GI Pathology - Exam 1 Flashcards
Carcinoid syndrome
-patho
-causes
causes: endogenous secretion of serotonin and kallikrein
patho-paraneoplastic syndrome from tumors
Carcinoid Syndrome
-s/s
flushing
N/V
diarrhea
-less often: HF, emesis, bronchoconstriction, hepatomegaly, endocardial fibrosis, retroperitoneal and pelvis fibrosis
Carcinoid Syndrome
-treatment
octreotide (somatostatin analogue)
-decreases serotonin release from tumor
-avoid beta blockers, will increase serotonin release from tumor (phenylephrine ok)
Hirshsprung’s Disease
-patho
-causes
patho: poor regulation of activity of colon, swollen colon, shrunken rectum; causes obstructions
causes: lack of ganglionic cells in myenteric (auerbach) plexus and submucosal (meissner) plexus
-more common in males, siblings of pts with this disease, and pts with Down Syndrome
Hirschsprung’s
-s/s
-tx
S/s: newborn fails to have BM in 48hr, swollen abdomen, green/brown vomit, constipation/diarrhea, failure to gain weight
Tx- high fiber, fluids, stool softeners, isotonic enemas, surgery
Mendelson’s Syndrome
-patho
-tx
patho: hypoxia, pulm edema, infiltrates following aspiration
Tx- vent support, bronchodilators prn, abx if culture is +
Mallory-Weiss Tear
-patho/causes
-tx
patho: laceration at junction of esophagus and stomach from mallory-weiss syndrome/ tearing from extreme vomiting
s/s-hemataemesis
tx- heals on its own, cautery/clip possibly, medications to decrease acid
Gastrinoma/ Zollinger-Ellison Syndrome
-patho
-s/s
patho: non-beta cell tumor of pancreas or G cell tumor; increased parietal cell mass constantly stimulates; low pH inactivates pancreatic lipase causing bile salts to increase
s/s: steatorrhea and hypokalemia; duodenal ulcers, diarrhea
Ketoacidosis
-causes
Lack of insulin
-body can’t use available glucose
-ketosis occurs, breaking down fat for fuel
Insulin deficiency
-excess of glucagon
-promotes breakdown of stored fats, producing ketones
-body thinks it needs more glucose so it breaks down other sources
Ketoacidosis
-effects
-excess glucose acts as osmotic diuretic
-polyuria
-polydipsia
-polyphagia
-possible weight loss
-Kussmaul breathing (acetone breath)
-high BG, ketonuria
-N/V abd pain
-confusion
-weakness/fatigue
-acidosis from anaerobic break down/ketones
Acute liver failure
-patho
patho: severe impairment/necrosis of liver cells WITHOUT preexisiting liver disease or cirrhosis
Leading cause of acute liver failure is _ _.
Acetaminophen overdose
-give N-acetylcysteine
Acute liver disease
-s/s
anorexia
vomiting
abd pain
progressing jaundice
ascites
GIB
coag issues
encephalopathy(ammonia accumulation-late)
portal HTN, elevated bilirubin
Acute liver failure
-tx
-antiviral therapy (improves cases of viral hepatitis)
-lower the serum ammonia level
-liver transplant
Portal HTN
-patho
HTN in portal vein (normal = 5-10mmHg, HTN is >10mmHg)
-increased resistance to portal flow from either obstruction in liver or reduction of flow in biliary channels
Portal HTN
-tx
beta blockers- prevent variceal bleeding
no definitive tx, liver transplant is best option
There is normally a _ - _ mmHg difference between CVP and portal venous system pressure, _ difference = bleeding/varices
0-5mmHg difference
increased
About _% of CO flows thru liver.
