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64 Cards in this Set

  • Front
  • Back
S&S of GI disease
outcome of a variety of disorders
may be representative of other systemic diseases
Constitutional Symptoms

vague and imply anything (point to a lot of diseases)
nausea and vomiting
diarrhea
malaise (not wanting to get up and out of bed)
fatigue
fever
dizziness
appetite loss
Aging and the GI system
constipation
ileus (decrease in GI motility)
absorption loss
incontinence (lose sphincter tone)
diverticular disease (outpocketing of valve, pouch bulges out due to weakening, when infected can casue bleeding, bowel death)
decreased gastric acidity
Atrophic Gastritis
chronic:
older age groups
atrophy of gastric mucosa
decreased gastric acidity
reduced intrinsic factor
extrinsic and intrinsic factors combine to help absorption of Vit B 12 into the system and leads to hematopoiesis and myelnation of axons
Vit B 12 deficiency
pernicious anemia
can't absorb vitamin B 12
bone marrow produces fewer RBC and increase cell size
Hematologic Disorders
Pernicious Anemia:
Macrocytic (RBC are way to big), normochromic (normal level in hemoglobin)
Neurologic Disorders
Peripheral neuropathy (lots of wasps stinging extremities, in hot water, burning, axon is being overstimulated, carrying stimulations that it shouldn't be carrying, loss of sensation means its advanced)
Subacute combined degeneration
Dementia (confusion, forgetfulness)
Subacute Combined Degeneration
affects spinal cord
lesion dorsal aspect of lateral white columns (UMN syndrome/spasticity) and dorsal white columns (touch/prop/tactile senses)
Dementia
B12 deficiency
megaloblastic madness
Esophageal Disorders symptoms
dysphagia (difficulty swallowing)
pyrosis (heart burn)
odynophagia (pain with swallowing)
waterbrash (reflex salivation)
Esophagitis
acute, nonspecific
pyrosis
reflux
cork-screw appearance (spasms)
GERD
(gastro esophageal reflux disease)
tx tries to decrease stomach acidity
incompetent LES (lower esophageal sphincter)
normally should be closed, swallow - opens sphincter through relaxation, allows acidic contents of stomach to be isolated from esophagus, pressure above and below forces sphincter to close, too much acid build pressure in stomach and force sphincter to open up, acid goes in esophagus and irritates it, may lead to esophageal cancer
Hiatal hernia
herniation of lower esophagus and stomach (stomach and contents are up in esophagus and keeps (LES) sphincter open)
esophageal hiatus
congenital diaphragmatic defect
feels like heart attack
scleroderma
hardening of esophageal and esophageal vascular collagen
esophageal dysmotility and dysphagia
lose elasticity of conn tiss and subcutaneous tiss
don't eat, malnourished
features of systemic sclerosis
drawn pursed lips
shiny skin over cheeks and forehead
atrophy of muscles of temple, face, and neck
facial chanes are known as Mauskopf (mousehead)
esophageal tumor

never benign
obstruction (difficulty swallowing)
bleeding
dysphagia and waterbrash
cachexia (malnourished)
achalasia
loss of myenteric plexus (Auerbach's)
failure of LES to relax
accumulation of food causes esophageal dilatation
accumulate food in bottom of esophagus (can't open sphincter)
mallory weiss syndrome
lower esophageal bleeding
alcohol, bulimia, antibiotics
tracheoesophageal fistula
communication between Trachia & Esophagus
3 c's (cough, choke, cyanosis)
aspiration pneumonia
acute Gastritis
diffuse inflammation
epigastric pain
pain-relief food pattern (put milk in your stomach when it hurts)
gastric mucosa becomes inflamed
causees (overindulgence in alcohol or eating, NSAIDS (aleve), ASA (asprin), GI viral infection
peptic ulcer disease (etiology)
discete lesion that invovles a specific part in stomach
not really causes:
hyperacidity
diet
stress
medications
cause:
helicobacter Pylori (house this bacteria in GI tract)
peptic ulcer disease (pathophysiology)
protective barriers fail
mucus
epithelium
hydrogen back diffusion (leak back into mucosa and destroys cells and causes ulcer)
peptic ulcer pathophysiology
decreased barrier function
histamine release with vasodilatation
gastric acid release
capillary and venule destruction
bleeding along with plasma loss and acid accumulation
incidence of peptic ulcers
1:1 male:female
80% in the duodenal bulb
20% pylorus of the stomach
helicobacter pylori (90-95%)
peptic ulcer disease (complications)
intractability
hemorrhage
perforation
obstruction
stress ulcers
occur after trauma (SC injury)
blood shunted to places that need healing
GI tract doesn't have blood
tissue death
stomach cancer
h. pylori present
lower socioeconomic status
chronic gastritis is risk factor
occur more in males
adenocarcinomas
linitis plastica
leather bottle stomach
the entire wall is cartilaginous and stiff (hard)
poor prognosis
esophageal tumor

