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Therapeutics Y2 Sem 2 > Liver > Flashcards

Liver Flashcards

1
Q

Where is the liver located?

A

Right upper quadrant of the abdomen

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2
Q

What are the lobules of the liver?

A

connected by small ducts and centered on a branch of the hepatic vein

Portal Triads at the corner of adjacent lobules

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3
Q

What is the hepatic duct?

A

Transports bile produced by the liver cells to the gallbladder and duedenum

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4
Q

Liver cells can generate at what %?

A

About 70% of thel iver tissue can be destroyed before the body is unable to eliminate drugs and toxins via the liver

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5
Q

What is average blood flow to the liver?

A

25% of cardiac output so 1500mL of blood/flow/minute

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6
Q

Where does venous flow from the portal vein do?

A

Venous blood from the SMALL intesitne which absorbs nutrients, drugs, toxins and is direct to the liver

Pancreatic venous drainage

Spleen

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7
Q

Arterial flow in the from the hepatic artery does what?

A

Liver oxygenation

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8
Q

Venous flow out through teh hepatic vein

A

BLood from both the portal vien and hepatic artery mixes together in the sunisoids and exits the liver through the hepatic vein.

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9
Q

What is excreted the from tliver?

A

Bile

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10
Q

What under goes metabolism in the liver?

A

Billirubin, drugs, nutrients, hormones,

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11
Q

What is storred in the liver?

A

Vitamins/minerals (b12, Iron) CHO

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12
Q

what is synthesizedin the iver?

A

Plasma proteins such as albumin coagulation proteins and other tranpsort proteins

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13
Q

What is the purpose of the gallbladder?

A

Stores and concentrates bile

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14
Q

What is the function of Bile?.

A

Emulsification of Dietary fat, chol, vitamins

Elimination of waste excess chol, xenobioitcs and bilirubin

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15
Q

What is the end product of heme degreadation

A

Breakdown of RBC in spleen/liver

Insoluble (Bound t o albumin for transport to liver

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16
Q

What is bilirubin metbabolism?

A

Glucuronidated in liver
Excreted in bile

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17
Q

What are the general patterns of hepatocellular injury?

A
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18
Q

What are the etiological causes of hepatic injury?

A

Viruses
Drugs
Environmental toxins
Alcohol

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19
Q

What is cholestasis?

A

A failure of normal amounts of bile to reach the duodenum

Leads to accumulation of bile in liver cells and biliary passages

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20
Q

What causes Cholestasis?

A

– Cholelithiasis (gall stones) - most common
– Tumor, viral hepatitis, alcohol-related liver disease, drugs
– Primary biliary cholangitis (PBC), primary sclerosing
cholangitis (PSC)

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21
Q

What can cause Primary biliary cholangitis?

A
  • Caused by the slow, immune-mediated destruction of
    small bile ducts within the liver
  • Leading cause of liver transplant in women in Canada
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22
Q

What is primary sclerosing cholangitis?

A
  • Involves progressive inflammation and fibrosis affecting
    any part of the biliary tree
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23
Q

What does PSC lead to?

A
  • Leads to the progressive destruction of bile ducts
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24
Q

What is PSC commonly associated with?

A
  • Commonly associated with inflammatory bowel disease
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25
Q

What is cholestatic syndrome? Signs/Symptoms?

A
  • Pruritis
  • Jaundice
  • Dark Urine
  • Light coloured stools
  • Steatorrhea
  • Xanthoma and xanthelasma
  • Hepatomegaly
  • Features specific to disease
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26
Q

What is URSO?

A

Naturally occurring bile acid

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27
Q

What is the MOA of URSO?

A

decrease chol saturation

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28
Q

What is URSO used for?

A

– Gradual dissolution of stones in 30-40%
– Stones often recur after drug d/c

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29
Q

What is OCA Obeticholic acid

A

Alternative for PBC

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30
Q

What is URSO used for in tersm of chronic forms of cholestasis?

A

such as PBC or PSC

– Improves serum biochemical tests
– Limited efficacy in preventing disease progression in PSC

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31
Q

What are the drug treatments for Pruritis?

A

Cholestyramine *Most efficacious)
Antihistamines
Naltrexone
Rifampin sertraline

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32
Q

What are the causes of hepatocellular damage?