30%
-if obstruction occurs, can drop CO or cause systemic HoTN from poor venous return
PUD is ulceration in the _ _ of the lower esophagus, stomach, or duodenum
mucosal lining
-when acid and pepsin overcome ability of mucosa to defend itself
PUD
-causes
Causes of:
high acid/peptic content
irritation
poor blood supply
poor secretion of mucus
infection (H. Pylori)
PUD
-risk factors
-genes
-H.Pyloir infection
-habitual use of NSAIDs
-excessive drinking, smoking
-acute pancreatitis
-COPD
-obesity
-cirrhosis
-age >65y
PUD-Gastric ulcers
-sites/patho
common site: antral region adjacent to acid-secreting mucosa
Patho:
-common cause=H.Pylori;
-primary defect is increased permeability to H+ ions
-pepsinogen converted to pepsin too early
-histamine release increases HCl
-gastric secretion is normal or less than normal
PUD-gastric ulcer
-s/s
pain IMMEDIATELY after eating
-chronic
-anorexia, vomiting, wt loss
PUD-BOTH GASTRIC AND DUODENAL ULCER
-tx
Antacids-neutralize gastric contents, pH, inactivate pepsin, relieve pain
PPI +anticholinergics- suppress acid secretion
Bismuth + combo abx + vit C- kill H.Pylori
Sucralfate and colloidal bismuth- coat ulcer
Surg resection
PUD-duodenal ulcers
-sites/patho
mosre common than gastric ulcers bc less protection than stomach
patho:
-higher # of parietal cells in duodenum secreting acid
-high gastrin level
-rapid gastric emptying (chyme is acidic_
-cigarette smoking increasing acid
PUD-duodenal ulcers
-s/s
chronic intermittent pain in epigastric region
-pain 30min-2hr AFTER eating when stomach is empty
-PAIN RELIEF WITH FOOD
Duodenal ulcer risk can be reduced with diet high in vitamin _ and _
vit A
fiber
Inflammatory bowel diseases have unknown origin, are immune related with _ cell responses and include _ _ and _’s disease
TCell
ulcerative colitis
crohn’s disease
Ulcerative colitis is an inflammatory disease that causes ulcers of the _ mucosa
colonic
-sigmoid and rectum usually
IBD - UC
-causes
-patho
causes: infectious, immunologic, dietary, or genetic
patho: continuous lesions, limited to mucosa and are not transmural (NOT SKIPPED)
IBD-UC
-s/s
-diarrhea (10-20 BM/day), bloody stool, cramp
-remission and exacerbations
-PAIN
IBD-UC
-tx
-FIRST LINE = 5-aminosalicylic acid (Mesalazine)
-steroids and salicylate
-immunosuppressive drugs
-broad spect abx
-colostomy or resection (increased risk colon cancer)
Diaphragmatic hernia
-patho
-s/s
-tx
patho: weakness in the diaphragm, congenital ~8wks
s/s: L sd most common; DIB, tachycardia, tachypnea, dim BS
tx: surg
Hiatal hernia
-patho
protrusion of upper part of stomach thru diaphragm into thorax
-BRINGS ON GERD, lowers LES resting pressure
Hiatal hernia
-s/s
-tx
s/s:L sd most common; DIB, tachycardia, tachypnea, dim BS
tx- wt loss, PPI, antacid, sug repair
GERD
-patho
acid and pepsin reflux into esophagus causing esophagitis
GERD
-causes
-resting LES tone is decreased either from TRANSIENT RELAXATION or WEAKNESS OF SPHINCTER
GERD
-risk factors
vomiting
lifting/bending
coughing
obesity
GERD
-s/s
heartburn/ indigestion
chronic cough
laryngitis
upper abd pain WITHIN 1hr eating
GERD
-complications
-scar tissue and stricture of esophagus
-aspiration
-chronic sinus infection
-dysplastic changes (Barrett’s esophagus)
GERD
-tx
-PPI <- most effective
-H2 antagonists, prokinetic meds, antacids, pain meds
-elevate HOB 6in
-wt loss
-quit smoking
-surg - lap fundoplication
Cholelithiasis
-patho
-too much water, cholesterol in bile
-decreased secretion of bile acids(reduced CCK)
-decreased resorption of bile salts from ileum (reduced CCK)
-gallbladder smooth musc stasis
-genes
-inflamed epithelium
Cholelithiasis
-s/s
-epigastric pain, R hypochondrium pain
-intolerance to fatty food
-biliary colic (stones lodge in cystic or common bile duct)
-jaundice
-abd tenderness/fever
Cholelithiasis
black v brown stones
black:
-formed in sterile environment
-made of calcium bilirubinate polymer from hyperbilirubinbilia
brown:
-bacterial infection of bile ducts
-made of calcium soaps, unconjugated bilirubin, cholesterol, FA, and mucin
Cholelithiasis
-tx
-lap chole -preferred
-transluminal endoscopy
-endoscopic retrograde cholangiopancreatography or sphincterotomy
