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USMLE Step 1 > GI Stuff Missed > Flashcards

GI Stuff Missed Flashcards

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USMLE® Step 1 flashcards
1
Q

Primary Billiary Cirrhosis

A

chronic liver disease characterized by autoimmune destruction of INTRA-hepatic bile ducts and cholestasis

  • common in middle aged women
  • elevated alkaline phosphotase
  • associated with severe pruritis at nice
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2
Q

Budd-Chiari Syndrome

A

secondary to thrombotic occlusion of hepatic veins and/or intra- or supra-hepatic IVC
- venous occlusion causes sinusoidal pressure to increase leading to portal hypertension, splenomegaly, ascites, hepatomegaly,

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3
Q

Elevated alkaline phosphotase of unknown etiology should be followed up what test

A

Gamma-glutamyl transpeptidase - enzyme predominantly found in hepatocytes and biliary epithelial.

Elevated alk phosphatase + elevated gamma=glutamyl transpeptidase = liver disease

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4
Q

Discuss presence of bi-modal distribution of drug plasma concentration

A
  • presence of two distinct groups within population and suggests polymorphism in drug metabolism
  • one rapidly converts drug to metabolite and other drug converts drug slowly leading to accumulation of original drug
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5
Q

Isoniazid metabolism

A

metabolized by acetylation to N-acetyl isoniazid.

  • genetically, people are fast “acetylators” thus metabolize drug quickly or slow “acetylators” and thus metabolize drug slowly.
  • Slow metabolizers are at increased risk of side effects
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6
Q

Methylation in drug metabolism

A
  • used in azathioprine and 6-mercaptopurine
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7
Q

Ulcerative Collitis complications

A
  • Toxic megacolon
  • Malutrition
  • Sclerosing cholangitis
  • Colorectal carcnimoa (worse with right sided colitis or pancolitis)
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8
Q

Sx: Patient diagnosed with UC but poorly controlled is presenting with abdominal pain and distention, fever, diarrhea, and shock. What’s the next step in work up?

A

Flat plain abdominal X- ray to identify toxic megacolon

  • Barrium enema and colonoscopy are contraindicated because it may cause perforation
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9
Q

Ulcerative Collitis

A
  • autoimmune disease
  • continuous colonic lesions, always with rectal involvement
  • MUCOSAL and SUBMUCOSAL involvement only
  • Friable mucosal “pseudopolyps”
  • Loss of haustra “lead pipe appearance”
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10
Q

Crohn’s Disease

A
  • disordered response to intestinal bacteria
  • any part of GI, usually terminal ileum and colon
  • Skip lesions and rectal sparing
  • TRANSMURAL inflammation
  • “Cobblestone” mucosa, creeping, bowel wall thckening, linear ulcers, fissures, and FISTULAS
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11
Q

Pathogenesis of hepatic steatosis

A
  • due to decrease in fatty acid oxidation to excess NADH production by alcohol dehydrogenase and aldehyde dehydrogenase
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12
Q

Sx: 5 month old presenting with poor feeding, weakness, and complete loss of extremity muscle tone. Aside from formula, fed with juice and honey. Likely diagnosis”

A

“Floppy baby syndrome” - from C. botilinum

  • infant botulinism results form eating C. botulinum spores found in spores due to honey consumption.
  • Don’t give honey to babies under 1
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13
Q

To reduce likelihood of cholesterol precription and gallstone formation, what should be the balance between bile acid and cholesterol

A

Cholesterol levels should be kept LOW
Bile acid levels should be help HIGH

  • High levels of phosphatidylcholine, will render cholesterol more soluble
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14
Q

Liver: embryological origins and arterial supply

A

Endoderm derived foregut

- arterial supply is celiac trunk derived from proper hepatic artery

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15
Q

Kidneys: embryological origins and arterial supply

A
  • retroperitoneal and derived from mesoderm

- renal arteries

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16
Q

Transverse Colon: embryological origin and arterial supply

A

Proximal 2/3 of transverse colon: derived from MIDgut and supplied by SMA via middle colic artery

