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Pathophysiology > 36. Digestive Alterations > Flashcards

36. Digestive Alterations Flashcards

1
Q

a non absorbable substance in the intestine draws excess water into the intestine and increases stool weight and volume; causes large-volume diarrhea

A

osmotic diarrhea

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2
Q

excessive mucosal secretion of fluid and electrolytes produces large volume diarrhea; can have infectious causes

A

secretory diarrhea

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3
Q

excessive motility decreases transit time and opportunity for fluid absorption resulting in diarrhea

A

motility diarrhea

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4
Q

characterized by frank bright red blood or dark, grainy digested blood (“coffee grounds”) that has been affected by stomach acid

A

upper GI bleeding (esophagus, stomach, duodenum)

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5
Q

bleeding from the jejunum, ilium, colon, or rectum

A

lower GI bleeding

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6
Q

usually caused by slow, chronic blood loss that is not obvious and results in iron deficiency anemia

A

occult bleeding

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7
Q

bright red stools

A

hematochezia

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8
Q

black tarry stools that are sticky and have a characteristic foul odor

A

melena

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9
Q

difficulty swallowing

A

dysphagia

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10
Q

2 types of dysphagia

A
  • mechanical obstruction - functional dysphagia (neural or muscular disorders)
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11
Q

rare form of dysphagia related to loss of inhibitory neurons in the myenteric plexus w/ smooth muscle atrophy in the middle/lower parts of esophagus

A

achalasia

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12
Q

What does achalasia lead to?

A

altered esophageal peristalsis and failure of lower esophageal sphincter (LES) to relax -> can cause distention/obstruction in esophagus

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13
Q

how do people manage symptoms of achalasia

A
  • eat small meals slowly - drink fluids with meals - sleep w/ head elevated to prevent regurgitation/aspiration
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14
Q

reflux of acid and pepsin or bile salts from the stomach into the esophagus that causes esophagitis

A

gastroesophageal reflux disease (GERD)

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15
Q

abnormalities in the LES, esophageal motility, and gastric motility or emptying can cause what?

A

GERD

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16
Q

type of diaphragmatic hernia w/ protrusion of the upper part of the stomach through the diaphragm into the thorax

A

hiatal hernia

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17
Q

proximal portion of stomach moves into the thoracic cavity through the esophageal hiatus

A

sliding hiatal hernia (type 1; most common)

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18
Q

herniation of the greater curvature of the stomach through a secondary opening in the diaphragm alongside the esophagus

A

paraesophageal hiatal hernia (type 2)

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19
Q

What can having a portion of the stomach above the diaphragm (type 2 hiatal hernia) cause?

A
  • congestion of mucosal blood flow -> gastritis and ulcer formation - strangulation of the hernia (medical emergency)
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20
Q

delayed gastric emptying in the absence of mechanical gastric outlet obstruction

A

gastroparesis

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21
Q

narrowing or blocking of the opening between the stomach and the duodenum (can be congenital or acquired)

A

pyloric obstruction (gastric outlet obstruction)

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22
Q

most common acquired cause of pyloric obstruction

A
  • peptic ulcer disease or carcinoma near pylorus - duodenal ulcers more likely to cause obstruction
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23
Q

caused by any condition that prevents the normal flow of chyme through the intestines; can occur in small or large bowel

A

intestinal obstructions

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24
Q

mechanical blockage of the intestinal lumen by a lesion (most common type of intestinal obstruction)

A

simple obstruction

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25
Q

failure of intestinal motility often occurring after intestinal or ABD surgery, acute pancreatitis, or hypokalemia

A

paralytic ileus (functional obstruction)

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26
Q

7 common causes of intestinal obstruction

A
  • hernia - intussusception - torsion (volvulus) - diverticulosis - tumors - paralytic ileus - fibrous adhesions (post-op; Crohn’s)
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27
Q

less common bowel obstruction that is usually related to cancer

A

large bowel obstruction

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28
Q

most common type of bowel obstruction

A

small bowel obstruction (SBO)

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29
Q

What does an intestinal obstruction lead to?

A

accumulation of fluid/gas proximal to obstruction

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30
Q

How would a bowel obstruction lead to pneumonia?

A
  • distention -> pressure on diaphragm -> decreased respiratory volume -> atelectasis -> pneumonia
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31
Q

How would a bowel obstruction lead to peritonitis?

A
  • distention and prolonged increased of wall tension -> decreased venous return -> bowel edema -> increased capillary permeability (fluid loss into peritoneum) -> bacterial translocation to peritoneum
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32
Q

How would a bowel obstruction lead to loss of water/electrolytes and dehydration?

A
  • ABD pain leads to N/V, decreased intake, decreased nutrient absorption, and decreased carb reserves (ketosis)
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33
Q

When does a bowel obstruction leads to alkalosis or acidosis?

