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KCSU17 Patho/Pharm Submodule 2 > GI > Flashcards

GI Flashcards

1
Q

contents of GI

A 
mouth
esophagus 
stomach 
small intestine 
large intestine 
rectum 
anus

7-9 meters

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2
Q

functions of GI

A
  1. digestion (break down of food for absorption)
  2. secretion (large volume of fluid secreted, some acidic and some basic)
  3. motility (coordinated movement)
  4. Absorption (nutrient extraction by passive active transport)
  5. Defense
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3
Q

Mechanisms that control the GI

A

intrinsic
extrinsic
hormonal

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4
Q

intrinsic control of GI

A

enteric nervous system

local control of GI

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5
Q

extrinsic control of GI tract

A

via nervous system

parasympathetic via vagus nerve

sympathetic input: thoracic spinal cord

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6
Q

hormonal control of GI

A

endocrine cells of stomach and intestine

paracrine control (multiple systems such as histamine and somatostatin release)

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7
Q

two stages of swallowing

A
  1. pharyngeal

2. esophageal

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8
Q

pharyngeal swallowing

A

food in pharynx stimulates closer of all openings except esophagus

food is moved to top of esophagus

UES relaxes and closes after bolus passage

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9
Q

where does voluntary control of swallowing stop?

A

when food is in pharynx

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10
Q

esophageal swallowing

A

begins once food bolus has passed to UES

vagus n. stimulates peristaltic contraction and LES is relaxed

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11
Q

clinical importance of oropharyngeal control and esophageal motility

A

can cause aspiration (good gets into the lungs)

found following stroke and dementia or brain tumor

systemic/distal cause, not often a cause of esophagus

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12
Q

cells that secrete stomach acid

A

parietal cells

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13
Q

parietal cells

A

secrete H+ in exchange for a K+ via ATPase pump

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14
Q

histamine

A

paracrine activator of stomach acid

binds to H2 receptors on parietal cells

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15
Q

gastric glands

A

secrete mucins that produce the gel layer

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16
Q

mucins

A

competent of mucus gel layer that adheres to the gastric epithelium

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17
Q

mucus gel layer

A

composed of mucins and small amounts of HCO3 to this layer

allows for pH to be around 7.0

irritation can cause gasatritis

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18
Q

irritation of mucus layer

A

stimulates additional mucin secretion

gastric juices are able to upset the stomach layer

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19
Q

which part of the stomach is a reservoir

A

corpus

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20
Q

antrum

A

part of the stomach that exerts powerful muscular contractions to break off food

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21
Q

what controls gastric emptying

A

stomach contraction

duodenal pyloric relaxation via the vagus nerve

chemical composition of the chyme

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22
Q

composition of chyme

A

acid, fat, hyperosmolar solutions will empty more slowly

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23
Q

major site of absorption

A

small intestine

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24
Q

part of the small intestine that gives it high absorption rates

A

brush border

carbohydrates, proteins, lipids, H2O, and electrolytes

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25
Q

if you can’t absorb something

A

increase in osmolarity within small bowel lumen

will cause diarrhea, cramps

GI moves it along quickly

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26
Q

slowing down of peristaltic contractions causes?

A

more complete absorption

constipation

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27
Q

most of GI microbes are found

A

in the colon

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28
Q

colon absorbs

A

most of the fluids and electrolytes

esp. water and potassium

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29
Q

common signs and symptoms of GI Dz

A

abdominal or chest pain

altered ingestion of food
altered bowel movements
GI tract bleeding
course of sepsis

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30
Q

complications of GI disease

A

dehydration
sepsis
bleeding

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31
Q

evaluation of GI symptoms

A 
labs
imaging (plain films, CT scan, ultrasound, EGD, sigmoidoscopy, colonscopy)
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32
Q

