Brainscape's Knowledge GenomeTM

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


See full index

VM722 Pharm > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

main mechanism for ACh termination

A

degradation by AChE

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

main mechanism for catecholamine termination

A

re-uptake by transporters

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

beta 1 adrenergic receptor

A

sympathetic

increase HR at SA node, conduction at AV node, conduction/contraction at ventricles

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

M2 receptor

A

parasympathetic
decrease HR at SA node, decreased conduction velocity; AV blocks at AV node
bronchoconstriction, bronchial gland secretion

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

alpha 1 receptor

A

sympathetic
constriction of arteries
mydriasis in eye

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

beta 2 receptor

A

sympathetic
dilation of arteries in skeletal m.
bronchodilation in bronchial smooth m.
increase aqueous humor in eye

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

M3 receptor

A

Parasympathetic
increase NO in arterial endothelium –> dilation
bronchoconstriction, bronchial gland secretion

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

In the GI, what do M3 and M2 receptors do

A

increase GI motility & secretions

relax sphincters, salivation

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

In the bladder what do M3 receptors do

A

detrusor contraction

trigone & sphincter relaxation

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

In the eye what do M3 and M2 receptors do

A

miosis of pupil (constriction)

lacrimal gland secretion

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

alpha 2 receptor

A

sympathetic
decrease NE release at ANS nerves (presynaptic)
CNS inhibition

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

anticholinergic

A

muscarinic antagonist

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

Cholinergic/parasympathomimetic

A

NT that affects muscarinic receptors only (aka parasymp)

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

SLUDGE

A

Signs suggesting excessive cholinergic (parasymp) stimulation
Salivation, Lacrimation, Urination, Defication, GI symptoms, Emesis

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

Acetycholine

A
  • endogenous cholinergic
  • acts on both musc and nico receptors –> widespread unpredictable response
  • short half life
  • not used much clinically, except opthalmic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Bethanechol (direct cholinergic agonist)

A

w/ selectivity for M3
GI secretions/motility, bladder contraction, slight decrease HR
Used to treat non-obstructive urinary retention

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

Pilocarpine (direct cholinergic agonist)

A

induces miosis, decreases intraocular pressure for glaucoma

sometimes to induce salivation

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

Indirect acting cholinergic agnoists

A

inhibit AChE to decrease ACh degradation

act on both muscarinic and nicotinic, less selective

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

inotropic

A

modifying force or speed on contraction

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

cAMP activates what? Stimulated by what?

A

PKA
Receptors M2, M4, alpha 2 cause decrease in cAMP
Beta 1, 2, 3 increase cAMP

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

DAG, IP3 activate what? Stimulated by what?

A

PKC

Receptors M1, 3, 5, alpha1 cause increase in DAG, IP3

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

Non-covalent AChE inhibitors

A

reversible competitive antagonists of AChE

Physostigmine, Neostigmine

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

Physostigmine

A

counters CNS signs of anticholinergic intoxication

can cross BBB, Neostigmine can’t

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

Cholinergic antagonist (anticholinergic, parasymptholytiv)

A

Blocks ACh at muscarinic (parasymp) receptors

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

Signs of anticholinergic toxicity

A

tachycardia, bronchodilation, dry mouth, decreased urination, decreased lacrimation, mydriasis, accomodation
aka anti-SLUDGE

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

Atropine (competitive anticholinergic)

A
  • non-discriminant, so affects multiple organ systems
  • enters CNS
  • used as adjunct during general anesthesia (decrease salivation, airway secretions, increases HR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Glycopyrrolate (synthetic competitive anticholinergic)

A
  • similar to atropine
  • quaternary, so can’t affect CNS
  • used as adjunct during general anesthesia (decrease salivation, airway secretions, increases HR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Ipratropium (anticholinergic)

A
  • Bronchodilation, decrease airway secretion

- used for lung disorders (asthma, RAO, chronic bronchitis)

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

Propantheline (anticholinergic)

A
  • promotes urine retention (reduces detrusor contraction, increases trigone contraction)
  • treats incontinence due to detrusor instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Ganglionic blocker

A

overstim nicotinic receptors –> inactive
widespread effects, no longer used
hypotension

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

Uses of NMJ blockers

A

tracheal intubation
orthopedic manipulations
balanced anesthesia (but hard to monitor)
skeletal muscle paralysis

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

What’s special about the NMJ

A

Spare receptors - not all need ACh stim for contraction to occur
May need to give more drug to fully block all receptors
May have absence/reversal of clinical blockade but still lots of circulating drug - lapse in and out of drug state

