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196 Cards in this Set

  • Front
  • Back
Methacholine used for:
dx of asthma: causes flushing, sweating, salivation, GI cramping, bronchoconstriction
Carbachol, bethanechol, methacholine more slowly metabolized than ACh
mnemonic = Can’t Be Metabolized, inhibitors of AChase only potentiate effects of ACh
Alzheimer’s disease appears to involve a deficit of ACh in CNS – tx w...
carbamate AChase inhibitors like donepezil
AChase inhibitors: physostigmine (3), neostigmine (4), edrophonium (4)
edophonium medical use
- diagnosis of myasthenia gravis (MG)
- to differentiate between “myasthenic” and “cholinergic” crisis in patients tx w neostigmine
- used w atropine in reversal of neuromuscular blockade (NmB) caused by non-depolarizing drugs (d-tc, pancuronium)
pilocarpine causes:
miosis and cycloplegia via contraction of ciliary muscle, effect decreases IOP via increased outflow of aqueous humor
- S/E = bronchoconstriction, salivation
acetylcholine, carbachol effect which receptors?
methacholine, bethanechol effect which receptors?
bethanechol used for
urinary retention in PD patient treated w benztropine,
- psychotic patient treated w typical antipsychotic drug (e.g., thioridazine) or
- a patient treated w TCA
choline esters i.v. decrease BP via
nitric oxide (NO) released from vascular endothelial cells (muscarinic receptors)

- the decrease in BP is blocked by atropine
nicotine effects
- induces cytochrome CYP450, so increases drug metabolism
- inc sympathetic activity with inc HR and BP, cutaneous vasoconstriction
- increased respiration and GI motility

- large doses - muscle fasciculations, followed by depolarization blockade
- CNS - convulsions with overdose (OD)

(metabolized by the liver)
neostigmine medical use:
- tx of MG (always used w atropine to prevent indirect muscarinic S/E’s)
- used w glycopyrrolate in reversal of NMB caused by non-depolarizing drugs.
Name 3 organophosphates
malathion, parathion, isofluophate (DFP)
S/S of organophosphate poisoning.
- person in agriculture, home, biochemistry laboratory who present with:
(looks like inc cholinergic with CNS effects)

lacrimation, salivation, miosis, dyspnea, nc BP (N1), skeletal muscle fasciculations (N2)
Tx for organophosphate poisoning
atropine and pralidoxime (2-PAM) (regenerates phosphorylated AChase)

Carboxylesterases in humans degrade organophosphates and prevent our death
Tertiary muscarinic antagonist
(cross BBB)
benztropine, cyclopentolate, atropine, scopolamine
Quaternary muscarinic antagonist (N-methyl-PIG)
propantheline - GI spasticity
ipratropium - prevent bronchoconstriction
over tx with atropine results in
blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone
MOA of drugs for tx of glaucoma
+ Muscarinic increases outflow in Canal of Schlemm
Contract shincter muscle, iris
Contract ciliary muscle
Ganglionic Blocking drugs 2 names and effects
trimethaphan, hexamethonium - block SNS and PSNS
Block increase in plasma Epi induced by hypoglycemia
neuromuscular blockers: Depolarizing (non-competitive)
2 names
succinylcholine and decamethonium
- phase I = MEP depolarized
- phase 2 = repolarized, but still refractory

- causes fasciculations prior to flaccid paralysis

- Uses: NM blockade, ECT
Neuromuscular blocking drugs, Non-depolarizing (competitive) 2 classes
d-tubocurarine (curare), pancuronium(the -curiums and -roniums)

MEP never depolarized

no fasciculations prior to flaccid paralysis

Use: NM blockade
In myasthenia gravis (MG) the N2-receptor density is

- tx effect of succinylcholine is decreased

- tx effect of curare is increased
in burns and denervation injury, the N2-receptor density is

- tx effect of succinylcholine is increased (hyperkalemia)

