Pharm Autonomic Nervous System, Cardiovascular Drugs

Front 1

Methacholine used for:

Back 1

dx of asthma: causes flushing, sweating, salivation, GI cramping, bronchoconstriction

Front 2

Carbachol, bethanechol, methacholine more slowly metabolized than ACh

Back 2

mnemonic = Can’t Be Metabolized, inhibitors of AChase only potentiate effects of ACh

Front 3

Alzheimer’s disease appears to involve a deficit of ACh in CNS – tx w...

Back 3

carbamate AChase inhibitors like donepezil

Front 4

carbamates

Back 4

AChase inhibitors: physostigmine (3), neostigmine (4), edrophonium (4)

Front 5

edophonium medical use

Back 5

- 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)

Front 6

pilocarpine causes:

Back 6

miosis and cycloplegia via contraction of ciliary muscle, effect decreases IOP via increased outflow of aqueous humor
- S/E = bronchoconstriction, salivation

Front 7

acetylcholine, carbachol effect which receptors?

Back 7

nicotinic/muscarinic

Front 8

methacholine, bethanechol effect which receptors?

Back 8

muscarinic

Front 9

bethanechol used for

Back 9

urinary retention in PD patient treated w benztropine,
- psychotic patient treated w typical antipsychotic drug (e.g., thioridazine) or
- a patient treated w TCA

Front 10

choline esters i.v. decrease BP via

Back 10

nitric oxide (NO) released from vascular endothelial cells (muscarinic receptors)

- the decrease in BP is blocked by atropine

Front 11

nicotine effects

Back 11

- 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)

Front 12

neostigmine medical use:

Back 12

- 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.

Front 13

Name 3 organophosphates

Back 13

malathion, parathion, isofluophate (DFP)

Front 14

S/S of organophosphate poisoning.
- person in agriculture, home, biochemistry laboratory who present with:

Back 14

(looks like inc cholinergic with CNS effects)

lacrimation, salivation, miosis, dyspnea, nc BP (N1), skeletal muscle fasciculations (N2)

Front 15

Tx for organophosphate poisoning

Back 15

atropine and pralidoxime (2-PAM) (regenerates phosphorylated AChase)

Carboxylesterases in humans degrade organophosphates and prevent our death

Front 16

Tertiary muscarinic antagonist
(cross BBB)

Back 16

benztropine, cyclopentolate, atropine, scopolamine

Front 17

Quaternary muscarinic antagonist (N-methyl-PIG)

Back 17

N-methylatropine
propantheline - GI spasticity
ipratropium - prevent bronchoconstriction
glycopyrrolate

Front 18

over tx with atropine results in

Back 18

blind as a bat, mad as a hatter, red as a beet, hot as a hare, dry as a bone

Front 19

MOA of drugs for tx of glaucoma

Back 19

+ Muscarinic increases outflow in Canal of Schlemm
Contract shincter muscle, iris
Contract ciliary muscle

Front 20

Ganglionic Blocking drugs 2 names and effects

Back 20

trimethaphan, hexamethonium - block SNS and PSNS
Block increase in plasma Epi induced by hypoglycemia

Front 21

neuromuscular blockers: Depolarizing (non-competitive)
2 names

Back 21

succinylcholine and decamethonium
- phase I = MEP depolarized
- phase 2 = repolarized, but still refractory

- causes fasciculations prior to flaccid paralysis

- Uses: NM blockade, ECT

Front 22

Neuromuscular blocking drugs, Non-depolarizing (competitive) 2 classes

Back 22

d-tubocurarine (curare), pancuronium(the -curiums and -roniums)

MEP never depolarized

no fasciculations prior to flaccid paralysis


Use: NM blockade

Front 23

In myasthenia gravis (MG) the N2-receptor density is

Back 23

decreased

- tx effect of succinylcholine is decreased

- tx effect of curare is increased

Front 24

in burns and denervation injury, the N2-receptor density is

Back 24

increased

- tx effect of succinylcholine is increased (hyperkalemia)

- tx effect of curare is decreased

Front 25

presynaptic receptors causing Increased overflow of NE

Back 25

Ang II & Beta2-stimulation, Alpha2-block, cocaine, TCA’s

Front 26

presynaptic receptors causing Decreased overflow of NE

Back 26

muscarinic (ACh) & alpha2-stimulation (clonidine; PGE’s

Front 27

metyrosine inhibits

Back 27

tyrosine hydroxylase (TH), dopamine-Beta-hydroxylase (DBH) & ATP released w NE from nerves

Front 28

DA CV effects

Back 28

increased RBF/mesenteric BF (block by haloperidol), increased dP/dT (alpha1), increased DBP (beta1)

Front 29

i.v. NE decreases HR via baroreflex, how is this blocked pharmacologically?

