GI Day #1 Flashcards
Neonatal Jaundice
-Physiologic jaundice presents on days ________ of life and bilirubin levels fall in about 50% of neonates in first week of life.
-Initial therapy of choice for all types of neonatal jaundice?
-In severe cases, what is needed?
-Jaundice associated with bilirubin levels > _____.
-Kernicterus associated with bilirubin levels > ______.
-Presents on days 3-5 of life
-Phototherapy is initial TOC
-Jaundice: > 5 mg/dL
-Kernicterus: > 20 mg/dL
Dubin-Johnson Syndrome
-What is it? What should you remember?
-What is seen on labs? Bilirubin can increase with illness, pregnancy, OCPs.
-what is seen on liver biopsy?
-Treatment?
-Hereditary conjugated (direct) hyperbilirubinemia due to decreased hepatocyte excretion of conjugated bilirubin (gene defect MRP2)
-Isolated conjugated (direct) hyperbilirubinemia (between 2-5 mg/dL most times)
-Liver biopsy: grossly black liver
-Treatment: None needed
Crigler-Najjar Syndrome
-What is it?
-What is the pathophysiology of it?
-Types (there are 2)
-What should you watch for?
-What is seen on labs?
-What does the liver look like on biopsy?
-Management of Type 1?
-Management of Type 2?
-Hereditary unconjugated (indirect) hyperbilirubinemia
-Patho: decreased activity of UGT (glucuronosyltransferase) needed to convert bilirubin to direct.
-Type 1: no UGT activity, Type 2: very little UGT activity
-Neonatal jaundice with severe progression in second week, leading to kernicterus
-Labs: isolated indirect (unconjugated) hyperilirubinemia + otherwise normal LFTs
-Type 1: Phototherapy, Liver transplant
-Type 2: no treatment needed, but Phenobarbitol can increase UGT activity
True or False: Type 1 of Crigler-Najjar Syndrome does NOT respond to Phenobarbitol?
True, Type 1 does not respond to this medication
Gilbert’s Syndrome
-What is it?
-What is the pathophysiology?
-Symptoms
-What is seen on labs?
-Management?
-Hereditary unconjugated (indirect) hyperbilirubinemia
-Patho: reduced UGT activity and decreased bilirubin uptake
-Symptoms: transient episodes of jaundice during periods of stress, fasting, alcohol, or illness
-Labs: increase in isolated indirect bilirubin levels + otherwise normal LFTs
-No treatment needed; mild, benign disease
Liver Injury Patterns
-ETOH Hepatitis:
-Viral/Toxic/Inflammatory Process:
-ETOH: AST: ALT > 2 (think S for Scotch)
-Viral/Toxic: ALT > AST (think L for Liver)
-AST & ALT < 1,000 = acute viral hepatitis (A, B, or C)
Liver Injury Patterns
-Biliary Obstruction or Cholestasis:
Increased alkaline phosphatase (ALP) and increased GGT suggests hepatic source or biliary obstruction
-GGT most sensitive of biliary injury
-If ALP high without elevated GGT, look for sources other than the liver
Explain what happens with Albumin and PT in liver injury
-PT is an earlier indicator of severe liver injury/prognosis than albumin.
-Prolonged PT seen when liver’s protein synthesizing ability is lost.
-Albumin: useful marker of overall liver protein synthesis. Levels decrease with liver failure
Anorectal Abscess and Fistula
-MCC of abscess
-MC site for abscess
-Management for both
-Staph Aureus MCC
-Posterior rectal wall MC site for abscess
-Incision and drainage followed by WASH (warm water cleansing, analgesics, sitz baths, high fiber diet)
Anal Fissures
-Etiologies
-Symptoms
-Where does it MC occur?
-What is seen in chronic condition?
-Management
-Low-fiber diets, passage of large/hard stools, constipation, anal trauma
-Severe painful rectal pain and bowel movements, refrain from defecating, BRBPR
-Skin tags seen in chronic
->80% resolve spontaneously
–Supportive (first-line): WASH, stool softeners, laxatives, mineral oil
–Second line: topical vasodilators (Nitroglycerin, Nifedipine ointment)
–Botox injections reduce internal sphincter spasm
–Lateral internal sphincterotomy for refractory
Internal Hemorrhoids
-Occur where?
-Symptoms of internal
-What are the four degrees?
-Risk Factors?
-Diagnostics
-Management
-originate from superior hemorrhoid vein and Occur proximal (above) the dentate line
-Tend to bleed and are painless, intermittent rectal bleeding (painless BRBPR), rectal itching and fullness, mucus discharge
-Degrees (1: does not prolapse, 2: prolapses but reduces spontaneously, 3: prolapses but requires manual reduction, 4: irreducible and may strangulate)
-Risk Factors: pregnancy, constipation, obesity, prolonged sitting, cirrhosis with portal hypertension
-Diagnostics: visual inspection, DRE, Anoscopy for internal
-Conservative treatment: WASH with topical rectal corticosteroids (lidocaine)
-Surgical: rubber band ligation MC, sclerotherapy, infrared coagulation if needed.
External Hemorrhoids
-Occur where?
-Symptoms of External
-Risk Factors?
-Diagnostics
-Management
-Originate from inferior hemorrhoids vein and Occur distal (below) the dentate line
-Perianal pain aggravated with defecation, tender palpable mass, skin tags
-Risk Factors: pregnancy, constipation, obesity, prolonged sitting, cirrhosis with portal hypertension
-Diagnostics: Visual inspection, DRE, fecal occult blood testing
-Conservative: WASH + topical rectal corticosteroids
-Hemorrhoidectomy for external hemorrhoids most times
Vitamin C Deficiency
-Other Name for the vitamin
-Risk Factors
-Symptoms (what to remember)
-Management
-Ascorbic Acid
-RF: diets lacking raw fruits and veggies, smoking, illicit drug use, elderly
-Scurvy (3 H’s): Hyperkeratosis = hyperkeratotic follicular papules surrounded by hemorrhage, coiled hairs; Hemorrhage = vascular fragility with recurrent hemorrhages in gums, skin, and joints and impaired wound healing; Hematologic = anemia, glossitis, malaise, weakness, increased bleeding time
-Management: ascorbic acid replacement
Vitamin A Deficiency
-Other name for this vitamin
-Vitamin A function
-Sources
-Risk Factors for Deficiency
-Symptoms
-Labs
-Retinol
-Function: vision, immunity, embryo development, skin, cellular health
-Sources: found in kidney, liver, egg yolk, butter, green veggies
-RF: liver disease, ETOH, fat-free diets, fat malabsorption (CF, Crohn, Bariatric Surgery)
-Visual changes (night blindness, xerophthalmia/dry eyes, retinopathy), impaired immunity, dry skin, taste loss; Squamous Metaplasia (conjunctiva, respiratory, urinary tract); Bitot’s Spots (white spots on conjunctiva)
-Labs: decreased serum retinol levels
What can happen with Vitamin A toxicity/excess?
Blurred vision, idiopathic intracranial hypertension, teratogenicity, vision changes
