Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > EXAM 2 - FULL REVIEW > Flashcards

EXAM 2 - FULL REVIEW Flashcards

1
Q

Autonomic nervous system

A

Systems not under conscious control, sympathetic/parasympathetic nervous system and enteric (gut with neurons?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Sympathetic responses

A

increased HR/BP, dilated bronchioles, shunting to needed muscles. fight or flight bruh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Parasympathetic response

A

Rest and digest, conserve energy, shunt blood to endocrine, gi, urogenital.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Function of chain ganglia, and how they are similar to PNS plexi

A

sympathetic chain ganglia run along sides of spinal cord and transmit information for the sympathetic response.

PNS plexi help distribute parasympathetic response to specific organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sympathetic NS response, NTs, receptors, anatomy

A

originates from thoracolumbar region of spinal cord, short preganglionic fibers that release ach and long postganglionic fibers that release NE.

Uses receptors A1/2, b1/2/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Paraympathetic NS response, NTs, receptors, anatomy

A

slow HR, promote digestion. Uses ach at both pre and post ganglionic neurons. Uses muscarinic and nicotinic receptors, and have long preganglionic fibers and short postganglionic fibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sympathomimetic

A

drugs that mimic effect of sympathetic ns (epi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Parasympathomimetics

A

drugs that mimic parasympathetic ns (acetyhlcholine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Parasympathoplegic

A

drugs that inhibit parasympathetic (atropine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sympathoplegic

A

Drug that inhibit sympathetic ns (alpha and beta blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Adrenergic (gQ, gI, gS) and their effects

A

alpha 1/2 and beta 1/2.
-Alpha 1 is gQ, and increases phospholipase C -> IG3/DAG
-Alpha 2 is gI, and decreases cAMP
-Beta1/2/3 are gS, increase cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cholinergic receptors

A

nicotinic: ligand-gated ion channels
muscarinic: g-protein coupled, varying subtypes (m1, m2, etc.

M1, 3 and 5 are excitatory (phospholipase C, gQ)

m2 and m4 are inhibitory, related to gI proteins to decrease cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where are alpha and beta receptors found? muscarinic and nicotinic?

A

alpha1 - blood vessels and eyes
alpha 2 - nervous system
beta-1 - heart
beta2-lungs and skeletal muscles (dilation for each)
muscarinic - heart and smooth muscle, glands
nicotinic - skeletal muscles and brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

6 classes of NTs and example

A

Esters - ACH
Monoamines - NE, serotonin, dopamine
Amino Acids - Glutamate, GABA
Purines - Adenosine, ATP
Peptides - Substance P, endorphins
Inorganic Gases - Nitric Oxide (NO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Types of synpases

A

Electrical juntion, chemical synapse, and axodendritic synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fate of NTs in synapse

A

Reuptake into neuron, degraded by enzymes, and diffusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

NE transport, storage, release and degradation

A

Synthesized from tyrosine into cell by CHT, combined by CHAT and stored in vesicles via VAT, and either taken back into presynaptic cell or degraded by monoamine oxidase (MAO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Major uses of cholinomimetic agonists include

A

glaucoma (pilocarpine), urinary retention (bethanechol), diagnostic tool for MG (edrophonium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pharmacodynamic differences between direct acting and indirect acting cholinomimetic agents

A

direct acting bind directly to receptor to produce effects while indirect acting will inhibit things such as acetylcholinesterase to have more effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Difference between nicotinic and muscarinic

A

nicotinic are ionotropic and found at NMJ and autonomic ganglia, super fast

muscarinic are GPCRs found in heart and smooth muscles, glands, mediate slower and longer lasting effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cholinomimetics effects in major organ systems

A

miosis and decreased intraocular prssure, decreased heart rate/contractility, increased GI motility/secretion, and increased bladder contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Types of glaucoma and drugs

