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x 6102 Pathophys > gastro > Flashcards

gastro Flashcards

1
Q

vomiting center (3)

A

medulla

  • reticular formation
  • tractus solitarius
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2
Q

vomiting center stimulated by

A

serotonin –> medulla

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3
Q

diarrhea: osmotic

A

malabsorption (too much water in lumen)

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4
Q

diarrhea: secretory

A

C. diff

  • spores cause inflammation
  • cells burst and die
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5
Q

diarrhea: motility

A

ex: irritable bowel syndrome
- overstimulated sympathetic
- accelerated peristalsis/intestinal movement

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6
Q

abdominal pain: parietal

A

along perineum (more specific to location of origin)

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7
Q

abdominal pain: visceral

A

actual organ (distention or inflammation)

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8
Q

abdominal pain: referred

A

examples:

urologic (calculi, bladder cancer)

cardiac (MI)

heartburn

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9
Q

dysphagia x2

A

mechanical (tumor, stricture)

functional (muscular or neuro problem, ex: myasthenia gravis)

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10
Q

achalsia

A

esophagus doesn’t relax, needs stent

common in elderly

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11
Q

hiatal hernia

A

bit of stomach fundus moves up through gap in diaphragm into thoracic cavity

surgical emergency when strangulation

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12
Q

GERD

A

reflux d/t decreased resting tone of lower esophageal sphincter

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13
Q

peptic ulcer: gastric

A

often antrum

  • H. pylori, stress, critical illness
  • histamine release = acid production increase = disrupted mucosa
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14
Q

peptic ulcer: duodenul

A

most common

d/t acid & pepsin penetrating mucosa

tx: H2 or PPI

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15
Q

upper GI bleed x3

+ sx + d/t

A

esophagus, stomach, duodenum

bright red blood, emesis, coffee ground stool

d/t esophageal varices + malory weiss tears, intractable vom

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16
Q

lower GI bleed

+ d/t

A

jejunum, ileum, colon, rectum

d/t inflammatory disease, hemorrhoids, diverticula

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17
Q

pyloric obstruction

A

“gastric outlet obstruction”
between stomach & duodenum

results in distention/discomfort and typically requires surgical repair

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18
Q

intestinal obstruction and ileus: herniation

A

prolapse/pouch through wall

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19
Q

intestinal obstruction and ileus: adhesions

A

common post-surgical - scarring or abnormal interaction of tissues (stuck to each other)

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20
Q

intestinal obstruction and ileus: volvulus

A

twisting
- can result in ischemia or death of chunk of tract = emergency

colectomy may result

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21
Q

intestinal obstruction and ileus: intussusception

A

telescoping

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22
Q

intestinal obstruction and ileus: intervention

A

SURGICAL!

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23
Q

gastritis: acute

A

destruction of mucosal barrier

- meds (NSAIDS!), chemicals, H. pylori

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24
Q

gastritis: chronic

A

chronic fundal gastritis = most severe
- t cell & autoantibodies involved = prolonged inflammatory response

common in geriatric

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25
Q

ulcerative colitis

A
  • continuous lesions
  • not transmural
  • inflammation leads to cytokines = VERY WATERY DIARRHEA (less absorptive area, decreased transit time)
  • most severe: rectum, sigmoid
  • remission/flare
  • can lead to toxic megacolon, perforation, abscess
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26
Q

crohn’s disease

A
  • idiopathic
  • ANYWHERE along tract (mouth - anus)
  • skip lesions
  • bloody or MUCOID stools (mucommon)
  • weight loss (poor absorption, slower motility)

CHRISTMAS

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27
Q

crohn’s CHRISTMAS

A 
c obblestones (radiology)
h igh temp
r educed lumen (inflamm)
i ntest fistula (desperexit)
s kip lesions
t ransmural (all layers, can ulcerate)
m alabsorption
a bdominal pain
s ubmucosal fibrosis
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28
Q

diverticular disease

A

colonic mucosa herniates through smooth muscle layers = outpouching

can be asymptomatic, inflammatory, or ruptred

flares common, 50s-60s common

mgmt: diet, bowel rest, abx, surgical (rupture = emergency)