Back 29

with atropine

Front 30

Epi CV effects

Back 30

= increased skeletal muscle BF; decreased skin, renal and GI BF; inc HR, dp/dt, CO, SBP and PP, decreased DBP with physiological doses

Front 31

DA used instead of NE or Epi to:

Back 31

maintain dp/dt post-MI bx DA inc RBF whereas NE and Epi dec RBF.

Front 32

Epi + halothane CV effect:

Back 32

arrhythmias

Front 33

Epi reversal with an alpha-blocker results in

Back 33

= only Beta effects = inc HR and RBF, dec TPR, BP, and ERP in heart
achieved by Epi + phentolamine

Front 34

Epi + Beta-blocker results in these CV effects:

Back 34

only alpha effects = increased BP
(eg propanolol)

Front 35

Epi added to local anesthetic agent to

Back 35

systemic absorption

Front 36

phenylephrine (PharmEffect) =

Back 36

alpha 1-agonist = mydriasis without cycloplegia (but still have pupillary light reflex)

Front 37

ritodrine (Beta2-agonist) decreases

Back 37

uterine contraciton in premature labor

Front 38

isoproterenol CV and Resp pharm effect

Back 38

(non-selective Beta1 & Beta2-agonist) so bronchodilation with increased HR

Front 39

albuterol, terbutaline resp pharm effect

Back 39

bronchodilation with less inc HR

Front 40

clonidine pharm effect

Back 40

pre- and post-synaptic alpha2-adrenoceptor agonist

Front 41

pre-tx with reserpine

Back 41

prevents indirect adrenergic agonism (no inc in BP with tyramine)

Front 42

tyramine-containing foods contraindicated in patients taking:

Back 42

phenelzine or tranylcypromine which non-selectively inhibit MAO-A and MAO-B

Front 43

methylphenidate, DOC for:
and S/E:

Back 43

tx ADHD/ADD
S/E's = depression, insomnia, decreased appetite and linear growth rate

Front 44

amphetamine toxicity =

Back 44

nervous, excited, agitated, increase HR/BP, toxic psychosis = paranoid schizophrenia, formication w excoriations, convulsions w OD;
difficult to distinguish from effects of cocaine

Front 45

tx amphetamine psychosis with:

Back 45

chlorpromazine

Front 46

ephedrine indirect adrenergic pharm effect=

Back 46

direct Beta1 and Beta2, indirect alpha - no alpha after reserpine

Front 47

Alpha blocker 3 P’s

Back 47

phentolamine, prazosin, phenoxybenzamine

Front 48

phentolamine/PBZ increases HR via baroreflex, which alpha blocker has no effect on HR

Back 48

prazosin

Front 49

ergotamine, dihydroergotamine
Pharm effect:
Used for tx of:

Back 49

partial alpha agonists
tx of migraine

Front 50

major S/E of alpha blockers

Back 50

orthostatic hypotension

Front 51

tamsulosin - blocks:
(which receptor and for what medical use)

Back 51

alpha1A-receptors in GU tract in patients w BPH to enhance voiding

Front 52

patient with pheo tumor - tx with:

Back 52

phentolamine = decreases BP = EPI reversal

Front 53

Epinephrine-reversal by:

Back 53

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

Front 54

atenolol/ metoprolol pharm effect

Back 54

block beta 1

Front 55

propranolol/timolol pharm effect

Back 55

block beta 1 and beta 2

Front 56

medical uses for beta blockers

Back 56

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]

Front 57

S/E of beta blockers

Back 57

CHF, bronchospasm, AV block, delayed recovery of [glucose] in pats w Type 1 DM after s.c. injection of too much insulin

Front 58

timolol medical use

Back 58

decreased IOP wo cycloplegia (do not use propranolol because it causes local anesthesia of cornea)

Front 59

beta blocker withdrawal syndrome

Back 59

patient tx w beta-blocker for angina -> discontinue drug -> increased cardiac Beta-receptor stimulation -> increased O2 demand -> angina and MI

Front 60

patient with hyperthyroidism, tx with

Back 60

with (PTU and) propranolol to decrease tachycardia and tremor and prevent the peripheral conversion of T4 to T3

Front 61

type I diabetic patient treated with glaucoma drug which causes hypoglycemia.

