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DEMS > Unit I, week 3 > Flashcards

Unit I, week 3 Flashcards

1
Q

Two types of hepatocyte death

A

1) Ballooning Degeneration

2) Necrosis and apoptosis

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2
Q

Ballooning degeneration in hepatocytes

What does it look like?
What type of liver disease is it seen in?
Reversible or irreversible?

A

hepatocyte swelling and clumping of hepatocyte organelles and keratin filaments with clearing of cytoplasm

Most often seen in steatohepatitis

Reversible injury

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3
Q

Necrosis and apoptosis of hepatocytes

What does it look like?
What type of liver disease is it seen in?
Reversible or irreversible?

A

decrease cell size with increased eosinophilia of cytoplasm with a small dark nucleus

Seen with ischemia and chronic viral hepatitis

Irreversible injury

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4
Q

Common Inflammation/Etiology Associations:

Neutrophils → ?
Eosinophils → ?
Plasma cells → ?
Lymphocytes → ?

A

Neutrophils → Steatohepatitis

Eosinophils → drug reaction

Plasma cells → autoimmune hepatitis

Lymphocytes → commonly viral (but also in many other hepatitises)

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5
Q

Location of infiltrate in liver and etiology:

Portal based → ?

Interface inflammation → ?

Zone 3 (around central vein)→ ?

A

Portal based → biliary disease

Interface inflammation → autoimmune and viral hepatitis

Zone 3 → autoimmune hepatitis or acute cellular rejection (transplant)

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6
Q

Cholestasis causes accumulation of _______ in hepatic parenchyma

This results it ____________

A

accumulation of BILE in hepatic parenchyma

Cytoplasmic bile in hepatocytes → ballooning degeneration

Can result from obstructive and nonobstructive causes

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7
Q

Fibrosis in the liver:

common end result of ________ within hepatic __________

_______ deposition by __________ in __________

A

common end result of inflammatory/injury within hepatic parenchyma

Type I Collagen deposition by activated stellate in space of Disse

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8
Q

Pathophysiology of fibrosis in the liver (4)

A

chronic cycles of injury and regeneration

→ activated stellate cells deposit type I collagen

→ architectural and vascular reorganization

→ cirrhosis

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9
Q

Acute Hepatitis

what is it?
causes? (2)

A

New onset of symptoms for less than 6 months + elevations in AST/ALT

Causes: acute viral hepatitis, adverse drug reaction

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10
Q

Acute hepatitis

histology

A

marked LOBULAR DISARRAY and inflammation with numerous necrotic hepatocytes and cholestasis

Does NOT have significant liver fibrosis in background (suggests chronic)

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11
Q

Chronic hepatitis

what is it?
causes? (3)

A

clinical, serologic, or pathologic evidence of hepatic injury / inflammation for greater than 6 months

Causes: chronic viral hepatitis, autoimmune hepatitis, adverse drug reaction

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12
Q

Histology of chronic hepatitis

A

less lobular disarray, less prominent inflammation, rare necrotic hepatocytes, slow progression of fibrosis over time - “Patchy”

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13
Q

Chronic hepatitis

Grade represents what?

Stage represents what?

A

Necroinflammatory activity (GRADE) - amount of inflammation/injury

Degree of fibrosis (STAGE) - cumulative result of injury over time, amount of fibrous tissue deposition

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14
Q

Cirrhosis

A

end stage histological stage of chronic liver disease of any cause characterized by regenerative nodules surrounded by fibrous tissue

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15
Q

Cirrhosis is characterized by diffuse __________ that divides the liver parenchyma into _______ as a result of _______, _________, and __________

A

Characterized by diffuse FIBROUS SEPTATION that divides the liver parenchyma into NODULES as a result of:

1) recurring death of hepatocytes
2) deposition of ECM

3) architectural and vascular reorganization

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16
Q

Hepatotropic viruses:

A

Hepatitis A, B, C, D, E viruses →primary site of infection is hepatocytes

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17
Q

Hepatitis A and Hepatitis E

1) ss/ds RNA/DNA?
2) transmission?
3) can chronic disease occur as a result?
4) Test for by looking for what?
5) HEV has a high mortality rate in who?

A

1) ssRNA virus
2) Spread via fecal-oral route
3) Never lead to chronic disease - only acute hepatitis
4) Test by looking for IgM and IgG specific antibodies
5) HEV → high mortality among pregnant women

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18
Q

Hepatitis B

1) ss/ds RNA/DNA?
2) transmission?
3) can chronic disease occur as a result?
4) histology - 1 main feature

A

1) dsDNA virus (integrates into host genome)
2) Blood and bodily fluid transmission - can also get vertical transmission

3) 10% of chronic liver disease - major cause of chronic liver disease worldwide
- Most patients will recover from acute infection, only 5-10% progress to chronic hepatitis

4) Histology: see “ground glass” viral inclusions in hepatocytes

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19
Q

Hepatitis C

1) ss/ds RNA/DNA?
2) transmission?
3) can chronic disease occur as a result? can acute disease result?

A

1) ssRNA virus
2) Blood and bodily fluid transmission

3) Rarely presents as acute hepatitis
* *Causes 80% of chronic liver disease - MOST patients with Hep C get chronic hepatitis (85% of those infected) (but only 20% of these patients go on to develop cirrhosis)

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20
Q

Histology of Hep C infection

A

lymphoid aggregates, inflamed portal tract with injury between portal tract and lobule

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21
Q

Hepatitis D

A

cannot replicate without concurrent HBV infection - can augment HBV infection

→ increases risk of fulminant hepatitis, and faster progression to end stage liver disease

Commonly associated with IV drug abuse

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22
Q

Autoimmune hepatitis: immune mediated attack directed at ________ resulting in ___________

Primary biliary cirrhosis (PBC): autoimmune mediated attack directed at _______________ resulting in ___________

Primary sclerosing cholangitis: autoimmune mediated attack directed at __________ resulting in ___________

A

Autoimmune hepatitis:

  • hepatocytes
  • resulting in acute flare that progresses to chronic hepatitis

Primary biliary cirrhosis:

  • intrahepatic small caliber bile ducts
  • -> inflammatory bile duct destruction

Primary sclerosing cholangitis:

  • intrahepatic and extrahepatic LARGE carliber bile ducts
  • -> obliterative fibrosis of large caliber bile ducts
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23
Q

Autoimmune hepatitis

Labs (3)
Treatment
More in females or males?

