You are on page 1of 7

PATHO 2 EXAM 1 STUDY GUIDE

GI A&P

Important secretions/gastric hormones and their role in digestion and absorption


o Mucus: protects gastric mucosa from acid and pepsin
o Gastrin: stimulates gastric glands to secrete hydrochloric acid and pepsinogen, growth of
gastric mucosa
o Bile: fat digestion and absorption, alkaline [independent], contains salts (conjugated bile
acids), cholesterol, bilirubin, electrolytes, and water, produced by hepatocytes of liver,
stored in gallbladder
o Trypsin: protein digestion into amino acids that are absorbed via small intestine villi
capillaries, produced by pancreas
o Acid: dissolve food fibers, act as bactericide against swallowed microorganisms, convert
pepsinogen to pepsin, made by parietal cells
o Pepsin: proteolytic enzyme- breaks down protein and forms polypeptides in stomach, chief
cells release pepsinogen which is converted into pepsin in acidic stomach enviro
o etc.
o Intrinsic Factor: needed for absorption of vitamin B12, secreted into blood
o Gastroferrin: facilitates small intestine absorption of iron, secreted into blood
o G cells: secrete gastrin
Relationship between Calcium and Vitamin D in the GI tract: Vitamin D promotes Ca
absorption in GI tract (along with parathyroid hormones, both also promote bone mineralization and
absorption of phosphate)
Liver A&P:
o Cell Types and roles:
Hepatocytes: functional cells of liver, located in liver lobules as cords or plates
Kupffer cells: tissue macrophages, bacteriocidal and important for bilirubin production
and lipid metabolism, destroy intestinal bacteria and prevent infection, located in
sinusoids (spaces between plates of hepatocytes)
S cells: produce secretin
Hepatic stellate cells: help regulate sinusoidal blood flow, participate in innate
immunity, located in Disse space between the lining of the sinusoid and hepatocyte
o Bilirubin
Formed from: byproduct of the destruction of aged RBCs (Kupffer cells destroy aged
RBCs and separate hemoglobin into heme and globin, globin is broken down into
amino acids and recycled to make new proteins, the heme is converted to biliverdin
and iron, iron is stored to make more RBCs, biliverdin is converted to bilirubin in the
macrophage)
Concepts of solubility r/t unconjugated and conjugated bilirubin: biliverbin is
converted to bilirubin in macrophage -released into plasma where it binds to albumin
(unconjugated bilirubin/free bilirubin)- goes from plasma in sinusoids to hepatocytes
where it binds with glucoronic acid (conjugated bilirubin)- secreted in bile- reaches
distal ileum ad colon bacteria deconjugate it to urobilinogen- excreted in urine as
urobilin and small amt excreted by kidneys
Unconjugated Bilirubin/Free Bilirubin: Lipid Soluble, moves from plasma in
sinusoids to hepatocytes
Conjugated Bilirubin: water soluble, secreted in bile
Urobilinogen: deconjugate bilirubin, excreted in urine as urobilin and small
amt in feces
o Albumin:
Synthesis: hepatocytes make from amino acids (from trypsin breaking down
proteins)
Role in Osmotic Pressure: maintains plasma oncotic pressure, protein- pulls water
o Liver Tests
AST: high- hepatocellular injury
ALT: high- hepatocellular injury
LDH: high- hypoxic injury, primary liver injury
Total Bilirubin Level: high- biliary obstruction