A

open angle: increased intraocular pressure due to improper drainage, treated with pilocarpine to increase aqeuous outflow

closed angle: sudden blockage of drainage, acute pressure increase, emergency treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

s/s of organophoshate poisoning

A

SLUDGE-M, resp failure, bradycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

s/s nictonic toxicity

A

N/V, muscle twitching, seizures/coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

effects on atropine across different organs

A

eyes: mydriasis and cycloplegia (dilation, dry eyes)
GI: decreases motility/secretions
Resp: reduces bronchial secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

s/s atropine overdose and treatment

A

Dry mouth, blurred vision, tachycardia, hallucinations, hyperthermia (reduced sweating)

treatment: cholinesterase inhibitors such as physostigmine to reverse effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

use of cholinomimetics in disease

A

MG (edrophonium to diagnose, stigmine to treat)
Glaucoma: pilocarpine
postop ileus: bethanechol to increase GI motility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

clinical indications and contraindications for muscarinic antagonist

A

indications: bradycardia, motion sickness, reduce secretions for surgery

contraindications: glaucoma, urinary retention, obstructive GI diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Effects of two types of nicotinic antagonists

A

Ganglionic blockers and neuromuscular blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

two types of muscle relaxants

A

depolarizing agents (sux) and non depolarizing agents (rocuronium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

catecholamine structure

A

consist of a benzene ring with hydroxyl groups at 3 and 4 position and amine group on the side chain. Removing hydroxyl groups (COMT), and MAO.

e.g. ephedrine is not degraded by these enzymes due to absence of OH groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MOA of direct and indirect acting catecholamines

A

direct acting: (norepi and epi) bind directly to adrenergic receptors.
indirect-acting: (amphetamines) increase release or block reuptake of NE leading to prolonged affects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

alpha-agonist, beta agonist, mixed agonist

A

alpha: phenylephrine - vasoconstrction, increased peripheral resistance, blood pressure
beta: isoproterenol - hr and contractility, reducing peripheral resistance.
mixed: epi - increase HR, contractility, vasoconstriction, increased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Nonselective alpha agonist
selective alpha 2
nonselective beta agonist
selective beta-1 agonist
selective beta 2 agonist

A
  1. epi
  2. clonidine
  3. isoproterenol
  4. dobutamine
  5. albuterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

tissues with alpa 1 and alpha 2 receptors

A

alpha 1 - blood vessels
alpha 2 - CNS and presynaptic nerve terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Tissues containing beta 1/2 receptors

A

beta 1 - heart
beta 2 - lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Major clinical applications of adrenoceptor agonists include

A

epi for anaphylaxis/cardiac arrest
dobutamine for heart failure
albuterol for asthma
phenylephrine for nasal decongestion/hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

triphasic effects of dopamine

A

low dose: D1 receptors, vasodilation in kidneys
mid dose: B1 contractility and hr
high dose: A1 vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

common toxicities with sympathomimetics

A

CV toxicity: arrythmias, hypertension
CNS toxicity: anxiety, tremors, seizures
OTher: hyperglycemia, hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe and compare the effects of an alpha blocker on BP/HR

A

cause vasodilation by inhibiting a1 receptors, reducing vascular resistance and lowering BP.
May lead to reflex tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Effects of alpha blocker in presence/absence of agonist

A

absence: there is nothing to block and has little to not effect
presence (in presence of epi): prevents epi effects i.e. vasoconstriction Hr/contractility, may cause reflex tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

list the alpha and beta blockers described in class and their clinical uses

A

Alpha:
Phentolamine - used in pheochromocytoma and hypertensive emergencies
prazosin - used for hypertension and BPH

Beta:
propanolol - non selective, for htn, angina, arrythmias
metoprolol - beta 1 selective, used for heart failure and hypertension (not in end stage HF, need contractility)
labetalol - mixed alpha/beta, used in hypertensive crises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

explain this sentence: phentolamine converts a pressor into a depressor

A

phentolamine is a competitive alpha blocker and it inhibits effects of epi on alpha receptors. By blocking these receptors, epi effects shift to beta-2 receptor mediated vasodilation, leading to a decrease in BP instead of increase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Define the difference between selective and non selective beta blockers

A

selective beta blockers primarily block beta-1 receptors, which are found int he heart

non-selective beta blockers block both beta1 and 2, affecting heart rate as well as lungs causing bronchoconstriction (propanolol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

clinical indications and toxicities of beta blockers

A

indication: htn, angina, hf, arrythmias

toxicities: bradycardia, fatigue, bronchoconstriction, worsening of peripheral vascular disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

clinical indications and toxicities of alpha blockers

A

indication: hypertension, BPH and pheochromocytoma

toxicity: orthostatic hypotension, reflex tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

regulators of BP

A

cardiac output (SV x HR) and PVR which is influenced by blood viscosity, vessel diameter, and vessel length.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

anatomic control sites for BP

A

Heart (CO), blood vessels (PVR), kidneys (fluid balance, RAAS), and CNS (symp vs parasymp)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Non-pharmacological interventions for elevated BP