A

Female > male

Labs:

  • Increased AST and ALT, normal ALP
  • Positive auto-ab test (ANA, ASMA, anti-LKMB)
  • elevated IgG

Treat with steroids

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24
Q

Primary biliary cirrhosis (PBC)

Presentation
more in females or males

A

insidious onset with pruritus appearing before jaundice

Females&raquo_space; males, middle aged

25% progress to liver failure

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25
Q

Primary biliary cirrhosis (PBC)

Labs

A

elevated ALP, GGT, and bilirubin with normal/slightly increased AST and ALT

Elevated IgM

Anti-mitochondrial antibody*** = HALLMARK

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26
Q

Primary biliary cirrhosis (PBC)

Histology

A

lymphocyte mediated bile duct damage, granulomatous duct destruction → no bile ducts left (ductopenia)

Intrahepatic SMALL caliber duct destruction

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27
Q

Primary Sclerosing Cholangitis (PSC)

associated with ________

Increases patients risk for _______

More common in males or females?

A

Associated with UC

Increased risk for cholangiocarcinoma

Male&raquo_space; female

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28
Q

Primary Sclerosing Cholangitis (PSC)

Presentation

A

Persistently elevated alkaline phosphatase and no other signs/symptoms

  • Serology nonspecific
  • Later → fatigue, pruritus, jaundice

Dx with radiology (ERCP or MRCP)

**Causes multiple biliary strictures and areas of dilation (string of pearls)

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29
Q

Primary Sclerosing Cholangitis (PSC)

Histology

A

periductal “onion-skin” fibrosis → fibrous obliteration of bile duct

Intra and extrahepatic LARGE caliber bile duct involvement

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30
Q

Drug induced liver injury

-intrinsic vs. idiosyncratic

A
  • Relatively common cause of liver injury
  • Many patterns of injury mimic other diseases

Intrinsic (dose related - e.g. Acetaminophen) or idiosyncratic (unpredictable)

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31
Q

Acetaminophen Liver Injury

Intrinsic or idiosyncratic?
Pattern of necrosis?

A

Major cause of ACUTE liver failure that leads to liver transplant in US

Intrinsic (dose-related) hepatotoxin

Centrilobular necrosis (zone 3) - death around central vein
-Amount of acetaminophen dictates level of damage
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32
Q

Steatosis

A

accumulation of fat in hepatocytes, metabolic derangement of hepatocytes

Lipid influx > lipid clearance

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33
Q

Steatohepatitis

A

hepatocellular injury in association with steatosis +/- overt inflammation

Often chronic and can lead to fibrosis and cirrhosis

TWO TYPES: alcoholic, and non-alcoholic

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34
Q

Causes of Steatohepatitis

A

alcohol metabolic syndrome, drug injury

Not all causes of steatosis also cause steatohepatitis

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35
Q

Triad of findings in steatohepatitis

A

steatosis, lobular inflammation, and hepatocyte ballooning degeneration

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36
Q

Alcoholic type Steatohepatitis

A

AST/ALT ratio > 2, normal ALP, increased GGT

-Alcohol is a large carbohydrate load → liver converts carbs into fats and shuts off B-oxidation of lipids and causes problems with export of lipids → accumulation of lipids in hepatocytes

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37
Q

Histology of Alcoholic vs. non-alcoholic type steatoheptatitis

A

Alcoholic: MALLORY hyaline and prominent NEUTROPHIL infiltrates

Non-Alcoholic: Fibrosis begins centrilobular (zone 3) → prominent sinusoidal pattern (CHICKEN-WIRE)

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38
Q

Non-Alcoholic type Steatohepatitis

A

Seen in patients with diabetes, metabolic syndrome, obesity, or adverse drug reaction

Causes hepatic fibrosis over time → cirrhosis

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39
Q

Hereditary hemochromatosis

______ overload due to mutation in _______ on chr ________

inheritance pattern?

Males or females more effected?

A

iron overload secondary to mutation in HFE gene on chr 6 (autosomal recessive)

Males&raquo_space; females (Northern European descent)

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40
Q

Pathogenesis of injury and damage to the liver in Heridatry Hemochromatosis

A

→ abnormal regulation of iron absorption in SI → deposition of iron in tissues and hepatocytes

→ injury and fibrosis via oxidative damage

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41
Q

Presentation of Hereditary Hemochromatosis (triad)

Histology?

A

liver disease, diabetes, heart failure

Histology: iron deposits (Prussian blue stain) in hepatocytes

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42
Q

Wilson’s Disease

______ overload due to mutation in _______ on chr ________

inheritance pattern?

A

copper overload secondary to mutations in ATP7B gene on chr 13 (autosomal recessive)

Problem with copper transport protein for biliary excretion of copper

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43
Q

Presentation of Wilson’s disease

Histology?

A

Presentation: neuropsychiatric symptoms + Liver disease and Kayser-Fleischer rings on eye exam

Histology: copper accumulation in hepatocytes

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44
Q

Alpha-1-antitrypsin deficiency

genetic disease characterised by decreased production of ____________

three possible genotypes?

associated with what pulmonary problem?