A

– Toxic agents: Alcohol, drugs, toxins
– Infections: Hepatitis
– Longstanding cholestasis
– Ischemic injury: Thrombosis
– Other Diseases (autoimmune, iron overload)

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33
Q

What does Hepatocellular damage depend on?

A

– Duration of assault (cells can regenerate)

– Intensity of assault (massive: fulminant hepatic failure vs
mild to moderate: hepatitis)

– Tremendous reserve capacity of liver

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34
Q

What happens when hepatoctes are destroyed?

A

– contents of cells are released into the circulation
– functional ability of the liver may be compromised (if
enough damage has occurred)

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35
Q

What liver enzyme measurements are released into circulation post injury?

A

– ALP, AST, ALT, GGT

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36
Q

What do the ALP, AST, ALT, GGT help us do?

A

– Helps to distinguish type of injury.
– Cholestatic
– Hepatocellular
– Other

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37
Q

What is the ALP test?

A

ALP (Alkaline phosphatase)
– Present in bile duct > hepatocytes
– High concentrations also found in bone

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38
Q

What is the GGT test?

A

GGT (Gamma glutamyl transpeptidase)
– All liver disorders
– Confirms hepatic origin of ALP
– Also: EtOH, pancreatitis, MI, COPD, renal

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39
Q

What is AST/ALT test?

A

Aminotransferases (AST, ALT)
– (aspartate aminotransferase, alanine
aminotransferase)
– ALT more specific than AST
– Poor correlation with severity, prognosis
– May be minimally elevated in cholestatic syndromes

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40
Q

What are the ABC tests for testing the synthetic capability of the liver?

A

Albumin, Bile, Clotting

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41
Q

What is the albumin level correlate/general information/

A

– Normal lifespan ~20 days
– Reduced after sustained assault
– Sx: edema, ascites
– Effects on calcium, highly bound drugs (phenytoin).
– Pre-albumin level

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42
Q

What is the bilirubin test?

A

Results of bilirubin retention leads to deposits in skin and tissues causing dark urine, pale stools, yellow skin

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43
Q

What causes Increased levels of bilirubin?

A

– Obstruction: Cholestasis
– Impaired metabolism: Hepatocellular
– Excessive production: e.g…….?

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44
Q

Unconjugated bilirubin is?

A

Bound to albumin, not soluble in water and measured as indirect

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45
Q

Conjugated Bilirubinemia is?

A

Conjugated by the liver, soluble in water, measured as direct

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46
Q

What is the clotthing prothrombin time?

A

Since the Liver synthesized coagulation factors (I, II, V, VII, IX, and X)

During states of liver damage we will this will lead to INR increases. 70% of liver capacity needs to be loss in order to see this change too.

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47
Q

Which Coagulation factor can be measured if we want to rule out Vitamin K deficiency?

A

Factor V

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48
Q

Generally what does AST correlate to?

A

RBC, Muscle, Liver

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49
Q

What does ALT correlate to?

A

Liver

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50
Q

What does ALP correlate to?

A

Liver Bone Placenta

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51
Q

What does GGT correlate to?

A

Liver*** This is very liver specific

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52
Q

Review the slide next

A
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53
Q

During hepatocellular and cholestatic describe the increases in ALP

A
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54
Q

During hepatocellular and cholestatic describe the increases in GGT

A
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55
Q

During hepatocellular and cholestatic describe the increases in AST

A
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56
Q

During hepatocellular and cholestatic describe the increases in ALT

A
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57
Q

During hepatocellular and cholestatic describe the increases in LDH

A
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58
Q

What is Cirrhosis?

A

A chronic diffuse disease characterized by fibrosis and
nodular formation

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59
Q

What does Cirrhosis result from?

A

continuous liver injury

– Ex: repeated acute liver injury in alcohol use disorder
– Takes a long time to develop

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60
Q

What happens to the liver in cirrhosis?

A

liver becomes hard, shrunken, and nodular
– Loss of normal structure and function
– Irreversible fibrosis (scarring)

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61
Q

What are the causes of liver cirrhosis?

A

Causes: alcohol, viral,
autoimmune, inherited,
drugs/toxins, Non-alcoholic fatty
liver disease, etc

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62
Q

What is non-alcoholic fatty liver disease?

