PANCE Prep- GI Flashcards
Describe the role of HCl and Pepsin and what stimulates their release
HCl (secreted by parietal cells in response to histamine, acetylcholine and gastrin) 1. dissolving food (solvent) 2. activating pepsin 3. stimulates duodenal release of other digestive enzymes 4. kills harmful bacteria in the food Pepsin: (secreted as inactive pepsinogen by chief cells and becomes activated by HCl acidic environment) 1. digests proteins into smaller peptides
____ stimulates stomach acid secretion and motility. This hormone is inhibited by ___
gastrin Somatostatin via negative feedback
What are the main functions of the large intestines
- absorb water from undigested food (main fxn) 2. transport undigested food for fecal removal (contains Haustra) 3. absorb vitamins produced by bacteria (Vit. K and biotin)
___ is associated w/ no suppression of gastrin levels with the secretin test
Zollinger-Ellison Syndrome (ZES) *gastrin producing tumor)
What are the main functions of the duodenum?
- most chemical digestion (via secretin and CCK) 2. regulates rate of gastric emptying
What are the functions of Secretin and CCK
Secretin: (released by duodenum), inhibits parietal cell gastric acid production and causes pancrease to release bicarb (to buff acid from chyme leaving the stomach entering the duodenum) CCK: aids in breakdown of fats and proteins by stimulating pancreatic release of digestive enzymes 2. increase bicarb release (neutralize stomach acid) 3. stimulates gallbladder contraction and bile release (bile salts help emulsify fats into smaller micelles
Biliary colic is usually worse when? this is due to ___
after a fatty meal -due to CCK mediated contraction of the gallbladder and release of bile
What organ has both endocrine and exocrine functions
pancreas
- ____ breaks down starches into simple sugars 2. __ neutralizes gastric acid in duodenum and activates enzymes. Secretion is stimulated by secretin. 3. ___ precursors to enzymes that break down proteins. 4. ___ breaks down fats into fatty acids 5. ___ increases blood glucose levels 6. ___ decreased blood glucose levels
- amylase 2. bicarbonate 3. proteases 4. lipases 5. glucagon (produced by alpha cells) 6. insulin (produced by beta cells)
Octreotide (somatostatin analog) is used in medical management of:
- GH producing tumors (acromegaly, gigantism) 2. some pituitary tumors 3. flushing and diarrhea associated w/ carcinoid tumors and VIP tumors 4. bleeding esophageal varices
Diagnostic test of choice for achalasia and nutcracker esophagus
Esophageal manometry (motility study)
MC causes of esophagitis and how do you diagnose
- GERD (MC) 2. infectious in immunocompromised (Candida, CMV, HSV) 3. meds DX: Upper endoscopy
What type of esophagitis do the following endoscopic findings suggest and how do you treat them? 1. Small, deep ulcers 2. Large superficial shallow ulcers 3. Linear yellow-white plaques 4. multiple corrugated rings
- HSV- acyclovir 2. CMV- Ganciclovir 3. Candida- PO fluconazole 4. Eosinophilic- remove foods that incite allergic response or inhaled topical corticosteroid w/o spacer
-Heartburn (pyrosis**) often retrosternal that is worse with supine position -Regurgitation, dysphagia -Chest pain
GERD (transient relaxation of LES) DX: clinical, endoscopy, esophgeal manometry, 24 hr pH monitoring (gold standard but only if sx are persistent) TX: 1. lifestyle modification 2. OTC H2 blocker or antacids PRN 3. H2 blocker, PPI (mod-severe) 4. Nissen fundoplication if refractory
What is Barrett’s Esophagus?
esophageal squamous epithelium replaced by precancerous metaplastic columnar cells *risk of developing adenocarcinoma
What are ALARM sx of GERD
- Dysphagia 2. Odynophagia 3. Weight loss 4. Bleeding
-Dysphagia w/ both solids and liquids vs -stabbing CP worse w/ hot or cold liquids/foods
achalasia -DX: esophageal manometry (GS)-increased LES pressure >40 -double contrast esophagram- “Birds beak” appearance of LES Diffuse esophageal spasm -DX: esophagram- “corkscrew”
dysphagia, sense of lump in the neck, neck mass, regurgitation of food, cough, halitosis (old, trapped food pouch)
Zenker’s Diverticulum (pharyngoesophageal pouch) *diverticulum only involves mucosal pouch
Full thickness rupture of the distal esophagus -associated w/ repeated forceful vomiting -retrosternal chest pain worse w/ deep breathing and swallowing -hematemesis -PE: creptius on chest auscultation due
Boerhaave Syndrome DX: Chest CT/CXR: pneumomediastinum Contrast esophagram (GS)
What is Mallory Weiss Syndrome/Tears?
