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Drugs COPY Flashcards

1
Q

How do the M odd receptors work?

A

M1, 3, & 5 (Modd): ­increased intracellular Ca2+ (Gq)

  • Activation results in stimulation of phospholipase C → PIP2 hydrolysis to IP3 (which acts on SR to increases [Ca2+]i) + DAG → DAG activates PKC to open Ca2+ channels on sarcolemma
  • ­increased intracellular Ca2+ increases muscle contraction via MLCK
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2
Q

How do the M even receptors work?

A

M2 & 4 (Meven): hyperpolarizes the cell (Gi)

activation results in inhibition of cAMP synthesis → causes K+ efflux which hyperpolarizes the cell

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3
Q

How can adrenergic transmission be terminated?

A

Termination of Adrenergic Transmission:

  • Reuptake: accounts for about 60%. NE, EPI transported back into nerve terminal. Inhibited by cocaine and drugs used for depression
  • Diffusion: accounts for about 20%. NE, EPI diffuse away from synaptic cleft
  • Metabolism: accounts for 20%. NE, EPI metabolized to inactive compounds (COMT & MAO)
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4
Q

How do alpha1 receptors work?

A

a1: increased ­intracellular Ca2+(Gq) by increased DAG and IP3

  • Vasoconstriction (BP increased­)
  • On smooth muscle of vessels, eye, and GI/urinary sphincters
  • Smooth muscle contraction by stimulating phospholipase C and Ca2+
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5
Q

What do alpha 2 receptors do?

A

a2: decreased cAMP (Gi), decreased Norepinephrine release (autoreceptor)

  • presynaptic nerve terminals and modulate nerve activity
  • inhibit cAMP synthesis; inhibits neuron activity by causing K+ efflux which hyperpolarizes the cell
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6
Q

What do beta 1 receptors do?

A

b1: increased ­cAMP (Gs), ­increased HR, ­increased Myocardial contractility

  • Found in heart; activation leads to increased ­contraction increased heart rate; causes renin secretion and lipolysis
  • coupled to Gproteins; increases ­adenylyl cyclase and cAMP
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7
Q

What do beta 2 receptors do?

A

b2: ­increased cAMP (Gs),

  • Vasodilation (non-innervated b2) lowering BP, bronchodialation
  • located on most tissues; activation leads to relaxation of smooth muscle (uterus, GI, bladder)
  • ­increased cAMP → activates PKA → phosphorylates MLCK, preventing it from phosphorylating myosin → decreases contraction
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8
Q

What do beta 3 receptors do?

A

b3: ­increased cAMP (Gs), ­increased lipolysis

  • least defined, but present on adipocytes; cause lipolysis coupled to Gproteins; ­increased adenylyl cyclase and cAMP
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9
Q

What are the side effects for muscarinic agonists?

A

Muscarinic Agonists:

  • Overall: “SLUD” (salivation, lacrimation, urination, defication) + hypotension / bronchoconstriction
  • Eyes: pupillary constriction (miosis)
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10
Q

What are the side effects for muscarinic antagonists?

A

Muscarinic Antagonists:

  • “Red as a beet, dry as a bone, blind as a bat, and mad as a hatter” (opposite of SLUD)
  • Eyes: mydriasis (relaxation causes wide pupils) and dry eyes
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11
Q

List some muscarinic agonists and antagonists and what are they used for?

A

Agonist: muscarine, nicotine, varenicline

Antagonist: atropine (treat bradyarrhythmias), ipratropium/tiotropium (treat asthma/COPD)

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12
Q

For Norepinephrine:

  • What is the receptor specificity?
  • What effect does it have/what is it used for?
A
  • alpha1 = alpha2 > beta1 > beta2
  • increases blood pressure
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13
Q

For Epinephrine:

  • What is the receptor specificity?
  • What effect does it have/what is it used for?
A
  • beta1 = beta2 > alpha1 = alpha2
  • increases HR
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14
Q

How does the reflex response occur for norepinephrine?

A

alpha1 and alpha2 stimulation causes BP to increase, causing baroreceptors to fire more, decreasing CNS response, leading to decrease in HR…beta1 stimulation causes increase in HR… overall neutral response

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15
Q

List some of the alpha1 agonists (3).

A

Phenylephrine, midodrine, methoxamine

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16
Q

For Phenylephrine, midodrine, methoxamine:

  • What action do they have?
  • What receptor do they act on?
A

Vasoconstriction leading to increased ­ BP

alpha1

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17
Q

How does the phenylephrine reflex response with baroreceptors work?

A

alpha1 stimulation causes BP to increase, causing baroreceptors to fire more, decreasing CNS response, leading to decrease in HR… overall decreased HR

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18
Q

What is the mechanism of action of psuedoepherine? What does it lead ot?

