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Pharmacology Flashcards

1
Q

Xenobiotic

A

Foreign to body

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2
Q

Phase I Metabolism - 3 jobs

A

To render lipophilic molecules more polar/hydrophilic, provide functional groups, and enzymatic oxidation, reduction, hydrolysis

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3
Q

Cyp 450s

A

principally responsible for phase I; most expressed in liver; Cyp1A2, Cyp2C9, Cyp2C19, Cyp2D6, Cyp3A4; most abundant is Cyp3A4; increased activity induced by many drug and chemicals; previous exposures to chemicals can dramatically later drug metabolism; acute or chronic use of one drug can alter metabolism of other drugs in a patient

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4
Q

Induction of Cyp 450

A

induced by nuclear receptors - examples include Aryl Hydrocarbon Receptor with ligands PAHs, caffeine; constitutive Androstanol Receptor with ligands rifampicin, warfarin; prengenolone X Receptor with ligand simvastatin

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5
Q

Phase II metabolism - job

A

involves conjugation of Phase I metabolites to large polar molecules

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6
Q

Glucuronidation

A

Most common phase II conjugation reaction; occurs in liver by UDP-GT enzyme - low activity at birth, rises linearly, and plateaus in adulthood, declines in old age

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7
Q

Clinical Manifestations of low Glucuronidation (3)

A

Neonatal hyperbilirubinemia - inability of newborn (esp. premature) to metabolize ilirubin - CNS damage due to buildup of bilirubin
Chloramphenicol (antibiotic) - deficiency in UDP-GT, excessive free drug in blood and tissues and drug associated toxcities
Crigler-Naijar Syndrome - almost total genetic deficiency in hepatic UDP-T babies are highly jaundiced, death occurs in early childhood

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8
Q

Beta Glucuronidate

A

present in mucosa of SI; hydrolyzes glucuronate conjugates, releasing free drug reabsorbed by GI - hepatic circulation of drug which prolongs retention time and biological effects

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9
Q

Phase II Conjugation Reaction

A

Sulfate conjugation; glutathione S-transferases; Methyl Conjugation; amino acid conjugation; N-acetylation conjugation (some are slow acetylators and some are fast

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10
Q

Factors influencing Drug Metabolism

A

Genetic factors; sex differences (not much in humans); Disease states; drugs and duration (EtOH - acute intake inhibits drug metabolism while chronic intake increases it); developmental age; nutrition

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11
Q

Nutritional Effects on Drug metabolism (3 of them)

A

Brussel sprouts, cabbage, cauliflower, dark green inducers of P450 - have potent inducers of P450

Grapefruit Juice - inhibits Cyp3A4 metabolism and increase bioavailability and toxicity of meds

Charcoal broiled beef diet induces AHR

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12
Q

Drug Transporters

A

ABC (ATP BInding Cassette):
P-Glycoprotein (Pgp) - primarily transport parent molecules out of cells; MRP and related - transport Phase II conjugates of drugs and/or conjugated drug metabolites

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13
Q

Generic vs. Brand drugs

A

same active ingredient, identical dose; comparable kinetics - 10% of AUC and Tmax of brand name ones

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14
Q

Pharmacokinetics

A

what the patient does to the drug - Absorption, Distribution, Metabolism, and Excretion

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15
Q

Pharmacodynamics

A

What the drug does to the patient - intended, unintended, and socio-economic

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16
Q

Ibuprofen (e.g. Motrin; related Naproxen)

A

Pharmacologic class - NSAID
Therapeutic - analgesic, antipyretic, anti-inflammatory, anti-gout, anti-dysmennorhea
Pharmacodynamics - inhibition of prostaglandin synthesis via COX1 and COX2
pharmacokinetics - extensive metabolism in liver
avoid in pts. allergic to ASA
caution in renal failure, geriatric pts
drug interactions - warfarin, ASA, diuretics, antiHTN
OTC - 200-400mg po q4h prn

