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Pathophysiology > Upper GI disorders > Flashcards

Upper GI disorders Flashcards

1
Q

cholelithiasis

A 
gallstones
bile states -> formed stones 
3 factors
- supersaturatoin of Bile w/ cholesterol 
- nucleation of crystals
- hypomotility
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2
Q

risk factors for cholelithiasis

A 
high spinal injury
TPN
prolonged fasting
rapid wt. loss
pregnancy
oral contraceptive
obesity
DM 
women 
IN CHILDREN
- cystic fibrosis
- sickle cell
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3
Q

chronic cholelithiasis

A

intermittent biliary colic, persistent epigastric or RUQ pain

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4
Q

chronic cholelithiasis s/s

A

pain radiates to back
N/V
sweating
gas

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5
Q

acute cholecystitis s/s

A 
severe RUQ pain radiates to back 
tenderness
fever
cystic duct obstruction 
bacterial infection
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6
Q

acalculous cholecysitis

A

without preexisting gallstones

  • major surgery
  • critical illness
  • trauma
  • burns
  • TPN
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7
Q

GERD

A 
function and structure alteration of the gastroesophageal junction 
anything that dec. LES pressure or inc. intraabdominal pressure
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8
Q

GERD risk factors

A 
fatty foods
caffeine
alcohol
smoking
sleep position 
obesity
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9
Q

GERD s/s

A

heartburn
regurgitation
chest pain
dysphagia

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10
Q

persistent GERD can lead to

A 
esophageal strictures
barrett esophagus 
pulmonary s/s
- cough
- laryngitis
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11
Q

N/V

A

disturbances in gastric motility

alteration in vestibular system/ taste/olfaction

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12
Q

gastric dysrhythmia

A

inc. release of nitric oxide
down-regulation of stimulatory G protein expression
up-regulation of inhibitory G protein expression
-> dec. gastric contractility and emptying

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13
Q

abdominal bloating and constipation

A 
changes in H2O absorption 
mechanical factors
dietary factors
dec. physical activity
hormonal effects
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14
Q

dysphagia d/t nervous system

A

postpolio syndrome
multiple sclerosis
muscular dystrophy
parkinsons

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15
Q

dysphagia d/t immune system

A

inflammation and weakness

  • polymyositis
  • dermatomyositis
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16
Q

dysphagia d/t scleroderma

A

tissues of the esophagus become hard and narrow

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17
Q

dysphagia d/t blockages

A

GERD
diverticula
tumors/growth

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18
Q

Achalasia

A 
LES fails to relax 
Loss of intrinsic inhibitory innervation 
- aperistalsis
- incomplete relaxation
- inc. resting tone
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19
Q

achalasia ->

A

dysphagia
mucosal inflammation and ulceration
squamous cell carcinoma

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20
Q

Sliding Hiatal hernia

A

portion of stomach and gastroesophageal junction slide into thorax
visceral peritoneum remains intact and restrains the size of hernia

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21
Q

paraesophageal hiatal hernia

A

greater curvature of stomach rolls through the diaphragmatic defect
membrane becomes thinned out or defection -> true peritoneal sac to protrude into the posterior mediastinum where negative intrathroacic pressure causes it to enlarge.

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22
Q

hiatal hernia risk factors

A

inc. intraabdominal pressure
- ascites
- preg
- obesity
- chronic straining/coughing

23
Q

hiatal hernia s/s

A

GERD

ulceration on the mucosal surface: cameron ulcers

24
Q

anorexia nervosa

A

lack of desire to eat despite stimuli that normally produces hunger

  • poor body image
  • can lose 25-30% of ideal body weight d/t fat and muscle depletion/atropy
  • can lead to starvation induced cardiac failure
  • females -> absence of menstruation
25
Q

Bulimia nervosa

A

body wt remains near normal but with aspirations for wt. loss

  • recurrent binge eating
  • self-induced vomiting -> pitted teeth, pharyngeal and esophageal inflammation, and tracheoesphageal fistulae
  • fasting to oppose the effect of binge eating, or excessive exercise
  • overuse of laxatives -> rectal bleeding and relying on laxatives
26
Q

Long-term starvation

A

Kwashiorkor
Marasmus
- stunted physical and mental development
- presence of subQ fat, hepatomegaly
- fatty liver differentiates between the 2

