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Abd Pain Flashcards

1
Q

Whats the MC cause of upper GI bleed?

A

peptic ulcer dx

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2
Q

what’s the MC cause of lower GI bleed?

A

Diverticulosis (then colitis)

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3
Q

what are the 2 types of chronic gastritis? (just names, what can cause them & location)

A
  1. Type A: Atrophic Gastritis - autoimmune - in body/fundus or multifocal (body, fundus & antrum)
  2. Type B: Nonatrophic Gastritis - H. plyori - in antrum
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4
Q

Describe multifocal atrophic gastritis? (what causes it, location, histo, risks)

A

Type A atrophic gastritis but involves antrum, body and fundus. Causes by H plyori, genetics & diet.

Histo: mucosal atrophy & loss of glands and intestinal metaplasia w/ goblet cells (risk for dysplasia and gastric adenocarcinoma)

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5
Q

Describe chronic autoimmune metaplastic atrophic gastritis (location, histo)

A

Location: body & fundus
Histo: atrophic mucosa w/ intestinal metaplasia, flattened gastric folds, thin body/fundic mucosa, increased antral G-cell hyperplasia (make gastrin)

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6
Q

what’s the most common cause of vit B12 deficiency?

A

chronic gastritis b/c of loss of IF so can’t absorb vit B12

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7
Q

what’s the difference btwn acute and chronic gastritis

A

acute gastritis: erosive acidic damage to stomach mucosa

chronic gastritis: chronic inflammation of stomach muocsa

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8
Q

What are risk factors for acute gastritis?

A

aspirin, NSAIDs, alcohol, cocaine, shock (stress ulcers), chemo, radiation, bile reflux, ischemia, uremia, burns (Curling ulcers), brain injury (increased intracranial pressure - Cushing ulcer w/ increased vagal N stimulation increasing acid production),

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9
Q

what 3 different things could be seen in a spectrum of acute erosive gastritis?

A
  1. Hemorrhage
  2. Erosions - loss of superficial epithelium
  3. Ulcers - loss of mucosa layer (multiple occur)
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10
Q

what’s the difference btwn peptic ulcer disease and erosion?

A

Peptic ulcer disease extends to muscularis mucosa

Erosion: extends to superficial lamina propria epithelium necrosis

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11
Q

what are the aggressive vs defensive substances secreted in the stomach? How do they relate to acute gastritis?

A

Aggressive: gastric acid and pepsin
Defensive: bicarb & mucin, prostaglandins
Acute gastritis can be due to increased acid secretion or decreased bicarb (also decreased BF)

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12
Q

what do prostaglandins do in the stomach?

A

increase mucosal BF, mucus & bicarb secretion & stimulate epithelial regeneration

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13
Q

What could cause gastric or duodenal peptic ulcer disease?

A

Gastric: H plyori or NSAIDs (could lead to gastric carcinoma)
Duodenal: H plyori or Zollinger-Ellison syndrome (acid producing tumor, see ulcers in abnorm places like beyond 2nd part of duodenum)

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14
Q

Describe characteristics of H pylori

A

GN curved bacilli, microaerophilic
Polar flagella so highly motile (passes thru gastric mucosa & adheres to epithelial cells)
Produces urease

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15
Q

What are the 6 most important virulence factors of H pylori? (just name them)

A
  1. Heat shock proteins
  2. Urease
  3. Mucinase & phospholipase
  4. CagA
  5. NAP - neutrophil activating protein
  6. VacA
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16
Q

what’s the function of the heat shock proteins in H pylori?

A

HSP - virulence factor of H pylori

in low pH it induces H pylori to express urease

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17
Q

what’s the function of urease in H pylori?

A

Urease - neutralizes gastric acid

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18
Q

what’s the function of mucinase and phospholipase in H pylori?

A

disrupt gastric mucus so H pylori can get to the epithelium

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19
Q

what’s the function of CagA in H pylori?

A

via type IV secretion it helps deliver H pylori to the cytoplasm of epithelial host cells to take over signaling. It’s pro-inflammation & anti-apoptotic.
It’s assoc w/ cell changes, increased inflammation and IL-8 production.
Increased risk of gastic adenonocarcinoma w/ this strain

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20
Q

what’s the function of VacA in H pylori?

A

cytotoxin that induces vacuolation in H pylori host cell.

proapoptotic (works against CagA)

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21
Q

What 4 main events occur w/ H pylori damage?

A
  1. Immune Response activation via IL-1, 6 & 8 & TNF. (IL-8 1st produced by epithelial cells, recruits neutrophils leading to damage)
  2. Bacterial products: urease, phospholipase, protease, VacA, CagA
  3. increased acid secretion, decreased duodenal bicarb and favors intestinal metaplasia
  4. T & B cell recruitment: T cell driven, activates B cells leads to increased lymphoma risk
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22
Q

what 4 ways could you test for H plyori?

