Upper GI disorders Flashcards by Chelsey Miller

cholelithiasis

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

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risk factors for cholelithiasis

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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chronic cholelithiasis

intermittent biliary colic, persistent epigastric or RUQ pain

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chronic cholelithiasis s/s

pain radiates to back
N/V
sweating
gas

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acute cholecystitis s/s

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

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acalculous cholecysitis

without preexisting gallstones

major surgery
critical illness
trauma
burns
TPN

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GERD

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

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GERD risk factors

fatty foods
caffeine
alcohol
smoking
sleep position 
obesity

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GERD s/s

heartburn
regurgitation
chest pain
dysphagia

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persistent GERD can lead to

esophageal strictures
barrett esophagus 
pulmonary s/s
- cough
- laryngitis

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N/V

disturbances in gastric motility

alteration in vestibular system/ taste/olfaction

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gastric dysrhythmia

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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abdominal bloating and constipation

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

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dysphagia d/t nervous system

postpolio syndrome
multiple sclerosis
muscular dystrophy
parkinsons

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dysphagia d/t immune system

inflammation and weakness

polymyositis
dermatomyositis

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dysphagia d/t scleroderma

tissues of the esophagus become hard and narrow

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dysphagia d/t blockages

GERD
diverticula
tumors/growth

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Achalasia

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

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achalasia ->

dysphagia
mucosal inflammation and ulceration
squamous cell carcinoma

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Sliding Hiatal hernia

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

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paraesophageal hiatal hernia

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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hiatal hernia risk factors

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

hiatal hernia s/s

GERD

ulceration on the mucosal surface: cameron ulcers

anorexia nervosa

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

Bulimia nervosa

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

Long-term starvation

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

Kwashiorkor

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

Marasmus

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

retching

nonproductive vomiting

projectile vomiting

spontaneous vomiting that does not follow nausea or retching

Abdominal pain

``` may be first sign of GI disorder 3 types - visceral - somatic - referred ```

visceral abd. pain

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

somatic abd. pain

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

referred pain

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

peptic ulcer disease

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

hydrochloric acid and injury to mucosa

potentiates pepsin and other injury substances with aspirin and NSAID use

duodenal ulcer

``` 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 ```

H. pylori virulence

unique, lengthy DNA sequences | - pathogenicity islands

peptic ulcer s/s

``` 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 ```

gastric ulcer

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

gastric ulcer patho

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

stress ulcer

peptic ulcer that is r/t severe illness, neural injury, or systemic trauma - ischemic - cushing: r/t burn injury

stress ulcer s/s

bleeding

gastritis

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

Acute gastritis

H. pylori | NSAIDs

Chronic gastritis

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

gastritis s/s

anorexia N/V postprandial discomfort

Peptic ulcer bed 4 layers

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

damaging forces to gastric mucosa

gastic acidity peptic enzymes H. pylori drugs

defensive forces of gastric mucosa

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

Esophageal varices

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

esophageal varices complication

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

cholesterol gallstone 3 phases

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