-lithotripsy for large stones
-drugs to dissolve small stones (CDCA and ursodeoxycholic acid)
Cholecystitis
-patho
-tx
inflammation of gallbladder (acute or chronic)
s/s- fever, leukocytosis, rebound tenderness, abd muscle guarding
tx- pain mgmt, fluids and lytes, fasting, abx, if GB is perffed, immediate chole
Pancreatitis
-patho
injury or damage to panc cells and ducts cause leakage of panc enzymes(trypsin, lipase, and chymotrypsin) into its tissue, inflaming and eating itself
-can leak into the bloodstream and injure vessels and other organs
Pancreatitis - Acute
-s/s
-resolves spontaneously
-epigastric or midabd pain
-N/V
-fever, leukocytosis
-elevated serum lipase - primary dx marker
Pancreatitis-Acute
-tx
narcotics
NG suctioning
IV fluids
Pancreatitis - Chronic
-patho
-most common cause = alcohol abuse
-repeated exacerbations ->chronic changes
-destroys ACINAR cells and ISLETS OF LANGERHANS
-parenchyma is destroyed and replaced with fibrous tissue, calcifications, obstructions, and cysts
Pancreatitis - Chronic
-s/s
-tx
continuous or intermittent abd pain
tx: corticosteroids (for autoimmune), smoking and alcohol cessation, analgesics, endoscopy, surg drainage of cysts
Pyloric stenosis
-patho
-s/s
-tx
patho: blocking/narrowing of pylorus, messes up gastric emptying
s/s: acidic projectile vomiting IMMEDIATELY AFTER eating, wt loss, persistent hunger
tx- surg - pyloromyotomy
Bowel obstruction
-causes
-cancer
-ulcer
-spasm
-paralytic ileus
-adhesions
Bowel obstruction can be _ or _.
intestinal
pyloric (acidic vomit)
Bowel obstruction at pylorus causes:
acid vomit
Bowel obstruction below duodenum causes:
neutral/basic vomit
Bowel obstruction that is in sm intestine causes:
extreme vomiting
Bowel obstruction that is in large intestine causes:
extreme constipation and less vomiting
Bowel obstruction - below duodenum
-patho
from fibrous adhesions
-neutral/basic vomit
-minor change in whole body acid/base status
Bowel obstruction
-Acute colonic pseudo-obstruction (Olgilvie syndrome)
massive dilation of large bowel
-happens in pts who are critically ill, and older immobilized pts
Bowel obstruction - large int.
-patho
most commonly from colorectal cancer, twisting (volvulus), or strictures from diverticulitis
-severe constipation can cause vomiting if sm intestine is full
Hepatitis can be _ or _
autoimmune or viral
Hepatitis - Autoimmune
-patho
-s/s
patho: rare, chronic, progressive T Cell inflammation
s/s: NO SYMPTOMS, or jaundice, fatigue, poor appetite, amneorrhea
Hepatitis- Autoimmune
-tx
immunosuppressive therapy (steroids or with azathioprine) with remission within 24mo
-relapses are common with tx withdrawal
Hepatitis- Viral
types
-systemic, primarily affects liver
-A(AKA infectious),B (AKA serum hepatitis),C,D,E
Hepatitis - Viral
-complications
-hepatic cell necrosis
-Kupffer cell (immune cell) hyperplasia
-phagocyte infiltration of liver (obstructing bile flow and hepatocyte function)
Chronic active hepatitis occurs with Hep _ and _ with a predisposition to _ and hepatocellular _
B and C
cirrhosis
carcinoma
Fulminant hepatitis causes widespread hepatic necrosis and is often fatal, occurs with Hep _ (with or without Hep D infection) and Hep _
B and C
Hepatitis - Viral
-phases
incubation
prodromal (preicteric)
Icteric
Recovery
Hepatitis - Viral
-Incubation phase
varies depending on virus
Hepatitis - Viral
-Prodromal (Preicteric) phase
**starts ~ 2wks after exposure, ends when jaundice appears **
-fever, malaise, anorexia, liver enlargement/tender
-HIGHLY TRANSMISSABLE
Hepatitis- Viral
-Icteric Phase
actual phase of illness
-jaundice and hyperbilirubinemia
-fatigue
-abd pain
Hepatitis - Viral
-Recovery phase
-begins with resolution of jaundice
-symptoms resolve after a few wks
-chronic or chronic active hepatitis can occur
Hepatitis - Viral
-tx
-restrict physical activity PRN
-low-fat, high carb diet if bile flow is obstructed
-avoid contact with blood/body fluids with pts with Hep B or C
Hep A
-source
feces, bile serum of infected pts
-risks: crowded areas, unsanitary, food/water contamination
Hep A
-transmission
fecal-oral
Hep A
-prevention/tx
handwashing
-immunoglobulin admin before exposure or early in incubation phase
-vaccines!!
