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Symptoms 2 > Edema 2 - Franco > Flashcards

Edema 2 - Franco Flashcards

1
Q
  • *In a patient with increased total bilirubin, elevated AST and ALT, normal alk phos, and low albumin: A decrease in which of the following would be the most likely cause of leg edema in a patient?**
    a. Capillary hydrostatic pressure
    b. Interstitial colloid osmotic pressure
    c. Interstitial hydrostatic pressure
    d. Plasma colloid osmotic pressure
    e. Pre-capillary arteriolar resistance
A

D - plasma colloid osmotic pressure d/t the low albumin state!

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2
Q

Liver anatomy review:

  1. What artery brings the majority of blood to the liver?
  2. What artery brings the rest of blood to the liver?
  3. What does having dual blood supply to the liver mean clinically?
A
  1. portal vein = 70% of blood flow
  2. proper hepatic artery = 30% of blood flow
  3. Its very difficult for liver to have ischemic injury d/t its dual blood supply, so even in sitatuations where a person with a hypercoaguable state clots off the portal vein, the person does fine because of their hepatic artery
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3
Q

Liver Anatomy Review:

  1. Draw out the classic lobule (Franco diagram)
  2. Where does the Central Vein lead?
  3. What part of the lobule filters out toxic substances from the blood?
A
  1. see diagram
  2. Central Vein leads to the Hepatic vein which leads to the IVC
  3. Hepatocytes
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4
Q

Liver anatomy review:

  1. What is the location and purpose of Kuppfer cells?
  2. What is the location and purpose of Stellate cells?
  3. What liver cell type is responsible for cirrhosis?
  4. What substances activate stellate cells?
A
  1. Macrophages in the sinusoids –> detoxifies blood
  2. In the space of disse - responsible for forming scar tissue (lays down collagen, causing fibrosis, causing cirrhosis)
  3. Stellate cells (since in charge of fibrosis) are responsible for cirrhosis
  4. Alcohol and hep C stimulate stellate cells to lay down collagen –> fibrosis –> cirrhosis
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5
Q

Liver anatomy Review:

  1. Draw out the zones you would see and their relation to the Central Vein + other veins in the lobules
    * Hint: there are 3 zones*
  2. Which zone would be most at risk / damaged first in cardiac arrest?
  3. Which zone would have the highest concentration of viral particles when exposed to viral hepatitis?
  4. What zone does acetaminophen cause damage to?
A
  1. see diagram
  2. Zone 3 (cardiac arrest = no blood flow to liver = damages zone farthest away from blood supply, CV, first)
  3. Zone 1
  4. Zone 3
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6
Q

A donor liver arrives in New York from Chicago 7 hours after harvest. A biopsy is performed on arrival to check for ischemic injury. The P450 system is very susceptible to ischemia. In which of the following histologic regions of the liver is this system located?

A. Bile ducts
B. Intermediate zone
C. “Ito” cells
D. Pericentral vein zone
E. Periportal zone

A

D – pericentral vein zone (another term for zone 3, close to the central vein)

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7
Q

Bilirubin Review:

  1. Understand (draw out if you can) bilirubin metabolism and the major enzymes
  2. What enzyme is responsible for conjugating bilirubin?
  3. What transporter is responsible for bilirubin excretion out of the hepatocyte?
  4. Where can bilirubin be metabolized and excreted from the body?
  5. What metabolite gives feces its brown color?
  6. What metabolite gives urine its yellow color?
A
  1. see diagram (hopefully it shows up, if not when i go through these i will email the diagram to you guys)
  2. UDP-glucuronyl transferase, specifically UGT1A1
  3. MOAT
  4. feces or urine
  5. stercobilin
  6. urobilin
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8
Q

A 43-year-old woman comes to the physician because of jaundice, abdominal pain and nausea. Endoscopic retrograde cholangiopancreatography is performed. Multiple common bile duct stones are seen, and the injected contrast material is retained within a dilated common bile duct proximal to the stones. The stones are removed and analysis shows they are composed primarily of cholesterol. Which of the following findings is most consistent with this patient’s symptoms?