Back 61

timolol

Front 62

reserpine pharm effect

Back 62

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

Front 63

guanethidine pharm effects

Back 63

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

Front 64

cocaine pharm effects

Back 64

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

Front 65

cocaine medical uses

Back 65

local anesthetic effect via blockade of Na+ channels in sensory neurons

Front 66

cocaine OD

Back 66

dilated pupils, euphoria, hallucinations, excitation, halo vision, itchy skin, increase BP/HR, convulsions - difficult to distinguish from amphetamine toxicity/OD

Front 67

cocaine withdrawal syndrome

Back 67

sleepiness, depression, anhedonia

Front 68

MAO inhibitors medical use

Back 68

depression

Front 69

drugs that inhibit MAO-A and MAO-B

Back 69

phenelzine, tranylcypromine

Front 70

selegiline pharm effect

Back 70

selectively inhibits MAO-B to prevent breakdown of DA in CNS

Front 71

“cheese” reaction

Back 71

inhibition of MAO-A in gut wall allows dietary tyramine to enter the circulation; tyramine releases NE to cause HT and tachycardia

Front 72

clonidine and alpha-methyldopa (alpha-MD) pharm effects as antihypertensives

Back 72

decrease SNS activity via stimulation of alpha2-receptors in CNS: decrease plasma NE & renin activity (PRA) , HR

Front 73

clonidine and
alpha-methyldopa (alpha-MD)
S/Es

Back 73

S/E = sedation, dry mouth, edema
- S/E of alpha-MD = hepatitis, “flu” syndrome, (+) Coomb’s test

Front 74

clonidine withdrawal syndrome

Back 74

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)

Front 75

Drugs that decrease plasma NE

Back 75

clonidine, alpha-MD, guanethidine, reserpine, ganglionic blockers

Front 76

Drugs that increase plasma NE

Back 76

alpha blockers, hydralazine, minoxidil, diazoxide, nifedipine, HCTZ, sodium nitroprusside

Front 77

3 Arterial vasodilators

Back 77

hydralazine, minoxidil, diazoxide

Front 78

hydralazine, minoxidil, diazoxide pharm effects

Back 78

dilate resistance vessels = decrease TPR & BP; increase HR, dP/dT, CO , PRA and plasma NE

Front 79

hydralazine S/E

Back 79

edema ;SLE = arthralgia, arthritis, fever, malar (butterfly) rash, glomerulonephritis- d/c hydralazine and tx with steroid

Front 80

minoxidil S/E

Back 80

hirsutism, effect additive w finasteride; edema

Front 81

diazoxide S/E

Back 81

inhibition of insulin release = hyperglycemia; edema

Front 82

3 Drugs for HT emergency

Back 82

diazoxide, sodium nitroprusside (SNP), labetalol

Front 83

sodium nitroprusside (SNP) pharm effects

Back 83

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

Front 84

thiocyanate (tx w thiosulfate) and CN (tx w nitrite/thiosulfate) toxicity with Sodium Nitroprusside

Back 84

after Sodium Nitroprusside infusion in patients w poor renal function = muscle weakness, & spasm, disorientation)

Front 85

3 Ca++ blockers

Back 85

nifedipine, diltiazem, verapamil

Front 86

nifedipine, diltiazem, verapamil pharm effects

Back 86

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

Front 87

nifedipine, diltiazem, verapamil med uses

Back 87

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)

Front 88

Drugs which decreased dP/dT

Back 88

Beta-blockers, Ca++ blockers, diisopyramide

Front 89

Effects of Ang II

Back 89

increase BP, increases SNS activity via CNS, presynaptic enhancement release of NE, blocks NE uptake, release of ADH, release of aldosterone, decreases mesenteric BF.