Distal 1/3: derived from HINDgut and supplied by IMA via left colic artery

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17
Q

Pancreas: embryological origin and arterial supply

A

Endoderm derived structure of FOREgut and MIDgut
- receives blood from superior and inferior pancreaticduodenal arteries as well as other arterial branches of celiac artery

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18
Q

VIPomas

A

non-beta cell pancreatic islet cell tumors that hypersecrete VIP

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19
Q

VIP

A
  • increases intestinal Cl- loss into stool which creates excess loss of water, sodium, and potassium
  • relaxes GI smooth muscle
  • inhibits gastric acid secretion
  • Somatostatin inhibits VIP secretion
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20
Q

WDHA syndrome

A
  • Watery Diarrhea Hypokalemia Achlorydia

- due to excess secretion of VIP

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21
Q

Gastrin

A
  • produced by G cells in stomach mucosa
  • stimulates gastric acid production and growth of gastric mucosa
  • excess secretion of gastrin cause Zollinger-Ellison synrom (intractable peptic ulcer diseae)
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22
Q

Metoclopramide

A
  • dopamine antagonist with both central and peripheral effects
  • has prokinetic and anti-emetic effects
  • used to treat gastroparesis, no real effect on PUD
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23
Q

Erosions

A
  • mucosal defects that don’t fully extend through muscularis mucosa
  • acute erosive gastropaty can cause upper GI bleeds –> tarry stools
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24
Q

Gastric ulcers

A
  • extend into submucoal layer and muscularis propria (inner circular layer and outer longitudinal smooth muscle layers)
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25
Q

Common causes of gastric ulcers

A
  • H. pylori (most common cause)

- NSAID use, due to inhibition of prostaglandins

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26
Q

Kaposi’s sarcoma (on colonoscopy)

A
  • derived from HHV-8
  • in colonoscopy: reddish/flat maculopapular lesions and hemorrhagic nodules
  • spindle-shaped tumor cells with small vessel proliferation
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27
Q

Ulcerative Colitis (on colonoscopy)

A

Colonoscopy: continuous areas of erythematous, fribable, granular mucosa with possible pseudopolyps

Biopsy: inflammatory infiltrate involving mucosa and submucoda

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28
Q

Entamoeba histolytica (on colonoscopy)

A

Colonoscopy: numerous discrete, flash-shaped ulcerative lesions
Biopsy: Trophozoits containing RBCs

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29
Q

Cryptosporidium (on colonoscopy:

A

Nonulcerative inflammation

- basophilic clusters een on surface of intestinal mucosal cells

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30
Q

Signs of metastasis of gastric cancer (hint: 3)

A

Virchow’s node (supraclavicular node)
St. Mary Joseph nodule (nodule bulging into umbilicus)
Krukenberg tumor of ovary (usually bilateral mucin-producing, “signet” ring cells in ovaries)

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31
Q

Adenoma to Carcinoma sequence

A
  1. APC mutation: progression from normal mucosa to small polyp
  2. K-ras mutation: increased size of polyps
  3. p53 and DCC mutation: malignant transformation
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32
Q

Ulcerative Colitis

A
  1. Rectum is always involved
  2. Inflammation limited to submucosa and mucosa
  3. Mucosal damage is continuous
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33
Q

Mallory Weiss Syndrome

A
  • longitudinal mucosal tears at esophagogatric-squamocolumnar junction
  • secondary to increased intraabdominal pressure and gastric pressure due to repeated retching and vomiting
  • seen in alcoholics and bulimics
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34
Q

Useful marker in evaluation of cirrhotic patients for hepatocellular carcinoma

A

Alpha-fetoprotein

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35
Q

CEA

A

serum marker associated with colorectal cancer

- not useful for screening but used in staging and determining prognosis

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36
Q

CA-125

A

serum marker elevated in majority of women with ovarian cancer
- not effective screening tool for ovarian cancer but helpful in determining recurrence of disease

