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STEP 1 Prep > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q 
Tetracycline
Bacteriostatic
First line treatment for severe acne
Indicated in renal pts.
Do not take with milk, antacids, or iron
Contraindicated in children due to bone growth disruption

Rx? MOA?

A

Rx: Doxycline
MOA: Binds 30s —> aminoacyl tRNA can’t attach

Milk, antacids, iron preparations ⬇️ absorption. Fecally excreted so no problem for renal failure pts.

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2
Q

Vinca alkaloids
M-phase specific
Indication: Hodgkin & Non-Hodgkin lymphomas, leukemia, solid tumors

MOA: Binds beta tubulin –> Stops microtubule polymerization –> Inhibition of mitotic spindle formation

Rx? A/E?

A

Rx: Vincristine
A/E: peripheral neuropathy, constipation

Rx: Vinblastine
A/E: Myelosuppression

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3
Q

First Generation
Reversible inhibitor
CNS entry
Indication: Allergies, motion sickness, morning sickness, sleep aid

Rx? MOA? A/E?

A

Rx: Diphenhydramine
Dimenhydrinate, Chlorpheniramine, Doxylamine

MOA: H1 histamine receptor blockers

A/E: Anticholinergic, antimuscurinic, anti-alpha-adrenergic, sedation (unless intended for sleep aid)

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4
Q

Which drugs show zero order kinetics?

A

Aspirin, Phenytoin, Ethanol

“APE” !

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5
Q

Antitumor Antibiotic - Anthracyclines

Indication: leukemia, lymphoma, solid tumors

Associated with cardiotoxicity presenting with reduced QRS voltage, prolonged systole & reduced ejection fraction

Rx? MOA (3)? A/E?

A

Rx: Doxyrubicin, daunorubicin

MOA:

  1. Intercalates into DNA —> DNA breaks
  2. Free radical generation
  3. Topoisomerase II inhibition

A/E: dialated cardiomyopathy (irreversible but preventable with dexrazoxane)

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6
Q

Which drugs are associated with Serum Sickness?

A 
Antitoxins
Captopril
Cefaclor (a cephalosporin)
Ciprofloxacin
Hormones from other species
Penicillins
Tetracyclines
TMP-SMX
Vaccines
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7
Q

Estrogen receptor modulator
Receptor antagonism: in breast
Receptor partial agonism: in endometrium and bone

Rx? Indication? A/E?

A

Rx: Tamoxifen
Indications: breast cancer, gynecomastia
A/E: Endometrial cancer, hot flashes, DVT, PE

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8
Q 
Antimetabolite
S-phase specific
PYRIMIDINE analog
Prodrug: Capecitabine
Effects enhanced w/ leucovorin (tetrahydrofolate precursor)

A/E: Palmar-plantar erythrodysesthesia (hand-foot syndrome) - redness, swelling and blistering of palms and soles

Rx? MOA?

A

Rx: 5-Fluorouracil

MOA: Thymidylate sythase inhibitor
⬇️dTMP synthesis —> ⬇️DNA synthesis

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9
Q

Antimetabolite
S-phase specific
Folic Acid analog
Indications (Neoplastic): ALL, lymphomas, choriocarcinoma, sarcomas
Indications (Non-Neoplastic): Ectopic pregnancy, abortion, rheumatoid arthritis

Rx? MOA? A/E?

A

Rx: Methotrexate
MOA: competitively inhibits dihydrofolate reductase; ⬇️ dTMP, ⬇️ DNA synthesis

A/E:

  1. Hepatotoxicity
  2. Nephrotoxicity
  3. Pulmonary fibrosis
  4. Folate deficiency (teratogenic)
  5. Mouth ulcers
  6. Myelosuppression (reversible with leucovorin)
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10
Q

Antimicrobial
Bacteriostatic
Bactericidal in combination with sulfonamides (Sulfamethoxazole)
Indications: UTI’s (pts. with penicillin allergy), Shigella, Salmonella, Pneumocystis j. pneumonia & prophylaxis, Toxoplasmosis prophylaxis

Rx? MOA? A/E?

A

Rx: Trimethoprim

MOA: Bacterial dihydrofolate reductase inhibitor

A/E:

  1. Hyperkalemia
  2. Megaloblastic Anemia
  3. Leukopenia & Granulocytopenia (preventable with leucovorin)
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11
Q

Antimicrobial - Sulfonamides
Bacteriostatic
Bactericidal in combination with Trimethoprim
Indications: Gram neg., Gram pos., simple UTI (with TMP)
Mechanism of resistance: Enzyme modification

Rx? MOA? A/E?

A

Rx: Sulfamethoxazole, sulfadiazine, sulfisoxazole

MOA: Dihydropteroate synthase inhibitor (first step in tetrahydrofolate production)

A/E:

  1. HSR (sulfa allergy)
  2. Hemolysis in G6PD Deficiency
  3. Steven Johnson Syndrome
  4. Tubulointerstitial nephritis
  5. Kernicterus
  6. Warfarin toxicity (displaces warfarin from albumin)
  7. Photosensitivity
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12
Q

MOA: Reversible inhibition of IMP dehydrogenase –> ⬇️ PURINE synthesis in B & T cells

A/E:

  1. Pancytopenia
  2. Hyperglycemia (Glucocorticoid sparing property)
  3. HTN

Complication: Invasive CMV infection

Rx? Indication?

A

Mycophenolate mofetil

Indication: Rheumatic disease

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13
Q

Immunosuppressant
Calcineurin inhibitor
Indications: rheumatoid arthritis, psoriasis

A/E:

  1. Nephrotoxicity
  2. Gingival hyperplasia
  3. Hirsutism
  4. Hyperlipidemia

Rx? MOA?

A

Rx: Cyclosporine

MOA: Binds cyclophilin –> prevents IL-2 transcription –> block T-cell activation

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14
Q

Immunosuppressant
Calcineurin Inhibitor
Indication: Post-op solid organ transplant

A/E:

  1. Increase risk of diabetes
  2. Nephrotoxicity
  3. Neurotoxicity

Rx? MOA?