A. Excessive hemolysis
B. Increased pigmentation of the stool
C. Increased urinary urobilinogen
D. Light brown urine
E. Unconjugated hyperbilirubinemia

A

D - common bile duct is blocked, so bilirubin is not being excreted properly through the intestines, only in urine, in which case there would be more urobilin in the urine than normal (yelow color normally, too much = light brown ie super pigmented)

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9
Q

In neonatal jaundice:

  1. Is it due to increased indirect or direct bilirubin?
  2. why does it occur?
  3. when does it normally resolve by?
  4. What is a possible complication?
A
  1. increased indirect bilirubin
  2. normally d/t delayed maturation of liver to dispose of bilirubin, there is low UGT1A1 at birth (i.e. the enzyme that conjugates bilirubin in the hepatocytes)
  3. normally resolves within 5 days
  4. Possible complication of neonatal jaundice is Kernicterus: specific brain damage, i.e. ‘bilirubin encephalopathy’ d/t hyperbilirubinemia –> causes athetoid (writing) cerebral palsy and hearing loss
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10
Q

Kernicterus:

1. is a possible complication of what in newborns?

  1. what are the consequences?
A
  1. conseuqence d/t neonatal jaundice, i.e. increased indirect bilirubin
  2. consequences = cathetoid (writing) cerebral palsy and hearing loss
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11
Q

State whether the following diseases are due to increased indirect (unconjugated) or direct (conjugated) bilirubin:

  1. Crigler Najar Type I
  2. Dubin-Johnson syndrome
  3. Rotor syndrome
  4. Gilbert Syndrome
A
  1. Crigler Najar Type I = indirect
  2. Dubin-Johnson syndrome = direct
  3. Rotor syndrome = direct
  4. Gilbert Syndrome = indirect
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12
Q

What is the defect in the following diseases that cause hyperbilirubinemia (direct or indirect):

  1. Crigler-Najar Type I
  2. Dubin Johnson Syndrome
  3. Gilbert syndrome
A
  1. Crigler-Najar Type I = UGT1A1 (i.e. the UDP glucuronyl transferase in hepatocytes that conjugates bilirubin) is absent
  2. Dubin Johnson Syndrome = defect in MOAT
  3. Gilbert syndrome = UGT1A1 is reduced (about 30%)
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13
Q

A 4-week-old baby has been undergoing phototherapy for jaundice that appeared on the first day after birth. Daily phototherapy has not resolved the jaundice, but so far has been sufficient to prevent kernicterus. Total bilirubin has remained between 21 and 23 (normal <1.2), but direct bilirubin is too low to be measurable. Which of the following explains this infant’s condition?

A. A deficiency in the hepatocyte basolateral membrane bilirubin transporter
B. A deficiency in the hepatocyte canalicular organic ion transporter (cMOAT)
C. A deficiency in UDP glucoronyl transferase
D. Biliary obstruction
E. Normal physiologic jaundice of the newborn

A

C

This is likely Crigler Najar Type I or Type II = UGT1A1 asbence = the specific UDP glucoronyl transferase (what conjugates bilirubin in the hepatocytes) – will cause an increase in indirect bilirubin

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14
Q

Reye Syndrome:

  1. How do children with this disease present? What is their clinical history?
  2. What is the mechanism of disease?
  3. What will an abnormal lab finding be in this disease?
  4. What disease in children is safe to treat with the medication at fault here?
A
  1. Children present with rash, severe vomiting, hypoglycemia, hepatomegaly, and coma. Associated with viral infection (especially VAV and influenza B) that has been treated with aspirin.
  2. Mechanism: aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes.
  3. Will cause increase ammonia levels in blood
  4. Avoid aspirin in children, except in those with Kawasaki disease
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15
Q

A 46-year-old woman comes to the physician because of dark urine and grayish stools. Physical exam shows mild scleral icterus and right upper quadrant abdominal tenderness. Lab studies show: Total bilirubin 3.2 (<1.2)
Direct bilirubin 2.1 (<0.3) Alkaline phosphatase 150 (<120) AST 9 (<45)
ALT 10 (<45). Which of the following is the most likely diagnosis?

a. Autoimmune hemolysis
b. Choledocholithiasis
c. Crigler-Najjar syndrome
d. Gilbert syndrome
e. Viral hepatitis

A

B

=choledocholithiasis, i.e. stones in the common bile duct

How to get this answer:

    • increased conjugated bilirubin, which takes out A, C, and D
  • Normal liver enzymes rules out E*
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16
Q

Gallstones:

  1. What are the risk factors for gallstones?
  2. Best test to diagnose gallstones?
A
  1. Risk factors = ‘forty, fat, female, fertile’ – and native american (poor steve)
  2. ultrasound of the right upper abdomen
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17
Q

Blockage of what space in the liver lobule by extracellular components (eg stellate cells) may result in what symptoms?