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37
Q

Acute acalculous cholecystitis

A

commonly seen in hospitalized patients who are :

  • septic
  • immunocompromised
  • on Total parental nutrition
  • major trauma

secondary to gallbladder stasis and ischemia which cause injury and inflammation to gallbladder BUT WITHOUT GALLSTONES

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38
Q

Porcelain gallbladder

A

seen on abdominal radiograph as rim of Ca deposits that outline gallbladder
- associated with gallbladder carcinoma

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39
Q

Fluke infection of biliary tree

A

associated with formation of brown pigment stones

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40
Q

Formula for drug half live (using clearance and volume distribution)

A

t 1/2 = (Vd X ln 2) / CL

Vd = volume distribution
CL = drug clearance

** Ln 2 = .7

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41
Q

Mesenteric adenitis

A

occurs in children 5-14 years old

  • may be associated with Yersinia Enterocolitica
  • non specific signs: abdominal pain in right lower quandrant
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42
Q

Ulcerative Colitis: Clinical Manifestations

A

BLOODY DIARRHEA, abdominal comfort

“Toxic megacolon” is complication

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43
Q

Crohn’s Disease: Clinical Manifestation

A

ABDOMINAL PAIN, diarrhea

“Fistulas, strictures (leading to intestinal obstructino)

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44
Q

Crigler-Najjar Syndrome

A

autosomal recessive disorder of bilirubin metabolism by lack of UGT enzyme need to catalyze bile glucuronidation
- uncojugated bilirubinemia develops causing kernicterus (bilirubin encephalopathy) and death

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45
Q

Sx: One month old with hx of persistent jaundice experiences muscle rigidity, lethargy and seizures. Presents with hyperbilirubinemia

A

Crigler-Najjar Syndrome

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46
Q

Dubin-Johnson syndrome

A

autosomal recessive disorder

  • absent biliary transport protein (MRP2), used in hepatocellular excretion of conjugated bile in bile canaliculi
  • liver appears dark but patients are assymptomatic
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47
Q

Rotor syndrome

A

autosomal recessive disorder

  • assymptomatic hyperbilirubinme results from defects in hepatic uptake and excretion of bilirubin pigments
  • patients are often jaundiced but have normal life expectancies
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48
Q

Discuss gut deconjugation of bilirubin

A

S. aureus and lots of anaerobes can decojugate bile in gut (removing glycine and taurine) of bile acids making them less soluble and unable to form micells
- no neuro symptoms associated with this

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49
Q

Campylobacter

A
  • common cause inflammatory gastroenteritis and can be acquired frrom domestic animals or contaminated food
  • inflammatory diarrhea accompanied by fever, abdominal pain, and tenesmus
  • associated with Guillain Barre syndrome
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50
Q

Traveler’s diarrhea

A
  • self contained, watery diarrhea

related to ETEC - produces heat labile (LT, cholera-like) and heat stable (ST) enterotoxins

LT - activates adenylate cyclase and increases cAMP
ST- activates guanylate cyclase and increases gGMP
- both cause water loss and watery diarrhea

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51
Q

EHEC

A

produces Shiga-like toxin, like Shiga toxin, inactivates 60S ribosomal subunit in human cells thus inhibiting cell protein production and eventually cell death

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52
Q

C. difficile

A
  • pseudomembranous colitis (yellow/white membranous plaque in colon
  • secondary to antibiotic use which disturb gut flora and lead to overgrowth of C. difficile
  • treated by metrodinazole
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53
Q

Discuss opioid use and right upper quadrant pain

A

Opioid analgesics can lead to biliary colic

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54
Q

Sx: 2 y.o presents with black tarry stool. Radioactive labeled accumulation in right lower abdominal quadrant.

Failed embryo process?