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17
Q

Dose -response

A

degree of response is a function of the amount of drug administered to the organism

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18
Q

Quantal Dose-Response Data

A

all or none effect; drug given to many animals at different doses and response is scored; information about the population; will have hyper-respondent and hyper-resistant individuals

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19
Q

Graded or continual dose-response

A

individual’s incremental response to increasing doses of drug

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20
Q

Drugs have 3 effects

A

1) primary effect - desired effect which is of therapeutic value
2) side effect or undesirable effect - not target effects, but not necessarily bad, and may be primary in other settings
3) toxic effects - bad!, loss of function, necrosis, organ failure, death

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21
Q

Important components of dose (5)

A

Amount, duration and frequency, chemical form, physical form, and route of exposure

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22
Q

Therapeutic Index

A

LD50/ED50 - should be greater than 1 and the bigger, the better; ideally want more than 10; based on population response, but importance is separatin of therapeutic benefit and toxic doses in individuals

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23
Q

Margin of Safety Index

A

LD1/ED99; more conservative; should be greater than 1 and bigger is better

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24
Q

Protective Index

A

ED50(desirable)/ED50(undesirable); should be greater than 1 and bigger is better

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25
Q

Chronicity Index

A

one dose LD50/ninety-dose LD50; 1 is best, 90 is worst (no clearance); cumulative toxicity

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26
Q

Threshold dose

A

all or none phenomenon at specific threshold dose; underlying biochem mechanisms may be a continual dose-response, but apparent threshold is observed at physiologic level; e.g. acetaminophen toxicity

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27
Q

Potency

A

relative dose required to produce a given effect; doesn’t equal affinity
Changed with non-competitive antagonists

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28
Q

Intrinsic Activity

A

referred to as efficacy in intact patient refers to magnitude of the maximal response (highest dose); doesn’t equal efficacy
changed with competitive antagonists

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29
Q

Chemical Antagonism

A

direct interaction of agonist and antagonist

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30
Q

Functional Antagonism

A

two agonists act independently but lead to opposite biological effects

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31
Q

Competitive Antagonism

A

antagonist binds to receptor but elicits no response and competes with agonist for binding and blocking against action - have equilibrium (reversible) and non-equilibrium (irreversible)

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32
Q

Two State Receptor Model

A

active and inactive state - ligands bind and shift equilibrium toward one state or the other - agonists shift it to active state and inverse agonists toward inactive state; true antagonists could interfere with binding of both agonists and inverse agonists

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33
Q

Partial Agonism and Antagonism

A

low intrinsic activity; can have properties of both agonist and antagonist; used to dampen responses

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34
Q

Additivity

A

effect of two drugs in combination is additive to either drug given alone

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35
Q

Simple Synergy

A

each drug acts alone and combination is greater than additive

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36
Q

Potentiation

A

one or both has no apparent effect alone, but dramatically alters effects of other drug in combination

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37
Q

Absorption

A

movement of drug from site of administration to the blood

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38
Q

Distribution

A

delivery of drug from blood to tissues and target site(s)

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39
Q

Bioavailability

A

most important parameter; amt of drug that actually reaches target site in pharmacologically active and bioavailable form

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40
Q

pH of compartment

A

degree of ionization affects partition coefficient and extent of diffusion; ionized forms of drugs (acidic drugs in ph more basic than pKa and basic drugs in pH lower than pKa) aren’t well absorbed
weak bases like Kanamycin that get trapped in stomach are great to treat GI infections

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41
Q

where to sample for drugs in OD?