A

Rx: Tacrolimus

MOA: Binds FK506 binding protein (FKBP) –> prevents IL-2 transcription –> blocks T-cell activation

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15
Q

Immunosuppressant
mTOR inhibitor
Synergistic w/ cyclosporine
Indication: Kidney transplant rejection prophylaxis

A/E:

  1. Pancytopenia
  2. Insulin resistance
  3. Hyperlipidemia

Rx? MOA?

A

Rx: Sirolimus/Rapamycin

MOA: binds FK506 binding protein (FKBP) –> prevents RESPONSE to Il-2 –> blocks T-cell activation and B-cell differentiation

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16
Q

Immunosuppressant

NF-kappa-B inhibitor

Permissive action when paired with adrenergic receptor agonist (increase amplitude of maximal response)

Indications: Autoimmune and inflammatory disorders, adrenal insufficiency, asthma, CLL, Non-Hodgkin Lymphoma

Rx? MOA? A/E?

A

Rx: Glucocorticoids
MOA: ⬇️ cytokine transcription –> inhibition of T and B cell function

A/E:

  1. Cushing syndrome
  2. Avascular necrosis of femoral head
  3. Osteoporosis
  4. Hyperglycemia
  5. Amenorrhea
  6. Atrophy of adrenal cortex
  7. Neutrophilic leukocytosis (due to demargination of WBCs)
  8. Poor wound healing (due to ⬇️ fibroblast activity and collagen synthesis)
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17
Q

Direct Muscarinic Agonist
Resistant to Ach esterase
Activates bladder and bowel smooth muscle

Rx? Indication?

A

Rx: Bethanechol
Indication: Urinary retention, post-op/neurological ileus

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18
Q

Direct Muscarinic agonist
Mild nicotinic receptor agonism
Susceptible to Ach esterase
Used to diagnose bronchial hyperactivity (asthma challenge test)

Rx?

A

Methacholine

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19
Q

Direct Muscarinic agonist
Tertiary Amine - Can cross blood brain barrier
Resistant to Ach esterase
Potent stimulator of sweat, lacrimal, and salivary glands

Rx? Indications?

A

Rx: Pilocarpine, cevimeline

Indications:

  1. Open angle glaucoma - contracts ciliary muscle
  2. Closed angle glaucoma - contracts pupillary sphincter
  3. Xerostomia/dry mouth (associated with Sjögren syndrome)
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20
Q

Indirect Muscarinic Agonist - Ach esterase inhibitor
Lipid soluble (CNS entry)
First line tx for Alzheimer

Rx?

A

Rx: Donepezil, rivastigmine, galantamine

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21
Q

Indirect Muscarinic Agonist - Ach esterase inhibitor
Short t ½
For DIAGNOSIS of myasthenia gravis

Rx?

A

Edrophonium

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22
Q

Indirect Muscarinic Agonist - Ach esterase inhibitor
Tertiary Amine (CNS entry)
Indication: Atropine OD, Glaucoma

Rx?

A

Physostigmine

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23
Q 
Indirect Muscarinic Agonist - Ach esterase inhibitor
Quarternary amine (NO CNS entry)

Indications:

  1. TREATMENT of Myasthenia gravis
  2. Reversal of NM receptor blockade (post-op)
  3. Ileus
  4. Urinary retention

Rx?

A

Neostigmine, Pyridostigmine

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24
Q

Indirect Muscarinic Agonist - Ach esterase inhibitors
Irreversible
Lipid soluable
Found in insecticides and nerve gas

Rx? Toxicity sx? Tx?

A

Compound: Organophosphates

  1. Malathion (insecticide)
  2. Parathion (insecticide)
  3. Sarin (nerve gas)

Sx of Toxicity: “DUMBBEELSS”:

  1. Muscarinic effects - diarrhea, urination, miosis, bradycardia, bronchoconstriction, emesis, lacrimation, salivation, sweating
  2. NM receptor effects - excitation (CNS + skeletal muscles) followed by paralysis

Tx:

  1. For M effects: atropine (competitive inhibitor); crosses BBB
  2. For NM effects: pralidoxime (time sensitive regeneration of Ach)
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25
Q 
Muscarinic Antagnoist
Tertiary amine (CNS entry)
Found in belladonna flowers and jimsonweed

Indications: Antispasmodic, antisecretory, antidiarrheal, tx of AchE inhibitor toxicity

Rx? Effects?

A

Rx: Atropine, Tropicamide

Effects:

  1. Hyperthermia
  2. Tachycardia
  3. Decrease secretions
  4. Flushed Skin
  5. Mydriasis + cycloplegia, Sedation
  6. Hallucinations
  7. Urinary retention, Constipation

(Hot, Fast, Dry, Red, Blind, Mad, Full)

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26
Q

Muscarinic Antagonist
No CNS entry
Indications: Asthma, COPD

Rx?

A

Tiopropium, Ipratropium

Note: Tiotropium has longer duration

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27
Q

Muscarinic Antagonist
Indications: motion sickness

Rx? A/E?

A

Rx: Scopolamine

A/E: short term memory loss, sedation

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28
Q 
Muscarinic Antagonist
Lipid soluble (CNS entry)

Indication: Parkinsonism, acute dystonia

Rx?

A

Benztropine, trihexyphenidyl

“Park your Benz in the 3rd (tri) spot”

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29
Q

Muscarinic Antagonist
Indication: Urge incontinence (overactive bladder), bladder spasms

Rx?

A

Oxybutynin

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30
Q

How does botulinum toxin effect cholinergic neurons?

A

Botulinum toxin interacts with synaptobrevin to in pre-synaptic neurons and prevents the release of Ach.

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31
Q

How do MAO inhibitors influence norepinephrine release?

A

Inhibition of MAO prevents NE metabolism in pre-synaptic nerve terminals. This increases the mobile pool of NE, meaning there is more NE available for release during the next nerve depolarization.

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32
Q

I damage storage vesicles required for dopamine conversion to norepinephrine, thus causing a decrease in norepinephrine.

Q: Who am I?

A

Reserpine

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33
Q

I inhibit the binding of norepinephrine containing vesicles to the presynaptic nerve terminal membrane, thus inhibiting norepinephrine release.

