Pharm - Kaplan Flashcards
Anti-GAD (glutamic acid decarboxylase deficiency)
Treatment?
DM type 1
Insulin
Enoxaparin…MoA?
Use?
Binds AT3, inhibits thrombin and factor Xa
DVT (treatment and prophylaxis)
HLA-DR3, DR4, DR3/4
Type 1 DM (anti-GAD antibodies)
HLA-DR5
Treatment?
Hashimoto’s thyroiditis
Levothyroxine
Functions of angiotensin 2
Thus, functions of ACEIs/ARBs
- Stimulate aldosterone (increase Na/H2O retention)
- Vasoconstrict (increase TPR)
Diuresis, vasodilation
Drugs causing oxidative stress, thus affecting G6PD
What does this mean?
TMP-SMX Nitrofurantoin Fluoroquinolones Isoniazid Dapsone Primaquine Quinine
Meaning = buildup of H2O2
Inhibitor of ergosterol synthesis via squalene epoxidase
Use?
Terbinafine
Dermatophytes – esp. tinea corporis
Inhibitor of beta glucan synthesis
Use?
Echinocandins (Caspofungin)
Invasive or resistant oral candidiasis
Anti-fungal w/ mitotic spindle function inhibition
Use?
Griseofulvin
Dermatophytes (oral)
How to remember which organs have which muscarinic receptors?
Most important organ (M1) = Brain
2nd most important (M2) = Heart
EVERYTHING ELSE = M3 (except glands - M1)
Anti-fungal that inhibits thymidylate synthetase
Use?
Flucytosine
Cryptococcus (but NOT in HIV – BM suppression)
Inhibitor of egosterol synthesis via lanosterol 14-alpha-demethylase
Use?
-azoles (antifungal)
Anti-fungal that binds to egosterol
Amphotericin B
A patient is treated for a UTI while taking an antacid. The UTI continues to get worse. What drug class was given?
Why did it get worse?
Fluoroquinolones
Iron and calcium inhibit the absorption of fluoroquinolones
Drugs for heart failure that improve mortality
Why?
ACEI’s, ARBs, Aldosterone antagonists, Beta blockers
Ang 2 is involved in heart remodeling during CHF
Prevention of uric acid crystals in tumor lysis syndrome
Allopurinol
A man taking a drug for depression starts having sweating, tachycardia, and headache after eating pizza. Explain.
Taking a MAO + eating tyramine foods (cheese, beer, wine) –> tyramine displaces NE from nerves and blocks its metabolism –> SYMPATHETIC CRISIS
Side effects of TCAs
3 C’s: Coma, Cardiotoxicity, Convulsions
Activation of PPAR-alpha
Side effect?
Fibrates (Gemfibrozil, Fenofibrate, Clofibrate)
Gallstones (increases cholesterol in bile)
Bile acid sequestrants
Side effect?
Cholestyramine, Colestipol
Constipation
Flushing, hyperglycemia, hyperuricemia…drug?
Niacin
Rhabdomyolysis…drug?
Statin
PPAR-gamma activators
Functions?
Side effects?
Contraindication?
Thiazolidinediones (-glitazone)
Increase insulin sensitivity, decrease gluconeogenesis
Decrease TGs, increase HDL, decrease CRP, decrease Glc
Hepatotoxicity, heart failure
Class 3-4 Heart Failure
A patient is given fentayl and midazolam for anesthesia. What is the best combo of drugs to fight the respiratory depression in this patient?
Naloxone (for the fentanyl) + Flumazenil (for the benzo)
Alkylating agent that attacks guanine N7
Side effect to note
Treatment? MoA?
Cyclophosphamide
Hemorrhagic cystitis
Mesna (traps acrolein in bladder)
Alkylating agent that cross-links DNA strands
Side effects
Treatment for the one?
Cisplatin
Nephrotoxic, Neurotoxic (deafness)
Amifostene (for nephrotoxicity)
Alkylating agent used in Hodgkin’s lymphoma
Procarbazine
Intercalating agent that causes DNA strand breakage
Side effect?
Treatment? MoA?