A

decreased production of protease inhibitor a1-antitrypsin (autosomal recessive)

PiMM = normal, PiMZ = heterozygote, PiZZ = disease genotype

Associated with pulmonary emphysema

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45
Q

Histology of a1-antitrypsin deficiency

A

Intracytoplasmic accumulation of PAS +, diastase resistant hyaline globules with progressive fibrosis (abnormally folded A1A)

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46
Q

Budd-Chiari Syndrome

A

liver enlargement, pain, ascites, with main hepatic vein occlusion

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47
Q

Hepatocellular carcinoma

A

most common primary MALIGNANT tumor of liver

Malignant neoplasm of hepatocytes

Almost exclusively occurs in patients with chronic liver disease and cirrhosis

-Presents as distinct mass in cirrhotic liver

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48
Q

Prognosis of hepatocellular carcinoma is based on what? (4)

A

1) size
2) presence of macroscopic and microscopic vascular invasion
3) focality
4) invasion of adjacent structures

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49
Q

Cholangiocarcinoma

malignant neoplasm of _______

major risk factor is _____

prognosis?

A

malignant neoplasm of bile ducts

Major risk factor is PSC

Poor long-term survival

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50
Q

Hemangioma

A

benign neoplasm of dilated vascular spaces

Most common primary hepatic tumor

More common in women

Usually small and symptomatic - larger ones may require resection

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51
Q

Focal Nodular Hyperplasia

A

benign mass-like proliferation of hepatocytes

Arises due to a local vascular flow anomaly

Second most common primary hepatic mass

More common in women

Usually asymptomatic

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52
Q

Hepatocellular adenoma

A

BENIGN neoplasm of hepatocytes

***Extremely low risk of malignant transformation

Occurs mostly in women of childbearing age
-Associated with contraceptive use

Usually no underlying chronic liver disease

Risk of rupture and abdominal hemorrhage

Usually asymptomatic

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53
Q

AST

  • normal function
  • Located where?
  • Expressed where?
A

catalyze transfer of amino groups to form hepatic metabolite pyruvate

Located in CYTOSOL and MITOCHONDRIA

Also expressed in NON-HEPATIC TISSUES (heart, skeletal muscle, blood)

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54
Q

When are AST and ALT released?

A

Released from damaged hepatocytes into blood after hepatocellular injury or death

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55
Q

ALT

  • normal function
  • Located where?
  • Expressed where?
A

catalyze transfer of amino groups to form hepatic metabolite oxaloacetate

Located in CYTOSOL of hepatocytes

More SPECIFIC FOR HEPATOCELLULAR INJURY than AST, but ALT can still be elevated in nonhepatic conditions

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56
Q

What can cause severe (>15x nml) AST and ALT elevations (7)

A

1) Acute viral hepatitis (A-E, herpes)
2) medications/toxins
3) ischemic hepatitis
4) autoimmune hepatitis
5) Wilson’s disease
6) Acute Budd-Chiari syndrome
7) hepatic artery ligation or thrombosis

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57
Q

Normal AST/ALT ratio = ______

AST/ALT > 1 –> ?

AST/ALT > 2 –> ?

A

normal = 0.8

AST/ALT > 1 seen in cirrhosis
AST/ALT > 2 → alcoholic hepatitis

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58
Q

Why is the AST/ALT ratio > 2 in alcoholic hepatitis?

A

Lower ALT from hepatic deficiency of pyridoxine (B6) in alcoholics which is a cofactor for enzymatic activity of ALT

Higher AST because of damage to mitochondria full of AST

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59
Q

Alkaline phosphatase

normal function
located where?

A

Removes phosphate groups from nucleotides, proteins and alkaloids

Present in nearly all tissues
(bone, placenta, liver, etc.)

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60
Q

Why would alkaline phosphatase be elevated?

A

cholestatic or infiltrative disease of the liver, and by disease causing obstruction of biliary system

Also due to bone disease, meds, pregnancy, hepatic and nonhepatic tumors

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61
Q

Where is alkaline phosphatase located in the liver?

how can you differentiate an elevated alk. phos. from liver vs. non-hepatic causes

A

In liver - isolated to microvilli of bile canaliculus

  • Liver alkaline phosphatase more heat stable
  • Use y-glutamyltransferase (GGT) or 5’nucleotidase serum levels to confirm liver-specific origin for elevation of alk. phos.
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62
Q

Isolated alkaline phosphatase elevation → (4)

A

1) Primary biliary cirrhosis (PBC)
- AMA (antimitochondrial antibody) positive → PBC

2) Bile duct obstruction - cholestatic disease (may also have elevated conjugated hyperbilirubinemia)
3) Primary sclerosing cholangitis (PSC)
4) Infiltrative diseases of liver

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63
Q

Bilirubin

A

Normal heme degradation product, excreted by body via secretion into bile

Requires conjugation (glucuronidation) into water soluble bilirubin forms before biliary secretion

Acts as an antioxidant

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64
Q

Bilirubin is typically elevated due to…

A

cholestasis, impaired conjugation, or biliary obstruction

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65
Q

Normal bilirubin secretion occurs how? (3 steps)

A

1) Unconjugated bilirubin taken up into hepatocyte
2) → conjugated into glucuronide form by ER enzyme bilirubin-UGT
3) → water soluble bilirubin (conjugated) secreted across canalicular membrane into bile

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66
Q

Gilbert Syndrome

causes _________ hyperbilirubinemia

A

diminished production of bilirubin-UGT → unconjugated hyperbilirubinemia

Jaundice occurs during times of stress

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67
Q

Hemolytic Jaundice is due to __________ hyperbilirubinemia

A

unconjugated hyperbilirubinemia

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68
Q

3 main causes of unconjugated (indirect) hyperbilirubinemia

A

Gilbert’s syndrome
Hemolysis
Crigler-Najjar syndrome

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69
Q

4 main causes of conjugated (direct) hyperbilirubinemia

A

Extrahepatic obstruction of bile flow
Intrahepatic cholestasis
Hepatitis
Cirrhosis

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70
Q

How does cirrhosis cause hyperbilirubinemia

A

Cirrhosis → bilirubin elevation due to increased peripheral RBC destruction and fibrosis of sinusoids

→ jaundice and conjugated hyperbilirubinemia

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71
Q

Prothrombin time and liver function

A

Assesses the extrinsic clotting pathway

Can asses synthetic function

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72
Q

2 reasons why PTT would be elevated

how do you differentiate these causes?

