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Step 1 Subjects > GI > Flashcards

GI Flashcards

1
Q

Midgut development

A

6th week: midgut herniates through umbilical ring

10th week: returns to abdominal cavity, rotates around SMA

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2
Q

Apple peel atresia

A

Vascular accident in utero:

  • Intestinal atresia distal to duodenum–> bilous vomit
  • SMA obstruction–> blind end to proximal jejunem, absence of part of small bowel and mesentary
  • Terminal ileum distal to atresia spirals around ileocolic vessel
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3
Q

Hepatoduodenal ligament

A

Connects liver to duodenum

Contains:
- Portal triad= hepatic artery, portal vein, common bile duct

  • *Pringle maneuver= compress ligament between thumb and forefinger to control bleeding
  • Connects greater and lesser sacs
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4
Q

Gastrohepatic ligament

A

Connects: Liver to lesser curvature of stomach

Contains: Gastric arteries

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5
Q

Gastrocolic ligament

A

Connects: greater curvature and transverse colon

Contains: gastroepiploic arteries (some L also contained in gastrosplenic ligament)

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6
Q

Plexi in digestive tract

A

Submucosa (internal)= Meissner’s plexus
- Controls secretory activity

Muscularis externa: Auerbach’s plexus= myenteric nerve plexus
- Controls inner circular and outer longitudinal muscle layers of muscularis externa

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7
Q

Hindgut supply/innervation

A

Artery= IMA

Parasympathetic innervation= Pelvic (vs Vagus for mid and foregut)

Vertebral level= L3

Structures:
- Distal 1/3 of transverse colon to upper portion of rectum

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8
Q

Pectinate (dentate) line in rectum

A

Formed by endoderm (hindgut) meeting ectoderm

Above:

  • Internal hemorrhoids (supplied by superior rectal (portal) and middle/inferior rectal (IVC))
  • Visceral innervation: non-painful hemorrhoids
  • Arterial supply= IMA (superior rectal artery)
  • Adenocarcinoma
  • Drains to deep lymph nodes

Below:

  • External hemorrhoids (painful)
  • Venous: Inferior rectal–> internal pudendal–> internal iliac–> IVC
  • Arterial= internal pudendal (inferior rectal artery)
  • Squamous cell carcinoma
  • Drains to superficial inguinal nodes
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9
Q

Hepatic zones

A

Zone 1= first affected by viral hepatitis

Zone 3= portal vein/hepatic artery—> venous drainage to hepatic vain

  • Affected first by ischemia
  • Contains P450 system
  • Sensitive to toxic injury
  • EtOH hepatitis
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10
Q

Direct hernia

A

Thru Hesselbach’s triangle:

- Between inferior epigastric vessels (lateral) and medial umbilical ligament (medial)

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11
Q

Hiatal hernia

A

Sliding= most common
- GE junction displaced (above diaphragm)

Paraesophageal=

  • Normal GE junction
  • Fundus of stomach protrudes into thorax
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12
Q

Gastrin

A

Source:
- G-cells in antrum of stomach

  1. Stimulates ECL (enterochromaffin-like cells) to secrete histamine–> stimulates parietal-cell acid secretion
  2. Stimulates Parietal cell acid release

Stimulated by vagus nerve via GRP (vs Ach to parietal cells)

  • Increased in Zollinger-Ellison syndrome
  • Increased by chronic PPI use
  • Stimulated by Phe, Tryptophan
  • Gastrinoma: can lead to jejunal ulcers, diarrhea, abdominal pain
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13
Q

CCK

A

Source: I cells in duodenum, jejunem

  • increase pancreatic secretion (all types), gallbladder contractions (emptying), relax sphincter of Oddi
  • Decrease gastric emptying
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14
Q

Secretin

A

Source: S cells in duodenum

  • Increases pancreatic bicarb secretion, bile secretion
  • Decreases gastric acid secretions
    • both allow pancreatic enzymes to function

Stimulated by fatty acids in duodenum

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15
Q

Somatostatin

A

Source: D cells in pancreatic islets, gastric mucosa

BLOCKS all the things! (stimulated by acid, blocked by vagal stimulation)
- Anti-growth hormone effects

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16
Q

Glucose-dependent insulinotropic peptide (GIP)

A

Source: K cells in duodenum

  • decrease H+ secretion
  • Increase insulin release (endocrine!)
    • Oral glucose used more rapidly than equivalent by IV due to GIP secretion
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17
Q

Vasoactive intestinal polypeptide (VIP)