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

Non-depolarizing (aka competitive) NMJ blockers

A
  • no motor endplate depolarization (no m. contraction)
  • see initial muscle weakness –> flaccid paralysis
  • Pancuroniu, Atracurium, Mivacurium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Pancuronium (non-depolarizing NMJ)

A

long lasting (2-3 hrs)
eliminated by kidneys
Also blocks muscarinic receptors –> tachycardia
no histamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Atracurium (non-depolarizing NMJ)

A 
Intermediate duration (.5 - 1 hr) 
degradation is temp, pH dependent (cold, acidosis = longer lasting)
does promote histamine release (decrease BP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Mivacurium (non-depolarizing NMJ)

A 
short acting (15 min) 
rapidly altered by plasma esterases
does promote histamine release (decrease BP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How would you reverse a non-depolarizing NMJ?

A

AChE inhibitor - Physostigmine, neostigmine

Outcompetes NMJ blocker, ACh accum’s and takes back over

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

Depolarizing (non-competitive) NMJ blockers

A
  • Cause prolonged motor endplate depolarization
  • see initial fasciculations –> muscle relaxation –> spontaneous flaccid paralysis with continued exposure
  • Succinycholine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Succinylcholine (depolarizing NMJ blocker)

A
  • Mimics ACh at nicotinic receptors at NMJ but resistant to AChE
  • not pharmacologically reversible (b/c receptors in state of constant depolarization)
  • rapid onset, short acting, so good for tracheal intubation
  • causes some histamine release
  • can cause hyperkalemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

NMJ block toxicity

A
  • respiratory paralysis, ganglionic blockade
  • histamine release - bronchospasm, hypotension (pre-treat with antihistamine)
  • can progress to apnea, cardiovascular collapse (b/c of histamine)
  • malignant hyperthermia b/c excess calcium = excessive contracture, heat production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

adrenergic agonist (sympathomimetic)

A

Mimic effect of catecholamines (NE, Epi, Dopamine) to alter symp activity
cardiac excitation, catabolic states, CNS stim, minimize alpha 2 receptor action

42
Q

PPA (phenylpropanolamine)

mixed-acting adrenergic antagonist

A
  • affects both alpha and beta receptors to promote NE release
  • increases urethral tone, manage urinary incontinence
  • opposite acting of Phentolamine, Phenoxybenzamine
43
Q

Do you have better selectivity at higher or lower doses?

A

Lower doses

44
Q

Epinephrine (direct-acting adrenergic agonist)

A
  • Increases CO (beta1) - contractility, HR, oxygen consump
  • Get combo of peripheral vasoconstriction (alpha 1), & vasodilation to increase skeletal m. blood flow (beta 2)
  • powerful bronchodilation (esp. if pre-constricted)
45
Q

Low dose of Epi

A

Beta 2 dominance –> decreased BP due to vasodilation

46
Q

High dose of Epi

A

alpha 1 dominance –> increased BP, CO due to vasoconstriction

47
Q

Therapeutic uses of Epi

A

hypersensitivity, restoring cardiac rhythm, control superficial bleeding, adjunct to keep local anesthetics local

48
Q

Epi toxicity

A

Cardiac arrhythmia, hypertensive crisis, cerebral hemorrhage

49
Q

How does NE potency differ from Epi?

A

Beta 1 = potency same
Beta 2 = EPI, NE basically no-existant
Alpha 1 = Epi better than NE

50
Q

Norepinephrine (direct-acting adrenergic agonist)

A
  • Increases CO (beta1) - contractility, HR, oxygen consump
  • Get combo of peripheral vasoconstriction (alpha 1), & vasodilation to increase skeletal m. blood flow (beta 2)
  • no effect on bronchodilation
51
Q

NE toxicity

A

intense vasoconstriction, robust in BP causing baroreceptor vagal response

52
Q

Therapeutic use of NE

A

Help maintain BP during shock but also may inadvertently decrease perfusion so of limited use

53
Q

Low dose Dopamine

A

Vasodilation (D1), Positive inotropy (beta 1 receptors)
good for hypovolemia following trauma
Good for short term fix for CHF w/ compromised renal fx

54
Q

High dose dopamine

A

Vasoconstriction (alpha 1)

55
Q

Dobutamine (Non-selective beta adrenergic agonist)

A

Increases contractility, but only minimally changes HR/BP
Positive inotrope for heart failure
toxicity - tachycardia

56
Q

Selective beta2 adrenergic agonist

A
  • Bronchodilators
  • Albuterol, Clenbuterol
  • Chronic administration can lead to down regulation of receptors, loss of efficacy
  • Can be used to increase muscle mass
57
Q

