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Exam #3 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Describe the physiology of the RAAS?

A
  • short and long term blood pressure regulation
  • regulation of plasma volume
  • modulation of sympathetic NS
  • stimulates thirst
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2
Q

What is renin?

A
  • proteolytic enzyme produced from the JG cells

- regulates the formation of Angiotensin II

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3
Q

What endogenous chemicals cause increases in angiotensinogen synthesis?

A
  • insulin
  • estrogens
  • glucocorticoids
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4
Q

What is the relationship of renin and sodium intake?

A
  • increases in sodium will cause decreases in renin release
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5
Q

How is renin secretion controlled?

A
  • Intrarenal baroreceptor pathway - measures blood vol.
  • Macula densa pathway - increase NaCl flux across MD decreases renin release
  • Beta adrenergic receptor pathway - increases release
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6
Q

What are the feedback inhibition pathways?

A
  • Ang II stimulates AT1 receptors on JG cells to decrease renin release
  • Ang II increases BP which decreases renin release
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7
Q

What are the effects of Ang II?

A
  • increases total peripheral resistance - direct vasoconstriction, sympathetic activation
  • alters renal funciton - aldosterone release, constriction of renal arterioles, contraction of mesangial cells
  • ## alters cardiovascular structure (via AT1 receptor activation)
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8
Q

What is the mechanism of action of ACE inhibitors?

A
  • inhibits conversion of Ang I to Ang II

- inhibits degradation of bradykinin

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9
Q

What are the pharmacological effects of ACE inhibitors?

A
  • increases release of renin (without effect)
  • increases circulating Ang I
  • decreases aldosterone release
  • prevents/reverses remodeling of cardiovasculature
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10
Q

What are the pharmacokinetics of ACE inhibitors?

A
  • cleared renally
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11
Q

What are the therapeutic uses of ACE inhibitors?

A
  • hypertension
  • congestive heart failure
  • acute myocardial infaction
  • high risk cardiovascular events
  • diabetic nephropathy - reduces glomerular capillary pressure, delays disease progression
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12
Q

What are some adverse effects associated with ACE inhibitors?

A
  • hypotension at first does
  • cough
  • angioedema
  • hyperkalemia
  • acute renal failure (w/ pre-existing bilateral renal arterial stenosis)
  • never use in pregnant patients
  • antacids reduce the bioavailability
  • NSAIDS reduce efficacy
  • NSAIDS, potassium sparing diuretics and potassium supplements can lead to hyperkalemia
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13
Q

What is the mechanism of action of ARBs?

A
  • competitive antagonist of the AT1 receptor
  • high affinity for the AT1 over the AT2
  • inhibits aldosterone secretion
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14
Q

How are ARBs differing from ACE inhibitors?

A
  • ARBs reduce AT1 receptor activation more effectively
  • ARBs maintain the AT2 receptor beneficial effects from Ang II binding
  • ARBs should have no effect on bradykinin
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15
Q

What are the therapeutic uses for ARBs?

A
  • hypertension
  • Reno-protective in type 2 DM
  • congestive heart failure
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16
Q

What are the adverse effects associated with ARBs?

A
  • slight cough and rare angioedema
  • don’t give to pregnant patients
  • hypotension and renal failure in pts w/ RAS-dependent BP (renal artery stenosis)
  • hyperkalemia
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17
Q

What is the mechanism of action of direct renin inhibitors?

A
  • block conversion of angiotensinogen to Ang I
  • increase in renin in plasma due to no Ang II feedback
  • no effect on bradykinin
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18
Q

What are the therapeutic uses of direct renin inhibitors?

A
  • hypertension (alone or in combo)
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19
Q

What some adverse effects associated with direct renin inhibitors?

A
  • slight cough and rare angioedema
  • don’t give to pregnant patients
  • hypotension and renal failure in pts w/ RAS-dependent BP (renal artery stenosis)
  • hyperkalemia
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20
Q

What are the different drugs used to inhibit RAS function?

A
  • Angiotensin Converting Enzyme Inhibitors (cptopril, enalapril and enalaprilat)
  • Angiotensin Receptor Blockers (losartan)
  • Direct Renin Inhibitors (aliskiren)
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21
Q

What are the different classes of diuretic drugs?