- tx effect of curare is decreased
presynaptic receptors causing Increased overflow of NE
Ang II & Beta2-stimulation, Alpha2-block, cocaine, TCA’s
presynaptic receptors causing Decreased overflow of NE
muscarinic (ACh) & alpha2-stimulation (clonidine; PGE’s
metyrosine inhibits
tyrosine hydroxylase (TH), dopamine-Beta-hydroxylase (DBH) & ATP released w NE from nerves
DA CV effects
increased RBF/mesenteric BF (block by haloperidol), increased dP/dT (alpha1), increased DBP (beta1)
i.v. NE decreases HR via baroreflex, how is this blocked pharmacologically?
with atropine
Epi CV effects
= increased skeletal muscle BF; decreased skin, renal and GI BF; inc HR, dp/dt, CO, SBP and PP, decreased DBP with physiological doses
DA used instead of NE or Epi to:
maintain dp/dt post-MI bx DA inc RBF whereas NE and Epi dec RBF.
Epi + halothane CV effect:
Epi reversal with an alpha-blocker results in
= only Beta effects = inc HR and RBF, dec TPR, BP, and ERP in heart
achieved by Epi + phentolamine
Epi + Beta-blocker results in these CV effects:
only alpha effects = increased BP
(eg propanolol)
Epi added to local anesthetic agent to
systemic absorption
phenylephrine (PharmEffect) =
alpha 1-agonist = mydriasis without cycloplegia (but still have pupillary light reflex)
ritodrine (Beta2-agonist) decreases
uterine contraciton in premature labor
isoproterenol CV and Resp pharm effect
(non-selective Beta1 & Beta2-agonist) so bronchodilation with increased HR
albuterol, terbutaline resp pharm effect
bronchodilation with less inc HR
clonidine pharm effect
pre- and post-synaptic alpha2-adrenoceptor agonist
pre-tx with reserpine
prevents indirect adrenergic agonism (no inc in BP with tyramine)
tyramine-containing foods contraindicated in patients taking:
phenelzine or tranylcypromine which non-selectively inhibit MAO-A and MAO-B
methylphenidate, DOC for:
and S/E:
S/E's = depression, insomnia, decreased appetite and linear growth rate
amphetamine toxicity =
nervous, excited, agitated, increase HR/BP, toxic psychosis = paranoid schizophrenia, formication w excoriations, convulsions w OD;
difficult to distinguish from effects of cocaine
tx amphetamine psychosis with:
ephedrine indirect adrenergic pharm effect=
direct Beta1 and Beta2, indirect alpha - no alpha after reserpine
Alpha blocker 3 P’s
phentolamine, prazosin, phenoxybenzamine
phentolamine/PBZ increases HR via baroreflex, which alpha blocker has no effect on HR
ergotamine, dihydroergotamine
Pharm effect:
Used for tx of:
partial alpha agonists
tx of migraine
major S/E of alpha blockers
orthostatic hypotension
tamsulosin - blocks:
(which receptor and for what medical use)
alpha1A-receptors in GU tract in patients w BPH to enhance voiding
patient with pheo tumor - tx with:
phentolamine = decreases BP = EPI reversal
Epinephrine-reversal by:
alpha-blockers such as phentolamine, phenoxybenzamine and prazosin = The vasopressor effect of a large (supraphysiological dose) of EPI is reversed to a vasodepressor effect by an alpha-blocker
atenolol/ metoprolol pharm effect
block beta 1
propranolol/timolol pharm effect
block beta 1 and beta 2
medical uses for beta blockers
1) angina = decreased oxygen requirement via decreased dP/dT and HR, but LV-EDV increases
2) decreased HR, AV conduction, dp/dt
3) block increase in HR caused by hemorrhage, minoxidil, hydralazine, diazoxide, nitroprusside, nitroglycerin
4) Beta-blocker (BB) decrease oxygen demand by decreasing HR, dp/dt and afterload (DBP) [NTG decreases oxygen demand by decreasing venous return and LV-EDV]
S/E of beta blockers
CHF, bronchospasm, AV block, delayed recovery of [glucose] in pats w Type 1 DM after s.c. injection of too much insulin
timolol medical use
decreased IOP wo cycloplegia (do not use propranolol because it causes local anesthesia of cornea)
beta blocker withdrawal syndrome
patient tx w beta-blocker for angina -> discontinue drug -> increased cardiac Beta-receptor stimulation -> increased O2 demand -> angina and MI
