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First Aid GI, Heme/Onc Flashcards

1
Q

Name the pancreatic enzymes used to digest

(a) Carb
(b) Lipids
(c) Protein

A

Pancreatic enzymes

(a) Alpha-amylase
(b) Lipase
(c) Proteases: trypsin, chymotrypsin, elastase- all secrete in zymogen form

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2
Q

What is Virchow node?

(a) MC cause

A

Virchow node = involvement of left supraclavicular node from metastatic cancer

(a) MC from gastric adenocarcinoma
- L supraclavicular node drains stomach region

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3
Q

What is ileus?

(a) Tx

A

Ileus = intestinal hypomotility w/o obstruction

a) Treat w/ bowel rest, electrolyte correction, and cholinergic drugs (pro-motility agents

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4
Q

Gastric vs. duodenal ulcer

(a) Prandial pain
(b) Wt change
(c) Association w/ H. pylori
(d) Secondary cause
(e) Risk of carcinoma
(f) Biopsy finding

A

Gastric ulcer

(a) Pain greater w/ meals
(b) Prandial pain => wt loss
(c) 70% cases have H. pylori infxn
(d) NSAIDs
(e) Elevated risk of carcinoma
(f) Do biopsy to see margins and r/o malignancy

Duodenal ulcer

(a) Pain decreased w/ meals
(b) Meal decreases pain => wt gain
(c) 100% association w/ H. pylori
(d) Zollinger-Ellison syndrome
(e) Generally benign
(f) Hypertrophy of Burnner glands

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5
Q

Explain the features of CREST syndrome

A

CREST syndrome = limited cutaneous form of systemic sclerosis (multi-system CT d/o)

  • Calcinosis: calcium deposition in the skin causes thickening/tightening
  • Raynaud’s: often one of the first manifestations, exaggerated vasoconstriction
  • Esophageal dysmotility: causing dysphagia to solids
  • Sclerodactyly = localized thickening/tightness of fingers or toes
  • Telangiectasias = dilated capillaries
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6
Q

What is the most important pancreatic enzyme for protein digestion?

(a) Fxn
(b) Activation (catalyzed by which enzyme?) and location of activation

A

Trypsinogen is the key protease

(a) Trypsinogen –> trypsin, then trypsin activates the other proteases (chymotrypsin and elastase) and positive feedbacks on itself to cleave more trypsinogen
(b) Trypsinogen converted into trypsin by enterokinase contained on the brush border of the duodenum and jejunum

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7
Q

Infant p/w bilious vomiting and gastric distention, see double bubble on Xray

(a) Dx?
(b) Associated condition

A

(a) Dx = duodenal atresia- failure of small bowel to recanalize during development
(b) Associated w/ Downs syndrome

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8
Q

Gastric acid from parietal cells

(a) Name 2 things that stimulate secretion
(b) Name 4 hormones that inhibit secretion

A

Gastric acid secretion by parietal cells

(a) Stimulated by histamine, ACh, and gastrin (mainly gastrin)
(b) Gastric acid secretion inhibited by: somatostatin, secretin, GIP (gastrin inhibitory peptide), prostaglandin

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9
Q

Most specific serum maker for

(a) Acute pancreatitis
(b) Wilson disease
(b) Liver/biliary disease over bone disease

A

Serum marker

(a) Lipase is more specific than amylase for acute pancreatitis
(b) Wilson disease: low ciruloplasmin (serum Cu-carrying protein)
(c) GGT is elevated in liver/biliary and NOT bone disease, while Alk phos can be elevated in both

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10
Q

Adverse events of omeprazole

A

Omeprazole (PPI) can increase risk of C. Dif and pneumonia

-can also cause hypomagnesemia w/ long term use

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11
Q

What is achalasia?