labs for GI symptoms

A

chemistry panel and CBC

LFTs or amylase/lipase levels to eval liver of pancreatic pathology

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33
Q

imaging done for GI

A

plain films

CT scan

ultrasound

EgD

flexible sigmoidoscopy

colonoscopy

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34
Q

plain films

A

KUB/upright

useful ut limited

used for bowel obstruction, ileus, or constipation

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35
Q

usually diagnostic study of choice

A

CT scan

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36
Q

ultrasound

A

increasingly used for appendicitis, kids, and decrease radiation exposure

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37
Q

EDG

A

evaluates esophagus, stomach, duodenum

direct visualisation

can biopsy specimens, pics, dilate, or inject substances

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38
Q

flexible sigmoidoscopy

A

evaluation of left colon

preform biopsy and removal of masses

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39
Q

colonoscopy

A

evaluation of colon

under direct visualization

can preform biopsy, pictures, and removal of masses

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40
Q

etiologies of esophageal achalasia

A

unknown

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41
Q

esophageal achalasia

A

loss of lower esophageal neurons and defective innervation

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42
Q

consequences of esophageal achalasia

A

lower sphincter fails to relax properly

tonic contraction of the LES is unusually harsh

causes defective peristalsis in esophagus eventually a dilated distal esophagus

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43
Q

symptoms of esophageal achalasia

A

vomiting (bc throat is full)

chest pain/discomfort

cough

aspiration

poor breath/foul breath

symptoms worsen when lighting down

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44
Q

treatment of esophageal achalasia

A

botulinum toxin

can rip esophagus, or stent it (both risk reflux) so both are secondary until Botox

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45
Q

how does Botox fix esophageal achalasia

A

relaxes the LES

paralyzes it slightly to let food pass

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46
Q

normal function to prevent acid reflux

A

gastric acid kept awn from esophagus by tonically contracted LES and peristalsis of esophagus

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47
Q

reflux

A

barrier is breached

reflex of caustic gastric acid

relatively unprotected esophagus results in burning substernal pain

48
Q

recurrent reflux

A

causes scarring and inflammation of esophagus

LES is is less competent

49
Q

causes of GERD

A

facilitated by weak LES or herniation of stomach thru diaphragm hiatus

50
Q

causes of hiatal hernia

A

obesity
overeating
pregnancy
ascites

anything that increases abdominal pressure

51
Q

mechanisms of GERD

A
  1. loss of LES tone or esophageal peristalsis (pregnancy, alcohol, overeating)
  2. increased stomach volume or pressure
  3. increased gastric acid production
52
Q

consequences of GERD

A

recurrent esophageal mucosa

  1. friable, bleeding ulcers/esophagitis
  2. hemorrhage and perforation
  3. fistula formaiton
  4. esophageal strictures
  5. replacement of normal squamous epithelium with columnar epithelium
53
Q

Barrett’s esophagus

A

when columnar epithelium of esophagus (caused by GERD) cause esophageal adenoCA

54
Q

processes of peptic and duodenal ulcer disease

A
  1. excessive acid secretion (acid not proper buffer)

2. inadequate mucosal defense (gel layer decreases)

55
Q

etiologies of peptic and duodenal ulcer disease

A 
H. pylori infection 
NSAID use
smoking
alcohol 
stress 
reflux of bile into stomach
56
Q

H. Pylori infection

A

colonizes more than 50% of people

spread is fecal oral

most show gastritis but only some develop clinical ulcer disease

57
Q

H. pylori pathology

A

increases gastric acid production

weakens mucosal defenses

if treated for ulcer but not H. Pylori dz will rapidly recur

58
Q

urease

A

H. pylori

neutralizes gastric acid

gastric mucosal injury via ammonia

ammonia creates a nest/protection of the bacteria from H. pylori

59
Q

pathophysiology of NSAID induced dz

A

inhibition of prostaglandin synthesis by NSAIDs causing diminished vasodilation and local relative ischemia of gastric mucosa

mucosa can not repair itself or produce mucus/bicarbonate = inadequate mucosal defense

makes ulcers and worsen if NSAID use continues

60
Q

spectrum of acid DX

A

first comes erosive gastritis followed by ulceration

61
Q

erosive gastritis

A

first manifesto of acid induce Dz

gastric mucosa is irritated up to shallowly ulcerated

maybe ne acute or chronic

62
Q

acute erosive gastritis

A

follows an episode of insult to the gastric mucosa

heavy EtOH and heavy NSAID use

63
Q

chronic erosive gastritis

A

caused by the same mechanisms

just not severe enough to cause more than shallow mucosal ulceration

64
Q

ulceration

A

eaten away top layer of exposed skin

surrounding rim of inflammation with yellow scar tissue in middle

can be duodenal or gastric

65
Q

gastric ulcer

A

ulceration penetrating through the mucosa to the submucosa and muscularis mucosa

surrounded by erosive gastritis

most common site is the lesser curvature of stomach

66
Q

duodenal ulcers

A

same thickness of penetration

more likely to be associated with H pylori infection and genetics

67
Q

signs of ulcers

A

gnawing pain in epigastrium or sub sternal chest pain

may radiate to back

relieved by food and antacids

can present atypical, painlessly (elderly)