Hep B
-source
blood, saliva, semen, body fluids of infected pt
Hep B
-transmission
contact with infected blood, body fluid, needles
-maternal transmission to fetus if mom is infected in 3rd tri
Hep B
-prevention/tx
Hep B vax
Hep C
-source
-commonly the cause of post-transfusion Hep
-implicated in infections from IV drug use and HIV
Hep C
-transmission
Co infection with Hep B is common
-80% with Hep C will have chronic liver disease
Hep C
-prevention/tx
no vax available
-antivirals
Hep D
-source
requires Hep B for replication
Hep D
-transmission
-
Hep D
-prevention/t
Tx: Pegylated interferon alpha
Hep E
-source
contaminated water, undercooked meat
-common in african and asian countries and developing countries
Hep E
-transmission
fecal-oral
Hep E
-prevention/tx
vaccine in china only
Cirrhosis
-types
-Alcoholic liver disease
-Nonalcoholic fatty liver disease
-biliary cirrhosis
-primary sclerosing cholangitis
Cirrhosis
-patho
irreversible inflammatory, fibrotic disease disrupting liver function/structure
-nodular and fibrotic tissue decreases hepatic function
-biliary channels become obstructed and cause portal HTN
-portal HTN shunts blood away and causes necrosis from ischemia
-most common causes: alcohol abuse and viral hepatitis
Cirrhosis- Alcoholic liver disease
-patho
-alcohol oxidizes and damages hepatocytes
-mild form: fatty liver (steatosis) - reversible if drinking stops here
-moderate: steatohepatitis - inflammation and necrosis is happening
-severe: alcoholic cirrhosis (fibrosis)- toxic effects from alcohol affect immune function, oxidative stress from lipid peroxidation, malnutrition; hormone degradation doesn’t occur properly, ammonia builds up, FA and enzyme/protein synth is decresed
Cirrhosis- Alcoholic liver disease
-s/s
Nausea
anorexia
fever
abd pain
jaundice
spider angiomas
amenorrhea
loss of body hair
gynecomastia
edema
varices
coag issues
anemia/ splenomegaly
hepatopulmonary syndrome
elevated AST, ALT, ALP bilirubin, PTT, LOW albumin
Cirrhosis - Alcoholic liver disease
-tx
-cessation of alcohol
-rest/ nutrient dense diet
-corticosteroids, antioxidants, drugs that slow fibrosis
-manage complications (ascites, GIB, infection, encephalopathy)
Cirrhosis - NA fatty liver disease
-patho
infiltration of hepatocytes with fat in absence of alcohol intake
-assoc with obesity
Cirrhosis - biliary (Bile Canaliculi)
-patho
cirrhosis begins in bile canaliculi and ducts
-autoimmune (primary biliary cirrhosis): T Cell and antibody mediated destruction of INTRAhepatic bile ducts
-obstructive (secondary biliary cirrhosis): obstruction of bile ducts
Cirrhosis - Primary sclerosing cholangitis
-patho
chronic inflammatory fibrotic disease of medium/large bile ducts OUT of liver
Acute Liver Failure
-patho
severe impairment or necrosis of liver without preexisting disease or cirrhosis
-main cause: acetaminophen OD
-hepatocytes become edematous, patchy areas of necrosis and inflammatory cell infiltrates disrupt parenchyma
-irreversible
Acute Liver Failure
-s/s
anorexia
vomiting
abd pain
progressive jaundice
Acute Liver Disease
-tx
N-acetylcysteine
antiviral drugs (for viral hepatitis)
reduce the ammonia serum levels
liver transplant
Porphyria
-patho
enzyme defect causing altered heme synth and overproduction/ accumulation of precursors in liver
-**Delta-aminolevulinic acid (ALA) and porphobilogen (PBG) **
-prophyrins or pophyrin precursors accumulate and type of porphyria depends on which accumulates
Porphyria
-triggers
hormonal changes during menstrual cycle
fasting
infections
exposure to triggering drugs (etomidate)
Porphyria
-s/s
vary widely between 9 different forms, non-specific
Most common presentation:
-acute abd pain
-seizures
-confusion
-hallucinations
-progressive motor neuropathy causing paralysis or resp failure
-tachycardia/HTN
-skin lesions/blisters/rash
-frailty
-red urine
Porphyria
-tx
-Hemin 3-4mg/kg Iv Q day for 4 days - fixes deficiency of regulatory heme and down regulates ALAS
-IV glucose for mild attacks (same effect)
-avoid triggering drugs (reglan, barbs, sulfa drugs, rifampin)
-treat other symptoms