Q: Who am I?

A

Guanethidine

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34
Q

D1 Receptor agonist indicated in severe hypertension (vasodilation properties)

Rx?

A

Fenoldopam

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35
Q

Alpha-1 agonist
Indications: nasal decongestant, hypotensive states, ophthalmologic use
Possible reflex bradycardia
No change in pulse pressure

Rx?

A

Phenylephrine

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36
Q

Alpha-2 agonists

Indications:

  1. Mild HTN
  2. Opioid withdrawal
  3. HTN management in pregnancy

Rx? MOA? A/E?

A

Rx: Methyldopa, Clonidine

  • Opioid withdrawal (clonidine)
  • HTN management in pregnancy (methyldopa)

MOA: stimulate presynaptic alpha-2 receptors to decrease NE release (negative feedback)

A/E:

  1. Positive Coombs test (methyldopa) –> hemolysis
  2. CNS depression
  3. Edema
  4. Rebound HTN with abrupt cessation

“Alpha = MC^2”

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37
Q

State the Beta-receptor preference of the following agonist:

  1. Isoproteronol
  2. Dobutamine
  3. Albuterol, Salmeterol, Terbutaline
A
  1. Beta 1 = Beta 2
  2. Beta 1 > Beta 2
  3. Beta 2 selective
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38
Q

I increase SV, HR, CO, and pulse pressure. What class am I?

I decrease TPR and BP. What class am I?

A

Beta 1 agonist

Beta 2 agonist

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39
Q

Why does Beta 1 agonism increase pulse pressure?

A

Preface: we have not studied beta-1 selective drugs. So any drugs that act as a beta-1 agonist also have beta-2 activity.

Beta-2 stimulation = vasodilation = decreased diastolic BP
Beta-1 stimulation = increase SV = maintained systolic pressure despite vasodilation

The widened different between the two accounts of widening of pulse pressure

Rule: anytime you stimulate Beta-1 receptors, pulse pressure will increase

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40
Q

Alpha-1, Alpha-2, Beta-1 agonist
Potential reflex bradycardia

Rx?

A

Norepinephrine

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41
Q

Why does norepinephrine lack Beta-2 activity?

A

Beta-2 receptors are not innervated and most norepinephrine released in the body is from nerve terminals.

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42
Q

Alpha-1, Alpha-2, Beta-1, Beta-2 Agonist
Low dose produces BP/HR tracing that looks like isoproterenol (Beta-1 & 2 stimulation)
High dose produces BP/HR tracing that looks like norepinephrine (Alpha-1, Beta-1 & 2 stimulation)

Q: Who am I?

A

Epinephrine

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43
Q

Why is epinephrine able to stimulate Beta-2 receptors?

A

Epinephrine is released systemically from the adrenal medulla and is therefore able to stimulate non-innervated beta-2 receptors.

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44
Q

Explain “Epinephrine Reversal”

A

Epinephrine reversal allows you tell the difference between norepinephrine and high dose epinephrine.

In a patient with HTN, provide an Alpha-1 blocker.

  • If the BP returns to normal, the cause of the HTN was norepinephrine
  • If the BP becomes hypotensive, the cause of the HTN was epinephrine

Why?

  • By blocking the alpha-1 activity of epinephrine, you expose the beta-2 activity (which is now unopposed on the blood vessels), leading to vasodilation.
  • Norepinephrine does not display beta-2 activity.
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45
Q

Indications of norepinephrine & epinephrine.

A

Both:
1. Cardiac arrest

Epinephrine:

  1. Adjunct to local anesthetic
  2. Anaphylaxis
  3. Asthma

Norepinephrine:
1. Hypotension

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46
Q

Releasers
Indirect Adrenergic Receptor Agonists
MOA: Displace NE from the mobile pool

Agents?

A
  1. Tyramine (found in red wine and cheese)
  2. Amphetamines
  3. Ephedrine (similar to amphetamines)
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47
Q

______ and ______ increase NE in the synapse by inhibiting NE re-uptake.

A

Cocaine

Tricyclic antidepressants

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48
Q
  1. COMPETITIVE nonselective Alpha receptor antagonist. Who am I? Indication?
  2. NONCOMPETITIVE nonselective Alpha receptor antagonist. Who am I? Indication?
  3. Selective Alpha-1 receptor antagonist. Who am I? Indication?
  4. Selective Alpha-2 receptor antagonist. Who am I? Indication?
  5. What are adverse effects of Alpha-1 receptor antagonist?
A
  1. Phentolamine. Pheochromocytoma.
  2. Phenoxybenzamine. Pheochromocytoma.
  3. Prazosin, Tamsulosin (BPH only), Doxazosin, Terazosin. BPH & HTN.
  4. Mirtazapine. Depression.

A/E:

  1. First dose syncope
  2. Orthostatic hypotension
  3. Urinary incontinence
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49
Q

Which drugs are selective Beta-1 antagonist? Indications?

A

Acebutolol (Anti-arrhythmic)
Atenolol (Anti-arrhythmic)
Metoprolol

Rule: “A-M olol”
Note: all beta blockers used for angina, hypertension, and post-MI

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50
Q

Which drugs are non-selective Beta blockers? Indications?

A

Pindolol
Propranolol (Antiarrhythmic, Migraine, anxiety, essential tremor)
Timolol (Glaucoma)

Rule: “N-Z olol”
Note: all beta blockers used for angina, hypertension, and post-MI

51
Q

Which beta blockers act as partial beta agonists and DO NOT increase blood lipids?

A

Acebutolol

Metoprolol

52
Q

Selective Beta-1 blocker with no CNS entry, therefore DOES NOT cause sedation.

Rx?

A

Atenolol

53
Q

Combined alpha-1 and beta blocker.

Rx? Indications?

A

Carvedilol (Angina of Effort, CHF)
Labetalol (Hypertensive emergencies)

N.B: Beta blockers contraindicated in vasospastic angina

54
Q

K+ and beta blocker.

Rx?

A

Sotalol

55
Q

Glaucoma

Which drugs decrease aqueous humor FORMATION? MOA?