A

acidic drugs in blood and sample for basic drugs in stomach regardless of route of admin

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42
Q

Oral Absorption of Drugs

A

high blood supply; rapid absorption; sublingual administration increases absorption as there’s more resident time; can be used to deliver rapidly and directly to blood stream and avoid metabolism

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43
Q

Stomach Absorption of Drugs

A

only weak acids abosrobed; can get ion trapping of weak bases

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44
Q

Small Intestine Absorption of Drugs

A

large surface area, rich and high blood supply; most drugs absorbed in proximal jejunum; predominant process is passive diffusion but depends on what pt. ate; shortened transit time can decrease absorption

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45
Q

Large Intestine Absorption of Drugs

A

less surface area and vascular stuff than SI; rectal useful for pts with vomitting, GI surgery, or obstruction; bypasses 1st route kinetics

46
Q

Factors affecting GI absorption

A

Gastric emptying time; Intestinal motility; food and food consumption; formulations of drugs; metabolism and digestion

47
Q

Drug Absorption by Lung

A

inhaled gases, anesthetics, smokes, etc; large SA, thin cell layer, highly vscularized; high partition coefficient (lipophilic) anesthetics cross very readily

48
Q

Drug absorption by Skin

A

creams and lotions for local dosing; effective for slow, long term dosing

49
Q

Absorption for IM or SC (advantages and disadvantages)

A

Advantages - rapid, precise, large volumes

Disadvantages - pain, tenderness, local tissue necrosis, microbial contamination, nerve damage

50
Q

Absorption for IV (advantages and disadvantages)

A

Advantages - direct to blood and circumvents entire absorption process; useful for drugs with narrow TI or poor absorption; very rapid
Disadvantages - in OD, can’t remove drug or block or slow absorption, risk of embolism, microbial contamination, local necrosis

51
Q

Selective Accumulation of Drugs (5 places)

A

Kidney - susceptible to toxicity due to high CO
Eye - retinal pigment binds drugs
Fat - accumulate drugs, low blood flow so slow in and out except if fasting
Lung - 100% of CO, selectively accumulate basic amines
Bone (including teeth) - very slow in and out

52
Q

Placental Barrier

A

MYTH! Not a barrier - lipophilic drugs can cross readily and assume fetus will get at least the dose you are giving mum

53
Q

Simple One Compartment Model

A

body is a single, homogenous fluid-filed compartment; drug instantly distributed homogenously - many drugs modeled this way

54
Q

Multi-Compartment Model

A

many drugs need 2, 3 or more compartments; drugs distributed rapidly to highly perfused tissues and more slowly to other tissues

55
Q

First Order Kinetics (including equation)

A

X = X0(e)^-kt; drugs is removed at the same rate not same amount; if route of elimination is saturated, it can follow zero order kinetics

56
Q

Zero order kinetics

A

constant amount of drug is removed per unit time (EtOH, aspirin, and phenytoin)

57
Q

Two phases of elimination for two compartment model

A

Redistribution between two compartments - can’t really measure rate of elimination - alpha slope

then measure rate of elimination once two compartments have equilibrated - beta slope

58
Q

Drug Half Life

A

T1/2 = 0.693/Kel

59
Q

Volume of Distribution

A

volume that appears to be based on concentration in central compartment - used to figure out how much you need to give to get a certain concentration
doesn’t correspond to actual physiological space but is a calculated value

60
Q

Clearance (including equation)

A

primary parameter that defines elimination rate

Clp = Kel X Vd

61
Q

Clearance from plasma

A

Clp; amount of plasma cleared per unit time, not the amt of drug removed

62
Q

Fractional Dose (and equation)

A

F = AUC (oral)/AUC (iv); needed for accurate dosing

63
Q

Steady State Concentration (and equation)

A

Css; dependent on infusion rate, K0, and clearance; takes ~4half lives to reach Css; to avoid delay use loading dose (D* = CssXVd)

64
Q

Norepinephrine (NE) metabolism

A

by 2 enzymes - Catecholamine O Methyltransferase (COMT) and Monoamine Oxidase (MAO)