A
  1. culture: 5-10% oxygen, urease +
  2. Urea breath test: consume radioactive urea, organism breaks it down into radioactive CO2
  3. Serology: IgG for H pylori (but not specific to present or past infection)
  4. Stool sample
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23
Q

what are the 4 main inflammatory gastritis disorders?

A
  1. acute gastritis
  2. chronic gastritis
  3. reactive gastropathy
  4. peptic ulcer disease
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24
Q

Describe chronic autoimmune metaplastic atrophic gastritis (S/S, Abs, what mediates it, risks)

A

S/S: achlorhydria (no acid production) w/ increased gastrin level (loss of neg fbk), hypergastrinemia, megaloblastic pernicious anemia (lack IF so can’t absorb vit B12) - MC in Scandinavia
Abs: Anti-IF, anti-parietal cell, anti-H/K ATPase (proton pump) Abs
Mediator: T cells - type IV hypersensivity
Risk: increased risk for gastric andenocarcinomia

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25
Q

Describe chronic H plyori gastritis (location, histo, S/S)

A

Location: antrum
Histo: bubbly H plyori
S/S: epigastric abd pain

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26
Q

What are increased risks w/ chronic H pylori gastritis?

A
  1. ulceration - Peptic ulcer disease
  2. gastric adenocarcinoma (intestinal metaplasia type)
  3. MALT lymphoma (increased germinal centers in walls leads to increased post GC B cells in marginal zone)
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27
Q

what are the 2 patterns of inflammation w/ H pylori gastritis?

A
  1. Antral mucosal inflam - high acid production & elevated duodenal ulcer risk (MC)
  2. Pangastritis - lower gastric acid, higher adenocarinoma risk, assoc w/ higher IL-1B response to infection
28
Q

what would be seen in histo of chronic active H plyori gastritis?

A

increased inflam btwn glands, some areas of neutrophils

29
Q

what’s the relationship btwn H pylori and GERD?

A 
infected pts (esp CagA strains) may be protected b/c bacterial ammonia neutralizes acid.
If H pylori is eradicated it may exacerabate GERD - rebound hyperacidity
30
Q

what’s reactive gastropathy?

Describe it’s histo

A

mucosal injury pattern caused by chemicals (NSAIDs, aspirin, alcohol, bile reflux)
Histo: surface foveolar epthelium is thick & corkscrew like but no inflammation

31
Q

what’s lymphocytic gastritis?

A

assoc w/ celiac dx in women, w/ varioliform appearance (small pox pitted appearance)

32
Q

what could cause granulomatous gastritis?

A

Crohns or sarcoid

33
Q

what could cause eosinophilic gastritis

A

food allergies is kids or drugs in adults

34
Q

what are some S/S of gastric peptic ulcers?

A

gnawing burning epigastric pain, worse at night and 1-3 hr post meal, anemia, weight loss, hematemesis, perforation w/ acute abdomen (pain refers to LUQ or chest)

35
Q

where is a peptic ulcer most likely to occur?

A

1st part of duodenum - anterior wall

stomach antrum is 2nd

36
Q

what’s gastritis cystica?

A

reactive epithelial proliferation w/in the wall of stomach. it may mimic adenocarcinoma. Possible complication of chronic gastritis

37
Q

what stimulates the H/K/ATPase proton pump in the parietal cells?

A

ACh (M3 receptor), histamine (H2 receptor) and gastrin (G receptor)

38
Q

what vessels make up the portal vein?

A

splenic vein and superior messenteric vein (also inferior)

39
Q

what’s the dual blood supply of the liver?

A

portal vein (mostly, 75%) and hepatic artery

40
Q

where do the hepatic artery and portal veins converge?

A

vascular channels called hepatic sinusoids lined w/ fenestrated epithelial cells that lack BM

41
Q

what’s the MC cause of increased portal P and by what mechanism?

A

Cirrhosis

increases resistance to flow from architectural distortion of liver and intrahepatic vasoconstriction from decreased NO

42
Q

what’s the hepatic vein pressure gradient and what can it predict?

A

diference btwn wedged hepatic venous P (sinusoidal P) & free hepatic V P (intraabdominal IVC pressure)

Can form varices if gradient > 10 mmHg, and variceal bleeding if gradient > 12 mmHg

43
Q

what’s Budd Chiari Syndrome?(just definition)

A

Posthepatic form of portal htn from hepatic venous outflow obstruction w/ a thormobosis of Hepatic V at opening of IVC

44
Q

what can Budd Chiari Syndrome lead to?

A

sinusoidal congestion, Portal V HTN and reduced Portal V blood flow.
S/S: hepatomegaly, pain, ascites, impaired hepatic fxn

45
Q

what’s Mallory-Weiss syndrome?

A

linear lacerations at the GE junction seen w/ increased intra-abdominal P and negative intrathoracic P above the diaphragm. Assoc w/ hiatal hernia
Often from bulemia or alcoholics from increased retching/vomiting

46
Q

what’s Boerhaave’s Syndrome?