A
  • Carbonic anhydrase inhibitors (acetazolamide)
  • Na-K-2Cl symport inhibitors (furosemide)
  • Na-Cl symport inhibitors (hydrochlorothiazide, chlorothiazide)
  • K-sparing diuretics - ENaC inhibitors (amiloride, triamterene), Aldosterone antagonists (spironolactone, eplerenone)
  • Osmotic diuretics (mannitol)
  • Vasopressin receptor antagonists (demeclocycline, tolvaptan)
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22
Q

What are the functions of the kidneys?

A
  • filter large quantities of plasma
  • maintain blood volume
  • maintain acid-base balance
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23
Q

What are the three components of the filter in the glomerular capillaries?

A
  • fenestrated capillary
  • basement membrane beneath the endothelial cells
  • filtration slit diaphragms
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24
Q

What is solvent drag?

A
  • solutes are flowing with filtered water
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25
Q

What are the characteristics of the proximal tubule?

A
  • 65% reabsorption of filtered Na

- highly permeable to water

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26
Q

What are the characteristics of the Loop of Henle?

A
  • Descending thin limb - highly permeable to water, low permeability to Na and urea
  • Ascending thin limb - permeability to NaCl and urea but not water
  • Ascending thick limb - actively reabsorbs NaCl and impermeable to water and urea
  • 25% of filtered Na is reabsorbed
  • Macula densa senses NaCl leaving the Loop
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27
Q

What is the significance of the Macula Densa?

A
  • senses NaCl leaving the Loop of Henle
  • when NaCl is high, constriction of the afferent arteriole of the nephron will occur
  • constriction of the afferent arteriole will protect from salt and volume wasting
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28
Q

What are the characteristics of the distal convoluted tubule?

A
  • actively transports NaCl
  • impermeable to water
  • “diluting segment of the nephron”
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29
Q

What are the characteristics of the collecting duct?

A
  • fine adjustments in electrolyte composition are made

- modulation done by aldosterone and ADH (modulating water permeability)

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30
Q

What are the seven mechanisms by which Na may cross the renal epithelium?

A
  • sovent drag
  • simple diffusion
  • channel-mediated diffusion
  • carrier-mediated diffusion
  • ATP mediated transport
  • symporters
  • antiporters
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31
Q

Describe renal handling of Cl?

A
  • reabsorption follows reabsorption of Na
  • occurs paracellularly in the proximal tubule and thick ascending limb of the Loop
  • occurs transcellularly in the proximal tubule, thick ascending limb, DCT and collecting duct
  • symport, antiport and Cl channels
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32
Q

Describe renal handling of K?

A
  • 80-90% reabsorbed in proximal tubule by diffusion and solvent drag
  • secreted in DCT and collecting duct (channel mediated)
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33
Q

Describe renal handling of Ca?

A
  • 70% is reabsorbed by proximal tubule by passive diffusion
  • 25% is reabsorbed by the thick ascending limb
  • 5% is reabsorbed in DCT
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34
Q

Describe renal handling of phosphate?

A
  • 80% reabsorbed by proximal tubule
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35
Q

Describe renal handling of Magnesium?

A
  • mainly reabsorbed in the thick ascending limb by a paracellular pathway due to a potential difference
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36
Q

Describe renal role in acid-base balance?

A
  • reabsorb HCO3 and secrete protons
  • substances not bound to protein are filtered
  • substances bound to proteins are actively transported into nephron
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37
Q

Why is it important to know medications effects on ion transporters in the nephron?

A
  • drug-drug interactions can occur because multiple drugs use same transporter (either for clearance or to get to activation site)
  • will decrease efficacy of drugs that must cross these transporters to get to site of activation (furosemide)
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38
Q

What are the main concepts of diuretic action?

A
  • disruption of sodium conservation (increase water excretion)
  • sodium transporters and channels are targets
  • will modify renal handling of other ions as well
  • the nephron will try and compensate by reabsorbing Na downstream (leads to loss of potassium)
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39
Q

What is the mechanism of action of the carbonic anhydrase inhibitors (CAIs)?

A
  • competitive inhibitor of carbonic anhydrase both within the cells and on the apical membrane
  • blocks formation of protons to be exchanged for the reabsorption of Na
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40
Q

What are the effects on the urinary electrolytes that are excreted?