GI Disorders

Effects of gastric suctioning on Acid-Base balance and Fluid & Electrolytes: hypokalemia,
metabolic alkalosis from Na, Cl, and H+ ion loss
Abdominal Pain:
o Parietal: from the parietal peritoneum (lines abdominal walls), sharp- localized and intense,
tends to be on 1 side of the other due to nervous system innervation
o Visceral: pain from abdominal organ, radiates, diffuse, vague since nerve endings sparse
Referred: visceral pain felt at distant location, well localized there, areas share same
pathway
Diarrhea/Constipation
o Constipation Dietary recommendations: drink more fluids, increase fiber intake
o Diarrhea Dietary Recommendations: restoration of fluid and electrolyte balance
Anorexia: lack of desire to eat despite physiologic stimuli that would normally produce hunger
o Causes: side effects of drugs and disorder of other organ systems including cancer, heart
disease, and renal disease
o S&S: nausea, abdominal pain, diarrhea, psychologic stress
Dysphagia: difficulty swallowing
o Causes: mechanical obstruction of esophagus or functional disorder that impairs
esophageal motility via neural or muscular disorders
o S&S: distention and spasm of esophageal muscles during eating or dirnking may cause mild
or severe stabbing pain at level of obstruction, discomfort 2-4 seconds after swallowingupper esophageal obstruction, 10-15 secs after swallowing- lower esophagus obstruction,
regurgitation of undigested food, unpleasant taste sensation, vomiting, aspiration, weight
loss, aspiration could lead to pneumonia
Hematochezia: bloody stools, bright red stools
o Causes: frank bleeding from rectum or lower GI tract
o S&S: fresh, bright red blood passed from rectum
Hematemesis: bloody vomitus
Hiatal hernia: protrusion of the upper part of the stomach through the diaphragm (esophageal
hiatus) into the thorax
o Causes:
Sliding/direct: congenitally short esophagus, trauma, weakening of the diaphragmatic
muscles at GE junction, slides into hernia while lying down, stomach slides back into
abdomen when standing, exacerbated by factors that increase intra-abdominal
pressure
Paraesophageal/indirect: through not norm diaphragm hole, GE junction not affected
and remains below the diaphragm, NO REFLUX
o S&S: GER, dysphagia, heartburn, epigastric pain, regurgitation and substernal discomfort
after eating are common
GERD: reflux of gastric contents (chyme- acid and pepsin) into esophagus
o Causes: incompetent lower esophageal sphincter- cause unknown, irritant effects of
refluxate, abnormal esophageal clearance ,hiatal hernia present, delayed gastric emptying
potentiates (gastroparesis, partial gastric outlet obstruction)
o S&S: heartburn, dysphagia, chronic cough, asthma, upper abdominal pain within 1 hr of
eating, if chronic and severe-strictures
Intestinal/Bowel Obstruction: something that prevents stools from moving through the
intestines
o Causes: hernia, mesenteric occlusion, torsion/volvulus, intusscesception, diverticulosis,
tumor/neoplasm, adhesions, paralytic ileus
Paralytic Ileus: from surgery, peritonitis, hypokalemia, ischemic bowel, spinal
trauma, or drugs
o S&S: colicky abdominal pain, vomiting, diarrhea, abdominal distention, bowel sounds,
dehydration, hypotension- shock (decreased venous return, intestinal edema, large amt of
peritoneal fluid sequestered, bacterial translocation-sepsis)
Ulcers: break in protective mucosal lining of lower esophagus, stomach, or duodenum, exposes
muscle layers to damage from autodigestion from gastric acids
o Duodenal Ulcers: caused by hypersecretion of acid and pepsin, H pylori, or NSAIDs, most
common