A

Vasoconstriction leading to ­increased BP

  • INDIRECT AGONIST: Stimulate release of pre-formed catecholamines, indirectly stimulating alpha1 receptor
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19
Q

List two alpha2 agonist drugs.

A

Clonidine and Methyldopa

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20
Q

How does clonidine work?

And what receptor does it act as an agonist for?

What happens if the drug is stopped abruptly?

A
  • Alpha 2
  • Blocks synthesis of catecholamines and hyperpolarizes cell to prevent depolarization
  • Chronic low [NE] release leads to upregulation of alpha 1 receptors (post-synaptic)
  • If drug is stopped abruptly, can lead to hypertension crisis because upregulated post-synaptic receptors will pick up the catecholamines that are being released
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21
Q
  • How does methyldopa work?
  • What are some physiological effects related to this drug?
A
  • PRODRUG analog precursor that is metabolized by the same enzymes as dopamine
  • Displaces norepiphrine and dopamine synthesis because it uses same enzymes.
  • Has higher affinity for receptor than NE, giving rise to negative feedback preventing synthesis of NE
  • Parkinsonian symptoms (tremors)
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22
Q

For Isoproterenol:

  • what is the receptor specificity?
  • What are the basic effects?
A
  • Beta1 = Beta2
  • Decreased BP and increased HR
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23
Q

How does the basoreceptor reflex work for isoproterenol?

A

beta2 stimulation causes BP to drop, causing baroreceptors to fire less, allowing CNS to reflexively increase HR…beta1 stimulation causes increase in HR… overall HR is doubly increased

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24
Q
  • What receptor does dobutamine work on?
  • What effect does dobutamine have?
  • What occurs with chronic use of beta agonists?
A
  • Beta1
  • Increases HR
  • Chronic use of beta-agonists will lead to downregulation of receptors
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25
Q

How does the basoreceptor reflex work for dobutamine?

A

Beta1 stimulation causes no change to BP, causing no response by baroreceptors… overall HR increase

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26
Q
  • What receptor does albuterol (short-acting)/salmeterol (large-acting) work on?
  • What effect does it have?
  • What are some physiological effects?
A
  • beta2
  • decreased BP; Vasodilation and bronchodialation
  • Increased blood flow due to smooth muscle relaxation causes hyperglycemia and tremors
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27
Q

Name three alpha antagonists.

A

Phentolamine

Phenoxybenzamine

Prazosin

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28
Q

For Phentolamine:

  • IV or oral? Fast or slow?
  • What is the receptor specificity?
  • What is its MOA?
  • What is it used for?
  • What is a big side effect of the drug?
A
  • IV and short acting (QUICK)
  • alpha1 = alpha2 ANTAGONIST
  • MOA: Competitive inhibitor
  • Hypertensive crisis
  • Reflex tachycardia due to resulting decreasing BP
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29
Q

For Phenoxybenzamine:

  • IV or oral? Fast or slow?
  • What is the receptor specificity?
  • What is its MOA?
  • What is it used for?
  • What is a big side effect of the drug?
A
  • Irreversible non-competitive inhibitor
    • Oral - slow
    • alpha 1 = alpha 2 ANTAGONIST
    • MOA: irreversible noncompetitive inhibitor
    • Use: Hypertensive crisis
    • Reflex tachycardia due to resulting decreased BP.
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30
Q

For Prazosin** and any other **-osin drugs:

  • What is the receptor specificity?
  • What is the use?
  • What is a possible side effect
A
  • Alpha1 Antagonist
  • Used for prostatic hypertrophy
  • Reflex tachycardia
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31
Q

Name 4 beta antagonists.

A

Propanolol

Metoprolol

Labetolol

Carvedilol

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32
Q

For propanolol:

  • What is the receptor specificity?
  • What are some possible physiological effects (2)?
  • What are some side effects?
A
  • Beta 1 = beta 2 antagonist
  • Effects
    • Negative inotropic (contractility) and chronotropic (HR) actions
    • Blocks renin release
  • Side Effects
    • Slows AV node firing
    • Crosses blood brain barrier - CNS effects (vivid dreams, depression, decreased libido)
    • Inhibits glycogenolysis
    • Vasoconstriction
    • Bronchoconstriction
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33
Q
  • What receptor blockage is specific for slowing of AV conduction?
  • What receptor blockage is specific for inhbiting glycogenolysis?
  • Bronchoconstriction?
  • Vasoconstriction?
A
  • slowing of AV conduction: Beta1
  • inhibition of glycogenolysis: Beta2
  • Bronchoconstriction: Beta2
  • Vasoconstriction: Beta2
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34
Q

For metoprolol:

  • What is the receptor specificity?
  • What is it used for?
  • What is a physiological effect?
A
  • Beta1 selective Antagonist (little beta2 activity)
  • Slows HR and therefore cardiac output is decreased
  • Bradycardia
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35
Q

For Labetolol and Carvedilol:

  • What is the receptor specificity?
  • What is it used in?
  • Is there a reflex tachycardia present? Why or why not?
A
  • Beta1 = beta2 > alpha1 = alpha2 antagonist
  • used in hypertensive crises and in heart failure
  • Does NOT have reflex tachycardia because beta1 is blocked
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36
Q

How are most beta blockers excreted and why is this important?

