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)*
how do you dx and tx acute pancreatitis
DX: abdominal CT* XRAY: sentinel loop = localized ileus, colon cut off Labs: increased TG, lipase (more specific than amylase), amylase, ALT, hypocalcemia TX: supportive/pancreatic rest -NPO, IV fluids, analgesia w/ Meperidine (Demerol) -Abx NOT routinely used- if necrotizing–> broad spectrum
What is Ranson’s criteria?
*used to determine prognosis of acute pancreatitis GET ON ADMISSION: Glucose Age LDH AST WBC GET W/N 48 HRS: Calcium, hematocrit fall, Oxygen, BUN, Base deficit, Sequestration of fluids
What are the manifestations, dx, and tx of chronic pancreatitis
s/s triad: 1. calcifications, 2. steatorrhea, 3. DM DX: XRAY: calcified pancrease* -amylase/lipase usually NOT elevated TX: oral pancreatic enzyme replacement
-Abdominal/back pain +/- relieved w/ sitting up and forward -Painless jaundice* -Weight loss -Pruritis -Palpable NONTENDER, distended gallbladder*
Pancreatic carcinoma (MC- adenocarcinoma ductal (70% found in pancreas head)) *Courvoisier’s sigb = Palpable NONTENDER, distended gallbladder* DX: CT* -increased CEA, CA 19-9 markers TX: Whipple procedure** -ERCP w/ stent placement as palliative tx for intractable itching
-Persistent portion of embryonic vitteline duct (yolk stalk)* -Rule of 2’s: 2x in males, 2y/o, 2 feet from ileocecal valve, 2 inches in length -often found incidentally during surgery for other cause -Painless rectal bleeding or ulceration*
Meckel’s (ileal) diverticulum TX: surgical excision if symptomatic
-Abdominal cramping, abdominal distention, vomiting, obstipation (absence of stool/flatus) -**high pitched tinkles on auscultation and visible peristalsis –>hypoactive bowel sounds later
small bowel obstruction MC cause: post-surgical adhesions*** then incarcerated hernia DX: XR: air fluid levels in step ladder pattern, dilated bowel loops TX: nonstrangulated: NPO (bowel rest), IV fluids, bowel decompression strangulated–> surgery
decreased peristalsis w/o structural obstruction -MC post-operative state, w/ opiates, metabolic hypokalemia, hypothyroidism -Decreased to no bowel sounds
Paralytic (adynamic) ileus
How do you dx celiac disease
*small bowel autoimmune inflammation 2/2 to alpha-gliadin in gluten–> loss of villi and absorption area–> impaired fat absorption DX: + endomysial IgA Ab and + transglutaminase Ab SB biopsy- definitive dx *May get dermatitis herpetiformis
How do you dx and tx lactose intolerance?
