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Pathophysiology > GI Cont. > Flashcards

GI Cont. Flashcards

1
Q

This is a much deeper peptic ulceration of the stomach wall

-may burrow through the muscular wall

A

Chronic peptic ulceration

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2
Q

What commonly causes Chronic peptic ulceration?

A

-H. Pylori
-NSAIDS
-Aspirin use
(damage the mucosal barrier)

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3
Q

______ junctions of the _______ cell lining of the stomach help prevent acidic stomach contents from damaging the deeper layers of the stomach wall

A
  • Tight junctions

- Epithelial cell lining

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4
Q

What are prostaglandins used for in the stomach?

A
  • Improving local blood flow in the stomach
  • Allows mucus production and bicarbonate secretion
  • This COUNTERBALANCES H+ secretion
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5
Q

What do aspirin and NSAIDS do to prostaglandin synthesis?

A
  • Inhibit arachadonic acid metabolic pathways
  • Decrease prostaglandin synthesis
  • Gastric mucosa=vulnerable
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6
Q

What are 3 ways hemorrhage can present with?

A
  • Melena (black poop)
  • Hematochezia
  • Hematemesis
  • Anemia
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7
Q

Ulcers increase the risk for _______

A

Adenocarcinoma of the stomach

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8
Q

Ulcer=loss of _______

A

mucosa

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9
Q

What does the floor of the ulcer contain

A
  • granulation tissue

- inflammatory debris

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10
Q

Describe the rim of the ulcer

A
  • Erythemateous

- Edematous

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11
Q

What are more likely, duodenal or gastric ulcers?

A

Duodenal ulcers

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12
Q

_______ is a rare disease characterized by a gastrinoma in the pancreas.

A

Zollinger Ellison syndrome

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13
Q

Excessive gastrin causes increased acid production =

A

recurrent ulcers in the stomach

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14
Q

What is the most common form of stomach cancer?

A

-Adenocarcinomas

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15
Q

What are risk factors for adenocarcinoma of the stomach?

A
  • Chronic atrophic gastritis
  • Smoked/pickled foods
  • Nitrate food preserves
  • Low fruit/veggie diets
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16
Q

This is a rare outpocketing of the jejunum

A

Meckel diverticulum

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17
Q

This is failure of the anterior abdominal wall to form and the intestines protrude

A

Gastroschisis

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18
Q

This is a less severe case of gastroschisis with less bowel protruding

A

Omphalocele

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19
Q

This is a very small deficit at the umbilicus

A

Umbilical hernia

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20
Q

This results from localized, genetic absence of the autonomic ganglionic plexus in the colon wall that controls peristalsis

A

Hirschsprung Disease

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21
Q

What effects does Hirschsprung’s disease have on the body

A
  • No peristalsis
  • Impaired fecal movement
  • Poop backs up upstream
  • Overgrowth of bacteria
  • Severe inflammation
22
Q

These are dilated anal varices?

A

-Internal and external hemorrhoids

23
Q

S&S of hemorrhoids

A
  • Bleed regularly
  • Leave bight red blood on stool surface
  • Painful
  • Itchy
24
Q

Who commonly has hemorrhoids?

A
  • Older people
  • Pregnancy (due to increased BV and venous stasis)
  • Portal hypertension
25
Q

This is the twisting of the bowel

A

-Volvulus

26
Q

Describe the internal and external infarcted bowel

A

Infarcted bowel is EDEMATOUS

- Internal= extensive hemorrhage in the mucosa and submucosa

27
Q

What happens to the damaged wall?

A

-Becomes leaky

28
Q

What results from the leaky damaged wall

A
  • Peritonitis

- Septicemia

29
Q

This occurs when C. Difficle overgrows

A

Pseudomembranous colitis

30
Q

Describe C. Dif

A
  • Gram Positive
  • Anaerobic
  • Spore forming bacteria
31
Q

Can C. Dif be part of the normal flora?

A

Yes

32
Q

What is a major cause of C. Dif infection?

A

-Broad spectrum antibiotic use

because it kills normal flora

33
Q

Pathogenesis of C. Diif

A
  • Secretes enterotoxin
  • Binds to epithelium of the colon
  • Causes an inflammatory response
  • Produces cellular, purulent exudate
  • Causes necrosis of colonic mucosa
34
Q

What is the #1 cause of nosocomial diarrhea

A

C. Dif

-secretes enterotoxin and produces a cellular purulent exudate and causes necrosis

35
Q

This is the poor absorption of fats, electrolytes, minerals, and water

A

Malabsorption

36
Q

This is malabsorption with fatty stools

A

Sprue

37
Q

S&S of Malabsorption

A
  • Large, bulky, greasy stools
  • Excessive bowel gas
  • Distention
38
Q

Describe luminal malabsorpion

A
  • Happens in the lumen
  • Usually due to deficiency of pancreatic or liver function
  • no lipase or defective bile acids
39
Q

What are causes of intestinal malabsorpion

A
  • Surgically shortened bowel
  • Lack of brush border enzyme
  • Gluten sensitivity
40
Q

Complications common to sprue

A
  • Anemia (poor B12, iron, or folate)
  • Bleeding (from decreased vitamin K)
  • Brittle, weak bones (from decreased Ca and Vitamin D)
  • Osmotic edema (from decreased proteins)
41
Q

Diverticula have a very _____ wall composed of _____ and ______ only

A

Thin wall

  • Mucosa and submucosa only
  • NO MUSCLE present
42
Q

Where do the mucosa and submucosa extrude through the musclular walls?

A

-Points where small arteries penetrate from the external surface

43
Q

T/F- Colonic diverticulosis is uncommon in people who eat a traditional diet rich in grains, fruits, and veggies

A

True

44
Q

Diets with small amounts of non-digestible bulk= more compact feces=

A

Easier to pass

45
Q

Straining at stool causes…

A

Increased pressure

46
Q

Stasis=

A

INFECTION

47
Q

Pathogenesis of a blockage in the lumen

A
  • Blockage
  • Increase pressure
  • Decreased blood flow
  • Ischemia
  • Infarction
  • Necrosis
  • Infection/inflammation
48
Q

What are complications for diverticulosis

A
  • Perforation
  • Peritonitis
  • Abcess
  • Hemorrhage
  • Fistulas
  • Stenosis
49
Q

Pathogenesis for appendicitis

A
  • Obstruction of orifice
  • Distension of lumen
  • Pressure increases
  • Stasis and ischemia
  • Proliferation of bacteria
  • Necrosis and perforation
  • Complications
50
Q

What is the most common cause of an abdominal emergency?

A

Appendicitis

51
Q

S&S of appendicitis

A
  • Periumbilical carmping/pain
  • Localizes to RLQ
  • Nausea, vomiting, anorexia
  • RLQ tenderness= irritated peritoneum –> ilius

Pathophysiology (18 decks)

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