A

Most beta blockers are excreted via the liver, making it likely that they have drug interactions due to biotransformation by P450 enzymes.

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37
Q

Outline the process from the baroreceptors to renin to aldosterone release.

A
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39
Q

With aldosterone release or inhibition, how can you get hyperkalemia?

  • Outline what occurs to Na+, H2O, K+ with Aldosterone.
  • Without aldosterone?
A
  • Normal: with aldosterone → increased expression of Na+ and Na+/K+ ATPase channels
  • Abnormal: without aldosterone → decreased expression of Na+ and Na+/K+ ATPase channels → excretion of Na+ and retention of K+ and H+ → hyperkalemia and metabolic acidosis
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40
Q

What 5 things causes renin release?

A
  • Renin release is stimulated by:
    • Sympathetic activation
    • Low pressure in renal vasculature
    • Sodium diuresis
    • Decreased blood volume
    • Decreased renal blood flow
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42
Q

In the renin-angiotensin-aldosterone system, what are the 4 classes of drugs used to reduce BP?

A
  • Angiotensin Converting Enzyme (ACE) Inhibitors
  • Angiotensin Receptor Blockers (ARBs)
  • Direct Renin Inhibitors
  • Aldosterone Receptor Antagonists
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43
Q

For Angiotensin Converting Enzyme (ACE) Inhbitors:

  • What are three important drugs to know?
  • What is the MOA?
    • What is a secondary MOA that occurs with ACEI’s?
  • What are three side effects?
  • What are 5 main advantages?
A
  • Lisinopril**, Enala_pril, Captopril_**
  • MOA: Prevents conversion of ATI to ATII, reducing peripheral resistance (ATII causes vasoconstriction)
    • Bradykinin (vasodilator) is inactivated via ACE
    • ACEI: by blocking ATII synthesis and bradykinin inactivation, you get a double whammy of decreasing BP
  • Side Effects:
    • Cough/angioedema
    • Decreases renal function
    • Hyperkalemia
      *
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44
Q

For Angiotensin Converting Enzyme (ACE) Inhbitors:

  • What are three side effects?
  • What are 5 main advantages?
A

Lisinopril, Enalapril, Captopril

  • Side effects
    • Cough/angioedema
    • Decreases renal function
    • Hyperkalemia
  • Advantages
    • No effects on HR
    • No reflex actions of the sympathetic nervous systme
    • Prevents stroke
    • Beneficial in HF
    • Slow progression of kidney disease
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45
Q

For Angiotensin Receptor Blockers:

  • What are three drug names?
  • MOA?
  • What are two side effects?
  • What is the main advantage?
A
  • Losartan, Valsartan, Olmesartan
  • MOA
    • angiotensin I receptor inhibitors
    • antagonizes angiotensin II through actions at angiotensin I receptor
  • Side Effects
    • decreased renal funtion
    • hyperkalemia
  • Advantage
    • Better tolerated than ACE inhbitors
      • Less likely to cause cough/angioedema
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46
Q

For direct renin inhbitor:

  • What is a drug?
  • What is the MOA?
  • What are three side effects?
  • What is a minor advantage?
A
  • Drug: Aliskiren
  • MOA: inhibits renin
  • Side effects: diarrhea, cough, angioedema
  • Advantage: Can be tolerated better
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47
Q

For aldosterone receptor antagonists:

  • Name two drugs.
  • What is the MOA?
  • What are three side effects?
  • What is an advantage of one of the drugs compared to the other?
A
  • Spironolactone, eplerenone
  • MOA: Inhibits aldosterone receptor → increases Na+ excretion (and H2O) and conserves K+
  • Side Effects:
    • For Spironolactone: Hyperkalemia, Metabolic acidosis, sexual dysfunction
    • Advantage of Eplerenone: ONLY hyperkalemia
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48
Q

All renin, angiotensin, aldosterone system drugs are contraindicated in what two situations and why?

A

All drugs are contraindicated in:

  • Renal artery stenosis (because it blocks ATII from causing vasoconstriction → decreases perfusion pressure through glomeruli)
  • Pregnancy
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49
Q

In the renin, angiotensin, aldosterone system drugs: What are the two main prodrugs to know and what class of drug are they?