A

jaundice, ascites, and liver failure

18
Q

Primary Biliary Cirrhosis:

  1. Etiology and pathology?
  2. What population is it commonly seen in?
  3. Labs you would look for?
  4. common signs and presentation
A
  1. autoimmune reaction –> causes lymphocytic infiltrate and granulomas, causing destruction of intralobular bile ducts
  2. middle aged white females
  3. increased alkphos, increased IgM, AMA+ (anti-mitochondrial antibody)
  4. fatigue, puritis, steatorrhea (d/t decreased bile salt excretion) and fat soluble vitamin deficiencies (vitamines ADEK)
19
Q

Autoimmune hepatitis

  1. Describe the pathophys behind the disease
  2. Labs you would expect to see
A
  1. autoantibodies against the liver, causes hepatocyte inflammation
  2. increased ALT/AST >1000, increased IgG, +ANA (antinuclear antibody) or +ASMA (antismooth muscle antibodies)
20
Q

Wilson’s Disease

  1. etiology
  2. Lab values you would expect
  3. clinical signs
A
  1. homozygous mutation for gene ATB7B
  2. increased Cu in urine, decreased serum ceruloplasmin
    * Reminder: ceruloplasmin is what binds copper in plasma and when not bound will deposit in the kidney, brain and cornea, as well as be excreted in the urine*
  3. Kayser Flescher Rings (copper deposits in cornea) + neuro and psych issues
21
Q

Hereditary Hemochromatosis

  1. Etiology
  2. Lab results you would expect
  3. clinical symptoms
A
  1. homozygous mutation C282Y/C282Y on HFE gene on chromosome 6
    * Reminder: HFE gene is what regulates absorption of iron from small intestine. normally when iron is needed, iron is absorbed and mobilized by transferrin, which is what HFE downregulates when levels are adequate. If HFE gene is defective, then iron is continuously absorbed from the intestine*
  2. increased ferritin, markedly elevated HCT, elevated liver function tests
  3. skin hyperpigmentation and diabetes (‘bronzed diabetes’), weakness, lethargy
22
Q

alpha-1 Anti-trypsin deficiency:

  1. purpose of alpha1-antitrypsin
  2. causes what in children?
  3. genetic type that is associated with lung and liver disease
  4. abnormal labs?
A
  1. inhibits proteolytic enzyme elastase, and is predominantly made in the liver
  2. this is the most comon cause of genetic liver disease in children and the most common genetic disease leading to liver transplant in children
    * However, reminder: the most overall reason for transplant (not genetic, developmental): biliary atresia*
  3. PiZZ (the other kinds only affect the lungs)
  4. liver function tests elevated, otherwise need to diagnose with liver biopsy
23
Q

A 52-year-old woman comes to the physician because of generalized itching. Exam shows mild jaundice. Labs show increased conjugated bilirubin and alkaline phosphatase. A liver biopsy shows granulomatous inflammation centered on small bile ducts within the portal spaces. Which of the following findings would confirm the most likely diagnosis?

A. Antimitochondrial antibody
B. Decreased serum ceruloplasmin
C. Elevated liver enzymes
D. Hypoalbuminemia
E. Markedly elevated hematocrit
F. PiZZ allele
G. Prolonged prothrombin time

A

A

= Primary biliary cirrhosis, almost always women complaining of itching – with antimitochondrial antibody

Ruling out the other options:

    • Autoimmune hepatitis – antinuclear and antismooth muscle antibodies
  • Wilsons disease = decreased serum ceruloplasmin
  • C, D, and G are non specific
  • Markedly elevated hematocrit = hereditary hemochromatosis
  • PiZZ = a1 anti-trypsin deficiency*
24
Q

Based on the following image, please label A through E

A

A is right hepatic duct

B Is left hepatic duct

C is common bile duct

D is pancreatic duct

E is cystic duct

25
Q

A 45-year-old man comes to the physician because of vomiting blood. He has no history of medical illnesses. Exam shows a distended abdomen, yellow discoloration of the skin and sclera, and gynecomastia. Neurologic examination shows mild cognitive and short-term memory deficiencies. Microscopic examination of a liver biopsy would most likely show which of the following?

