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GI Test 2 > Banderas Pharm > Flashcards

Banderas Pharm Flashcards

1
Q

Some antivirals target DNA polymerase. How do these drugs selectively target viral DNA polymerase instead of host DNA polymerase?

A

They’re not selective; instead, they take advantage of the much more rapid viral nucleic acid synthesis vs. host, so viral inhibition > host

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2
Q

Some viruses manifest symptoms only after most replication has already occurred. What is an appropriate antiviral therapy for these cases?

A

Chemoprohphylaxis

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3
Q

What stage of viral events do hepatitis drugs target?

A

Repilication

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4
Q

What forms of hepatitis do we have immunizations for?

A

A and B

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5
Q

When do we receive hep A vax?

A

At 12 months; 2 dose series

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6
Q

When do we receive hep B vax?

A

At birth; 3 dose series

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7
Q

If a baby is born to a mother who is HBsAg+, how do we prevent hep B infection in the infant?

A

Administer the first of the 3 dose Hep B series at birth, along with HBIG

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8
Q

What is given to a seropositive transplant patient to prevent hepatitis infection?

A

Nucleotide analog drugs for HBV and HCV

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9
Q

HBIG provides protection for how long?

A

3-6 months

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10
Q

A healthcare provider had pre-employment Hep B titers drawn and they came back at 9 milli-IU/mL. At work, they had an exposure to a patient with unknown Hep B status. What steps should be taken for the provider?

A

The provider should have completed a vaccine course before patient care, since titer needs to be 10+ to be considered immune.

The exposure to a patient with unknown status should be considered a positive exposure.

The provider should be given HBIG and their vax series should be completed.

They would be considered a “non-responder” if titer does not exceed 10 milli-IU/mL after 2 complete series are given.

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11
Q

How is Hep A treated?

A

Supportive therapy

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12
Q

Why are we unable to cure Hep B with current therapies?

A

Hep B has a relaxed circular DNA genome until entering hepatic cells, where it enters the nucleus and converts to a covalently closed circular DNA (cccDNA), which cannot currently be targeted.

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13
Q

What is a major difference between Hep B and Hep C that allows us to cure Hep C but not B?

A

Hep C (ssRNA+) replicates in the cytoplasm and does not establish latency.

Hep B converts to cccDNA when it enters the cell nucleus, and we are unable to target it.

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14
Q

How do we treat acute Hep B?

A

Usually we do not treat acute Hep B, as most (95%) patients will clear it naturally.

Some progress to chronic Hep B. Those we treat with nucleoside analogs.

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15
Q

What are the two classes of drugs that are used to treat chronic Hep B?

A

Peg-interferon or nucleoside analog drugs

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16
Q

Patients who are being started on immunosuppressants should be started on what kind prophylactic therapy to prevent chronic Hepatitis B?

A

Begin nucleoside analogs 1 week before starting immunosuppressants

Continue for one year after immunosuppressant therapy ends

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17
Q

What two types of patients receive prophylactic treatment with nucleoside analogs?

A

Patients undergoing immunosuppressive therapy

Seropositive patients undergoing liver transplant

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18
Q

Compare the pros and cons of peg-interferon and nucleotide analogs in the treatment of Hep B

A

Peg-intererons:
Pro: finite (but long, 48 week) course. No resistance because it does not target viral enzyme (instead bolsters immune response).
Con: Not well tolerated - more AEs; and subQ administration

Nucleotide analogs:
Pro: Well tolerated and easy PO administration
Con: Have to take indefinitely and reliably, and there is a risk of resistance because we’re targeting viral enzymes.

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19
Q

What is the (general) MOA of peg-interferon?

A

Targets host cells and acts similarly to cytokines, binding receptors to stimulate endogenous antiviral response; specifically, inducing interferon-specific genes.

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20
Q

What are the AEs of peg-interferon? What is its most limiting effect?

A
  • Flu like symptoms with each administration
  • Bone marrow suppression, leading to leukopenia or thrombocytopenia
  • Thyroid disease
  • ***CNS effects: depression, fatigue, seizures < this is the most limiting effect; some providers Rx antidepressants with peg-interferon
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21
Q

What is the target of the nucleot(s)ide analogs used to treat Hep B?

A

DNA polymerase in the relaxed circular DNA.

It does not target the cccDNA in the nucleus, which is why we need life-long therapy.

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22
Q

What enzyme mutates resulting in resistance to the nucleot(s)ide analogs used to treat Hep B?

A

DNA polymerase

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23
Q

What labs should be monitored while treating a patient with peg-interferon for Hep B?