  • What is different about prodrugs?
A
  • Enalapril: ACE Inhibitor
  • Olmesartan: ARB (Angiotensin receptor blocker)

Must be metabolized before and therefore has a shorter half-life

50
Q

Hydrachlorothiazide/chlorthialidone

MOA?

A

MOA

  • Inhibit Na+/K+/Cl-/H+ reabsorption in the distal tubule by inhibiting Na+/Cl- symporter → increased excretion of water → lowers BP
  • Stimulates Ca++ reabsorption
51
Q

Hydrachlorothiazide/chlorthialidone

Side Effects?

A
  • Hypokalemia
  • Glucose intolerance (lower K+ → less depolarization → less insulin release)
  • Gout
  • Metabolic alkalosis
52
Q

Triamterene

MOA?

Side Effects?

A

MOA

  • Inhibits sodium reabsorption through ion channels

Side Effects

  • Hyperkalemia
  • Acidosis
53
Q

Dihydropyridines

Nifedipine**, amlo_dipine_**

MOA?

Side Effects?

A

MOA

  • Causes relaxation of vessels (used for angina, Raynaud’s phenomenon)

Side Effects

  • Peripheral edema
  • Gingival hyperplasia
54
Q

Non-dihydropyridines:

Verapamil, diltiazem

MOA?

Side Effects?

A

MOA

  • Blocks main depolarizing ion in SA and AV nodes to decrease contractions

Side Effects

    • Contraindicated in patients with HF and conduction defects/SA node arrest

Inhibit P450s

55
Q

Non-dihydropyridines:

Verapamil, diltiazem

MOA?

Side Effects?

A

MOA

  • Blocks main depolarizing ion in SA and AV nodes to decrease contractions

Side Effects

    • Contraindicated in patients with HF and conduction defects/SA node arrest

Inhibit P450s

56
Q

Hydralazine

MOA? Side Effects?

A

MOA

  • Relaxes smooth muscle in vasculature to decrease total peripheral resistance
  • Used in resistant hypertension

Side Effects

  • Lupus-like syndrome
57
Q

Nitroprusside (IV)

MOA? Side Effects?

A

MOA

    • Relaxes smooth muscle in vasculature to decrease total peripheral resistance
      • Prodrug = NO and cyanide
        Used in hypertensive crises because fast-acting

Side Effects

  • Cyanide toxicity
58
Q

Drug interactions with diuretics

A

NSAIDs and Steroids cause Na+ retention

59
Q

Why aren’t loop diuretics a first-line choice for hypertension?

A

Because they must be give 2x daily due to short duration of activity and activation of RAAS

60
Q

Statins

MOA

Side effects

Utility

A
  • MOA: HMG-CoA Reductase inhibitor; thereby increasing LDL clearance
  • Adverse effects: Myalgias and rhabdomyolysis (muscle breakdown)
  • Utility: Primary and secondary prevention
61
Q

What is your body’s reflex to long term statin use

A
  • Reflex: compensation for statin therapy
    • GI cholesterol absorption increases
    • Cellular production of HMG CoA reductase increases
    • The PCSK9 gene is activated
62
Q

Ezetimibe

MOA

A
  • MOA: inhibits cholesterol transport into enterocytes
  • When given with statins, Ezetimibe has a better effect on preventing CV events
63
Q

Bile acid sequestrants (i.e. Cholesevalam, Choleystyramine)

MOA?

A
  • MOA: inhibit bile acid reabsorption in the ileum → more bile is secreted → more LDL is secreted → lower LDL
64
Q

Plant stanols/sterols

MOA?

A

MOA: lowers reabsorption of LDL

65
Q

PCSK-9 inhibitors (Evolocumab)

MOA?

Drawbacks?

A

MOA: monoclonal antibodies that bind to PCSK9 → inhibiting LDL receptor degradation → increasing LDL resorption into cells for degradation

Negative: $$$$$

66
Q

Explain Unusual therapies for homozygous FH (HoFH)

  • Lomitapide
  • Mipomersen
  • LDLpheresis
A
  • Lomitapide
    • MOA: blocks the apolipoprotein B from attaching to VLDL
  • Mipomersen
    • MOA: blocks the loading of triglycerides on apolipoprotein B
  • LDLpheresis
    • MOA: dialysis that removes LDL from your blood
67
Q

For nitroglycerin:

  • What is the class?
  • What are the methods of intake and what effects do they have?
  • What is the mechanism of action?
A
  • Class: Nitrate
  • Can take sublingually, po, or IV
    • PO/SL both work on veins
    • IV works on coronary arteries (hence the Nitro drip post-MI)
  • MOA: Nitrates → NO @ vessel walls → stimulates guanylate cyclase → produce cGMP → dephosphorylating of MLC → venodilation → decreases preload
    • REQUIRE THIOL FOR ACTIVATION
68
Q

For nitroglycerin:

  • What are some side effects?
  • What are contraindications to worry about?
A
  • Side Effects:
    • Hypotension with reflex tachycardia
    • Tolerance can develop
  • Contraindications
    • Keep in glass bottle (reacts with plastic)
    • No Viagra
      • Inhibits PDE 5, which allows for no way to terminate action of cGMP, causing it to accumulate → fatal hypotension
69
Q

For isosorbide mononitrate:

  • What is the method of ingestion?
  • What class is this drug?
  • What is the MOA?
  • What are some side effects?
  • What is a contraindication?
A
  • Ingested po
  • Class: Nitrate
  • MOA: NO @ vessel walls → stimulates guanylate cyclase → produce cGMP → dephosphorylating of MLC → venodilation → decreases preload
    • Completely bioavailable – no need for metabolism
  • Side Effects:
    • Hypotension with reflex tachycardia
    • Tolerance can develop
  • Contraindications:
    • No Viagra
      • Inhibits PDE 5, which allows for no way to terminate action of cGMP, causing it to accumulate → fatal hypotension
70
Q

For -olol drugs:

  • What class are these drugs?
  • What is their MOA?
  • What are some side effects?
  • Who are they indicated in?
A
  • Beta-blockers
  • MOA:
    • Act on beta adrenergic receptors in SA/AV node and vessels
    • Decreases HR, contractility, BP (Increasing O2 delivery by increasing diastolic time)
  • Side Effects
    • Hypotension
    • Beta2 blockage is bad for several reasons:
      • Inhibits glycogenolysis (beta 2)
      • Vasoconstriction
      • Bronchoconstriction
  • Indicated in people with cardiac conditions
71
Q

For -DHP drugs:

  • What class are these drugs?
  • What is their MOA?
  • What are some side effects?
  • Who are they contraindicated in?
A
  • Calcium channel blockers
  • MOA: Works at vessels: blocks Ca2+ from entering cell → blocking constriction of smooth muscles in vessels → arteodilation
    • *decreases afterload
  • Side Effects: hypotension
  • Contraindicated in: patients taking beta blockers
72
Q

For non-DHP drugs:

  • What class are these drugs?
  • What is their MOA?
  • What are some side effects?
  • Who are they contraindicated in?
A
  • Class: calcium channel blockers
  • MOA: Works at SA/AV nodes: blocks Ca2+ from entering cells → slows contraction of heart → decreased HR
  • Side Effects: hypotension
  • Conraindicated in people taking beta blockers
73
Q

For Ranolazine:

  • What class are these drugs?
  • What is their MOA? There are two.
  • Side effects?
  • Contraindications?
A
  • Class: Metabolic modifier (used for patients with angina)
  • MOA:
    1. Inhibits late sodium currents → decreased Ca channel activation → therefore decrease Ca2+ in the cell → less diastolic stress → improved coronary blood flow
    2. Partial fatty oxidation inhibitor → tissues switches to glucose metabolism → creates more ATP
    3. *prolongs QT interval
  • Side Effects: Dizziness, headaches, nausea
  • Contraindications: Metabolized by P450s
74
Q

For aspirin:

  • What is the class?
  • What is the MOA?
  • What are some side effects?
  • What are some contraindications?
A
  • Class: Platelet Aggregation
  • MOA: Irreversibly inhibits COX-1/2 → reduces TXA → prevents platelet aggregation
    • *COX-1 found in platelets
  • Side Effects: GI bleeding/GI irritation
  • Contraindications: Patients taking NSAIDS
75
Q

For clopidogrel:

  • What is the class?
  • What is the MOA?
  • What are some side effects?
  • What are some contraindications?
A
  • Class: Platelet aggregation
  • MOA: Prodrug that inhibits to the P2Y (ADP receptor) → allows for Prostacyclin to have anti-platelet activity
  • Side Effects: rash diarreah, bleeding
  • Contraindication: metabolized by CYP540
76
Q

For Tenecteplase:

  • What is the class?
  • What is the MOA?
  • In what time period should it be administered following an MI?
  • What are some side effects?
  • What are some contraindications?
A
  • Class: Thrombolytic:
  • MOA: Binds to fibrin at clot site → activating plasminogen → degrades fibrous clot
  • Administer within 70 minutes
  • Side Effects: Bleeding Thrombocytopenia, allergy/hypotension/fever
  • Contraindicated: patients with active bleeding
77
Q

Quineidine

Type? MOA? Effects? Use? Adverse Effects?

A

Type:Ia

MOA:Na+ channel blocker and K+ rectifier channel blocker

Effects:

  • Prolonged Phase 0 depolarization and prolonged Phase 3 repolarization
  • QT and QRS prolongation
  • Raises depolarization threshold

Use: Historic drug for reentrant arrhythmias

AE:

  • QT prolongation – Torsades de Pointes
  • Anticholinergic properties
  • Cinchonism – tinnitus, dizziness, blurred vision, headache,
78
Q

Flecainide

Type? MOA? Effects? Use? Adverse Effects?