Front 90

Drugs which decrease mesenteric BF to tx GI bleeding:

Back 90

NE & Ang II (get escape), ADH (a.k.a. AVP) & octreotide (no escape)

Front 91

2 ACE inhibitors

Back 91

captopril, enalapril - prevent conversion of Ang I to Ang II

Front 92

ACE inhibitor pharm effects

Back 92

) decrease TPR and BP with no change in HR and CO
2) block formation of Ang II, block enzymatic destruction of bradykinin (BK)

Front 93

ACE inhibitor S/E

Back 93

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

Front 94

ACE inhibitor MOA in tx of CHF

Back 94

increase CO by decreasing preload and afterload; reverses cardiac remodeling caused by angiotensin II (ang II)

Front 95

HT patient with DM, which drug to use

Back 95

tx w ACEI to decrease BP and decrease proteinuria (protects kidneys)

Front 96

acetazolamide pharm effect

Back 96

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

Front 97

acetazolamide MOA

Back 97

inhibits carbonic anhydrase in PT and DT to prevent reabsorption of bicarbonate

Front 98

acetazolamide med use

Back 98

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

Front 99

acetazolamide S/E

Back 99

hyperchloremic metabolic acidosis

Front 100

Simulators of respiration

Back 100

acetazolamide, nicotine, Epi, theophylline, caffeine

Front 101

Inhibitors of respiration

Back 101

EtOH
opiates - morphine
benzodiazepines - diazepam
barbiturates

Front 102

To make urine alkaline

Back 102

CAI or Na bicarbonate = increase renal Cl of acidic drugs

Front 103

To make urine acidic

Back 103

ammonium chloride = increase renal Cl of basic drugs

Front 104

2 Loop diuretic drugs, MOA

Back 104

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

Front 105

furosemide, ethacrynic acid pharm effects

Back 105

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

Front 106

furosemide, ethacrynic acid medical use

Back 106

used in tx of acute pulmonary edema, CHF, peripheral edema, hypercalcemia

Front 107

furosemide, ethacrynic acid S/E

Back 107

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

Front 108

Thiazides, hydrochlorothiazide MOA

Back 108

acts in distal tubule and  GFR in all patients

Front 109

Thiazides, hydrochlorothiazide pharm effects

Back 109

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

Front 110

Thiazides, hydrochlorothiazide med uses

Back 110

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%)

Front 111

hydrochlorothiazide S/Es

Back 111

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

Front 112

K+-Sparing diuretics

Back 112

TASK = triamterene, amiloride, spironolactone (aldosterone receptor antagonist)

All are contraindicated in renal insufficiency bx they can cause fatal hyperkalemia

Front 113

amiloride and triamterene MOA

Back 113

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

Front 114

spironolactone MOA

Back 114

aldo antagonists; partial agonist at androgen/progesterone receptors

Front 115

spironolactone pharm effects

Back 115

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

Front 116

spironolactone med uses

Back 116

4) used in tx of secondary hyperaldosteronism ass w cirrhosis, nephrotic syndrome;
5) reverses cardiac remodelling caused by aldosterone in patients with HF

Front 117

spironolactone S/Es

Back 117

hyperkalemia, gynecomastia (males), menstrual irregularities, hirsutism, deeped
voice (females)

Front 118

patient tx with OCP containing estrogen + norethindrone develops hirsutism - why? how to tx?

Back 118

hirsutism results from androgenic effects of the progestin norethindrone which is a derivative of 19-nortestosterone; tx with spironolactone

Front 119

postmenopausal female develops hirsutism - how to tx?

Back 119

spironolactone

Front 120

patient with an adrenal tumor has increase BP and plasma [HCO3-], decrease plasma [K+] and PRA; plasma [Na+] is normal -> dx? and tx?

Back 120

Conn's syndrome = aldosterone-secreting adrenal tumor; tx with spironolactone

Front 121

hypokalemia from furosemide and HCTZ prevented by:

Back 121

K+-sparing diuretic drugs, ACE inhibitors, Beta-blockers, and, to a certain extent, by p.o. K+ supplements

Front 122

digoxin kinetics:
digitoxin kinetics:

Back 122

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

Front 123

Cardiac Glycosides:

Back 123

digoxin, digitoxin

Front 124

cholestyramine and digoxin

Back 124

chole and antacids binds digoxin and decrease absorption and effect

Front 125

digoxin in older pts

Back 125

decrease Vd, so decrease loading dose: decrease GFR, so decrease maintenance dose older patients can have decrease GFR with normal serum [Cr]

Front 126

quinidine effect on digoxin

Back 126

increase plasma digoxin by displacing digoxin from skeletal muscle and decreasing renal Cl