A

Fatty liver disease that looks like it was alcohol induced

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63
Q

What is Non-alcoholic steatohepatitis

A

A disease that looks like alcohol disease but not caused by it. Instead more so related to insulin resistance.

Just more fatty liver then actual fatty liver

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64
Q

How much alcohol is required to cause liver cirrhosis?

A

women more susceptible then men, but once >5 drinks per day both men and women are at increased risk substantially

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65
Q

WHat is the diagnosing criteria for cirrhosis?

A

Biochemical markers

Fib-4 score

AST to platelet ratio index

Abdominal aultrasound

Elastrography

Liver biopsy

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66
Q

what are biochemical markers used for?

A

Screening

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67
Q

What is the Fib-4 score used for>

A

helps to estimate the amount of scarring in the liver/risk of
fibrosis using age, platelet count, AST and ALT

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68
Q

What is the AST to platelet ratio index used for>

A

Used to estimate liver fibrosis specifically in patients with
hepatitis C

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69
Q

What is the abdominal ultrasound used for?

A

generally the first imaging modality recommended when liver
disease is suspected

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70
Q

What is elastropgraphy?

A

Relatively new, non-invasive way to determine liver stiffness
– Measures propagation speed of mechanical waves through
liver parenchyma

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71
Q

WHat is the stage 2-3 fibrosis of a elastography indicate?

A

Stiffness = 7-11kPa

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72
Q

What is stage 4 fibrosis?

A

Cirrohiss >11-14kPa

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73
Q

What are the limitations of elastrography?

A

low reliability in patients with obesity, ascites and
artificially elevated stiffness due to severe liver inflammation or
steatosis

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74
Q

What is a liver biopsy and its role?

A

Rarely needed now for diagnosis

Still has a role in definitive diagnosis of underlying cause

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75
Q

what does liver cirrhosis result form?

A

Decreased funcitoning liver tissues and impaired function and diminished reserve

Portal hypertension too!

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76
Q

What is the prognosis of liver cirrhosis?

A

Patients will die in 5-15 years after dx of cirrhosis?

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77
Q

What is the treatment of liver cirrhosis?

A

– Of the specific disease
– Of the complications (bleeding esophageal varices, ascites,
encephalopathy)
– Liver transplantation

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78
Q

What is compensated Liver Cirrhosis?

A

Body may continue to function well/normal

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79
Q

What is decompensated liver cirrhosis?

A

– severe scarring & disruption of function

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80
Q

What are the symptoms of compensated liver cirrhosis?

A

Asymptomatic

Non-specific symptoms inclusive of: * Anorexia, weight loss, weakness, NV, GI upset, muscle
wasting
* LETs may be abnormal

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81
Q

What are the symptoms of decompensated liver cirrhosis?

A

confusion, edema, fatigue, bleeding

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82
Q

What are the abnormal lab functions of decompensated?

A

INR, albumin, bilirubin

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83
Q

What else may occur due to decompensated liver cirrhosis?

A
  • Signs of chronic liver disease
  • Portal HTN, ascites, varices, encephalopathy
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84
Q

What are the potential labratory presentations of cirrhosis?

A

– Hypoalbuminemia
– Elevated prothrombin time (PT)
– Thrombocytopenia
– Elevated alkaline phosphatase (ALP)
– Elevated aspartate transaminase (AST), alanine
transaminase (ALT), and γ-glutamyl transpeptidase
(GGT)
– Elevated bilirubin

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85
Q

What is the portal system?

A

Normally self-contained, low-pressure venous system

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86
Q

What is portal HTN

A

Results from increase in resistance to portal flow and
increase in portal venous inflow

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87
Q

What is splanchnic dilation related to?

A

Portal htn

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88
Q

What does RAAS do during Portal HTN?

A

Activate

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89
Q

What is the vicious cycle of portal hypertension?

A

End up with “back flow” of blood and widening of the
venous channels that connect the portal and
systemic circulation

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90
Q

What is splenomegaly?

A

Spleen enlarges 3-6x
– May be uncomfortable/painful to patient

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91
Q

What causes splenomegaly?

A

↑ sequestering and destruction of RBCs
– anemia
– thrombocytopenia

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92
Q

What are the 4 consequences of portal to systemic shunting?