A
  • symptomatic of Merkel’s diverticulum
  • contains ectopic gastric mucosa which produces acid causing possible uleration and bleding
  • 99mm Tc-pertechenate scan identidies ectopic gastric epithelium an
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55
Q

Merkel’s diverticulum

A
  • derived from vitelline duct (yolk sac)
  • present in first 2 years of life, usually with lower GI bleeding (red stools)
  • true diverticulum (involves all three layers of bowl)
  • may contain acid-secreting gastric mucosa and/or pancreatic tissue
  • ## may lead to intussusception or volvulus
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56
Q

Hirschsprung disease

A
  • caused by failure of neural crest migration into bowel wall
  • absence of ganglion cells of Auerbach and Meissner plexi
  • manifests with obstruction in the first few days of life
  • unable to pass meconium, bilious vomiting, abdominal distention
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57
Q

Pancreatic pseudocyst

A

common complication of acute pancreatitis.

  • commonly found in lesser peritoneal sac, bordered by stomach, duodenum, and pancreas
  • collection of fluid rich in enzymes and inflammatory debris
  • walls consist of granulation tissue and fibrosis.
  • NOT lined by epithelium like true cysts
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58
Q

Major side effects of statins

A
  • Myopathy
  • Liver toxicity

** careful monitoring of liver function is useful with treatment with hypolidemic drus

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59
Q

Common causes of esophagitis in HIV patients

A
  • Candida albicans (most common)
  • CMV
  • HSV-1
  • patients present with dysphagia and pain upon swallowing
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60
Q

Microscopic findings of Crohn’s disease

A
  1. Chronic inflammation that involves ENTIRE thickness of intestinal wall
  2. NONCASEATING GRANULOMAS that may be present in all tissue layers
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61
Q

Hepatitis B virus infection (hint: 2 phases)

A
  1. PROLIFERATIVE phase - entire virion and related antigens of episomal HBV DNA are present. HBsAg and HBcAg w/ MHC class molecules activate CD8+ T lymphocytes which destroy infected hepatocytes.
  2. INTEGRATIVE phase - HBV DNA is incorporated into hepatocytes that survived immune response. Those re-infectivity remains low, patients still at risk for hepatocellular carcinoma.
62
Q

Hepatitis D virus

A

replication defective RNA virus that is only capable of causing infection when encapsulated by HBsAg

  • or superinfection of chronic carrier
63
Q

Discuss aflatoxins and cancer risk

A

Aspergillus flavus and Aspergillus parasiticus make AFLATOXINs which associated with a G:C –> T:A transversion in p53 gene that increases risk of HEPATOCELLULAR CARCINOMA

64
Q

Diverticula

A
  • abnormal pouches that protrude from wall of GI tract
  • most commonly affected part is sigmoid colon (> 60 years old)
  • attributed to increased luminal pressure, commonly due constipation
  • may be assymptomatic, acute diverticulitis, or painless bleeding
  • PULSION, by mechanism and FALSE, but nature
65
Q

Traction diverticula

A

occur to inflammation and subsquent scarrings

- are TRUE diverticulaw

66
Q

Pathogenesis of acute necrotizing pancreatitis

A
  • caused by abnormal activation of TRYPSIN which activate ALL proteolytic pancreatic enzymes
  • also proteolytic enzymes lead to activation of other proteolytic enzymes and autodigestion
67
Q

Positive Predictive Value

A

TP / FP + TP

  • depends on prevalence of a disease
  • more common a disease is in the population, the more likely the person tested positive HAS the disease
68
Q

Discuss negative predictive value and disease prevalence

A

NPV = TN / FN + TN

  • as prevalence increases, NPV becomes lower
  • more common a disease is within a population, the probability of a true negative result for a person who doesn’t have the test is low
69
Q

Calories per gram

  • in protein
  • in carbs
  • in fat
A

Protein: 1g produces 4 calories
Fat: 1g produces 9 calories
Carbohydrate: 1 g produces 4 calories

70
Q

Which part of GI tract is always affected by Hirschsprung’s disease?

