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Fall 2024 > Pharm test 2 Exam review Erin's > Flashcards

Pharm test 2 Exam review Erin's Flashcards

1
Q

Afferent

A

Going towards the CNS

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2
Q

Efferent

A

Going away from the CNS

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3
Q

Ganglia

A

Cell bodies in the PNS

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4
Q

Nuclei

A

Cell bodies in the CNS

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5
Q

Which are parasympathetic fibers originating from?

A

Craniosacral region

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6
Q

Where are sympathetic fibers originating from?

A

Thoracolumbar

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7
Q

Where are the ganglia located in the sympathetic division?

A

Close to the spinal cord

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8
Q

Where are the ganglia located in the parasympathetic division?

A

In the visceral effector organs

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9
Q

Which receptors are GQ?

A

Alpha 1, M1, M3, M5

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10
Q

What does GQ activate?

A

Phospholipase C

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11
Q

What is the end result of GQ activation?

A

Contraction

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12
Q

What receptors are G inhibitory (Gi)

A

Alpha 2, M2 and M4

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13
Q

What does Gi inhibit?

A

Adenylyl cyclase

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14
Q

Which receptors are G stimulatory?

A

Beta 1 and 2

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15
Q

What is the end result of G inhibitory?

A

Decreased cAMP

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16
Q

What is the end result of G stimulatory?

A

Increased cAMP

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17
Q

What happens when a G stimulatory signal is activated? (first thing)

A

Stimulates adenylyl cyclase

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18
Q

Briefly explain the hormonal feedback loop

A

Kidneys sense drop in BP –> renin release –> renin converts angiontensinogen (liver) into angiotensin I –> angiontensin I converted to angiotensin II by ACE (lungs) –> Angiotensin II causes vasoconstriction as well as stimulating the adrenal cortex to release aldosterone –> aldosterone release causes water and sodium reabsorption –> this increases blood volume –> increases venous return –> increases CO and finally increases MAP

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19
Q

Briefly explain autonomic feedback loop

A

Baroreceptors sense drop in BP and talk to the vasomotor center to increases sympathetic outflow and decrease parasympathetic outflow. (HR, PVR, Contractile force, Venous tone) End result is increased MAP

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20
Q

Neurotransmitter fates (4)

A

Diffuse away
Broken down in the synapse
Taken back up into presynaptic cell
Taken up by surrounding cells

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21
Q

What is an example of an ester?

A

Acetylcholine

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22
Q

What are the three monoamines?

A

Norepi, serotonin, dopamine

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23
Q

What does CHT do?

A

Transports choline into the neuron

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24
Q

What does CHAT do?

A

Combines acetyl-coa and choline into acetylcholine

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25
Q

What does VAT do?

A

Transports ACh into the vesicle

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26
Q

What are the steps in neurotransmitter release from vesicle?

A

Docking, priming, fusion

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27
Q

What does the SNARE complex do?

A

Anchors vesicles near release site

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28
Q

What is synaptogamin and what is its purpose?

A

Calcium sensor that serves for the release of neurotransmitter

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29
Q

Where is VAMP located?

A

On the vesicle

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30
Q

Where is SNAP-25 located?

A

Presynaptic membrane

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31
Q

Name the four components of the SNARE complex?

A

Syntaxin, SNAP-25, VAMP and Synaptogamin

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32
Q

Explain priming for a neurotransmitters

A

Prepares neurotransmitter for release (think pulling back hammer on gun) It is ATP dependent

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33
Q

Why does the neuron not become giant with docking, priming and fusion?

A

Two hypotheses: Kiss and run and clatherin coated pit

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34
Q

How does botulinum toxin mess with neurotransmitter release?

A

Prevents fusion by acting on SNAPs and VAMPs

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35
Q

How does Sarin nerve gas mess with neurotransmitters? Treatment?

A

Blocks AChE, too much acetylcholine. Treatment is atropine

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36
Q

Tyrosine is a precursor to ___

A

dopamine

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37
Q

How does cocaine and tricyclic antidepressants effect the reuptake of norepinephrine?

A

Block the NET –> excess of norepinephrine at the synapse

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38
Q

What are the direct acting cholinomimetics (class) ?

A

Choline esters and alkaloids

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39
Q

What are the indirect acting cholinomimetics?

A

Inhibit AChE, can be reversible or irreversible

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40
Q

Are esters of choline soluble or insoluble in lipids? How does this impact their absorption?