65
Q

Norepinephrine

A

noradrenaline, levophed; stimulate alpha 1 - increases CO, SVR, MAP, decrease blood flow to skin, muscle and kidney; stimulate beta 1 - in heart, increasing HR and contractility
given IV only; half life 1-2 minutes; excessive vasoconstriction in mesenteric vessels, peripheral arterioles; use cautiously in pt taking MAO inhibitor; risk of HTN in pt with propranolol; for acute hypotension and shock; monitor BP, HR, infusion site, evidence of extravasation; correct volume depletion with IV fluids before giving NE infusion

66
Q

Epinephrine

A

Adrenaline, EpiPen; Vasopressor, cardiac stimulant, bronchodilator, adjunct to local anesthetics, treatment for anaphylaxis;
Alpha 1 - vaso and venoconstriction
Beta 1 - tachycardia and increased contractility
beta 2 - bronchodilation; help in severe anaphylaxis by stabilizing mast cells
given IV, IM, SC, inhaled, ophthalmic topical
can be HTN, hemorrhagic stroke, angina, arrhythmias
risk of excessive HTN in pts taking propranolol
monitor BP, HR, rhythm, infusion site

67
Q

Dopamine

A 
can't get through the blood brain barrier; agonist at DA, beta1, and alpha 1 receptors
DA agonist at low dose, then beta 1 comes in, and then alpha1
increased contractility (beta1), vasoconstriction (alpha1), improved mesenteric and renal perfusion (DA)
given IV, short term
68
Q

Phenylephrine (alpha)

A

neosynephrine; alpha 1»alpha 2; vasoconstriction and venoconstriction by stimulating contraction of vascular smooth muscle cells
nasal decongestant, mydriatic, increase BP in vasodilated state
not inactivated by COMT
don’t use longer than 3 days - nasal congestion can get worse if stop suddenly

69
Q

Clonidine (alpha)

A

Catapres; synthetic, selective alpha2 agonist, stimulates alpha 2 receptors in brainstem causes down regulation of SNS; treat HTN, treat or prevent migraine
given orally or patch, causes sedation or dry mouth

70
Q

Isoproterenol (beta)

A

synthetic beta 1 and 2 agonist; increase cardiac contractility, increase HR, increase cardiac conduction; will cause vasodilation and hypotension and tachyarrhythmias

71
Q

Dobutamine (beta)

A

beta1 receptor agonist; increases contractility more than HR; useful in ICU for patients in cardiogenic shock when don’t want to produce tachycardia; can have HTN and ectopy

72
Q

Albuterol (beta)

A

beta2 agonist; SM cells in airways, rescue inhaler for asthma, COPD, inhibit premature labor; rarely given as IV infusion to delay labor; side effects - anxiety, tachycardia, tremor

73
Q

Mirabegron

A

myrbetric; beta 3 receptor agonist; SM of bladder, reduces detrusor muscle tone; treatment of overactive bladder; increases bladder capacity; administered orally, don’t use for BPH

74
Q

Ephedrine

A

acts indirectly to release NE from adrenergic nerve endings, mild to moderate hypotension during surgery, nasal congestion, potent CNS stimulant, side effects include HTN, insomnia

75
Q

Pseudoephedrine

A

Sudafed; synthetic derivative of ephedrine; indirectly releases NE and some direct agonism at alpha and beta adrenergic receptors; nasal and sinus decongestant, less ability to dilate bronchioles than ephedrine; don’t take if have HTN

76
Q

Amphetamine

A

indirectly releases NE from adrenergic nerve endings; no FDA approved indications; can be used for obesity, narcolepsy, ADHD (adderall); very high risk of dependence, insomnia, restlessness, tremor

77
Q

Tyramine

A

not prescribed, but in a lot of food and could have food-drug interactions; present in aged/fermented foods like red wine, smelly cheeses, pickled herring; acts indirectly to release NE; metabolized in liver by MAO; watchout in pts on MAO inhibitor drugs

