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GI > Review Session > Flashcards

Review Session Flashcards

1
Q

What blood vessels come off the splenic artery?

A
  • Greater and dorsal pancreatic (body and tail)

- Left Gastroomental (greater curvature) and short gastric

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2
Q

What blood vessels come off the common hepatic

A
  • R gastric (lesser omentum
  • Gastroduodenal artery
  • Panc duodenal artery
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3
Q

Portal/systemic for estoph

A

-gastric vein to esoph

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4
Q

Portal/systemic for caput

A

paraumbilical to superficial abd

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5
Q

Portal/systemic for rectum

A

superior rectum–>middle and inferior rectal vein

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6
Q

List pathophys of GERD

A
  • TLESR (most impt)
  • LES hypotonia
  • Hiatal hernia
  • Obesity
  • Pregnancy (pressure and estrogen)
  • Poor esophageal peristalsis
  • Reduced saliva production
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7
Q

Two risk factors for adenocarcinoma

A

GERD and Barrett’s esoph

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8
Q

Treatment of GERD

A
  • Lifestyle modification
  • Antacids
  • H2 blockers (Ranitidine and Famotidine)
  • PPI
  • Surgery (not as common anymore)
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9
Q

List the aggressive factors of peptic ulcer

A

Acid, pepsin, bile salts

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10
Q

List defensive factors of peptic ulcer

A
  • Mucus/mucosal barrier
  • bicarb
  • blood flow
  • cell regeneration
  • PGs (aspirin and NSAIDs inhibit these)
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11
Q

Major etiologies of peptic ulcer disease

A
  • H pylori
  • NSAIDs
  • Hypersecretory states (ZES)
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12
Q

NSAIDs have what effect?

A

PG inhibition and antiplatelet (systemic)

Topical events also

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13
Q

Symptoms of DU?

A
  • Epigastric burning pain dev 1-3 hrs after meal
  • Pain relieved by food or antacids (food triggers activations, end up getting bicarb sec via secretin etc which provides relief and neut of acid after eating, transient)
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14
Q

Complications of DU?

A

Bleeding, obstruction, perforation

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15
Q

What bv is in danger with DU?

A

Gastroduodenal artery

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16
Q

Is ZES common?

A

Rare

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17
Q

Clinical ZES

A
  • Aggressive PU disease
  • Diarrhea
  • Heartburn
  • Hemorrhage
  • Perforation
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18
Q

What syndrome is ZES associated with

A

MEN1 syndrome

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19
Q

How fast are gastric slow waves?

A

3/min

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20
Q

What causes gastroparesis

A
  • idiopathic
  • post surgical
  • diabetic
  • meds related
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21
Q

Causes of esophagitis

A
  • GERD
  • Pill
  • Allergy
  • Crohn’s dis
  • Viral CMV/HSV
  • Radiation
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22
Q

What causes esophageal disease?

A
  • Herpes (punched out ulcers)
  • CMV (nuclear/cytoplasmic inclusions, large ulcers)
  • Candida (white plaques on endoscopy)
  • KS (AIDS)
  • Lymphoma (immunosupp, rare)
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23
Q

Eosinophilic Esophagitis

A

-Allergic response to antigen, dysphagia

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24
Q

Risk factors of squamous cell carcinoma

A

Smoking, alcohol, achalasia, lye ingestion

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25
Q

Risk factor of barretts

A

GERD

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26
Q

How are carbs transported in?

A

Na coupled transport of monosaccharides

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27
Q

List the factors necessary for lipid absorption

A
  • bile salts
  • panc lipase
  • bicarb
  • panc colipase
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28
Q

What forms a chylomicron?

A

TG and apoproteins

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29
Q

How much liters of fluid/d does small intestine see?

A

9-10 L

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30
Q

How much water is abs in small bowel?

A

all but 1.5L

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31
Q

Where is water absorbed fastest in small bowel?

A

Ileum

32
Q

Ion transport by crypt cells

A
  • Cl secretion by apical membrane

- Regulated by cAMP

33
Q

How much water does colon see and abs?

A

sees 1.5L and abs 1.4L

34
Q

Describe abs and sec of colon

A

Surace cell:

  • abs: water, Cl, Na
  • sec: K+, bicarb

Crypt:
-sec: Cl

35
Q

Does the small bowel secrete bicarb or k?

A

no

36
Q

What is SCFA?

A

Short chain fatty acids produced by colonic bacteria that nourish colonocytes from undigested carbs

37
Q

What infectious disease can cause colitis?

A
  • Shigella
  • Salmonella
  • Campylobacter
38
Q

What is microscopic colitis?

A

Lymphocytic colitis
Collagenous colitis

–>get watery diarrhea

–Chronic mucosal inflammation in absence of endoscopic or radiologic abnormalities

39
Q

What is ischemic colitis?