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29
Q

appendicitis

A

inflamed appendix

common 20-30s

medical emergency

s/s: n/v fever, periumbilical pain radiating to RLQ

tx: abx, appendectomy

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30
Q

appendicitis pain

A

periumbilical radiating to RLQ

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31
Q

irritable bowel syndrome

A

w/ c or d or BOTH

dx of exclusion

tx: diet, anti-spasmodics, etc

no specific pathology:

  • visceral hypersensitivity
  • abnormal GI permeability, mobility, secretion
  • post-infectious
  • overgrown intestinal flora
  • food/allergy intolerance
  • psychosocial
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32
Q

obesity BMI

A

> 30 kg/m2

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33
Q

obesity: adipokines

A

secreted by adipocytes,

assist in regulation of intake, lipid metab/storage, insulin sensitivity

visceral fat leads to adipokine dysfunction

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34
Q

leads to adipokine dysfunction

A

visceral fat

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35
Q

brain bit related to obesity and what it does

A

arcuate nucleus (hypothalamus)

balances energy intake and metabolism

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36
Q

refeeding syndrome

A

severely malnourished pts must have nutrition restarted slowly with close monitoring

starvation causes lyte shift out of cell into plasma, aggressive nutrition = insulin causes glucose + ions to move back into cell = profoundly low serum lyte concentrations
- PO4, K, Mg, Ca

20kcal/kg/day with lyte monitoring

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37
Q

leading cause of acute liver failure in the US

A

acetaminophen

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38
Q

acute liver failure: complications

A 
portal htn
esophageal varices
splenomegaly
hepatopulmonary syndrome
ascites
hepatic encephalopathy
jaundice
hepatorenal syndrome
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39
Q

hep B

A

autoimmune or viral
- vertical or horizontal, sex, parenteral (IV), needle stick

damaged hepatocytes

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40
Q

hep C

A

contaminated needles

- less common: sex, vertical transmission

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41
Q

hep B damaged hepatocytes x3 mechanisms

A
  1. HLA Class I restricted cytotoxic T-cell response intended for HBV-infected hepatocytes
  2. cytopathic effect of Hep B viral protein antigen (HBcAg) expression in affected hepatocytes
  3. over expression, ineffective secretion HbsAg (compensatory mechanism)

C = core
S = surface
both r/t protein

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42
Q

hep C mechanism of damage

A

direct cellular toxicity d/t release of cytokines intended to kill virus

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43
Q

cirrhosis

A

irreversible damage to liver d/t inflammation and fibrosis

leading causes: EtOH abuse, hepatitis

fibrotic lesions (d/t Kuppfer cells) alter biliary/blood flow = jaundice, portal htn

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44
Q

kuppfer cells

A

part of reticular endothelial cells (system) - stellate macrophages in liver

in cirrhosis, can promote deposition of fibrotic products by releasing inflammatory mediators & growth factors

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45
Q

non-alcoholic fatty liver disease (NAFLD)

A

occurs in absence of alcohol

most commonly associated with obesity, HLD, metabolic syndrome, DM2

most common chronic liver disease (US)

may progress to NASH

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46
Q

non-alcoholic steatohepatitis (NASH)

A

can result from NAFLD

may progress to cirrhosis, ESLD, hepatocellular carcinoma

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47
Q

biliary cirrhosis: primary

A

t lymp & ab-mediated destruction of intrahepatic bile ducts
- often accompanies other autoimmune diseases

dx: 2/3 -
1. biochem evidence of disease (min 6 mo)

