Drugs (Random Order) Flashcards
(115 cards)
1
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
- Better tolerated than ACE inhbitors
2
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)
3
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
4
Q
For Phenylephrine, midodrine, methoxamine:
- What action do they have?
- What receptor do they act on?
A
Vasoconstriction leading to increased BP
alpha1
5
Q
List some of the alpha1 agonists (3).
A
Phenylephrine, midodrine, methoxamine
6
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
7
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
8
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,
9
Q
Albuterol (short-acting)
Salmeterol (long-acting)
Class, MOA, Use, AE
A
Class:Beta-2 agonists
MOA:Beta-2 agonist
Use: Bronchodilation
AE:
- Tachycardia
10
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
11
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
12
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+
13
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
14
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
15
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
16
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
17
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
18
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
19
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
20
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
21
Q
Name 2 decongestants
A
- Pseudoephedrine
- Phenylephrine
22
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
23
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
24
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
25
For mucolytic agents:
* Name one.
* What is the MOA?
* What is its use?
* Example: acetylcysteine
* MOA: Splits the disulfide linkages that holds mucus together
* Use: Reduces sputum viscosity to improve secretion clearance
26
How do you treat Stage B HF?
* 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**
27
Digoxin
MOA? Effects? Use? Adverse Effects?
**MOA:** Blocks Na+/K+ ATPase
**Effects:**
* Increases vagal activity
* Slows AV conduction
**Use**:
* AV reentrant arrhythmias
* Chronic AFIB
**AE:**
28
How do you treat Stage D HF?
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**
29
For Praz**_osin**_ and any other _**-osin_** drugs:
* What is the receptor specificity?
* What is the use?
* What is a possible side effect
* Alpha1 Antagonist
* Used for prostatic hypertrophy
* Reflex tachycardia
30
For opioid antitussives:
* Name three.
* What are the MOAs?
* What is its use?
* Adverse effects?
* 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
31
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?
* Lisino**_pril**_, Enala_**pril**_, Capto_**pril_**
* 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
*
32
Cromyln
Class, MOA, Use, AE
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
33
What are the uses of antihistamines?
What are the adverse effects of antihistamines?
Use: Allergy-mediated pathologies
Adverse Effects: Diphenhydramine and hydroxyzine have anticholinergic effects (aka sedating)
34
Theophylline, caffeine
Class, MOA, Use, AE
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
35
PCSK-9 inhibitors (Evolocumab)
MOA?
Drawbacks?
MOA: monoclonal antibodies that bind to PCSK9 → inhibiting LDL receptor degradation → increasing LDL resorption into cells for degradation
Negative: $$$$$
36
For Labetolol and Carvedilol:
* What is the receptor specificity?
* What is it used in?
* Is there a reflex tachycardia present? Why or why not?
* Beta1 = beta2 \> alpha1 = alpha2 antagonist
* used in hypertensive crises and in heart failure
* Does NOT have reflex tachycardia because beta1 is blocked
37
Bupropion
MOA, Use, AE
MOA:Inhibits dopamine reuptake (lasting feeling of pleasure)
Use: Smoking cessation aid
AE:
* Tremors
* Insomnia
38
How do you treat stage C HF?
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**
39
For aspirin:
* What is the class?
* What is the MOA?
* What are some side effects?
* What are some contraindications?
* 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
40
What do beta 1 receptors do?
**b****1****:** 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
41
For non-opioid antitussives:
* Name one.
* What is the MOA?
* What is its use?
* Adverse effects?
* Example: Benzonatate
* MOA: Topical anesthetic action on respiratory stretch receptors (blocks sodium channels)
* Use: Decreases cough (so people with colds can sleep)
* AE: Sedating
42
For propanolol:
* What is the receptor specificity?
* What are some possible physiological effects (2)?
* What are some side effects?
* 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
43
Name 4 beta antagonists.
Propanolol
Metoprolol
Labetolol
Carvedilol
44
Non-DHP CCBs (verapamil and diltiazem)
Type? MOA? Effects? Use? Adverse Effects?
**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
45
What are the side effects for muscarinic antagonists?
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
46
For Hydralazine/Isosorbide (combo drug), in HF:
* What MOA/effect do they have?
* What is the rationale of that effect?
MOA:
* Hydralazine: vasodilates arteries
* Isosorbide: vasodilates veins
Rationale
* Reduces BP
* Decreases preload and afterload → reduces myocardial oxygen demand
* Limits remodeling (aldosterone)
47
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?
* Enala**_pril_**: ACE Inhibitor
* Olme**_sartan_**: ARB (Angiotensin receptor blocker)
Must be metabolized before and therefore has a shorter half-life
48
Drug interactions with diuretics
NSAIDs and Steroids cause Na+ retention
49
Bile acid sequestrants (i.e. Cholesevalam, Choleystyramine)
MOA?
* MOA: inhibit bile acid reabsorption in the ileum → more bile is secreted → more LDL is secreted → lower LDL
50
For -DHP drugs:
* What class are these drugs?