A

Type:Ic

MOA: Na+ channel blocker (potent)

Effects:

  • AV Node: prolonged refractory period
  • Atrial, ventricular, Purkinje fibers: prolonged Phase 0 with no change in refractory period
  • Raises depolarization threshold

Use:

  • Ventricular arrhythmias
  • AFIB
  • Paroxysmal supraventricular arrhythmias

AE:

  • Metallic taste
  • Visual disturbances
79
Q

Beta Blockers

Type? MOA? Effects? Use? Adverse Effects?

A

Type: II

MOA: Blocks beta-adrenergic receptors

Effects:

  • Slows conduction velocity
  • Decreases automaticity, thus increasing PR interval (due to slowed AV conduction)

Use:

  • Atrial tachycardia because slows conduction at AV node
  • Ca++ dependent arrhythmias at AV and SA nodes

AE:

80
Q

Amiodarone

Type? MOA? Effects? Use? Adverse Effects?

A

Type: III

MOA: Blocks Na+, Ca++, and K+ channels

Effects:

  • Delay repolarization (prolonged QT interval)

Use:

  • Sustained life-threatening arrhythmias

AE:

  • Thyroid issues
  • “Smurfism”
81
Q

Sotalol

Type? MOA? Effects? Use? Adverse Effects?

A

Type: III

MOA: Blocks K+ channels and beta-blocker

Effects:

  • Delay repolarization (prolonged QT interval)

Use:

  • Atrial and ventricular tachycardia

AE:

  • Bradycardia, bronchospasm
82
Q

Dofetilide

Type? MOA? Effects? Use? Adverse Effects?

A

Type: III

MOA: Blocks K+ channels

Effects:

  • Delay repolarization (prolonged QT interval)

Use:

  • Continuing atrial tachycardia after ablation

AE:

  • QT prolongation – contraindicated for hypokalemia
83
Q

Non-DHP CCBs (verapamil and diltiazem)

Type? MOA? Effects? Use? Adverse Effects?

A

Type: IV

MOA: Blocks calcium channels at SA and AV nodes

Effects:

  • Prolonged Phase 0 depolarization in nodal tissue
  • Prolonged QT interval

Use:

  • AFIB

AE:

  • Bradycardia
  • Hypotension
84
Q

Digoxin

MOA? Effects? Use? Adverse Effects?

A

MOA: Blocks Na+/K+ ATPase

Effects:

  • Increases vagal activity
  • Slows AV conduction

Use:

  • AV reentrant arrhythmias
  • Chronic AFIB

AE:

85
Q

Adenosine

MOA? Effects? Use? Adverse Effects?

A

MOA: Blocks Ca++ channels at SA and AV nodes

Effects:

  • Prolonged QT interval because prolonged Phase 0 depolarization

Use:

  • Acute reentrant supraventricular tachycardia

AE:

  • Bronchospasm
86
Q

How do you treat Stage A HF?

A
  • Stage A: High risk for developing HF
    • Treatment:
      • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)
87
Q

How do you treat Stage B HF?

A
  • Treatment used for A:
    • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)

PLUS

  • Treatment for B:
    • ACEI (indicated in PMHx of MI or decreased EF)
    • Beta-blockers (indicated in recent MI)
    • ICD
    • Digoxin: reduces progression of HF
88
Q

How do you treat stage C HF?

A

Treatment used for A:

  • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)

PLUS

Treatment for B:

  • ACEI (indicated in PMHx of MI or decreased EF)
  • Beta-blockers (indicated in recent MI)
  • ICD
  • Digoxin: reduces progression of HF

PLUS

  • Treatment for C
    • Hydralazine-Isosorbide Dinitrate Combo (balanced vasodilator)
    • Biventricular Pacing/Cardiac Revascularization Therapy (CRT): device placed that stimulates ventricular contraction at same time
      • Indicated in QRS ≥ 120ms and LVEF ≤ 35%
    • Neprilysin inhibitor
89
Q

How do you treat Stage D HF?