A
  • Sudden and temporary reduction of blood flow to the colon

- Due to vasculitis, mechanical, thrombotic, embolic, hemodynamic instability, neutrophilic infiltration and edema

40
Q

NOD2

A

younger pts

41
Q

How long after pancolitis does cancer begin?

A

7-10 years after pancolitis

42
Q

Where do abscesses form with CD?

A

Into the peritoneal cavity

43
Q

TPMT mutation

A

Check for this because otherwise make too much 6-TGN which is the active drug and get adverse events like leukopenia/death

44
Q

What drugs do we use to treat c dif?

A

Oral metronidazole, vancomycin and fecal transplant in refractory cases

45
Q

How are lipids absorbed?

A
  • Formation of chylomicrons that enter lacteal

- Medium chain TGs enter portal vein

46
Q

Sucralfate

A
  • Binds to GI mucosa and stimulates bicarb and PGE2 production
  • Not absorbed
  • Inc resistance to proteolysis by pepsin
  • No effect on gastric acid production
47
Q

List two H2 pump inhib

A

Ranitidine and Famotidine

-use for GERD, GU and DU

48
Q

Omeprazole

A
  • PPI
  • stomach–>small intestine (basic)–>absorbed–>taken in–>Protonated and sulfonated
  • Duration 17 hrs
49
Q

PPIs uses

A

GERD, DU, GU, H. pylori, ZES

50
Q

Are antacids synergistic with other drugs?

A

no

51
Q

When should you take misoprostol?

A

Along with NSAIDs to prevent GU

-bloating and diarrhea=side effects

52
Q

Antibodies for celica

A

EMA, TTG

53
Q

HLA for celiac

A

HLA-DQ2 and DQ8

54
Q

What is celiac associated with?

A

Dermatitis herpetiformis

55
Q

Oral manifestations of IBD

A

Pyostomatitis vegetans

oral lesions that precede intestinal findings

56
Q

Melanosis coli

A

Brown mucosa caused by accumulation of lipofuscin in macrophages of lamina propria due to lax

-anthraquinone

57
Q

CMV disease

A
  • Immunosuppressed patients

- watery or bloody diarrhea

58
Q

Diagnostic tests of CMV

A
  • CMV rapid antigen, PCR or culture of blood

- Sigmoidoscopy or colonoscopy with biopsy (viral inclusions on pathology)

59
Q

How do you treat CMV?

A

Ganciclovir

60
Q

Treatment for cholerae

A
  • IV or oral rehydration
  • Particular attention to bicarb and K+
  • Abx: tetracycline, fluoroquinolones, TMP-SMX
61
Q

IBS definition

A
  • Recurrent abdominal discomfort for at least 3 days per month in preceding 3 mo with at least 2/3…
  • Relief with defecation
  • onset associated with change in stool form or appearance
  • change in stool freq
62
Q

Causes of IBS

A
  • Brain gut interactions
  • Abnormal motility
  • Visceral hypersensitivity
  • Altered gut flora
  • Psychosocial factors
63
Q

What do you have that says you don’t have IBS?

A
  • Rectal bleeding
  • Nocturnal or progressive abdominal pain
  • Wt loss
  • Anemia, elevated inflammatory markers, electrolyte abnormalities
64
Q

Sessile serrated adenoma

A

Base of glands are broad and expanded and serration goes down to the base of the crypt. Have malignant potential

Always remove

65
Q

Juvenile Polyp

A
  • Not dysplastic
  • Gland dilation
  • SMAD4 mutation
66
Q

Colonic polyps

A
  • Hyperplastic
  • Most common diminutive polyp
  • No malignant potential
  • Serrated appearance
67
Q

FAP inc risk of what kinds of cancers?

A

SB and colonic adenocarcinomas also have extra-intestinal manifestations

68
Q

Lynch syndrome has what kinds of colic lesions?

A

Right sided colonic lesions

69
Q

What mutation in lynch syndrome?

A

DNA mismatch repair, germline

70
Q

What mutation in peutz-jegher syndrome?

A

STK11/LKB1

  • ->pigmentation and hamartomatous polyps
  • ->arborizing smooth muscle
71
Q

Where else does STK11/LKB1 inc cancer for?

A

pancreas, liver, lungs, breast, ovaries, uterus, testicles

72
Q

Hep A serologic course

A

ALT then IgM then IgG

73
Q

Hep B serologic course, acute

A

HBsAg then IgM and total anti-HBc inc at the same time then anti HBs

74
Q

Hep B serologic course, chronic

A
  • HBsAg and total anti-HBc reaches peak as IgM decreases

- HBeAg stays high throughout

75
Q

Hep C serologic course chronic

A

Symptoms come with anti-HCV

76
Q

Biliverdin

A

from heme

GI (12 decks)

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