A

– metabolites/toxins in the blood have not been processed
by the liver first

– ↑ sensitivity to noxious substances absorbed from the GI
tract (encephalopathy)

– malabsorption of fat in the stool (↓ bile flow)

– Contributes to all other complications as well: ascites,
SBP, varices, hepatorenal sx

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93
Q

What are noxious substances?

A

pollutants

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94
Q

Waht is ascites?

A

Collection of fluid in the peritoneal cavity

– Many liters may collect (up to 20L +)
– Can cause massive distension

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95
Q

What is the pathogenesis of asictes?

A

– Hydrostatic pressure
– Hypoalbuminemia (reduced oncotic pressure)
* Causes relative hypovolemia→aldosterone secretion in response
– Renal retention of Na+ and water

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96
Q

What is SAAG

A

serum-ascites albumin gradient

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97
Q

What does it mean if someones SAAG value is >11g/L?

A

indicates portal hypertension

  • Likely responsive to diuresis
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98
Q

What if someones SAAG value is <11g/L?

A

likely other causes (e.g. infection, malignancy
* Not typically responsive to diureses

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99
Q

If you have a total protein concentration of >25g/L and SAAG >11 what does this suggest?

A

Cardiac dysfunction as the etiology of ascites

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100
Q

What is the goal of ascites management?

A

Remove abdominal fluid and prevent sx ant maintain reasonable QOL

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101
Q

What are the management strategies of ascites?

A

– Salt restriction
– Diureses
– Paracentesis
– TIPS
– Liver Transplant

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102
Q

What is the generally flow of management of ascites?

A
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103
Q

What is TIPS?

A

Transjugular intrahepatic portosystemic shunt

Helps blood bypass diseased liver

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104
Q

What are the two medications used for diureses?

A

Spironolactone and furosemide

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105
Q

What is paracentesis?

A

– Aspiration of peritoneal fluid with a needle
– Large volume aspiration may result in “fluid steal” from
the vascular space
– Paracentesis + Albumin may be helpful
– May help ↓ discomfort
– Risk of abdominal perforation and infection

106
Q

What should be monitored with spironolactone therapy?

A

Hyperkalemia
Dehyrdation
Estrogen like side effects

107
Q

What are the drug interactions of spironolactone?

A

Digoxin levels may increase because of the excess in K

108
Q

What may occur when on Furosemide and Spironolactone therapy?

A

Hypovolemia

109
Q

What is the general dosing for spironolactone and furosemide?

A

100mg and 40mg po od

110
Q

What are the highest values that we can go up with spironolactone and furosemide?

A

400mg and 160mg

111
Q

What diuretic can be added with spironolactone and furosemide?

A

Metolazone

112
Q

Which drug may sub spironolactone?

A

Amiloride

113
Q

What should be monitored when on Spironolactone and furosemide?

A

SCr, Na, K, weight, BP

114
Q

What is refractory ascites?

A

Unresponsive to sodium-restricted diet and high-dose
diuretic treatment

  • (400 mg/day of spironolactone and 160 mg/day of furosemide)

Essentially occurs rapidly after occuring

115
Q

What is the treatment of Refractory Ascites?

A

– serial therapeutic paracentesis, (+/- albumin)
– transjugular intrahepatic portasystemic shunt (TIPS),
– or liver transplantation

116
Q

What is the goal of Ascites?

A

Gradual weight loss

Monitor creatinine serum Na and K frequently, Consider SBP

117
Q

What is Spontaneous bacterial peritonitis?

A
  • Infection in ascitic fluid without obvious cause
  • Thought to be from bacteria translocation (the passage of bacteria
    from the gut to the bloodstream and other extraintestinal sites,
    together with decreased host defenses
118
Q

What are the symptoms of Spontaneous bacterial peritonitis?

A

Fever, chills, abd pain, etc…

119
Q

What are the general mortality rates of SBP?

A

Very high so when individuals present to emerge with ascites they should be evaluated and tests should be performed

120
Q

When should we treat spontaneous bacterial peritonitis?

A

Empirically treat:
– Culture positive
– PMN >250/uL OR a high degree of suspicion for SBP (do not wait
for culture if you don’t have one)

Hence, TREAT ASAP

121
Q

What is the common treatment for community acquired SBP?