A

Source: parasympathetic ganglia in sphincters, gallbladder, small intestine

  • Moves things along in GI system
  • Increases intestinal water, electrolyte secretion
  • Relaxes smooth m., sphincters

Stimulated by distention, vagal stimulation
- Inhibited by adrenergic input

    • VIPoma= non-alpha, non-beta islet cell pancreatic tumor
  • -> watery diarrhea, hypokalemia, metabolic acidosis (and achlorhydria)
    • Treatment= somatostatin
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18
Q

Motilin

A

Source: small intestine

Produces MMCs (increased in fasting state)

** Erythromycin= motilin receptor agonist–> stimulates intestinal peristalsis

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19
Q

Saliva

A

Parotid gland (IX)
Submandibular and sublingual gland (VII)
- Stimulated by sympathetic and parasympathetic activity
- Amylase–> hydrolyzes alpha1,4 linkages–> disaccharides (maltose, alpha-limit dextrins)
- HCO3- –> bacterial acid
- Lipase (also pancreatic)–> digest medium chain triglycerides—> monoglycerides

Hypotonic d/t reabsorption of ions (CFTR protein) but at high flow is isotonic due to decreased time for reabsorption

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20
Q

Chief cells

A

Located in stomach

  • Secrete pepsinogen
  • Converted from pepsinogen–> pepsin by stomach acid
  • -> cleaves polypeptides at aromatic aa sites
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21
Q

Brunner’s glands

A

Duodenal submucosa

Secrete alkaline mucous

Hypertrophied in peptic ulcer disease

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22
Q

Trypsinogen

A

Converted to trypsin (from zymogen)

  • Enterokinase/enteropeptidase (duodenal mucosa enzyme) cleaves trypsin
  • Activated trypsin cleaves more trypsinogen (positive feedback)
    • Inhibited by serum alpha-1-antitrypsin and BPTI (basic-pancreatic trypsin inhibitor)
    • Alcoholic pancreatitis= damage to acinar cell–> abnormal trypsin activation
    • Hereditary pancreatitis= mutation in trypsinogen–> not inhibited by BPTI
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23
Q

Amylase

A

Salivary amylase: starts digestion
- Hydrolyzes alpha-1,4 linkages to yield disaccharides (maltose, alpha-limit dextrans)

Pancreatic amylase:
- Hydrolyzes starch in duodenum: oligosaccharides and disaccharides

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24
Q

Oligosaccharide hydrolases

A

Brush border of intestine: rate-limiting step in carb digestion–> monosaccharides from oligo/di-saccharides

    • Only monosaccharides can be absorbed
  • SGLT1 (Na+-dependent): glucose, galactose
  • GLUT-5: facilitated diffusion of fructose
  • Transport sugar to blood via GLUT-2

**D-xylose absorption test= distinguish GI mucosal damage from other malabsorption problems

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25
Q

Bile

A
  • Bile salts: bile acid conjugated to glycine, taurine
  • Phospholipids
  • Cholesterol
  • Bilirubin (conjugated heme and glucuronic acid via UDP glucuronosyl transferase)
  • Water and ions

** Cholesterol 7-alpha hydroxylase catalyzes rate-limiting step

Functions:

  1. Digest/absorb lipids/fat-soluble vitamins
  2. Cholesterol excretion
  3. Antimicrobial: membrane destruction via emulsification of gram-negative outer membranes
    * * Enterococci + Strep bovis can grow in bile
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26
Q

Cimetidine
Ranitidine
Famotidine
Nizatidine

A

H2-blockers (reversible)–> decreased parietal cell H+ secretion due to decreased histamine stimulation

Tox:

  • Cimetidine= potent inhibitor of P450; antiandrogenic (prolactin–> gynecomastia, impotence, decreased libido); can cross BBB (confusion, dizziness, h/a) and placenta
  • Rantidine + Cimetidine–> decreased renal creatinine excretion
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27
Q

Omeprazole, -prazole

A

Proton pump inhibitors

MOA: irreversible inhibtion of H+/K+ ATPase in stomach parietal cells

Use: ulcers, reflux, Zollinger-Ellison

Tox: increased risk of C. diff (decreased aciditiy), pneumonia
- Hip fractures, decreased Mg+2 with long-term use

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28
Q

Bismuth, sucraflate

A

Bind ulcer base: physical protection
- Allow HCO3- secretion to reestablish pH gradient in mucosa

Use: Ulcer healing, traveler’s diarrhea

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29
Q

Misoprostol

A

PGE1 analog: increases production and secretion of gastric mucous, decreased acid production

