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CRRAB II- FINAL > Pharmacology- Regal/Trachte > Flashcards

Pharmacology- Regal/Trachte Flashcards

1
Q

What viral envelope protein binds to CD4 on host T-cells?

A

gp120

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2
Q

What are the co-receptors found on T-cells that the HIV virus also needs to bind?

A

CXCR4 (later) or CCR5 (early)

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3
Q

What host transcription factor binds to LTR and acts as a promoter for the HIV viral genome?

A

NFkB!!!!! is a transcription factor that binds to long terminal repeats and acts as a promoter for viral genes

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4
Q

CD4+ count less than what is considered AIDS?

A

less than 200

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5
Q

What is the main cause of reduced T-cells in HIV?

A

Provirus (envelope proteins inserted in host membrane) can bind to non-infected cells to induce autophagy

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6
Q

What is the difference between a nuceloside reverse transcriptase inhibitor and a nucleoTide reverse transcriptase inhibitor?

A

The nucleoside inhibitors require phosphorylation by cellular enzymes to the triphosphate form to be active

Happens in cytosol where RT is

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7
Q

Zidovudine

A

nuscleoSide reverse transcriptase inhibitor

competitively inhibits RT and terminates DNA production

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8
Q

Lamivudine

A

nuscleoSide reverse transcriptase inhibitor

competitively inhibits RT and terminates DNA production

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9
Q

Emtricitabine

A

nuscleoSide reverse transcriptase inhibitor

competitively inhibits RT and terminates DNA production

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10
Q

Abacavir

A

nuscleoSide reverse transcriptase inhibitor

competitively inhibits RT and terminates DNA production

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11
Q

Tenofovir

A

nucleoTide reverse transcriptase inhibitor

*already phosphorylated!!

competitively inhibits RT and terminates DNA production

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12
Q

What are the major toxicities of NRTIs?

A

Mitochondrial toxicity= lactic acidosis
Hepatic steatosis = fatty liver
Fat redistribution
Hyperlipidemia

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13
Q

Efavirnez

A

Non-nucleoside RT inhibitor

Binds DIRECTLY to RT (at a site distinct from the NRTI)

  • Does NOT require phosphorylation to be effective
  • No cross resistance with NRTIs
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14
Q

Etravirine

A

Binds DIRECTLY to RT (at a site distinct from the NRTI)

  • Does NOT require phosphorylation to be effective
  • No cross resistance with NRTIs
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15
Q

Atazanavir

A

Protease inhibitor

-Inhibits the protease responsible for post-translational cleavage of the Gag-Pol polyprotein (cannot fold properly).

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16
Q

Ritonavir

A

Protease inhibitor

-Inhibits the protease responsible for post-translational cleavage of the Gag-Pol polyprotein (cannot fold properly).

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17
Q

Darunavir

A

Protease inhibitor

-Inhibits the protease responsible for post-translational cleavage of the Gag-Pol polyprotein (cannot fold properly).

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18
Q

Enfuviritde (T-20)

A

Fusion inhibitor

Binds to gp41 (transmembrane envelope glycoprotein) and prevents conformational change so fusion with host does not occur

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19
Q

Raltegravir

A

Integrase inhibitor

Binds to integrase, and inhibits strand transfer (the final step for provirus integration)

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20
Q

Maraviroc

A

CCR5 antagonist

Binds specifically and selectively to host CCR5 (one of the co-receptors used by HIV to gain entry into the host cell)

**note will not work against HIV that utilizes CXCR-4
Resistance if HIV switches chemokine receptors

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21
Q

Why would you add a low does of ritonavir to an HIV regimen?

A
  • Ritonavir is a protease inhibitor that is poorly tolerated
  • It is used at lower doses to increase the serum concentrations of other protease inhibitors and decrease the dosage frequency of other protease inhibitors
  • POTENT INHIBITOR or CYP3A4 which is the cytochrome that metabolizes a number of other protease inhibitors and decreases their effectiveness
22
Q

Rifampin

A

Specifically binds to and inhibits mycobacterial DNA-dependent RNA polymerase

Blocks RNA synthesis/ transcription

Most active mycobacterial agent available- bactericidial activity against dividing and non-dividing M. tuberculosis with sterilizing activity

23
Q

Isoniazid

A

Blocks myobacterial reductase and inhibits mycolic acid synthesis (essential requirement for cell wall)