A
  • increase in Na excretion
  • increase in K excretion due to compensation for the early loss of Na in the tubule
  • increase in HCO3 = decrease in urinary pH
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41
Q

What is the effect of CAIs on the macula densa?

A
  • increases NaCl passing the macula densa

- reducing GFR

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42
Q

What are the therapeutic effects of CAIs?

A
  • open angle glaucoma
  • altitude sickness
  • Epilepsy
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43
Q

How does acetazolamide treat altitude sickness?

A
  • makes the plasma more acidic which increases the breathing rate to try and bring back to homeostasis which will increase the amount of oxygen to the brain
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44
Q

What are the adverse effects of CAIs?

A
  • hypokalemia - due to renal compensation
  • urinary alkalization leading to renal stones, potassium wasting and worsen hepatic encephalopathy by diverting ammonia into systemic circulation
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45
Q

What is the mechanism of action of the Loop diuretics?

A
  • inhibit the Na-K-Cl symporter

- removes the potential across the epithelial cell stopping Ca++ and Mg++ reabsorption

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46
Q

What are the effects of Loop diuretics on the urinary electrolytes being excreted?

A
  • major increase in Na
  • increase in K
  • increase in Cl
  • no change in HCO3 excretion
  • increase in Ca++ and Mg++
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47
Q

How does a Loop diuretic effect renal blood flow?

A
  • stimulation of renin release leads to increase of RBF (GFR)
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48
Q

How is a Loop diuretic delivered to its site of action?

A
  • bound to proteins so it is not filtered

- passes through anionic transporters

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49
Q

What are the therapeutic uses for Loop diuretics?

A
  • Acute pulmonary edema (increasing venous capacitance)
  • Congestive heart failure (depleting volume)
  • Hypercalcemia (removing gradient)
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50
Q

What are some adverse effects of Loop diuretics?

A
  • hyponatremia and hypokalemia
  • hypocalcemia
  • ototoxicity - alteration in inner ear electrolytes
  • hyperuricemia
  • hyperglycemia
  • NSAIDs will reduce efficacy
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51
Q

What is the mechanism of thiazides and thiazide-like diuretics?

A
  • inhibition of the Na-Cl symporter

- weakly inhibits the carbonic anhydrase

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52
Q

What effect does thiazides have on urinary excretion of electrolytes?

A
  • increase Na
  • increase K - due to renal compensation
  • increase Cl
  • small increase in HCO3 - due to weak CAI
  • decreases excretion of Ca++
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53
Q

How is a thiazide drug brought to its site of action?

A
  • delivered via an anion transporter
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54
Q

What are the therapeutic uses of thiazides?

A
  • Hypertension
  • mild edema
  • Nephrogenic diabetes insipidus
  • Calcium nephrolithiasis and osteoporosis
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55
Q

What are some adverse effects of thiazides?

A
  • hypokalemia, hyponatremia
  • hyperuricemia
  • hyperglycemia and hyperlipidemia
  • erectile dysfunciton
  • NSAIDs will reduce efficacy
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56
Q

What are two types of Potassium sparing diuretics?

A
  • ENaC inhibitors (triamterene and amiloride)

- Aldosterone antagonists (spironolactone and eplerenone)

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57
Q

What are the mechanisms of action of ENaC inhibitors?

A
  • block Na reabsorption by blocking the Na channels on the apical side of the cell
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58
Q

What are the mechanisms of action of Aldosterone antagonists?

A
  • block cytosiolic mineralocorticoid receptors and reduces expression of the ENaC transporters
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59
Q

What are the therapeutic uses for potassium sparing diuretics?

A
  • prevent hypokalemia
  • Liddle syndrome and cystic fibrosis
  • primary hyperaldosteronism, hepatic cirrhosis, CHF
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60
Q

What are some adverse effects associated with potassium sparing diuretics?

A
  • hyperkalemia
  • gynecomastia, impotence, hirsutism, dicreased libido
  • metabolic acidosis
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61
Q

What is an example of an osmotic diuretic and where does it effect the nephron?

A
  • mannitol

- entire nephron length

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62
Q

What is the mechanism of action of osmotic diuretics?

A
  • increases the osmolality of tubular fluid
  • reducing passive reabsorption of NaCl in ascending lip of the Loop
  • inhibits the release of renin
63
Q

How does mannitol effect urinary excretion and renal hemodynamics?