A

Insoluble in lipids, permanently charged, poorly absorbed

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41
Q

This ester of choline is primarily used for pupillary constriction (miosis)

A

ACh

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42
Q

This ester is used for the diagnosis of asthma

A

Methacholine

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43
Q

This ester is used to decrease intraocular pressure

A

Carbachol

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44
Q

This ester is used for bladder dysfunction and reflux disease

A

Bethanechol

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45
Q

Why is atropine contraindicated in narrow angle glaucoma?

A

It relaxes the ciliary muscle which obstructs drainage from the canal of schlem causing a build up of aqueous humor, which increases IOP

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46
Q

Name the indirect (block AChE) cholinomimetics

A

Simple alcohols (edrophonium)
Carbamic acid esters of alcohols (neostigmine)
Organic derivatives of phosphoric acid (organophosphates)

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47
Q

This drug is used for MG diagnosis

A

Edrophonium

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48
Q

Explain cholinomimetic effects (SLUDGE-M)

A

Salivation, lacrimation, urination, GI motility, Emesis, Miosis

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49
Q

What do antimuscarinics block?

A

Parasympathetic nervous system response, they block ACh receptors

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50
Q

What would you use tropicamide for?

A

Mydriasis (dilation) and cycloplegia (paralysis of ciliary muscle)

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51
Q

Explain symptoms and tx for organophosphate exposure

A

SLUDGE-M (blocks AChE)
Tx: atropine and pralidoxime
Give ASAP because bond between organophosphate and AChE ages and becomes harder to break

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52
Q

Treatment for atropine OD and symptoms

A

BRAND (blind, red, absent bowel sounds, nuts, dry)
Tx: Neostigmine

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53
Q

Explain phase I and II for succinylcholine

A

Phase I - depolarization of post synaptic cell
Phase II - If we continue giving this drug for a long period of time and we give larger and larger doses of it, the end plate will actually repolarize over time
When this happens, we enter phase II block
In the phase II block, the succinylcholine is still there but the muscle is no longer reacting to that succinylcholine binding to that receptor
Phase II is a deeper block and we get more repolarization and phase I keeps the muscle in a depolarized state
Sodium channels never reset

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54
Q

Reversal for non depolarizing muscle relaxants:

A

Neostigmine, pyridostigmine and suggamadex (Roc, Vec)

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55
Q

What is an example of a direct and indirect acting adrenergic agonist?

A

Ephedrine

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56
Q

What does COMT do?

A

Inactivates catecholamines in the gut

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57
Q

What does MAO do?

A

Inactivated catecholamines in the presynaptic cell

58
Q

What happens when you substitute the alpha carbon on a catecholamine?

A

Alpha carbon substitutions are not recognized by MAO and therefore not broken down as readily as something like norepinephrine.

59
Q

Tell me the receptors that the following drugs work on:
Phenylephrine (neo)
Epinephrine
Isoproterenol

A

Neo - alpha agonist
Epinephrine - mixed (alpha and beta)
Isoproterenol - beta agonist

60
Q

How does isoproterenol impact the blood vessels?

A

Vasodilates them

61
Q

What receptor does midodrine hit? What is it used for?

A

Postural hypotension, alpha 1 receptor agonist

62
Q

Name the reversible and irreversible alpha antagonists

A

Phentolamine (reversible) and Phenoxybenzamine (irreversible)

63
Q

What is a pheochromocytoma? What class of drugs is given for this?

A

A tumor of the adrenal medulla producing excess epinephrine
Treatment: alpha antagonists such as phentolamine and phenoxybenzamine

64
Q

-osins are what class? What are they used for?

A

Alpha antagonists
Used for BPH to shrink prostate
Highly selective for alpha 1

65
Q

Explain labetolol

A

Racemic mixture that is both an alpha and beta blocker

66
Q

Why avoid propranolol in an asthmatic?

A

It’s non selective and can block Beta 2 and cause bronchoconstriction

67
Q

Why is esmolol good for surgery?

A

Ultra short acting and beta one selective

68
Q

Hydraulic equation

A

BP = CO X PVR

69
Q

Four anatomical control sites and how we can manipulate them for BP control

A

Resistance Arterioles: can dilate these
Capacitance Venules: increase capacitance by relaxing them
Pump output Heart: use BB to decrease CO
Volume Kidneys: can block excess renin, ang 1, ang 2, aldosterone (RAAS system)

70
Q

Name the four antihypertensives and how they work

A

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

71
Q

Define: Pre HTN, HTN, HTN urgency, HTN emergency

A

Pre HTN: >140
HTN >160
HTN urgency: >180 with no organ damage
HTN emergency: >180 with organ damage

72
Q

What class is methyldopa? What is it used for?

A

Sympathoplegic (alpha 2 agonist), used for pregnancy induced HTN - works like clonidine

73
Q

What does cAMP do in the heart?