  1. antimitrochondrial antibody (AMA) positivity
  2. histologic features of liver biopsy
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48
Q

biliary cirrhosis: secondary

A

d/t partial or complete obstruction of common bile duct (or branches)

can be d/t gallstones, tumors, strictures, chronic pancreatitis

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49
Q

alcoholic cirrhosis

A

d/t toxic effects on liver metabolism, immunologic changes, oxidative stress and malnutrition

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50
Q

cholelithiasis

A

formation of gallstones

cholesterol or pigmented

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51
Q

cholelithiasis: risk factors

A 
obesity
rapid weight loss
middle age
female gender
oral contraceptives
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52
Q

cholelithiasis: cholesterol

A

form in bile that is supersaturated with cholesterol, forming crystals

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53
Q

cholelithiasis: pigmented

A

black: hard, associated with hyperbilirubinemia
brown: soft often d/t bacterial infection of bile ducts

54
Q

cholecystitis

A

usually caused by gallstone in cystic duct leading to obstruction (distends & inflames gallbladder)

55
Q

acute pancreatitis x4

A

1) obstruction of bile or pancreatic duct, preventing outflow or pancreas digestive juices
2) alcohol abuse
3) drugs
4) viral infection

digestive enzymes activated in pancreas = autodigestion = inflammation

56
Q

chronic pancreatitis

A

repeated occurences, may be d/t gallstones (** especially), autoimmune disease, gene mutations, smoking, chemical exposure, obesity

57
Q

third most common cause of cancer death in US both men & women

A

colon cancer

58
Q

hepatocellular carcinoma

A

closely related to cirrhosis

HCV, HBV, cirrhosis lead to this d/t cellular proliferation, effects of growth factor, cytokine, oxidative stress

MELD score for transplant

59
Q

pancreatic cancer

A

most arise from exocrine cells (secretory cells provide enzymes for digestion) but can from endocrine (alpha, beta)

ductal adenocarcinomas most common

WHIPPLE PROCEDURE - temporizes, not curative (digestive capabilities still lacking, malnutrition, poor healing, underlying cancer)

60
Q

whipple procedure

A

temporizing surgical procedure for pancreatic cancer

not curative bc digestive capabilities still lacking, malnutrition, poor healing, underlying cancer

61
Q

four layers of GI tract

A

mucosa (mucus membrane)

submucosa

smooth muscle (circular then longitudinal)

serosa (serous membrane)

62
Q

GI smooth muscle electrical activity:

waves + responsible + result

A

SLOW

  • interstitial cells of Cajal (pacemaker) stim by parasymp vs symp
  • not action potential, pulsation resting membrane potential

SPIKE

  • Ca/Na channel (slow open = prolonged action potential)
    • Ca = contraction
  • true action potential
63
Q

enteric nervous system + 2 plexes & function

A

GI-specific nervous system

myenteric (outer, between longitudinal & circular)
- fxn: movement

vs

submucosal (inner)
- fxn: secretion & blood flow

64
Q

myenteric plexus aka

A

Auerbach’s plexus

65
Q

submucosal plexus aka

A

Meissner’s plexus

66
Q

ANS neuron neurotransmitters working in conjunction with enteric neurons x2

A

parasympathetic: ACh
(excites - take ACh-tion!!)

sympathetic: Norepineprhine
(inhibits - NO action!)

67
Q

cranial nerve of mastication

A

V

68
Q

deglutition

A

voluntary swallowing (ex: oropharyngeal bit of esophagus)