A
  • Rectum
  • Hirschsprung’s is abnormal migration of neural crest cells as they are supposed to migrate caudally
  • in proximal colon by 8th week
  • in rectum by 12th week
71
Q

Natural Killer cells

A
  • express CD16 and CD56
  • don’t require thymus for maturation and are present in athymic patients
  • have no antigen-specific activities, and don’t require antigen exposure or process antigen memory
  • are activated by IFN-gamma and IL-12
72
Q

Natural Killer Cells are activated by which cytokines?

A

IFN-gamma and IL-12

73
Q

Which immune effector cell kill cells with decreased MCH class I antigen cell surface expression?

A

NK cells

  • they’re like bouncers at a club
  • they periodically check the IDs (MHC I) of cells to determine if they belong there.
  • Virus-infected cells and tumor cells are killed by NK cells
74
Q

Gallstone ileus

A

mechanical bowel obstruction caused when a large gallstone erodes intestinal lumen
- air in biliary tract is suggestive for this

75
Q

Lesser omentum

A
  • double layer of perinteum that extends from liver to lesser curvature of stomach and beginning of duodenum
  • composed of hepatogastric and hepatoduodenal ligaments
76
Q

Greater omentum

A
  • peritoneum that extends form greater curvature of stomach, travels inferiorly over small intestine and then reflects on itself and ascends to encompass transverse colon
  • gastrocolic ligament extends from greature curvature of stomach to transverse colon
77
Q

Main side effects of all protease inhibitors

A

Lipodystrophy: increased deposition of fat on back and abdomen but less fat on extremities

Hyperlglycemia: results from increased insulin resistance form protease inhibitors may lead to diabetes

Inhibition of P450 -

78
Q

Whipple disease

A
  • caused by gram + actinomycete, Tropheryma whippelli
  • involves small intestines, joints, and CNS
  • proliferates within macrophages of tissues, thus no inflammatory response
79
Q

Histological signs of Whipple’s disease-

A
  • caused by Topheryma whippelli
  • findings in small intestine mucosa containing foamy macrophages packed with rod-shaped bacilli and PAS-positive, diastase-resistant granules
80
Q

Identifying pancreas on abdominal CT

A

head of panceas is in close association with second part of duodenum

  • body overlies left kidney, aorta, IVC and superior mesenteric vessels
  • tail lies in splenorenal ligament
81
Q

Sx: young man coming back from India presents with low-grade fever, dark urine, nausea, anorexia and mild right upper abdominal quandrant tenderness

A

Acute viral hepatitis

- likely caused by Hepatitis A, virus endemic in INdia

82
Q

Histological features of viral hepatitis

A

Diffuse ballooning degeneration (hepatocyte swelling)
Mononuclear cell infiltrates
Councilman bodies (eosinophillic apoptotic hepatocytes

83
Q

Carcinoid tumors

A

made from enterochromaffin cells of intestinal mucosa

  • produce vasoactive substances, such as %-HT, bradykinin, prostaglandins, and others
  • when confined to intestine, secretory products go to portal system and are metabolized by liver
  • if they metastasize to liver, then they enter systemic circulation
84
Q

Sx of Carcinoid tumors

A
  1. Vasomotor instability: cutaneous flushing, dizziness
  2. GI symptoms: secretory diarrhea, crampy abdominal pain
  3. Bronchoconstriction: dyspnea with wheezing
  4. Right sided (pulmonary, triscuspid) valvular heart disease
85
Q

Celiac sprue

A
  • malabsorption disease characterized by IgA antibodies to gliadin
  • patients present with diarrhea, steatorhea, weight loss, fat-dependent vitamins (A,D,E,K)
  • small intestinal biopsy shows severe atrophy and blunting of villi
86
Q

Alpha-1 trypsin deficiency

A
  • often young mailes
  • protein reduces tissue damage caused by inflammation through the inhibition of neutrophil elastase
  • histologically associated with reddish-pink, periodic acid-Schiff-positive granules of unsecreted, polymerized A1AT in periportal hepatocytes
87
Q

80% of acute pancreatitis is caused by what two things?