A

full thickness lacerations/perforation of the esophagus (Mallory- Wiess syndrome turns into this)

47
Q

what happens w/ esophageal varices? where is it MC located?

A

dilation of submucosal esophageal Vs (drain into Azygous to SVC) b/c of collaterals formed btwn hepatic & caval systems connecting them to L Gastric V b/c of portal HTN (usu from cirhosis)
MC - distal 1/3 esophagus

48
Q

what’s an angioectasia?

Where’s it MC located

A

MC vascular abnormalitiy of GI tract, acquired (elderly) ectatic (dilated submucosal Vs), distorted, thin-walled venules/caps/arterioles. Can cause GI bleed.
Usu in cecum or ascending colon

49
Q

What’s Hereditary Hemorrhagic Telangiectasia? What’s mutated? What would be seen by age 10?

A

Aka Olser-Weber-Rendu syndrome
AD mutated endoglin (ENG) & activin receptor like kinase 1 (ALK-1) leads to teleangiectasia of skin & mucus membranes (mouth to anus). Can have iron def anemia b/c of slow blood loss
By age 10, 1/2 have GI bleed

50
Q

What’s Dieulafoy’s Lesion?
Where do they occur?
S/S?

A

large (1-3 mm) submucosal A protrudes thru mucosa (differs from ulcer)
Occurs in stomach (usually), SI or LI
S/S: massive hematemesis or melena

51
Q

What’s Colonic diverticulosis?
Where would bleeding occur?
where’s it MC seen

A

(pseudodiverticulosis) herniation (outpouching) of colonic mucosa & submucosa thru musuclar layers of colon btwn taenia on mesenteric side (where vasa recta enter) due to increased intraluminal P, low fiber diet (decreasing peristalsis) or muscular wall weakness
Bleed from vessels at neck/base of diverticulum
MC in sigmoid colon

52
Q

what 3 places are GI sensory neuroreceptors located?

A
  1. Mucosa & muscularis of hollow viscera
  2. Serosal structures in peritoneum
  3. within mesentery
53
Q

How’s visceral pain transmitted? Describe the pain and location

A

C fibers
dull, cramping, burning pain
poorly localized

54
Q

What are the 3 types of nociceptors that transmit C fiber visceral GI pain?

A
  1. Abd visceral nociceptors - responding to mechanical and chemical stimuli
  2. Mechanical nociceptors - stretch
  3. Chemical nociceptors - inflammation, tissue ischemia & necrosis, noxious thermal or radiation
55
Q

How’s somatic parieta pain transmitted? Describe the pain and location (and example of location)

A

A-delta fibers (in skin and muscle)
Sharp sudden pain
Location - well localized pain (ex: McBurney’s pt for appendicitis)

56
Q

what causes referred pain?

A

visceral and somatic afferents from different anatomic regions converge on second-order neurons in SC at same segment

57
Q

what’s dyspepsia?

S/S

A

difficulty w/ digestion (indigestion)

S/S: epigastric pain, postprandial fullness, early satiety, anorexia, belching, N/V, bloating, heart burn & regurg

58
Q

what’s functional dyspepsia?

A

presence of early satiety, postprandial fullness, epigastric pain & burning in absence of organic, systemic or metabolic dx

59
Q

4 steps of normal gastric emptying

A
  1. fundic relaxation to accommodate food
  2. antral contractions (grind food down)
  3. pyloric relaxation
  4. antropyloroduodenal coordination
60
Q

what’s gastroparesis?

S/S

A

paralysis of stomach; delayed emptying in absence of obstruction
S/S: early satiety, N/V, bloating, epigastric discomfort

61
Q

3 subtypes of gastroparesis
which is MC?
what can cause each of them?

A
  1. Diabetic Gastroparesis: DM > 10 yrs, due to neruopathy, nephropathy & CVD (increased glucose can reduce stoamch release)
  2. Idiopathic Gastroparesis: MC, reduced interstitial cells of Cajal (stomach pacemakers); viral prodrome (CMV, EBV, Varicella)
  3. Post surgical Gastroparesis (damaging vagus N)
62
Q

what’s chronic mesenteric ischemia?

S/S

A

intestinal angina from occlusion of 2+ splanchinc As (Celiac, SMA or IMA)
S/S: abd cramping w/in 30 min of eating, gradual increase in severity, slowly resolves over 1-3 hr, weight loss. H/O vascular dx

63
Q

what are the 3 branches of celiac A?

what do they supply

A

left gastric, splenic & common hepatic arteries

supplies stomach, duodenum, pancreas and liver (and spleen)

64
Q

what are the branches of the IMA?

A

L colic, Sigmoid and Superior Rectal As

65
Q

What would the AST to ALT ratio be in alcoholic hepatitis?

A

AST: ALT ratio > 2:1

GI (8 decks)

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