Anthracyclines (Doxorubicin)
Delayed CHF
Dexrazoxane - Prevents formation of free radicals
Treatment of methotrexate BMS? MoA?
Leukovorin - Folinic acid rescue
Pyrimidine antimetabolite that inhibits thymidylate synthetase (2)
5-FU, Capecitabine
Purine antimetabolite activated by HGPR transferase
6-mercaptopurine
Complexes with Fe and O2 to cause DNA strand scission
What cell cycle phase?
Side effects?
Bleomycin
G2
Pulmonary fibrosis, pneumonitis
Inhibitor of microtubule polymerization (2)
Side effect to note?
Vincristine, Vinblastine
Neurotoxicity
How to remember how beta blockers work?
A-M = beta-1 selective (EXCEPT C and L) N-Z = beta non-selective
**Carvedilol and Labetolol = beta-1, beta-2, and alpha-1
What do beta blockers do to blood pressure?
DECREASE it (prevents glycogenolysis by skeletal muscle and liver)
Dopamine…
- Low dose?
- Medium dose?
- High dose?
Low = D1 (renal artery dilation) Medium = Beta-1 (heart) High = alpha-1 (vessels, etc.)
Which are more sensitive to stimulation: alpha or beta?
BETA (beta response predominant at low dose, alpha response predominant at high dose)
Phenylephrine…MoA
Alpha-1 agonist
How to remember the alpha-2 agonist drugs?
A = MC^2
A = alpha ^2 = alpha-2 M = methyldopa C = clonidine
Beta-1 selective agonist
Beta-2 selective agonists (3)
Dobutamine
Salmeterol, albuterol, terbutaline
In a sympathetic BP/HR tracing, an increase in BP = ?
An increase in pulse pressure = ?
Bradycardia?
Alpha-1
Beta-1
Reflex
Epinephrine…
- Low dose
- Medium dose
- High dose
Low = beta-1 and beta-2 (like isoproterenol) Medium = beta-1 only (alpha-1 and beta-2 cancel out) High = alpha-1, beta-1, beta-2 (looks like norepinephrine)
Differentiating NE vs. High Dose Epinephrine
Give alpha-1 blocker…
- NE – BP goes back to normal
- Epi – BP drops below normal (beta-2 effect)
Selegiline…MoA
Use?
Can you get tyramine hypertension w/ this?
Inhibition of MAO type B (brain – blocks dopamine metab.)
Parkinson’s
NO – tyramine is metabolized by MAO-A only
A patient has Horner’s syndrome. What is the difference between putting cocaine in the eye, vs. putting amphetamine in the eye?
Cocaine – prevents re-uptake – will work if NE is already being released
Amphetamine – promotes release – will work as long as that last nerve in the pathway is in tact
Phenoxybenzamine vs. Phentolamine
Phentolamine = competitive alpha antagonist Phenoxybenzamine = non-competitive alpha antagonist
Alpha-1 selective antagonists
Use?
How is tamsulosin different than the rest?
Benefit of it?
Prazosin, Terazosin, Tamsulosin, etc.
BPH, other things
No Z in the name = alpha-1A selective = prostate (BPH)
Does NOT affect the BP like the others do
Alpha-2 selective antagonist
Use?
Mirtazepine
Antidepression
Treatment for pheochromocytoma
Phenoxybenzamine (BOTH HAVE 16 LETTERS)
When is blocking beta-2 beneficial?
Glaucoma (reduced aqueous humor production)
Side effect of beta blockers
Dyslipidemias
Beta blockers with partial agonist activity (ISA)
Acebutolol, Pindolol
Most and least sedating beta blockers
Most = propranolol Least = atenolol
Sotalol…MoA
Beta-blocker + K+ channel blocker
Being treated for asthma, develops tremor, tachycardia, and seizure…possible cause?
MoA?
Theophylline toxicity
Phosphodiesterase inhibitor
Alpha-1 agonist vs. muscarinic antagonist…which one can cause cycloplegia?
Why?
Muscarinic antagonist
Accommodation = M3 on ciliary muscle = PARASYMP ONLY
Open-angle glaucoma…treatments of choice?