(a) Distinguishing clinical feature
(b) Loss of what innervation?
(c) Increased risk of what malignancy?
(d) Diagnostic test and finding
(e) Possible infectious cause of secondary achalasia

A

Achalasia = failure of LES to relax

(a) Dysphagia to both liquids and solids, not just solids like obstruction
(b) Loss of Auerbach plexus (btwn muscle layers of the walls of the LES)
(c) Increased risk of esophageal squamous cell carcinoma
(d) Bird’s beak phenomenon on barium swallow
(e) Chagas disease (T. cruzi infection)

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12
Q

Which stain can identify hemochromatosis on liver biopsy

A

Hemosiderin (Fe) deposition stains under Prussian blue stain

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13
Q

Direct vs. indirect inguinal hernia

(a) through deep inguinal ring
(b) thru superficial inguinal ring
(c) covered by all 3 layers of spermatic fascia
(d) seen in older men

A

Inguinal hernias

(a) Only indirect inguinal hernias go thru the deep inguinal ring
(b) Both indirect and direct inguinal hernias come out the superficial inguinal ring
(c) Indirect inguinal hernias descent in the same path of the testes => are covered by all 3 layers of spermatic fascia
- while direct inguinal hernias are only covered by external spermatic fascia
(d) Direct seen in older men (2/2 wall weakening), while indirect are more likely to be seen in younger children (2/2 failure of transversalis fascia to fuse)

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14
Q

Describe the Pringle maneuver used in trauma to control bleeding

A

Pringle maneuver = clamping of the hepatoduodenal ligament to clamp the portal triad (CBD, portal vein, proper hepatic artery) to prevent someone from bleeding out of their liver
-obvs a rather temporizing measure until get to the OR

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15
Q

Differentiate true vs. false diverticulum

(a) Give an example of each

A

True diverticulum is when all 3 layers of the gut wall outpouch
(a) Meckels

Pseudodiverticulum (false) is when only the mucosa and submucosa (not muscularis) outpouch
(a) Zenkers

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16
Q

Crohns vs. UC

(a) Location
(b) Transmural inflammation
(c) Granulomas
(d) Pseudopolyps
(e) Higher risk of obstruction
(f) Association w/ PSC
(g) More likely to have bloody diarrhea

A

Crohns vs. UC

(a) Chrons MC terminal ileum but can be anywhere, UC always involving rectum
(b) Transmural inflammation in Crohns
(c) Noncaseating granulomas in Crohns
(d) Pseudopolyps in UC
(e) Higher risk of obstruction in Crohns (transmural inflammation => strictures)
(f) UC is associated w/ primary sclerosing cholangitis
(g) UC => bloody diarrhea

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17
Q

Zenker diverticulum

(a) Clinical features
(b) Typical age group

A

Zenker diverticulum = pharyngoesophageal false diverticulum

(a) Halitosis (bad breath from trapped food), dysphagia, obstruction
(b) MC in elderly males

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18
Q

Clinical presentation of gastrinoma

A

Gastrin = hormone that stimulates gastric acid secretion by parietal cells => chronic elevation in gastrin (2/2 gastrinoma) causes medically refractory gastric ulcers

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19
Q

What is the remnant of the fetal umbilical vein?

(a) Part of what ligament?

A

Fetal umbilical vein => ligamentum teres hepatis which is contained within the (a) falciform ligament = connects liver to the anterior abdominal wall

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20
Q

Fxn of secretin from duodenal S-cells

A

Secretin works to stimulate pancreatic release of bicarb, b/c bicarb needed to neutralize duodenal lumen so pancreatic enzymes have basic environment in which to work

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21
Q

2 manifestations of alpha-1 antitrypsin deficiency

A
  1. Panacinar emphysema 2/2 uninhibited elastase in lungs

2. Cirrhosis due to deposition of abnormally folded proteins in the hepatocellular ER

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22
Q

What are anal fissures?

(a) Location- anterior or posterior?
(b) Relationship to pectinate line
(c) Clinical features

A

Anal fissures = tear in anal mucosa

(a) Posteriorly b/c that is where perfusion is worse
(b) Below the pectinate line
(c) Pain w/ pooping, blood on the TP

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23
Q

Main mechanism by which Peyer’s patches work to

A

IgA!!! ‘secretory’ IgA

Peyer’s patches contain specialized M-cells that present antigens to immune cells, activated B cells differentiate into IgA secreting cells
-then IgA is transported across epithelium into the gut lumen to deal with intraluminal antigen

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24
Q

What is ileus?