A

PKA –> Ca release from SR –> contraction

74
Q

What does cAMP do in the blood vessel?

A

Inhibits MLCK –> can not phosphorylate myosin –> relaxation

75
Q

How does monoxidil work? What is the end result?

A

K channel opener, vasodilation

76
Q

How does Hydralazine work?

A

Dilates arterioles, K channel activation, possible NO production

77
Q

Hydralazine toxicity

A

HA, nausea, flushing, worse in slow activator, symptoms similar to SLE

78
Q

What are the concerns with sodium nitroprusside toxicity? What is the treatment?

A

Cyanide toxicity (metabolic acidosis, arrhythmias, death)
Treat with sodium thiosulfate

79
Q

Mechanism of sodium nitroprusside

A

Release NO to relax vascular smooth muscle and increase intracellular cGMP

80
Q

What receptors does Fenoldopam act on? What is it useful for?

A

Vasodilator that is good for HTN emergencies
Agonist of D1 receptors and good for renal perfusion

81
Q

What is a major side effect of ACE inhibitors? Why?

A

Cough, because bradykinins are not broken down and this causes inflammation

82
Q

What does alliskiren do?

A

Renin inhibitor

83
Q

What class is losartan and valsartan? How do they work?

A

ARBs
blocks angiotensin II from binding to its receptors, so no vasoconstriction or aldosterone is released

84
Q

What is the mechanism of action of ACE inhibitors? What is their common name ending?

A

inhibits ACE enzymes so angiotensin I is not converted to angiotensin II
-pril

85
Q

How does aldosterone inhibitors lower BP?

A

Block aldosterone, essentially a diuretic effect to lower BP

86
Q

What class is bonsentan? How does it work? What is it used for?

A

Endothelin receptor antagonist
Prevents endothelin from binding to its receptor which prevents proliferation and vasoconstriction
Pulmonary HTN treatment

87
Q

How much blood does the venous system contain? (%)

A

70%

88
Q

Most common type of angina? How is it relieved?

A

Stable / angina of effort
Relieved by rest

89
Q

What is variant angina?

A

Angina caused by vasospasms, pain at rest

90
Q

What is unstable angina?

A

Pain at rest, caused by ACS - an emergency

91
Q

What does cGMP do to MLCK

A

dephosphorylates it can causes relaxation

92
Q

Steps of contraction in relation to calcium in the heart

A

For contraction - calcium influx binds to calmodulin and forms the calcium calmodulin complex. Calcium calmodulin complex activates myosin light chain kinase (MLCK) → MLCK is phosphorylated → interacts with actin and causes a contraction.

93
Q

Define concerns with overexposure to nitrates and nitrites.

A

Overtime, you develop a resistance to nitric oxide.
Can develop tolerance with complete continuous exposure→ blood vessels stop dilating → this is why you have an off period to clear nitric oxide form system
History of high nitrate/nitrite exposure can cause headaches
Problematic for workers on meat processing plants and fertilizer plants because they have a lot of nitrate that gets into air and they breathe it in.
Farmers around crops sprayed with this had problems with this
Nitrite ion can attach to hemoglobin to form methemoglobin (excess of amount of nitrite Attached to it)
Very low affinity for oxygen
Pseudocyanosis at very high levels (Raynaud’s essentially)
Benefit: very high affinity for cyanide so inducing pseudocyanosis can be useful in treating cyanide poisoning.
Methemoglobin can facilitate the removal of cyanide.

94
Q

Describe targets of pFOX inhibitors
What pFOX inhibitor is approved in the US?

A

By using the pFOX inhibitors (like ranolazine), this decreases fatty acid oxidation and causes the heart to switch over to glucose utilization (more efficient); less likely to flip into anaerobic metabolism

Ranolazine

95
Q

4 drug classes to treat angina

A

CCBs, pFOX inhibitors, Beta blockers, nitrates

96
Q

Explain systolic HF patho

A

Heart itself is not pumping effectively due to THIN heart muscle walls → could be due to infection or drugs ex.

97
Q

Describe patho of diastolic HF

A

Hypertrophy of myocardium– heart muscle too THICK

98
Q

Does diastolic or systolic HF have a reduced ejection fraction?

A

Systolic

99
Q

Describe the normal process of cardiac contractility

A

Depolarization causes voltage gated calcium channels to open and “Trigger calcium” enters the cell.

Trigger Calcium binds to channels in SR and calcium is then released from the SR

Calcium frees actin to interact with myosin. This causes a contraction.