A

significant hepatocellular dysfunction, or vitamin K deficiency

How to differentiate?

-Administer subcutaneous vitamin K and assess response

No correction → liver dysfunction
Normalization → vitamin K deficiency

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73
Q

Patterns of liver chemistry tests:

Hepatocellular injury or necrosis → predominant _________ elevation

Cholestatic pattern → predominantly __________ elevation

A

Hepatocellular injury or necrosis → predominant AST and ALT elevation

Cholestatic pattern → predominantly alkaline phosphatase elevation

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74
Q

What does it mean if you are positive for…

HBsAg

A

Hepatitis B surface antigen = marker for ACTIVE INFECTION or CHRONIC INFECTION (if present for > 6 months)

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75
Q

What does it mean if you are positive for…

HBsAb

A

Antibody to HBsAg

Marker of immunity to hepatitis B

**Either vaccinated, or successfully cleared HepB infection

76
Q

What does it mean if you are positive for…

HBcAb

A

Hepatitis B core antibody

ONLY in people infected with HepB - marker of ACTIVE or PRIOR INFECTION (not present for vaccinated people)

77
Q

What does it mean if you are positive for…

HBeAg

A

Hepatitis B “e” antigen

Marker of high viral load, ACTIVE VIRAL REPLICATION

Goal of treatment is to turn this OFF - E ANTIGEN SEROCONVERSION

78
Q

What does it mean if you are positive for…

HBeAb

A

Antibody to hepatitis B “e” antigen

Associated with LOWER VIRAL LOAD

79
Q

What does it mean if you are positive for…

HBV DNA

A

presence means active viral replication

80
Q

Indications for treatment of a Hepatitis B infection (4)

A

1) HBsAG (+) > 6 months
2) Serum HBV DNA > 10^5 copies/mL

3) Persistent or intermittent elevations in ALT and AST levels
- -> Unlikely to get seroconversion with low ALT

OR if Advanced liver disease (cirrhosis) present

81
Q

Treatment of HBV infection (2)

A

1) Interferon (not used anymore - lots of side effects)

2) Nucleoside/nucleotide analogs

82
Q

Nucleoside/nucleotide analogs used to treat HBV infection (4)

A

lamivudine, adefovir, entecavir, tenofovir

Fewer side effects

Resistant mutations in some strains

83
Q

Goal of HBV treatment

A

achieve HBeAg seroconversion

Goal is NOT to get rid of surface antigen

84
Q

When is an HCV infection considered chronic and treatment should be initiated?

A

presence of HCV RNA in blood for > 6 months after infection

85
Q

Goal of HCV antiviral therapy

A

clear HCV RNA and remain HCV RNA negative for 12 weeks = Sustained Virological Response (SVR) = CURE

**big difference with HepB - all you are trying to get is seroconversion

86
Q

Treatment of hereditary hemochromatosis (2)

A

Therapeutic phlebotomy (1x weekly for one year) + maintenance phlebotomy every 2-4 months

OR chelation therapy with deferoxamine*

87
Q

Treatment of autoimmune hepatitis

A

1) Corticosteroids

2) Azathioprine - inhibit T cell replication
- Side effects = reduce WBCs, nausea, pancreatitis

Must continue treatment - 50% chance of flare of AIH with cessation of therapy after achieving 2 year remission

88
Q

Treatment of primary biliary cirrhosis

A

Ursodiol (ursodeoxycholic acid)

89
Q

Treatment of primary sclerosing cholangitis

A

No effective medical therapy

Treatment = management of complications of biliary obstruction with stenting of strictures and ERCP

Liver transplantation is only long term treatment

90
Q

Treatment of Wilson’s Disease

A

chelators (D-penicillamine, trientine)

Zinc can be used once successful chelation of copper has occurred

91
Q

Treatment of non-alcoholic statohepatitis

A

Treatment = modify risk factors

-Obesity, type II diabetes, dyslipidemia

92
Q

How many teeth do adults have?

what age do kids get teeth?

A

Adult dentition = 8 incisors + 4 canines + 8 premolars + 12 molars = 32 teeth

What age do kids get teeth: age 6 months → full complement of primary teeth by age 3

93
Q

Periodontal ligament

A

Periodontal ligament binds tooth to alveolar bone

94
Q

Early childhood caries (ECC)

3 characteristics

A

Infectious and transmissible, destroys tooth structure

95
Q

Etiology of Early Childhood Caries

A

Bacteria (mutans strep) break down dietary sugars into acids which eat away the tooth

How OFTEN sugar is ingested is more important than how MUCH sugar is eaten at once

96
Q

First clinical sign of caries

Kids need help brushing teeth until what age?