68
Q

complications of an ulcer

A

bleeding
perforation
obstruction (due to scaring)

69
Q

treatment of acid disorders

A

antacids/Tums
H2 blocks (Famotidine/Pepcid)
Proton pump inhibitors (Lansoprazole/Prevacid)

70
Q

antacids

A

Tums

contains ions that soak up the acid within the stomach, rendering it neutral (decreases the amount of acid that is there)

meant to be PRN

excessive use can cause metabolic acidosis

71
Q

H2 Blockers

A

Famotidine/Pepcid

blocks effects of histamine in gastric mucosa – no H+ activation over time

72
Q

Proton pump inhibitors

A

Lansoprazole/Prevacid

block the H+/K pump that creates the acidic environment
strongest acid treatment

need a bit of acid to work, so can’t be taken with food or concurrent with H2 blockers

73
Q

ligament of Treitz

A

separates upper and lower GI

74
Q

upper GI bleed

A

melena

black tarry and smelly stools

consequence of blood digestion in GI tract

coffee ground emesis or hemetemasis (vomiting red blood)

75
Q

Lower GI bleed

A

hematochezia

maroon BM to bright red bleeding BM

76
Q

why is the GI tract so prone to bleeding?

A

lots of vasculature on surface

if you have a platelet disorder this is particularly problematic bc GI tract can be easily damaged

77
Q

dumping sundrome

A

too rapid transit of chime to small intestine

causes cramping, diarrhea, and light headedness

osmotic load induced fluid shifts from vasculature to intestine (not going slowly instead taking a big load and pulling water in)

MC cause surgical alteration, neurologic issues, diabetes

78
Q

gastroparesis

A

prolonged transit of chyme to intestine

causes bloating, nausea, bacterial overgrowth, erratic blood glucose and bezoars

MC cause: autonomic neuropathy

79
Q

2 pathophysiological mechanisms of diarrhea

A

osmotic diarrhea

secretory diarrhea

80
Q

osmotic diarrhea

A

failure to absorb osmotically active substance from the intestine

causes water retention by intentional contents

takes water with it

deficient absorption, pancreatic deficiency

81
Q

secretory diarrhea

A

secreted hormones by untested cause water secretion form intestinal epithelial cells

pushes water out of cell into stool

enterotoxins, tumor products, lacatives

82
Q

gateroenteritis

A

stomach flu

acute inflammation of stomach and intestines

typically caused by virus

s/s: N/V/D, cramps

disease is self limiting and treatment is supportive

norovirus is likely cause, typically don’t give anti diarrheal bc they need to get it out

83
Q

autoimmune reaction to normal bowel flora

A

Inflammatory bowel dz

causes collateral damage to GI

results in cramping, abdominal pain, weight loos, irregular bowels

infection response

84
Q

two types of IBD

A

churn’s

ulcerative colitics

85
Q

Crohn’s Disease

A

Full thickness bowel wall involvement from mouth to anus with skip lesions (random spots of inflammation)
-impacts muscularis, cirrosal outer layer

often causes perirectal abscess snd fistula formation

commonly found in distal illeum

slightly higher CA chances

86
Q

ulcerative colitis

A

found in colon and rectum only

often causing proctitis with bloody stools with tenesmus (fee like you have to poop but don’t)

affects ONLY mucusoal layer

higher potential for CA due to higher cell turnover

87
Q

Crohn’s disease causes

A

transmural inflammation causes lympatic obstruction and eventually edema, mucosal ulceration, and fissures

88
Q

pathophysiologic consequences of Crohn’s

A
  1. inflammation that interferes with nutrient absorption
  2. bowel wall thickens decreasing lumen diameter (prone to blockage)
  3. inflammation promotes adhesion formation (scar tissue connecting tissue)
  4. inflammation causes abscess and fistula formation
89
Q