(a) Tx

A

Ileus = intestinal hypomotility w/o obstruction

a) Treat w/ bowel rest, electrolyte correction, and cholinergic drugs (pro-motility agents

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25
Q

Name 2 fxns of bile in addition to fat digestion/absorption

A
  1. Cholesterol excretion- this is the body’s only way of secreting cholesterol
  2. Antimicrobial- disrupts microbe membranes

(also for fat-soluble vitamins but that goes w/ fat absorption)

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26
Q

Differentiate true vs. false diverticulum

A

True diverticulum (ex: Meckel) is when all 3 layers of the gut wall outpouch

Pseudodiverticulum (false) is when only the mucosa and submucosa (not muscularis) outpouch

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27
Q

Hirschsprung disease

(a) What is it?
(b) Associated mutation
(c) Clinical features
(d) Tx

A

Hirschsprung disease

(a) Congenital megacolon- lack of enteric nervous plexus in a segment of the colon 2/2 failure of neural crest cell migration
(b) Associated w/ mutations in RET gene
(c) Clinically: bilious emesis, abdominal distention, chronic constipation
(d) Bowel segment resection

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28
Q

Receptor responsible for

(a) Absorbing glucose into enterocyte
(b) Absorbing galactose into enterocyte
(c) Absorbing fructose into enterocyte
(d) Secreting monosacharrides into blood stream

A

Receptor on enterocytes

(a) Absorb glucose in = SGLUT1 (Na+ dependent)
(b) Absorb galactose = SGLUT1 (Na+ dependent)
(c) Absorb fructose = GLUT5
(d) All 3 monosaccharides get into bloodstream by GLUT2

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29
Q

Onadestron

(a) Mechanism
(b) Fxn
(c) Toxicity

A

Onadestron = Zofran

(a) 5-HT3 antagonist, decreases vagal tone and works centrally as a powerful anti-emetic
(b) Nausea
(c) Prolonged QT, HA, constipation

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30
Q

Analog of what hormone is used in tx of acromegaly? (and why)

A

Somatostatin (hormone) from D-cells of pancreatic islets inhibit growth hormone (as well as insulin and glucagon secretion)

So octreotide (somatostatin analogue) used in tx of acromegaly (excess GH)

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31
Q

Composition of gallstones

(a) MC
(b) Other

A

(a) 80% of gallstones are cholesterol
- radiolucent (white on Xray) b/c of calcification
- dx w/ US

(b) Others are pigment stones

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32
Q

Indication of sulfasalazine

A

Sulfasalazine = combo antibacterial and anti-inflammatory used in UC, Crohns, and RA

-Anti-inflammatory that is less immunosuppressive than corticosteroids

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33
Q

Meckel diverticulum

(a) What is it?
(b) Complications
(c) Location, age of onset

A

Meckel diverticulum

(a) Persistence of vitelline duct causing true diverticulum
(b) Melena, intussusception, volvulus, obstruciton
(c) 2 inches long, 2 ft from the ileocecal valve, 2% of the population, presents in first 2 years of life

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34
Q

Conjugated or unconjugated hyperbilirubinemia?

(a) Dubin-Johnson
(b) Gilbert
(c) Crigler-Najjar
(d) Rotor syndrome
(e) Phsyiologically in newborns
(f) Pancreatic cancer
(g) Liver fluke

A

Unconjugated (indirect)

  • Gilbert, Crigler-Najjar
  • Phsyiologic

Conjugated (direct)

  • Dubin-Johnson, Rotor
  • Pancreatic cancer (or any obstructive cause)
  • Liver fluke
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35
Q

Clinical triad of hemochromatosis

A
  • cirrhosis
  • diabetes mellitus
  • skin pigmentation

‘bronze diabetes’

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36
Q

Key characteristics of Wilson disease

A
  • low serum ceruloplasmin (Cu-binding protein)
  • cirrhosis, increased risk of HCC
  • corneal deposits = Kayser-Fleischer rings
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37
Q

What is a Krukenberg tumor?

(a) MC cause

A

Krukenberg tumor = b/l mets to the ovaries

(a) MC cause = gastric adenocarcinoma

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38
Q

Fxn of intrinsic factor

A

Intrinsic factor secreted by parietal cells (same ones that secrete gastrin) in stomach bind B12 and allow it to be absorbed in the terminal ileum

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39
Q

MC source of blood in a bleeding gastric ulcer

A

Left gastric artery

-L gastric bleeds when a gastric ulcer on the lesser curvature of the stomach bleeds

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40
Q

Peyer’s patch- what are they?