78
Q

Cocaine

A

indirectly to block reuptake of NE at synapse and stimulates release of NE, Epi, DA; acts as local anesthetic and CNS stimulant; nose bleeds, anesthesia for corneal surgery; can be smoked, snorted, or injected; side effects HTN, tachycardia, arrhythmias, seizures, MI

79
Q

Prazosin

A

Minipress; selective alpha 1 blocker; anti HTN, treatment of BPH, treatment of Raynaud’s, treatment of kidney stones; blocks alpha 1 receptors on arterioles and veins; available po or transdermal; variable oral bioavailability; extensively metabolized in liver;
toxicity - excessive hypotension , esp. orthostatic esp in pts on diuretics; start gradually and at bedtime; monitor BP, weight, edema; tend not to use as monotherapy due to potential reflex of tachycardia, increased RAAS, given with diuretics

80
Q

Tamsulosin

A

Flomax; alpha 1 blocker; rx of obstructive symptoms of BPH; relaxation of SM in bladder neck and prostate - improving urine flow; >90% metabolized by Cyp450enzymes; toxicity - excessive hypotension with syncope; additive effects with most other antihypertensives; rule out prostate carcinoma before beginning treatment

81
Q

Phentolamine

A

Regitine; competitive alpha blocker; antihypertensive drug for pts with pheochromocytoma; only IV, short half life; excessive hypotension with syncope; rule out prostate carcinoma; can be used for treatment of ureter spasm in renal colic; used for intra op management of pheochromocytoma

82
Q

Atenolol

A

Tenormin, metoprolol, toprol; beta 1 blocker; anti HTN, antiarrhythmic, primary and secondary prevention of MI, antianginal; preference for beta 1 over beta 2; po or iv; renally excreted; metoprolol is hepatic metabolims and shorter half life; excessive hypotension, bradycardia, heart block; less efective in preventing stroke; renally excreted; may be esp. useful in HTN patients with exertional angina, MI, a-fib, watch for abrupt withdrawal

83
Q

Propranolol

A

Inderal; non specific beta blocker; anti HTN, antiarrhythmic, primary and secondary prevention of MI, anti-anginal; po or iv; cleared by hepatic metabolism; toxicity - excessive hypotension, bradycardia, heart block can worsen severe CHF;

84
Q

Labetalol

A

Trandate; also Carvedilol/coreg; mixed alpha-beta receptor blocker; anti HTN, treatment of stable CHF; reduces BP by blocking access of NE to beta receptors; high first-pass effect; toxicity - avoid in pts with bradycardia, heartblock, CHF, asthma, shock, use with caution in patient with cardiomyopathy, pheochromocytoma, use in pregnancy when woman has severe HTN; most commonly given IV small boluses; reduced doses in patients with impaired liver function

85
Q

Normal HTN

A

SBP

86
Q

Pre HTN

A

SBP 120-139; DBP 80-89

87
Q

Stage 1 HTN

A

SBP 140-159 or DBP 90-99

88
Q

Stage 2 HTN

A

SBP >160 or DBP >100

89
Q

Four classes of anti-HTN drugs

A

Thiazide diuretics (HCTZ); long acting CEB (amlodipine); ACE inhibitor (lisinopril); Angiotensin Receptor Blocker (losartan)

90
Q

Treatment Goals for HTN

A

general population 80y/o - goal is

91
Q

Pathophysiology of HTN

A

When BP drops, sensed by baroreceptors at aortic arch and carotid body → signal to medulla which sends nerve down to T1-L2 spinal levels (glutamine synapse here) → sympathetic nerve which synapses at a ganglion and releases ACh onto Nn receptors → nerves out to arteries (vasoconstriction via NE at alpha1 receptors), veins (venoconstriction via NE at alpha1 receptors), SA node (increase HR via NE at beta1 receptors), AV node (increase conductivity via NE at beta1), Ventricular muscle (increase contractility via NE at beta1), and kidney → kidney retain NaCl and water and produces renin, which produces angiotensin I → converted to angiotensin II (by Angiotensin Converting Enzyme) → Angiotensin II acts on vasoconstriction via angiotensin receptor I