A

Cefotaxime of ceftriaxone for 5 days

122
Q

What si the common treatment for hospital acquired SBP?

A

Piperacillin/tazobactam
Meropenem+- Vanvomycin

123
Q

What are the clinical signs that infection has decreased?

A

PMN count decreased by 25% (polymorphonuclear leukocyte)

124
Q

Who should be considered for SBP prophylaxis?

A

pts having survived an episode of
SBP (secondary prophylaxis), or those at high risk (primary
prophylaxis)

125
Q

What is considered high risk for SBP prophylaxis?

A

low ascitic fluid total protein ascites or variceal
hemorrhage

126
Q

What is hepatorenal syndrome?

A

Renal failure in patients with severe liver disease

127
Q

How is Hepatorenal syndrome categorized?

A

Severe vasoconstriction of the renal
circulation

128
Q

What is the treatment of Hepatorenal syndrome?

A

Stop diuretics and avoid all potential nephrotoxins such as NSAIDS and aminoglycosides

129
Q

What is Varcies?

A

High pressure in portal vein
– Creates “bypasses” or shunts (collaterals)

Relatively small veins become engorged with an
excess of blood

130
Q

What are the principle sites of varices?

A

– Veins in rectal area (hemorrhoids)
– Abdominal wall (umbilicus)
– Esophageal varices

131
Q

How common are esophageal varices?

A

65% of patients with advanced cirrhosis

132
Q

What is the issue with esophageal varices?

A

High risk of recurrent hemorrhage and possible require prophylaxis

133
Q

What is the medical treatment for Variceal bleed?

A

– Adequate blood volume resuscitation

– Protection of airway from aspiration of blood

– Prophylaxis against SBP and other infections

– Control of bleeding

– Prevention of re-bleeding

– Preservation of liver
function/prevention of hepatic
encephalopathy
– Prevention of acute kidney injury

134
Q

What are the treatment strategies of variceal bleeding?

A

Packed red blood cells to help resuscitate blood volume

Abx prophylaxis for SBP

Octreotide or somatostatin (Vasoconstrictors)

135
Q

What is the prevention of variceal bleeding?

A

Propranolol and nadolol,, which are used. They are non-selective

136
Q

What is the dosing regimen of Nadolol and propranolol?

A
137
Q

What is the othern on-pharmacological prevention of varcieal bleeding?

A

Endoscopic variceal ligation

138
Q

What isthe secondary prophylaxis of Variceal bleeding prevention?

A

– Non-selective beta blocker + EVL
– TIPS for those who have re-bleeding despite therapy

139
Q

What is hepatic encephalopathy?

A

CNS dysfunction observed in late-stage cirrhosis

140
Q

What causes hepatic encephalopathy?

A

– Accumulation in the bloodstream of neurotoxic
substances that are normally removed by the liver
– MOA not entirely clear but a number of substances
have been implicated
* Ammonia
* Tryptophan
* GABA’ergic compounds

141
Q

What is the presentation of Encephalopathy?

A

Presentation variable

– Drowsiness, personality changes, confusion, motor sx’s
– Many sx are reversible with appropriate therapy
– Severity of sx is “graded”

142
Q

What is the txt of Encephalopathy?

A

Lactulose

143
Q

What are alternative therapies to Lactulose?

A

Metronidazole
Rifaximin

144
Q

Patients with cirrhosis often lack which vitamins?

A

ADEK (Fat soluble

145
Q

What vitamins need to supplemented due to nutrient deficiencies associated with heavy alcohol use?

A

B1, B6, and Folate

146
Q

What is asymptomatic Hepatitis generally associated with?

A

Elevated AST and ALT levels

147
Q

What is acute hepatitis symptoms?

A

flu-like symptoms, abdominal pain, jaundice, scleral
icterus, pale stools, dark urine

148
Q

What is acute fulminant hepatitis?

A

Rare but may be fatal

149
Q

What is chronic persistent hepatitis

A

Delayed recovery with minimal liver damage but failure to develop antibody

150
Q

What is chronic active hepatitis?

A

Progressive liver damage, failure to develop antibody, may be asymptomatic

151
Q

What is Hep A/

A

RNA virus that can be transmitted via fecal-oral route,

More likely to occur in travel to countries with higher rates or poor conditions and hygine

152
Q

Is Hep A vaccine?