* What is their MOA?
* What are some side effects?
* Who are they contraindicated in?
* 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
51
How can adrenergic transmission be terminated?
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)
52
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?
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
53
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?
MOA
* Increase cAMP by phosphodiesterase-3 → activation of Ca channels → positive inotrope
Rationale:
* Vasodilation → decrease BP, preload, afterload
Side Effects
* Teratogenicity, hypotension, hyperkalemia
54
For expectorant:
* Name one.
* What is the MOA?
* What is its use?
* Guaifenesin
* MOA: Increase respiratory tract fluid secretions and helps loosen phlegm
* Use: Sinusitis (may help – “expect” it to help)
55
For nitroglycerin:
* What is the class?
* What are the methods of intake and what effects do they have?
* What is the mechanism of action?
* 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
56
* How does methyldopa work?
* What are some physiological effects related to this drug?
* 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)
57
Triamterene
MOA?
Side Effects?
MOA
* Inhibits sodium reabsorption through ion channels
Side Effects
* Hyperkalemia
* Acidosis
58
Omalizumab
Class, MOA, Use, AE
Class:MAB
MOA:Binds to IgE
Use: allergic asthma
AE:
* expensive
59
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?
* 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
60
Dihydropyridines
Nife**_dipine**_, amlo_**dipine_**
MOA?
Side Effects?
MOA
* Causes relaxation of vessels (used for angina, Raynaud’s phenomenon)
Side Effects
* Peripheral edema
* Gingival hyperplasia
61
For nitroglycerin:
* What are some side effects?
* What are contraindications to worry about?
* 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
62
For -olol drugs:
* What class are these drugs?
* What is their MOA?
* What are some side effects?
* Who are they indicated in?
* 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
63
Name 5 anti-histamines.
* Diphenhydramine
* Hydroxyzine
* Fexofenadine
* Loratadine
* Cetirizine
64
How do you treat Stage A HF?
* Stage A: High risk for developing HF
* **Treatment:**
* **Treat risk factors (i.e. HTN, smoking, cholesterol, alcohol)**
65
Why aren’t loop diuretics a first-line choice for hypertension?
Because they must be give 2x daily due to short duration of activity and activation of RAAS
66
How do the M even receptors work?
**M2 & 4 (Meven):** hyperpolarizes the cell (Gi)
activation results in inhibition of cAMP synthesis → causes K+ efflux which hyperpolarizes the cell
67
What do alpha 2 receptors do?
**a****2**: 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
68
For Ranolazine:
* What class are these drugs?
* What is their MOA? There are two.
* Side effects?
* Contraindications?
* 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
69
Montelukast
Class, MOA, Use, AE
Class:Leukotriene modifiers
MOA:Acts on leukotriene receptors C4, D4, E4, decreasing LT effect on Gq receptors
Use: Decreases bronchoconstriction
AE:
* Well Tolerated
70
What is your body's reflex to long term statin use
* Reflex: compensation for statin therapy
* GI cholesterol absorption increases
* Cellular production of HMG CoA reductase increases
* The PCSK9 gene is activated
71
How do the M odd receptors work?
**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
72
Fluticasone
Budesonide
Class, MOA, Use, AE
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
73
What 5 things causes renin release?
* Renin release is stimulated by:
* Sympathetic activation
* Low pressure in renal vasculature
* Sodium diuresis
* Decreased blood volume
* Decreased renal blood flow
74
For Nitroprusside, in HF:
* What MOA/effect do they have?
* What is the rationale of that effect?
MOA:
* Balanced vasodilators (arteries and veins)
Rationale:
* Reduces BP
* Decreases preload and afterload → reduces myocardial oxygen demand
* Limits remodeling (aldosterone)
75
For Isoproterenol:
* what is the receptor specificity?
* What are the basic effects?
* Beta1 = Beta2
* Decreased BP and increased HR
76
How are most beta blockers excreted and why is this important?
Most beta blockers are excreted via the liver, making it likely that they have drug interactions due to biotransformation by P450 enzymes.
77
For decongestants (pseudophedrine, phenylepherine):
* What is the MOA?
* What are the uses?
* What are some adverse effects?
* MOA: Alpha 1 agonists (Gq) – vasoconstriction
* Uses: Used to decrease mucus production
* Adverse effects: Tissue necrosis if use extends past 3 days
78
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?
MOA
* Beta-1 agonist
Rationale
* Increases SV by increasing contractility
Side Effects
* Tachycardia, arrhythmias, angina, myocardial ischemia
79
* What receptor blockage is specific for slowing of AV conduction?
* What receptor blockage is specific for inhbiting glycogenolysis?
* Bronchoconstriction?
* Vasoconstriction?
* slowing of AV conduction: **Beta1**
* inhibition of glycogenolysis: **Beta2**
* Bronchoconstriction: **Beta2**
* Vasoconstriction: **Beta2**
80
Explain Unusual therapies for homozygous FH (HoFH)
* Lomitapide
* Mipomersen
* LDLpheresis
* 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
81
How does clonidine work?