27
Q

Kwashiorkor

A

lack of proteins causes liver to swell due to the inability to produce lipoproteins for cholesterol synthesis

28
Q

Marasmus

A

liver function continues, but overall caloric intake is too low to support cellular protein synthesis
- deficiency of all nutrients

29
Q

retching

A

nonproductive vomiting

30
Q

projectile vomiting

A

spontaneous vomiting that does not follow nausea or retching

31
Q

Abdominal pain

A 
may be first sign of GI disorder 
3 types
- visceral 
- somatic
- referred
32
Q

visceral abd. pain

A

stretching/distending abd. organ
inflammation
- diffuse, poorly localized
- gnawing, burning, cramping

33
Q

somatic abd. pain

A

injury to abd. wall, parietal peritoneum, root of mesentery, or diaphragm
- sharper more intense, localized

34
Q

referred pain

A

felt at distant location from source
- same dermatome/neurosegments
sharp, well localized, skin or deeper tissues

35
Q

peptic ulcer disease

A

break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum
- superficial: erosions
- deep: true ulcer
caused by hydrocholoric acid and pepsin

36
Q

hydrochloric acid and injury to mucosa

A

potentiates pepsin and other injury substances with aspirin and NSAID use

37
Q

duodenal ulcer

A 
most common peptic ulcer
development factors
- H. pyloryi
-> lower bicarb levels in duodenum 
- inc. stomach acid and pepsin 
- NSAIDS
- inc. gastrin 
- acid production by smoking 
- stress: glucocorticoid release -> inc. acid production 
- heredity
38
Q

H. pylori virulence

A

unique, lengthy DNA sequences

- pathogenicity islands

39
Q

peptic ulcer s/s

A 
epigastric burning, relieved with eating or antacids 
- worse with empty stomach (gastric)
- worse 2-3 hr after meal (duodenal)
nausea
abd. pain/upset
chest discomfort
40
Q

gastric ulcer

A

tends to be in antral region of stomach, adjacent to the acid-secreting mucosa

  • inc. mucosal permeability to H+
  • gastric secretion is normal or less than nml
41
Q

gastric ulcer patho

A

damaged mucosal barrier

  • > dec. function of mucosal cells, loss to tight junctions
  • > back diffusion of acid into gastric mucosa
  • > pepsinogen converts to pepsin
  • > further mucosal erosion, destruction of blood vessels, bleeding
  • > ulceration
42
Q

stress ulcer

A

peptic ulcer that is r/t severe illness, neural injury, or systemic trauma

  • ischemic
  • cushing: r/t burn injury
43
Q

stress ulcer s/s

A

bleeding

44
Q

gastritis

A 
inflammation of stomach lining /mucosa 
Triggered by toxins
- ETOH
- aspirin
- irritating substances (viral, bacterial, autoimmune)
- tobacco
45
Q

Acute gastritis

A

H. pylori

NSAIDs

46
Q

Chronic gastritis

A 
chronic fundal gastritis
chronic antral gastritis 
- s/s often do not correlate with disease severity. 
Atrophy
intestinal metaplasia
lymphoid aggregates
neutrophil infiltrates
47
Q

gastritis s/s

A

anorexia
N/V
postprandial discomfort

48
Q

Peptic ulcer bed 4 layers

A

necrotic debris (top most)
inflammatory layer
granulation tissue
fibrous scar (deepest)

49
Q

damaging forces to gastric mucosa

A

gastic acidity
peptic enzymes
H. pylori
drugs

50
Q

defensive forces of gastric mucosa

A 
mucus secretion
bicarbonate
mucosal blood flow
apical surface membrane transport
epithelial regenerative capacity 
Elaboration of prostaglandins
51
Q

Esophageal varices

A

impaired hepatic portal blood flow
- associated with alcoholic cirrhosis
~ 2/3 of cirrhosis pts

52
Q

esophageal varices complication

A

rupture
-> hematemesis
20-30% die on each episode
70% recurrence rate

53
Q

cholesterol gallstone 3 phases

A
  • superstauration of bile with cholesterol -> precipitation
  • nucleation of crystals
  • hypomotility (stasis of bile) allow for stone growth

Pathophysiology (80 decks)

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