Internal Anki

What are the main types of gastrointestinal bleeding?

Upper GI bleeding (80-90%) and lower GI bleeding (10-20%).

What is the most common cause of upper GI bleeding?

Peptic ulcer bleeding (~50%).

What percentage of upper GI bleeds are variceal?

5-20%.

What is the mortality rate of upper GI bleeding?

10-14%.

What is the mortality rate of lower GI bleeding?

2-4%.

Where does upper GI bleeding occur in relation to the ligament of Treitz?

Proximal to the ligament of Treitz.

Where does lower GI bleeding occur in relation to the ligament of Treitz?

Distal to the ligament of Treitz.

List common causes of upper GI bleeding.

Peptic ulcer, varices, erosive lesions, Mallory-Weiss tear, cancer, Dieulafoy lesion, AV malformation.

List common causes of lower GI bleeding.

Diverticulosis, polyps, cancer, IBD, ischemia, angiodysplasia, hemorrhoids.

What are the typical symptoms of acute GI bleeding?

Hematemesis, melena, hematochezia, occult bleeding, anemia.

What scoring systems are used for upper GI bleed risk assessment?

Glasgow-Blatchford score (GBS) and Rockall score.

When is early vs emergency endoscopy indicated in upper GI bleeding?

Early <24h for stable patients, emergency <12h for unstable patients.

Which Forrest classifications need endoscopic therapy?

Forrest I, IIa, IIb.

What medications are used for peptic ulcer bleeding management?

IV PPI bolus + continuous infusion.

What is the target hemoglobin in restrictive transfusion during GI bleed?

70-90 g/L.

What is the most common cause of peptic ulcer bleeding?

H. pylori infection and NSAID use.

What are the main complications of peptic ulcer bleeding?

Rebleeding, perforation, gastric outlet obstruction.

How does terlipressin affect mortality in variceal bleeding?

Reduces relative mortality risk by 34%.

What is the role of antibiotic prophylaxis in variceal bleeding?

Prevent infection in cirrhotic patients (e.g. ceftriaxone or quinolone for 5-7 days).

What is the endoscopic treatment of choice for esophageal variceal bleeding?

Endoscopic band ligation (EBL).

When should endoscopy be performed for variceal hemorrhage?

Within 12 hours of presentation after resuscitation.

What is the rescue therapy for persistent variceal bleeding?

Urgent TIPS (transjugular intrahepatic portosystemic shunt).

What is the treatment for gastric variceal bleeding (GOV2, IGV1)?

Endoscopic cyanoacrylate (glue) injection. endoscopic sclerotherapy

What is the most feared complication after EBL?

Ligation-induced ulcer bleeding (3%; 30-50% mortality).

What is the most common etiology of lower GI bleeding?

Diverticulosis.

How is hemodynamic instability with hematochezia interpreted?

Suggests possible upper GI source.

What imaging is useful for localizing small bowel bleeding?

CT angiography, RBC scintigraphy, or capsule endoscopy.

What is first-line investigation for suspected small bowel bleeding?

Video capsule endoscopy (VCE).

When is deep enteroscopy indicated?

After VCE, for diagnosis and therapy.

Which hemostatic techniques are used for varices?

Band ligation, sclerotherapy, cyanoacrylate injection.

What is the mortality rate for variceal bleeding?

Approximately 20%.

Which condition is characterized by bleeding from telangiectasias or angiodysplasia?

Lower GI bleeding, often in older adults.

When should anticoagulants be reversed in GI bleeding?

If actively bleeding and INR >1.5-2.5.

What is the initial lab workup in suspected GI bleed?

CBC, BUN, creatinine, electrolytes, PT/INR, type & crossmatch.

What are the main risk factors for GI bleeding?

H. pylori, NSAID use, anticoagulants, cirrhosis, comorbidities.

What are the Forrest classifications Ia-III?

Ia: spurting bleed, Ib: oozing bleed, IIa: current non-bleeding ulcer w/ visible vessel, IIb: ulcer covered by adherent clot, IIc: non bleeding ulcer with (hematin) black base, III: non bleeding (clear, fibrinous) ulcer clean base.

What are the key steps in managing upper GI bleeding?

Resuscitation, risk stratification, endoscopy, IV PPI, stop NSAIDs, restart antiplatelets if needed.

What are first-line vasoactive drugs for variceal bleeding?

Terlipressin, octreotide, somatostatin.

What are endoscopic hemostatic techniques?

Epinephrine injection, sclerotherapy, clips, band ligation, APC, thermal therapy, Hemospray.

What are common complications of severe GI bleeding?

Hypovolemia, shock, anemia, multi-organ failure.

Turner syndrome

45,X karyotype; short stature, webbed neck, streak ovaries → primary amenorrhea.

Klinefelter syndrome

47,XXY karyotype; tall stature, gynecomastia, small testes, infertility.

Polycystic ovary syndrome (PCOS)

Oligomenorrhea, hirsutism, acne, polycystic ovaries on ultrasound, insulin resistance.

Gout — Acute management

Colchicine, NSAIDs, corticosteroids. (Allopurinol or febuxostat only for long-term prevention, not during an acute attack.)

Tophi

Deposits of uric acid crystals in soft tissues, typically around joints, ears, or tendons in chronic gout.

