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Energetics & Homeostasis > Exam 5 > Flashcards

Exam 5 Flashcards

1
Q
A

Cirrhosis

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2
Q

What is Wilson’s Disease?

A

Excess accumulation of copper (ATP7B mutation)

Copper is deposited in:

  • Liver
  • Kidneys - Joints
  • Brain (i.e. basal ganglia)
  • Eyes (i.e. corneas: Kayser Fleischer ring)
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3
Q
A

Hepatocellular Carcinoma

  • Notice the cirrhotic liver around the carcinoma
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4
Q

Hepatitis B transmission

A

Blood and Sex

Blood (needles/IVDU, old transfusions), Sex, vertical transmission (mom to baby)

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5
Q

Direct Bilirubin

A

Direct = Conjugated

Conjugated Bilirubin is excreted in the urine

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6
Q

Functional unit of the liver

A

Lobule

  • Portal tract (triad)
  • Hepatocytes
  • Central Vein
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7
Q

What is Hereditary Hemochromatosis

A

Excess accumulation of Iron (bronze diabetes).

  • Due to low levels of Hepcidin.
  • Hepcidin lowers iron absorption by reducing iron transport across gut mucosa and reduces iron exit from the liver.
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8
Q

Pathology?

A

Hereditary Hemochromatosis

  • Autosomal recessive disorder of the HFE gene
  • Leads to excessive intestinal absorption of iron from low Hepcidin

Classic triad

  • Cirrhosis
  • Diabetes mellitus
  • Increased skin pigmentation, AKA, bronze diabetes.
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9
Q

Indirect Bilirubin

A

Indirect Bilirubin = Unconjugated Bilirubin

  • Has not been conjugated in the liver yet (pre-hepatic bilirubin)
  • Bound to albumin, which makes it slightly less toxic than if it wasn’t bound

(Total - Direct = Indirect)

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10
Q

Kuppfer cells

A

Macrophages that sit in the sinusoids

Little Kups of inflammation that cause big problems if you knock them over

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11
Q

Hepatitis C transmission

A

Blood (old transfusions, IV drug/needles)

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12
Q

What happened here?

A

Primary Sclerosing Cholangitis (slide of what was the portal triad)

  • Bile duct is destroyed and replaced with fibrosis
  • Mara Rendi says need to be able to recognize
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13
Q
A

Metastatic Carcinoma invading the liver

  • Notice the normal liver architecture around the cancer (no cirrhosis)
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14
Q

Treatment for Wilson’s Disease

A

copper chelation and inhibition of copper absorption

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15
Q

What’s going on here?

A

Chronic Cholecystitis

(Thick Wall)

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16
Q

Diagnosis and Treatment for HH

A

Dx:

  • increased serum iron
  • increased transferrin saturation
  • increased ferretin levels

Tx: phlebotomy to reduce iron load

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17
Q

Alpha-1-antitrypsin deficiency (A1AT)

A

​Can’t inactivate neutrophil elastase, so it goes crazy and runs around the lung and liver destroying tissues.

  • function of A1AT is to inhibit the action of destructive neutrophil proteases, particularly in the lung.
  • Autosomal co-dominant
  • Can lead to liver and lung disease
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18
Q

Stellate Cells

A

Store vitamin A

Make collagen

Stellate Stalactites: Make fibrotic stalactites in the liver leading to cirrhosis

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19
Q

Hepatitis E main points

A

Fecal oral transmission Bad in pregnancy

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20
Q

Hepatitis D main points

A

Transmission: Blood and Sex

Only replicates if you already have hepatitis B already

  • Up to 20% mortality if you have both
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21
Q

Progression of liver damage from alcohol

A

Alcoholic Liver Disease–>alcoholic hepatitis–> alcoholic cirrhosis–> Increased risk of liver cancer