SR calcium goes back into SR via SERCA pump (ATP dependent)

NCX pump allows exchange of sodium into cell for trigger calcium to be pumped out of cell

100
Q

What are the four factors of cardiac performance?

A

Preload, after load, contractility, and HR

101
Q

What three factors contribute to SV?

A

Preload, after load, contractility

102
Q

This is the end diastolic pressure that stretches out the ventricles

A

Preload

103
Q

What things contribute to EDV?

A

Passive filling, atrial contraction and ESV

104
Q

Drugs used for heart failure

A

Calcium
Cardiac glyocosides (digoxin)
PDE inhibitors (milrinone)
Catecholamines
Others:
Vasodilators
Beta blockers

105
Q

What is the only oral positive inotrope for heart failure?

A

Digoxin

106
Q

MOA PDE3 inhibitors

A

Stop the inactivation of cAMP and cGMP. This results in more cAMP and cGMP to have vasodilatory effects as well as positive inotropic effects

107
Q

What are the M and H gates doing during the resting state of a Voltage gated sodium channel?

A

M gates closed, H gates open

108
Q

What are the M and H gates doing during the activated state of a Voltage gated sodium channel?

A

Both are open

109
Q

What are the M and H gates doing during the inactivated state of a Voltage gated sodium channel?

A

H gate closed
M gate open

110
Q

What ion is moving during phase 0? Is it going in or out of the cell?

A

Sodium, into cell

111
Q

What ion is moving during phase 1? Is it going in or out of the cell?

A

Potassium, out of the cell

112
Q

What ion(s) are moving during phase 2? Is it going in or out of the cell?

A

Calcium in, potassium out

113
Q

What ion is moving during phase 3? Is it going in or out of the cell?

A

Potassium out

114
Q

What is happening during phase 4?

A

Sodium/potassium ATPase pump resets the concentration gradient of sodium/potassium

115
Q

Two main classifications of arrhythmias

A

Disturbances in impulse formation
Disturbances in impulse conduction

116
Q

What are the three things that can cause disturbances in impulse formation?

A

SA/AV node abnormalities
Ion changes
SNS stimulation

117
Q

What are the two things that can cause disturbances in impulse conduction?

A

Block and reentry

118
Q

What does vagal discharge do to the pacemaker rate? How does it impact the phase 4 slope?

A

Slows PM rate
Reduction in phase 4 slope

119
Q

How does acceleration of the pacemaker rate impact phase 4?

A

Increases the phase 4 depolarization slope

120
Q

Explain the three requirements for a reentry disturbance of impulse conduction

A

There must be an obstacle (scar tissue)
Block must be unidirectional
Conduction time must be long enough to reenter same areas after the refractory period

121
Q

Class I antiarrhythmics

A

sodium channel blockade

122
Q

Class II antiarrhythmics

A

sympatholytics

123
Q

Class III antiarrhythmics

A

prolong action potential duration (other mechanisms besides sodium channels - blocks K channels)

124
Q

Class IV antiarrhythmics

A

block cardiac calcium channel currents

125
Q

Examples of Class IA anti antiarrhythmic agents

A

Quinidine, procainimide, disopyramide

126
Q

What effect do Class IA drugs have on the APD and ERP?

A

prolong APD and increase ERP

127
Q

Examples of Class IB anti antiarrhythmic agents

A

Lidocaine

128
Q

What effect do Class IB drugs have on the APD and ERP?

A

Shorten APD, decrease ERP

129
Q

Examples of Class IC anti antiarrhythmic agents

A

Flecainide, propafenone

130
Q

What effect do Class IC drugs have on the APD and ERP?

A

No effect on APD or ERP but causes slow dissociation

131
Q

What W-V class is satolol?

A

Class II

132
Q

What W-V class is amiodarone?

A

III

133
Q

What W-V class is verapamil?

A

IV

134
Q

Risks of amiodarone toxicity

A

-Bradycardia/ heart block
-Precipitate HF
-Fatal pulmonary fibrosis
-Concentration in tissues, found in almost every organ

135
Q

How does verapamil work?

A

Blocks activated and inactivated calcium channels to slow SA node. Also has a hypotensive action

136
Q

Initial treatment for bradycardia

A

Treat underlying cause, d/c drugs

137
Q

Treatment for symptomatic bradycardia

A

1st - atropine
2- epinephrine, dopamine

138
Q

Treatment for chronic symptomatic bradycardia

A

Pacemaker

139
Q

Treatment for symptomatic heart block

A

Atropine, pacing

140
Q

Treatment for symptomatic SVT

A

Adenisone

141
Q

Treatment for wide complex Tach

A

amiodarone

142
Q

V fib treatment (drugs)

A

amio, lido

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