92
Q

Thiazide Diuretics (3 types)

A

Thiazides (HCTZ, chlorthalidone); Loop diuretics (Furosemide); K sparing diuretics (spironolactone)

93
Q

Inhibitors of RAAS systems (2 types)

A 
ACE inhibitors (lisinopril)
Angiotensin receptor blockers (losartan)
94
Q

Vasodilators (2 types)

A 
Direct acting (Nitroprusside, hydralazine)
Calcium entry blockers (amlodipine, verapamil, nifedipine)
95
Q

Sympathlolytic Agents (4 types)

A

act within CNS (clonidine)
act on autonomic ganglia (trimethaphan)
act on post-ganglionic neurons (reseprine)
block peripheral adrenergic receptors (atenolol, prazosin, labetalol)

96
Q

Hydrochlorothiazide

A

HydroDiuril; also chlorthalidone
diuretic, antihypertensive; blocks reuptake of Cl and Na from tubular fluid after glomerular filtration, also causes decrease in SVR via altering [Ca] in SM of endothelial cells by altering [Na]
lower BP by 10-15mmHg
F~70%; toxicity - excessive hypotension, allergy to sulfa antibiotics, cause K and Mg depletion, cause Na and Cl depletion, metabolic alkalosis, volume depletion
more side effects in geriatric patients
Chlorthalidone might be preferable - greater reduction, better control, longer half life

97
Q

Lisinopril

A

Prinivil, Zestril, Captopril; ACE inhibitor; anti HTN, treatment of CHF, preserving renal function, preserving LV function after MI, acute management of MI; inhibits conversion of AT I to ATII by ACE, diminishes vasoconstriction and stimulation of aldosterone
toxicity - orthostatic hypotension, use with caution in patients with impaired renal function or renal artery stenosis, angioedema (in african americans esp.), dry cough due to destruction of bradykinin
category C/D in pregnancy due to abnormal cartilage development in fetus

98
Q

Losartan

A 
CoZaar; angiotensin 1 receptor blocker; antihypertensive, preserve renal function, treatment of CHF
blocks stimulation of AT1 receptor by angiotensin II, reducing vasoconstriction and production of aldosterone
F!30%; toxicity - dizziness, orthostatic hypotension, worsening of renal failure
pregnancy class C/D - use care in patients on diuretics, those with renal artery stenosis, those with mitral or aortic stenosis
Pts who had angioedema with ACE inhibitor - some will have it with this as well
99
Q

Nitroprusside

A

Nipride, Nitropress; not given chronically; vasodilator; antihypertensive, management of severe CHF, management of pulmonary HTN, produce controlled hypotension to reduce bleeding during surgery; acts directly on vascular SM to cause dilatation; relase Cn and NO to activate gunaylate cyclase - production of cGMP; only route is IV, CN metabolite converted to SCN in liver and excreted in urine; toxicity - excessive hypotension, accumulation of CN and thiocyanate, headache, decreased blood flow to brain; monitor patient closely!; for treatment of HTN crisis only

100
Q

Hydralazine

A

Apresoline; rarely given chronically; peripheral vasodilator; antihypertensive, treatment of CHF, vasodilator; acts by inducing endothelium to produce NO; given po, im, iv; toxicity - more dangerous in patients with renal disease, prior stroke, angina; watch for hypotension, edema, occassionally drug-induced lupus; never use as chronic oral monotherapy since edema and reflex tachycardia will result; used in pregnancy - safe for fetus but causes fluid accumulation

101
Q

Amlodipine besylate

A

Norvasc; dihydropyridine calcium entry blocker; antihypertensive, antianginal; reduces BP by inhibiting influx of Ca through slow channels, dilating peripheral arterioles; produces negative inotropic effect; inhibits spasm of coronary arteries in vasospastic angina; toxicity - hypotension, AV block, worsening CHF, watch out for pts with aortic stenosis, heart failure, severe liver disease; shorter acting nifedipine can increase risk of MI; pregnancy class C