69
Q

prevents backflow of food from stomach into esophagus

A

lower esophageal sphincter

70
Q

why anticholinergics cause constipation

A

depress myenteric plexus

71
Q

GI movements x2

A

propulsive (peristalsis)
- must have active myenteric plexus

mixing (segmentation)
- chopping, violent

72
Q

stomach: 3 parts

A

fundus, body, antrum

73
Q

stomach: absorption

A

very little

exceptions: NSAIDS, alcohol, aspirin

74
Q

x2 hormones stimulate gastric motility & what mediates them

A

gastrin & motilin

- PS mediated vagal nerve

75
Q

inhibits gastric motility & how

A

secretin

- symp nerve mediated

76
Q

gastric secretion: gastric glands

A

along mucosa, primary secretory units

77
Q

gastric secretion: parietal cells

secretes what & stimulated by

A

aka oxyntic

secretes: HCl, IF, gastroferrin

stim by ACh & gastrin & histamine
- ACh released by vagus nerve, stims g & h

78
Q

gastric secretion: chief cells

A

secretes: pepsinogen

79
Q

pepsinogen

A

secreted by gastric chief cells, inactive precursor to PEPSIN
- protein to peptide

responsible for GERD & esophageal degradation

80
Q

gastric secretion: enterochromaffin cells secrete what

A

histamine

H2 blockers work here

81
Q

gastric secretion: D cells secrete what

A

somatostatin

82
Q

gastric secretion: somatostatin

stimulated by & result

A

stimulated by: acid

result: inhibits acid, pepsinogen release

83
Q

strongest stimulation for pepsin secretion

A

ACh

84
Q

gastric secretion: gastrin

A

stimulates gastric glands to secrete HCl, pepsinogen

growth of mucosa
promotes motility

85
Q

gastric secretion phases x3

A

cephalic (sensory responses to food)
- mediated by vagus/myenteric plexus

gastric (food enters stomach = distension)
- mediated by vagus/enteric plexus

intestinal (chyme enters duodenum, GI motility slows)

86
Q

duodenum ends at

A

ligament of Treitz

87
Q

duodenal villi composed of x3

A

columnar epithelial
goblet cells
enterocytes

88
Q

small intestine countercurrent exchange

A

arterial and venous flow in villi opposite directions, blood often goes from art to ven directly without being carried into tip of villi

89
Q

short gut syndrome

A

after large resected gut chunk

  • blood shunted
  • disrupted countercurrent exchange
  • poor absorption
90
Q

crypts of Lieberkuhn

A

between villi of small intestine (duod) - goblet + enterocytes reside here

91
Q

Paneth cells

A

built in immunity in small intestine

Paneth like Janeth T, ID MD

92
Q

hepcidin

A

iron buffer preventing iron trafficking

93
Q

fat digestion/absorption phases x4

A
  1. emulsification/lipolysis
  2. micelle formation
  3. fat absorption
  4. resynthesis of trigs & phospholipids
94
Q

main types of lipids & function x3

A

triglyceride - energy

phospholipid - membrane structure

cholesterol - not a lipid but has lipophilic head or something / membrane structure

95
Q

where chylomicron is synthesized & what it does

A

made in small intestine by enterocytes

with VLDL, delivers TAG to cells

96
Q

enterocytes remind you of: x2

A

chylomicron makers

live in the Crypts of Lieberkuhn (between duodenal villi)

97
Q

on chylomicron cell surface

A

Apoprotein B so they can be suspended and not stick to shit

98
Q

TAG - what and what happens to it

A

energy rich molecule delivered by chylomicron/VLDL to cells

broken down by lipoprotein lipase into fatty acids and monoglycerides so they can diffuse into cell to be oxidized

99
Q

how is adipose tissue mobilized to be used as energy?

A

hydrolysis turns triglyercides into fatty acids and glycerol

100
Q

what happens to free fatty acids that leave fat cells

A

immediately bind with albumin

101
Q

hydrolysis stimulated by

A

inadequate glucose (primary energy means)

hormones (endocrine glands)

102
Q

where are lipoproteins made and what do they NOT do

A

made in liver

DON’T transport free fatty acids

103
Q

liver role in storage of lipids

A

degrade fatty acids into smaller units for energy use

desaturates triglycerides lowering their melting point = they can stay liquid and are easy to transport

uses little of fatty acids made and turns remainder into acetoacetic acid to be sent to cells