Front 127

digoxin MOA

Back 127

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

Front 128

digoxin med use

Back 128

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

Front 129

digoxin S/E

Back 129

bradycardia, AV block, PVC’s; n/v (CTZ); CNS-abnormal color vision, halo vision, esp. in elderly

Front 130

Antidysrhythmic drugs

Back 130

quinidine, procainamide, disopyramide, lidocaine, amiodarone, verapamil

Front 131

quinidine MOA

Back 131

MOA: blocks Na+ channels in fast fibers

Front 132

quinidine pharm effects

Back 132

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)

Front 133

quinidine med uses

Back 133

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

Front 134

quinidine S/E

Back 134

hypotension (alpha-blockade),decrease dp/dt, diarrhea (limits use), tinnitus w OD

Front 135

pt w atrial fibrillation given quinidine to slow ventricular rate, but ventricular rate increases
soon after quinidine. Why? What to do about it?

Back 135

immediate atropine-like effect of quinidine increase AV conduction; tx w verapamil or diltiazem to decrease AV conduction and slow ventricular rate

Front 136

lidocaine MOA

Back 136

block of Na+ channels in fast fibers - given i.v. due to low F

Front 137

lidocaine pharm effect

Back 137

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

Front 138

lidocaine S/E

Back 138

seizures, tx w benzodiazepine (BZ)

Front 139

disopyramide pharm effects

Back 139

marked decrease in dp/dt
marked antimuscarinic effects: dry mouth, constipation; contraindicated in BPH & glaucoma

Front 140

amiodarone MOA

Back 140

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)

Front 141

amiodarone medical use

Back 141

recurrent ventricular tachycardia/fibrillation

Front 142

amiodarone S/E

Back 142

pulmonary fibrosis, hypo- or hyperthyroidism; blue, purple or slate gray skin; corneal microdeposits

Front 143

verapamil MOA

Back 143

blocks L-type Calcium channels at SA and AV nodes and cardiac myocytes

Front 144

verapamil pharm effects

Back 144

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

Front 145

verapamil medical use

Back 145

used to tx AV nodal re-entry tachycardia

Front 146

verapamil S/E

Back 146

decrease dp/dt; decreased CO in HF, AV block

Front 147

patient with atrial fibrillation and no HF has palpitations and dizziness -> tx with verapamil -> MOA?

Back 147

increase ERP of AV node slows ventricular rate -> improved AV filling -> increase CO

Front 148

aspirin as an antiplatelet drug

Back 148

irreversibly inhibits COX-1 of platelets to prevent the
synthesis of TXA2

Front 149

abciximab, eptifibatide, tirofiban

Back 149

antagonists of the platelet IIb/IIIa which uses fibrinogen to bind platelets together

Front 150

ticlopidine and clopidogrel

Back 150

antagonist of platelet purinergic (ADP) receptors

Front 151

a patient requires an antiplatelet drug after MI or stroke, but the patient has aspirin hypersensitivity. How to Tx?

Back 151

ticlopidine or clopidogrel

Front 152

heparin MOA

Back 152

accelerates binding of antithrombin III (AT III) to activated clotting factors 2, 9-12, increases aPTT

Front 153

heparin kinetics/pharm effect

Back 153

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

Front 154

heparin medical uses

Back 154

MI and DVT’s

Front 155

heparin S/E

Back 155

bleeding, antiplatelet effect additive w aspirin, thrombocytopenia

Front 156

heparin antagonist

Back 156

protamine sulfate

Front 157

3 LMW heparins

Back 157

ardeparin, dalteparin, enoxaparin

Front 158

LMW heparins kinetcs/pharm effects
(as different from heparin)

Back 158

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

Front 159

warfarin, dicumarol MOA

Back 159

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

Front 160

warfarin, dicumarol antidote

Back 160

vit K1 (phytonadione), fresh frozen plasma, factor IX concentrate (contains factors 2,7,9 & 10)

Front 161

warfarin, dicumarol pharm effects

Back 161

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

Front 162

warfarin, dicumarol medical uses

Back 162

DVT’s, prevent emboli with prosthetic cardiac valves and A-fib

Front 163

warfarin, dicumarol metabolism

Back 163

metabolized by CYP450

Front 164

inhibitors of CYP450
(increasing plasma warfarin and PT)

Back 164

cimetidine, ketoconazole, isoniazid, erythromycin and grapefruit juice

Front 165

inducers of CYP450
(decreasing plasma warfarin and PT)

Back 165

carbamazepine, phenobarbital, phenytoin, rifampin, chronic EtOH, benzopyrene (cigarette smoke)

Front 166

patient OD's with warfarin are attempts suicide with rat poison -> which clotting factors and lab tests affected?