Is this a slow or fast onset of disease?
- *Latanoprost (PG analog – increases outflow)
- *Beta-blockers (Timolol) (inhibit production)
Slow
Closed-angle glaucoma…treatments of choice?
Is this a slow or fast onset of disease?
**Acetazolamide (decreases production)
Mannitol (increases drainage)
Pilocarpine (increases drainage)
Fast
Pupil constriction
Airway constriction
BV dilation
Muscarinic agonism (ex. Pilocarpine)
Mecamylamine
Ganglion blocker
Major drugs with a side effect of hyperuricemia (3)
Why?
Aspirin, loop diuretics, thiazide diuretics
Compete for weak acid secretion at the PCT w/ urate
Potassium sparing diuretics
Amiloride, Triamterene
Aldosterone receptor antagonists
Spironolactone, eplerenone
Renal side effect of Lithium
How?
Treatment? Why?
Nephrogenic diabetes insipidus
Enters principal cells via NAC, then block V2 receptors
Amiloride - blocks uptake through NAC
Spironolactone vs. Eplerenone - side effects
Spironolactone - hirsutism/gynecomastia (AR agonist)
Eplerenone - no androgen side effects
Patient with tinnitus or fullness sensation in ear. Recently started being treated for heart failure. Drug class?
Drugs that increase this risk?
Loop diuretics
Aminoglycosides
Calcineurin inhibitor
How does it work?
Side effects?
Cyclosporin
Binds cyclophilin and inhibits IL-1 and IL-2 production and T-cell activation
Nephrotoxicity, severe hypertension, gingival hyperplasia, hyperlipidemia, hyperglycemia
Ulcerative stomatitis side effect…cancer drug?
Methotrexate
Nephrogenic DI…drug of choice?
Explain
Thiazides
Decrease Na+ levels in the blood –> compensatory increase in reabsorption in the proximal tubular –> water follows
Function of thiazides on vessels and insulin
**Hyperpolarize SM –> vasodilation (long term)
Hyperpolarize beta cells –> decreased insulin
MoA…
- Flutamide
- Leuprolide
- Octreotide
- Finasteride
Flutamide = androgen receptor competitive antagonist
Leuprolide = GnRH analog
Octreotide = somatostatin analog
Finasteride = 5-alpha reductase inhibitor (BPH)
Why do thiazides cause hyperglycemia (part of hyperGLUC)?
Can loop diuretics do this?
Hypokalemia –> decreased insulin secretion –> increased blood glucose
Yes, but not as much
Aliskiren..MoA
Renin antagonist
6-mercaptopurine…activated into what?
2 enzymes needed for metabolism of these drugs?
So?
What is contraindicated in these patients?
Azathioprine
HGPRT, X.O.
Must reduce dose if taking allopurinol or febuxostat
Live virus vaccines (b/c decreased T-cell immunity)
Binds to 30S ribosome and inhibits binding of aminoacyl-tRNA
Uses?
Tetracyclines
Cholera, lyme disease, acne, Rickettsia, others…
Prevention of initiation complex, causing mRNA misreading and inhibiting protein synthesis
Side effects?
Aminoglycosides
Nephrotoxic, ototoxic, teratogen
Inhibition of DNA gyrase (topoisomerase 2), preventing negative supercoils
Side effects?
Fluoroquinolones
Tendon rupture, arthropathy, phototoxic, CNS stimulation
When are ACEI’s and ARB’s BAD for the kidney?
Renal artery stenosis –> decreased GFR –> renal failure
Calcium channel blockers…how to remember?
How to remember where these work?
“VD Dipines” – Verapamil, Diltiazem, Amlodipine
In order of HEART –> VESSELS
- Verapamil = most cardiac
- Dipines = most vascular
Gingival hyperplasia…drugs?
- Cyclosporin
- Phenytoin
- Dipines (CCBs)
Functions of alpha-1 antagonists (-zosin)
- Arteriolar dilation
- VENOUS dilation
Side effects of alpha-1 blockers (3)
- First dose syncope
- Orthostatic hypotension (bc of VENOUS dilation)
- Urinary incontinence
Function of alpha-2 agonists
Uses? (3)
DECREASE sympathetic outflow (POWERFUL)
- HTN
- Opiate withdrawal (clonidine)
- HTN management in pregnancy (methyldopa)
Side effect of methyldopa
Hemolytic anemia (positive Coombs test)
Function of Hydralazine
MoA?