A
  • alkalosis (early or high obstruction) - acidosis (late or low obstruction)
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34
Q

What 2 electrolytes are affected most by a bowel obstruction?

A
  • K (hypokalemia) - Cl (hypochloremia)
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35
Q

How would a bowel obstruction lead to shock?

A
  • distention -> increased capillary permeability - dehydration from loss of water/electrolytes - both lead to hypovolemia -> shock
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36
Q

inflammatory disorder of the gastric mucosa; can be acute or chronic

A

gastritis

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37
Q

break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum

A

peptic ulcer

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38
Q

2 most common causes of ulcers

A

NSAIDs and H. Pylori infection (both are erosive factors)

39
Q

most common type of peptic ulcer

A

duodenal ulcer (also caused by NSAIDs and H. Pylori)

40
Q

ulcers that occur in the stomach; often associated w/ chronic gastritis

A

gastric ulcers

41
Q

How do gastric ulcers form?

A
  • caused H. Pylori, NSAIDS, bile salts, alcohol, or ischemia - damage to mucosal barrier -> decreased function of mucosal cells -> diffusion of acid into gastric mucosa - formation of histamine -> increased acid production, increased capillary permeability and mucosal edema - conversion of pepsinogen to pepsin causes further erosion and bleeding -> ulcer
42
Q

Consequences of upper and lower GI bleeding

A
  • blood volume depletion -> decreased CO -> compensatory constriction of peripheral arteries - decreased blood flow to kidneys (renal failure) - decreased blood flow to GI structures -> bowel/liver infarction/necrosis - decreased blood flow to brain and heart - metabolic acidosis -> lactic acidosis -> death
43
Q

7 postgastrectomy symptoms

A
  • dumping syndrome - alkaline reflux gastritis - afferent loop obstruction - diarrhea - weight loss - anemia - bone/mineral disorders
44
Q

rapid emptying of hypertonic chyme from surgically residual stomach into the small intestine 10-20 minutes after eating; can cause N/V, osmotic diarrhea, pain, and hypotension

A

dumping syndrome

45
Q

stomach inflammation caused by reflux of bile and alkaline pancreatic secretions containing proteolytic enzymes

A

alkaline reflux gastritis

46
Q

cause of anemia after gastrectomy

A

loss of IF -> B12 deficiency -> pernicious anemia

47
Q

lactose intolerance is due to what?

A

deficiency in lactase (enzyme that breaks down lactose)

48
Q

Chief problem of pancreatic insufficiency

A

fat malabsorption -> steatorrhea

49
Q

chronic inflammatory disease that causes ulceration of the colonic mucosa (most common in rectum and sigmoid colon)

A

ulcerative colitis (UC)

50
Q

idiopathic inflammatory disorder that affects any part of the GI tract from the mouth to the anus; spreads with discontinuous transmural involvement (skip lesions)

A

Crohn’s disease (CD)

51
Q

most common sites of CD

A

ascending colon and transverse colon

52
Q

symptom based disease characterized by recurrent ABD pain w/ altered bowel habits

A

Irritable bowel syndrome (IBS)

53
Q

herniations or saclike outpouchings of the mucosa and submucosa through the muscle layers usually in the wall of the sigmoid colon

A

diverticula

54
Q

asymptomatic diverticular disease

A

diverticulosis

55
Q

diverticulosis w/ inflammation of diverticula

A

diverticulitis

56
Q

inflammation of the vermiform appendix (projected from the apex of the cecum)

A

appendicitis

57
Q

Internal vs external hemorrhoids

A
  • internal: may see bright red blood (not painful) - external: dilation of veins below the pectinate line (painful)
58
Q

obesity’s affect on adipocytes

A
  • insulin resistance - increased lypolysis - increased inflammation
59
Q

obesity’s affect on pancreas and liver

A
  • pancreas: increased insulin secretion (due to insulin resistance) - liver: insulin resistance, increased gluconeogenesis and glycogenolysis
60
Q

increased ghrelin from the stomach causes what?

A

increased appetite -> signals hypothalamus

61
Q

common complications of obesity

A
  • cardiovascular problems (HTN, CAD, stroke, MI) - pulmonary (sleep apnea, asthma) - endocrine (NIDDM, infertility) - MSK (OA, low back pain, plantar fasciitis) - GI (GERD, gallstones, fatty liver)
62
Q

4 cancers associated w/ obesity

A
  • breast - colon - renal - endometrial
63
Q

abnormally high blood pressure in the portal venous system caused by resistance to blood flow

A

portal HTN

64
Q

portal HTN commonly causes what?