A. Dilated bile ducts with normal hepatocytes
B. Multiple nests of disorganized hepatic parenchyma containing biliary components
C. Multiple small nodules with intracellular Russell bodies
D. Single disorganized collection of atypical hepatocytes with multiple mitosis
E. Sites of fibrosis and disorganization of hepatic parenchyma

A

E

principle cell in charge of hepatic fibrosis = stellate cell (occurs in the sinusoids)

26
Q

A 55-year-old man with a history of alcoholism is admitted to the hospital because of hematemesis. Exam shows jaundice and a distended abdomen with large, tortuous, distended anterior abdominal wall veins radiating from the umbilicus. The liver cannot be palpated secondary to the abdominal girth. An US of the abdomen reveals more than 1.5 liters of peritoneal fluid. Bleeding at which of the following anastomoses is the most likely cause of the patient’s hematemesis?

A. Inferior phrenic veins-esophageal veins
B. Left gastric vein-esophageal veins
C. Left gastric vein-right gastric vein
D. Left gastro-omental vein-right gastro-omental vein
E. Paraumbilical veins-superficial veins of the anterior abdominal wall

A

B

27
Q
  1. In a patient with active esophageal variceal bleeding, what is the medication used for treatment and mechanism of action?
  2. In a patient with non-bleeding esophageal varices, what is the medication used for treatment and the mechanism of action?
A
  1. Active = Octreotide = somatostatin analog –> it decreases compression of the mesenteric artery, decreasing the amt of blood coming into the portal vein
  2. Non-bleeding = Propranolol or Nadolol = non-selective (Beta1 and 2) beta blockers = decrease cardiac output by blocking beta receptors, and produce splanchnic vasoconstriction by beta 2 blockade (goal is to reduce risk of first bleed, re-bleed, and to increase survival)
28
Q

Spontaneous Bacterial Peritonitis:

  1. is a complication of what disease?
  2. presents with what symptoms?
  3. How to diagnose?
  4. Is caused by what major organisms? (3)
A
  1. complication of cirrhosis
  2. presents with abdominal pain + fever
  3. diagnosed with PMN > 250
  4. All G- bugs that come from Gi tract: E-coli (45%) > Strep (30%) > Klebsiella
29
Q
  1. Ascites d/t cirrhosis is most commonly managed by what medication? What is the mechanism of action?
  2. another treatment option for ascites?
  3. Why wouldn’t you want to choose one of the medications?
A

1. Spironolactone –> inhibits aldosterone

  1. Other option being furosemide –> loop diuretic
  2. Spironolactone is known to increase K+ and cause male gynecomastia, but Furosemide is known to lower K+
30
Q

Ascites:

  1. caused by what disease?
  2. what is the effect on circulating volume
  3. do you have hypo or hypernatremia?
A
  1. cirrhosis
  2. decreased circulating volume
    * Reminder: cirrhosis = increases resistance to portal flow = portal HTN = splanchnic vasodilation = decreasing effective circulating volume*
  3. Hyponatremia
    * decreasing effective circulating volume = increasing vasopressin and activatin renin-angiotensin-aldosterone system*
    * Vasopressin causes H2O retention*
    * RAA system causes Na+ retention*
    * H2O retention >> Na+ retention = hyponatremia*
31
Q

A 65-year-old man with a long history of alcohol abuse and a history of cirrhosis is brought to the ED in a confused and disoriented state. He is started on lactulose and admitted to the hospital, where he is maintained on a protein-restricted diet. Lactulose acts to minimize a metabolic abnormality that results from decreased function of which of the following processes?

A. Amino acid synthesis
B. Fatty acid metabolism
C. Gluconeogenesis
D. Glycogenolysis
E. Lactate metabolism
F. Urea cycle

A

F

  • Urea cycle = ammonia –> into the gut*
  • Lactulose helps trap the ammonia (NH3) in the colon. It does this by using gut flora to acidify the colon, transforming the freely diffusible ammonia into ammonium (NH4+) which can no longer diffuse back into the blood.*
32
Q
  1. What medications are used in the treatment of Wilson’s disease? what is the mechanism?
  2. which is more often used? why?
A
  1. Penicillamine or Trientene–> chelator, binds free copper and induces cupuria (excretion of copper in the urine)
  2. Trientene > penticillamine d/t less side effects
33
Q