A

Treatment used for A:

  • Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)

PLUS

Treatment for B:

  • ACEI (indicated in PMHx of MI or decreased EF)
  • Beta-blockers (indicated in recent MI)
  • ICD
  • Digoxin: reduces progression of HF

PLUS

Treatment for C

  • Hydralazine-Isosorbide Dinitrate Combo (balanced vasodilator)
  • Biventricular Pacing/Cardiac Revascularization Therapy (CRT): device placed that stimulates ventricular contraction at same time
    • Indicated in QRS ≥ 120ms and LVEF ≤ 35%
  • Neprilysin inhibitor

PLUS

  • Treatment/Care for stage D:
    • Surgical therapy: cardiac transplantation, valve repair/replacement
    • Drugs
    • Palliative care
90
Q

For ACEi, ARB, Aldosterone Antagonists in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are side effects?
  • Can you combine ACEI and ARBs?
A
  • What effect do they have?
    • Balanced vasodilators (dilate arteries and veins both)
  • What is the rationale of that effect?
    • Reduces BP
    • Decreases preload and afterload → reduces myocardial oxygen demand
    • Limits remodeling (aldosterone)
  • What are side effects?
    • Monitor potassium, especially if combining!
  • CANNOT COMBINE ACEI AND ARBs
91
Q

For Hydralazine/Isosorbide (combo drug), in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
A

MOA:

  • Hydralazine: vasodilates arteries
  • Isosorbide: vasodilates veins

Rationale

  • Reduces BP
  • Decreases preload and afterload → reduces myocardial oxygen demand
  • Limits remodeling (aldosterone)
92
Q

For Nitroprusside, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
A

MOA:

  • Balanced vasodilators (arteries and veins)

Rationale:

  • Reduces BP
  • Decreases preload and afterload → reduces myocardial oxygen demand
  • Limits remodeling (aldosterone)
93
Q

For beta blockers (Metoprolol succinate, Carvedilol, bisoprolol), in HF:

  • What MOA/effect do they have (Acutely and chronically)?
  • What is the rationale of that effect?
A

MOA

  • Acute: decreases contractility and HR
  • Chronic: increases contractility (due to up-regulation of beta receptors)

Rationale

  • In HF, beta receptors are down-regulated due to chronic compensatory sympathetic stimulation
  • Beta blockers can up-regulate beta receptors à resulting in increased contractility
94
Q

For loop diuretic like Furosemide, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

_**PNEUMONIC ALERT BIATCHES: Furosemide (FURY has no wrath aka potent)**_

MOA:

  • Inhibits sodium reabsorption at the Loop of Henle blocking Na/K/Cl

Rationale

  • Reduces BP – works well in renal failure
  • More potent, helps with edema

Side Effect

  • Dehydrating
  • Hypokalemia
  • Hyperuricemia
  • Ototoxicity
95
Q

For digoxin, in HF:

  • What MOA/effect do they have? LONG
  • What is the rationale of that effect?
  • What are the side effects of this drug?
    • How do you treat digoxin toxicity? TWO WAYS
A

MOA:

  • Blocks Na/K ATPase → resulting in greater driving force for Na/Ca exchanger → increased intracellular Ca
  • Positive Inotrope
  • Hypokalemia – increases effectiveness (risk Digoxin toxicity)
  • Hyperkalemia decreases effectiveness

Rationale

  • Increase in contractility → Increase SV and CO → leads to increased reflex vagal tone → reduce O2 demand

Side Effects

  • Chromatopsia
  • Drug Interaction:
    • Diuretics
    • P-glycoprotein inhibitors
      • Quinidine, Verapamil
  • Tx toxicity: w/ potassium or Digibind
96
Q

For dobutamine, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

MOA

  • Beta-1 agonist

Rationale

  • Increases SV by increasing contractility

Side Effects

  • Tachycardia, arrhythmias, angina, myocardial ischemia
97
Q

For dopamine, in HF:

  • What MOA/effect do they have?
    • Specifically for Low dose, intermediate dose, high dose!
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

Dobutamine and dopamine are similar in MOA, Rationale, and Side Effects

MOA

  • Low dose: stimulate dopamine receptors to vasodilate (Ehhh)
  • Intermediate dose: stimulate beta-1 receptors (GOOD)
  • High dose: stimulate alpha-1 receptors (BAD)

Rationale

  • Increases SV due to increased contractility

Side Effects

  • Tachycardia, arrhythmias, angina, myocardial ischemia
98
Q

For Milirinone, in HF:

  • What MOA/effect do they have?
  • What is the rationale of that effect?
  • What are the side effects of this drug?
A

MOA

  • Increase cAMP by phosphodiesterase-3 → activation of Ca channels → positive inotrope

Rationale:

  • Vasodilation → decrease BP, preload, afterload

Side Effects

  • Teratogenicity, hypotension, hyperkalemia
99
Q

Fluticasone

Budesonide

Class, MOA, Use, AE

A

Class:Glucocorticoid

MOA:Acts as a nuclear transcription factor to antagonize mucous production and inflammatory mediators

Use: Prophylaxis, Upregulation of beta receptor

AE:

  • Thrush (can avoid with water)
  • Change in vocal chords (can avoid with water)
  • Decrease in bone density
  • Abruptly stopping drug is bad because cortisol inhibits HPA
100
Q

Cromyln

Class, MOA, Use, AE

A

Class:Mast cell inhibitor

MOA:Stabilize plasma membrane of mast cells and basophils and eosinophils to prevent degranulation and release of histamine and leukotrienes