(a) Present in what layers of the gut wall?
(b) Fxn of M-cells

A

Peyer’s patch = unencapsulated aggregate of lymphoid tissue in the gut wall

(a) In the lamina propria and submucosa of the ileum
(b) Peyer’s patches contain specialized M-cells that present antigens to immune cells

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41
Q

Management for inguinal vs. femoral hernias

A

Inguinal can potentially be non-operable if they’re asymptomatic (b/c then very minimal risk of bowel incarceration)

While femoral hernias always need surgical management 2/2 risk of bowel incarceration

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42
Q

Complications of congenital malrotation

A

Anomaly of midgut rotation => improper bowel position and formation of Ladd bands (fibrous bands)

Can lead to volvulus (bowel twisting on its mesentery/blood supply) and obstruction

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43
Q

Complications of volvulus

(a) Type in children vs. elderly

A

Volvulus (bowel twisting on its mesentery/blood supply) => obstruction and infarction

(a) Midgut volvulus seen in children, sigmoid volvulus seen in elderly

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44
Q

Two clinical features of pyloric stenosis

A
  • non-bilious projective vomiting around 2-6 wks of life

- ‘olive’ shaped palpable mass in the abdomen

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45
Q

MC location for diverticulum

A

Sigmoid colon

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46
Q

Which 3 carbohydrate molecules can be absorbed by enterocytes?

A

Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes

=> break all other larger carbs down to these building blocks

47
Q

Crohns vs. UC

(a) Cobblestone mucosa
(b) Creeping fat w/ bowel wall thickening
(c) Loss of haustra
(d) Association w/ erythema nodosum
(e) Association w/ gallstones

A

Crohns vs. UC

(a) Cobblestoning = Crohns
(b) Creeping fat w/ bowel wall thickening = Crohns
(c) Loss of haustra = UC
(d) Both are associated w/ erythema nodosum
(e) Crohns associated w/ increased risk of gallstones

48
Q

How can acute pancreatitis lead to impaired calcium homeostasis ?

A

Ca2+ collects in pancreatic Ca2+ soap deposits

-in lifequfactive necrosis of pancreatic parenchyma

49
Q

Somatostatin

(a) Secreted by what
(b) Fxn
(c) Positive regulator
(d) Negative regulator

A

Somatostatin = basically shuts down digestion

(a) Secreted by D-cells of pancreatic islets
(b) Fxns to decrease gastric acid/pancreatic/and intestinal fluid secretion, decreases GB contraction, decrease both insulin and glucagon secretion

(c) Somatostatin stimulated by acid
- negative feedback regulator

(d) Somatostatin inhibited by vagal tone
- when in rest and digest mode you want to inhibit hormone that depresses digestion

50
Q

Clinical presentation of diverticulitis

(a) 2 complications and their manifestations

A

Diverticulitis => LLQ pain, fever, leukocytosis (‘left sided appendicitis’ b/c overlapping clinical presentation

(a) Complications
- perforate => free air in abdomen (see on CXR w/ air under diaphragm)
- fistulize, possibly w/ bladder (colovesical fistula) => pneumaturia

51
Q

Hormone/product of the following GI cells

(a) Parietal cells
(b) Mucus cells
(c) D cells
(d) K cells
(e) I cells
(f) Chief cells
(g) S cells
(h) G cells
(i) ECL cells

A

GI cell products

(a) Parietal cells secrete gastric acid (H+) and intrinsic factor
(b) Mucus cells secrete bicarb
(c) D cells secrete somatostatin
(d) K cells secrete GIP (gastric inhibitory peptide)
(e) I cells secrete CCK to stimulate pancreatic juice secretion
(f) Chief cells secrete pepsinogen (activated to pepsin)
(g) S cells secrete secretin (activate duodenal cell release of HCO3-)
(h) G cells release gastrin that indirectly stimulate parietal cells to secrete more acid
(i) ECL cells are stimulated by gastrin and release histamine to activate parietal cell acid secretion

52
Q

Metoclopramide

(a) Mechanism of action
(b) Tox
(c) Contraindications

A

Metoclopramide = Reglan

(a) D2 receptor antagonist to increase upper GI contractility/motility
(b) Parkinsonian effect
(c) Contraindicated in SBO and Parkinson due to D1 receptor blockade

53
Q

Differentiate the 2 outward layers of the gut wall intra vs. retroperitoneal

A

Intraperitoneally

Retroperitoneal parts of the GI tract = parts 2,3,4 of duodenum, ascending and descending colon
-outermost layer is adventitia

54
Q

What two types of polyps increase risk of CRC?

(a) Which two don’t?