A

CBC every few months
Thyroid panel every few months

*Monitor neuropsych effects

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24
Q

Patients on nucleot(s)ide analogs should be monitored for what metabolic AE?

A

Lactic acidosis

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25
Q

Tenofovir is available as TDF and TAF. What is a major difference between these?

A

Both require assessment of creatinine clearance at baseline.

TDF requires annual monitoring in patients with risk for renal impairment. It also requires bone density monitoring in certain patients.

TAF is better tolerated and only requires ongoing monitoring as indicated by symptoms; it has less nephrotoxicity.

26
Q

Name the nucleot(s)ide analogs used in treatment of Hep B.

A

Entecavir
Tenofovir (TAF** and TDF)
Adefovir - not preferred

(TAF is preferred between the tenofovirs)

27
Q

Patients born between what years should all be screened for Hep C?

A

1945 - 1965

28
Q

What Hep C genotype is most common in the US? What genotype(s) respond best to our treatment?

A

1 is MC in US

1 and 4 respond best

29
Q

What is the old regimen for treating Hep C?

A

Peg-interferon + ribavirin for 24-48 weeks.

30
Q

What is the current, general model for treating Hep C?

A

Interferon-free regimens: combination therapy of direct acting agents.

31
Q

Name the classes and associated suffixes of drugs used to treat Hep C.

A
  • previr = protease inhibitors
  • asvir = NS5A inhibitors
  • buvir = NS5B inhibitors
32
Q

Drugs with the suffix -previr have what MOA and indication?

A

The protease inhibitors (“-previr”) inhibit clevage of viral polyproteins so the viral replication complex cannot be formed.

It is used to treat Hep C.

33
Q

Drugs with the suffix -asvir have what MOA and indication?

A

The NS5A inhibitors (“-asvir”) inhibit viral replication machinery so new viral particles cannot be assembled.

It is used to treat Hep C.

34
Q

Drugs with the suffix -buvir have what MOA and indication?

A

The NS5B inhibitors (“-buvir”) inhibit replication/synthesis of viral RNA by shutting down RNA polymerase.

It is used to treat Hep C.

35
Q

What drug is sometimes used to supplement DAA therapy in the treatment of Hep C?

A

Ribavirin

36
Q

What are some important AE associated with ribavirin?

A

Hemolytic anemia: CBC should be taken at baseline and monitored throughout treatment
Teratogenic: Patients should not conceive while on ribavirin & 6 months after therapy ends

37
Q

Efficacy of ribavirin is closely associated with what two elements of treatment?

A

Dose and duration

The dose is weight-based

38
Q

Two patients have Hep C and have never been treated for it before. One has compensated cirrhosis and one has no cirrhosis. Both have genotype 1. In what way with their treatment regimens likely differ?

A

The patient without cirrhosis may be on an 8-12 week course.

The patient with cirrhosis will be on a 12 week course.

39
Q

We never use _____ to treat Hepatitis C.

A

Monotherapy. Always a combination of different classes of DAAs.

40
Q

Before starting treatment for Hep C, we should screen for …?

A

Hep B. Treating Hep C can cause a Hep B flare.

41
Q

What baseline labs should be ordered before initiation DAA therapy?

A

CBC
Renal fxn
Hepatic fxn
INR

–
Repeat the first 3 at four weeks; after that, order as appropriate if symptoms occur.

** You can remember these with the mnemonic RICH. Thanks, Kayla! :)

42
Q

Drugs with the suffix -previr have what AE when used in patients with existing cirrhosis?

A

Hepatic decompensation

43
Q

What are some AEs of DAAs?

A
  • Reactivation of Hep B
  • Deceased elimination of bilirubin –> jaundice
  • Protease inhibitors –> hepatic decomp in patients with existing cirrhosis
  • $$$
  • Drug interactions
44
Q

What is the first line treatment for ascites that is not causing respiratory distress of trouble ambulating?

A

Spironolactone + furosemide; monitor weight and urine output, want slow movement of ascitic fluid

45
Q

What is the MOA of the pharmacologic treatment for ascites?

A

Diuretics: prevent resorption of Na+ causing more Na+ to be lost in urine; water follows

46
Q

What is the treatment for refractory ascites? What are some AEs and how are they managed?

A

Paracentesis; performed when ascites causes respiratory distress or impaired ambulation

Draw >4L of fluid off abdomen

Can cause PICD: paracentesis-induced circulatory dysfunction (24-48 hours after paracentises, fluid starts moving out of vasculature back into abdomen). To manage this, give IV albumin to correct oncotic balance.

47
Q

What is a complication of chronic ascites that we discussed, and how is it treated?