S&S: epigastric pain- visceral or referred, chronic, intermittent, 2-3 hrs after eating,
empty stomach, may occur at night then gone in am, pain-food-relief pattern,
remission- exacerbation, hemorrhage may be first sx, perforation
o Gastric Ulcers: NSAIDs, H pylori, increased mucosa permeability to H+ ions, often preceded
by chronic gastritis since reduces mucosal barrier
S&S: pain immediately after eating, chronic (no remissions/exacerbations), more
N&V and weight loss
o Stress Ulcers: acute form of peptic ulcer caused by severe stress, decreased mucosal
blood flow major factor
Ischemic ulcer: within hrs of trauma, critical illness
Cushing Ulcer: severe head injury or brain surgery causes overstimulation of vagus
nerve= increased acid production
o What blood in the vomit or stool can indicate about ulcer location (also shade of
blood: bright red vs. dark or brown):
Upper GI bleed: esophagus- bright red blood, stomach- coffee grounds (bc interacts
with H in stomach which oxidizes the iron in hemoglobin), duodenum
Lower GI bleed: jejunum on, hemorrhoids- bright red blood, farther up- occult, black,
tarry
Gastritis: inflammation of gastric mucosa, acute or chronic, affects fundus and/or antrum
o Causes:
Acute Gastritis: alcohol, NSAIDs, Chemicals/toxins [urea]
Chronic Fundal Gastritis-Type A: most severe, have antibodies to parietal, gastric
cells, and intrinsic factor (so cant maintain mucosal lining), associated with other
auto-immune diseases, gastric atrophy, loss of chief and parietal cells, pernicious
anemia, risk for gastric cancer
o S&S: bleeding, anorexia, N&V, fullness, epigastric pain
Pancreatitis: norm secretes trypsins/proteolytic enzymes to break down proteins into duodenum
in inactive form but leads to autodigestion
o Causes: activation of trypsins while still in pancreas- biliary obstruction like gallstones,
activated proteases (trypsins), autodigestion
Alcohol: causes sphincter of Odi to swell which obstructs pancreatic enzyme release
into the duodenum
o S&S: pain, fever, N&V, abdominal distention, 3rd spacing of fluid-peritoneal edema, acute
renal failure (protein breakdowns go into circulation and clog glomerulus), increased WBCneutrophils, increased amylase and lipase in bloodstream
Chronic pancreatitis: chronic pain, pancreatic enzyme deficiency, glucose control
issues
Inflammatory Bowel Disease: ulcerative colitis and crohns disease
o Compare/Contrast Ulcerative Colitis versus Crohns disease
o Ulcerative Colitis: chronic inflammatory disease usually of rectum and sigmoid colon (but
can affect entire large bowel) causing ulcer formation
Cause: anticolon antibodies T lymphocyte cytotoxic reaction, genetic, infectious, or
unknown
S&S: ulcerations, skip lesions, pseudopolyps, cramping abdominal pain, bloody
diarrhea, remissions and exacerbations, increased colon cancer risk, severe- fever,
anemia, weight loss, 10-20 stools/day
o Crohns Disease: AKA regional enteritis/granulomatous colitic
Cause: inflammatory process by activated neutrophils and macrophages- immune,
genetic, infectious, unknown, stress may exacerbate but doesnt cause, no increased
colon cancer risk
Affects ascending and transverse colon
S&S: thickening of wall, cobble stoning, diarrhea, fever, abdominal pain, weight loss
Cholelithiasis: gallstones
o Causes: chronically elevated rate of bilirubin excretion (binds with calcium, associated with
chronic liver disease), supersaturated cholesterol bile- crystal aggregation
o S&S: RUQ pain that radiates to scapular and associated with N&V secondary to/stimulated
by fatty meals
Liver Disorders: Definitions, Causes, Clinical Manifestations, lab changes/assessment
findings

Jaundice: accumulation of bilirubin in tissues


Obstructive:
Intrahepatic: increased both conjugated and unconjugated bc hepatocytes
function altered- unable to conjugate bilirubin and bile canaliculi obstructed
from fibrosis
Extrahepatic: increase in conjugated bilirubin that accums in liver and enters
bloodstream to deposit in tissues, and go out in urine outside of liver, gall
bladder disease, pancreatic disease
Hemolytic: increased level of unconjugated bilirubin bc cant keep up with the
increased RBC hemolysis rate, physiologic jaundice of newborn transient but dtoxic to
brain >15 mg/dL old RBC breakdown rate
S&S: hyperbilirubinemia total>2.5-5 mg/dL, yellow sclera then skin
Portal Hypertension: obstruction from damaged liver scar tissue and fibrosis to venous
flow through portal system results in high hepatic venous pressure and development of
collateral blood vessels
How pressures of the liver influences fluid balance: increased capillary
permeability in portal venous system leads to fluid push out of mesenteric venous
system into the peritoneal cavity and decreased oncotic pressure from decreased
albumin synthesis- ascites
S&S: esophageal varices, splenomegaly, ascites, hepatic encephalopathy
Esophageal varices: distended torturous collateral veins in lower
esophagus, stomach, and rectum, if rupture will hematemesis and high
mortality rate 30-60% (no pressure keeping in check bc esophagus hollow
lumen)
Ascites: accumulation of fluid in peritoneal cavity, reduces circulatory volume
o Cause: usually cirrhosis, CHF, cancer, infections, portal HTN,
decreased albumin synthesis, increased RAA- increased aldosterone
and ADH bc hypovolemia compensation
o S&S: weight gain, abdominal distention, dyspnea, tachypnea, pleural
effusion, hepatic encephalopathy
Hepatic encephalopathy: accumulation of substances toxic to brain- mainly
ammonia (others- fatty acids, serotonin, tryptophan) from incomplete protein
metabolism and bacterial action in bowel on unabsorbed amino acids, protein
in diet, and blood in GI tract= more ammonia absorbed to blood
o Norm: stomach pepsin breaks down proteins- small intestine trypsin
breaks down protein into amino acids- hepatocytes use amino acids to
make proteins/albumin and remove ammonia from other amino acids
and convert it to urea to- excreted by kidneys
o S&S: personality changes, memory loss, irritability, lethargy, sleep
disturbances, asterixis (flex hand, pulsing tremor)
Hepatitis pathophysiology
Types A: 30 day incubation, acute onset, mild disease, fecal, oral, IV, sex, vaccine,
children and young adults [day care]
Type B: 60-180 incubation, insidious onset, severe disease, IV or sex (highest blood,
wounds, semen, vaginal fluid, then saliva), vaccine, anyone affected [bodily fluids]
Type C: 35-60 incubation, insidious onset, variable disease- chronic disease common
80%, cirrhosis 20%, IV and sex (drug users 60-90% infected by 5 yrs), no vaccine,
causes 50% of chronic liver disease, any group infected-highest males mid-30s [drug
users]
S&S: elevated AST and ALT, febrile illness, malaise, lethargy, jaundice
Phases of disease
Prodromal: 2 wks after exposed, general sx (fatigue, anorexia, N&V, HA,
fever), lasts 2 wks
Icteric (Jaundice): jaundice skin, dark urine, clay colored stools, enlarged
tender liver, lasts 2-6 wks
Recovery: jaundice gone, liver still enlarged- norm function up to 12 wks from
start of jaundice
Focus on how each type is different from the others

