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Review / Wrong Answers > 6/7 UWorld > Flashcards

6/7 UWorld Flashcards

1
Q

Symptoms of carcinoid syndrome

A
  • Symptoms = BFDR
    • Bronchospasm
    • Flushing
    • Diarrhea
    • Right-sided heart disease/murmur
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2
Q

What is angiodysplasia?

A
  • Tortuous dilation of vessels within the bowel, leading to hematochezia
  • Unexplained GI bleeding and anemia
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3
Q

What is proctitis

A
  • Inflammation of perianal region and rectum
  • Usually due to fecal matter in the area for an extended period of time
  • Also associated with ulcerative colitis
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4
Q

Describe the progression from adenoma to carcinoma in colorectal cancer

A
  • Order of events = AK=53
  • Normal colon
    • = APC (adenomatous polyposis coli) gene mutation (loss of APC)
  • Colon at risk for polyps
    • = KRAS mutation (oncogene)
  • Development of polyps/adenoma
    • = p53 mutation (loss of tumor suppressor)
  • Progression to carcinoma
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5
Q

What is Turcot syndrome

A
  • FAP + malignant CNS tumor (medulloblastoma)
    • THINK: TURcot = TURban
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6
Q

What is the defect in hereditary nonpolyposis colorectal cancer (HNPCC)

A

Aka Lynch Syndrome

Defect in DNA mismatch repair (MMR)

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7
Q

Most common location of diverticulitis

A

Sigmoid colon (LLQ pain)

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8
Q

Most common location of Crohn’s

A

Terminal ileum; rectal sparing

Vs. UC which can only affect the colon and rectum is always involved

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9
Q

Crohn’s vs. Ulcerative colitis

Histology

A

Crohn - noncaseating granulomas with lymphoid aggregates

UC - crypt abscesses with neutrophils

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10
Q

Crohn’s vs. UC - X-ray imaging

A

Crohns:

  • Cobblestone mucosae
  • Creeping fat
  • Strictures = “string sign” appearance

UC:

  • Loss of haustra = “lead pipe” appearance
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11
Q

Describe excretion of bilirubin (urobilinogen, stercobilin, and urobilin)

A
  • Colonic bacteria converts bilirubin to urobilinogen
    • Most (80%) Urobilinogen is oxidized to stercobilin and excreted in the stool – makes stool brown
  • Small amount (20%) of urobilinogen is reabsorbed by the gut
    • 90% Enters mesenteric veins and goes back into the liver and into bile – enterohepatic circulation
    • Tiny amount (10%) of reabsorbed urobilinogen is converted to urobilin and excreted in the urine – makes urine yellow
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12
Q

Describe primary sclerosing cholangitis (histology, imaging, complications)

A
  • Unknown cause
  • Concentric fibrosis of the intra- and extra-hepatic bile ducts (“onion skin” fibrosis)
  • Contrast imaging will show “beaded” appearance due to alternating fibrotic and dilated regions
  • Mostly occurs in men around age 40
  • Associated with (+) pANCA and Ulcerative colitis
  • Can lead to secondary biliary cholangitis
  • Increased risk for cholangiocarcinoma
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13
Q

Describe the source of bilirubin

A
  • Bilirubin metabolism:
    • Hemoglobin broken down into heme and globin
    • Heme then broken down into iron and protoporphyrin
    • Protoporphyrin converted into unconjugataed bilirubin (water insoluble)
    • UCB binds to albumin to be brought to the liver
    • Liver conjugates UCB into CB (water soluble)
      • UDP glucuronyl transferase (UGT) is the enzyme in the hepatocytes that conjugates bilirubin
    • CB dumped into bile canaliculi to be sent to the gallbladder
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14
Q

What is the cause and histology of Primary biliary cirrhosis (PBC)

A
  • Autoimmune destruction of intra-hepatic bile ducts
    • Associated with other autoimmune conditions
  • Lymphocytic infiltrate + granulomas
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15
Q

What is Charcot’s triad of cholangitis?

A
  • Inflammation/infection of the biliary tree
  • Charcot’s triad:
    • Jaundice
    • Fever
    • RUQ pain
  • Reynold’s pentad:
    • Jaundice, fever, RUQ pain, Hypotension, AMS
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16
Q

Antibody associated with Primary biliary cirrhosis

A
  • Autoimmune destruction of intra-hepatic bile ducts
    • Associated with other autoimmune conditions
  • (+) anti-mitochondrial antibody (AMA)
17
Q

Causes of acute pancreatitis

A
  • Autodigestion of pancreas by pancreatic enzymes
  • Causes:
    • Most common:
      • Gallstones
      • Alcohol
    • I GET SMASHED:
      • Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypertriglyceridemia/Hypercalcemia, ERCP, Drugs (e.g. Sulfa, NRTIs, protease inhibitors)
        • ERCP = endoscopic retrograde cholangio pancreatogram
18
Q

What is Trousseau sign

A
  • Hypercoagulability
  • Venous thrombosis
  • Migratory thrombophlebitis

Caused by adenocarcinoma of the pancreas or lung

19
Q

How do you differentiate between Type I vs. Type II Crigler-Najjar syndrome

A
  • Type I is more severe
  • If you give phenobarbital, it will cause decreased UCB in Type II and no change in Type I
20
Q

Presentation of Dubin Johnson syndrome

A
  • Deficiency of bilirubin canalicular transport protein
    • Cannot transport CB from liver to bile ducts
  • Black liver (due to build up of bilirubin in hepatocytes)
  • Increased CB
  • Clinically benign
21
Q

What are Mallory bodies and what disease are they seen in

A
  • Intracytoplasmic eosinophilic inclusions of damaged keratin filaments
  • Seen in alcoholic hepatitis
22
Q

Why would you see bleeding and bruising in liver failure

A

Loss of coagulation factors - Coagulopathy and elevated PT and PTT

23
Q

Why do you see edema and ascites in liver failure?