Review: Hepatitis B

  1. Go over the timeline of when the different surface antigens are present
  2. what serum marker indicates immunity?
  3. What serum marker can diagnose Hep B infection in the window period?
A
  1. Antigens (indicate active disease): HBsAg, starts to decrease at 24 weeks; HbeAg (large amount of virus in blood); Window period of about 8 weeks, only way to dx Hep B in this time is to detect IgM anti-HBc; Antibodies: AgE to anti-HBe (indicates seroconversion); Anti-HBs (indicates immune, either from vaccine or natural infection)
  2. Anti-HBs
  3. IgM Anti-HBc
34
Q

A 34-year-old man develops malaise, fatigue, and anorexia after returning from a trip to Calcutta, India. His symptoms slowly resolve and he does not seek treatment. Three months later, labs of the serum show: HBcAb Positive, HBeAb Positive, HBeAg Negative, HBsAg Negative, HBsAb Negative. The absence of HBsAg and HBsAb is likely indicative of which of the following?

A. The patient has been successfully vaccinated against hepatitis B
B. The patient is anergic to hepatitis B
C. The patient is immune to hepatitis B
D. The patient is in the window period
E. The patient is making an excess of HBsAb

A

D

35
Q

A 39-year-old African-American man comes to the physician because of anorexia, malaise, dark urine, and upper abdominal discomfort. His temperature is 100.2F. Exam shows scleral icterus and moderate RUQ tenderness. The liver is palpable below the right costal margin. Labs show: HBsAg positive, HBsAb negative, Anti-HBc IgM positive, HBeAg positive. Which of the following will most likely change in his serologic findings when the patient enters the window period?

A. He will become HBcAg-positive
B. He will become HBc IgG-positive
C. He will become HBeAg-negative
D. He will become HBsAb-positive
E. He will become HBsAg-negative

A

E

36
Q

Alcohol Metabolism review:

  1. An increase in what metabolite in alcoholic is often what causes the damage to the liver?
  2. Why is taking acetaminophen at the same time as alcohol a bad idea?
A
  1. increase in acetaldehyde
  2. Both are CYP2E1, so used up more quickly when trying to metabolize both alcohol and tylenol –> at risk for hepatic necrosis
37
Q

Alcoholic liver disease:

  1. What lab values are going to indicate this?
  2. What is the progression of disease?
A
  1. AST:ALT ratio of >2:1 (ALT usually <300)
  2. Normal liver –> fatty liver (steatosis on biopsy) which can either go to alcoholic hepatitis (steatosis + inflammatory cells) or cirrhosis (devo of nodules, stage 4 disease)
    * alcohol hepatitis can also progress to cirrhosis after about 20 years*
38
Q

Primary Sclerosing Cholangitis:

  1. Describe the pathophysiology:
  2. What would you expect to see on ERCP? (Endoscopic retrograde cholangiopancreatography)
  3. What population is this common in?
  4. what disease is it commonly associated with?
  5. What lab values would you expect to see?
A
  1. Unknown cause of concentric “onion skin” bile duct fibrosis
  2. alternating strictures and dilation with “beading” of intra- and extrahepatic bile ducts on ERCP
  3. Young men with IBD
  4. ulcerative colitis
  5. MPO-ANCA/p- ANCA +
39
Q

In a patient that has primary sclerosing cholangitis AND ulcerative cholitis, what are they at increased risk for? (3)

A
  1. cholangiocarcinoma
  2. gallbladder carcinoma
  3. colorectal carcinoma
40
Q

A 52-year-old woman comes to the physician because of fatigue, pruritus, and light-colored, greasy stools for the past two months. Prior to the appearance of these symptoms, she was in good health. Family history is noncontributory. Vital signs are within normal limits. Exam shows mild hepatomegaly. Rectal exam shows stool that is guaiac-negative. Serum IgM is elevated and additional studies show the presence of antimitochondrial antibodies. If untreated, she is at increased risk for which of the following?

A. Markedly decreased serum alanine aminotransferase
B. Markedly decreased serum alkaline phosphatase
C. Markedly decreased serum bilirubin
D. Markedly increased serum albumin
E. Markedly increased serum cholesterol

A

E

41
Q

Liver tests:

  1. which is more specific, ALT or AST?
  2. what is the best liver function test?
A
  1. ALT is more specific than AST
  2. INR is the best liver function test
42
Q

Spider angiomata, caput medusae, palmar erythema, and dupuytrens contractures are common symptoms of what disease?

A

cirrhosis

Symptoms 2 (11 decks)

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