A

Yes! havrix, Acaxim, Vaqta

153
Q

What is the general symptomalgy of Hep A?

A

Fever, jaundice, scleral icterus

Hepatomegaly upon physical examination

154
Q

How long do Hep A symptoms generally last?

A

3 months

155
Q

Is Sequelae of Hep a common?

A

No Fulminant hepatitis is rare

156
Q

Mortality of Hep A?

A

Low

157
Q

Is Hep A chronic?

A

No

158
Q

What is the treatment of HepA?

A

Supportive therapy, avoiding hepatotoxic drugs and Etoh

No clear pharm therapy

159
Q

What can be done to prevent hep a?

A

Vaccines

160
Q

What can be given post-exposure for prophylaxis?

A

Hep A vaccine 14 days within 14 days of exposure,

Immunoglobulin if patient is under 1 or vaccine unabailable

161
Q

What are the serological markers of Hep A?

A

Total anti-HAV
anti-HAV IgG
anti-HAV IgM

162
Q

What does Total anti-HAV mean?

A

Total IgG and IgM antibodies to HAV

May indicate acute, resolved infection or immunity

163
Q

What does anti-HAV IgG represent?

A

Immunity from vaccine or previous exposure (Life long protection)

164
Q

What does anti HAV IgM indicate?

A

Acute HAV infection

165
Q

What is HepB?

A

DNA virus that is transmitted either perinatal, sexual, or blood

166
Q

What is the prevention of HepB?

A

Vaccibes!

167
Q

What are the symptoms of HepB?

A

Young people will generally be asymptomatic, but older patients will be jaundice, dark urine, white stool, abdominal
pain, fatigue, fever, chills, loss of appetite, and pruritus possibly.

Mostly asymptomatic

168
Q

What are the serological markers of HepB? (All)

A

HBsAg
Anti-HBs
Anti-HBc total
Anti-HBc IgM
HBeAg
anti-HBe
HBV-DNA

169
Q

What are the three serological markers we should know for HepB?

A

HBsAg
Anti-HBs
HBV-DNA

170
Q

What is HBsAg?

A

Indicated HBV infection, acute or chronic

171
Q

What is Anti-HBs

A

marker of HBV
immunity; in cases where both HBsAg and anti-HBs are present, HBV
infection persists

172
Q

What is HBV-DNA?

A

a marker of viral replication/infectivity detectable at the
start of acute infection and used to assess and monitor the
treatment of chronic HBV infection

173
Q

When is screening recommended for HBV?

A

Once atleast when you are over 18

High risk groups

174
Q

What is the treatment of HBV?

A

Interferon or Nucleoside analogues

175
Q

What is the treatment goal of HepB treatment?

A

Permanent suppression/elimination of the virus and prevent cirrhosis, liver failure and hepatocellular carcinoma

176
Q

What is duration of therapy for IFN treatment of HepB?

A

16-48wk course, 30% successful in developing immunity

177
Q

What are the pros/cons of IFN treatment?

A
  • Shorter course of therapy
  • Absence of resistance
  • A chance at full seroconversion
178
Q

What are the cons of IFN treatment?

A

– Contraindicated in decompensated cirrhosis
* Increased risk of life-threatening infections and
possible worsening of hepatic decompensation
– Subcutaneous injection
– Many side effects!
* Influenza-like illness, emotional lability,
myleosuppressive effects, hyper/hypothyroidism

179
Q

What are the treatment outcomes of nuceloside analogues?

A
  • > 90% response, 10-15% success in developing immunity
    (40-50% seroconversion in 5 years, varies with agent)
180
Q

What are the advantages of nucleoside analogues?

A

– Safer
– fewer side-effects
– Po

181
Q

What are the disadvantages of Nuceloside analgoues?

A

– chronic therapy –
* endpoint is seroconversion + 12 months(durability
75%)
* This can take years and some may require
treatment indefinitely
– drug resistance

Renal dysfunction dose adjustment

182
Q

What are the nucleoside analogues used for HepB treatment?

A

Lamivudine
Adefovir
Tenofovir
Entecavir

183
Q

What is LAMIVUDINE MOA?

A

Pyrimidine nucleoside analogue inhibitor of HBV

184
Q

What is LAMIVUDINE generaly used for?

