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Pathophysiology > GI: Stomach > Flashcards

GI: Stomach Flashcards

1
Q

define gastroparesis

A

delayed gastric emptying in absence of mechanical gastric outlet obstruction

*common in DM

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2
Q

Gastritis

-acute vs chronic

A

*inflamm disorder of the gastric mucosa
ACUTE: caused by injury of protective mucosal barrier–superficial inflammation—- “rug burn” of the stomach aka SUPERFICIAL

CHRONIC:

  • chronic fundal gastritis (type A–IMMUNE)–pernicious anemia for ex
  • chronic antral gastritis (type B–NONimmune)–aka infectious–>HP infection for ex or chronic NSAID use
*symps are vague for both* 
anorexa
fullness
n/v
epigastric pain
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3
Q

patho behind

Autoimmune Metaplastic Atrophic Gastritis

A
  • T cell mediate auto destruction of the gastric mucosa
  • Autoimmune gastritis leads to chronic gastritis–anti-parietal and anti-intrinsic factor antibodies–leads to development of pernicious anemia (B12 malabsoprtion)

*lack of parietal cells can lead to: hypochlorhydria + hypergastrinemia

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4
Q

list/explain the stress-related mucosal dz

*general cause

A

Acute form of PUD–related to severe illness or major trauma

  1. ischemic ulcers–>w/in hours of trauma, burns, hemorrhage, HF or sepsis
  2. curling ulcers–>dev as a result of burn injury
  3. cushing ulcers–>result of brain injury or brain surgery
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5
Q

stress gastritis

  • MC causes/major RFs
  • what can reduce the risk?
  • focus should be on?
A

RFs:

  • mechanical ventilation
  • coagulopathy
  • truama
  • burns
  • shock
  • sepsis
  • CNS injury
  • liver failure
  • kidney dz
  • multiorgan failure

***use of enteral nutrition reduces the risk of stress related bleeding

Focus should be on PREVENTION

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6
Q

Atrophic (Chronic) gastritis

  • due to ?
  • explain the types
  • inr risk of what
A

due to gland atrophy + intestinal metaplasia **

  • ->small intestine bacterial overgrowth
  • ->decr IF secretion–>B12 deficiency–>pernicious anemia
  • ->risk of adenocarcinoma increase THREE fold**
  • ->achlorhydia too

types:
1. Immune AKA pernicious Anemia aka Type 1
- –>auto immune disorder involving the fundic glands

  1. Non-immune AKA type 2 aka HP infection
    - ->malabsorption secondary to chronic HP infection
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7
Q

Autoimmune gastritis affects what part of stomach and spares whihc?

A

affects– fundus (top part)

spares–antrum (lower part)

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8
Q

parietal cells produce
*what will happen if this cell is damaged

Antral G cells produce?

A

IF–B12 absoprtion
acid–help with iron asboprtion

damage leads to:

  1. iron def anemia
  2. pernicious anemia

Antral G cells produce gastrin

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9
Q

deifine PUD

A
  • a break or ulceration in the protective mucosal lining
  • disruption of mucosal integrity of stomach lining or duodenal lining—- leads to local defect due to active inflammation
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10
Q

define dyspepsia

A

epigastric pain exacerbated by fasting— improves with meals
basically upset stomach

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11
Q

do majority of PTs with dyspepsia have PUD?

A

NO—- over 90% do not have ulcers

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12
Q

how do majority of PTs with PUD present

A

asympto..

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13
Q

occurance of acid peptic disorders in US

  • lifetime prevalnce in US?
  • death rate?
A

very common–4 million individuals/yr

Lifetime prevalence–about 12% men and 10% women

15,000 deaths/yr due to complications

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14
Q

how to differentiate b/w gastric and duodenal ulcer?

A

change in PT’s symptoms with food is key

  1. Duodenal ulcer–s/s get better with food
  2. gastric ulcer–s/s get worse when eating
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15
Q

which is MC– duodenal or gastric ulcers?

A

duodenal–4 times more common

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16
Q

which is usually benign– duodenal or gastric ulcers

A

proximal duodenal MC benign

Gastric–4% associated with gastric adenocarcinoma

17
Q

duodenal ulcer

*developmental factors (2)

A

Dev Factors

  • HP infection**
  • NSAIDs
18
Q

gastritis tends to develop where in stomach vs gastric ulcers?

A

gastritis– fundus
ulcer–antrum (lower) next to the acid-secreting mucosa of the body—why it can be associatd with adenocarcionoma (intestinal cells met to stomach)

19
Q

primary defect in gastric ulcers?