Cirrhosis: irreversible inflammatory disease in liver that disrupts liver structure and
function
Stages:
Fatty liver (reversible)
Alcoholic hepatitis (scar tissue remains but can recover, hepatocytes necrosis)
Cirrhosis (alcohol changed to toxin that irreversible damage all liver functions,
CT growth, and nodules)
Types:
Alcoholic (hepatocyte damage)
Biliary (canaliculi or bile duct damage)
o Primary: viral or autoimmune anti-mitochondrial antibodies [transplant]
o Secondary: obstruction of bile ducts
S&S: damage to all cell processes, altered metabolism of nutrients, liver
inflammation- pain and fever, N&V, anorexia, fatigue, liver fibrosis and scarring lead
to portal hypertension, ascites, edema, splenomegaly (anemia and
thrombocytopenia), and varices (esophageal, hemorrhoids, caput medusa- abdominal
veins superficial), fatty infiltrates, liver necrosis (hyperbilirubinemia, jaundice, clay
colored stools, bleeding, dark urine, hypoglycermia, ascites and edema,
gynecomastia, loss of body hair, menstrual dysfunction, palmar erythema, increased
ADH and aldosterone to try to compensate for hypovolemia)
Liver Failure
Most common causes: acetaminophen toxicity or overdose [alcohol gets rid of the
liver enzyme (glucothionate) thats needed to break down the toxic metabolite made
from Tylenol metabolism]

GI Disorders in Children

Cleft lip/harelip and Cleft Palate


o Incidence: Asian> white >black, cleft lip more, male- cleft lip more, female- isolated cleft
palate more
o Pathophysiology: multiple gene-enviro interactions, mom Vit B deficiency, mom tobacco or
alcohol, mom hyperhomocysteinemia, mom DM, genetic variations of growth factors,
associated w/ trisomy 13 and other malformations, overall- reduced amount of neural crest
mesenchyme that migrates to area that develops into embryo face
Cleft lip: incomplete fusion of nasomedial or intermaxillary process 4 th wk embryo
Cleft palate: fissure of uvula and soft palate and/or nostril, hard palate, and maxillary
alveolar ridge
o S&S: feeding difficulty
Pyloric Stenosis: obstruction of pyloric sphincter caused by hypertrophy of the sphincter muscle
o Incidence: common, 1-2 wks and 3-4 months old, male>female, white>black or Asian, full
term> preterm
o Pathophysiology: cause unknown- increased mom gastrin secretion, stress related, family Hx
o S&S: forceful vomit without apparent reason immediately after eating, may be bloody
vomitus, prolonged retention of food, constipation, weight loss
Tracheoesophageal Fistula: connection btwn esophagus and trachea
o Incidence: Esophageal Atresia with distal TEF 87%, isolated TEF 4%, EA with proximal TEF
1%, EA with double TEF 1% (prox and distal connection btwn them)
o S&S: bubbling, drooling, aspiration, abdominal distention, coughing with feeding