A

Dietary changes (DASH diet, reduced sodium intake)
Weight loss
physical activity
stress management
reduction of alcohol intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Major groups of antihypertensive medications

A

diuretics (hydrochlorothiazide, furosemide, spironolactone)
beta blockers (metoprolol, propanolol)
calcium channel blockers (diltiazem, amlodipine, verapamil)
ACE inhibitors (lisinopril)
Renin inhibitors (aliskiren only one)
ARBs (losartan, valsartan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Targets of centrally acting sympathoplegics

A

clonidine and methyldopa act on a2 receptors in CNS, specifically medulla oblongata, to reduce sympathetic outflow, lower BP, and decrease peripheral resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

major sites of action of peripheral sympathoplegics

A

beta receptors in heart (propanolol) and alpha 1 receptors (Prazosin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

doses for metoprolol, atenolol, and esmolol

A

metoprolol: 50-100mg/day (oral)
atenolol: 25-100mg/day (oral)
Esmolol: 50-300mcg/kg/min (IV infusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

mechanism of action of vasodilator drugs and 4 classifications

A

work by relaxing vascular smooth muscle to reduce PVR

direct-acting vasodilators (hydralizine)
calcium channel blocker (amlodipine)
nitrates (nitoglycerin)
potassium channel openers (minoxidil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

compensatory response to vasodilators

A

tachycardia due to baroreceptor reflex and fluid retention due to RAAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Major antihypertensive vasodilator drug and effects

A

Hydralazine (arterial dialation)
Minoxidil (Arteriolar dilation)
Sodium nitroprusside (arterial and venous dilation, used in hypertensive EMERGENCIES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

concerns with sodium nitroprusside and dosing

A

used in htn emergencies but may cause cyanide toxicity with prolonged use. 0.3-10mcg/kg/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

three classes of CBBs and major target

A

Dihydropyridines (peripheral vasculature, amlodipine)
Phenylalkylamines (Heart, verapamil)
Benzothiazepines (mixed heart/vessel, diltiazem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

RAAS pathway and treatment targets

A

Renin converts angiotensin to angiotensin I, ACE converts angiotensin I to angiotensin II, which increases BP by vasoconstriction and aldosterone release. Treatment targets ACE inhibitors such as lisinopril and ARBs (losartan)

There is one Renin inhibitor, called aliskiren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Differences between 2 angiotensin antagonists

A

ACE-I: block the conversion of angiotensin I to angiotensin II. (lisinopril)

ARBs: Block angiotensin II receptors (losartan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MOA for pulm hypertension therapeutics

A

Prostacyclin analogs (epoprostenol), endothelin receptor antagonist (bosentan) and PDE-5 inhibitors (sildenafil)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Hypertensive urgency and hypertensive crisis (emergency)

A

Urgency: >180/100, no end organ damage (fix in hours to days)

Emergency: >180/110, with end organ damage, this is an emergency. (fix immediately)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Treatments for mild/mod/severe hypertension

A

mild: lifestyle mods and monotherapy
moderate: combination of two drugs (beta blocker + diuretic)
Severe/emergent: IV antihypertensives (sodium nitroprusside, cardene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Differences in arterial, capillary, and venous tone

A

Arterial tone: controls BP
Venous: influences venous return and preload
Capillary: can completely shunt to bypass blood and make it go to more important parts of body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Pathophysiology of effort angina and vasospastic angina

A

Effort: occurs with physical activity due to increased myocardial demand

Vasospastic: occurs at rest due to coronary artery spasm, determinants of oxygen consumption include HR, contractility and wall tension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Coronary blood flow and diastole

A

directly related to duration of diastole because thats when the coronary arteries fill with blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Strategies for anginal pain relief

A

Drugs reducing oxygen demand such as beta blockers and nitrates, and increase oxygen supply (calcium channel blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

molecular pathways of vascular tone and drug targets

A

Pathways include nitric oxide, calcium, cAMP/cGMP, with targets like CCBs and nitrates.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Primary nitrates and nitrites

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

they cause vasodilation by increasing cGMP, used in angina and HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Concerns with nitrate overexposure

A

Tolerance and methemoglobinemia (reduced oxygen binding) are major concerns with prolonged use of nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Receptor differences in epicardial arteries

A

Alpha receptors cause vasoconstriction (reducing blood flow to heart and increasing BP, and beta 1 receptors cause increased heart rate and contractility.