A
  1. Timolol (beta blocker - works on ciliary epithelium)

2. Acetazolamide (carbonic anhydrase inhibitor)

56
Q

Glaucoma

Which drugs increase aqueous humor outflow? MOA?

A
  1. Pilocarpine (M3 receptor activation –> ciliary muscle contraction –> increase outflow through canal of Schlemm)
  2. Mannitol (osmotic diuretic)
  3. Latanoprost (Prostaglandin F2-alpha receptor activation)
57
Q

Group: Diuretic
MOA: Carbonic anhydrase inhibitor
Indications: Acute mountain sickness, metabolic alkalosis, glaucoma

A/E:

  1. Bicarbonaturia
  2. Acidosis
  3. Hypokalemia
  4. Hyperchloremia
  5. Renal stones
  6. Sulfonamide HSR

Rx? Site of Action?

A

Rx: Acetazolamide, Dorzolamide
Site: Proximal Tubule (minor action in collecting duct intercalated cells)

CA inhibitors prevent intracellular H+ formation –> No H+ available to run to Na+/H+ antiporter –> increased Na+ in tubular lumen –> water follows Na+

Acidosis secondary to bicarb wasting.

58
Q

Group: Diuretic
MOA: Inhibition of water reabsorption throughout the nephron
Indications: Oliguria, decrease intraocular pressure
A/E: Acute hypovolemia

Rx?

A

Mannitol

59
Q

Group: Diuretic
MOA: Inhibition of Na+/K+/2Cl- co-transporter
Indications: Severe edema, Acute pulmonary edema, hypercalcemia, heart failure
Toxicity increased by digoxin and lithium (decreased clearance)
Strongest natriuretic effect of all diuretics

A/E:

  1. Ototoxicity (enhanced by aminoglycosides)
  2. Hypokalemia + alkalosis
  3. Hypocalcemia
  4. Hypomagnesemia
  5. Hyperuricemia
  6. Sulfonamide HSR (except which?)

Rx? Site of Action?

A

Rx: Furosemide (less ototoxic), Torsemide, Ethacrynic Acid (very ototoxic)
Site: Thick Ascending Limb

Na+, K+ and Cl- stay in lumen. H20 follows Na+
Decreased intracellular accumulation of K+ –> Decrease K+ backflow to lumen –> Decrease paracellular drive to reabsorb Mg2+ and Ca2+
Hyperuricemia because drug competes with uric acid for organic acid transporters in PCT

Sulfonamide HSR except Ethacrynic Acid

Rule: Diuretics that waste K+ also waste H+ (except CA inhibitors)

60
Q

Explain the rationale for using glucagon to treat beta blocker overdose.

A

Beta receptors are Gs coupled. Blocking Beta receptors decreases cAMP.
Glucagon receptors are also Gs coupled. Stimulating glucagon receptors increases cAMP. 9

61
Q

Group: Diuretics
MOA: Inhibition of Na+/Cl- cotransporter
Indications: Nephrogenic diabetes insipidus, Calcium stones, HTN, CHF
Toxicity increased with digoxin

A/E:

  1. Hypokalemia + alkalosis
  2. Hypercalcemia
  3. Hyperglycemia (contraindicated in diabetes mellitus)
  4. Hyperuricemia
  5. Hyperlipidemia (contraindicated in hyperlipidemics)
  6. Sulfonamide HSR

Rx? Site of action?

A

Rx: Hydrochlorothiazide, Chlorthalidone, Indapamide
Site: Distal tubule

Rule: Diuretics that waste K+ also waste H+ (except CA inhibitors)

62
Q

How do thiazide diuretics and amiloride help with nephrogenic diabetes insipidus?

A

Increase loss of Na+ –> decrease plasma Na+ –> triggers PCT to reabsorb more Na+ (renal compensation in area with highest Na+ reabsorption potential) –> H20 follows Na+

Result: Decreased urine output (paradoxical because decreased urine is caused by diuretic in this case)

63
Q

Why do thiazide diuretics cause hyerglycemia?

A

K+ wasting –> decreased extracellular K+ –> increased concentration gradient for K+ outflow from Beta-cells of the pancreas –> Hyperpolarization –> No insulin release

64
Q

Group: Diuretics
MOA: Aldosterone receptor antagnoist
Indications: Hyperaldosteronism, Hirsutism, Hypokalemia, Hepatic ascites, CHF

Rx? Site of action?

A

Rx: Spironolactone, Eplerenone (no anti-androgen effects)
Site: Collecting duct principle cells

Aldosterone receptor blockade –> decrease Na+ and H20 reabsorption, decrease K+ wasting

65
Q

Group: Diuretic
MOA: Inhibition of Na+ channels
Indications: Nephrogenic diabetes insipidus, Hypokalemia, HF

Rx? Site of action?

A

Rx: Amiloride, Triamterene
Site: Collecting duct principle cell

66
Q

What are the adverse effects of K+ sparing diuretics?

A
  1. Hyperkalemia –> Arrhythmia

2. Gynocomastia (Spironolactone)

67
Q

What is the action of lithium in the principle cells of the collecting duct? How can it be corrected?

A

Lithium (Li+) can use Na+ channels to enter principle and damage V2 receptors (no response to ADH).

Tx: Amiloride (Na+ channel blockade)

68
Q

Group: Antihypertensive
MOA: Angiotensin converting enzyme inhibitor
Indications: Autosomal Dominant Polycystic Kidney Disease (Renal protection), Diabetic nephropathy (Renal protection) , CHF, HF

Rx? A/E?

A

Rx: Lisinopril, Captopril

Decreased angiotensin II –> decrease aldosterone –> Na+ wasting, H2O follows

A/E:

  1. Dry cough (increased bradykinin)
  2. Hyperkalemia
  3. Angioedema
  4. Teratogen
  5. Renal Failure
69
Q

Group: Antihypertensive
MOA: Angiotensin receptor blocker
Indications: HTN, Renal protection against diabetic nehropathy, CHF

A/E:

  1. Hyperkalemia
  2. Angioedema
  3. Teratogen
  4. Renal failure

Rx?