Prodrug that is activated my mycobacterial enzyme
Bactericidial
For latent and TB disease
Effects dividing cells

24
Q

Pyrazinamide

A

Exact MOA unclear

Prodrug with metabolite active only in acidic environments

More active against slowly replicating organisms

Hepatoxicity

25
Q

Ethambutol

A

Inhibition of arabinosyltransferases involved in cell wall synthesis

BACTERIOSTATIC!!!!
Provides synergy with other drugs
Least potent against M. tuberculosis among first line drugs

Ocular toxicity

26
Q

Streptomyocin/ Aminoglycosides

A

Inhibits protein synthesis by binding at site on 30S mycobacterial ribosome

Low level bactericidial activity
Administered only IV or IM
Used infrequently because of toxicity, inconvience, etc.

Ototoxicity, neuropathy, renal toxicity

27
Q

Pyridoxine

A

Vitamin B6! Supplemental

Should be given to all HIV pts being treated with isoniazid to reduced CNS & PNS adverse effects

28
Q

What are the four first-line drugs used for tuberculosis?

A

Rifampin
Isoniazide
Pyrazinamide
Ethambutol

29
Q

Which of the 4 first line drugs for tuberculosis is bacterioSTATIC?

A

Ethambutol

30
Q

Lispro Insulin

A

Rapid Acting insulin
Onset is 15 mins
Duration 3-5 hours

31
Q

Aspart Insulin

A

Rapid Acting insulins
Onset is 15 mins
Duration 3-5 hours

32
Q

What is the short acting insulin called?

A

Regular insulin
Onset 30 mins
Duration 4-8 hours

33
Q

NPH Insulin

A

Intermediate Acting
Onset 2-4 hours
Duration 10-20 hours

34
Q

Glargine Insulin

A

Long Acting
Onset 1-2
Duration 18-24 hours

35
Q

When is the peak of long acting insulin?

A

TRICKED YA!

Theres isn’t one!!!! Hehehehe

36
Q

Mannitol

A

Osmotic diuretic
Increases tubular fluid osmolarity
Increases urine flow

37
Q

Acetazolamide

A

Carbonic Anhydrase inhibitor
Acts in the PCT
Not used clinically

38
Q

Furosemide

A

Loop diuretic
Inhibits NKCC pump in thick ascending limb
Stimulates PGE release (vasodilatory affect on afferent arteriole)

39
Q

Bumetanide

A

Loop diuretic
Inhibits NKCC pump in thick ascending limb
Stimulates PGE release (vasodilatory affect on afferent arteriole)

40
Q

Clorthalidone

A

Inhibits NaCl reabsorption in the early CT

41
Q

Hydrochlorothiazide

A

Inhibits NaCl reabsorption in the early CT

42
Q

Spironolactone

A

Competitive aldosterone receptor antagonist

43
Q

Epleronone

A

Competitive aldosterone receptor antagonist

44
Q

Amiloride

A

Directly block ENaC Channel in principle cells of collecting duct

45
Q

Triamterene

A

Directly block ENaC Channel in principle cells of collecting duct

46
Q

How do the thiazide diuretics cause hyperglycemia?

A

Thiazide binds SUR on K+ channel and opens it

Leads to hyperpolarization of cell (Ca+ does NOT enter, NO increase in cAMP)

Prevents insulin secretion

NOTE* same MOA of how thiazides cause vasodilation to decreases systemic resistance and lower BP

47
Q

How does glucose binding to GLUT 2 normal cause insulin release?

A 
Glucose binds GLUT 2
Broken down into ATP
ATP blocks K+ channel
Leads to depolarization
Depolarization activates Ca+ channel
Ca+ enters cell- increases cAMP
Increased camp causes insulin stored in vesicles to be released!
48
Q

Demecocyclin

A

Antibiotic that has ADH antagonist properties

49
Q

Probenicid

A

Inhibits renal organic acid transporter to facilitate excretion of (excretes more uric acid, treatment for gout)

50
Q

Sulfinpyrazone

A

Inhibits renal organic acid transporter to facilitate excretion of (excretes more uric acid, treatment for gout)

51
Q

Colchicine

A

Microtubule inhibitor to treat gout

52
Q

Allopurinol

A

Xanthine oxidase inhibitor to treat gout

CRRAB II- FINAL (20 decks)

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