DX: hydrogen breath tests* TX: lactase enzyme preparations, lactose free diet
Diverticula most commonly occurs where? How do you dx and tx
sigmoid colon associated w/ low fiber diet, constipation, obesity DX: CT, increased WBC TX: -itis: clear liquid diet, Abx (Cipro or Bactrim + Metronidazole) -osis: high fiber diet, fiber supplement
MC cause of acute lower GI bleeding
diverticulitis
MC site of volvulus
*sigmoid
- RLQ pain w/ LLQ palpation= __ 2. RLQ pain w/ internal and external hip rotation w/ flexed knee = __ 3. RLQ pain w/ right hip flexion/extension (raise leg against resistance) =__ 4. point 1/3 from the distance from the anterior sup. iliac spine and navel= __
- rovsing sign 2. Obturator sign 3. Psoas sign 4. McBurneys point tenderness
How do you dx IBS
Recurrent abdominal pain on average at least 1 day a week in the last 3 months associated w/ at least 2 of the following: 1. releated to defecation 2. onset associated w/ change in stool FREQUENCY 3. onset associated w/ change in stool FORM/APPEARANCE
How do you tx IBS
- life style modification- quit smoking, low fat/unprocessed food diet 2. tx diarrhea w/ anticholinergics/spasms (Dicyclomine) or Loperamide 3. tx constipation w/ bulk-forming laxatives 4. TCAs or serotonin for intractable pain
-chronic dull abdominal pain worse AFTER meals “intestinal angina” -weight loss/anorexia -Dx w/ angiogram and Colonoscopy: muscle atrophy w/ loss of villi
Chronic mesenteric ischemia *mesenteric atherosclerosis of the GI tract
“severe” abdominal pain out of proportion to PE findings** -poorly localized pain, N/V -Hx of Afib, MI or atherosclerosis
Acute mesenteric ischemia Dx: angiogram TX: surgical revascularization w/ stent
abdominal pain, fever, N/V, diarrhea, electrolyte disorder -XR: dilated colon >6cm*
Toxic megacolon TX: bowel decompression, bowel rest, NG tub *surgery if severe or refractory
Compare and contrast ulcerative colitis and crohns disease
UC: -limited to colon (begins in rectum and spreads proximally), CONTINUOUS, mucosa or submucosa only -LLQ pain, colicky, -bowel urgency w/ bloody diarrhea -Pseudopolyps on colonscopy -Stovepipe sign on barium study (loss of haustral) *surgery is curative CD: - any segment of GI tract (anus to mouth, MC in TERMINAL ILEUM), SKIPPED lesions, transmural -RLQ pain, crampy -NONbloody diarrhea -skipped lesions w/ cobblestone appearance on colonoscopy -String sign on barium study *surgery is not curative
Complications of UC and CD
UC: PSC, colonn CA, toxic megacolon, *smoking decreases risk for UC *MUCOSA/SUBMUCOSA only CD: perianal dz: fistulas, strictures, abscess, granulomas*, B12 def *TRANSMURAL
How do you dx UC and CD
UC Colonoscopy: uniform inflammation, pseudopolyps Barium study: “stovepipe sign” Lab: + P-ANCA CD: Colonoscopy: skipped lesions, cobblestone appearance Barium study: string sign Lab: + ASCA
How do you tx IBD (UC and CD)
Aminosalicylates –> corticosteroids–> immune modifying agents 1. 5-ASA (sulfasalazine-works primarily in colon, mesalamine- oral best for maintenance) 2. Corticosteroids- used for flares 3. immune modifying agents
colorectal CA is typically caused from progression of __ polyps into malignancy *MC site of metastatic spread= __
adenomatous polyps (10% of polyps w/in 10-20 yrs) Liver
How do you dx CRC
- Colonoscopy w/ biopsy* 2. barium enema: apple core lesion 3. CEA level monitoring
When should ppl be screened for colorectal CA
- FOB: annually at 50 or colonsocpy q10y or flex sig q5y up to 75y/o 2. + 1st degree relative 60y/o or older: annually at 40 or colonscopy q10y 3. + 1st degree relative less than 60y/o : annually at 40 or 10 yrs prior to diagnosed age or colonscopy q5y
What type of hernia? 1. through pelvic floor in which abdominal/pelvic contents protrude through obturator foramen 2. through abdominal wall weakness 3. through abdominal cavity through femoral canal below inguinal ligament 4. protrude at the internal inguinal ring LATERAL to inferior epigastric artery 5. protrude MEDIAL to inferior epigastric vessels WITHIN hesselbachs triangel (rectus abdominis, inferior epigastric vessels, Pouparts ligament (RIP)
- Obturator hernia 2. Incisional (ventral) hernia 3. Umbilical hernia 4. femoral hernia (MC seen in women) 5. Indirect inguinal (MC overall in M and F and kids) 6. Direct inguinal (does not reach the scrotum)
How to differentiate internal and external hemorrhoids
Internal: intermittent rectal bleeding (bright red blood per rectum) -uncomplicated internal are usually non-tender and nonpalpable External: perianal pain* aggravated w/ defecation + tender palpable mass
anorectal abscess and fistulas are treated by:
MC on posterior rectal wall TX: I&D followed by WASH (warm water cleansing, Analgesics, sitz baths, High fiber diet)
-severe painful rectal pain and bowel movements causing patient to refrain from having BM leading to constipation, bright red blood per rectum -skin tags seen w/ chronic (MC at posterior midline)
anal fissures >80% resolve spontaneously with supportive measures
what is PKU and how do you tx?