Use: Prevents degranulation and release of histamine and leukotrienes

AE:

  • Well Tolerated
101
Q

Montelukast

Class, MOA, Use, AE

A

Class:Leukotriene modifiers

MOA:Acts on leukotriene receptors C4, D4, E4, decreasing LT effect on Gq receptors

Use: Decreases bronchoconstriction

AE:

  • Well Tolerated
102
Q

Albuterol (short-acting)

Salmeterol (long-acting)

Class, MOA, Use, AE

A

Class:Beta-2 agonists

MOA:Beta-2 agonist

Use: Bronchodilation

AE:

  • Tachycardia
103
Q

Theophylline, caffeine

Class, MOA, Use, AE

A

Class:Methylxanthines

MOA:

  • Inhibits PDE3, activating PKA and causing vasodilation
  • Inhibits PDE4, inhibiting inflammatory processes
  • Enhance catecholamine secretion to work on beta-2

Use: Used if other drugs do not work, Nocturnal asthma

AE:

  • Stimulant
  • Diuretic affects
104
Q

Ipratropium

Tiotropium

Class, MOA, Use, AE

A

Class:Anticholinergics

MOA:Block M3 receptors (Gq receptors)

Use: Bronchodilation

AE:

  • Dry mouth (opposite of SLUD)
105
Q

Omalizumab

Class, MOA, Use, AE

A

Class:MAB

MOA:Binds to IgE

Use: allergic asthma

AE:

  • expensive
106
Q

Bupropion

MOA, Use, AE

A

MOA:Inhibits dopamine reuptake (lasting feeling of pleasure)

Use: Smoking cessation aid

AE:

  • Tremors
  • Insomnia
107
Q

Varenicline

MOA, Use, AE

A

MOA:Nicotine receptor agonist

Use: Eases withdrawal symptoms and blocks pleasurable effects

AE:

  • Transient nausea
108
Q

Name 5 anti-histamines.

A
  • Diphenhydramine
  • Hydroxyzine
  • Fexofenadine
  • Loratadine
  • Cetirizine
109
Q

What is the general mechanism of action of antihistamines?

A

Competitive H1 receptor (Gq receptor); although increase in intracellular Ca2+, histamine stimulation causes production of prostacyclin and NO, outweighing histamine’s vasoconstrictive effects

110
Q

What are the uses of antihistamines?

What are the adverse effects of antihistamines?

A

Use: Allergy-mediated pathologies

Adverse Effects: Diphenhydramine and hydroxyzine have anticholinergic effects (aka sedating)

111
Q

Name 2 decongestants

A
  • Pseudoephedrine
  • Phenylephrine
112
Q

For decongestants (pseudophedrine, phenylepherine):

  • What is the MOA?
  • What are the uses?
  • What are some adverse effects?
A
  • MOA: Alpha 1 agonists (Gq) – vasoconstriction
  • Uses: Used to decrease mucus production
  • Adverse effects: Tissue necrosis if use extends past 3 days
113
Q

For intranasal corticosteroid:

  • Name one.
  • What is the MOA?
  • What is its use?
  • What are 3 adverse effects?
A
  • Example: fluticasone
  • MOA: Transcription factor that decrease capillary permeability, stabilize lysosomes, decrease mucus production
  • Uses: Sinusitis
  • AE: Candida infection, perforation of nasal septum, bone necrosis
114
Q

For expectorant:

  • Name one.
  • What is the MOA?
  • What is its use?
A
  • Guaifenesin
  • MOA: Increase respiratory tract fluid secretions and helps loosen phlegm
  • Use: Sinusitis (may help – “expect” it to help)
115
Q

For mucolytic agents:

  • Name one.
  • What is the MOA?
  • What is its use?
A
  • Example: acetylcysteine
  • MOA: Splits the disulfide linkages that holds mucus together
  • Use: Reduces sputum viscosity to improve secretion clearance
116
Q

For opioid antitussives:

  • Name three.
  • What are the MOAs?
  • What is its use?
  • Adverse effects?
A
  • Example: Codeine/Hydrocodone/Dextrmethorphan
  • MOA: Acts on Gi receptors to hyperpolarize cell membranes – prevents neurotransmitter release
  • Uses: Decreases cough (so people with colds can sleep)
  • Adverse effects: Dextromethorphan (seen as DM in cold medications) is very weak; honey more effective
117
Q

For non-opioid antitussives:

  • Name one.
  • What is the MOA?
  • What is its use?
  • Adverse effects?
A
  • Example: Benzonatate
  • MOA: Topical anesthetic action on respiratory stretch receptors (blocks sodium channels)
  • Use: Decreases cough (so people with colds can sleep)
  • AE: Sedating

CardioResp (14 decks)

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