superficial longitudinal mucosal erosions following persistent retching/vomiting typically after ETOH DX: upper endoscopy TX: supportive - acid suppression to help promote healing
Dysphagia + esophageal webs + iron def. anemia= ___
Plummer-Vinson Syndrome *often has atrophic glossitits DX: barium esophagram
esophageal varices are dilation of the gastroesophageal collateral submucosal veins mostly likely due to ___
portal HTN and cirrhosis
TX of acute active esophageal varices bleeds, and prevention of rebleeds
Acute tx: 1. endoscopic ligation** 2. Octreotide: vasoconstricts portal venous blood flow 3. Vasopressin 4. Baloon tamponade 5. Trans jugular intrahepatic portosystemic shunt (TIPS)* Prevention: 1. nonselective BB: Propranolol, nadolol 2. Isosorbide: long acting nitrate Abx Prophylaxis: fluoroquinolones or ceftriaxone
MC cause of esophageal CA worldwide:___ (MC in ___ esophagus) MC cause of esophageal CA in US: ___ (MC in ___ esophagus) MC cause of gastric CA worldwide: ___
squamous cell- in upper 1/3rd of esophagus adenocarcinoma- in lower 1/3rd of esophagus adenocarcinoma
MC causes of gastritis
- H. pylori (MC) 2. NSAID/ASA (2nd MC) 3. Acute Stress 4. alcohol, reflux **1 and 2 are also most common causes of PUD DX: endoscopy (GS)
MC cause of upper GI bleed
PUD
Compare and contrast gastric ulcers and duodenal ulcers
Gastric: -decreased mucosal protective factors (mucus, bicarb, prostaglandins, NSAIDS) -4% malignant -Worse w/ meals Duodenal: -increased damaging factors (acid, pepsin, H.pylori) -MC- almost always benign -Better w/ food
How do you diagnose H. pylori
- endoscopy w/ biopsy is GS 2. rapid urease test 3. Urea breath test 4. Stool antigen 5. Serology Abs (CANT USE for eradication test) *must stop PPI 2-4 weeks prior to recheck urea breath test
TX of H. pylori eradication TX of H. pylori neg. PUD
H. pylori: tripe therapy (CAP) 1. Clarithromycin 2. Amoxicillin (metronidazole if PCN allergy) 3. PPI HP neg: acid suppression: PPI or H2 blocker, sucralfate
Side effects of PPIs
-B12 def. -CP450 inhibition–> increases levels of theophylline, warfarin and phenytoin (H2 blockers are also CP450 inhibitors)
multiple “kissing ulcers” -increased fasting gastrin level -Positive secretin test: increased gastrin release w/ secretin
Zollinger-Ellison Syndrome (ZES) TX: surgical resection of the tumor
What is Dubin-Johnson Syndrome?
hereditary direct hyperbilirubinemia TX: none needed Think: D’s “Dubin, Direct hyperbili, Dark liver on biopsy
What is Crigler Najjar Syndrome
Hereditary unconjugated (INDIRECT) hyperbili with normal LFTs Type I: NO UGT activity tx: phototherapy Type II: Very little UGT activity tx: usually not needed- could us phenobarbital to increase UGT activity
Transient episodes of jaundice during periods of stress, fasting, ETOH, or illness
Gilberts Syndrome *reduced UGT activity- indirect hyperbili *normal LFTs No tx needed
What labs are used to measure: 1. hepatocellular damage 2. cholestasis 3. liver “synthetic” function
- hepatocellular damage: ALT*, AST 2. cholestasis: alkaline phosphate, GGT, bili 3. liver “synthetic” function: PT, albumin
What do the following labs suggest? 1. ALT >1,000, + ANA, +smooth muscle Ab*, increased IgG and response to corticosteroids 2. Increased ALP (alkaline phosphatase) and GGT 3. AST and ALT >1,000, ALT>AST 4. AST: ALT >2
- autoimmune hepatitis 2. biliary obstruction or intrahepatic cholestasis 3. viral/toxic hepatitis 4. ETOH hepatitis (think S =scotch)
What are the 5 F’s of cholelithiasis and how do you dx and tx
Fat, fair, female, forty, fertile DX: US TX: elective cholecystectomy
What is choledocholithiasis? complications? Dx? TX?
gallstone in the common bile duct Complications: acute pancreatitis or acute cholangitis DX: abdominal US or ERCP (diagnostic and therapeutic) TX: ERCP
What is acute cholangitis? Dx?