AR disorder *enzyme cannot metabolize–> accumulation–> phenylketone neurotoxicity *s/s- vomiting, mental delays, convulsions–>blonde, blue-eyed w/ fair skin MC TX: restrict phenylalanin (milk, cheese, nuts, fish, chicken, meats, eggs, legumes, aspartame)
Risk factors and sx of Vit. A deficiency
Risk factors: liver dz, ETOH, fat free diets S/S: 1. visual changes (esp. at night**/nighttime blindness*) and dry eyes (xerophthalmia) 2. squamous metaplasia (conjunctiva, respiratory epithelium, urinary tract)– Bitot’s spots*: white spots on conjunctiva due to metaplasia of cornea 3. impaired immunity and poor healing
Risk factors and sx of Vit. C deficiency
Risk factors: smoking, alcohol, malnourished/poor diet S/s: (3 H’s) 1. Hyperkeratosis: hyperkeratotic follicular papules (often surrounded by hemorrhage) 2. Hemorrhage: vascular fragility w/ recurrent hemorrhages in gums, skin, joints, and impaired wound healing 3. Hematologic: anemia, glossitis, weakness, increased bleeding time
Vit. D deficiencies in adults and in kids? TX?
Kids: Ricketts- bone softening/ bowing adults: Ostomalacia- looser lines on xray TX: ergocalciferol (Vit. D)*
- nervous system changes: paresthesia, demyelination, neuropathy, muscle cramps or wasting 2. High output HF, dilated cardiomypathy
Beriberi Vit. B1 (thiamine) def. 1. Dry 2. wet **ETOH MC CAUSE!!
- Ataxia 2. global confusion 3. ophthalmoplegia
Wernicke’s Encephalopathy (Triad of sx) *Mc cause is ETOH
-Memory loss (esp. short term) -Confabulation (mis interpreation/recall of memory)
Korsakoff Dementia (vit. B1 (thiamine) def **IRREVERSIBLE
-Oral lesions, magenta colored tongue, angular cheilitis, pharyngitis -Photophobia, corneal lesions -Scrotal dermatitis
Riboflavin (B2) Def. *Oral-Ocular-Genital syndrome
-diet high in corn or lack tryptophan -Pellagra -Diarrhea -Dementia -Dermatitis
Niacin/Nicotinic Acid (B3) def. *Pellagra– 3 D’s (diarrhea, dementia, dermatitis)
Common etiologies and sx of Pyridoxine (B6) def.
Etiologies: chronic alcoholism, Isoniazid***, OCP S/s: peripheral neuropathy, seizures, HA, stomatitis
___ is the primary natural source of vitamin B12. Stomach acid releases B12 from food and binds it to ____ for later absorption in the ___
Animal foods Intrinsic factor terminal ileum
Etiologies of B12 (Cobalamin) def.