patient with hyperthyroidism, tx with
with (PTU and) propranolol to decrease tachycardia and tremor and prevent the peripheral conversion of T4 to T3
type I diabetic patient treated with glaucoma drug which causes hypoglycemia.
reserpine pharm effect
1) decrease NE release via depletion of neuronal NE stores, poisons NE storage vesicles
2) no effect of TAP drugs (tyramine, amphetamine, phenylpropanolamine) after
pretreatment w reserpine; no alpha effects of ephedrine after reserpine
guanethidine pharm effects
1) decreased nerve-stimulated NE release
2) competitive inhibitor of NE uptake1
3) anti-HT effect blocked by TCA’s bx TCA’s block entry of guanethidine into neuron
cocaine pharm effects
1) blocks uptake1 of NE, Epi, DA, 5-HT in CNS
2) blocks uptake in peripheral sympathetic neurons - potentiates effects of NE and Epi, but not isoproterenol (ISO)
3) Euphoria via release of DA in nucleus accumbens
cocaine medical uses
local anesthetic effect via blockade of Na+ channels in sensory neurons
cocaine OD
dilated pupils, euphoria, hallucinations, excitation, halo vision, itchy skin, increase BP/HR, convulsions - difficult to distinguish from amphetamine toxicity/OD
cocaine withdrawal syndrome
sleepiness, depression, anhedonia
MAO inhibitors medical use
drugs that inhibit MAO-A and MAO-B
phenelzine, tranylcypromine
selegiline pharm effect
selectively inhibits MAO-B to prevent breakdown of DA in CNS
“cheese” reaction
inhibition of MAO-A in gut wall allows dietary tyramine to enter the circulation; tyramine releases NE to cause HT and tachycardia
clonidine and alpha-methyldopa (alpha-MD) pharm effects as antihypertensives
decrease SNS activity via stimulation of alpha2-receptors in CNS: decrease plasma NE & renin activity (PRA) , HR
clonidine and
alpha-methyldopa (alpha-MD)
S/E = sedation, dry mouth, edema
- S/E of alpha-MD = hepatitis, “flu” syndrome, (+) Coomb’s test
clonidine withdrawal syndrome
sweating, increase HR, abrupt return of BP to HT value, abdominal pain, tremor, headache, apprehension (differs from beta-blocker withdrawal syndrome = no tremor, sweating, abdominal pain or increase BP)
Drugs that decrease plasma NE
clonidine, alpha-MD, guanethidine, reserpine, ganglionic blockers
Drugs that increase plasma NE
alpha blockers, hydralazine, minoxidil, diazoxide, nifedipine, HCTZ, sodium nitroprusside
3 Arterial vasodilators
hydralazine, minoxidil, diazoxide
hydralazine, minoxidil, diazoxide pharm effects
dilate resistance vessels = decrease TPR & BP; increase HR, dP/dT, CO , PRA and plasma NE
hydralazine S/E
edema ;SLE = arthralgia, arthritis, fever, malar (butterfly) rash, glomerulonephritis- d/c hydralazine and tx with steroid
minoxidil S/E
hirsutism, effect additive w finasteride; edema
diazoxide S/E
inhibition of insulin release = hyperglycemia; edema
3 Drugs for HT emergency
diazoxide, sodium nitroprusside (SNP), labetalol
sodium nitroprusside (SNP) pharm effects
dilates arteries and veins via release of nitric oxide (NO) from SNP molecule
2) balanced vasodilation NT patient = decreases TPR and venous retrun -> CO = n.c.
CHF = decreases preload and afterload -> leads to increase in CO
thiocyanate (tx w thiosulfate) and CN (tx w nitrite/thiosulfate) toxicity with Sodium Nitroprusside
after Sodium Nitroprusside infusion in patients w poor renal function = muscle weakness, & spasm, disorientation)
3 Ca++ blockers
nifedipine, diltiazem, verapamil
nifedipine, diltiazem, verapamil pharm effects
block Ca++ channels at SA/AV nodes, cardiac myocytes, arterial VSM
2) decrease in BP: nifedipine>diltiazem>verapamil
3) decrease AV conduction via increase in ERP: verapamil>diltiazem
4) nifedipine - slight increase in HR with increase or n.c. in AV conduction
nifedipine, diltiazem, verapamil med uses
angina - decrease oxygen demand (decrease dp/dt, HR and afterload) w increased
oxygen delivery via dilation of coronary arteries and arterioles