A

Prophylaxis

185
Q

What is LAMIVUDINE issue now a days?

A

Resistance

186
Q

What is Adefovir MOA?

A

Nucleotide analogue

187
Q

How is Adefovir used?

A

– Less potent & does not achieve viral suppression in most in
the first year (likely from low approved daily dose)

– Useful add on in lamivudine resistance

188
Q

What are the side effects of Adefovir?

A

Nephrotoxicity, hypophosphatemia

189
Q

What is Tenofovir MOA?

A

Theres 2 forms

▪ Tenofovir disoproxil fumarate (VIREAD )(TDF)
▪ Tenofovir alafenamide (VEMLIDY ) (TAF)

Many MOA

190
Q

What is Tenofovir usage?

A

Most poten with the lowest chance of resistance development

191
Q

What is Entecavir MOA?

A

Selective guanosine analogue and potent inhibitor of HBV DNA
replication

192
Q

What is the difference between TAF vs TDF?

A

TAF produces higher levels of TDF in the cells and can be administered in lower doses

193
Q

What is the benefit of Entecavir?

A

More effective than lamivudine but should not be used to
rescue in lamivudine resistance (as may confer resistance)

194
Q

When should combo therapy be used of HepB drugs?

A

People with cirrhosis who have resistance may have a flare,
which could be fatal

Lamiviudine+ Tenofovir for example

195
Q

What is HepC?

A

Single stranded RNA virus

196
Q

How is HepC transmitted?

A

Perinatal, sexual, blood

197
Q

Which of the transmission is highest?

A

Parenteral

198
Q

What is the symptomology of hepC?

A

Approximately 70% of patients are asymptomatic. If
symptoms occur, jaundice, dark urine, white stool,
abdominal pain, fatigue, fever, chills, loss of appetite, and
pruritus are possible.

199
Q

What is the Sequelae of HepC?

A

chronic disease (75%; 25% spontaneously resolve), cirrhosis,
hepatocellular cancer 5%,

Accelerated presentation when co-infected with HIV

estimated that 70% of those in sask are co-infected with HCV

200
Q

Which genotypes are most common in canada?

A

Genotype 1-6, 1a, 1b, 2, 3

201
Q

What are the serological markers of HCV?

A

Anti-HCG
HCV RNA

202
Q

What is anti-HCV?

A

(antibody to HCV): indicates infection, either acute
or chronic

203
Q

What is the issue with the anti-HCV test?

A
  • It may be negative during the first 6 weeks after exposure.
  • Needs additional HCVRNA to confirm an acute infection.
  • This test will remain positive for life despite clearance of infection.
204
Q

What is the HCV RNA Test?

A

(HCV RNA by polymerase chain reaction):
indicates virus replication activity; it appe

205
Q

What does the HCV RNA test mean?

A

Its presence indicates ongoing viremia whereas a negative result
indicates no active infection.

206
Q

How often should individuals we screened?

A

annually with an anti-
HCV; if previously successfully treated or spontaneously cleared
the infection, HCV RNA should be performed

207
Q

What was the traditional treatment of HepC?

A

Ribavarin and Interferon

208
Q

What is Harvoni drugs?

A

Ledipasvir and sofosbuvir

209
Q

Ledipasvir and sofosbuvir

A

Harvoni

210
Q

What are the side effects of Harvoni?

A

Mild to moderate fatique, headache, insomnia, nausea

211
Q

What is a limitation of harvoni?

A

Decreased absorption if administered with acid suppressing drugs (PPI)

212
Q

What genotypes does harvoni cover?

A

G1,4,5,6

213
Q

What is the drugs of Zepatier?

A

Grazoprevir and Elbasavir

214
Q

Grazoprevir and Elbasavir

A

Zepatier

215
Q

What is unique about Zepatier?

A

Studies targeting patients that are difficult to treat, or have
lack of data in literature(PWID, Renal) have been done

216
Q

What drug is added to Zepatier to cover G3 paitents?

A

Sofosbuvir

217
Q

What may occur when on Zepatier treatment?

A

Transient increase in ALT around 8 weeks and need monitoring

218
Q

What genotypes does Zepatier target?

A

G1, 4

219
Q

Who should avoid the use of Zepatier?

