric mucosa, increase gastric motility

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22
Q

What produces somatostatin and where are they located?

A

D cells (pancreatic islets, GI mucosa)

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23
Q

Action of somatostatin

A

Decrease gastric acid and pepsinogen secretion, decrease pancreatic and SI fluid secretion, decrease gallbladder contraction, decrease insulin and glucagon release

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24
Q

What produces cholecystokinin and where are they located?

A

I cells (duodenum, jejunum)

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25
Q

Action of cholecystokinin

A

Increase pancreatic secretion, increase gallbladder contraction, decrease gastric emptying, increase sphincter of Oddi relaxation

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26
Q

What produces secretin, and where are they located?

A

S cells (duodenum)

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27
Q

Action of secretin

A

Increase pancreatic HCO3- secretion, decrease gastric acid secretion, increase bile secretion

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28
Q

What produces GIP and where are they located?

A 
GIP= Glucose-dependent insulinotropic peptide (aka Gastric inhibitory peptide)
K cells (duodenum, jejunum)
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29
Q

Function of GIP

A

Exocrine: decrease gastric H+ secretion
Endocrine: Increase insulin release

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30
Q

Symptoms of a VIPoma

A

Watery Diarrhea, hypokalemia, and achlorhydria

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31
Q

What produces Intrinsic factor, and where are they located?

A

Parietal cells (upper glandular layer of the stomach)

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32
Q

What produces gastric acid, and where are they located

A

Parietal cells (upper glandular layer of the stomach)

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33
Q

What produces pepsin, and where are they located?

A

Chief cells (in the deep glands of the stomach)

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34
Q

What is the action of pepsin?

A

Protein digestion

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35
Q

Primary mechanism of gastrin increasing acid secretion

A

Through its effects on enterochromaffin-like cells (leading to histamine release)

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36
Q

How are glucose and galactose taken up from the gut?

A

SGLT1 (Na-dependent)

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37
Q

How is fructose taken up from the gut?

A

GLUT-5 (facilitated diffusion)

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38
Q

How do glucose, galactose, and fructose get into the blood from the enterocytes?

A

GLUT-2

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39
Q

What catalyzes the rate-limiting step in bile synthesis?

A

Cholesterol 7-alpha-hydroxylase

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40
Q

What is heme metabolized by?

A

Heme oxygenase to biliverdin (which is reduced to bilirubin)

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41
Q

What enzyme is used to conjugate indirect bilirubin?

A

UDP-glucuronosyl-transferase (in the liver)

Direct bilirubin is conjugated with glucuronic acid

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42
Q

Most common salivary gland tumor?

A

Pleomorphic adenoma
Composed of chondromyxoid storm and epithelium
Recurs if incompletely excised or ruptured intraoperatively

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43
Q

What is a benign cystic tumor with germinal centers?

A

Warthin tumor (papillary cystadenoma lymphomatosum)

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44
Q

What is MC malignant salivary tumor?

A

Mucoepidermoid carcinoma (has mutinous and squamous components)

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45
Q

What is a curling ulcer?

A

Burns–> decreased plasma volume –> sloughing of gastric mucosa

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46
Q

What is a Cushing ulcer?

A

Brain injury–> increased vagal stimulation –> increased ACh –> increased H+ production

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47
Q

What is Menetrier disease

A

Gastric hyperplasia of mucosa-> hypertrophied rugae, excess mucus production with resultant protein loss and parietal cell atrophy with decreased acid production. Precancerous

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48
Q

What do you see in Whipple disease?

A

Gram positive, rod-shaped bacilli, PAS + foamy macrophages in intestinal lamina propria, mesenteric nodes. Cardiac symptoms, arthralgias, and neurologic symptoms are common

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49
Q

Treatment for Crohn disease

A

Corticosteroids, azathioprine, antibiotics (eg. ciprofloxacin, metronidazole), infliximab, adalimumab

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50
Q

Treatment for Ulcerative colitis

A

5-aminosalicylic preparations (eg. mesalamine), 6-mercaptopurine, infliximab, colectomy

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51
Q

Which IBD is associated with sclerosing cholangitis?

A

Ulcerative colitis

52
Q

What is a Zenker diverticulum?

A

Pharyngeoesophageal false diverticulum. Herniation of mucosal tissue at Killian triangle between the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor

53
Q

Where is the APC gene located?

A

Chromosome 5q

54
Q

What is Gardner syndrome?

A

FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth

55
Q

What is Turcot syndrome?

A

FAP + malignant CNS tumor

56
Q

What is Peutz-Jeghers syndrome associated with?

