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GI > Pathophysiology (Prunuske) > Flashcards

Pathophysiology (Prunuske) Flashcards

1
Q

Zollinger-Ellison Syndrome (gastrinoma)

A
  • -Caused by gastrin-secreting tumor (usually)
  • -Excess H+ secretion and hyperplasia and hypertrophy of parietal cells
  • -95% of patients get gastric ulcers
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2
Q

Gastric and duodenal ulcers

A
  • -H. pylori infection
  • -Poor secretion of mucus, bicarb by surface epithelium
  • -Stress can contribute (not cause)
  • -Irritation w/EtOH, acid, digestive enzymes, bile
  • -Treat w/antibiotics and PPI, stop NSAIDS
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3
Q

GI peptic ulcer pathophysiology

A
  • -Gastrin levels increased (somatostatin inhibition during fasting state not activated)
  • -Increased gastrin can cause acid hypersecretion, pepsin secretion, hyperplasia of ECL and parietal cells and stomach contractions
  • -NSAIDs further exacerbate due to inhibition of protective factors from PG
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4
Q

Achlorhydria

A
  • -Reduced acid secretion
  • -Possible causes: aging , gastric resection, genetics, auto-immune attack of H+/K+ ATPase, PPIs, infection
  • -Bacterial overgrowth, diarrhea, pneumonia
  • -Hip fractures, iron deficient anemia (decreased Ca++ and iron absorption)
  • -Decrease in pepsin activation doesn’t cause problems
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5
Q

Pyloric stenosis

A

Congenital condition where pylorus fails to relax after meal–> malnutrition and dehydration
–Treat with surgical myotomy

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6
Q

Gastroparesis

A
  • -Reduced gastric emptying often because of diabetic neuropathy
  • -Vagus and enteric nerves fail to generate enough force to empty stomach contents
  • -Treat with prokinetic drugs
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7
Q

Dumping syndrome

A
  • -Rapid, gastric emptying (often from gastric bypass, vagotomy, high-sugar meals)
  • -Rapid entry of contents into duodenum represents osmotic challenge and water moves to lumen causing hypovolemia and reduced BP
  • -Nausea, weakness, dizziness, sweating, shakiness, diarrhea, heart palpitations
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8
Q

Peptic ulcer disease

A
  • -Scarring and ulcers near pylorus can delay emptying

- -Duodenal ulcers can lead to rapid gastric emptying from loss of duodenal negative feedback mechanism

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9
Q

Vomiting (emesis)

A
  • -Expulsion of contents of stomach contents through reverse peristalsis of the intestine
  • -Often preceded by nausea (sensation vomiting will happen)
  • -Can cause Mallory-Weiss tear if forceful enough
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10
Q

What coordinates emesis mechanisms?

A
  • -Vomiting center in medulla
  • -Increased salivation (bicarb) protects teeth enamel
  • -Retro-peristalsis (starting from middle of small intestine) into stomach through relaxed pyloric sphincter
  • -Can be preceded by retching
  • -Glottis closes to prevent aspiration of vomit
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11
Q

Does the stomach contract during process of vomiting?

A

No, except at the annular notch. Control is mediated by extrinsic nerves

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12
Q

What inhibitors are used to suppress vomiting?

A

Inhibitors of DA, Histamine and 5-HT

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13
Q

What are some emetic stimulants?

A
  • -Stimulation of pharynx
  • -Sensory input from higher centers
  • -Vestibular info
  • -Irritants or blockage in GI tract
  • -Blood-borne emetics
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14
Q

Hereditary pancreatitis

A
  • -Mutation in trypsinogen PRSS1 gene–> activates digestive enzymes in pancreas
  • -Autosomal dominant
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15
Q

Pancreatitis causes

A
  • -Cystic fibrosis
  • -Occlusion of pancreatic duct
  • -EtoH
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16
Q

Pancreatitis effects

A
  • -Upper abdominal pain from autodigestion of pancreatic tissue
  • -Vomiting and sympathetic activation
  • -Elevated serum amylase and lipase levels
  • -Malabsorption of fat and fat-soluble vitamins
  • -Steatorrhea
  • -Malignancy, diabetes, infections
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17
Q

Cirrhosis

A

Hardening of liver from irreversible deposition of excess collagen

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18
Q

Cirrhosis effects

A

Jaundice, abdominal ascites, esophageal varices, hepatic encephalopathy, GI bleeding

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19
Q

Cirrhosis pathology

A

–Oxidative stress (alcohol, infection) –> Kupffer cells release cytokines–> collagen production by stellate cells–> collagen accumulates–> increases resistance to blood flow and reduces hepatocyte function