tx uses: HT, exertional and vasospastic angina, AV nodal re-entry tachycardia (V+D)
Drugs which decreased dP/dT
Beta-blockers, Ca++ blockers, diisopyramide
Effects of Ang II
increase BP, increases SNS activity via CNS, presynaptic enhancement release of NE, blocks NE uptake, release of ADH, release of aldosterone, decreases mesenteric BF.
Drugs which decrease mesenteric BF to tx GI bleeding:
NE & Ang II (get escape), ADH (a.k.a. AVP) & octreotide (no escape)
2 ACE inhibitors
captopril, enalapril - prevent conversion of Ang I to Ang II
ACE inhibitor pharm effects
) decrease TPR and BP with no change in HR and CO
2) block formation of Ang II, block enzymatic destruction of bradykinin (BK)
ACE inhibitor S/E
fetal toxicity (category X) , K+ retention, cough; cough caused by BK & PG and is blocked by aspirin (ACEI’s block metabolism of bradykinin)
4) ACEI’s potentiate the decrease in BP caused by i.v. bradykinin
5) ACEI's increase the plasma concentration of BK
5) losartan = Ang II receptor antagonist - no cough
ACE inhibitor MOA in tx of CHF
increase CO by decreasing preload and afterload; reverses cardiac remodeling caused by angiotensin II (ang II)
HT patient with DM, which drug to use
tx w ACEI to decrease BP and decrease proteinuria (protects kidneys)
acetazolamide pharm effect
inhibits formation of aqueous humor and CSF, some effect to decrease gastric acid secretion
2) increased excretion of Na+, K+, bicarbonate - urinary pH increases to 8-8.5
acetazolamide MOA
inhibits carbonic anhydrase in PT and DT to prevent reabsorption of bicarbonate
acetazolamide med use
used to increase urinary pH to enhance renal clearance of acids, e.g., salicylates,
4) used to tx glaucoma and altitude sickness - acidosis, via renal loss of bicarbonate, stimulates respiration
acetazolamide S/E
hyperchloremic metabolic acidosis
Simulators of respiration
acetazolamide, nicotine, Epi, theophylline, caffeine
Inhibitors of respiration
opiates - morphine
benzodiazepines - diazepam
To make urine alkaline
CAI or Na bicarbonate = increase renal Cl of acidic drugs
To make urine acidic
ammonium chloride = increase renal Cl of basic drugs
2 Loop diuretic drugs, MOA
furosemide, ethacrynic acid; inhibit Na+:K+:2Cl- symporter in ascending limb of the loop of Henle; also blocks Na+ transport in macula densa of DT
furosemide, ethacrynic acid pharm effects
increased urinary excretion of Na+, K+, Ca++, Mg++, C- , and water
2) Increased delivery of Na+ to LDT/CD causes K+ loss
3) blocks Na+ transporter in macula densa cells of DT -> no sodium sensed -> increase PRA and Ang II -> secondary hyperaldosteronism -> exacerbates K+ loss
4) Cl- loss caused hypokalemic, hypochloremic metabolic alkalosis
5) urine isotonic in presence and absence of ADH
6) PG-dependent increase in RBF and GFR
7) increases hematocrit via decreased plasma volume
furosemide, ethacrynic acid medical use
used in tx of acute pulmonary edema, CHF, peripheral edema, hypercalcemia
furosemide, ethacrynic acid S/E
bilateral hearing loss via toxicity to CN VIII; potentiated by aminoglycosides (e.g., gentamicin)