- Pernicious anemia: autoimmune destruction/loss of gastric parietal cells** (they secret intrinsic factor) 2. Strict vegans 3. Malabsorption (ETOHism, Celiac, Crohns) 4. decreased intrinsic factor production (bypass surgery, PPIs and H2RA blockers)
How do you dx pernicious anemia
-Ab testing -Schilling test (Vit. B12 (Cobalamin) def)
-Paresthesia, gait abnormalities, memory loss, dementia -GI upset, anorexia, diarrhea, glossitis -Macrocytic anemia w/ hypersegmented neutrophils****
B12 (Cobalamin) def. TX: IM or oral B12 *pernicious anemia needs IM B12
Management of Diarrhea
- IV fluid repletion (mainstay tx of gastroenteritis)– PO preferred 2. Diet: bland low-residue die (BRAT) 3. Anti-motility agents: if pt <65y w/ mod-severe signs of volume depletion (DONT give for invasive diarrhea) 4. Antiemetics
Types of anti-motility agents
- Bismuth subsalicylate (pepto-bismol, kaopectate)–> SE: Reyes in kids, dark stools and tongue 2. Opioid agonists (Diphenoxylate (lomotil), loperamide (immodium) 3. Anticholinergics (Phenobarbital/Hyoscyamine/Atropine/ Scopolamine)
What antimotility agent is best to used for dysentery (bloody diarrhea w. fever) and what what is CI w/ dysentery
Use: Bismuth Subsalicylate (pepto or Kaopectate) CI: Loperamide (immodium)
Types of anti-emetics
- 5-HT3 Blocker (serotonin receptor blocker) (Ondansetron, Granisetron, Dolasetron) 2. CNS dopamine receptor blockers (Prochlorperazine (compazine), Promethazine (phenergan), Metoclopramide (reglan))
SE of Dopamine blockers
*anti-emetic drugs (prochlorperazine, promethazine, metoclopramide) 1. QT prolongation 2. Anticholinergic 3. Antihistamine SE (drowsy) 4. EPS sx (rigidity, bradykinesia, tremor, akathisia, Dystonic rxns/dyskinesia, Parkinsonism sx)
MC overall cause of gastroenteritis in adults in N. America -associated w. outbreaks ex. cruise ships, hospitals, restaurants
Norovirus
MC cause of diarrhea in children
Rotavirus
How can you differentiate non-invasive vs invasive types of diarrhea
non-invasive: vomiting, watery, voluminous (involves SI), no fecal WBCs or blood invasive: high fever, + blood and fecal leukocytes, not as voluminous (LI) mucus
-prominent vomiting, abdominal cramps, HA, noninvasive diarrhea -h/o eating dairy products, mayonnaise, meats, or eggs w/in last 6 hrs (short incubation period)
Staphylocccus aures
-vomiting*, cramps, noninvasive diarrhea -h/o eating fried riced w/in last 1-6 hrs
Bacillus cereus
-Copious watery diarrhea “rice water stools” (grey, no fecal odor, blood or pus) that rapidly produces severe dehydration–> hypovolemia -h/o contaminated food and water- outbreaks may occur during poor sanitation and overcrowding conditions
Vibrio Cholera and parahemolyticus TX: supportive- fluid replacement**, Abx if severely ill or w/ high fever (tetracyclines) Vibrio parahemolyticus- associated w/ eating raw shellfish esp. in Gulf of Mexico
MC cause of travelers diarrhea s/s: abrupt onset of watery diarrhea, abdominal cramps, vomiting (IP 24-72 hrs)
enterotoxigenic E. coli *risks: unsanitary drinking water/ice TX: Fluids +/- Bismuth–> if severe use fluoroquinolone
s/s of C. difficile
- abdominal cramps, diarrhea, fever, tenderness 2. Strikingly increased lymphocytosis* 3. Psudomembranous colitis 4. Toxic mega colon 5. H/o Abx use (Clindamycin or chemo)
tx of C. difficile
- Metronidazole 1st line for mild 2. Vancomycin 2nd line (but 1st line if severe)
Causes of bloody diarrhea
- Campylobacter 2. Shigella 3. Salmonella 4. Yersinia 5. Enterohemorrhagic E. coli 6. Campylobacter
___ MC cause of bacterial enteritis in US.
Campylobacter jejuni
___ MC antecedent event in post-infectious Guillain-Barre Syndrome
Campylobacter jejuni
-fever, HA, abdominal pain (mimics acute appendicitis) -Diarrhea initially watery then bloody -h/o undercooked poultry*, raw milk, water, diary cattle
Campylobacter jejuni DX: stool, gram neg “S, COMMA, or SEAGULL shaped” organism TX: fluids -if severe, Erythromycin
-lower abdominal pain, high fever*, tenemus -Explosive watery diarrhea then mucoid, bloody (may cause toxic megacolon) -Febrile seizures in young children*
Shigella *fecal/oral transmission- HIGHLY VIRULENT DX: stool cultures CBC +/- Leukemoid reaction WBC >50,000 2. sigmoidoscopy: punctate areas of ulcerations TX: fluids -if severe: trimethoprim-sulfamethoxazole
-abdominal pain, fever, cramping, vomiting -Mucus + bloody diarrhea -h/o eating poultry products (dairy, meat, eggs) w/in last 6-48 hrs exotic pets (reptiles ex. TURTLES) -MC in summer months
Salmonella gastroenteritis (S. typhimurium) TX: fluids -if severe, Fluoroquinolones
-HA, constipation, pharyngitis, cough –> crampy abominal pain, diarrhea “pea soup stools*** -intractable fever, relative bradycardia* -Hepatosplenomegaly, blanching “Rose Spots” appears in 2 weeks
Typhoid (enteric) Fever (S. typhi) TX:fluids -if severe, Fluoroquinolones
-Watery diarrhea early–> bloody crampy diarrhea w/ abdominal pain, vomiting, low grade or absent fever -h/o ingestion of undercooked ground beef, unpasteurized milk/apple cider, day care centers, contaminated water
Enterohemorrhagic E. Coli H0157:H7 *produces cytotoxin TX: fluids -Abx use is controversial (increased risk of HUS in kids)
-fever, abdominal pain mimic acute appendicitis (can cause mesenteric adentits* -producing abdominal tenderness, guarding
Yersinia enterococlitica tx: fluids if sever fluoroquinolones
-Frothy, greasy, foul diarrhea (no blood or pus) and malabsorption w/ cramping, bloating -h/o ingestion of contaminated water from remote streams or well
Giardia lamblia DX: stools- protozoan TX: fluids -Metronidazole -Furazolidone in children* *Boil water x 1 minute to kill cysts
-GI colitis, dysentery, liver abscesses* -MC seen in travelers to developing nations or immigrant population
Amebiasis DX: stool ova and parasites TX: fluid 1. colitis and abscess metronidazole
MC cause of chronic diarrhea in patients with AIDS
cryptosporidium
Causes of osmotic diarrhea *malabsorption of nonabsorbable substances in the intestinal lumen *Decreased diarrhea w/ fasting, increased osmotic gap, and increased fecal fat
- Rapid transit of GI contents (meds- lactulose, sorbitol, antacids) 2. Bacterial overgrowth (Whipples diase, Tropical Sprue) 3. Malabsorption (Celiac, lactose intolerance)
Cause os secretory diarrhea *normal osmotic gamp, large volume, no change in diarrhea w/ fasting
- Hormonal: serotonin (carcinoid), ZES) 2. Laxative abuse
-Weight loss, steatorrhea, nutritional def, fever, lymphadenopahty -nondeforming arthritis, neuro sx -rhythmic motion of eye muscles while chewing** -H/o farmer around contaminated soil
Whipples Disease (Tropheryma whippelii) DX: duodenal biopsy- Periodic aci Schiff (PAS)- positive macrophages and dilation of lacteals TX: PCN
Types of meds to help w/ constipation
- fiber 2. Bulk forming laxatives (psyllium, methylcellulose, polycarbophil, Wheat dextran) 3. Osmotic laxatives (polyethylene glycol (PEG), miralax, lactulose, sorbitol, milk of magnesia, or magnesium citrate) 4. Stimulant laxative- bisacodyl (Dulcolax), Senna
-Vitamins ___ are absorbed in the jejunum and ileum. -Vitamins ___ are absorbed throughout the small intestine. -__ absorbed in the proximal jejunum. -___ absorbed in the distal small intestine. -__ is absorbed primarily in the proximal intestine. -___ is absorbed mainly in the ileum.
B1, B5, B6= jejunum and ileum B2, and B3= throughout SI Folic Acid= prox. jejunum Vitamin C= distal SI Iron= prox. intestine Zinc= ileum
What are the fat soluble vitamins?
Fat: A,D,E,K
____ is due to a combination of insufficient secretion of zymogens from the pancreas leading to incomplete protein digestion and an immature, leaky gut in the infant. The poorly digested proteins irritate the lining of the intestinal tract causing pain when the infant eats.
Milk protein intolerance TX: 1. educating the family that this is a self-limiting condition. As the child grows and matures, the pancreas will reach adult secretory levels by a year of age and the tight junctions between the cells will work more effectively. *Parents typically start to see improvement around 4-6 months of age but some kids can take up to 10 months for improvement in their 2. maternal elimination diet can help. Start with a two week trial of eliminating one food at a time—dairy first, then soy and finally peanuts. If no improvement is seen after eliminating those three foods, you can do a trial of a soy formula for 2 weeks. *Unfortunately 50% of kids that react to breast milk or regular formula will also react to soy. 3. If soy formula does not change the condition, you can do a 2 week trial of a semi-elemental formula like Nutramigen or Alimentum where the proteins are more hydrolyzed. 4. If the child is still highly fussy, you can try a two week trial of elemental formula such as EleCare and Neocate.
What is the definition of chronic constipation and when are the 3 peak times of occurence
delay or difficulty in defecation present for 2 or more weeks 1. 6 months w/ introduction of solids 2. 1-2 y/o w/ introduction of cows milk 3. 3-5 y/o w/ kids not wanting to go at school
tx regimen for kids <1y/o w/ constipation
- educate on process 2. diet: introduce 2-4oz of sorbitol containing fruit juice into diet or feed pureed prunes 3. meds: trial of osmotic laxative- ex. lactulose or karosyrups 1-2x daily
tx regimen for kids >1y/o w/ constipation
- Educate 2. diet: decrease milk intake increase fiber, increase clear fluids 3. behavioral changes: toilet time 15-20 min after meals 4. meds: lactulose or miralax
as involuntary passage of fecal material in the underwear; typically the child has anywhere from 3-8 bowel movements in their underwear that they can’t control
encopresis (fecal incontinence due to long standing diarrhea *tx aggressively w/ education, diet, behavioral changes, disimpaction and meds
Intussusception most commonly occurs in the ____
terminal ileum near the ileocecal junction
-undernourished infant with hypochloremic metabolic alkalosis -Vomiting is immediately post-prandial and infant will feed following emesis (“hungry vomiter”)
Pyloric stenosis DX: abdominal us Tx: correct electrolytes and pyloromyotomy
4 factors that predict level of dehydration
- cap refill >2 sec 2. absence of tears 3. dry mucous membranes 4. ill general appearance
What lab values can help assess dehydration
BUN Creatinine BUN/creatinine urine specific gravity
Volume resuscitation formula for kids
start w/ LR or NS at 20ml/kg IV over 1 hr
Rehydration formula (if electrolytes are normal) for kids
*do after volume resucitation 1. administer ORT at 100ml/kg over 3-4 hrs if tolerated OR 2. D5 1/4 NS IVF w/ 20mEq/L K+ over 3-4 hrs 3. D5 1/2 NS with 20mEq/L K_ to replace losses on top of maintance levels
formula for calculating maintenance fluid
Holliday-Segar Method 1. determine the total ml per day and then calculate ml per hour to determine the rate of IV flow Simplifed for home ORT: infant <1y/o: 1oz/hr Toddler 1-3y/o: 2oz/hr Older kids 3-5y/o: 3oz/hr