102
Q

Verapamil

A

Ca entry blocker; antihypertensive, antianginal, antiarrhythmic; reduces BP by inhibiting influx of Ca through slow channels and dilating peripheral arterioles; negative inotropic effect; toxicity - hypotension, AV block, worsening of CHF, bradycardia; use reduced doses in patients with both renal and hepatic diseases; short acting nifedipine can increase risk of MI

103
Q

Clonidine

A

Catapres; central alpha 2 agonist, acts in brainstem to turn down output of NE; need to drip into brainstem for optimal use but give tablet/patches; antihypertensive, adjunct to Rx of opioid withdrawal, prophylaxis of migraine; withdraw gradually b/c of risk of rebound HTN, risk of bradycardia in sinus node disease, lethargy, fatigue, depression; additive sedation with other CNS drugs; special consideration - pregnancy clas C

104
Q

Trimethaphan

A

Arfonad; use as IV infusion briefly (only in OR or ICU); ganglionic transmission blocker; antihypertensive; blocks nicotinic transmission within both sympathetic and parasympathetic ganglia; produces veno- and vasodilation; useful only when given IV; fall in BP within minutes; watch out for sudden, severe drop in BP, fall in HR; only used during general anesthsia; given by IV infusion, only to treat HTN crisis; minute-to minute monitoring of BP and HR; given in neurosurgery, esp. when clipping an aneurysm

105
Q

Reserpine

A

no brand name; antihypertensive; binds to vesicles with NE or 5HT preventing uptake - ultimately dpelete neuron of NE or 5HT - effect takes 2-3weeks to develop; decreases NE in all neurons in CNS; good oral bioavailability; dizziness, orthostatic hypotension, depression; NOT used for long term management due to side effects

106
Q

Sympathetic NS Anatomy

A

thoracolumbar nerve roots T1-L3; noradrenergic sympathetic neurons from sympathetic ganglia to effector organs; cholinergic sympathetic neurons run from thoracolumbar segments of spinal cord to ganglia

107
Q

Parasympathetic NS Anatomy

A

Craniosacral - CNs III, VII, IX, X and S2-S4 nerve roots; both have cholinergic neurons from CNS–> ganglia and ganglia –> organ

108
Q

Somatic motor NS goes to

A

to skeletal muscle for physical movement under conscious control; has motor neurons and sensory nerves may travel in same nerve

109
Q

Autonomic NS goes to

A

to smooth muscle, cardiac muscle, exocrine glands, other organs (kidney) to regulate and is mostly under unconscious control; motor neurons only

110
Q

Adrenoreceptors (6 types)

A

Alpha 1 in smooth muscles, glands; Gq increase IP3, DAG, increase Ca2+
Alpha 2 in nerve endings, Gi, decrease cAMP, decrease transmitter release
Beta 1 in cardiac muscle, JGA, Gs, increase cAMP, increase HR and contractility
Beta2 in SM, liver, and heart, Gs, increase cAMP, relax bronchiolar SM
Beta 2 in adipose tissue, Gs, increase cAMP, increase lipolysis
Dopamine 1 in SM, Gs, increase cAMP, relax vascular SM in renal arterioles

111
Q

Cholinergic Receptors (5 types)

A

M1 on nerve endings - Gq coupled, increase IP3, DAG cascade
M2 in heart and on some nerve endings, Gi coupled
M3 in smooth muscle, glands, endothelium, Gq coupled
Nn (nicotinic, NT type) in ANS ganglia
Nm (muscular) in neuromuscular end plate

112
Q

Sarin nerve gas

A

increases effects of ACh throughout body by inhibiting AChE; kills due to bronchorrhea and skeletal muscle paralysis

Board prep (2 decks)

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