S/E - hypokalemia w alkalosis, hypomagnesemia, hyperglycemia, dilutional hyponatremia = cannot make a dilute urine in order to excrete free water

S/E - hyperuricemia (bad for gout) and Li+ toxicity caused by their enhanced reabsorption in PT

enhances digoxin toxicity via hypokalemia - less K+ to compete w digoxin for Na+-K+ ATPase binding sites
Thiazides, hydrochlorothiazide MOA
acts in distal tubule and  GFR in all patients
Thiazides, hydrochlorothiazide pharm effects
1) block NaCl symporter in principal cells of DT: increase excretion Na+, K+, Mg++, Cl- and water
2) decrease excretion of Ca++ in hypercalcinuria: used to decrease formation of kidney stones
3) decrease free water clearance: urine always hypertonic; causes dilutional hyponatremia
4) Increased delivery of Na+ to LDT/CD causes K+ loss
5) blocks Na+ transporter in macula densa cells of DT -> no sodium sensed -> increase PRA and Ang II -> secondary hyperaldosteronism -> exacerbates K+ loss
Thiazides, hydrochlorothiazide med uses
used in tx of HT, edema, kidney stones and DI (distal loss of Na and water enhances the reabsorption of filtrate in the PT; less volume sent distally; urine vol decrease by 50%)
hydrochlorothiazide S/Es
7) S/E - hypokalemia w alkalosis, hypomagnesemia, hyperglycemia, hyponatremia; uniformly decreases GFR
8) S/E - hyperuricemia (bad for gout) and Li+ toxicity caused by their enhanced reabsorption in PT
9) enhances digoxin toxicity via hypokalemia - less K+ to compete w ith digoxin for Na+-K+ ATPase binding sites
10) diuretic effect contracts the blood volume & therefore potentiates the fall in BP caused by anti-HT drugs, especially sympatholytic drugs (e.g., clonidine and alpha-blockers like prazosin
K+-Sparing diuretics
TASK = triamterene, amiloride, spironolactone (aldosterone receptor antagonist)

All are contraindicated in renal insufficiency bx they can cause fatal hyperkalemia
amiloride and triamterene MOA
1) block Na+ channels in principal cells of LDT/CD
2) increased Na+ excretion with decreased K+ excretion
3) make urine alkaline by inhibiting H+ ion secretion from intercalated cells of DT
spironolactone MOA
aldo antagonists; partial agonist at androgen/progesterone receptors
spironolactone pharm effects
1) blocks aldosterone receptors in the principal cells of the LDT and CD
2) increases urinary loss of Na+ and water w decrease in K+ excretion
3) no effect in adrenalectomized patient
spironolactone med uses
4) used in tx of secondary hyperaldosteronism ass w cirrhosis, nephrotic syndrome;
5) reverses cardiac remodelling caused by aldosterone in patients with HF
spironolactone S/Es
hyperkalemia, gynecomastia (males), menstrual irregularities, hirsutism, deeped
voice (females)
patient tx with OCP containing estrogen + norethindrone develops hirsutism - why? how to tx?
hirsutism results from androgenic effects of the progestin norethindrone which is a derivative of 19-nortestosterone; tx with spironolactone
postmenopausal female develops hirsutism - how to tx?
patient with an adrenal tumor has increase BP and plasma [HCO3-], decrease plasma [K+] and PRA; plasma [Na+] is normal -> dx? and tx?
Conn's syndrome = aldosterone-secreting adrenal tumor; tx with spironolactone
hypokalemia from furosemide and HCTZ prevented by:
K+-sparing diuretic drugs, ACE inhibitors, Beta-blockers, and, to a certain extent, by p.o. K+ supplements
digoxin kinetics:
digitoxin kinetics:
digoxin= t1/2 = 1-1.5 d: renal Cl, decreased GFR decreases Cl and inc t1/2