A
  • increases all electrolytes being excreted

- increases RBF and maintains GFR

64
Q

How is mannitol used therapeutically?

A
  • minimize acute tubular necrosis

- reduces pre/post op CSF and intraocular pressure

65
Q

What are some adverse effects associated with osmotic diuretics?

A
  • contraindicated in heart failure and active cranial bleeding
  • flash pulmonary edema
66
Q

What are the effects of vasopressin (ADH)?

A
  • vasoconstriciton with V1a stimulation
  • increase Na and urea reabsorption transporters as well as the movement of aquaporins in the collecting duct (with V2)
  • net result is increased water retention and concentration urine
67
Q

What are some vasopressin receptor antagonists?

A
  • demeclocycline

- tolvaptan

68
Q

What is the mechanism of aciton of vasopressin receptor antagonists?

A
  • competitive antagonists of the V2 receptors

- increase water excretion without change in electrolyte excretion

69
Q

How is a vasopressin receptor antagonist used therapeutically?

A
  • hyponatremia associated with SIADH
70
Q

What adverse effects are associated with demeclocycline and tolvaptan?

A
  • demeclocycline - all tetracycline side effects and diabetes insipidus
  • tolvaptan - hyperglycemia
71
Q

Losartan

A
  • ARB
72
Q

Aliskiren

A
  • direct renin inhibitor
73
Q

Captopril, Enalipril, Enaliprilat

A
  • ACE inhibitor
74
Q

Acetozolamide and Methazolamide

A
  • Carbonic Anhydrase Inhibitors
75
Q

Demeclocycline and Tolvaptan

A
  • Vasopressin receptro antagonists
76
Q

Furosemide

A
  • Loop diuretic
77
Q

Chlorothiazid and Chlorothiadone

A
  • Na-Cl inhibitor
78
Q

Triamterene and amiloride

A
  • ENaC inhibitor
79
Q

Spironolactone and eplerenone

A
  • aldosterone antagonist
80
Q

Mannitol

A
  • osmotic diuretic
81
Q

What are some drugs that are used as anti-influenza medications?

A
  • amantadine
  • oseltamivir
  • zanamivir
82
Q

What are some drugs that are used as anti-herpes medications?

A
  • acyclovir
  • valacyclovir
  • ganciclovir
  • valganciclovir
  • cidofovir (with probenecid)
  • foscarnet
83
Q

What are some drugs that are used as anti-viral hepatitis medications?

A
  • interferon alpha
  • ribavirin
  • simeprevir
  • sofosbuvir
  • entecavir
84
Q

What are three general properties of antiviral drugs?

A
  • often have higher host toxicity than antibiotics
  • most are nucleosides, used to prevent replication of viral nucleic acids
  • they are predominantly virustatic and host immune system clears the infection
85
Q

What is the most effective approach to prevent influenza infection?

A
  • vaccination
86
Q

What is the mechanism of action of amantadine?

A
  • blocks influenza A M2 ion channel

- interferes with viral uncoating

87
Q

What are the pharmacokinetics of amantadine?

A
  • orally available and well absorbed in GI

- eliminated renally

88
Q

WHat are the therapeutic uses of amantadine?

A
  • not currently recommended because of resistance
89
Q

What are the adverse effects associated with amantadine?

A
  • lowers the seizure threshold
  • no use in pregnancy
  • interacts with anticholinergics
90
Q

What is the mechanism of action of oseltamivir?

A
  • competitive inhibitor of neuraminidase

- interferes with spread by preventing release

91
Q

What are the pharmacokinetics of oseltamivir?

A
  • orally available
  • metabolized in the liver
  • excreted by the kidneys
92
Q

What are the therapeutic effects of oseltamivir?

A
  • prevention/treatment of influenza A and B

- must be given with 48 hours of symptom onset

93
Q

What are the adverse reactions and degree of resistance for oseltamivir?

A
  • slight nausea and bomiting

- variable resistance in seasonal flu

94
Q

What are some characteristics of zanamivir?

A
  • neuraminidase inhibitor
  • low or bioavailability
  • inhalation administration - can cause bronchospasms
95
Q

What are the characteristics of HSV infection?