A

White spots indicate acids have demineralized enamel (first clinical signs of caries)

Kids need help with brushing until age 6

97
Q

Oral cancer and precancer

often located in what 3 places

A

Alcohol and tobacco increase risk of oral cancers

Early lesions may be asymptomatic

MUST LOOK at lateral tongue, floor of mouth, inside of lips = NEGLECTED AREAS

98
Q

Periodontal disease

etiology

A

chronic plaque at gum line, bacterial infection, host inflammatory response

99
Q

Periodontal disease

3 types

A

Gingivitis: mild gum swelling, tenderness, erythema, bleeding gums with brushing - first most mild stage

Chronic periodontitis: more severe than gingivitis
-Infection and inflammation induce loss of bone and tooth attachment

Aggressive periodontitis: otherwise healthy individual with rapid attachment loss and bone destruction

100
Q

What makes diabetic glycemic control worse?

A

Periodontal disease

Poor glycemic control = 3x increased risk of periodontitis and periodontal disease worsens glycemic control → viscous cycle

101
Q

Periodontal disease and pregnancy

A

Periodontal disease associated with preterm birth and preeclampsia- dental treatment IS SAFE during pregnancy

102
Q

Xerostomia

what is it?
what causes it?

A

Decreased saliva promotes periodontal disease

Typically iatrogenic!

Meds (Steroids, antihistamines, diuretics, anti-HTN, anticholinergic, antidepressants)

103
Q

Physical exam of patient with cirrhosis (9)

A

1) Ascites (sign of portal hypertension)
2) Variceal hemorrhage (signs of portal hypertension)
3) Hepatic encephalopathy (sign of portal HTN and liver dysfunction)
4) Jaundice (sign of compromised liver function)

5) Muscle wasting
6) Splenomegaly
7) Enlargement of left lobe of liver
8) Spider angiomata
9) Caput Medusae

104
Q

Labs in a patient with cirrhosis (4)

A

1) Hypoalbuminemia
2) Prolonged PTT
3) Hyperbilirubinemia
4) Low platelet count - due to portal HTN and hypersplenism

105
Q

Radiographic findings in cirrhosis

A

Nodular liver with caudate lobe hypertrophy, ascites, splenomegaly, venous collaterals, recanalization of umbilical vein, and hepatocellular carcinoma

106
Q

2 main pathophysiologic causes of portal HTN

A

portal HTN from

1) increased intra-hepatic resistance (at level of SINUSOIDS in patient with cirrhosis)
2) increased portal venous inflow from splanchnic vasodilation

107
Q

Increase in intrahepatic vascular resistance (sinusoidal region) in cirrhosis caused by what?

A

1) Deposition of fibrous tissue and formation of nodules that disrupt architecture of liver → increased resistance to portal blood flow
2) Active vasoconstriction within liver + reduced endothelial NO release → increased resistance

In cirrhosis, portal HTN is at level of sinusoids

108
Q

What is the mechanism causing splanchnic vasodilation in cirrhosis?

A

→ Increased shear stress in splanchnic vasculature → increase NO production → splanchnic vasodilation → increased portal blood inflow
→ increases portal HTN

109
Q

Measurement of Portal Pressure

A

Hepatic venous pressure gradient (HVPG) = WHVP - FHVP

Wedged hepatic venous pressure (WHVP)

Free Hepatic venous pressure (FHVP) → internal zero (corrects for extravascular, intra abdominal pressure increases)

110
Q

Patterns of hepatic venous pressure gradient for:

Presinusoidal portal HTN

Sinusoidal portal HTN

Post-sinusoidal portal HTN

Posthepatic portal HTN

A

Pre-sinusoidal portal HTN (e.g. in schistosomiasis) → no pressure gradient, with portal HTN

Sinusoidal pattern → elevated HVPG (can’t dissipate pressure through liver)

Post-sinusoidal HTN → sinusoids intact, but have outflow obstruction, can’t dissipate pressure → elevated HVPG

Posthepatic portal HTN (e.g in heart failure)
-Have high FHVP - don’t get gradient because the whole system is at higher pressure

111
Q

Formation of varices

A

formation of portal systemic collaterals → dilation of coronary and gastric veins → gastroesophageal varices

112
Q

Variceal hemorrhage

what is the most important predictor of hemorrhage?

A

occurs when expanding force exceeds its maximal wall tension

Most important predictor of hemorrhage is variceal SIZE

113
Q

Treatment of varices

A

1) Pharmacotherapy (vasoconstrictors, venodilators)
2) Endoscopic Variceal Band Ligation - can be used prophylactically
3) Shunt therapy (TIPS)

114
Q

Octreotide

THIS WILL BE ON TEST

A

Vasoconstrictor - reduce portal blood inflow

Decreases splanchnic flow by causing splanchnic vasoconstriction → reduce portal pressure

Give to a patient when they come into the ER with variceal bleeding

115
Q

Transjugular Portosystemic Shunt (TIPS)

A

corrects portal HTN by creating communication between hypertensive portal system and low pressure systemic veins, bypassing the liver

Connects hepatic vein and portal vein

Can cause complications due to liver bypass → encephalopathy, liver failure

116
Q

Pathophysiology of ascites

A

Elevated portal pressure → increase in NO production in splanchnic and systemic circulations → potent vasodilation

→ decreased effective arterial blood volume

→ activate neurohumoral systems (renin, angiotensin, aldosterone), and sodium and water retention → ASCITES

In advanced cirrhosis get translocation of bacteria from gut that further increases NO production

117
Q

Causes of ascites (3)

how do you differentiate these?

A

cirrhosis
peritoneal pathology (malignancy or TB)
heart failure

Differentiate with pericentesis (SAAG + total protein)

118
Q

Complications of ascites (2)

A

Spontaneous bacterial peritonitis

Hepatorenal syndrome

119
Q

Paracentesis

A

used to determine if infected and differentiate between causes of ascites - should be done in anyone with ascites

Assess SAAG, total protein, PMN count, and cultures

120
Q

Serum-ascites albumin gradient***

SAAG > 1.1 g/dL –> ?
SAAG < 1.1 g/dL –> ?