A

Decompensated Cirrhosis

220
Q

What are the drugs in Epclusa?

A

Sofosbuvir and Velpatasvir

221
Q

Sofosbuvir and Velpatasvir

A

Eclusa

222
Q

What are the cure rates of Epclusa?

A

99-100%

223
Q

What genotypes does Epclusa cover?

A

Pan-genotypic, some exceptions with G3 though

224
Q

What conditions may require Ribavirin+Epclusa?

A

Cirrhotic and G3 where it is resistance testing Y93H

225
Q

What drugs should be avoided when taking Epclusa?

A

Acid suppressing drugs

226
Q

What is the drugs composed of in Maviret?

A

GLECAPREVIR + PIBRENTASVIR

227
Q

GLECAPREVIR + PIBRENTASVIR

A

Maviret

228
Q

What is unique about Maviret in terms of treatment?

A

May be used in severe kidney failure (Even dialysis), and patients who receive a Hep C kidney transplant

229
Q

What are the special dosing recommendations of Maviret?

A

take with food

230
Q

What is the coverage of maviret?

A

All genotypes 1-6

231
Q

What is the drugs composed of in Vosevi?

A

SOFOSBUVIR + VELPATASVIR + VOXILAPREVIR

232
Q

SOFOSBUVIR + VELPATASVIR + VOXILAPREVIR

A

Vosevi

233
Q

What is the role of Vosevi?

A

Treatment failures

234
Q

When should Vosevi be avoided?

A

Decompensated cirrhosis

235
Q

What is the general treatment course of HepC drugs in general?

A

8-12 weeks

236
Q

Which drugs should we focus on?

A

Harvoni, Zepatier, Epclusa, Maviret, Vosevi

237
Q

What is the transmission of HepD?

A

Perinatal, sexual, blood

238
Q

What protect us from HepD infection?

A

Vaccines for HepB

239
Q

What is the treatment for HepD?

A

PEG INF for 12 months at standard dosing

240
Q

What is Hep E?

A

Transmitted via fecal-oral, high mortality for pregnant women otherwise patients fare very well

241
Q

What is the incidence of acute liver failure due to DIH?

A

50%

242
Q

What is the general pattern of injury of liver damage?

A

Hepatocellular
Cholestatic
Steatosis
Mixed

243
Q

What does Cholestatic mean?

A

Reduced bile development

244
Q

What does steatosis mean?

A

Fat build up in the liver

245
Q

What are the classifications of DILI?

A

By the damage generally

246
Q

How is DILI diagnoses?

A

Generally by a temporal relationship with drug use

247
Q

How would we identify DILI Hepatocellular?

A

– ↑ AST/ALT (preceds incr total bilirubin and ALP)
– Usually occurs w/in 1yr of starting drug
– Can result in fulminant hepatitis

248
Q

How would we identify DILI Steatonecrosis?

A

– ↑ synth of FA→hepatocytes engorged with FA, burst open
– Inflammation

249
Q

How would we identify DILI Fibrosis?

A

– Mild, chronic hepatitis→fibrosis→cirrhosis if drug not d/c

250
Q

How would we identify DILI Fibrosis?

A

– Prevents proper elimination of bile by liver→accumulation
– ↑ ALP

251
Q

What is the definition of hepatotoxicity>

A

ALT >3x the upper limit AND total bilirubin >2x the upper limit of norm

252
Q

How do we calculate R?

A
253
Q

What does an R value of >5 indicate?

A

Hepatocellular injury

254
Q

What does an R value of between 2-5 indicate?

A

Mixed

255
Q

What does an R value of <2 indicate?

A

Cholestatic injury

256
Q

What are the intrinsic causes of DILI?

A

direct hepatotoxin, which has inherent propensity to induce
injury in all individuals; dose dependent or time dependent &
reproducible

257
Q

What are the idiosyncratic causes of DILI?

A

causes injury in a small # of uniquely susceptible patients;
variable presentation
* further classified into allergic or non-allergic type

258
Q

What re the toxic doses of Acetampinophen in adults?

A

7.5g

259
Q

What are the toxic doses of acetaminophen in children?

A

> 150mg/kg

260
Q

What do we consider when DILI is suspected?

A

Considera ll sources

261
Q
A

Therapeutics Y2 Sem 2 (17 decks)

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