biliary tract infection secondary to obstruction *MC to gram neg organism (E. coli MC then Klebsiella and enterococci) DX: 1. leukocytosis, increased ALP w/ GGT, increase bili> ALT and AST 2. US or CT 3. Cholangiography via ERCP (GS)
What is Charcots triad and Reynolds pentad
Charcots: fever/chills, RUQ pain, jaundice Reynolds: Charcots + shock + AMS **acute cholangitis
how do you treat acute cholangitis
- Abx 2. Common bile duct decompression/stone extraction via ERCP
What is Boas sign What is Kerr’s sign
Boas: referred pain to R shoulder/subscapular area (phrenic nerve irritation) (seen in acute cholecystitis) Kerrs: referred pain to L subscapular area (phrenic nerve irritation) (seen in splenic rupture)
How do you dx and tx acute cholecystitis
DX: US is initial test 2. HIDA is gold standard TX: NPO, IV fluids, Abx (Ceftriaxone + Metronidazole) -cholecystectomy
-Rapid liver failure (w/in 8 weeks) + hepatic encephalopathy -Vomiting, coma, asterixis (flapping tremor of the hand w/ wrist extension) -Coagulopathy -Hepatomegaly, jaundice
Fulminant hepatitis DX: Increase ammonia, PT/INR, LFTs and hypoglycemia TX: 1. Lactulose: neutralizes ammonia 2. Rifaximin, neomycin: decrease ammonia producing bacteria in GI 3. protein restriction 4. Liver transplant (definitive)
Etologies of Fulminant hepatitis
- Acetaminophen (MC) 2. Drug reaction (isoniazid) 3. viral hepatitis 4. Reye Syndrome
Rash (hands and feet) in children, intractable vomiting, liver damage, encephalopathy, dilated pupils with minimal response to light and multi-organ failure s/p ASA use
Reye Syndrome
What viral hepatitis’s are asociated w/ chronicity and may lead to ____
HepB HepC (80% have chronic) HepD *increase ALT>AST lead to ESLD or hepatocellular carcinoma
How are the following hepatitis transmitted? and what is their hallmark/distinguishing feature? Hep A Hep B Hep C Hep D Hep E
A: fecal-oral: Only one associated w/ spiking high fever (self limiting) B: Parental-sexual (tx w/ alpha-interferon 2b) C: parenteral-IVDU (tx w/ pegylated interferon alpha-2b and ribavirin) D: requires HepB to cause coinfection E: fecal-oral (self limiting)
How do you screen for hepatocellular carcinoma with viral hepatitis
serum AFP* and US *needle biopsy usually avoided to prevent seeding
When do you give HepB vaccine and when is it contraindicated
0, 1, 6 months CI: allergy to bakers yeast
Classic triad: Ascites, hepatomegaly, RUQ abdominal pain -idiopathic or hypercoaguable state
Hepatic vein obstruction (Budd-Chiari syndrome) DX: US- screening test Venography (GS) TX: 1. Shunts (TIPS) 2. Balloon angioplasty w/ stent 3. anticoagulation 4. Management of ascites: diuretics
-Ascites, gynecomastia, pruritis, spider angioma, caput medusa, muscle wasting, hepatosplenomegaly, palmer erythema, jaundice, Dupuytren’s contracture
Cirrhosis DX: US, liver biopsy Tx: 1. Encephalopathy: lactulose or rifaximin 2. Ascites: Na+ restriction, diuretics 3. Pruritis: Cholestyramine* 4. Liver transplant- definitive
Etiologies of Cirrhosis
*irreversible liver fibrosis w/ nodular regeneration secondary to chronic liver disease 1. ETOH (MC cause in US) 2. chronic viral hepatitis (HepC*, HepB, HepD) 3. nonalcoholic fatty liver 4. hemochromatosis
-Fatigue–> pruritus, RUQ discomfort, hepatomegaly, jaundice -MC middle aged women -Labs: elevated ALP and GGT, + Anti-mitochondrial Ab
Primary biliary cirrhosis (PBC) *idiopathic autoimmune disorder of INTRAhepatic small bile ducts DX: labs and biopsy TX: 1. Ursodeoxycholic acid 1st line to reduce progression 2. Cholestyramine (bile acid sequestrant) and UV lights for pruritus
-Jaundice, pruritus, fatigue, RUQ pain, hepatomegaly, splenomegaly*, -associated w. IBD, UC -MC in men 20-40 -Labs: increase ALP and GGT, + P-ANCA
Primary sclerosing cholangitis (PSC) *autoimmune progressive cholestasis, diffuse fibrosis of INTRAhepatic and EXTRAhepatic ducts DX: labs and ERCP (gold standard) TX: liver transplant (meds not helpful)
-Parkinson-like symptoms (bradykinesia, rigidity) dementia. -Arthralgia -Hepatosplenomegaly, cirrhosis, hemolytic anemia -Brown or green pigment in the cornea*
Wilson’s disease (Hepatolenticular degeneration) *cornea pigmentation= Kayser-Fleischer rings *free copper accumulation in liver, brain, kidey, cornea
How do you dx and treat wilson’s disease
DX: decreased ceruloplasmin (serum carrier molecule for copper) -increased urinary copper excretion TX: 1. D-Pencillamine (chelates copper) 2. Zinc: enhances fecal copper excretion and blocks copper absorption
Etiologies of acute pancreatitis and common manifestations
Etiologies: 1. gallstones* 2. alcohol* 3. scorpion bite 4. Mumps in children* S/S: -epigastric pain that is boring and constant w/ radiating to the back and relieved w/ leaning forward or in fetal position - N/V, -Cullen’s sign (periumbilical ecchymosis)* -Turner sign (flank ecchymosis)*