A

SAAG = serum albumin - ascites albumin

SAAG > 1.1 g/dL → ascites due to sinusoidal HTN (or Heart failure)

SAAG < 1.1 g/dL → ascites due to peritoneal malignancy
-NOT due to sinusoidal HTN, or HF

121
Q

Ascites total protein:***

Total protein > 2.5 g/dL →?

A

Total protein > 2.5 g/dL → Heart failure or peritoneal malignancy

-Loss of protein through normal “leaky” sinusoid as opposed to capillarized sinusoids seen in cirrhosis = Heart failure cause

122
Q

Total protein < 2.5 and SAAG > 1.1 → ascites due to _______

Total protein > 2.5 and SAAG > 1.1 → ascites due to ______

Total protein > 2.5 and SAAG < 1.1 → ascites due to _______

A

Total protein < 2.5 and SAAG > 1.1 → ascites due to cirrhosis

Total protein > 2.5 and SAAG > 1.1 → ascites due to heart failure

Total protein > 2.5 and SAAG < 1.1 → ascites due to peritoneal malignancy

123
Q

Treatment of ascites (4)

A

1) Diuretics and sodium restriction
2) Albumin
3) Large volume paracentesis
4) TIPS - can be used to deal with ascites refractory to diuretic tx

124
Q

Hepatorenal Syndrome: (HRS)

A

Occurs in advanced cirrhosis due to drop in effective arterial blood volume and renal vasoconstriction → renal dysfunction and reduced GFR

Liver transplant is curative if transplant performed within 4-6 weeks before irreversible ischemic damage occurs

Kidney themselves are not damaged, they just get reduced blood flow due to significant systemic vasodilation

125
Q

Criteria for diagnosis of hepatorenal syndrome

A

Cr > 1.5 or CrCl l< 40 ml/min

No improvement of renal function after plasma volume expansion

Ascites + Hyponatremia universal in HRS

126
Q

Spontaneous Bacterial Peritonitis

A

infection of ascitic fluid

Pathophysiology: migration of viable microorganisms from intestinal lumen to mesenteric lymph nodes and other extraintestinal organs and sites

Typically caused by E. Coli

127
Q

Treatment and diagnosis of spontaneous bacterial peritonitis

A

TX: abx (avoid aminoglycosides - nephrotoxic)

Dx: ascites with PMN count > 250 /mm^3

128
Q

Hepatic encephalopathy

A

neuropsych manifestations of cirrhosis

Due to portosystemic shunting and failure to metabolize neurotoxic substances

  • Astrocytes are only cells in brain that can metabolize ammonia
  • Ammonia crosses BBB → dysregulation of GABA-BD receptors

Can’t use ammonia levels to diagnose

129
Q

Risk factors that worsen hepatic encephalopathy (6)

A

1) High protein load
2) GI bleeding
3) Infection
4) Over diuresis → azotemia and hypokalemia
5) Narcotics and sedatives
6) TIPS ** commonly causes HE

130
Q

Treatment of hepatic encephalopathy - reasoning?

A

Lactulose (laxative that acidifies stool, trapping NH4+ in stool and increases bowel movement)

131
Q

Model for End-Stage Liver Disease (MELD score)

A

estimates 3 month mortality in pts with cirrhosis

Used to rank patients on liver transplant list

Derived from total bilirubin, creatinine, and INR (now sodium also)

132
Q

Th1 T helper cells

2 main functions?

secrete _______ and activate __________

_______ helps CTL get activated when they recognize antigen

A

recognize antigen, attract macrophages

IFNy → activate M1 (inflammatory, “angry”) macrophages

IL-2 → helps CTL get activated when they recognize antigen

133
Q

Th17 helper T cells

secrete _______

Dendritic cells can make _______ –> pushes differentiation into Th17
-This is considered a central cytokine in what two diseases?

A

inflammatory role, more potent than Th1 cells

Secrete IL-17
Dendritic cells can make IL-23 → pushes differentiation into Th17

IL-23 considered a central cytokine in Crohn Disease and UC

134
Q

Th2 helper T cells

stimulate ______ to promote ___________ and __________

A

stimulate macrophages to become M2 (alternatively activated) → wall off pathogens, promote healing

135
Q

Th2 helper cells make ______ to attract ________ and _______

important for _________

A

Make IL-4 → attract eosinophils and macrophages

Important in parasite immunity if Th1’s M1 macs can’t kill invader

-Typically occurs after pathogen killing Th1 response

136
Q

Follicular helper T cells (Tfh)

A

stimulated by antigen and migrate from T cell areas of lymph nodes into B cell follicles → help B cells get activated and make IgM, IgG, IgE, and IgA

137
Q

Regulatory T cells (Treg)

make cytokines (_____ and _____) –> do what function?

This is the predominant T cell type where?

A

Make cytokines (IL-10, TGF-B) → suppress activation and function of Th1, Th17, and Th2 cells → keep immune response in check

Predominant T cell type in healthy gut

138
Q

Cytotoxic killer T cells (CTL)

make ______ –> attract ______

A

Make IFNy → attract macrophages that eat cells induced to die via apoptosis

139
Q

Cytotoxic killer T cells (CTL)

A

destroy any body cell they identify as foreign or abnormal antigen on surface presented on class I MHC

140
Q

T cell development

A

Pre T cells in thymus proliferate → express T cell receptor via random V(D)J → use TCR to examine stromal cell surfaces with 3 possible outcomes:

1) Nonselection
2) Negative selection
3) Positive selection

141
Q

1) Non-Selection
2) Negative Selection
3) Positive Selection

A

1) Non-Selection: no affinity between TCR and MHC
2) Negative-Selection: high affinity for self peptide in MHC → T cell dies by apoptosis (prevent autoimmunity) OR turns into a Treg
3) Positive selection: low affinity, T cell selected to mature

142
Q

Th0 cells (undecided precursors) located in _________ –> APC presents correct antigen in lymphoid tissues –> ?