Use: prevent NSAID-induced peptic ulcers

  • Maintain PDA
  • Induces labor (but don’t use in pregnant women before this!–> abortifactant)

Tox: diarrhea

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30
Q

Octreotide

A

Somatostatin analog

Use: variceal bleeds, VIPoma, carcinoid tumors

Tox: nausea, cramps, steatorrhea

31
Q

Antacids

A

Can affect absorption, bioavailability, urinary excretion of other drugs: alters gastric, urinary pH, delays gastric emptying
ALL cause hypokalemia

Overuse:

  • Aluminum hydroxide–> constipation, hypophosphatemia, muscle weakness, osteodystrophy, seizures
  • Magnesium hydroxide: diarrhea, hyporeflexia, hypotension, cardiac arrest
  • Calcium carbonate: hypercalcemia, rebound acid increase (can also chelate and decrease effectiveness of other drugs, like tetracycline)
32
Q

Brunner’s glands

A

Submucosal glands in Duodenum

33
Q

Peyer’s patches

A

Lymphoid nodules in lamina propria/submucosa of Ileum

34
Q

Vitamin/mineral absorption

A

Iron= Fe+2 in duodenum

Folate+ Fats= jejunem

B12 + bile acids= ileum

35
Q

ECL cells

A

Enterochromaffin-Like Cells

  1. Vagal stimulation (+Phe, Tryptophan) to G cells–> gastrin released into circulation
  2. Parietal cell direct stimulation (CCKb receptor) and ECL stimulation
  3. ECL cells–> histamine–> H2 receptor on parietal cell–> acid
36
Q

Gastric parietal cell

A

Directly stimulated by:

  1. Gastrin (via vagus stimulation of G cell)–> CCKb receptor
    - Activates Gq–> IP3
  2. Vagal stimulation–> M3 receptor
    - Activates Gq–> IP3
  3. Histamine (via ECL cell)–> H2 receptor
    - Activates cAMP production

Inhibited by:

  1. Prostaglandins/misoprostol
    - Gi–> inhibition of cAMP
  2. Somatostatin
    - Gi–> inhibition of cAMP

Lumen side: Cl- channel and H+/K+ ATPase (proton pump)

37
Q

Pancreatic secretions

A

Isotonic fluid (same K+/Na+ as serum)

  • Low flow–> increased Cl- (pumped out)
  • High flow–> increased HCO3- (stomach emptying acidic contents into duodenum offset by bicarb)
38
Q

Unconjugated bilirubin

A

Indirect bilirubin= 0.8 of bilirubin (vs 0.2 direct)

  • Breakdown product of heme
  • Elevated–> black pigment gallstones due to hemolysis

Bacteria contain beta-glucuronidase–> breaks down conjugated–> unconjugated bilirubin
- Brown pigment stones

39
Q

Conjugated bilirubin

A

Direct bilirubin (water soluble)

  • Unconjugated bilirubin taken up from bloodstream (bound to albumin)- passive
  • Converted to conjugated by UDP glucuronosyl-transferase
40
Q

Urobilinogen

A

Liver-excreted direct bilirubin converted by gut bacteria to urobilinogen

  • 80% excreted in feces
  • 20% moves to either: enterohepatic circulation (90%), or kidney (10%- yellow color to urine)
41
Q

Osmotic laxatives

A

Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose
- Osmotic: draw water into colon

Treatment for constipation

42
Q

Infliximab

A

Monoclonal ab to TNF-alpha

Use: crohn’s, UC, RA

Tox: infection (reactivate latent TB), fever, hypotension

43
Q

Sulfasalazine

A

Sulfapyridine (antibacterial) and 5-ASA (antiinflammatory)
- Activated by colonic bacteria

Use: UC, Crohn’s, mild RA

Tox: malaise, nausea, sulfonamide toxicity, reversible oligospermia

44
Q

Ondansetron

A

5-HT3 antagonist; acts on CTZ trigger zone in dorsal medulla (antiemetic)

Use: post-op N/V, chemotherapy

Tox: H/A, constipation

45
Q

Metoclopramide

A

D2 receptor antagonist (increases resting tone, contractility, LES tone, motility)
- No influence on colon transport time

Use:

  • Diabetic, post-op gastroparesis
  • Antiemetic

Tox:

  • Increased parkinson effects (contraindicated in Parkinson’s disease)
  • Restlessness, drowsiness, fatigue, depression, Nausea, diarrhea
  • Drug interaction with digoxin and diabetic patients
  • Contraindicated in small bowel obstruction
46
Q

Whipple’s disease

A

Tropheryma Whipplei infection
- Foamy PAS-positive macrophages in intestinal lamina propria, mesenteric nodes