And what receptor does it act as an agonist for?
What happens if the drug is stopped abruptly?
* 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
82
In the renin-angiotensin-aldosterone system, what are the 4 classes of drugs used to reduce BP?
* Angiotensin Converting Enzyme (ACE) Inhibitors
* Angiotensin Receptor Blockers (ARBs)
* Direct Renin Inhibitors
* Aldosterone Receptor Antagonists
83
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?
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
84
What are the side effects for muscarinic agonists?
Muscarinic Agonists:
* Overall: “SLUD” (salivation, lacrimation, urination, defication) + hypotension / bronchoconstriction
* Eyes: pupillary constriction (miosis)
85
How does the basoreceptor reflex work for dobutamine?
Beta1 stimulation causes no change to BP, causing no response by baroreceptors… overall HR increase
86
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?
* 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
87
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?
* Spironolact**_one_**, epleren**_one_**
* _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
88
Nitroprusside (IV)
MOA? Side Effects?
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
89
Hydrachlorothiazide/chlorthialidone
Side Effects?
* Hypokalemia
* Glucose intolerance (lower K+ → less depolarization → less insulin release)
* Gout
* Metabolic alkalosis
90
For direct renin inhbitor:
* What is a drug?
* What is the MOA?
* What are three side effects?
* What is a minor advantage?
* _Drug_: Aliskiren
* _MOA_: inhibits renin
* _Side effects_: diarrhea, cough, angioedema
* _Advantage_: Can be tolerated better
91
How does the basoreceptor reflex work for isoproterenol?
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
92
List two alpha2 agonist drugs.
Clonidine and Methyldopa
93
For Norepinephrine:
* What is the receptor specificity?
* What effect does it have/what is it used for?
* alpha1 = alpha2 \> beta1 \> beta2
* increases blood pressure
94
Flecainide
Type? MOA? Effects? Use? Adverse Effects?
**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
95
For Angiotensin Converting Enzyme (ACE) Inhbitors:
* What are three side effects?
* What are 5 main advantages?
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
96
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?
*_**\*\*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
97
Plant stanols/sterols
MOA?
MOA: lowers reabsorption of LDL
98
Non-dihydropyridines:
Verapamil, diltiazem
MOA?
Side Effects?
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
99
Ezetimibe
## Footnote
MOA
* MOA: inhibits cholesterol transport into enterocytes
* When given with statins, Ezetimibe has a better effect on preventing CV events
100
For clopidogrel:
* What is the class?
* What is the MOA?
* What are some side effects?
* What are some contraindications?
* 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
101
All renin, angiotensin, aldosterone system drugs are contraindicated in what two situations and why?
All drugs are contraindicated in:
* Renal artery stenosis (because it blocks ATII from causing vasoconstriction → decreases perfusion pressure through glomeruli)
* Pregnancy
102
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?
* 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.
103
For metoprolol:
* What is the receptor specificity?
* What is it used for?
* What is a physiological effect?
* Beta1 selective Antagonist (little beta2 activity)
* Slows HR and therefore cardiac output is decreased
* Bradycardia
104
Varenicline
MOA, Use, AE
MOA:Nicotine receptor agonist
Use: Eases withdrawal symptoms and blocks pleasurable effects
AE:
* Transient nausea
105
Beta Blockers
Type? MOA? Effects? Use? Adverse Effects?
**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:**
106
How does the reflex response occur for norepinephrine?
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
107
For Epinephrine:
* What is the receptor specificity?
* What effect does it have/what is it used for?
* beta1 = beta2 \> alpha1 = alpha2
* increases HR
108
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
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
109
Ipratropium
Tiotropium
Class, MOA, Use, AE
Class:Anticholinergics
MOA:Block M3 receptors (Gq receptors)
Use: Bronchodilation
AE:
* Dry mouth (opposite of SLUD)
110
Amiodarone
Type? MOA? Effects? Use? Adverse Effects?
**Type:** III
**MOA:** Blocks Na+, Ca++, and K+ channels
**Effects:**
* Delay repolarization (prolonged QT interval)
**Use**:
* Sustained life-threatening arrhythmias
**AE:**
* Thyroid issues
* “Smurfism”
111
Outline the process from the baroreceptors to renin to aldosterone release.
112
* What receptor does dobutamine work on?
* What effect does dobutamine have?
* What occurs with chronic use of beta agonists?
* Beta1
* Increases HR
* Chronic use of beta-agonists will lead to downregulation of receptors
113
Non-dihydropyridines:
Verapamil, diltiazem
MOA?
Side Effects?
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
114
Name three alpha antagonists.
Phentolamine
Phenoxybenzamine
Praz**_osin_**
115
Statins
MOA
Side effects
Utility
* MOA: HMG-CoA Reductase inhibitor; thereby increasing LDL clearance
* Adverse effects: Myalgias and rhabdomyolysis (muscle breakdown)
* Utility: Primary and secondary prevention