Mierbegron (selective beta3 adrenergic agonist)

A

relaxes detrusor m. to improve bladder capacity

fixes incontinence in humans, but toxic to dogs

58
Q

Selective alpha 1 adrenergic agonist

A

vasoconstriction –> increased BP

Phenylephrine - decongestant, vasopressor (constrictor), toxicity = hypertension

59
Q

Selective alpha 2 adrenergic agonist

A

CNS inhibition, decreased symp outflow, decreased NE release (alpha 2 receptors)
Dexmedetomadine, Xylazine - sedation/anesthesia, decrease BP, very safe (opposite of Atipamezole)

60
Q

Adrenergic antagonist (Sympatholytic)

A

Block NE, Epi, Dopamine catecholamine effect

61
Q

direct-acting sympatholytic

A
  • reversibly block NT’s from stimulating alpha and beta receptors
  • get decreased BP b/c decreased vasoconstriction
62
Q

Phentolamine (non-selective alpha adrenergic antagonist)

A
  • reversibly blocks both alpha 1 & 2 receptors

- opposite effect of PPA, used to manage urethral blockage (reduces sphincter tone)

63
Q

Prazosin (selective alpha 1 adrenergic antagonist)

A
  • vasodilation, decreased cO, decreased preload

- antihypertensive, treat CHF

64
Q

Atipamezole (selective alpha 2 adrenergic antagonist)

A
  • rapid reversal for Dexmedetomadine with minimal risk of relapse (b/c longer half life)
  • relieves CNS, pre-synaptic inhibition
  • increased NE release, less sedation, etc
65
Q

Atenolol (selective beta 1 adrenergic antagonist)

A
  • Blocks NE, Epi –> decreased CO, bp, cardiac arrhythmia
  • safer for patients with bronchospastic dz
  • Potential use for slowing feline hypertrophic cardiomyopathy
66
Q

Selective beta 2 adrenergic antagonist

A

would block Epi, increase bronchoconstriction

No scenario to need this, no drugs for it

67
Q

Propanolol (non-selective beta adrenergic antagonist)

A 
decreased Co (beta1 blockade), antiarrhythmic, bronchoconstriction (beta 2)
not much use when you have Beta1 selective drugs
68
Q

Timolol (non-selective beta adrenergic antagonist)

A

decreases aqueous humor production with glaucoma

69
Q

Carvedilol (non-selective beta adrenergic antagonist)

A

Blocks beta 1, beta 2 AND alpha 1 so REALLY good at lowering work of heart (decreased CO, vasodilation)
Used for congestive heart failure, vavlular dz

70
Q

Phenoxybenzamine (direct acting non-competitive adrenergic antagonist)

A

Irreversibly blocks alpha1 & 2 receptors
Effect lasts until new receptors are synthesized
Reduced urethral sphincter tone, used to manage urethral blockage (opposite PPA)

71
Q

Strategy to treat primarily vascular shock or a mix

A

promote vasoconstriction
high dose dopamine –> vasoconstrict, some increased CO
Maybe NE - max vasoconstriction
Mix - moderate dopamine

72
Q

How to treat primarily myocardial shock

A 
increase CO (beta one)
Dobutamine - increase contractility, minimal change to vasculature, HR
73
Q

Treat anaphylactic shock

A

Epi + antihistamine
beta 2 (bronchodilate, inhibit mast cell degranulation)
alpha 1, beta 1 cardio support

74
Q

Which part of the heart is the pacemaker

A

SA node

75
Q

Differences about pacemaker action potential

A

Technically no true resting membrane potential, just a slow depolarization of phase 4/0
No plateau phase (phase 2)
funny current

76
Q

funny current

A

Slowly depolarizing inward current activated by hyperpolarization causing phase 4 in pacemaker cells

77
Q

Class 1 antiarrhythmics

A

Sodium channel blockers

3 subgroups

78
Q

Class 2 antiarrhythmics

A

beta blockers
Slow av node conduction
Atrial fibrillation
Sotalol - non selective beta antagonist, most common antiarrhythmic, blocks K channels too

79
Q

Class 3 antiarrhythmics

A

K channel blocking
Prolong AP
Sotalol, Amiodarone (blue skin)

80
Q

Class 4 antiarrhythmics

A

Ca channel blocking to slow AV node conduction
Vascular (dihydropyridines) or non-vascular specific - inhibit both cardiac myocytes AND nodal cells (Diltiazam, Verapamil)