A
  • Gallstones
  • Chronic alcoholism

** One should measure hypertriglyceride levels

88
Q

Appearance of intestinal mucosa for someone with lactase deficiency

A

Appears normal on histological examinatino

89
Q

Whipple disease on histological exam

A

Distended macrophags in intestinal lamina propria

90
Q

Th1 cells

A
  • mediated release of IL-2 and IFN-gamma and activate macrophages to synthesize TNF (tumor necrosis factor)
  • key factor for development of granulomas
91
Q

Echinococcus granulosus

A

tapeworm that is most common cause of hyatid cysts in humans

  • endemic regions are in Middle East, South America, Iceland, Oceania
  • initially assymptomatic.
  • Liver is most affected, including lung, muscle, or bone
  • cysts look like egg-cell cal
92
Q

Gallstone hypomotility

A
  • slow response to cholecystokinin
  • risk factors: pregnancy, rapid weight loss, prolonged TPN, octeotride, or high spinal cord injuries
  • results in biliary sludge
93
Q

Brown pigment stones

A

arise in cases of biliary tract infection

94
Q

Black pigment stones

A

seen in intravascular hemolysis

95
Q

Initial presentation of Hep B

A

“serum sickness-like” with patients experiencing malaise, fever, skin rash, pruritis, lymphadenpathy and joint pain

  • may see elevations in ALT and AST (ALT > AST) followed by rise in bilirubin and alkaline phosphatase
96
Q

Cholecystokinin (CCK)

A

hormone responsible for gallbladder contraction

- made in duodenum and jejunum in response to fatty acids

97
Q

Secretin

A

promotes HCO2 secretion from pancreatic ductal epithelium

98
Q

Imperforate anus

A

result of abnormal development of anorectal structures

  • manifests during 1st days life by inability to pass meconium
  • if fistula is present, may pass meconium through umbilicus or urethra
  • often seen with urogenital tract abnormalities
99
Q

Pus

A

thin, protein-rich fluid is composed of dead leukocytes (mostly neutrophils)

100
Q

IL-8

A

secreted by macrophages and surrounding epithelial cells to attract neutrophils

101
Q

IL-10

A

antinflammatory cytokine secreted by macrophages and TH2.

limited production of pro-inflammatory cytokines (IFN-gamma, IL-2, IL-3, TNF-alpha)

102
Q

C3a

A

part of complement system
- along with C4a, C5a are anaphylotoxins that trigger histamine release from mast cells, resulting in vasodilation and enhanced vascular permeability

103
Q

IL-3

A

cytokine produced by activated T-cells, stimulated growth of cells in bone marrow

104
Q

Vibrio cholerae

A
  • along with ETEC cause toxin-mediated watery diarrhea
  • toxins don’t cause cell desth
  • activate adenylate cyclase to increase cAMP and increase efflux of Na and Cl
105
Q

Discuss UC and colon cancer

A

Long-standing UC is associated with increased risk of colorectal cancer

  • unlike sporadic colon cancer, UC carcinomas are more likely arise from:
  • non-polypoid dysplastic lesions
  • be multifocal
  • early p53 mutations and late APC mutations
  • higher histological grade
106
Q

Causes of malabsorption

A
  1. Pancreatic exocrine insufficiency
  2. Intestinal mucosal defects
  3. Bacterial proliferation
107
Q

First step after suspected malabsorption

A

Sudan III stain of stool

- identifies fecal fat and can be used to identify malabsorption

108
Q

Tubular adenomas

A
  • ## composed of dysplastic colonic mucosal cells that form tubular-shaped glands
109
Q

Villus adenomas

A

dysplastic epithelial cells form villi-like projections (“cauliflower-like”) that extend from polyp surfaces to stroma
- cause bleeding, secretory diarrhea, and partial intestinal obstruction