Presentation:

  • Cardiac, arthralgias, neurologic symptoms
  • Older men
  • Malabsorption
47
Q

Abetalipoproteinemia

A

Decreased synthesis of ApoB

  • -> inability to generate chylomicrons in intestine
  • -> decreased cholesterol, VLDL in bloodstream
  • -> fat accumulation in enterocytes

Early childhood presentation: malabsorption, neurologic disease

48
Q

Intestinal stomach cancer

A

Associated with:

  • H. pylori infection
  • Dietary nitrosamines (smoked food)
  • Chlorhydria
  • Chronic gastritis
  • Type A blood

Seen on lesser curvature: ulcer with raised margins

Signs:

  • Virchow’s node (L supraclavicular)
  • Sister Mary Joseph nodule (subcutaneous periumbilical mets)
49
Q

Diffuse stomach cancer

A

NOT associated with H. pylori

Histo:

  • Signet ring cells (mucin pushes nucleus to periphery)
  • Stomach wall= thickened, leathery (linitis plastica)

Signs:

  • Virchow’s node (L supraclavicular)
  • Sister Mary Joseph nodule (subcutaneous periumbilical mets)
  • Krukenberg’s tumor= bilateral mets to ovaries (abundant mucus, signet ring cells)
50
Q

H. pylori therapy

A

Triple: PPI, Clarithromycin, Metronidazole/amoxicillin

Quad: PPI, bismuth subsalicylate, metronidazole, tetracycline

51
Q

Ulcer vs erosion

A

Ulcer= penetrates into (not thru) submucosa

Erosion= does not extend thru muscularis mucosa
- Acute erosions= NSAID, surgical stress, Cushing/Curling, smoking EtOH

52
Q

Ulcer complications

A

Hemorrhage:

  • Gastric, duodenal (posterior > anterior)
  • Ruptured gastric ulcer= lesser curvature (bleed from L gastric artery)
  • Posterior duodenal ulcer–> gastroduodenal artery

Ulcer: Duodenal (anterior > posterior)

53
Q

Infectious diarrhea: microbe inoculum

A 
Lowest:
- Giardia (few)
- Entamoeba, Campylobacter jejuni, Shigella (~200)
- Clostridium perfringens (~500)
- Vibrio parahaemolyticus (~10^6)
- Salmonella (10^7)
- ETEC (10^9)
Highest
54
Q

Meckel’s diverticulum

A

Five 2’s: 2 inches long, 2 feet from ileocecal valve, 2% population, 2 years, 2 types of epithelia

True diverticulum

  • Persistance of vitelline duct
  • May contain ectopic gastric/pancreatic mucosa (secrete acid)

Symptoms:

  • melena (young children)
  • RLQ pain
  • Intususception
  • Volvulus
  • Terminal ileum obstruction

Diagnosis:
Pertechnetate study for ectopic uptake

55
Q

Angiodysplasia

A

tortuous dilation of vessels–> hematochezia
- Cecum, terminal ileum, ascending colon

Seen in elderly
- Confirm with angiography

56
Q

Adenomatous polyp

A

Precancerous (precursor to CRC)
- Malignancy associated with size, histology, dysplasia of epithelium

Symptoms:

  • Asymptomatic
  • Lower GI bleed
  • Partial obstruction
  • Mucous secretory diarrhea
57
Q

Hyperplastic polyp

A

Non-neoplastic

- 50% in rectosigmoid colon

58
Q

Juvenile polyposis

A

Sporadic lesions in children < 5 years (80% in rectum)
- NOT malignant if SINGLE

Juvenile polyposis syndrome= multiple juvenile polyps in GI tract–> increased risk of adenocarcinoma

59
Q

Peutz-Jeghers

A

Single polyp= not malignant

Peutz-Jeghers= AD syndrome, multiple nonmalignant hamartomas (can bleed, cause intussiception)
- Hyperpigmented mouth, LIPS, hands, genitalia

Mutation in serine/threonine kinase 11 (STK11) on Chromosome 19
- Increased risk of CRC, other malignancies

60
Q

Familial adenomatous polyposis (FAP)

A

AD mutation of APC on chromosome 5q

  • 2 hit hypothesis
  • 100% progress to CRC
  • 1000s of polyps, pancolonic, always in rectum

Gardner’s= FAP + osseous, soft tissue tumors, congenital hypertrophy of retinal pigment epithelium

Turcot’s syndrome= FAP + malignant CNS tumor

61
Q

Hereditary nonpolyposis coloretal cancer (HNPCC/ Lynch syndrome)