104
Q

how to turn triglycerides into ATP x6

A
  1. hydrolysis
  2. fatty acids & glycerol oxidized
  3. glycerol enters glycolytic pathway
  4. fatty acids degraded in mitochondria
  5. beta oxidation into Acetyl CoA
  6. Acetyl CoA enters Kreb’s
105
Q
  • what does beta oxidation do to fats? *
A

turns into acetyl CoA

106
Q

the story of acetoacetic acid

A

it is siamese Acetyl CoA forme din the liver

they go to tissues, get broken back into 2 Acetyl CoA to enter Kreb’s

if there’s tons of acetoacetic acid (higher than normal) = ketosis

107
Q

ketosis

A

acetoacetic acid levels are higher than normal

108
Q

acetoacetic acid + not enough carbs

A

not enough carbs = not enough oxaloacetic acid = Krebs is hindered

acetoacetic acid steps in and makes ketons

109
Q

lack of insulin or TH - what effect does it have on lipids?

A

increases plasma concentration of cholesterol

110
Q

atherosclerosis vs arteriosclerosis

A

athero: fatty lesions on inner surface of arterial walls (macrophage oxidize lipoproteins = foam cells = fatty streak)
arterio: thick/stiff vessels

111
Q

deamination

A

removes an amino group from protein

it is breakdown of proteins into smaller molecules for energy purposes

activated by aminotransferases

releases ammonia which is turned into urea in the liver and removed through urine

112
Q

activate deamination

A

aminotransferases

113
Q

urea cycle

A

deamination releases ammonia

liver turns ammonia into urea

5 enzymes involved

urea excreted in urine

114
Q

how are deaminated amino acids mobilized for energy

A

KETO ACID turned into substance that can enter Kreb’s Cycle

the substance is used for energy the same way Acetyl CoA is

115
Q

ketogenesis

A

conversion of amino acids into keto or fatty acids

116
Q

blood supply to large intestine

A

superior and inferior mesenteric arteries

117
Q

divides liver into 2 lobes

A

falciform ligament

118
Q

liver blood supply

A

hepatic artery (branches from celiac, 25% CO)

portal vein (75% liver blood supply)

119
Q

functional unit of liver

A

lobules aka acini (50-100k total)

120
Q

central vein

A

branch of hepatic artery that goes through the middle of the liver

empties into IVC

121
Q

venus sinusoids lined with 3 cell types

A 
hepatic
endothelial
reticuloendothelial (Kupffer)
122
Q

reticuloendothelial cells

A

aka Kupffer cells

macrophages of the liver

123
Q

spaces of disse

A

permeable and allow fluids and proteins into parasinusoidal space - connect liver to lymphatic system

drainage & immunity

124
Q

sphincter of Oddi

A

the gatekeeper of the gallbladder! decides when to let bile out

contracted during interdigestive period, causes bile to flow into gallbladder (thanks to increased pressure in common bile duct)

open during digestive period thanks to CCK

125
Q

sphincter of Oddi stimulated by (and result)

A

cholecystokinin! stimulates gallbladder contraction + relaxation of sphincter of Oddi

126
Q

what breaks down old RBCs (+ 2 things RBCs are broken into)

A

spleen or Kupffer cells in liver

+ globin = aa
+ heme = biliverdin

127
Q

unconjugated vs conjugated bilirubin

A

un: lipid soluble
conj: water soluble & excreted as bile

128
Q

liver stores which vitamin the most?

A

A!

129
Q

liver stores iron as

A

ferritin

130
Q

ampulla of Vater

A

common bile duct meets duodenum

131
Q

acinar cells & what they secrete (specific) + function

A

secrete digestive enzymes in pancreas

tripsin, chylotripsin
+ carboxypepsidase, elastase

function:
- alkaline and help neutralize chyme
- hydrolyze protein, carbs, fats

x 6102 Pathophys (6 decks)

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