A

located in PARACORTEX of lymph nodes

→ APC presents correct antigen in lymphoid tissues

→ divide and differentiate into Th1, Th17, Th2, Tfh, or Treg

143
Q

Determinants of differentiation of Th0 cells

A

conditions in periphery when APC was stimulated, what TLRs were engaged, and what cytokines/chemokines predominate

144
Q

Normal Peyer’s Patches

A

Th0 in gut binds peptide/MHC in presence of TGF-B → ONLY turns into a Treg (iTreg)

Local dendritic cells made IL-10 → favor Treg development

Abundant Tfh cells that drive B cells towards IgA production

145
Q

Recognition of normal commensal gut organisms

A

recognition of organisms by innate immunity via pattern recognition receptors that bind PAMPs

→ formation of iTregs (induced by exposure to normal flora) → prevent chronic inflammation

146
Q

Abnormal Peyer’s Patches

A

TGF-B + IL-6 → downregulate Treg and upregulate Th1 and Th17

IL-6 produced in response to stress or damage

Th0 cell in gut binds peptide/MHC in presence of TGF-B + IL-6 turns into a Th1, Th2, or Th17

147
Q

Celiac disease and HLA

A

HLA-DQ2, HLA-DQ8 → specially present peptides derived from gliadin to Th1 and Th17 cells (MUST have these HLA to get Celiac’s)

→ B cells with anti-TTG2 antibodies activated by Tfh cells to make IgA anti-tTG

148
Q

Is celiac disease an autoimmunity?

A

Celiac disease itself is NOT autoimmune, but dermatitis herpetiformis is

Anti-tTG ab (self) only made when gliadin (foreign peptide) also present

149
Q

Non-celiac gluten sensitivity:

A

Negative blood tests for celiac disease AND no sign of damage on intestinal biopsy

Symptoms improvement when gluten is removed from diet

Recurrence of symptoms when gluten is reintroduced

No other explanation for symptoms

NOT HLA-DQ2 and 8 associated but may be a food allergy

150
Q

Cephalic phase:
________ enzyme in saliva digests carbs

_______ sequesters iron to limit bacterial growth

________ neutralizes refluxed gastric acid

_________ pore forming antimicrobial enzyme

Stimulation of pancreatic release of digestive enzymes via the ENS is mediated primarily by _______

A

AMYLASE

LACTOFERRIN

HCO3-

LYSOZYME

ACH

151
Q

Salivary innervation:

_________ increased acinar cell secretion and vasodilation of blood vessels surrounding the acini (results in protein rich and fluid/ion rich solution)

_________ increased acinar cell secretion (results in high protein/low fluid solution)

A

Parasympathetic

Sympathetic

152
Q

Slow or fast, or both?

Saliva contains less HCO3- → ?

Acinar secretions are isotonic → ?

Ductal cells absorb more Na+ → ?

Ductal cells absorb less Cl- → ?
Ductal cells secrete K+ → ?

A

Saliva contains less HCO3- → SLOW

Acinar secretions are isotonic → BOTH

Ductal cells absorb more Na+ → SLOW

Ductal cells absorb less Cl- → FAST

Ductal cells secrete K+ → BOTH

153
Q

Involuntary phase of swallowing begins at ____________

A

closing of epiglottis

154
Q

Spasmogen or relaxant:

Substance P → ?
VIP → ?
ATP → ?
Acetylcholine → ?
Nitric oxide → ?
A

Spasmogen or relaxant:

Substance P → Spasmogen
VIP → relaxant
ATP → relaxant
Acetylcholine → Spasmogen
Nitric oxide → Relaxant
155
Q

Stimulation of gastric acid secretin:
Neurocrine → ?
Paracrine → ?
Endocrine → ?

A

Stimulation of gastric acid secretin:

Neurocrine → ACh (M3 receptors)
Paracrine → Histamine (H2 receptors)
Endocrine → Gastrin

156
Q

Intestinal phase:

___________ enzymes secreted from __________ cells to break down proteins into AAs

_______ is generated by proton pumps and secreted by parietal cells

________ breaks down the a1-4 bond of amylose and amylopectin yielding maltotriose and glucose

A

Protease, Acinar

HCl

Amylase (not B-1,4)

157
Q

Intestinal phase

_______ cells produce bicarbonate solution to liquify and neutralized the _________ in the duodenum that has a low pH

Decreased intestinal pH stimulates release of the enzyme __________ which in turn drives bicarbonate release from the pancreas

A

Ductal, chyme

Secretin

158
Q

Duodenal detection:

Fats and AA in the intestine compete for the enzyme trypsin allowing for signaling by ________ and __________ to increase the release of _________ from duodenal I cells

______ then acts back on the pancreas to increase release of digestive enzymes into the duodenal lumen via relaxation of the __________

A

CCK-RF and Monitor Peptide, CCK

CCK, Sphincter of Oddi

159
Q

Duodenal detection:

This causes contraction of the __________ to facilitate the release of __________ which aids fat digestion and absorption

It also has a negative effect on _________ motility and __________ emptying

A

Gallbladder, bile

Gastric, gastric

160
Q

Salivary vs. Pancreatic

Myoepithelial cells → ?
ACh drives secretion → ?
Partially hormonally regulated → ?
Responds to blood flow → ?
Rich in KHCO3 → ?
A

Myoepithelial cells → salivary

ACh drives secretion → salivary and pancreatic

Partially hormonally regulated → pancreatic

Responds to blood flow → salivary

Rich in KHCO3 → salivary

161
Q

Fat absorption:

Primary bile acids are produced in the liver from __________

Secondary bile acids are formed by ___________ in the intestines and colon

Bile acids are complexed with glycine or taurine to make ____________

A

Cholesterol

Bacteria

Bile salts

162
Q

Bile is recycled during a meal by uptake in the _____________
-Mechanism mediated by _________

Dietary fats are broken down by _________ and ___________ lipase

__________ lipase hydrolyses triglycerides into FFAs

A

Distal ileum

enterohepatic circulation

Lingual and gastric

Pancreas

163
Q

Bile salts solubilize fats into _____________ and FFAs are transported into enterocytes

FFA are esterified into triglycerides bound to proteins such as apolipoproteins and exported out of the cells through __________ in the form of ___________

A

Micelles

Lacteals, chylomicrons

164
Q

Fat soluble vitamins such as ____________

While water soluble vitamins either use ______________ e.g. biotin or folic acid or are taken up via specific transporters e.g. ______________

A

ADEK

Simple diffusion, B12

165
Q

Iron absorption:

Mostly absorbed in the jejunum, ______ absorption is often linked with the transport of other dietary components

Intracellular concentration of _____ is made artificially high by the __________ pump

Secretion of ________ into the lumen draws water with it during secretory diarrhea

A

Na+

K+, Na+/K+

Cl-

166
Q

Severe diarrhea or dehydration can cause significant loss of ______ leading to cardiac dysrhythmia

Both ______ and __________ compete for absorption into enterocytes

A

K+

Mg2+ and Ca2+

167
Q

________ sphincter is closed to prevent reflux of bacteria

Opened by distention of the distal ________ (local reflex)

Closed by distention of the proximal ________ (local reflex)

The _______ has the lowest paracellular permeability to water in the GIT due to its role in solidifying waste

A

Ileocecal

Ileum

Colon

Colon

168
Q

_________ are muscles that run along the colon but are shorter than it

__________ folds allow expansion while supporting the weight of the digesta

The ___________ is a small pouch that give the colon its segmented appearance

The colon does not experience _______________ but rather mass movements which is a good thing

A

Taenia Coli

Semilunar

Haustrum

MMC

169
Q

Defecation:

Filling of the _________ with stool causes relaxation of the _________ anal sphincter

This is mediated via intrinsic neuron derived _________ and ______

A

Rectum, Internal

VIP and NO

170
Q

This causes automatic contraction of the ________ anal sphincter also known as ___________ reflex

Voluntary relaxation of the _______ anal sphincter and increased ________ pressure result in ___________

A

External, Rectoanal inhibitory

External, abdominal, defecation

171
Q

___________= intrinsic hepatotoxin

Causes confluent ________ necrosis in the_________ region (zone ?), with significant inflammatory cell infiltrate

One of the more common causes of __________

A

Acetaminophen

coagulative

centrilobular (zone 3)

acute liver failure

172
Q

Hepatitis A (main points from review sesh)

A

can be from EATING CONTAMINATED STRAWBERRIES

ONLY CAUSES ACUTE HEPATITIS

A and E are fecal/oral - vowels hit your bowels

173
Q

Hepatitis B (main points from review sesh)

A

Transmitted in blood/bodily fluids, vertical transmission
DNA virus

Progress to chronic liver disease in only a minority of adult infected patients

There is a vaccine

174
Q

Hepatitis C (main points from review sesh)

A

Transmitted by blood/bodily fluids

RNA virus

Most progress to chronic hepatitis

Diagnosis via anti-HCV abs or by serum HCV PCR

NO vaccine

Asymptomatic in acute infection, then can progress to chronic hepatitis 80-85% of time (only 20% then progress to cirrhosis)

175
Q 
Hepatitis D 
(main points from review sesh)
A

requires coinfection

176
Q

Hepatitis E

main points from review sesh

A

Fecal-oral

RNA virus

Higher mortality with pregnant women

Does not cause chronic disease in otherwise healthy people

177
Q

PAS-positive diastase resistant globules in hepatocytes

emphysema

what am I?

A

Alpha-1-antitrypsin

178
Q 
IgM
Anti-Mitochondrial abs
Mostly middle aged women
Female predominance
Granulomatous lymphocytic cholangitis/florid duct lesion

what am I?

A

Primary biliary cholangitis (cirrhosis)

179
Q

IgG

anti-smooth muscle antibody

Plasma cell rich interface and centrilobular hepatitis

female predominance

what am I?

A

Autoimmune hepatitis

180
Q

UC

large bile duct strictures

male predominance

cholangiography is a primary diagnostic test

presents with obstructive/cholestatic labs

what am I?

A

Primary sclerosing cholangitis

181
Q

tumor of bile ducts

malignant, gland forming (adenocarcinoma) tumor with marked desmoplasia

associated with PSC

malignant neoplasm of bile duct cells**

what am I?

A

Cholangiocarcinoma

182
Q

tumor of hepatocytes

malignant, thickened hepatic plates + trabeculae with unpaired arteries

occurs almost exclusively in cirrhosis

most common malignant primary hepatic tumor

what am I?

A

Hepatocellular carcinoma

183
Q

tumor of hepatocytes

benign

female predominance

normal hepatic plate thickness with unpaired arteries

associated with oral contraceptives

what am I?

A

Hepatocellular adenoma

184
Q

primary tumor of blood vessels, benign

most common benign hepatic tumor

what am I?

A

Hemangioma

185
Q

proliferation of hepatocytes
non neoplastic, benign

*central scar and malformed blood vessels

vascular malformation/anomaly etiology

what am I?

A

Focal nodular hyperplasia

186
Q

What is STAGE of cirrhosis?

A

amount of fibrous tissue deposition which tracks the progression of patient towards cirrhosis

Grade = amount of inflammation

DEMS (10 decks)

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