A

AD mutation in MSH2 (DNA mismatch repair gene)

  • 80% progress to CRC
  • ALWAYS in proximal colon
62
Q

Site of colorectal cencer

A

Rectosigmoid > Ascending > Descending

  • Ascending= exophytic mass, iron deficiency anemia, weight loss (right colon has larger diameter- less likely to see obstruction)
  • Descending= infiltrating mass, partial obstruction, colicky pain, hematochezia

** Rare presentation with strep bovis

CEA good for monitoring recurrence (not good screening test)

63
Q

APC/beta-catenin (chormosomal instability pathway of CRC

A

Normal colon–>
Loss of APC–> At-risk colon
- APC maintains low beta-catenin (oncogenic), and intracellular adhesion
- Decreased intracellular adhesion, increased proliferation (seen in all sporadic, most familial CRC)
- See tubulovillous adenomatous polyps

Loss of k-RAS–> Adenoma

  • Unregulated intracellular signal transduction
  • See increased size in polyps

Loss of p53–> Carcinoma
- loss required for tumorigensis

64
Q

Carcinoid tumor

A

MUST metastasize outside GI system to observe effects of 5-HT production (serotonin)
- Wheezing, R-sided heart murmurs, diarrhea, flushing

Originates as neuroendocrine cell “dense core bodies” (EM) in appendix, ileum, rectum

Tx:

  • Resection
  • Octreotide
  • Somatostatin
65
Q

Hepatic encephalopathy

A

Glutamate released by neurons–> astrocytes–> convert to glutamine

Neurons take glutamine:

  • Recycle to glutamate–> neurotransmitters
  • Convert to alpha-ketoglutarate–> TCA

Encephalopathy= Ammonia toxicity–> depletion of glutamate and alpha-ketoglutarate–> excess glutamine
- Glutamine= hyperosmolarity in neuron cell, mitochondrial dysfunction (no Alpha-ketoglutarate)–> astrocyte swelling

66
Q

Liver markers of pathology

A

AST, ALT:

  • Viral hep ALT > AST
  • Alcoholic hep AST > ALT

Alk Phos: obstructive liver disease (HCC), bone disease, bile duct disease

Gamma-glutamyl transpeptidase (GGT): measure if LFTs increased to rule out bone disease

67
Q

Reye’s syndrome

A

Aspirin + viral infection
Symptoms:
- Mitochondrial abnormalities (decreased beta-oxidation d/t reversible inhibition of enxyme)
- Hypoglycemia
- fatty liver (microvesicular fatty change)
- Vomiting, hepatomegaly, coma

ONLY use aspirin in children with Kawasaki’s disease

68
Q

Hepatocellular carcinoma

A

Due to:

  • Hep B, Hep C
  • Wilson’s
  • Hemochromatosis (HLA-A3)
  • Alpha-1-antitrypsin
  • Alcoholic cirrhosis
  • Carcinogens (alflatoxin B1 from aspergillus–> p53 mutations (G:C–> T:A))
69
Q

Angiosarcoma

A

Malignant tumor of endothelial origin

- Associated with arsenic, polyvinyl chloride exposure

70
Q

Crigler-Najjar syndrome

A

Absent UDP-glucouronyl transferase
- Early in life: patients die early

Findings:

  • jaundice, kernicterus (bilirubin in brain)
  • Increased unconjugated bilirubin

Tx: plasmapheresis, phototherapy
- Type 2 respods to phenobarbital (increases liver enzyme synthesis)

71
Q

Dubin Johnson/Rotor syndrome

A

Conjugated hyperbilirubinemia (defective liver secretion

  • Benign
  • Black liver in Dubin-Johnson
72
Q

Gallstone ileus

A

Fistula between gallbladder and small intestine (large gallstone)

  • Air in biliary tree
  • Gallstone obstructing ileocecal valve

Women, 70+ years
- Symptoms= crampy abdominal pain, vomiting, abdominal distention, hard mass at ileocecal valve

73
Q

Pancreatic adenocarcinoma

A

CA-19-9 tumor marker (CEA less specific)

Presents:

  • Abdominal pain to back
  • Weight loss
  • *Trousseau’s syndrome**= migratory thrombophlebitis; redness, tenderness on palpation of extremities (CANCER)
  • -> hypercoagulability due to adenocarcinoma (pancreas, colon, lung)–> thromboplastin-like substance production
74
Q

Glucagonoma

A

Gluconeogenesis, lipolysis (weight loss)

Necrolytic migratory erythema, erythematous rash of groin

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