A

Hyper pigmented mouth, lips, hands, genitalia. Increased risk of colorectal, breast, stomach, small bowel, and pancreatic cancers

57
Q

What is Lynch syndrome?

A

AD mutation of DNA mismatch repair genes with subsequent micro satellite instability; associated with endometrial, ovarian, and skin cancers

58
Q

Most common molecular pathogenesis of colorectal cancer

A

Loss of APC gene causes decreased intercellular adhesion and increased proliferation –> methylation abnormalities–> COX-2 overexpression–> KRAS mutation causing unregulated intracellular signal transduction –> adenoma –> Loss of tumor suppressor genes (p53, DCC) causing increased tumorigenesis –> carcinoma

59
Q

Mechanism of Reye syndrome

A

Aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes

60
Q

What are Mallory bodies?

A

Intracytoplasmic eosinophilic inclusions of damaged keratin filaments, seen in alcoholic hepatitis

61
Q

Diagnosis of HCC?

A

Increased alpha-fetoprotein, 3 phase MRI

62
Q

Causes of unconjugated hyperbilirubinemia

A

Hemolytic, physiologic, Crigler-Najjar, Gilbert syndrome

63
Q

Causes of direct hyperbilirubinemia

A

Biliary tract obsruction (gallstone, cholangiocarcinoma, pancreatic or liver cancer, liver fluke); biliary tract disease (primary sclerosis cholangitis, primary biliary cirrhosis), excretion defect (Dubin-Johnson syndrome, Rotor syndrome)

64
Q

Crigler-Najjar syndrome, type I

A

Absent UDP-glucuronoyl transferase. Presents early in life; patients die within a few years. Findings: jaundice, kernicterus, increased unconjugated bilirubin. Tx: plasmapheresis and phototherapy

Type II is less severe and response to phenobarbital

65
Q

Dubin-Johnson syndrome

A

Conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign

66
Q

Rotor syndrome

A

Conjugated hyperbilirubinemia. Does NOT cause a black liver

67
Q

Pathology of PBC

A

Autoimmune rxn –> lymphocytic infiltrate +granuloma -> destruction of interlobular bile ducts

68
Q

Pathology of PSC

A

Unknown cause of concentric “onion skin” bile duct fibrosis -> alternating strictures and dilation with “beading” and intra- and extra-hepatic mile ducts

69
Q

Associated with PSC

A

Ulcerative colitis. May also see hypergammaglobulinemia (IgM). MPO-ANCA/p-ANCA positive. Can lead to secondary biliary cirrhosis, cholangiocarcinoma

70
Q

Charcot triad of cholangitis

A

Jaundice, fever, RUQ pain

71
Q

Causes of acute pancreatitis

A

idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hypertriglyceridemia, ERCP, Drugs . (GET SMASHED)

72
Q

Why do patients with sarcoid or Beryllium exposure have hypercalcemia?

A

Because the epithelioid histiocytes of the non-caveating granulomas produce 1-alpha hydroxyls that converts vitamin D to its active form

73
Q

Triad of Behcet syndrome

A

Aphthous ulcers, genital ulcers, and uveitis

74
Q

What is anisocytosis?

A

Varying size

75
Q

What is poikilocytosis?

A

Varying shapes

76
Q

What does the platelets contain?

A

Dense granules (ADP, Ca) and alpha granules (vWF, fibrinogen)

77
Q

What are the neutrophil chemotactic agents?

A

C5a, IL-8, LTB4, kallikrein, platelet-activating factor

78
Q

What are causes of eosinophilia?

A

Neoplasia, Asthma, Allergic processes, Chronic adrenal insufficiency, Parasites

79
Q

What do eosinophils produce?

A

histaminase and major basic protein (a helminthotoxin)

80
Q

What do basophil granules contain?

A

Heparin and histamine

81
Q

When might you see basophilia?

A

Myeloproliferative disease, especially CML

82
Q

What does cromolyn sodium do?

A

Prevents mast cell degranulation

83
Q

What type of immunoglobulin are Anti-A and Anti-B

A

IgM

84
Q

What does warfarin inhibit?

A

Vitamin K epoxide reducatase

85
Q

What drugs inhibit ADP induced expression of GpIIb/IIIa?

A

Clopidogrel, prasugrel, and ticlopidine

86
Q

What has a failure of agglutination with rstocetin assay?

A

von Willebrand disease and Bernard- Soulier syndrome

87
Q

When might you see basophilic stippling?