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22
Q

Hepatitis B

A
  • Transmitted via sex, blood (needles), vertical transmission (mom to baby)
  • Can be clinical or subclinical infection
  • 5-10% will go on to chronic Hepatitis
  • 5-10% of those –> cirrhosis & cancer
  • Immunization available
  • No curative treatment
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23
Q

Hepatitis C

A

Hepatitis C(hronic)

  • Transmitted via blood (transfusion, IV drug/needles) 50% of the time will go on to chronic hepatitis
  • Not usually a problem until it progresses (elevated LFT’s on routine lab work
  • Curative treatment available: almost $100,000 (Harvoni)
  • Can lead to cirrhosis and increased risk of liver cancer
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24
Q

Hepatitis A

A

​A for Acute & Asymptomatic

  • fecal oral: contaminated food & water, restaurants, daycares
  • Often undetected, can get better on its own
  • AST/ALT: High 100’s low 1000’s
  • Does not cause chronic liver disease
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25
Q
A

Kayser Fleischer ring: copper around cornea from Wilson’s Disease

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26
Q

Bronze Diabetes

A

Heriditary Hemochromatosis

Increased iron saturation leads to darkening of the skin and diabetes. Also see iron deposition throughout the body.

Elevated transferrin saturation

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27
Q
A

Chronic Cholecystitis

(Thick Wall)

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28
Q

A1AT causes

A

Liver and Lung Disease

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29
Q

If you get cancer in the gallbladder is can?

A

easily break through the thin wall and/or invade the liver

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30
Q
A

Gall stones (looks like in the common bile duct)

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31
Q

Gallstones can lead to?

A

Acute Cholecystitis

  • Acute obstruction of duct by stone leads to edema, congestion, hemorrhage and exudates.
  • Impacted stones cause ulceration.
32
Q

Chronic Cholecystitis

A

Thick gallbladder wall!

  • Multiple episodes of inflammation cause gallbladder thickening and contraction with variable wall thickness and appearance.
33
Q
A

Carcinoma of Gallbladder

34
Q
A

Porcelain Gallbladder

  • With longstanding inflammation gallbladder wall becomes fibrotic and calcified : “porcelain gallbladder”
  • Associated with gallbladder carcinoma in 20% of cases
35
Q
A

A) Mass of carcinoma

B) Gall stones

36
Q
A

Porcelain Gallbladder

Worry about Gallbladder carcinoma

37
Q

Consequence of thin gallbladder wall?

A

Carcinoma of the gallbladder has a really poor prognosis, because it usually presents at a late stage

  • usually no symptoms
  • easily spreads through thin wall of gallbladder out into the body or into the liver
38
Q

Label

A

Liver Lobule

39
Q
A
40
Q

Function of Hepatocytes

A

Protein Synthesis: (Albumin, Clotting & Anticoag factors)

Storage: (Carbohydrates, Lipids, Vitamins)

Bile Production

Detoxification:

  • Ammonia
  • Bilirubin
  • Drugs
  • Toxins
41
Q

Cell Type?

A

Hepatocytes

42
Q
A

Portal Triad (Portal Tract)

A) Portal Vein (venous blood from GI tract)

B) Bile Duct

C) Hepatic Artery (brings O2 rich blood to liver)

43
Q

Name and Function

A
44
Q

Liver Zones & Importance of Each

A
45
Q

Hepatitis virus types (DNA or RNA)?

A

Hep B is DNA virus

All others are RNA

46
Q
A

ground glass hepatocytes: Hepatitis B

47
Q

Diagnosis?

A

Chronic Hepatitis C

  • Lymphoid aggregates or follicles with germinal centers in the portal areas
  • Clear areas are steatosis (fat in hepatocytes)
  • Mara Rendi says “must know histology”
48
Q

What’s going on here?