A
  • Loss of albumin = decreased osmotic pressure causing to fluid to leak out of vessels
24
Q

Describe the TIPS procedure used to treat portal HTN

A
  • Transjugular intrahepatic portosystemic shunt
    • Shunt between the portal vein and hepatic vein relieves portal HTN by shunting blood to the systemic circulation, bypassing the liver
25
Q

Tumor markers of pancreatic adenocarcinoma

A

CA19-9

CEA

26
Q

Causes of nutmeg live

A

Backup of blood into the liver

Caused by Budd-Chiari and R heart failure

27
Q

Presenation and treatment of Wilson disease

  • Autosomal recessive
  • Mutation in hepatocyte copper-transporting ATPase (ATP7B gene)
  • Inadequate copper excretion into bile and blood
    • Decreased serum ceruloplasmin
    • Increased urine copper
    • Copper accumulation in: liver, brain, cornea, kidney, joints
  • Presentation:
    • Liver disease, Kayser-Fleischer rings, renal disease (Fanconi syndrome)
  • Treatment:
    • Chelation with Penicillamine
A
  • Mutation in hepatocyte copper-transporting ATPase (ATP7B gene)
  • Presentation:
    • Liver disease, Kayser-Fleischer rings, renal disease (Fanconi syndrome)
  • Treatment:
    • Chelation with Penicillamine
28
Q

Presentation of hemochromatosis

A
  • Classic triad:
    • Cirrhosis
    • Diabetes mellitus
    • Skin pigmentation
  • “Bronze diabetes”
29
Q

Describe the pathogenesis of A1ATD in liver disease

A
  • Liver:
    • Misfolded gene produce protein aggregates in hepatocellular endoplasmic reticulum à cirrhosis with PAS (+) globules
  • Lungs:
    • Decreased a1-antitrypsin = uninhibited elastase in alveoli = decreased elastic tissue = panacinar emphysema
30
Q

Diseases of what body systems will cause and increase in alkaline phosphatase

A

Liver, biliary, bone

31
Q

Associated risk factors for:

  • Hepatic adenoma
  • Hepatic angiosarcoma
  • Hepatocellular carcinoma
A
  • Hepatic adenoma:
    • Rare, benign liver tumor
    • Associations: oral contraceptive, anabolic steroid use
  • Hepatic angiosarcoma:
    • Malignant tumor of endothelial origin
    • Association: exposure to arsenic or vinyl chloride
  • Hepatocelllular carcinoma:
    • Most common primary malignant liver tumor in adults
    • Association:
      • Hepatitis B
      • Hepatitis C
      • All associations with cirrhosis
      • Hemochromatosis
      • A1-antitrypsin deficiency
      • Aflatoxin from Aspergillus
32
Q
A
33
Q

What drugs often provoke Prinzmetal angina

A

Triptans/dihydroergotamin

Cocaine/amphetaimes

34
Q

What is the function of zinc fingers in signal transduction

A

They directly bind DNA

Often incorporated into intracellular receptors (VETT CAP) that act directly as transcription factors

35
Q

How does pyruvate kinase deficiency lead to anemia?

A
  • Glycolytic enzyme deficiency (formation of pyruvate) = inability to generate ATP
  • Cannot maintain Na+/K+ ATPase = RBC swelling and lysis
36
Q

What structure courses through the angle between the aorta and superior mesenteric artery

A

Transverse portion of the duodenum

  • Superior mesenteric artery syndrome:
    • SMA usually forms a 45 degree angle with the aorta, with the transverse portion of the duodenum coursing horizontally between the two
    • If the angle diminished to less than 20 degrees, the transverse duodenum can get entrapped, leading to small bowel obstruction
37
Q

Which bacterial pathogens are the most common cause of intraabdominal infections (e.g. within fluid released from appendiceal rupture)

A

Bacteroides fragilis

E. Coli

38
Q

How does systemic blood flow effect cerebral circulation, and therefore intracranial pressure

A
  • BP between 60-140 has little effect on cerebral blood volume
    • Autoregulation (via cerebral blood vessel dilation and contraction) keeps flow constant
  • BP > 150 causes increased cerebral vascular volume and blood flow = increased ICP
  • BP < 50 causes cerebral hypoperfusion and potential ischemia
39
Q

How does arterial blood gas (specifically PaCO2) affect cerebral circulation, and therefore ICP

A
  • A drop in PaCO2 due to hyperventilation causes vasoconstriction = decreased cerebral blood flow = decreased ICP
  • So lowering PaCO2 is a treatment option for reduction ICP in patients with cerebral edema

Review / Wrong Answers (140 decks)

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