A

Adenomatous and serrated polyps increase risk

(a) While hyperplastic and hamartomatous are non-neoplastic

55
Q

Clinical presentation of diverticulitis

(a) 2 complications and their manifestations

A

Diverticulitis => LLQ pain, fever, leukocytosis (‘left sided appendicitis’ b/c overlapping clinical presentation

(a) Complications
- perforate => free air in abdomen (see on CXR w/ air under diaphragm)
- fistulize, possibly w/ bladder (colovesical fistula) => pneumaturia

56
Q

Differentiate indirect and direct bilirubin

(a) Location
(b) Conjugation
(c) Water solubility
(d) How does bilirubin travel in the bloodstream?

A

RBC –> Heme –> Indirect bilirubin

(a) Inside macrophage
(b) Unconjugated
(c) Water insoluble

(a) In the liver bilirubin is (b) conjugated into direct
(c) Water soluble

(d) Travels bound to albumin as unconjugated bilirubin-albumin complex when going btwn macrophage and liver

57
Q

What cells secrete CCK?

(a) Fxn of CCK
(b) Positive regulator of CCK
(c) Mechanism of CCK activity

A

CCK secreted by I cells of the duodenum and jejunum (proximal small intestines)

(a) CCK stimulates pancreatic juice secretion and gall bladder contraction
- also inhibits gastric emptying
(b) CCK activated by FFA and amino acids in the duodenal lumen
(c) CCK works on pancreas via neural muscarinic pathways

58
Q

Differentiate Boerhaave and Mallory-Weiss

(a) Key feature

A

Boerhaave syndrome = transmural (full thickness) tear in esophagus from violent wretching

(a) Pneumomediastinum
- this is a surgical emergency

Mallory-Weiss = esophageal tear, not transmural (so no pneumomediastinum)
(a) Hematemesis

59
Q

Triad of Plummer-Vinson syndrome

A

“plumbers DIE”

  • dysphagia
  • iron-deficiency anemia
  • esophageal web
60
Q

Differentiate clinical presentation of left vs right sided colon cancer

A

Left sided present w/ obstruction

Right sided present w/ blood in stool, maybe even iron deficiency anemia

61
Q

Differentiate Dubin-Johnson and Rotor syndromes

A

Both are hereditary causes of hyperbilirubinemia and both are benign

DJ causes a grossly black liver
Rotor is even milder and does not cause black liver

62
Q

Primary sclerosing cholangitis

(a) ERCP appearance
(b) Typical demographic
(c) Associated conditions
(d) Molecular markers
(e) Increased risk of what malignancy

A

PSC

(a) Beads on a string alternating strictures and dilations of both intra and extra hepatic bile ducts
(b) Young men w/ IBD
(c) UC
(d) Hyper-IgM, p-ANCA, MPO-ANCA
(e) Increased risk of cholangiocarcinoma

63
Q

Fxn of chief cells in the stomach

(a) Involvement of H+

A

Chief cells release pepsinogen which is (a) activated from proenzyme into active enzyme (pepsin) by H+

Fxn of pepsin = digestion of proteins in the stomach

64
Q

What is a Sister Mary Joseph nodule?

A

Palpable nodule/node bulging into the umbilicus from mets of malignant cancer in the pelvis or abdomen

Most often from gastric cancer, colon cancer, or pancreatic cancer

65
Q

2 MC causes of pancreatitis

A

EtOH and gallstones

66
Q

Serum marker for CRC

A

CEA tumor marker- monitoring for recurrence (not for screening)

67
Q

Describe 2 key parts of the embryologic development of the midgut

(a) Week 6
(b) Week 10

A

(a) Week 6- midgut herniates thru the umbilical ring
- failure to come back in may => omphalocele

(b) Week 10- midgut returns to the abdominal cavity and rotates around the SMA
- defective => malrotation

68
Q

Orlistat

(a) Mechanism of wt loss
(b) Side effects/toxicity

A

Orlistat

(a) Inhibits gastric and pancreatic lipase => decreases breakdown and absorption of dietary fat
(b) Steatorrhea, decreased absorption of fat-soluble vitamins

69
Q

Buzzword dx for pt presenting w/ painless jaundice

A

Tumor of the pancreatic head (that compresses the CBD)

70
Q

FAP vs. Lynch syndrome

(a) Mutation
(b) Risk of progression to CRC

A

FAP = familial adenomatous polyposis

(a) Mutation in APC tumor suppressor gene on chrom 5
(b) 100% progress to CRC => ppx remove colon before 20