110
Q

Discuss estrogen and gallstone formation

A

Estrogen facilitates gallstone synthesis by increasing hepatic HMG-CoA reductase activity.
- Suppressing 7-alpha hydroxylase (by medications such as fibrates) reduces conversion of cholesterol to bile acids, resulting in excess cholesterol secretiion

111
Q

Fibrates

A

inhibit 7-alpha hydroxylase - which reduces conversion of cholesterol to bile acids, resullting in increased secretion of cholesterol in bile

112
Q

Most likely outcome for someone infected with Hepatitis C

A
  • stable chronic hepatitis

- chronic hepatitis progressing to cirrhosis

113
Q

Appearance of Hep B histologically

A

hepatocyte cytoplasm is filled with spheres and tubules of HBsAg and the cytoplasm takes on granular, eosinophilic appearance described as “ground glass”

114
Q

Superior mesenteric artery syndrome

A

when transverse portion of duodenum is entrapped between SMA and aorta, causing symptoms of partial intestinal obstruction

  • aorticmesenteric angle lessens, secondary to diminished mesenteric fat, pronounced lordois, or surgical correction of scoliosis
115
Q

Most common malignant neoplasm of the liver

A

Metastasis

  • major site for metastatic spread because of its size, dual blood supply, high perfusion rate, and filtration function of Kupffer cells
  • appears as multiple nodules in the liver with marked hepatomegaly
  • more common than hepatocellular carcinoma
116
Q

Hepatic angiosarcomas

A

associated with recent or remote exposure to vinyl chloride, arsenic, or Thorostate
- commonly aggressive

117
Q

When is the omphalomesenteric (vitilline duct) obliterated during gestation?

A

7th week of embryonic development

118
Q

Crohn’s disease is associated with what type of kidney stones

A

Oxalate kidney stones

Impaired bile acid absorption in terminal ileum leads to loss of bile acids in feces with subsequent fat malabsorption.

  • Lipids then bind Ca ions and resulting soap complex forms
  • Free oxalate (which is normally bound by calcium to form unabsorbable complex) is absorbed and forms urinary calculi
119
Q

HNPCC

A

aka Lynch Syndrome

  • leads to occurrence of colon adenocarcinomas at young age (< 50 years old), along with extraintestinal malignancies
  • due to mutations of DNA mismatch repair genes (MLH1 and MSH2)
120
Q

Greatest markers of alcoholic liver injury

A

Serum albumin and prothrombrin time reflect liver dunction and are greastest determiners of prognosis

  • increased AST and ALT indicate hepatocellular amage
121
Q

Patient is drunk and/or intoxicated and demands to leave with no treatment. What do you do?

A

Patients who are temporarily intoxicated are not allowed to make medical conditions.

He is not allowed to leave until he is sober

122
Q

Chronic mesenteric anemia

A
  • often caused by atherosclerotic narrowing of celiac trunk, SMA, and IMA
  • these changes diminish blood flow, they cause postprandial abdominal pain, weight loss, and pain out proportion with physical findings
123
Q

Splenic artery

A

originates from celiac artery and gives off branches to stomach and pancreas (pancreatic, short gastric, left gastroepiploic arteries) before getting to spleen

  • if splenic artery is blocked, gastric tissues supplied by these arteries will be ischemic
124
Q

APC mutation

A

most common mutation required for emergence of adenomatous polyps from normal mucosa

125
Q

Diphenyloxate

A

opiate anti-diarrheal related to meriperdine

- binds to mu opiooids in GI tract and slows motility

126
Q

Rapid urease tests are used to diagnose what?

A

H. pylori
* pink color indicates alkaline solution or pH increase

urease will convert urea to carbon dioxide and ammonia and cause pH increase

127
Q

Triad of hemochromatosis

A
  • Hyperpigmentation
  • Diabetes Mellitus
  • Pigment Cirrhosis

“Bronze Diabetes”

128
Q

Most common outcome for someone infected with Hepatitis B

A

Acute hepatitis or subclinical symptoms that eventually resolve

129
Q

What type of ectopic tissue is usually present in Meckel’s diverticulum?