A

Rx: Losartan

No bradykinin increase –> no dry cough

70
Q

Group: Antihypertensive
MOA: Renin inhibitor
Indications: HTN

A/E:

  1. Hyperkalemia
  2. Angioedema
  3. Teratogen
  4. Renal failure

Rx?

A

Rx: Aliskiren

71
Q

Group: Antihypertensives/Calcium Channel Blockers
MOA: Inhibition of L-type Ca2+ channels in heart and vessels
Indications: Vasospastic angina, HTN, Arrhythmia, Raynaud Syndrome
Rx? Adverse effects?

A

Rx: Nifedipine, other “-dipine” drugs (vessel selective), Verapamil, Diltiazem (cardio selective),

A/E:

  1. Heart failure exacerbation (cardio selective)
  2. Gingival hyperplasia (non-cardio selective)
  3. Constipation (verapamil)
  4. Reflex tachycardia (non-cardio selective)

Blood vessel selective = dihydropyridines
Cardio-selective = non-dihydropyridines

72
Q

Direct acting vasodilator involving nitric oxide
MOA: Decrease TPR through ATERIOLAR dilation
Indication: mild HTN
A/E: SLE-like syndrome in slow acetylators

Rx?

A

Hydralazine

73
Q

Which drug classes reduce mortality in heart failure patients?

A
  1. ACE Inhibitors

2. Beta blockers

74
Q

What are the (1) adverse effects and (2) contraindications/cautions for beta blockers?

A

A/E:

  1. Decreased HR, SV, CO, contractility, conductivity
  2. Increased blood LDL and TG
  3. Sexual dysfunction

Contraindications/Cautions:

  1. Vasospastic disorders
  2. Asthma
  3. Diabetes mellitus (masks tachycardia/palpitations that would normally alert patient to a hypoglycemic event)
75
Q

Direct acting vasodilator involving nitric oxide
MOA: Decrease TPR via ATERIOLAR AND VENOUS vasodilation
Indication: Hypertensive emergency
A/E: Cyanide toxicity

Rx?

A

Nitroprusside

76
Q

What are the treatment options for cyanide poisoning? MOA?

A

Sodium nitrite/amyl nitrite + Sodium thiosulfate + Methylene Blue:

  • Administer sodium nitrite –> promotes formation of methemoglobin (MetHb)
  • MetHb + cyanide = cyanomethemoglobin –> cannot inhibit complex 4 of ETC
  • Administer Sodium thiosulfate –> Cyanomethemoglobin converted to thiocyanate (non-toxic) + MetHb
  • Administer methylene blue to convert MetHb to oxyhemoglobin
77
Q

Tx for chronic (preexisting) HTN in pregnancy?

Tx for preeclampsia?

A

Chronic: Methyldopa, Labetalol
Preeclampsia management: Labetalol, Hydralazine
Definitive preeclampsia tx: Deliver baby

78
Q

Direct acting vasodilator
MOA: Opens K+ channels –> hyperpolarization of smooth muscle –> arteriolar vasodilation
Indications: Insulinoma, severe HTN, baldness

A/E:

  1. Hypertichosis
  2. Hyperglycemia
  3. Edema
  4. Reflex tachycardia

Rx? Explain insulinoma and baldness indications.

A

Rx: Minoxidil, Diazoxide

Insulinoma: K+ channels remaining open –> hyperpolarization of beta cells of pancreas –> no insulin release

Baldness: vasodilation –> increase blood flow –> increased nutrient delivery to follicles –> promotion of hair grown

79
Q

For ethanol intoxication give ______? For ethylene glycol or methanol?
For ethanol abuse give ______?
For ethanol withdrawal give ______?

A

Intoxication:

  1. Fomepizole - long acting inhibitor of alcohol dehydrogenase
  2. Ethanol - competes with other alcohols for alcohol dehydrogenase (highest affinity)

Abuse:
1. Disulfiram - inhibitor or acetaldehyde dehydrogenase (mitochondrial enzyme) -> acetaldehyde build up responsible for headache, nausea, vomiting

Withdrawal:

  1. Benzos
  2. Thiamine + Folic acid
80
Q

MOA: Endothelin-1 A receptor antagonist
Indication: Pulmonary HTN

Rx? A/E? Contraindication?

A

Rx: Bosentan
A/E: flushing, headache, hypotension
Contraindicated in pregnancy

81
Q

Sildenafil

MOA? Indications? Contraindication? A/E?

A

MOA: Phosphodiesterase-5 & 6 inhibitor –> increased cGMP –> vasodilation

Indications: Pulmonary HTN, erectile dysfunction

Contraindication: Co-administration w/ isosorbide dinitrate/mononitrate

A/E: Blue green color blindness (PDE-6 inhibition)

82
Q

Rx: Digoxin
Indications: CHF, supraventricular tachycardia
Contraindications: Wolff-Parkinson White Syndrome
Note: Low therapeutic index.

Pharmacokinetics:

  • Renal clearance
  • Displacement of other drugs from tissue proteins
  • Long t 1/2

Direct Effect? Indirect Effect? A/E? Toxicity management?

A

MOA:

  1. Direct effect: inhibition Na+/K+ ATPase in cardiac myocytes (competes with K+ for Na/K+ ATPase)–> decrease Na+/Ca2+ exchange –> increase intracellular Ca2+ –> increase Ca2+ release from the sarcoplasmic reticulum –> increased contractile force
  2. Indirect effect: inhibition of neuronal Na+/K+ ATPase –> depolarization –> increased vagal activity

A/E:

  1. Yellow-green, blurry vision
  2. AV block, V. tach (toxic doses)

Toxicity:
Fab antibodies towards drug + supportive therapy

83
Q

Why is slowing AV conduction contraindicated in Wolff-Parkinson White Syndrome?

A

Slowing AV conduction can enhance re-entrance circuit activity, worsening the condition.

84
Q

Phosphodiesterase 3 Inhibitors
Indication: ACUTE chronic heart failure

Rx? MOA? Chronic use complication?