A

Lead poisoning

88
Q

Orotic aciduria

A

Defect in UMP synthase. Inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway). No hyperamonemia (vs. ornithine transcarbamylase deficiency)

89
Q

Treatment of orotic aciduria

A

Uridine monophosphate

90
Q

Hemolytic anemia in a newborn

A

Pyruvate kinase deficiency

91
Q

Treatment of PNH

A

eculizumab

92
Q

Warm agglutinin

A

Chronic anemia seen in SLE and CLL with certain drugs (e.g., alpha-methyldopa)

93
Q

Cold agglutinin

A

Acute anemia triggered by cold, seen in SLL, mycoplasma pneumonia infections, and infectious mono

94
Q

Corticosteroid effect on WBCs

A

Neutrophilia (because decreased margination), but eosinopenia (sequester in lymph nodes) and lymphopenia (cause apoptosis)

95
Q

When does OR=RR?

A

If prevalence is low

96
Q

What can predispose to long QT interval

A

Drugs (antiarrhythmics 1a and 3, antibiotics like macrolides, antipsychotics, antidepressants like TCAs, and antiemetics like ondansetron), hypokalemia, hypomagnesemia

97
Q

Inheritance of the long WT syndromes

A

Romano-Ward is autosomal dominant. Jervell and Lange-Nielson is autosomal recessive (with sensorineural deafness)

98
Q

What is Brugada syndrome

A

Autosomal dominant disorder in Asian mAles. Pseudo-right bundle branch block and ST segment elevations in V1-V3. Tx:ICD

99
Q

Potential cardio effect of Lyme disease

A

3rd degree heart block

100
Q

What local metabolites in the heart cause vasodilation

A

Adenosine, NO, CO2, decreased O2

101
Q

What local metabolites in the brain cause vasodilatation

A

CO2

102
Q

What local metabolites in the muscle control auto regulation

A

Lactate, K+, H+, CO2

103
Q

Most common cause of ASD

A

Osmium secundum defects

104
Q

How are PFO and ASD different

A

In ASD the septa are missing rather than unfused

105
Q

Heart defects associated with infants of diabetic mothers

A

Transposition of great vessels

106
Q

Heart defect associated with Williams syndrome

A

Supravalvular aortic stenosis

107
Q

Heart defects associated with 22q11 syndromes

A

Truncus arteriosus, tetralogy of Fallot

108
Q

What causes the onion skinning in severe hypertension

A

Proliferation of smooth muscle cells

109
Q

Most common presenting symptom of post-procedure atheroembolism

A

AKI

110
Q

What is AAA associated with

A

Transmural inflammation

111
Q

What is thoracic aortic aneurysm associated with

A

Cystic medial degeneration

112
Q

What causes thoracic aortic aneurysm in syphillis

A

Obliterating endarteritis of the vasa vasorum

113
Q

Triggers of Prinzmetal angina

A

Tobacco, cocaine, and triptans

114
Q

Tx of Prinzmetal angina

A

Ca channel blockers, nitrates, and smoking cessation

115
Q

Gross path of a heart after MI 4-24 hrs, 1-3 days, 3-14 days, and >2 weeks

A

4-24 hrs: dark mottling; pale with tetrazolium stain, 1-3 day: hyperemia , 3-14 days:hyperemia border, central yellow-brown softening, and >2 weeks: grey-white

116
Q

What is the scar composed of after an MI

A

Type 1 collagen

117
Q

What is Loffler syndrome?

A

Endomyocardi fibrosis with a prominent eosinophilia infiltrate, associated with restrictive/infiltration cardiomyopathy

118
Q

Endocarditis is IV drug user

A

S. Aureus OR pseudomonas, Candida

119
Q

Culture negative endocarditis

A

Coxiella brunette, Bartonella app. HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

120
Q

What is an Aschoff body?

A

Granuloma with giant cells

121
Q

What is an Anitachkow cell

A

Enlarged macrophage with ovoid, waxy, rod-like nucleus. Associated with rheumatic fever

122
Q

Tree bark appearance of the aorta

A

Tertiary syphillis

123
Q

Txt of Raynaud phenomenon

A

Ca channel blockers

124
Q

Which small vessel vasculitis does not have granulomas

A

Microscopic polyangiitis

125
Q

Presentation of microscopic polyangiitis

A

Necrotizing vasculitis commonly involving lung, kidneys, and SKIN with pauci/immune glomeruli nephritis and palpable purpura. Similar to Wegners (granulomatosis with polyangiitis) but WITHOUT NASOPHARYNGEAL INVOLVEMENT

126
Q

Presentation of eosinophilia granulomatosis with polyangiitis

A

Asthma, sinusitis, skin nodules or purpura, peripheral neuropathy

127
Q

MOA of fenoldopam

A

Dopamine D1 receptor agonist- coronary, peripheral, renal, and splanchnic vasodilation. Decreases BP and increases natriuretic

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