Beta-2 receptors in the smaller vasculature of the heart can dilate smaller arterioles and increase blood flow to heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Targets of pFOX inhibitors and what drug?

A

Target fatty acid oxidation to reduce oxygen consumption in ischemic heart disease.

Drug is called Ranolazine and it acts on sodium channels to improve myocardial relaxation, not available in the US currently.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Therapeutic and adverse effects of nitrates, beta blockers, and calcium channel blockers

A

Nitrates reduce preload but cause headaches, orthostatic hypotension, and reflex tachycardia.
BB reduce heart rate but cause bradycardia, fatigue/depression, and bronchoconstriction.
CCBs reduce afterload but cause hypotension, peripheral edema, bradycardia.

74
Q

Combination therapy for angina

A

combining nitrates with BBs or CCBs is more effective as it reduces oxygen demand and preventing reflex tachycardia.

75
Q

Medical vs surgical therapy for angina

A

medical: drugs to manage symptoms
surgical: involves procedures like CABG, stent placement.

76
Q

Define Heart failure and its pathogenesis

A

Heart is unable to meet myocardial demands of tissues, either due to systolic or diastolic dysfunction. Results in myocardial damage, high blood pressure, hyperthyroidism (and elevates myocardial demand). Congestion may occur, leading to pulmonary or peripheral edema.

77
Q

Four factors of cardiac performance and how they are altered in HF

A

Preload: increased in HF due to fluid retention.
Afterload: elevated due to high blood pressure and vascular resistance
Contractility: Decreased due to damage or thinning of myocardium.
HR: increased as compensatory mechanism but exacerbates HF over time.

78
Q

Define starling law

A

more the heart muscle is stretched, more forceful the contraction. In HF, excessive stretching leads to decreased contractility over time.

79
Q

How ESV, passive filling, and atrial contraction contribute to EDV

A

End systolic volume is volume of blood left in ventricle after contraction

Passive filling occurs as blood flows into ventricle before atrial contraction, contributing to end diastolic volume

Atrial contraction adds a small additional volume to EDV, which is the total volume of blood before next contraction.

80
Q

Strategies and drug groups for acute and chronic HF

A

Acute: diuretics, vasodilators, inotropes (dobutamine)

chronic: treat with ACE inhibitors, beta blockers, diuretics, aldosterone antagonists (ARBs)

81
Q

Molecular mechanisms controlling normal cardiac contractility

A

Controlled by calcium entering cell, triggering calcium release from SR. This frees actin to interact with myosin, leading to contraction.

82
Q

MOA of digitalis and major effects

A

digoxin inhibits na/k pump, leading to increased intracellular volume, enhancing contractility but also increases vagal tone, slowing heart rate.

83
Q

Nature and mechanism of dig toxicity

A

Arrythmias, such as Vfib, due to calcium overload. Has a very narrow therapeutic index.

84
Q

Positive inotropic drugs other than dig

A

dobutamine, dopamine, milrinone

85
Q

Beneficial effects of non-inotropic drugs in HF

A

Diuretics reduce fluid overload

Vasodilators decrease afterload

ACE-I/ARBs decrease afterload

86
Q

Rationale for BBs in HF

A

Reduce HR and myocardial oxygen demand, allowing heart to pump more efficiently.

87
Q

Non-pharmacological interventions for HF

A

CABG, transplant, VADs. Lifestyle changes is crucial for managing early stages.

88
Q
A
89
Q

Neurotransmitter class - Esters examples

A

Acetylcholine

90
Q

Neurotransmitter class - Monoamines example

A

NE, serotonin, dopamine

91
Q

Neurotransmitter class - Amino acids example

A

Glutamate, GABA

92
Q

Neurotransmitter class - Purines example

A

Adenosine, ATP

93
Q

Neurotransmitter class - Peptides examples

A

Substance P, endorphins

94
Q

Neurotransmitter class - Inorganic Gases example

A

Nitric Oxide (NO)

95
Q

Original of Sympathetic NS fibers, length, location of ganglia

A

Thoracolumbar region of spinal cord, short preganglionic, long postganglionic, close to spinal cord.