A
  • esophageal varices - splenomegaly - caput medusae (ABD varices) - hemorrhoidal varices (internal hemorrhoids)
65
Q

most common cause of ascites

A

cirrhosis

66
Q

Mechanisms that cause ascites

A
  • portal HTN -> increased lymph production -> leakage into peritoneal space and decreased plasma volume - hepatocyte failure -> decreased albumin synthesis -> decreased oncotic pressure in capillaries - altered metabolism + decreased renal flow -> increased RAAS
67
Q

complex neurologic syndrome caused by accumulation of toxins normally removed from the liver and circulation into the brain

A

hepatic encephalopathy

68
Q

most hazardous toxin not removed from liver during hepatic ecephalopathy

A
  • ammonia (end produce to protein digestion) -> usually converted to urea
69
Q

What plasma concentration of bilirubin is considered hyperbilirubinemia

A

greater than 2.5-3.0 mg/dL

70
Q

causes of hyperbilirubinemia

A
  • post hepatic obstruction to bile flow - intrahepatic obstruction - prehepatic excessive production of unconjugated biluribn (hemolysis of RBC)
71
Q

increased destruction of erythrocytes causes what type of jaundice

A

prehepatic (unconjugated)

72
Q

decreased liver ability to excrete bilirubin causes what type of jaundice

A

intrahepatic obstructive jaundice (both conjugated and unconjugated)

73
Q

bile duct obstruction (cholestasis) causes what type of jaundice

A

extra hepatic obstructive jaundice (conjugated)

74
Q

rare clinical syndrome resulting in severe impairment of liver cells without preexisting liver disease or cirrhosis

A

acute liver failure (fulminant liver failure)

75
Q

most common causes of acute liver failure

A
  • acetaminophen overdose (most common) - Hepatitis B
76
Q

irreversible inflammatory, fibrotic liver disease

A

cirrhosis

77
Q

clinical manifestations of cirrhosis

A
  • portal HTN (ascites, varices, splenomegaly) - decreased bilirubin metabolism (jaundice) - decreased bile in GI tract (light colored stools) - decreased vitamin K absorption (bleeding) - decreased hormone metabolism and increased androgens/estrogens - decreased protein, fat, and carb metabolism - toxin accumulation (hepatic encephalopathy)
78
Q

lab changes seen with cirrhosis

A
  • increased AST and ALT - increased bilirubin - low serum albumin - prolonged PT - elevated alkaline phosphatase
79
Q

infiltration of hepatocytes with fat (primarily triglycerides) in the absences of alcohol intake; associated w/ obesity

A

nonalcoholic fatty liver disease

80
Q

What forms before cirrhosis

A
  • alcoholic fatty liver (steatosis) - alcoholic steatohepatitis (alcoholic hepatitis)
81
Q

systemic viral disease that mainly affects the liver

A

viral hepatitis

82
Q

5 types of hepatitis and their routes

A
  • Hep A (fecal-oral; most common), parenteral, sexual - Hep B (parenteral, sexual, transplacental) - Hep C (parenteral, sexual, transplacental) - Hep D (Hep B coinfection, fecal-oral, sexual) - Hep E (fecal-oral)
83
Q

clinical phases of hepatitis

A
  • incubation - prodromal (highly transmissible) - icteric (acute illness) - recovery
84
Q

types of hepatitis that cause chronic active hepatitis

A
  • Hep B - Hep B/Hep D coinfeciton - Hep C
85
Q

formed from impaired metabolism of cholesterol, bilirubin, and bile acids

A

gallstones

86
Q

cardinal manifestations of cholelithiasis

A
  • epigastric and right hypochrondrium pain - intolerance of fatty foods
87
Q

cause of cholecystitis

A

gallstone lodged in the cystic duct -> causes gallbladder to become distended and inflamed

88
Q

pathophysiology of acute pancreatitis

A
  • duct obstruction -> acing cell injury - intracellular and extracellular activation of enzymes - lipase -> fat necrosis - trypsin, chymotrypsin, phospholipase, and elastase along w/ inflammation (complement and cytokines) cause cell injury, edema, thrombosis, hemorrhage, and necrosis
89
Q

What can acute pancreatitis lead to?

A
  • shock - SIRS - ARDS - acute tubular necrosis (ATN) - coagulation disorders - translocation of intestinal bacteria -> sepsis - pancreatic abscess
90
Q

most common cause of chronic pancreatitis

A

chronic alcohol abuse

91
Q

closely associated w/ development of colorectal cancer

A

colorectal polyps

92
Q

premalignant lesions

A

neoplastic polyps (tubular most common)

93
Q

most common type of colorectal polyps

A

hyperplastic (nonneoplastic or benign)

94
Q

signs and symptoms of colorectal cancer

A
  • pain - mass - change in bowel habits - blood in stool - anemia

Pathophysiology (20 decks)

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