A
  • genital warts
  • infection in mouth
  • miningitis
  • encephalitis
96
Q

What are the characteristics of VZV infection?

A
  • chickenpox

- shingles

97
Q

What are the characteristics of CMV?

A
  • infects immunocompromised

- retinitis, lung and GI infection

98
Q

What is the drug type of acyclovir?

A
  • nucleoside analog for HSV and VZV
99
Q

What is the mechanism of action of acyclovir?

A
  • conversion by viral kinase into acyclo-GMP
  • conversion of acyclo-GMP by host kinase into acyclo-GTP
  • acyclo-GTP will cause chain termination by inhibiting viral DNA polymerase
100
Q

How does resistance develop for acyclovir?

A
  • viral kinase deficiency or mutation
101
Q

What are the pharmacokinetics of acyclovir?

A
  • orally effective with low bioavailability

- widely distributed and eliminated unchanged by kidneys

102
Q

What are the characteristics of valacyclovir?

A
  • it is a prodrug that increases the bioavailability
103
Q

What are the therapeutic uses of acyclovir?

A
  • HSV all infections
  • VZV can lessen the infection time
  • used for more severe cases
104
Q

What are the adverse effects associated with acyclovir?

A
  • neurotoxicity

- reversible renal dysfunction

105
Q

What type of medication is ganciclovir?

A
  • nucleoside analog for CMV
106
Q

What is the mechanism of action of ganciclovir?

A
  • converted by the viral kinase and then by host kinase and then inhibits viral DNA polymerase
107
Q

What are the pharmacokinetics of ganciclovir?

A
  • orally effective with low bioavailability

- eliminated unchanged in the kidneys

108
Q

What are the characteristics of valganciclovir?

A
  • increased oral bioavailability
109
Q

What are the therapeutic uses of ganciclovir?

A
  • restricted due to toxicity
  • treats CMV retinitis
  • prevention of CMV in transplant pts
110
Q

What are the adverse effects associated with ganciclovir?

A
  • myelosuppression (neutropenia, thrombocytopenia)

- CNS (fever, convulsions)

111
Q

What type of drug is cidofovir?

A
  • nucleotide analog for CMV
112
Q

What is the mechanism of action of cidofovir?

A
  • converted only by host kinase

- inhibits viral DNA polymerase

113
Q

What are the pharmacokinetics of cidofovir?

A
  • poor oral bioavailbility

- used with probenecid to increase efficacy

114
Q

What is the therapeutic use of cidofovir?

A
  • CMV retinitis in AIDS pts
115
Q

What are the adverse effects associated with cidofovir?

A
  • nephrotoxicity because of probenecid use
  • neutropenia
  • possible carcinogen
116
Q

What type of drug is forcarnet?

A
  • non-nucleoside analog for HSV and CMV
117
Q

What is the mechanism of action of forcarnet?

A
  • effective on all herpesviruses and HIV
  • inhibits herpes DNA polymerase
  • inhibits HIV reverse transcriptase
118
Q

What are the pharmacokinetics of forcarnet?

A
  • poor oral bioavailability

- most eliminated unchanged by the kidney

119
Q

What is the therapeutic effect of forcarnet?

A
  • only for drug resistant herpes viruses
120
Q

What are the adverse effects associated with forcarnet?

A
  • nephrotoxicity

- electrolyte disturbances (hypocalcemia)

121
Q

What are some characteristics associated with HCV?

A
  • considered curable because no genomic integration
  • no vaccine
  • major risk for hepatocellular carcinoma
122
Q

What is the standard treatment for HCV?

A
  • 24-48 week treatment with combination of interferon alpha and ribavirin
123
Q

What is the mechanism of action of Ribavirin?

A
  • broad spectrum against DNA and RNA viruses
  • converted by host kinases
  • depletes GTP pools within cells
  • unknown causing lethal mutations in RNA viruses
124
Q

What are the pharmacokinetics of Ribavirin?

A
  • given orally or inhalation
  • high Vd and long half life
  • eleminated by hepatic metabolism and renal excretion
125
Q

What are the therapeutic uses of Ribavirin?

A
  • in fixed dose with INF alpha for HCV

- pediatric RSV brochiolitis and pneumonia

126
Q

What are the adverse effects associated with Ribavirin?