digitoxin= = t1/2 = 7 d: hepatic Cl, dec Cl and inc t1/2 in patient w cirrhosis and CHF
Cardiac Glycosides:
digoxin, digitoxin
cholestyramine and digoxin
chole and antacids binds digoxin and decrease absorption and effect
digoxin in older pts
decrease Vd, so decrease loading dose: decrease GFR, so decrease maintenance dose older patients can have decrease GFR with normal serum [Cr]
quinidine effect on digoxin
increase plasma digoxin by displacing digoxin from skeletal muscle and decreasing renal Cl
digoxin MOA
inhibition of Na+-K+ ATPase - increases dp/dt, but decreases resting membrane potential (Vm) and lack of pumping Na+ out causes automaticity in fast fibers
- low K+: potentiates inhibition of ATPase: causes automaticity and decrease ERP in ventricles
- low Mg++: same as Ca++ overload inside cells - causes automaticity
- high Ca++: Ca++ overload inside cells causes automaticity

MOA - acts in CNS to increase vagal tone:decrease HR, atrial contraction and AV conduction
digoxin med use
Used to control (decrease) ventricular rate in patients w atrial flutter or fibrillation: increase in vagal tone decreases AV conduction, so fewer atrial signals pass the AV node
digoxin S/E
bradycardia, AV block, PVC’s; n/v (CTZ); CNS-abnormal color vision, halo vision, esp. in elderly
Antidysrhythmic drugs
quinidine, procainamide, disopyramide, lidocaine, amiodarone, verapamil
quinidine MOA
MOA: blocks Na+ channels in fast fibers
quinidine pharm effects
Na+ channel block decrease phase 4 automaticity and phase O slope (decrease conduction velocity so it widens the QRS)
2) Delays ventricular repolarization via K+ channel block:increase APD, ERP and Q-T interval
3) SA node: no direct effect, anticholinergic effect causes tachycardia
4) AV node: atropine-like effect increases conduction, but direct effect decreases
conduction (P-R increases)
quinidine med uses
Tx atrial and ventricular dysrhythmias

6) give digoxin before quinidine in tx of atrial flutter and atrial fibrillation so digoxin prevents increase in AV conduction from atropine-like action of quinidine
quinidine S/E
hypotension (alpha-blockade),decrease dp/dt, diarrhea (limits use), tinnitus w OD
pt w atrial fibrillation given quinidine to slow ventricular rate, but ventricular rate increases
soon after quinidine. Why? What to do about it?
immediate atropine-like effect of quinidine increase AV conduction; tx w verapamil or diltiazem to decrease AV conduction and slow ventricular rate
lidocaine MOA
block of Na+ channels in fast fibers - given i.v. due to low F
lidocaine pharm effect
2) decrease phase 4 automaticity to prevent PVC’s: only used for ventricular arrhythmias
3) no effect at SA or AV nodes, BP or dP/dT
4) local anesthetic effect via Na+ channel block in sensory fibers
lidocaine S/E
seizures, tx w benzodiazepine (BZ)
disopyramide pharm effects
marked decrease in dp/dt
marked antimuscarinic effects: dry mouth, constipation; contraindicated in BPH & glaucoma
amiodarone MOA
increase APD, ERP interval in fast fibers by inhibiting K+ channels: increase Q-T
- powerful suppression of phase 4 automaticity (blocks Na+ channels)
- non-competitive beta- and alpha-blockade (hypotension & bradycardia)
- slows sinus rate and AV conduction (P-R increased)
amiodarone medical use
recurrent ventricular tachycardia/fibrillation
amiodarone S/E
pulmonary fibrosis, hypo- or hyperthyroidism; blue, purple or slate gray skin; corneal microdeposits
verapamil MOA
blocks L-type Calcium channels at SA and AV nodes and cardiac myocytes
verapamil pharm effects
SA node = decrease HR; AV node = decrease conduction velocity & increase ERP = fewer atrial signals pass through the AV node to the ventricles; myocardium = decrease dp/dt = decrease CO
verapamil medical use
used to tx AV nodal re-entry tachycardia
verapamil S/E
decrease dp/dt; decreased CO in HF, AV block
patient with atrial fibrillation and no HF has palpitations and dizziness -> tx with verapamil -> MOA?
increase ERP of AV node slows ventricular rate -> improved AV filling -> increase CO
aspirin as an antiplatelet drug
irreversibly inhibits COX-1 of platelets to prevent the
synthesis of TXA2
abciximab, eptifibatide, tirofiban
antagonists of the platelet IIb/IIIa which uses fibrinogen to bind platelets together
ticlopidine and clopidogrel
antagonist of platelet purinergic (ADP) receptors
a patient requires an antiplatelet drug after MI or stroke, but the patient has aspirin hypersensitivity. How to Tx?
ticlopidine or clopidogrel
heparin MOA
accelerates binding of antithrombin III (AT III) to activated clotting factors 2, 9-12, increases aPTT
heparin kinetics/pharm effect
not effective p.o.; works in vivo and in vitro
3) not metabolized by the liver: removed from circulation by reticuloendothelial system
4) increase lipoprotein lipase (hydrolyzes TG’s to glycerol + FFA) to decrease postprandial lipemia