A

Rx: Inamrinone, Milrinone

MOA: Prevents cAMP breakdown –> increased cAMP

  1. In heart: increased inotropy (contractility)
  2. In smooth muscle: vasodilation –> decreased TPR

Long term use contraindicated due to associated with increased mortality.

85
Q

Which sympathomimetics (sympathetic nervous system stimulants) are indicated for ACUTE treatment of chronic heart failure?
MOA?
Why is chronic use contraindicated?

A

Rx: Dobutamine
MOA: B1 receptor stimulation –> increased cAMP –> increased protein kinase A –> phosphorylation of Ca2+ channels (actives) –> increased intracellular Ca2+

Chronic use contraindicated due to tachyphylaxis (rapid tolerance within minutes to hours), rendering the drug ineffective

86
Q

Recombinant human B-type natriuretic peptide (rh BNP)
Indication: Acute decompensated CHF, Edema

MOA:

  1. Increases cGMP –> vasodilation
  2. Promotes diuresis
  3. Promotes natriuresis

Rx?

A

Nesiritide

87
Q

Rule: Fast response fibers of the heart are found in the ____ and the ____. The cardiac action potential of these fibers makes them most susceptible to ____ and ____ blockers, which effect phase ____ and ____ of the action potential curve, respectively.

A

Rule: Fast response fibers of the heart are found in the HIS-PURKINJE SYSTEM and the VENTRICLES. The cardiac action potential of these fibers makes them most susceptible to NA+ and K+ blockers, which effect phase ZERO and THREE of the action potential curve, respectively.

88
Q

Rule: Slow response cardiomyocytes found in the ____ and ____ would be most effected by ____ and ____ blockers, which would effect phase ____ and ____ of the action potential curve, respectively. These cells are also influenced by ____ and ____ outflow.

Q: What is the effect on ECG?

A

Rule: Slow response cardiomyocytes found in the SA and AV NODE would be most effected by CALCIUM CHANNEL and BETA blockers, which would effect phase 0 and 4 of the action potential curve, respectively. These cells are also influenced by SNS and PSNS outflow.

Q: What is the effect on ECG?
A: Prolonged PR interval (atrial depolarization)

89
Q

What are the classes of antiarrhythmic drugs?

A

“Saved By Pharm Class”

Sodium (Class I a-c)
Beta Blockers (Class II)
Potassium Channel Blockers (Class III)
Calcium Channel Blockers (Class IV)

90
Q

Antiarrhythmic Class I A
Indication: Atrial and ventricular arrhythmias

MOA:

  • Moderate blockade of fast Na+ channels during ACTIVATED state (M and H gate open)
  • Some K+ blocking activity
  • Antimuscarinc properties
  • Alpha blocking properties

Note: Effects enhanced in hyperkalemia, displaces digoxin from tissue proteins (increased risk of toxicity)

Rx? Tissue effected? ECG effect? A/E?

A

Rx: Quinidine
Tissue: His-Purkinje & ventricular, SA & AV node

ECG: increase action potential duration (decreased slope of phase 0 + phase 4), increase HR

A/E:

  1. Torsade de Pointes (any K+ blocking antiarrhythmic)
  2. Cinchonism (hearing loss, tinnitus, dizziness, flushing, and blurry vision)
91
Q

Antiarrhythmic Class I A
Indication: Atrial and ventricular arrhythmias

MOA:

  • Moderate blockade of fast Na+ channels during ACTIVATED state (M and H gate open)
  • Some K+ blocking activity (due to active metabolite NAPA)

Rx? Tissue effected? ECG effect? A/E?

A

Rx: Procainamide (NAPA = N-acetyl-procainamide)
Tissue: His-Purkinje & ventricular

ECG: Prolonged action potential (decreased slope of phase 0 + phase 4)

A/E:

  1. Torsade de Pointes (any K+ blocking antiarrhythmic)
  2. Drug induced SLE in slow acetylators (reversible)
  3. Thrombocytopenia
  4. Agranulocytosis
92
Q

Antiarrhythmic Class I B
Indications: Post MI ventricuar arrhythmia (preference for ischemic tissue), Digitalis induced arrhythmia

MOA:

  • Weak blockade of fast Na+ channels during INACTIVATED state (M and H gate closed) –> prolonged inactivation state –> decreased tissue excitability
  • Block of late (phase 1) Na+ slow channels (window period)

Rx? Tissue effected? ECG effect? A/E?

A

Rx: Lidocaine, Mexiletine, Phenytoin
Tissue: His-Purkinje & ventricular

ECG: Slight decrease in action potential duration (phase 1 Na+ block) ; slight decrease in phase 0 slope

A/E: CNS & cardiovascular depression

93
Q

Antiarrhythmic Class I C
Indications: Post MI ventricuar arrhythmia (preference for ischemic tissue), Digitalis induced arrhythmia

MOA:

  • Strong blockade of INACTIVATED fast Na+ channels (M and H gate closed)
  • Prolonged effective refractor period in AV node and accessory bypass tracts (no stimulus of any magnitude can elicit response)

Rx? Tissue effected? ECG effect? A/E?

A

Rx: Flecainide, Propafenone
Tissue: His-Purkinje tissues, AV node accessory bypass tracts

ECG: Prolonged QRS (severely decreased slope of phase 0)

A/E: Proarrhythmic, especially post MI (contraindicated)

94
Q

Antiarrhythmic Class II
Indications: Post-MI prophylaxis, SVTs

Rx? MOA? Tissue effected? AP effect? A/E?

A

Rx: Propranolol, Acebutolol, Esmolol (IV, acute SVT only)
MOA: Beta blockers –> decreased cAMP
Tissues: SA & AV node
AP Effect: Decrease slope of phase 4 of nodal AP

95
Q

Antiarrhythmic Class III
MOA: Decrease K+ rectifier current –> slows phase 3
ECG: Increased action potential duration, increased effective refractory period in all cardiac tissues

A/E:
1. Pulmonary fibrosis
2. Smurf skin (blue pigment)
3. Thyroid dysfunction
4, Hepatic necrosis
5. Corneal deposits
6. Phototoxicity

Rx?