Side effect?
ARTERIOLAR dilation ONLY
Via N.O.
Drug-induced SLE
Functions of Nitroprusside
MoA?
Use?
Side effect?
Arteriolar AND venule dilation
Via N.O.
HTN emergencies
Cyanide poisoning
Minoxidil, Diazoxide
K+ Channel agonists –> ARTERIAL dilation ONLY
Side effects of minoxidil and diazoxide (useful ones)
- Hypertrichosis (minoxidil – used for baldness)
- Hyperglycemia (diazoxide – used for insulinoma)
Angina + HTN…drugs to use?
Beta blockers, CCBs
Diabetes + HTN…drugs to use?
ACEIs, ARBs
HF + HTN…drugs to use?
ACEIs, ARBs, Beta blockers
Post-MI + HTN…drugs to use?
Beta blockers
BPH + HTN…drugs to use?
Alpha blockers
**HTN drugs contraindicated in dyslipidemias
Beta blockers, thiazides (both raise lipid levels)
Treatment mechanism for pulmonary hypertension
Drugs and mechanisms? (3)
Vasodilation
- Bosentan (endothelin blocker)
- Epoprostenol (PGI2)
- **Sildenafil (PDE-5 inhibitor)
5 strategies to treating heart failure
- Decrease sympathetics (control it)
- Decrease afterload (ACEIs, ARBs, arterial dilators)
- Decrease preload (diuretics, ACEIs, ARBs, venodilators)
- Increase contractility (Digoxin, beta agonists)
- **Stopping cardiac remodeling (ACEI’s, ARBs, Spironolactone, beta blockers)
How to substitute if you can’t take ACEIs/ARBs?
Hydralazine (arteriolar dilation) + Nitrate (venous dilation)
MoAs of Metoclopramide
Contraindicated in who?
What else is contraindicated in these people? (3)
- Sensitizes tissues to acetylcholine (ex. GI smooth muscle)
- Blocks dopamine receptors (anti-emesis)
Mechanical GI obstruction
Senna (GI stimulants), CCBs (Verapamil), anticholinergics
Function of dopamine and dobutamine on the heart?
Use?
Side effect?
Activates beta-1 receptors –> opening of Ca++ channel –> increase contractility
ACUTE heart failure ONLY
Tachyphylaxis (quick loss of response)
What type of PDE functions in the heart?
Drugs that block that?
PDE type 3
Inamrinone, Milrinone
2 functions of Digoxin
Benefits of each?
Side effects to note?
- DIRECT = increase heart contractility (CHF)
- INDIRECT = increase vagal output (SVTs)
Blurry yellow vision, halos around lights, bad arrhythmias
Intermittent claudication…drug to use?
MoA?
Contraindication?
Cilostazol
PDE3 inhibitor
CHF – increased mortality
Drugs that work on the ventricular action potential (MoAs)
Which parts of the EKG do they control?
Used for what types of arrhythmias?
Na+ channel blockers – prolong phase 0 – prolong QRS
K+ channel blockers – prolong phase 3 – prolong QT
For VENTRICULAR arrhythmias
See “rhythm control” drugs…think what?
Ventricular control (Na+ or K+ channel blockers)
Drugs that work on the SA/AV node action potential (MoAs)
Which part of the EKG do they control?
Used for what type of arrhythmias?
Calcium channel blockers – prolong phase 4
Beta blockers – prolong phase 4
PR interval
SVTs
Function of carotid massage and valsalva on the heart
Increase vagal firing –> PSNS on the heart –> slow SVTs
Polymorphic ventricular tachycardia…other name?
Caused by what?
Drugs that do this?
Torsades de pointes
Prolonging the QT
K+ channel blockers
Quinidine…
- Class?
- Additional bad effects?
Side effects?
Class 1A – Na+ and K+ channel blockers
- Muscarinic block –> increased HR
- Alpha-1 block –> reflex tachycardia
- Displaces digoxin, increasing its toxicity
- Cinchonism (GI, **tinnitus, ocular issues, CNS excitation)
- Hypotension (alpha-1 block)
- Torsades (increased QT)
MoAs of Class 1B antiarrhythmics
Do NOT cause what?
Classic drug?
- Block inactivated Na+ channels in hypoxic/ischemic tissue
- Block slow Na+ channels in phase 4, increasing recovery
NO TORSADES (unlike Class 1A)
Lidocaine
Use for Lidocaine
Oral version?
V tach
Mexiletine
MoA of Class 1C antiarrhythmics
Drug?
Use?
Contraindication?
Block fast Na+ channels in His-Purkinje tissues
Flecainide
A-fib – RHYTHM control (not rate)
Ventricular tachycardia
Class 2 antiarrhythmics
Use?
Unique one?
Beta blockers
SVTs (prolong PR interval)
Esmolol - super short - used for ACUTE treatment only
Class 3 antiarrhythmics
MoA?
Why do they prolong the effective refractory period?
K+ channel blockers
Prolong phase 3 repolarization –> prolong QT interval
Prevent voltage-gated Na+ channel re-opening b/c preventing repolarization
Amiodarone - class?
MoA?
Use?
Side effects? (5)
Class 3 (K+ channel blockers)
Mimics ALL classes (Na, Ca, K, and beta blocker)
ALL ARRHYTHMIAS
Pulmonary fibrosis, hepatic necrosis, thyroid dysfunction, blue skin, corneal deposits
Benefits of Dronedarone over Amiodarone
No iodine = no blue skin or thyroid problems
Sotalol - class?
MoAs?
Side effect?
Class 3 (K+ channel blockers)
Beta blocker w/ K+ channel blocker too – slows phase 3 and HR and AV conduction
TORSADES (MOST likely)
Class 4 – MoA
Results?
Drugs?
Use?
Ca++ channel blockers
Slow phase 0, phase 4, SA and AV nodal conduction
Verapamil, Diltiazem
SVTs
Adenosine - MoA
Half life?
Use? What else can be tried first?
Activates adenosine receptors in SA/AV NODES – Gi causes K+ efflux and hyperpolarization
10 seconds
Paroxysmal SVTs – carotid sinus and valsalva first
SVTs - drugs?
VTs - drugs?
Class 2, Class 4, Adenosine, Digoxin
Class 1, Class 3
A. fib - treatments
Rhythm control?
- Rate control
- Anticoagulation
Flecainide (1C)
Wolff-Parkinson-White…treatment idea?
Slow the fast muscle action potential (class 1)
Treatments for stable angina
Nitrates - vasodilation (BUT reflex tachycardia)
**Beta blockers – slow heart, reduce oxygen demand rise
CCBs (VD) – slow heart, reduce oxygen demand rise
Treatments for vasospastic angina
Nitrates - vasodilation
CCBs (DIPINES) - vasodilation
Drugs used in stable angina NOT used in vasospastic
Beta blockers (don’t vasodilate, might vasoconstrict)
Why do M3 receptors cause RELAXATION of vessels?
Coupled to N.O. synthase, which causes NO to go into the muscle, cause cGMP rise, causing muscle relaxation
How to prophylax for attacks of stable angina?
MoA?
- Transdermal nitroglycerine
- Isosorbide nitrates
NO –> cGMP –> dephosphorylation of MLC (inactivation)
How do PDE5 inhibitors work?
Why not take with nitrates?
Decrease inactivation of cGMP –> more dephosphorylation of MLCK –> more vascular relaxation
Nitrates work the SAME way
Angina drug that is contraindicated in long QT
Ranolazine
Why does cAMP cause SM relaxation?
Why does cGMP cause SM relaxation?
Why do CCBs cause SM relaxation?
PKA –> phosphorylated MLCK –> can’t activate MLC
PKG –> phosphatase –> dephosphorylate MLC –> inactive
No Ca+ –> no Ca-Calmodulin –> no MLCK activation