96
Q

Origin of fibers in Parasympathetic NS, length of fibers, location of ganglia

A

Brain and sacral spinal cord, long preganglionic and short postganglionic, in the visceral effector organs.

97
Q

Autonomic feedback loop in blood pressure

A

Sympathetic/parasympathetic NS response (PVR, HR, Contractility, Venous tone)

98
Q

Hormonal feedback lap in blood pressure

A

RAAS system pretty much

99
Q

CHT, CHAT, VAT

A

CHT: choline transporter into neuron
CHAT: acetyl CoA + choline = ACh
VAT: Transports ACh into vesicle

100
Q

Order of NE release in presynaptic neuron

A

Tyrosine gets into cell via Na+/Tyrosine channel, turns into tyrosine hydroxylase -> Dopamine -> dopamine -> into vesicle via VMAT -> Vesicle moves down to cell wall via SNAP and VAMP

101
Q

Cholinomimetics - Alkaloids

A

Plants - Betel nut and muscarine, Nicotine

These all increase ACh

102
Q

Cholinomimetics agents - Choline esters

A

ACh, Methanicholine, Carbechol, Methanechol

103
Q

Are alkaloids and choline esters direct acting or indirect acting Cholinomimetic agents?

A

Direct acting

104
Q

How does an Indirect-acting cholinomimetic work?

A

By inhibiting hydrolysis of ACh and inhibiting action of acetylcholinesterase. Both increase duration of ACh activity.

105
Q

ADM in esters of choline

A

A: poor
D: poor
M: Varies

106
Q

Use for ACh (in the eyes), Methacholine, Carbachol, Bethanechol

A

ACh: pupil constriction (miosis)
Methacholine: Diagnosis of asthma
Carbachol: Decrease intraocular pressure
Bethanechol: Bladder dysfunction, reflux disease

107
Q

Which type of glaucoma is atropine contraindicated? Why?

A

Closed-angle/Narrow angle. Atropine relaxes the ciliary muscle and causes complete drainage obstruction of aqueous humor, may result in blindness.

108
Q

Indirect cholinomimetic drugs

A

Simple alcohols: edrophonium (MG testing)

Carbamic acid esters of alcohols: Neostigmine

Organic derivatives of phosphoric acid: organophosphate

109
Q

Myasthenia gravis diagnostic drug and dose

A

Edrophonium 2mg IV, check for neg reaction, then give 8mg IV, and if improvement lasts 5 minutes, boom, diagnosed.

110
Q

Duration of action for tropicamide

A

4 hours

111
Q

How to reverse cholinergic toxidrome

A

Atropine

112
Q

Tx for organophosphate exposure

A

Atropine and Pralidoxime

113
Q

Reversal for atropine

A

-stigmine

114
Q

Nondepolarizing muscle relaxants have 3 categories

A

Short, intermediate and long acting

115
Q

succinylcholine has how many phases?

A

phase 1 and phase 2

116
Q

Reversal for non-depolarizing muscle relaxants

A

Neostigmine and pyridostigmine

sugammadex reverses steroid molecule curare derivatives

117
Q

Indirect acting adrenergic agonists

A

Amphetamine and cocaine

118
Q

Whats the one adrenergic agonist that is both direct and indirect acting

A

Ephedrine

119
Q

Cardiac output equation

A

SV (70ml) x HR (75bpm) = 5250ml/min

120
Q

Match these drugs to these receptors: Phenylephrine, Epinephrine, isoproterenol to Mixed, B agonist, A agonist

A

Alpha agonist: Phenylephrine
Beta agonist: Isoproterenol
Mixed: Epi

121
Q

Norepinephrine receptors

A

alpha, B1, little B2

122
Q

Isoproterenol receptors

A

Potent B agonist - vasodilator
Little effect on beta receptors, will increase HR/Contractility and reduce afterload/preload

123
Q

Dopamine

A

D1, B1, and A1 depending on dose. Triphasic.