A

Spontaneous bacterial peritonitis; high mortality rate. Often caused by E coli, Klebsiella, Staph or Strep.

If fluid shows PMNs > 250, start empiric cefotaxime (or ceftriaxone) and albumin

(after recovery, start prophylactic antibiotic - nofloxacin)

48
Q

What is the primary preventative treatment for a patient with esophageal varices?

A

Non-selective beta blockers: Propranolol or nadolol.

Start low, titrate to HR of 55-60 OR a 25% reduction of their baseline.

Remember that their liver disease = increased bioavailability of the B-blocker.

49
Q

After the patient has been stabilized and airway secure, what is the pharmacological therapy for bleeding esophageal varices?

A

Vasoconstrictors:
**Octreotide: mimics endogenous somatostatic, fairly specific for splanchnic vessels

Vasopressin is an older agent; not commonly used, causes more AE including renal dysfunction

Terlipressin - not in US, probably not on test

50
Q

Your patient presents with n/v, abdominal pain, and altered mental status. He has a history of EtOH abuse and examination reveals ascites, edema of the lower extremities, and hepatomegaly. LFTs are elevated.

What is the cause of the altered mental status, its pathophys, the tx we discussed, and its MOA?

A

Hepatic encephalopathy

Liver is unable to process ammonia (from byproducts of protein metabolism) –> urea for renal elimination.

Treat with Rifaximin or neomycin; these antibiotics kill off the gut bacteria that are responsible for metabolizing protein. Less protein metabolism = less nitrogenous byproduct, and therefore less ammonia.

Lactulose is also used; it is a disaccharide that gets metabolized by gut bacteria to various acids, lowing the gut pH and ion-trapping the NH3 as NH4+, allowing for elimination in stool.

51
Q

What is the MOA and indication of lactulose/lactilol?

A

Lactulose is used in hepatic encephalopathy; it is a disaccharide that gets metabolized to acids, lowering colon pH, converting NH3 –> NH4+, trapping it and allowing elimination in stool.

52
Q

What are some drugs commonly associated with DILI?

A 
Antibiotics, esp amox/clav and FQs
Antiepileptic drugs
Valproic acid
Acetaminophen 
NSAIDs
TNF-a, with or without methotrexate
Statins

Plus herbs/supplements

53
Q

What are some major differences between idiosyncratic DILI and intrinsic DILI?

A

Drugs that cause intrinsic DILI usually have predictable courses, fast onset, and are dose-dependent.

Drugs that cause idiosyncratic DILI are less related to dose, have variable courses or onset/latency, and only affect (rare) susceptible individuals.

54
Q

What is an R value and how is it calculated?

A

The R value is used to define hepatotoxicity injury patterns.

Hopefully we won’t actually have to calculate it BUT the formula is:

R = [ALT/ULN] / [AP/ULN]

If the denominator (AP) is elevated more significantly over it’s upper limit of normal, the R will be smaller.
If the numerator (ALT) is elevated more significantly, the R will be larger.

R < 2 indicates cholestatic injury pattern
R 2-5 = mixed pattern
R > 5 indicates hepatocellular injury

55
Q

RUCAM is a tool that helps assess what?

A

The likelihood of a causal connection between a drug and DILI
0 = excluded
3-5 = possible
>8 = highly probable

56
Q

When do we screen AST/ALT in patients on hepatotoxic drugs?

A

Baseline AST/ALT when beginning a potentially hepatotoxic drug is indicated. Many patients will have elevated results; anything <3x ULN is acceptable.

After that, only screen if there are symptoms (jaundice, B symptoms, etc)

57
Q

What is the indication and general MOA of cholestyramine?

A

Helps with pruritis associated with elevated bilirubin.

Works by binding cholesterol and bilirubin in the gut, increasing its excretion.

58
Q

What’s the most important thing that Banderas emphasized about DILI?

A

Documentation and counseling the patient. Don’t just list as an allergy. Specific DILI.

59
Q

What is the antidote for acetaminophen toxicity and what is its MOA?

A

N-acetyl cysteine (NAC)

Substitutes glutathione; helps eliminate the reactive intermediate in acetaminophen metabolism when the CYP450 pathway gets overwhelmed and endogenous glutathione is depleted.

60
Q

What are the timeline parameters for administering N-acetyl cysteine to a patient who is experiencing acetaminophen toxicity?

A

Must wait until at least 4 hours after ingestion to check serum levels.

At that point, refer to the Matthews-Rumack nonogram and assess the need for antidote.

If indicated, give immediately. If started 8-10 hours post exposure, good outcomes.

After 10 hours, 50% change of liver damage.
After 16 hours, pretty bleak.

GI Test 2 (2 decks)

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