Lynch syndrome

(a) Microsatellite instability = mutation in DNA repair enzyme
(b) 80% to CRC

71
Q

Mechanism by which NSAIDs can increase risk of gastric ulcers

(a) Protective tx

A

NSAIDs inhibit PGE1 synthesis, PGE1 stimulates increased production and secretion of mucosal barrier in the stomach

(a) Misoprostol = PGE1 analog that can be given w/ NSAID to prevent NSAID-induced ulcers

72
Q

Below the pectinate line

(a) Pain of hemorrhoids
(b) Innervation
(c) Type of cancer that develops
(d) Arterial supply

A

Below the pectinate line (ectoderm)

(a) Hemorrhoids are painful when thrombosed b/c somatically innervated
(b) inferior rectal branch of the pudendal nerve
(c) Squamous cell carcinoma
(d) Inferior rectal artery from the internal pudendal artery

73
Q

Explain why same load of glucose orally will cause more insulin secretion that IV load

A

Oral load stimulates release of GIP (gastric inhibitory peptide) which stimulates insulin secretion

While IV load won’t stimulate K-cells of small intestines to release GIP => one less positive regulator of insulin on board

74
Q

Misoprostol- mechanism

Functions

(a) 1 GI
(b) 1 Peds/GYN

A

Misoprostol = PGE1 analog

(a) Stimulate mucus barrier and decreased acid production in the stomach, can be given w/ NSAIDs to prevent NSAID-induced gastric ulcers
(b) Misoprostol to keep PDA patent, also can be given to induce labor

75
Q

Charcot triad of clinical features of cholangitis

A

RUQ pain, jaundice, fever

76
Q

Name the blood supply and parasympathetic innervation to the

(a) Foregut
(b) Midgut
(c) Hindgut

A

(a) Foregut: celiac trunk, vagus nerve
(b) Midgut: SMA, vagus nerve
(c) Hindgut: IMA, pelvic splanchnic (S2,3,4)

77
Q

Where in the GI tract are the following absorbed

(a) Iron
(b) B12
(c) Folate
(d) Bile acids
(e) Surgery in which this becomes very relevant

A

Nutrient/mineral absorption

(a) Iron absorbed as Fe2+ in the duodenum
(b) B12 terminal ileum
(c) Folate in small bowel
(d) Bile acids in terminal ileum
“Iron first bro”
(e) This becomes clinically relevant in small bowel resections, where you have to replace depending on which part of bowel is removed

78
Q

Gastrin

(a) Secreted by what?
(b) Fxn of hormone
(c) Pathologically elevated in what two disease states?
(d) Stimulated by what 2 things
(e) Mechanism of activity

A

Gastrin

(a) G-cells in the antrum of the stomach and duodenum
(b) Fxns to stimulate gastric acid secretion by parietal cells
(c) Elevated in Zollinger-Ellison and H. pylori (and gastrinoma)
(d) Gastrin secretion increases in response to vagal innervation (rest and digest) and by gastric distention (bolus of food)
(e) Stimulates parietal cells indirectly by activating ECL (enterochromaffin-like cells) to release histamine

79
Q

What is CREST syndrome?

(a) Antibodies present
(b) Key difference from systemic version

A

CREST syndrome = limited cutaneous form of systemic sclerosis (multi-system CT d/o)

(a) Anti-centromere antibodies
(b) Less commonly see kidney involvement (which is often seen in systemic sclerosis)

80
Q

Why should aspirin be avoided in children?

A

Risk of Reye syndrome- rare but often fatal childhood hepatic encephalopathy when viral infection is tx w/ aspirin

81
Q

Primary biliary cirrhosis

(a) Etiology
(b) Typical demographic
(c) Associated conditions
(d) Molecular marker

A

PBC

(a) Autoimmune rxn causing destruction of intralobular bile ducts
(b) Middle-aged F
(c) Other AI d/o: CREST, Sjogren, RA, celiac
(d) Anti-mitochondrial antibody

82
Q

Cause of esophagitis when on scoping you see

(a) White pseudomembranes
(b) Punched-out ulcers
(c) Linear ulcers

A

Esophagitis etiology

(a) White pseudomembranes = candida
(b) Punched-out ulcers = HSV-1
(c) Linear ulcers = CMV

83
Q

Above the pectinate line

(a) Pain of hemorrhoids
(b) Type of cancer that develops
(c) Arterial supply

A

Above the pectinate line (hindgut endoderm)

(a) Hemorrhoids are painless b/c there is only visceral innervation
(b) Adenocarcinoma (glandular derivative)
(c) Superior rectal artery (from IMA)

84
Q

What area is a watershed btwn the SMA and IMA blood supply?