GI Pharmacology

Hepatic drug metabolizing enzymes and how they affect drug inactivation: enzymes can
inactivate
Acetaminophen and liver toxicity: CYP2E1- NAPQI- protein adducts, lipid peroxidation- liver
failure, hepatocyte necrosis
Drugs for ulcer disease (reduce acids/neutralize acids) and how they should be taken
together

Antacids raise pH>4 so prevents sucralfate from crosslinking, inhibit absorption of H2


receptor blockers and PPI- so give anatacids 1 hr apart from acid
reduction/neutralization/mucosa enhancing drugs
Drugs that reduce the production of acids [Antiscretory]
o Proton Pump Inhibitors: [prazoles]
Indications for use: peptic ulcer disease, most effective for reducing gastric acid
secretion (97%)
Mechanism of action: is a prodrug activated in parietal cell, inhibits H+ and
K+ATPase enzymes that generates gastric acid irreversibly, reduces basal and
stimulated acid secretion
o H2 Receptor Blockers: [Cimetadine, ranitidine, famotidine, nizatidine]
Indications for use: peptic ulcer disease
Mechanism of action: selective blockade of histamine 2 receptor (norm- secretion
of gastric acid, promotes acid release by direct action on parietal cells) so decreases
gastric acid production, reduces basal, food stimulated, ad nocturnal gastric acid
secretion by 90% with single dose, short half life- 2 hrs
Check BUN and creatinine routinely
Drugs that neutralize acid antacids
o Indications for use: should not be primary therapy for PUD
o Mechanism of action: neutralize stomach acid (raises gastric pH to >5), stimulate
prostaglandins, dont coat ulcer- helps protect ulcer
o When they should be taken r/t meals and other drugs: should be taken on regular
schedule not prn usually 7x/day, 1-3 hrs after meals and at bedtime
Anti-inflammatory drugs for inflammatory bowel disease: [Sulfasalazine, Mesalamine,
Olsalazine], metabolized by intestinal bacteria into active compound 5-ASA which is antiinflammatory
Prokinetic drugs: Reglan
o Indications for use: gastroesophageal relux, diabetic gastroparesis, chemo induced N&V,
to move enteric tubes, short term bc can lead to tardive dyskinesia
o Mechanism of action: suppresses emesis by blocking dopamine and serotonin receptors,
increases acetylcholine action (increases upper GI mobility- increases gastric emptying)
Cytoprotective agents (used for GERD or duodenal ulcers specifically) [enhance mucosal
defenses]
o Sucralfate: creates bandaid barrier against acid and pepsin, crosslinks in acidic enviro
pH<4 and becomes viscous to adhere to ulcer crater up to 6 hrs, doesnt neutralize or
decrease acid
Laxatives
o Types and How they accomplish a laxative effect
Bulk Forming: swell in water to increase fecal mass and stimulate peristalsis, not
absorbed (act similarly to dietary fiber) [methycellulose, psyllium]
SEs: few since not absorbed, esophageal obstruction if swallowed without
water
Surfactants: lower surface tension of stool, helps water move into feces, decreases
water absorption from stool [docusate, Colace]
Stimulants/Contact: stimulate intestinal motility, act on intestinal wall to increase
fluid and electrolytes in lumen, decrease water and electrolyte absorption from stool,
produce semifluid stool in -12 hrs [dulcolax, exlax, castor oil]
Widely abused
Osmotics: poorly absorbed salts that create osmotic action and draw fluid into
intestine, enlarged stool mass increases peristalsis [milk of magnesia, magnesium
citrate]
Others-Lactulose: poorly absorbed and not digested so metabolized into acids by
colon bacteria which causes osmotic action and acidity causes ammonia to be pulled
from plasma into GI tract then eliminated to reduce ammonia
o Side effects/ADRs (in addition, think about how each type could be dangerous if
overdosed):
o Types that are frequently abused and how they can be abused: Stimulant/Contact
laxatives widely abused, misconception that normal is daily BM, strong laxatives purge
bowel which delays BM causing more use, chronic use decreases defecatory reflexes
o

Dietary recommendations that could complement or replace the need for


laxatives