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20
Q

Cholestasis

A

Impaired bile secretion

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21
Q

Primary biliary cirrhosis

A

Destruction of cholangiocytes

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22
Q

Primary sclerosing cholangitis

A

Inflammation of bile ducts

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23
Q

Pregnancy and relation to cholestasis

A

Progesterone reduces gallbladder smooth muscle tone

24
Q

Cholestasis effects

A
  • -Bile accumulates in liver–> metabolic dysfunction
  • -Itch (bile regurgitates into plasma)
  • -Hypercholesterolemia
  • -Deficiency of fat soluble proteins
25
Q

Cholelithaisis size, symptoms, prevalence

A
  • -Grain of sand to golf ball size
  • -RUQ pain, fever, many lack symptoms
  • -20% of people have
26
Q

Cholesterol stones

A

Caused by increased cholesterol or decreased bile acids treat with bile acid

27
Q

Pigment stones

A

Calcium salts of unconjugated bilirubin, can be caused by hemolytic anemia, infection of biliary tract that leads to deconjugation

28
Q

Treatment for cholelithiasis

A

Laparoscopic cholecystectomy

29
Q

Diverticulum

A

Single pouch protruding from alimentary tract. Usually false, not true.

30
Q

Diverticulosis

A

Multiple diverticula

31
Q

Diverticulitis

A

Impacted with feces, inflamed, painful, hemorrhage (if blood vessel erodes)

32
Q

Causes of mesenteric ischemia

A
  • -Occlusive mechanisms

- -Non-occlusive mechanisms (include prolonged reflex vasoconstriction or vasodilator toxins from gut)

33
Q

Effects of mesenteric ischemia

A
  • -Postprandial pain
  • -Sitophobia
  • -Necrosis of tops of villi
  • -Loss of barrier function of wall of gut an uptake of vasodilator toxins (endotoxin) from gut causing septic shock
34
Q

Consequences of removal of ileum

A

Can’t transport bile salts back to liver–> steatorrhea

35
Q

Osmotic diarrhea

A

Small bowel overgrowth of bacteria leading to increased production of organic acids that pull water from blood stream by osmosis

36
Q

Secretory diarrhea

A

Infection leads to excess secretion of Cl-, drawing water into lumen

37
Q

What is fluid flux in diarrhea dependent on?

A

Surface area available for ion transport and residence time in lumen

  • -East-West vector: increased by surface area
  • -North-South vector: influenced by motility–>transit time.
38
Q

What antidiarrheal works to slow transit time to increase fluid absorption?

A

Loperamide

39
Q

Borborygmi

A

Rumbling noise created by movement of gas in bowels

40
Q

Causes of small intestine bacterial overgrowth syndrome

A

Delayed small intestine transit time and diverticulum

41
Q

Small intestine bacterial overgrowth syndrome presentation

A
  • -Gas and bloating (due to fermentation)
  • -Anemia (competition for B12 uptake)
  • -Steatorrhea (deconjugate bile acids)
  • -Toxins alter epithelium
42
Q

How do you diagnose small intestine bacterial overgrowth?

A

Hydrogen breath test

43
Q

Xerostomia definition

A

Subjective sensation of dryness in oral mucosa

44
Q

Xerostomia causes

A
  • -Sjogren syndrome
  • -Lots of meds (esp. muscarinic antagonists)
  • -Secondary to head and neck radiation
  • -Dehydration
  • -Sialolithiasis
  • -Nerve damage related to injury or diabetes
  • -Postmenopausal hyposalivation
45
Q

Xerostomia consequences

A
  • -Increased likelihood of opportunistic infections
  • -Halitosis
  • -Tooth decay (decreased oral pH)
  • -Decreased taste
  • -Speech problems
  • -Dysphagia > malnutrition
46
Q

Treatment of xerostomia

A

Gum, artificial saliva, switch meds, parasympathomimetics

47
Q

What leads to halitosis in xerostomia?

A

Production of hydrogen sulfide by bacteria and accumulation of dead cells

48
Q

Dysguesia

A

Abnormal taste changes. Can occur from infection, aging, nutritional deficiencies

49
Q

Dysphagia/Odynophagia (causes and consequences)

A

Causes: structural abnormalities (cancer, diverticula) or functional abnormalities (stroke etc.)
Consequences: can lead to aspiration and malnutrition

50
Q

Primary diagnostic technique of dysphagia/odynophagia?

A

Videofluroscopic swallowing study. Barium swallowed with food and observed with x-ray

51
Q

GERD definition

A

Reflux of gastric acid contents into esophagus due to relaxation of lower esophageal sphincter

52
Q

Causes of GERD

A

Obesity, pregnancy, eructation, hiatal hernia

53
Q

Achalasia definition

A

Failure of LES to relax and in some cases lack of proximal peristalsis

54
Q

Manometry

A

Measures how tightly muscles contract when swallowing

55
Q

Portal hypertension

A

Gastric blood flow diverts and leads to formation of varices

GI (12 decks)

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