A

Rx: Amiodarone (contained iodine –> linked to blue skin + hypo/hyperthyroidism)

N.B: Before administration, check pulmonary function, liver function, thyroid function.

Alternative: Dronedarone (iodine free)

96
Q

Antiarrhythmic Class III
MOA: Decrease K+ rectifier current –> slows phase 3; decreased HR and AV conduction
ECG: Increased action potential duration, increased effective refractory period especially in Purkinje & ventricular fibers

A/E:
1. Torsades de Pointes (normal sinus beat –> long QT interval –> polymorphic v. tach)

Rx?

A

Sotalol

97
Q

Antiarrhythmic Class IV
MOA: Slow Ca2+ channel blockade –> decrease phase 0 & 4 –> decrease SA and AV node activity
Indication: SVT

A/E:

  1. Constipation
  2. Flushing
  3. AV Block
  4. Digoxin toxicity (How?)

Rx?

A

Rx: Verapamil, Diltiazem

Digoxin toxicity: Verapamil displaces digoxin from tissue binding sites, increasing free serum conc.

98
Q

MOA: Gi coupled receptor activation –> decreased cAMP –> decreased SA & AV node activity
Indications: DOC for paroxysmal supraventricular tachy & AV node arrhythmias
Kinetics: Receptor antagonized by methylxanthines (theophylline and caffeine)

A/E:

  1. Flushing
  2. Sedation
  3. Dyspnea

Rx?

A

Adenosine

99
Q

How do you treat Torsades?

A
  1. Correct hypokalemia
  2. Correct hypomagnesemia
  3. Discontinue drugs that prolong the QT interval
100
Q

Indication: Angina
Nitric oxide prodrug
MOA : Decrease myocardial oxygen requirement and increase oxygen delivery via VENOdilation (decrease preload –> decrease cardiac work)

N.B: decrease infract size. decrease post-MI mortality.

Rx? A/E? Contraindications?

A

Rx:

  1. Nitroglycerine (sublingual - rapid action; transdermal - preventative)
  2. Isosorbide (extended release for chronic use)

A/E:

  1. Headache
  2. Flushing
  3. Orthostatic hypotension
  4. Reflex tachycardia + fluid retention

Contraindications:

  1. Chronic use (due to tachyphylaxis)
  2. Coadministration w/ Sildenafil (severely decreased BP may cause MI)
101
Q

Indication: Refractory Angina
Rx: Ranolazine

MOA? A/E?

A

Block of late inward Na+ current in cardiac myocytes –> decrease Ca2+ accumulation –> decreased end diastolic pressure –> improved diastolic coronary flow

A/E increased QT interval, constipation

102
Q

Atorvastatin, Rosuvastatin, other “-statins”

Class? MOA? A/E?

A

Class: HMG-CoA Reductase Inhibitors

MOA:

  1. HMG CoA reductase inhibition –> HMG CoA not converted to Mevalonate –> de novo cholesterol synthesis stops
  2. Increased LDL receptors of hepatocytes –> increased LDL uptake from the blood
  3. Decreased VLDL synthesis

A/E:

  1. Rhabdomyolysis (increased risk with Gemfibrozi)
  2. Myalgia
  3. Hepatotoxicity (increased risk with cytochrome P450 inhibitors)
103
Q

Cholestyramine, Colestipol

Class? MOA? A/E?

A

Class: Bile acid sequestrants

MOA:

  1. Inhibition of bile acid reabsorption –> hepatocytes must synthesize more de novo –> deceased cholesterol in hepatocytes
  2. Increased LDL receptor expression –> LDL uptake into hepatocytes –> cholesterol released used to synthesize bile acids

A/E:

  1. Increased VLDL and TG synthesis (hypertriglyceridemia)
  2. Lipid soluble vitamin malabsorption
104
Q

Niacin/Nicotinic Acid (Vitamin B3)

Class? MOA? A/E?

A

Class: -

MOA:

  1. Inhibition of VLDL synthesis –> Decreased plasma VLDL and LDL
  2. Inhibition of lipolysis via hormone sensitive lipase in adipocytes
  3. Increased plasma HDL

A/E:

  1. Flushing
  2. Pruritus
  3. Burning pain
  4. Hepatotoxicity
  5. Hyperglycemia

N.B. First 3 A/E are prostaglandin mediated. Pretreat w/ NSAIDS to prevent.

105
Q

Gemfibrozil, Fenofibrate

Class? MOA? A/E?

A

Class: Fibrates

MOA: Binds PPAR-alpha

  1. Upregulation of lipoprotein lipase –> greatly increased chylomicron, VLDL and IDL triglyceride breakdown
  2. Upregulation of HDL synthesis
  3. Inhibition of cholesterol 7-alpha-hydroxylase

A/E:

  1. Cholesterol gallstones (due to 7-a-hydroxylase inhibition)
  2. Myositis
106
Q

Ezetimibe

Class? MOA? A/E?

A

Class: -
MOA: Inhibits intestinal absorption of cholesterol
A/E: Diarrhea

107
Q

Orlistat

Class? MOA? A/E?

A

Class: -

MOA: Inhibition of pancreatic lipase –> decrease triglyceride breakdown in intestines –> increased triglyceride excretion

A/E:

  1. Steatorrhea
  2. Decrease ADEK vitamin absorption
  3. Diarhea
108
Q

Alirocumab, Evolocumab

Class? MOA? A/E?

A

Class: PCSK9 Inhibitors
MOA: Inhibits action of PCSK9 (which destroys LDL receptors) –> increased LDL receptor activity –> significant serum LDL decrease
A/E: Neurocognitive effects

109
Q

What is the result of GABA-A activation? GABA-B activation?

A
  1. Increased Cl- influx

2. Increased K+ influx

110
Q

Class properties:
Binds to GAMMA subunit of GABA-A Complex
Potentiates GABA activity
Increases FREQUENCY of Cl- channel opening
No effect if GABA is absent (no GABA mimetic activity)
Receptor 1 mediates sedation; Receptor 2 mediates anti-anxiety and impaired cognitive function
Indicated for management of barbiturate and alcohol withdrawal

Class? Rx? Indications? Metabolism? Overdose Tx? Withdrawal sx? A/E?