A
  • hemolytic anemia

- contraindicated during pregnancy

127
Q

What is the mechanism of action of INF-alpha2a?

A
  • not directly acting on viral proteins
  • activates Jak-STAT signalling to increase immune response to stop viral replication
  • stimulates MHC class I and II
128
Q

What are the characteristics of pegylated INF-alpha2a?

A
  • interferon attached to large polyethylene glycol

- increases the half life

129
Q

What are the pharmacokinetics of INF-alpha2a?

A
  • well absorbed in SC or IM injection

- pegylation increases serum concentration and prolongs duration

130
Q

What are the therapeutic uses for INF-alpha2a?

A
  • chronic HCV and HBV in combo with other drugs
  • genital warts associated with HPV
  • cancers - Kaposi’s, lymphomas, melanoma
131
Q

What are some adverse effects associated with INF-alpha 2a?

A
  • Flu-like syndrome
  • Neuropsychiatric - depression
  • Myelosuppression
132
Q

What type of drug is simeprevir?

A
  • direct acting antiviral for HCV
133
Q

What is the mechanism of action of simeprevir?

A
  • inhibits viral protease

- analogous to HIV protease inhibitors

134
Q

What are the pharmacokinetics of simeprevir?

A
  • given in combo with ribavirin/INF

- metabolized by CYP3A4

135
Q

What are the adverse effects associated with simeprevir?

A
  • photosensitivity and rash

- contraindicated in pregnancy

136
Q

What type of drug is sofosbuvir?

A
  • direct acting antiviral for HCV
137
Q

What is the mechanism of action for sofosbuvir?

A
  • nucleotide prodrug metabolized to inhibit viral RNA polymerase
138
Q

What are the pharmacokinetics of sofosbuvir?

A
  • in combo with ribavirin and INF

- efficacy across all HCV genotypes and low resistance

139
Q

What are some characteristics of HBV?

A
  • DNA virus that integrates into host genome
  • vaccination available and effective
  • therapy used for persistant elevated serum ALT and HBV DNA
140
Q

What are the treatment options for HBV?

A
  • Pegylated INF
  • entecavir
  • Tenofovir
  • Lamivudine
141
Q

What is the mechanism of action of Entecavir?

A
  • converted by host cell kinase

- inhibits HBV DNA polymerase

142
Q

What are the pharmacokinetics of entecavir?

A
  • orally available

- excreted unchanged in urine

143
Q

What are the therapeutic uses of entecavir?

A
  • first line treatment for chronic HBV (administered for 1 year)
  • not active against HIV
144
Q

What are the adverse effects associated with entecavir?

A
  • risk of lactic acidosis and hepatomegaly when fatty liver
145
Q

What drugs are classified as nucleoside revers transcriptase inhibitors?

A
  • zidovudine
  • lamivudine
  • emtricitabine
  • tenofovir
146
Q

What drugs are classified as non-nucleotide revers transcriptase inhibitors?

A
  • efavirenz

- nevirapine

147
Q

What drugs are classified as protease inhibitors?

A
  • lopinavir/ritonavir

- atazanavir

148
Q

What drugs are classified as integrase inhibitors?

A
  • raltegravir
149
Q

What drugs are classified as fusion inhibitors?

A
  • enfuvirtide

- maraviroc

150
Q

What are the goals for antiretroviral treatment?

A
  • maximal suppression of plasma HIV RNA
  • restoration and/or preservation of immune function
  • limitation of drug adverse effects
  • reduction in HIV-associated morbidity and mortality
151
Q

What are the antiretroviral treatment guidlines?

A
  • treatment recommended for all symptomatic and asymptomatic HIV infected patients
  • a 3 drug regimine is the minimum standard of care
  • therapeutic failure is an increase in viral load
  • treatment failure requires initiation of a completely new regimen
152
Q

What are some consequences of antiretroviral therapy?

A
  • lifelong therapy
  • HIV lipodystrophy syndrome
  • complex pharmacokinetics with drug associations
  • immune reconstitution inflammatory syndrome
153
Q

What is IRIS?

A
  • reversal of immunodeficiency in pts with low CD4 counts
  • usually occurs in initial treatment phase
  • usually due to opportunistic infection with an accelerated inflammatory reaction

Exam #3 (9 decks)

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