81
Q

Class 1 antiarrhythmics subgrp IA

A

moderate conduction slowing, prolongs AP duration
Procainamide blocks repolarizing K channels
Used for Supraventricular tachycardia

82
Q

Class 1 antiarrhythmics subgrp IB

A

little conduction slowing if healthy cells, shortens AP duration
Lidocaine or Mexiletine blocks keeps inactivated Na channels inactivated

83
Q

Class 1 antiarrhythmics subgrp IC

A

profound conduction slowing, little change to AP duration

Flecainide used for life-threatening tachycardia etc b/c cure worse than dz

84
Q

Digoxin

A

decreases AV node conduction similar to Ca channel blocks b/c inhibits Na/K ATPase pump to decrease Ca efflux
very arrhythmogenic, very narrow therapeutic window, hypokalemia can = toxicity

85
Q

How do you treat CHF

A

reduce work of heart (beta blockers, diuretics, vasodilators)
increase heart performance (contractility)

86
Q

3 ways to increase cardiac performance

A
  1. increase beta 1 stim - but careful of ceiling effect - Dopamine, dobutamine
  2. Increase intracellular Ca in myocytes - beta 1, PDE-3 inhibitors (Milrinone, esp. if beta blockers on board)
    2b. Decrease Ca efflux - inhibit na/ca pump, Digoxin
  3. Enhance contraction - Pimobendan increases sensitization to Ca, vasodilator
87
Q

How do vasodilators work?

A

disrupt excitation-contraction coupling in vascular smooth m. either by blocking receptors or limiting Ca in some way

88
Q

Inhibitors of Renin-Angiotensin Aldosterone system

A

Aliskiren - renin antaognist, no conversion to Ang I
Enalapril - ACE antagonist, no conversion to Ang II
Lsoartan/Telmisartan - AT1 antagonist, no ADH or vasoconstriction (aldosterone)
See vasodilation, less water/na retention

89
Q

How do you disrupt the baroreceptor reflex?

A

Block alpha 1 –> vasodilation
Prazosin or alpha antagonist
See immediate drop in BP, then increase, but vasodilation remains

90
Q

Ca channel antagonists and vasodilation

A

decreased Ca = decreased contraction = dilation
Dihydropyradines - act in vasculature only, don’t affect AV node conduction
Non-vascular specific - Diltiazem, verapamil antiarrhythmics

91
Q

NO

A

NO –> cGMP –> PKG –> PROFOUND vasodilation
Nitroglycerin (venous dilation only)
Sodium nitropursside (arterial and venous dilation)

92
Q

PDE-5

A

inhibition = prolonged cGMP –> increased PKG –> vasodilation
Lung smooth m, the pene
Sildenafil

93
Q

K channel activators and NO

A

prolonged open K channels = vasodilation, decreased TPR/BP

Minoxidil - rarely used

94
Q

In the kidney, what’s typically secreted, what’s reabsorbed?

A

Secreted - H+, K+

Reabsorbed - Nacl, bicarb (HCo3), Ca

95
Q

Most Na & water reabsorption occurs where in the kidney?

A

proximal tubule&raquo_space;> loop of henle > distal nephron

96
Q

Reasons to use diuretics

A

reduce ECF vol
Oliguric renal failure
Hypertension (e.g. EIPH)

97
Q

Osmotic diuretics

A

Thin descending limb
MOA: amount filtered excess tubular transport changes osmolarity of filtrate
e.g. diabetes (glu in filtrate = water stays in urine)
Mannitol - freely filtered, for oliguric renal failure, cerebral edema

98
Q

Carbonic anhydrase inhibitors

A

-proximal tubule & acidification in collecting duct
- MOA: Na, bicarb loss = water loss
Acetazolamide - may cause hypokalemia
Glaucoma, altitude sickness

99
Q

Loop diuretics

A
  • thick ascending limb of loop of henle
  • inhibit Nacl reabsorption via na/k/cl pump –> increased Na excretion
  • Furosemide, may cause hypokalemia
  • treats EIPH, CHF, oliguric renal failure (causes vasodilation)
100
Q

Thiazide diuretics

A
  • distal tubule
  • blocks Na, Cl reabsoprtion by blocking co-transporter
  • Chlorothiazide
  • hypertension
101
Q

K+ sparing diuretic

A

Collecting duct
1. Blocks aldosterone = no na/K atpase acitivty, Na secretion
Spironolactone - competitive antagonist, may cause hyperkalemia
2. Blocks Na channels
Amiloride - use w/ loop diuretic

102
Q

Aquaretics

A

increase water clearance with little effect on ion secretion

Demeclocycline

VM722 Pharm (5 decks)

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