Heparin resistance results from decreased [AT III] in blood
heparin medical uses
MI and DVT’s
heparin S/E
bleeding, antiplatelet effect additive w aspirin, thrombocytopenia
heparin antagonist
protamine sulfate
3 LMW heparins
ardeparin, dalteparin, enoxaparin
LMW heparins kinetcs/pharm effects
(as different from heparin)
1) LMW = 2-6 K; LMW acts primarily on Xa, so little effect to increase the aPTT
2) anticoagulant effect only partially reversed by protamine sulfate
3) cleared by the kidneys instead of the RE system; longer half-life than heparin
warfarin, dicumarol MOA
inhibits post-translational vitamin K1-dependent gamma-carboxylation of glutamate residues on factors 2,7,9 & 10 via inhibition of enzyme
vitamin K1 epoxide reductase
warfarin, dicumarol antidote
vit K1 (phytonadione), fresh frozen plasma, factor IX concentrate (contains factors 2,7,9 & 10)
warfarin, dicumarol pharm effects
Only works in vivo, slow onset of action (2-3 d, full effect at 5 d) increases PT (INR)(greatest effect on factor 7)
- highly bound to plasma proteins: many drug-drug interactions: displacement of warfarin from plasma proteins has two effects: increase PT and increase clearance of warfarin
warfarin, dicumarol medical uses
DVT’s, prevent emboli with prosthetic cardiac valves and A-fib
warfarin, dicumarol metabolism
metabolized by CYP450
inhibitors of CYP450
(increasing plasma warfarin and PT)
cimetidine, ketoconazole, isoniazid, erythromycin and grapefruit juice
inducers of CYP450
(decreasing plasma warfarin and PT)
carbamazepine, phenobarbital, phenytoin, rifampin, chronic EtOH, benzopyrene (cigarette smoke)
patient OD's with warfarin are attempts suicide with rat poison -> which clotting factors and lab tests affected?
decrease activity of factors 2,7,9 and 10; increase aPTT and PT; no effect of factors 8 or 13 or bleeding time
Which type of cardiac dysrhythmia requires tx with warfarin?
Thrombolytic (fibrinolytic) drugs general MOA
all ultimately convert plasminogen to plasmin: plasmin destroys fibrin to lyse clots
urokinase MOA
direct activation of plasminogen
when tPA and plasminogen bind to fibrin in close proximity, plasminogen converted to plasmin by tPA = normal, intrinsic activation of plasmin
streptokinase MOA
changes conformation of plasminogen to expose an active protease site that hydrolyzes another plasminogen molecule to plasmin
streptokinase S/E
(same with all fibrinolytic drugs)
systemic destruction of clotting factors 5 & 8 causes bleeding, esp. in CNS (hemorrhagic stroke)
pt with MI treated with several drugs -> develops intracranial bleeding -> which drug caused it?
aminocaproic acid MOA
a lysine analog that binds to the lysine-binding sites on plasmin which blocks the binding of plasmin to fibrin
statins MOA
the inhibition of hepatic HMG CoA reductase reduces an intracellular hepatic sterol pool which suppresses the promotor region of the genes which code for HMG CoA reductase and LDL receptors; lack of sterol results in the increased synthesis of HMG CoA reductase and LDL receptors; increased hepatic LDL receptors take up LDL cholesterol to lower Tc