UC most commonly begins

A

at rectum and spreads proximally to colon

UC is mild dz with few exacerbations

bc this only effects MUCOSA it is not quite as severe

90
Q

s/s of IBD flare

A

sharp, cramping abdominal pain

bloody diarrhea (frankly blood)

break down of mucosa

infection symptoms (Fever, cills)

toxic megacolon

91
Q

toxic megacolon

A

colon gets so infected it dilates and moves air thru

increases in size then it gets thinner so it might perforate

92
Q

IBD flare ups outside bowels

A

10-20% of pts

arthritis or uveitisi

93
Q

arthritis and IBD

A

begins with LBP and morning stiffness

more common in crohn’s

best treated by treating IBD (manifestation)

94
Q

uveitis

A

painful inflammation of middle eye wall causing blurred vision, redness and sensitivity to light

95
Q

treatment for IBD

A

5-Asa derivatives
prednisone/solumedrol
azathioprine/imuran
inflizamab/remicade

96
Q

5- ASA Derivatives

A

aminosalicylates

mesalamine (Asacol)

initial treatment for IBD (non flare)

multiple, some enema, some oral and suppository

more helpful in UC than Crohn’s

mainstay of treatment for both (esp. mild)

97
Q

steroids

A

work really well but don’t want to have them on it for life

Prednisone/Solumedrol

treat acute flare of IBD

given IV at high dose for a dew days

de-escalated to oral for a taper

98
Q

azathioprine (Imuran)

A

immunomodulary agent that is used to tread IBD

refractory to 5ASA

2-3 months to begin working so CI for flares

SE: cytopenias, hepatitis, fever can occur so you need CBC and LFT often

increase risk of developing lymphoma and non melanoma skin CA

99
Q

inflixamab (remade)

A

immunomodulary agent that is used to tread IBD

more effective in Crohn’s can be used to induce remission in acute flare or maintenance

increases risk for infection

100
Q

most common cause of small bowel obstruction

A

adhesions

iatrogenic cause via surgery or inflammation

causes finding of small intestine

101
Q

SBO can also be caused by

A

tumor or hernia that is incarcerated

102
Q

treatment of partial SBO

A

watchful waiting

don’t want surgery bc it can lead to more adhesions

partial SBO is painful but not obstipation or distention

103
Q

treatment of complete SBO

A

surgery to remove obstruction

104
Q

SBO s/s

A 
constipation/obstipatoin 
cramping (due to peristaltic rushes) 
infection symptoms (Fever chills, elevated WBC, hypotension)

distal SBO= distention of abdomen
proximal SBO = vomiting

105
Q

MC cause for LBO

A

most common cause is colon CA

could be a volvulus, adhesions (rare)

106
Q

Volvulus

A

bowel twisting

107
Q

LBO

A 
increased distention 
feculant vomiting (vomiting actual shit)
108
Q

treatment of LBO

A

surgical treatment

109
Q

diverticulum

def. + caused by

A

herniation of mucosa and submucosal layers of the colon thru the muscularis layer

caused by low fiber, highly refined diet, chronic constipation/squeezing

110
Q

most common spot of diverticulum

A

L side of bowel

111
Q

complications of diverticulosis

A

diverticulitis

diverticular bleeding

112
Q

diverticulitis

A

blockage of the entrance of pouch by swelling or fecal matter

causes bacterial overgrowth, distention, and venous congestion

local infection, perforation, and abscesses may occur within 3-5 days

113
Q

diverticulitis s’s

A

slowly progressive abdominal pain

fevers (infection rxn)

BM changes

114
Q

diverticulitis outpatient treatment

A

oral antibiotics covering GRAM NEGATIVES and anaerobes (i.e. augmentin) and clear liquid diet

115
Q

diverticulitis hospital treatment

A

IV abx to cover GRAM NEGATIVES and ANAEROBES (i.e. metronidazole)

patients are NPO

116
Q

diverticular bleeding

A

thin walls of diverticular sac and stretching to blood vessel occasionally rupture and painless bleeding occurs

hematochezia

KCSU17 Patho/Pharm Submodule 2 (14 decks)

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