never benign
obstruction (difficulty swallowing)
bleeding
dysphagia and waterbrash
cachexia (malnourished)
achalasia
loss of myenteric plexus (Auerbach's)
failure of LES to relax
accumulation of food causes esophageal dilatation
accumulate food in bottom of esophagus (can't open sphincter)
mallory weiss syndrome
lower esophageal bleeding
alcohol, bulimia, antibiotics
tracheoesophageal fistula
communication between Trachia & Esophagus
3 c's (cough, choke, cyanosis)
aspiration pneumonia
acute Gastritis
diffuse inflammation
epigastric pain
pain-relief food pattern (put milk in your stomach when it hurts)
gastric mucosa becomes inflamed
causees (overindulgence in alcohol or eating, NSAIDS (aleve), ASA (asprin), GI viral infection
peptic ulcer disease (etiology)
discete lesion that invovles a specific part in stomach
not really causes:
hyperacidity
diet
stress
medications
cause:
helicobacter Pylori (house this bacteria in GI tract)
peptic ulcer disease (pathophysiology)
protective barriers fail
mucus
epithelium
hydrogen back diffusion (leak back into mucosa and destroys cells and causes ulcer)
peptic ulcer pathophysiology
decreased barrier function
histamine release with vasodilatation
gastric acid release
capillary and venule destruction
bleeding along with plasma loss and acid accumulation
incidence of peptic ulcers
1:1 male:female
80% in the duodenal bulb
20% pylorus of the stomach
helicobacter pylori (90-95%)
peptic ulcer disease (complications)
intractability
hemorrhage
perforation
obstruction
stress ulcers
occur after trauma (SC injury)
blood shunted to places that need healing
GI tract doesn't have blood
tissue death
stomach cancer
h. pylori present
lower socioeconomic status
chronic gastritis is risk factor
occur more in males
adenocarcinomas
linitis plastica
leather bottle stomach
the entire wall is cartilaginous and stiff (hard)
poor prognosis
esophageal tumor

never benign
obstruction (difficulty swallowing)
bleeding
dysphagia and waterbrash
cachexia (malnourished)
achalasia
loss of myenteric plexus (Auerbach's)
failure of LES to relax
accumulation of food causes esophageal dilatation
accumulate food in bottom of esophagus (can't open sphincter)
mallory weiss syndrome
lower esophageal bleeding
alcohol, bulimia, antibiotics
tracheoesophageal fistula
communication between Trachia & Esophagus
3 c's (cough, choke, cyanosis)
aspiration pneumonia
acute Gastritis
diffuse inflammation
epigastric pain
pain-relief food pattern (put milk in your stomach when it hurts)
gastric mucosa becomes inflamed
causees (overindulgence in alcohol or eating, NSAIDS (aleve), ASA (asprin), GI viral infection
peptic ulcer disease (etiology)
discete lesion that invovles a specific part in stomach
not really causes:
hyperacidity
diet
stress
medications
cause:
helicobacter Pylori (house this bacteria in GI tract)
peptic ulcer disease (pathophysiology)
protective barriers fail
mucus
epithelium
hydrogen back diffusion (leak back into mucosa and destroys cells and causes ulcer)
peptic ulcer pathophysiology
decreased barrier function
histamine release with vasodilatation
gastric acid release
capillary and venule destruction
bleeding along with plasma loss and acid accumulation
incidence of peptic ulcers
1:1 male:female
80% in the duodenal bulb
20% pylorus of the stomach
helicobacter pylori (90-95%)
peptic ulcer disease (complications)
intractability
hemorrhage
perforation
obstruction
stress ulcers
occur after trauma (SC injury)
blood shunted to places that need healing
GI tract doesn't have blood
tissue death
stomach cancer
h. pylori present
lower socioeconomic status
chronic gastritis is risk factor
occur more in males
adenocarcinomas
linitis plastica
leather bottle stomach
the entire wall is cartilaginous and stiff (hard)
poor prognosis
appendicitis
fecalith etiology (bits of dried stool that work their way into the lumen of appendix and cause obstruction)
unknown etiology (occurs spontaneously)
symptoms of appendicitis
marked leukocytosis (increase # of WBC)
rebound pain over McBurney's point (push on it and when you let go it hurts like hell)
nauea and vomiting
fever
rupture = peritonitis (infection of peritoneum with intestinal bacteria)
S&S of disorders with colon
constipation
diarrhea
altered stool size/color
hematochezia (blood in stool)
cramping (colicky pain)
Diverticulosis
aging-weakness in bowel wall
90% occur in the sigmoid colon
-outpoketings along the large bowel, occurs due to age, hydrostatic pressure inside bowel causes the weakened area to bulge (diverticulum)
-diverticuli becomes inflamed
S&S of diverticulosis
fever
abdominal pain
hematochezia
rupture causes leakage of intestinal contents into abdominal cavity (peritonitis)
Idiopathic Ulcerative Colitis
most common bowel disease in US
females>males
jewish ancestry
autoimmune disease
mucosa only (not full thickness of bowel like before)
hematochezia
abdominal cramps
toxic megacolon
bowel become spastic and cause S&S of obstruction and develop this
large, dilated colon
colorectal carcinoma
prevalence
65% rectosigmoid colon
35% ascending or transverse colon
S&S colorectal carcinoma
hematochezia
colicky pain
weight loss
anemia
alternating diarrhea/constipation
abdominal distention
irritable bowel syndrome
colon alternate between hyperactivity and sluggishness
return to normal in a few hours to a few days
relax
exercise
counseling