statins net effect
decrease Tc, LDL and TG's; slight increase in HDL
statins S/E
myositis/myopathy = muscle pain and weakness ass with increase CPK; muscle damage can progress to rhabdomyolysis
ezetimibe MOA
the inhibition of cholesterol absorption from the GI tract decreases an intracellular hepatic sterol pool leading to increased gene expression of hepatic LDL receptors; increased hepatic LDL receptors take up LDL cholesterol to lower Tc
ezetimibe net effect
selective for LDL cholesterol, so only Tc and LDL decrease
ezetimibe medical use
to tx patients who develop muscle weakness on a statin
gemfibrozil and fenofibrate MOA
activates lipoprotein lipase (esp. in skeletal muscle) to increase hydrolysis of VLDL
gemfibrozil and fenofibrate net effect
decrease Tc, LDL, VLDL and TG's; slight increase in HDL
gemfibrozil and fenofibrate medical use
to tx hypertriglyceridemia
gemfibrozil and fenofibrate S/E
myositis/myopathy = muscle pain and weakness ass with increase CPK; muscle damage can progress to rhabdomyolysis
niacin medical use
to increase HDL cholesterol
niacin S/E
flushing and itching in face and upper body
MOA of Antianginal drugs
all decrease oxygen demand and/or increase oxygen supply; all increase endocardial blood flow
atenolol, metoprolol, propranolol, timolol MOA for angina
negative chronotropic & inotropic effects decreases the rate-pressure product (HR x SBP); also decrease cardiac afterload (= decreased DBP)
atenolol, metoprolol, propranolol, timolol net effect for tx of angina
decreased cardiac oxygen demand
nitroglycerin a.k.a. glyceryl trinitrate, isosorbide mono- and dinitrate MOA
NO donors which selective venodilate; venodilation decrease venous return to decrease LV wall tension during diastole and systole
nitroglycerin a.k.a. glyceryl trinitrate, isosorbide mono- and dinitrate net effect
decreased cardiac oxygen demand
problem with using nitroglycerin
drug tolerance is a big problem
verapamil, diltiazem MOA for angina
negative chronotropic & inotropic effects decreases the rate-pressure product (HR x SBP); also decrease cardiac afterload (= decreased DBP); also dilates large epicardial vessels and small endocardial resistance vessels
amlodipine, felodipine MOA for angina
decreased cardiac afterload (DBP) and increased blood flow through large epicardial vessels and small endocardial resistance vessels
verapamil, diltiazem, amlodipine, felodipine net effect
net effect in both cases: decreased oxygen demand and increased oxygen supply
Tx of Congestive Heart Failure = systolic dysfunction

1) decrease preload with diuretic drugs
2) decrease both preload and afterload (balanced vasodilation) with an ACEI or ARB
3) enhance cardiac contractility (dp/dt) with digoxin
4) reverse cardiac remodeling caused by ang II with an ACE or ARB
5) reverse the cardiac remodeling caused by aldosterone with spironolactone
6) reverse the cardiac remodeling caused by the SNS with carvedilol
7) add digoxin to tx when ACEI + diuretic not working or when patient is in chronic atrial fibrillation