A

increased mucosal permeability to hydrogen ions

—gastric secretion tends to be normal or less than normal

20
Q

Helicobacter Pylori

  • what kind of bacteria
  • affect on body?
  • what happens during acute infection
  • what happens after acute infection
  • when is eradication achieved?
A

Spiral, gram (-) rod
*causes gastric mucosal inflammation

acute infection:
-causes transient illness of nausea and abdominal pain for several days–>acute gastritis with polymorphonuclear neutrophils (PMNs)

After infection or once s/s resole:
-majority progress to a chronic infection–>chronic diffuse mucosal inflammation characterized by PMNs and lymphocytes

eradication is achieved when:
ABX leads to >85% resolution of the chronic gastritis

Majority of chronic infection are asympto***** and no sequelae

21
Q

why does eating make gastric ulcer more painful?

A

because food stimulates production of MORE acid

22
Q

HP infection’s affects on:

  1. Gastrin
  2. acid production
A

since the HP infections usually attack the antrum– this can lead to:
1. increased gastrin–>turns on parietal cells–>secrs more acid

  1. Increased acid production

***all this leads to incr risk of devl PUD–esp duodenal

23
Q

gastric ulcers are mostly caused by imbalance with?

A

decreased protective mechanisms (decr mucus, bicarb, prostaglandins)

24
Q

duodenal ulcers are mostly caused by imbalance with?

A

aggressive factors (HP infection, incr HCL production)

25
Q

chronic HP infection gastritic leads to:

A

duodenal or gastric ulcers–10%
gastric CA–.1-3%
Low grade B cell gastric lymphoma–SUPER rare

26
Q

how to test for HP infection

-two genral ways

A

Noninvasive

  1. Fecal antigen immunoassay
  2. C-urea breath test

Invasive:
endoscopic + biopsy

27
Q

patho behind urea breath test

A

urea pill–>pill has carbon-urea (tagged carbon/radioactive)

NPO and off PPI****

normally NO urea in the stomach…. but HP makes urease–which breaks down urea into CO2 and ammonia– so if + HP infection… the CO2 will be breathed out WITH the carbon isotope.

+ test is breathing out the radioactive isotope
- test is just peeing out the substance and not breathing out any tagged C in CO2

28
Q

other conditions that cause PUD:

A 
Zollinger-Ellison syndrome 
CMV 
CD 
Lymphoma 
Medications
Chronic medical illneses like cirrhosis or CKD
29
Q

prevalence of HP infection with duodenal ulers?

A

70-90%

30
Q

chance of developing ulcer dz with an active HP infection?

A

10%

31
Q

HP infection increases risk of?

A

NSAID induced ulcers and complications

32
Q 
Zollinger-Ellison Syndrome 
-also called? 
-what is it 
MC found where 
-asoc with what dz?
A

(Gastrinoma)
gastrin-secreting neuroendocrine tumor that often leads to severe PUD and diarrhea DUE TO HYPERSECRETION OF GASTRIC ACID
>90% of PTs develop PUD
the s/s are identical to PUD– so this dz might go undiagnosed for years

MC in duodenal wall (45%), pancreas (25%), lymph nodes (5-15%) or other sites

Associated with MEN 1

33
Q

NSAIDs can cause PUDs by?

A

their prostaglandin production— leads to impaired defenses

34
Q

what is the MCC of UGIB

A

PUD

35
Q

Avg age for:

  1. duodenal ulcers
  2. Gastric ulcers
A

Duodenal: 30-55
Gastric: 55-70

36
Q

why does diarrhea occur in 1/3 of PTs with Zolliner-Ellison syndrome

A

Gastric acid hypersecretion–>direct intestinal mucosal injury –> pancreatic enzyme inactivation–> resulting in diarrhea, steatorrhea, and weight loss

37
Q

Gastric CA

  • MC assoc with?
  • other Rfs
  • MC ??
  • four types? (most favorable and worst prognosis?)
A

assoc with HP and atrophic gastritis—>gastric adenocarcinoma

other RF

  • consumption of heavily salted and preseved foods
  • low intake of veg/fruits
  • smoking
  • etoh

MC: adenocarcinoma–90%

TYPES:

  1. Polypoid carcinoma–solid mass projects into the stomach luemn
  2. ulcerative–looks like PUD
  3. superficial spreading–most favorable diagnosis
  4. Linitis plastica or “leather bottle”–infiltrates early– all layers–stomach wall becomes thick and rigid–poor prognosis

Pathophysiology (13 decks)

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