Back 166

decrease activity of factors 2,7,9 and 10; increase aPTT and PT; no effect of factors 8 or 13 or bleeding time

Front 167

Which type of cardiac dysrhythmia requires tx with warfarin?

Back 167

A-fib

Front 168

Thrombolytic (fibrinolytic) drugs general MOA

Back 168

all ultimately convert plasminogen to plasmin: plasmin destroys fibrin to lyse clots

Front 169

urokinase MOA

Back 169

direct activation of plasminogen

Front 170

tPA MOA

Back 170

when tPA and plasminogen bind to fibrin in close proximity, plasminogen converted to plasmin by tPA = normal, intrinsic activation of plasmin

Front 171

streptokinase MOA

Back 171

changes conformation of plasminogen to expose an active protease site that hydrolyzes another plasminogen molecule to plasmin

Front 172

streptokinase S/E
(same with all fibrinolytic drugs)

Back 172

systemic destruction of clotting factors 5 & 8 causes bleeding, esp. in CNS (hemorrhagic stroke)

Front 173

pt with MI treated with several drugs -> develops intracranial bleeding -> which drug caused it?

Back 173

streptokinase

Front 174

aminocaproic acid MOA

Back 174

a lysine analog that binds to the lysine-binding sites on plasmin which blocks the binding of plasmin to fibrin

Front 175

statins MOA

Back 175

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

Front 176

statins net effect

Back 176

decrease Tc, LDL and TG's; slight increase in HDL

Front 177

statins S/E

Back 177

myositis/myopathy = muscle pain and weakness ass with increase CPK; muscle damage can progress to rhabdomyolysis

Front 178

ezetimibe MOA

Back 178

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

Front 179

ezetimibe net effect

Back 179

selective for LDL cholesterol, so only Tc and LDL decrease

Front 180

ezetimibe medical use

Back 180

to tx patients who develop muscle weakness on a statin

Front 181

gemfibrozil and fenofibrate MOA

Back 181

activates lipoprotein lipase (esp. in skeletal muscle) to increase hydrolysis of VLDL

Front 182

gemfibrozil and fenofibrate net effect

Back 182

decrease Tc, LDL, VLDL and TG's; slight increase in HDL

Front 183

gemfibrozil and fenofibrate medical use

Back 183

to tx hypertriglyceridemia

Front 184

gemfibrozil and fenofibrate S/E

Back 184

myositis/myopathy = muscle pain and weakness ass with increase CPK; muscle damage can progress to rhabdomyolysis

Front 185

niacin medical use

Back 185

to increase HDL cholesterol

Front 186

niacin S/E

Back 186

flushing and itching in face and upper body

Front 187

MOA of Antianginal drugs

Back 187

all decrease oxygen demand and/or increase oxygen supply; all increase endocardial blood flow

Front 188

atenolol, metoprolol, propranolol, timolol MOA for angina

Back 188

negative chronotropic & inotropic effects decreases the rate-pressure product (HR x SBP); also decrease cardiac afterload (= decreased DBP)

Front 189

atenolol, metoprolol, propranolol, timolol net effect for tx of angina

Back 189

decreased cardiac oxygen demand

Front 190

nitroglycerin a.k.a. glyceryl trinitrate, isosorbide mono- and dinitrate MOA

Back 190

NO donors which selective venodilate; venodilation decrease venous return to decrease LV wall tension during diastole and systole

Front 191

nitroglycerin a.k.a. glyceryl trinitrate, isosorbide mono- and dinitrate net effect

Back 191

decreased cardiac oxygen demand

Front 192

problem with using nitroglycerin

Back 192

drug tolerance is a big problem

Front 193

verapamil, diltiazem MOA for angina

Back 193

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

Front 194

amlodipine, felodipine MOA for angina

Back 194

decreased cardiac afterload (DBP) and increased blood flow through large epicardial vessels and small endocardial resistance vessels

Front 195

verapamil, diltiazem, amlodipine, felodipine net effect

Back 195

net effect in both cases: decreased oxygen demand and increased oxygen supply

Front 196

Tx of Congestive Heart Failure = systolic dysfunction

(IMPORTANT!)

Back 196

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