A

Chronic Hepatitis C

49
Q

Pathology of Alcoholic Liver Disease

A
  1. Fat accumulation in hepatocytes (steatosis)
  2. Mallory Bodies
  3. Progresses to Fibrosis & Cirrhosis
50
Q
A

A) Fat

B) Inflammatory aggregates (ants)

C) Mallory Bodies (smudgy pinks)

  • alcohol is damaging liver cells and cytoskeletal elements get broken down
  • these cytoskeleton peices clump up (bright pink piles of debris)
51
Q

Non-Alcoholic Steatohepatitis (NASH) Pathology

A

Looks like Alcoholic Fatty Liver Disease without the Mallory bodies

Characteristic pathology with zone 3 hepatocellular injury pattern

  • Steatosis
  • Lobular inflammation
  • Fibrosis

Associated with insulin-resistance

52
Q

Primary Biliary Cirrhosis (PBC)

A

Key Point to remember: Bile ducts in the portal triads get destroyed –> can’t get bile out –> inflammation –> cirrhosis

  • Middle-aged females
  • Associated with autoimmune disorders
  • Positive anti-mitochondrial antibodies (AMA) and elevated alkaline phosphatase.
  • Florid duct lesion on pathology (granulomatous/inflammation attack on bile ducts)
53
Q

Primary Sclerosing Cholangitis (PSC)

A

​Destruction of the bile ducts

  • Commonly affects young males
  • 70% patients have coexisting idiopathic inflammatory bowel disease (UC)
  • Elevated alkaline phosphatase and bilirubin
  • ERCP shows beaded strictures of the bile ducts
  • Risk of cholangiocarcinoma
54
Q

Diagnosis?

A

Primary Sclerosis Cholangitis: Beads on a string

55
Q

Diagnosis?

A

Primary Sclerosing Cholangitis

  • Fibroinflammatory destruction of the bile ducts leading to Concentric periductal (“onion-skin”) fibrosis
  • Eventual fibroobliteration of the bile ducts
  • Cirrhosis develops subsequently
56
Q

Pathology?

What gene is mutated?

A

Kayser-Fleisher (copper) rings = Wilson Disease

  • Autosomal recessive disorder of copper metabolism resulting in accumulation of copper in organs including liver, brain, and eye.
  • ATP7B mutation: can’t put copper into bile
  • See decreased serum ceruloplasm
57
Q

Main Functions of the Liver

A

Stores: B12, copper, iron, A, D, E, K

Detoxifies: bilirubin, alcohol, drugs, toxins, Ammonia

Synthesizes: Transport proteins, plasma albumin, clotting factors, urea, glycogen, cholesterol, phospholipids, bile salts, lipoproteins

58
Q

Liver Function Tests and What They Generally Indicate

A

AST/ALT

  • Elevated = Active damage to hepatocytes (happening right now)

Alkaline Phosphate

  • Elevated = Biliary obstruction

Albumin & Clotting Factors

  • Elevated = Hepatocytes are dead and not making things
  • Clotting factors have a shorter half life than albumin and are thus low first
59
Q

Steps of Bilirubin conjugation image

A
60
Q

Label the boxes

A
61
Q

LFT’s in Acute Hepatocyte Necrosis

  • Type of Hyperbillirubinemia?
  • Urine Bilirubin?
  • Aminotransferases?
  • Alkaline Phosphatase?
  • Prothrombin/INR?
  • Albumin?
A
  • Conjugated (direct)
  • Urine Bilirubin: Present
  • Very High AST/ALT
  • Elevated Alkaline phosphatase (< 3 x normal)
  • Prothrombin/INR could be elevated or normal, depending on severity
  • Albumin would be normal (does not become elevated until hepatocytes dead for a while, because of long half-life)
62
Q

LFT’s in Cholestasis

  • Type of Hyperbillirubinemia?
  • Urine Bilirubin?
  • Aminotransferases?
  • Alkaline Phosphatase?
  • Prothrombin/INR?
  • Albumin?
A
  • Conjugated (Direct Bilirubin)
  • Urine Bilirubin: present
  • AST/ALT: slight elevation
  • Alkaline Phosphatase: Very High ( > 3x normal)
  • Clotting: Normal
  • Albumin: Normal
63
Q

LFT’s in Gilbert’s Syndrome

Type of Hyperbillirubinemia?