Wilson's vs Hemochromatosis — Key difference

Wilson's = copper accumulation; Hemochromatosis = iron accumulation.

Acute pancreatitis — Diagnostic criteria

(1) Characteristic abdominal pain, (2) Serum amylase/lipase >3× normal, (3) Imaging findings consistent with pancreatitis (need 2 of 3).

Antibiotics in pancreatitis

Only indicated in cases of sepsis or biliary tract infection, not routinely.

Biliary tract infection — Imaging/Treatment

ERCP or MRCP used for diagnosis and management.

Hepatitis B — Key serologic markers

HBsAg = current infection; Anti-HBs = immunity; Anti-HBc IgM = acute infection; Anti-HBc IgG = past infection.

Hepatitis C — Diagnosis

Anti-HCV antibodies and HCV RNA PCR.

Drug-induced liver injury — Causes

Commonly from acetaminophen, amiodarone, isoniazid, methotrexate.

Wilson's disease

Copper accumulation due to ATP7B mutation; low ceruloplasmin, high urinary copper, Kayser-Fleischer rings.

Hemochromatosis

Iron overload; high ferritin, high transferrin saturation, normal CRP (to exclude acute phase elevation).

FIB-4 score

Non-invasive score to assess liver fibrosis using age, AST, ALT, and platelet count.

Ascitic fluid — Exudate vs Transudate

Transudate: low protein, low WBC, low LDH; Exudate: high protein, high LDH, often malignancy or infection.

Spontaneous bacterial peritonitis

Ascitic fluid WBC >0.25 × 10⁹/L (250 cells/µL), mainly neutrophils.

Hepatocellular carcinoma — Marker

Alpha-fetoprotein (AFP) — used mainly for follow-up, not screening.

Acute liver failure — Causes

Viral hepatitis, drug-induced (acetaminophen), ischemic, autoimmune.

Pituitary adenoma

Benign tumor of the pituitary gland that can cause endocrine hyperfunction (e.g., prolactinoma, acromegaly, Cushing's disease) or local compression effects.

Acromegaly-Classic symptoms

Organ enalrgement -macroglossia, cardiomegaly Development of insulin resistance Headache ontop of head Excessice sweating due to hypertrophy of glands etc.

Acromegaly — Screening test

Measure IGF-1 levels (insulin-like growth factor 1); if elevated, confirms GH hypersecretion suspicion.

Acromegaly — Confirmatory test

Oral Glucose Tolerance Test (OGTT) with GH measurement — failure of GH to suppress after glucose load confirms diagnosis.; measured every 30mins

Acromegaly — Alternative in diabetic patients

Avoid OGTT; use 24-hour GH or IGF-1 monitoring instead (check 5/day).

Prolactinoma — Endocrine symptoms in women

Amenorrhea, galactorrhea, infertility.

Prolactinoma — Endocrine symptoms in men

Decreased libido, erectile dysfunction, infertility.

Prolactinoma — Mass effect symptoms

Bitemporal hemianopia (optic chiasm compression), headache.

Diabetes insipidus — Central

Deficiency of ADH due to hypothalamic or pituitary damage → polyuria and polydipsia.

Diabetes insipidus — Nephrogenic

Renal insensitivity to ADH; may be genetic (V2 receptor or AQP2 mutation) or acquired (e.g., lithium, hypokalemia).

Acquired nephrogenic DI — Causes

Lithium therapy, prolonged hypokalemia.

Cushing's disease vs. Cushing's syndrome

Cushing's disease = pituitary ACTH-secreting adenoma; Cushing's syndrome = excess cortisol from any cause (pituitary, adrenal, or exogenous).

Addison's disease — Diagnosis

Low cortisol levels and inadequate rise after ACTH (Synacthen) stimulation test; autoimmune antibodies may confirm etiology.

Addisons Disease- Treament + Dosage

Replacement therapy Secondary: Hydrocortisone (dont give methyprednisone doesn't have MR effect) Primary: Hydrocortisone and fludroortisone (both cortisol and mineralcorticoid must be replaced) Dosage: 2/day morning and noon (mimics bodies endogenous production)

Addisons disease - Dosing during illness

Must be increased to mimic the bodies natural response to stress situation

Addisons disease- Most Common Cause

Autoimmune adreanalitis

WBC

4-10 G/L

neu

45-70%

hgb

135-170 g/L in males, 120-150 g/L in females

hct

0.4-0.5 in males, 0.35-0.45 in females

MCV

80-100 fL

PLT

150-400 G/L

Na

135-145 mmol/L

K

3.5-5.1 mmol/L

Ca

2.25-2.65 mmol/L

PO4

0.8-1.45 mmol/L

creat

60-100 umol/L (2 digit number)

BUN

3-7 mmol/L (1 digit number)

Urate

200-430 umol/L

Glucose

4.1-5.9 mmol/L

Cholesterol

2.0-5.2 mmol/l

Triglyceride

< 1.7 mmol/l

Total bilirubin

5-20 umol/L

GOT

< 50 U/L

GPT

< 50 U/L

GGT

< 55 U/L

ALP

LDH

< 250 U/L

Total protein

65-80 g/L

Albumin

35-50 g/L

CRP

< 5 mg/L - < 20-30 means basically normal, 30-100 should be followed in 3-4 days