A

Benzodiazepines (The Lams and Pams)

Rx:

  1. Alprazolam (acute) - panic/anxiety attack, phobias
  2. Midazolam (short acting) - Anesthesia (IV), pre-op sedation
  3. Diazepam (long acting) - Anxiety, muscle relaxation, withdrawal states, sedation
  4. Temazepam - sleep disorders
  5. Lorazepam - status epilepticus (IV)

Metabolism: Hepatic
EXCEPT for oxazepam, temazepam, lorazepam (OTL: Outside the liver)

Overdose Tx: Flumazenil - nonspecific BZ (benzodiazepine) receptor antagonist

Withdrawal: Rounding insomia, anxiety, seizures

A/E: Dependence, additive CNS depression w/ barbiturates and alcohol

111
Q 
BZ1 receptor agonist
Short duration
Lipid metabolism
Indication: sleep disorders
A/E: Ataxia, headache, confusion

Rx?

A

Zolpidem, Zaleplon, Eszopiclone (Catch some ZZZ’s)

112
Q

Abruptly stopping which drug groups causes REM rebound?

A

Barbituates
Alcohol
Phenothiazines
MAO inhibitors

113
Q 
Class properties: 
Binds BETA subunit of GABA Receptor 
Prolongs GABA activity
Increases DURATON of Cl- channel opening
Mimics GABA at high doses
Inhibit complex I of ETC
CYP450 inducers

Class? Rx? Indications? Metabolism? Contraindication? Withdrawal? A/E?

A

Class: Barbiturates (The Barbitals)
Rx: Phenobarbital, Pentobarbital, Thiopental
Indications: Anxiety, Anti-seizure, Insomnia, sedation (thiopental)
Metabolism: Hepatic
Contraindication: Porphyrias (induce porphyrin formation)
Withdrawal: anxiety, agitation, seizures
A/E: Resp. & cardio depression (potential cause of death), dependence

114
Q

5-HT-1A partial agonist
Slow onset (effect begin after 1-2 weeks of intake)
Indication: generalized anxiety disorder
No affect on GABA, no sedation, no addiction, no tolerance

Rx?

A

Buspirone

115
Q

Selective blockade of 5HT reuptake
Takes 4-8 weeks of ingested to show appreciable antidepressant effects
CYPR50 inhibitors

Contraindications: MAOIs, TCAs, Merperidine

Indications: Depression, bulimia, binge-eating disorder, OCD, anxiety, premenstrual dysphoric disorder, premature ejaculation, PTSD

Class? Rx? A/E?

A

Class: SSRIs

Rx: fluoxetine, fluvoxamine, paroxetine, escitalopram, citalopram

A/E:

  1. Serotonin syndrome (sweating, rigidity, hyperthermia, ANS instability)
  2. Mania precipitation in pts with underlying bipolar disorder
  3. SIADH
  4. Decreased libido
  5. Bruxism
116
Q

Inhibition of 5HT and NE reuptake
Indications: depression, diabetic neuropathy, fibromyalgia, anxiety, PTSD, OCD

Rx? A/E?

A

Class: SNRIs

Rx: Venlafaxine, duloxetine

A/E:

  1. Increased BP
  2. Stimulant effect
  3. Sedation
117
Q

Inhibition of 5HT and NE reuptake

Indications: major depressive disorder, chronic neuropathic pain, migraine prophylaxis, OCD, nocturnal enuresis

A/E:

  1. Increased BP
  2. Stimulant effect
  3. Sedation

Class? Rx? A/E? Toxicity and Tx?

A

Class: Tricyclic antidepressants

Rx: Amitriptyline, nortriptyline, imipramine, clomipramine, amoxapine

A/E:

  1. Prolonged QT
  2. Postural hypotension
  3. Atropine-like effects

Toxicity:

  1. Convulsion, Coma, Cardiotoxicity, Confusion
  2. Respiratory depression
  3. Hyperpyrexia
  4. Hallucinations

Toxicity tx: NaHCO3 (sodium bicarbonate) - helps prevent arrhythmia

118
Q

Class: MAO Inhibitors
MOA: Irreversible inhibitors of MAO-A and MAO-B –> Increases levels of NE, 5-HT, Dopamine
Contraindications: SSRIs, TCAs, St. John’s wart, Linezolid
Indications: Parkinson disease, depression, anxiety

Rx? A/E?

A

Rx: Selegiline (selective MAO-B inhibitor), phenelzine, isocarboxazid

A/E:

  • Hypertensive crisis (especially with tyramine ingestion)
  • Serotonin syndrome (if taken with SSRIs, TCAs, or merperidine)
119
Q

Atypical Antidepressent
Indication: Insomnia, Depression
A/E: Priaprism, postural hypotension, sedation

Rx? MOA (2)?

A

Rx: Trazodone

MOA:

  1. Inhibition of serotonin reuptake
  2. Receptor antagonist for serotonin, alpha-1, and H1
120
Q

Class: Atypical Antidepressants
MOA: Inhibits NE and DA reuptake
Indications: Smoking cessation

Rx? Toxicity?

A

Rx: Bupropion
Toxicity: Stimulant effect (tachycardia & insomnia), headache, seizures

121
Q

Class: Atypical Antidepressants
MOA: Alpha-2 antagonist -> increased NE and 5-HT release; H1 antagonist

Rx? Toxicity?

A

Rx: Mirtazapine

Toxicity: Weight gain, increased appetite, sedation

122
Q

Indication: Bipolar disorder
Contraindication: Renal disease
Metabolism: Renal
MOA: Unknown

A/E:

  • Hypothyroidism
  • Hyperthyroidism
  • Tremor
  • Teratogenicity (causes Ebstein anomaly - malformed tricuspid valve)
  • Nephrogenic Diabetes insipidus

Rx?

A

Lithium

123
Q

Rx: Methylphenidate

MOA? Indication?

A

Methylphenidate: amphetamine-like; increases NE and DA in synaptic cleft.
Indication: ADHD

STEP 1 Prep (6 decks)

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