124
Q

Dobutamine

A

B1 selective agonist – used in cardiac shock, acute HF

125
Q

Non-catecholamine adrenergic agonists

A

Midodrine, phenylephrine, ephedrine, pseudoephedrine, amphetamines, methampethamines, cocaine, tyramine

126
Q

Midodrine

A

alpha 1 receptor selective, primarily postural hypotension

127
Q

Alpha antagonist drugs

A

Phentolamine (reversible) and Phenoxybenzamine (irreversible)
- used for treatment of pheochromocytoma

Prazosin - BPH and hypertension, highly selective to Alpha 1, tachycardia ABSENT

128
Q

Beta blocking agents general characteristics

A

A: well absorbed orally, peak 1-3 and half life 3-10 hours
D: Rapid
M: Major first-pass metabolism - low bioavailability
E: Varied

129
Q

Beta blockers effect on blood vessels

A

Acutely increases peripheral resistance, but chronically decreases peripheral resistance.

130
Q

Beta blockers in eyes

A

Decreased IOP

131
Q

Adverse affect with chronic use of beta blockers

A

Increased VLDL and decreased HDL

132
Q

Propanolol characteristics

A

B antagonist, non selective.
Extensive 1st pass metabolism

133
Q

Metoprolol and atenolol

A

Mainly B1 selective
Safer in COPD/asthmatics, diabetics

134
Q

Labetalol

A

Has racemic mixtures

S,R isomer: potent alpha blocker, alpha 1 selective
R,R isomer: potent beta blocker.

135
Q

Esmolol

A

Ultra short acting, Beta 1 selective, infusion. Terminated rapidly with D/C, safer in critically ill patients.

136
Q

Hydraulic equation

A

BP = CO x PVR

137
Q

4 types of antihypertensive agens

A

Diuretics: deplete sodium
Sympathoplegics: decrease PVR, Reduce CO
Direct vasodilators: relax vascular smooth muscle
Anti-Angiotensins: block activity or production

138
Q

Drug used for pregnancy induced hypertension

A

Methyldopa! safe to cross placental barrier

138
Q

Methyldopa

A

Acts alot like clonidine, analog of L-dopa, replaces NE in adrenergic nerve vesicles.
-Agonist at CNS alpha receptors.

139
Q

General vasodilator mechanism

A

Relax smooth muscle of arterioles and veins: Nitroprusside and nitrates

-Best given in conjunction with other antihypertensive medications that combat reflex tachycardia induced by vasodilation

140
Q

Minoxidil

A

Opens K+ channels in smooth muscles, less likely to contract and dilates arteries and arterioles. well absorbed orally/topically.

141
Q

Hydralazine effects and toxicity

A

Dilates arterioles - Nitric oxide production MAYBE?

Toxicity: HA, Nausea, sweating, flushing

142
Q

Sodium nitroprusside

A

HT emergencies, dilates arterial and venous vessels , rapidly lowers BP.

-INCREASES INTRACELLULAR cGMP
-cyanide accumulation after 48 hours causing arrythmias, acidosis, and death. Worse in renal insufficient pts.

143
Q

Fenoldopam

A

Peripheral arteriolar dilator, HTN emergencies, post-op htn.

Agonist of D1 receptors for kidney perfusion.

144
Q

Renin inhibitor

A

Aliskiren

145
Q

ACE inhibitors

A

block angiotensin 1 from turning into angiotensin 2

captopril - can lead to severe cough from bradykinin accumulation.

146
Q

ARBs

A

Block AT2 receptor to inhibit aldosterone secretion and therefore inhibit vasoconstriction, and decreasing sodium/water retention and decreased PVR

Losartan and Valsartan

147
Q

Treatments for Pulm HTN

A

Endothelin receptor antagonists such as bosentan, which block endothelin (vasoconstrictor)

Prostacyclin analogs such as epoprostenol, promoting vasodilation and inhibit platelet aggregation.

148
Q

Actions on Vascular smooth muscle by drug class: NO/nitrates, Beta-2 agonists, Beta blockers, CCBs

A

NO: increase cGMP
B2 agonists: increase cAMP - relaxation (dilation)
BB: Decrease demand
CCB: less total calcium - relaxation (dilation)

149
Q

Types of heart failure

A

Systolic failure: Decreased CO, Decreased ejection fraction. typical of acute HF.

Diastolic failure: reduced filling. Decreased CO, normal ejection fraction.