A

Splenic flexure

85
Q

MC type of gastric cancer

A

Gastric adenocarcinoma

86
Q

Define the pectinate line

A

Pectinate line = where the endoderm of the hindgut meets ectoderm

87
Q

Mechanism of physiologic neonatal jaundice

(a) Tx

A

Physiologic neonatal jaundice = immature UDP-glucoronosyltransferase => indirect/unconjugated hyperbilirubinemia

(a) Phototherapy to converted unconjugated –> conjugated (water soluble form)

88
Q

MC location of intussusception

(a) Clinical hallmarks

A

Commonly at the ileocecal jxn

(a) current jelly stools, intermittent abdominal pain

89
Q

Esophageal squamous cell vs. adenocarcinoma

(a) MC
(b) Location
(c) RF

A

Squamous cell carcinoma

(a) MC worldwide
(b) Upper 2/3 of esophagus
(c) RF: EtOH, diverticula (Zenker’s), esophageal web (Plummer’s), hot liquids

Adenocarcinoma

(a) MC in America
(b) Distal 1/3 of esophagus
(c) RF: GERD, obesity, Barrett’s

90
Q

Breakdown where the glucose energy is used in a RBC

A

RBC can only use glucose for energy! Can’t even use ketones like the brain

  • 90% used in glycolysis (only do anaerobic metabolism)
  • 10% used in HMP shunt (remake NADPH to detox H2O2 to glutathione)
91
Q

Main site of platelet storage in the body

(a) Lifespan of platelet
(b) Contents of dense granules vs. alpha granules

A

1/3 of the body’s plts are stored in the spleen

(a) Plts last 8-10 days
(b) Dense granules contain ADP and Ca2+

Alpha granules contain vWF and fibrinogen

92
Q

Platelet receptors for

(a) vWF
(b) Fibrinogen

A

Plt receptors for

(a) Adhesion to exposed collagen = plt Gp1b binds to vWF
(b) Aggregation of plts via fibrinogen binding to multiple plt’s Gp2b3a

93
Q

D/o where on histology you see

(a) Neutrophils w/ more than 5 lobes
(b) Increased number of immature neutrophils

A

Histologic abnormalities of neutrophils

(a) Hypersegmented neutrophils seen in folate and vitamin B12 deficiency
- b/c DNA synthesis is limited, so essentially cells divide one less time

(b) Increased blasts in leukemias
- over 20% blasts indicates acute leukemia

94
Q

Macrophages

(a) Derived from what cells?
(b) Activated by what factor?
(c) Lifespan

A

Macrophages

(a) Come from monocytes
(b) Activated by interferon gamma from Th4 helper-T cells
(c) Long lifespan once inside tissue

95
Q

Indication of RhoGAM

(a) When to give during pregnancy

A

RhoGAM prevents maternail production of anti-Rh IgG

(a) Give during third trimester to Rh- mother w/ potential of Rh+ baby, want to prevent production of anti-Rh IgG b/c these IgG (not IgM) can cross placenta in future pregnancies and cause hemolytic disease of the newborn (erythroblastosis fetalis)

96
Q

How does factor V Leiden mutation cause disease?

A

Factor V Leiden mutation produces a factor V (common pathway) that is resistant to inhibition by activated protein C (anticoagulant)

97
Q

Activity in thrombogenesis of ristocetin

A

Ristocetin activates vWF binding to Gp1b, so failure for blood to agglutinate in a ristocetin assay = von Willebrand disease (absent vWF) and Bernard-Soulier syndrome (Gp1b deficiency)

98
Q

Activity in thrombogenesis of ristocetin

A

Ristocetin activates vWF binding to Gp1b, so failure for blood to agglutinate in a ristocetin assay = von Willebrand disease (absent vWF) and Bernard-Soulier syndrome (Gp1b deficiency)

99
Q

Differentiate Hb barts and HbH seen

A

Both are abnormal Hb seen in alpha thalassema

Hb barts seen when all 4 alleles of alpha-globin are deleted => gamma chains tetramerize

HbH seen when 3 of 4 copies of alpha globin chain are deleted => excess beta chains form beta tetramers

100
Q

Differentiate the types of alpha-thalassemia trait seen in Asians vs. African populations

A

Alpha-thalassemia can have 1-4 alpha alleles deleted, when 2 alleles are deleted they can be on the same (cis) or opposite (trans) chromosomes

Cis seen in Asian populations (more dangerous for offspring) while trans seen in Africans

101
Q

What dose elevated HbA2 on electrophoresis indicate?

A

HbA2 (alpha2gamma2) production increased when HbA (alpha2beta2) production is defective, see both HbA and HbA2 in beta thalassemia minor (when one beta globin gene is defective)

102
Q

Reversible causes of sideroblastic anemia

A

Sideroblastic anemia (ringed sideroblasts seeing Fe accumulation in macrophages 2/2 defective heme synthesis)

Can be congenital (ALA synthase mutation), acquired, or reversible

Reversible 2/2 alcoholism, liver disease, isoniazid tx causing vit B6 deficiency, vit B6 deficiency (B6 necessary cofactor for ALA)

103
Q

Megaloblastic anemia refracotyr to both vit B12 and folate deficiency

A

Orotic aciduria = AR defect in UMP synthase that blocks conversion of orotic acid to UMP in pyrimidine de novo synthesis

Failure to thrive, developmental delay in child

104
Q

Megaloblastic anemia refracotyr to both vit B12 and folate deficiency

A

Orotic aciduria = AR defect in UMP synthase that blocks conversion of orotic acid to UMP in pyrimidine de novo synthesis

Failure to thrive, developmental delay in child

105
Q

Effect of corticosteroids on neutrophil and eosinophil count

A

Corticosteroids decrease activation of neutrophil adhesion molecules => impaired migration of neutrophils out to sites of inflammation so induces neutrophilia

But corticosteroids also sequester eosinophils in lymph nodes and cause apoptosis of lymphocytes => lymphopenia and eosinopenia despite neutrophilia

106
Q

Type of anemia seen in Pb poisoning (and why)

A

See microcytic anemia (w/ basophilic stippling) in lead poisoning b/c lead inhibits ALA dehydratase (needed for heme synthesis)

107
Q

Type of anemia seen in Pb poisoning (and why)

A

See microcytic anemia (w/ basophilic stippling) in lead poisoning b/c lead inhibits ALA dehydratase (needed for heme synthesis)

108
Q

D/o where antithrombin deficiency is acquired

A

Antithrombin III (ATIII) is filtered than needs to be reabsorbed, in renal failure/nephrotic syndrome ATIII is lost in urine

Decreased ATIII = less inhibition on factors II (thrombin) and X

109
Q

Differentiate FFP from cryoprecipitate

A

FFP replaces coagulation factors (so give in DIC, cirrhosis, immediate warfarin reversal)

While cyroprecipitate contains fibrinogen, factor 9 and 13, vWF, and fibronectin

110
Q

Hodgkin vs. NHL

(a) Constitutional symptoms
(b) Associated w/ EBV
(c) Reed-Sternberg cells
(d) Prognosis

A

(a) Much more likely to see B symptoms (fever, night sweats, wt loss) in Hodgkin
(b) EBV infection associated w/ Hodgkin
(c) Reed-Sternberg cells seen in Hodgkin
(d) Prognosis much better in Hodgkin

111
Q

What is porphyria?

A

Porphyria = defect in porphyrin synthesis (can be congenital, acquired, drug-induced) that causes build up of porphyrins

-mainly affects CNS and skin

MC type = porphyria cutaneous tarda
2nd = acute intermittent porphyria

112
Q

Differentiate the two MC types of porphyria:
porphyria cutaneous tarda vs.
acute intermittent porphyria

A

MC = porphyria cutaneous tarda = blistering or itchiness upon sunlight exposure (blistering photosensitivity)

2nd MC = acute intermittent porphyria
5 P's: most prevalent symptom is painful abdomen 
-port-wine colored urine
-polyneuropathy
-psychological disturbance
-precipitated by drugs
113
Q

Tx for acute porphyria

A

Porphyria = accumulation of porphyrins (some defect in heme synthesis)

Tx = glucose (usually 10% glucose IV infusion) and heme, both of which inhibit ALA synthase which inhibit first step in porphyrin synthesis (so prevent back up)

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