A

Gastric mucosa

  • gastric acid production leads to ulceration and subsequent bleeding
130
Q

Dorsal pancreatic bud

A

forms majority of pancreatic tissue (body, tail, and most of head)

131
Q

Ventral pancreatic pu

A

precursor for uncinate process, inferior/posterior potion of head, and major pancreatic duct

132
Q

Pancreas divisim

A
  • failure of pancreatic buds to fuse

- pancreatic ductal systems remain separate with accessory duct draining majority of pancreas

133
Q

Secretin

A

secreted by duodenal S cells in response to increased H+ concentrations

  • Chloride content of pancreatic secretions decrease as Bicarb concentration increases
134
Q

Risk factors for squamous cell esophageal cancer

A

Alcohol use
Tobacco smoking
Consumption of N-nitroso-containing foods (smoked) foods

135
Q

Risk factors for esophageal adenocarcinoma

A

Barrett’s esophagus
GERD
Obesity
Tobacco use

136
Q

In situations in which patient is unable to make decisions for themselves and there is no written directive stating their intentions for end of life care, who is responsible for making decisions.

A

Next of kin.

If married: spouse is next of kin followed by adult children

137
Q

Reye syndrome

A

occurs in children with febrile illness treated with salicylates

  • consists of hepatic failure and encephalopathy
  • associated with microvesicular steatosis of hepatocytes without inflammation and cerebral edema
138
Q

PPIs (“prazoles”)

A

acts on H+/K+/ATP inhibits gastric secretion from parietal cells from 3 pathways:

  • ACh (resists vagal stimulation)
  • Histamine
  • Gastrin
139
Q

common environmental risk factors for pancreatic cancer

A 
Smoking (MOST IMPORTANT)
> 50
chronic pancreatitis
diabetes mellitus
genetic predisposition
140
Q

Cephalic phase of gastric secretion

A

mediated by cholinergic and vagal mechanisms

- triggered by thought, sight, smell, and taste of food

141
Q

Gastric phase of gastric secretion

A
  • mediated by presence of gastrin (which stimulates histamine secretion)
142
Q

Intestinal influences

A
  • initiated when protein containing food enters duodenum

- can influence gastric secretion, but more importantly DOWNGRADES gastric secretion

143
Q

Parietal cells

A

secrete HCl and intrinsic factors

  • found in superficial region of gastric glands
  • autoimmune destruction leads to pernicious anemia
144
Q

Chief cells

A

synthesize and secrete pepsinogen

primarily found in deeper region of gastric glands

145
Q

Vancomycin resistance in VRE

A

substitution of D-lactate in place of D-alanine during peptioglycan cell wall synthesis.
-prevents binding of vancomycin to usual D-alanyl-D-alanine

146
Q

Abetalipoproteinemia

A

inherited inability to synthesize apolipoprotein B, important component of chylomicrons

  • lipids absorb in small intestine cannot be transported and therefore accumulate in intestinal epithelium
  • lack of lipids in cell membrane cause abnormal blood cells (acanthocytes) and neurological deficits
147
Q

Curling ulcers

A

ulcers arising in proximal duodenum in association with severe trauma or burns

148
Q

Cushing ulcers

A

ulcers arising in esophagus, stomach, or duodenum in patients with high ICP are particularly prone to perforation

149
Q

Markers of active Hep B viral infection

A
  • HBsAg
  • HBeAg
  • HBV DNA
150
Q

Discuss the changes in HBcAg overtime

A

Initially starts as HBcAg IgM and then changes to HBcAg IgG

151
Q

H. pylori infection

A

associated with duodenal ulcers caused by decrease in somastatin- secretin cells in gastric mucosa leading to unchecked gastrin production

USMLE Step 1 (34 decks)

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