Urine Bilirubin?

Aminotransferases?

Alkaline Phosphatase?

Prothrombin/INR?

Albumin?

A

Gilbert’s syndrome: decreased UGT1A1 enzyme activity

  • Unconjugated (indirect Bilirubin)
  • Urine Bilirubin: absent
  • AST/ALT: normal
  • Alkaline Phosphatase: normal
  • Clotting: Normal
  • Albumin: Normal

Gilbert just can’t conjugate anything…

64
Q

LFT’s in Cirrhosis

  • Type of Hyperbillirubinemia?
  • Urine Bilirubin?
  • Aminotransferases?
  • Alkaline Phosphatase?
  • Prothrombin/INR?
  • Albumin?
A
  • Conjugated = Direct Bilirubinemia
  • Urine Bilirubin: Present
  • AST/ALT: slight elevation
  • Alkaline Phosphatase: slight elevation to normal
  • Clotting (PTT/INR): Slow/Long
  • Albumin: Low
65
Q

LFT’s in increased UCB (e.g. RBC damage, neonatal jaundice)

  • Urine Bilirubin?
  • Aminotransferases?
  • Alkaline Phosphatase?
  • Prothrombin/INR?
  • Albumin?
A
  • Urine Bilirubin: No
  • AST/ALT: slight elevation in AST, ALT: normal
    • because dying RBC’s release AST
  • Alkaline Phosphatase: normal
  • Clotting: Normal
  • Albumin: Normal
66
Q

What does each of these tell you?

  • Urine Bilirubin
  • Aminotransferases
  • Alkaline Phosphatase
  • Prothrombin/INR
  • Albumin
A
  • Urine Bilirubin: Is it conjugated (post-hepatic)
  • Aminotransferases: Are liver cells being actively damaged
  • Alkaline Phosphatase: Is there obstruction or bone breakdown
  • Prothrombin/INR: Are hepatocytes dead
  • Albumin: Have hepatocytes been dead for a few days
67
Q

Palmar Erythema & Spider Angiomata mean?

A

Cirrhosis (consequences of excess estrogen)

The Liver clears/detoxifies estrogen

68
Q

Asterixis

A

Flapping tremor of the extended hands

Sign of Hepatic Encephalopathy (Ammonia)

69
Q
A

Caput Medusae

Consquence of Portal Hypertension

70
Q
A

Cirrhosis

Trichrome stain (where collagen is blue)

71
Q

Hepatocellular Adenoma

A
  • Associated with OCP (usually young women)
  • Regression after discontinuation of OCP
  • Benign, usually not associated with cirrhosis
72
Q
A

Cirrhosis

73
Q

Gilbert’s Syndrome

A

A benign condition where unconjugated bilirubin rises in the presence of stress (e.g. fever, sepsis, fasting and staying up all night)

  • episodic jaundice, with no other symptoms
  • autosomal recessive
74
Q

Pregnant women with itching of palms and soles

A

Think Intrahepatic Cholestasis (stasis of bile) of Pregnancy (ICP)

  • flow of bile (containing conjugated bilirubin) is stopped somewhere between hepatocytes and duodenum
  • mechanism not really understood (could be hormonal)
  • can see tea colored urine (conjugated hyperbilirubinemia)
75
Q

A woman in her third trimester of pregnancy presents to your clinic with tea-colored urine, and several days of intense itching of her palms and soles.

What is the appropriate treatment for this condition?

A

Ursodeoxycholic acid (you’re so deoxy, Cholic….)

  • reduces itching, bilirubin serum bile acid

Inducing her or C-section are common options

  • especially if her serum bile acid > 40 umol/L, due to the increased risk of complications it causes
76
Q

Treatment of Acetaminophen Overdose

A

Acetylceysteine

Restores pool of reduced Glutathione (GSH), which detoxifies toxic metabolite before it can do damage

Energetics & Homeostasis (1 decks)

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