150
Q

HAlf life of nitroglycerin

A

2-8 minutes

151
Q

Congestive heart failure results in

A

Increased LV pressure at end diastole
results in increased pulmonary pressure - pulmonary edema

152
Q

Normal cardiac contractility

A

Trigger calcium enters cell

Binds to channel in SR, releasing stored calcium

Frees actin to interact with myosin

153
Q

4 factors of cardiac performance

A

Preload, afterload, contractility, heart rate

CO = SV x HR

154
Q

Heart rate is controlled by 5 things

A

CNS, ANS, Neural reflexes, atrial receptors, hormones

155
Q

Stroke volume is made up of

A

Preload, afterload, contractility.

156
Q

Left ventricle numbers that total end diastolic volume

A

Passive filling 75ml + Atrial contraction 25ml + ESV 50ml = 140ml total

157
Q

Stroke volume = EDV - ESV

What is ESV?

A

ESV = 50ml

SV = 140ml - 50ml = 90ml

158
Q

Altered preload

A

> 20-25mm HG = pulmonary congestion.

This is increased in HF, which increases blood volume and venous tone.

159
Q

How to decrease preload

A

Salt restriction, diuretics, venodilation

160
Q

Afterload: what is it and it increases as _______?

A

Resistance against which heart must pump blood
Increases as cardiac output decreases.

161
Q

Digoxin

A

positive inotropic with narrow therapeutic index. The only oral pos inotropic for HF

162
Q

Milrinone

A

PDE3 inhibitors - these are the enzymes that inactive cAMP and cGMP

causes inotropic effects, vasodilation.

163
Q

Beta adrenergic stimulants

A

Dopamine and dobutamine: increase CO and decrease ventricular filling pressure

164
Q

Active cardiac cell membrane (sodium activity and gates)

A

Influx of sodium, rapid closer of H gate and inactivation.

165
Q

Explain the AP graph for cardiac action potentials

A

Sodium in as AP goes up, then at top of AP K+ and Cl- start flowing out, during plateau you got Ca++ coming in with K+ going out, and then on the downward line its K+ going out

166
Q

Early and delayed afterdepolarization

A

Early: arises from the plateau, called re-entry circuits, common in torsades, exacerbated by drugs that prolong QT interval.

delayed: arises from the resting membrane potential. common in dig toxicity from elevated intracellular calcium.

These are both arrythmias

167
Q

Four classes of antiarrhythmic agents

A

Class I: Sodium channel blockade
Class II: Sympatholytic
Class III: Prolong AP duration (K+ blockers)
Class IV: Block cardiac calcium channel currents

168
Q

Class I antiarrhythmic

A

Class IA: Sodium channel blockade to prolong AP duration (APD)

e.g. quinidine, procainimide

Class IB: shorten APD

e.g. lidocaine

Class IC: slow dissociation, minimal effect on APD

e.g. Flecainide

169
Q

Amiodarone

A

K channel blocker, prolongs APD

also dilates peripheral vasculature, and toxicity can cause bradycardia or heart block.

170
Q

Half life of amio

A

13-100 days

171
Q

Verapamil

A

CCB that blocks both activated and inactivated calcium channels
Prolongs AV node conduction while slowing SA node
hypotensive action

172
Q

Miscellaneous agents that dont fit into 4 classes of anti-arrhythmics

A

Digoxin

Adenosine: enhanced K+ conductance, inhibition of cAMP induced calcium influx, 10 second half life.

Magnesium: dig induced arrythmias

Potassium: normalize k+ levels

173
Q

Treatments for bradycardia

A

Underlying cause, D/C drugs, 1st line atropine, 2nd line epi/dopamine, and if chronic use pacemaker.

174
Q

Treatments for heart block

A

initial: 1st degree not usually treated bc its asymptomatic
symptomatic: atropine, transcutaneous pacing
Chronic: pacemaker

175
Q

Treatments for SVT

A

Assess cause, adenosine, and chronically treat with CCB and beta blockers

176
Q

Treatments for sinus tach

A

Assess cause, adenosine, CCBs/cardioversion acutely, and chronically catheter ablation.

177
Q

Treatments for vtach

A

amiodarone acutely and chronically, satolol chronically

178
Q

Treatments for afib

A

Diltiazem, verapamil (CCBs) acutely and then beta blockers/amio chronically

179
Q

Treatments for Vfib

A

CPR, defibrillation acutely. Amio/lidocaine chronically.

180
Q

How does Botox work?

A

Blocks SNAPs in the neuron.

Pharmacology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions