Brainscape's Knowledge GenomeTM

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


See full index

Pharm Dr. T > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Different types of nervous system

A

Somatic Nervous System (SNS)
Autonomic Nervous System (ANS)
Sympathetic Nervous System (SNS)
Parasympathetic Nervous System (PNS)
Enteric Nervous System (ENS)

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

Controls voluntary movements via skeletal muscles. It relays sensory and motor information to and from the CNS.

A

Somatic Nervous System (SNS)

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

Governs involuntary functions (e.g., heart rate, digestion). It is subdivided into the sympathetic and parasympathetic systems.

A

Autonomic Nervous System (ANS)

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

Activated in “fight-or-flight” responses, controlling stress reactions (e.g., increasing heart rate, dilating pupils).

A

Sympathetic Nervous System (SNS)

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

Engages in “rest-and-digest” activities, promoting relaxation (e.g., slowing heart rate, enhancing digestion).

A

Parasympathetic Nervous System (PNS)

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

Regulates gastrointestinal functions, often considered a “second brain” that operates mostly independently but interacts with the ANS.

A

Enteric Nervous System (ENS)

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

Activated by the parasympathetic system during relaxation, promoting activities such as digestion, decreased heart rate, and energy storage.

A

Rest-and-Digest

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

Triggered by the sympathetic nervous system in stressful situations, leading to responses like increased heart rate, blood pressure, and energy mobilization (glucose release). Adrenaline (epinephrine) and norepinephrine are key mediators.

A

Fight-or-Flight

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

increases heart rate, dilates pupils

A

o SNS: Fight-or-flight response

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

slows heart rate, constricts pupils

A

o PNS: Rest-and-digest

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

Uses norepinephrine (NE) at target organs, with acetylcholine (ACh) at preganglionic synapses

A

o SNS

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

Primarily uses acetylcholine at both pre- and postganglionic synapses

A

o PNS

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

Receptors used for SNS

A

Adrenergic receptors (alpha and beta types).

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

Receptors used for PNS

A

Muscarinic and nicotinic receptors

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

o SNS anatomy

A

Preganglionic neurons originate from the thoracolumbar region, with short preganglionic and long postganglionic fibers

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

o PNS anatomy

A

Preganglionic neurons arise from craniosacral regions, with long preganglionic and short postganglionic fibers

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

Functions of Chain Ganglia (Sympathetic)

A

Paravertebral ganglia where sympathetic neurons synapse, distributing sympathetic signals throughout the body

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

Functions of PNS Plexi

A

Networks of intersecting nerves that govern localized autonomic functions in the body. Both the chain ganglia and PNS plexi act as hubs for neural signal distribution.

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

Drugs that mimic the effects of the sympathetic nervous system (e.g., epinephrine).

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

Drugs that mimic the parasympathetic system (e.g., pilocarpine).

A
  • Parasympathomimetic (Cholinomimetic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Drugs that inhibit the parasympathetic nervous system (e.g., atropine).

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

Drugs that inhibit sympathetic system activity (e.g., alpha blockers like prazosin, beta blockers like propranolol).

A
  • Sympathoplegic (α and β blockers):
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  • Adrenergic receptors (SNS)
A

o Alpha (α1, α2) and Beta (β1, β2, β3) receptors. Second messengers: cAMP, IP3, DAG.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  • Cholinergic receptors (PNS)
A

o Nicotinic (ionotropic) and muscarinic (M1–M5, metabotropic). Second messengers: cAMP, IP3/DAG.

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

Vascular smooth muscle (vasoconstriction).

A

o Alpha-1

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

Heart (increased heart rate). Receptor

A

o Beta-1

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

Bronchi (bronchodilation). Receptor

A

o Beta-2

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

Heart (slows heart rate).

A

o Muscarinic M2

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

Receptor for Skeletal muscles (muscle contraction).

A

o Nicotinic-Ach-R

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

SNS increases MAP by constricting vessels, increasing heart rate, while PNS lowers MAP via vasodilation and decreased heart rate.

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

Hormones like renin-angiotensin-aldosterone influence MAP by controlling blood volume and vascular tone, often over a longer timescale than autonomic changes.

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

Increased heart rate, bronchodilation, decreased digestive activity.

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

Slowed heart rate, bronchoconstriction, increased digestive activity.

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

Primarily innervated by sympathetic fibers using beta-2 adrenergic receptors (vasodilation during exercise).

A

Skeletal Muscle Blood Vessel Innervation

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

Consists of dendrites (input), soma (cell body), axon (signal conduction), and axon terminals (output).

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

Junction between two neurons where neurotransmitters are released to transmit signals.

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

Six Main Classes of Neurotransmitters

A
  1. Amino acids
  2. Monoamines
  3. Peptides
  4. Purines
  5. Esters
  6. Gasses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Type of neurotransmitter, (e.g., nitric oxide).

A

Gas

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

(e.g., endocannabinoids).

A

Lipids

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

(e.g., ATP) type of neurotransmitter

A

Purines

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

(e.g., substance P).

A

Peptides

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

(e.g., dopamine, norepinephrine).

A

Monoamines

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

(e.g., glutamate, GABA). Type of neurotransmitter

A

Amino Acids

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

CNS Neurotransmitters and Emotion

A

*Dopamine: Reward and pleasure.
*Serotonin: Mood regulation.
*Norepinephrine: Arousal and stress response.

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

3 Types of Synapses

A
  1. Axodendritic: Between axon and dendrite.
  2. Axoaxonic: Between two axons.
  3. Axosomatic: Between axon and soma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q
  • Reuptake: (e.g., serotonin) is performed by
A

By the presynaptic neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q
  • Degradation: (e.g., ACh by acetylcholinesterase).
A

By enzymes

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

Away from the synapse

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

What causes depolarization

A
  • EPSP; Excitatory (e.g., glutamate).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Cause hyperpolarization in CNS

A
  • Inhibitory (e.g., GABA).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Choline acetyltransferase

A
  • Formation: Choline + Acetyl-CoA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q
  • Transport:
A

Stored in vesicles.

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

Enzymatic Cleavage of Acetylcholine

A

Broken down by acetylcholinesterase into acetate and choline

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

Packaged in vesicles, released into the synapse, and degraded by acetylcholinesterase.

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

Stored in vesicles, released into the synapse, reuptake by presynaptic neurons, degraded by monoamine oxidase (MAO) or catechol-O-methyltransferase (COMT).

A
  • Norepi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q
  • types of Receptor blockers (metoprolol, olol’s)
A

beta blockers

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

SSRIs for serotonin

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

e.g., MAO inhibitors for NE

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

Pilocarpine is used for___

A

o Glaucoma: used to reduce intraocular pressure.

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

Pilocarpine and cevimeline are used ___

A

o Xerostomia (Dry Mouth): used to stimulate salivary secretion.

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

Neostigmine and pyridostigmine is used ___

A

o Myasthenia Gravis: improve neuromuscular transmission.

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

Bethanechol is used ___

A

o Postoperative Ileus and Urinary Retention: to stimulate GI and bladder activity.

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

These directly activate cholinergic receptors (e.g., pilocarpine, bethanechol). They mimic the action of acetylcholine by binding to muscarinic or nicotinic receptors.

A

o Direct-Acting Cholinomimetics

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

These inhibit acetylcholinesterase (AChE), which breaks down acetylcholine, thereby increasing acetylcholine levels at synapses (e.g., neostigmine, physostigmine).

A

o Indirect-Acting Cholinomimetics

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

Ionotropic receptors found in neuromuscular junctions (NMJ) and autonomic ganglia. Activation leads to rapid depolarization via Na+ and K+ influx.

A

o Nicotinic Receptors

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

G-protein-coupled receptors (GPCRs) found in parasympathetically innervated organs. They have slower responses and modulate various cellular pathways like cAMP or IP3.

A

o Muscarinic (Cholinergic) Receptors

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

Effects of Cholinomimetics on eyes

A

Miosis (pupil constriction) and reduced intraocular pressure

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

Effects of Cholinomimetics on the heart

A

Decreased heart rate (bradycardia).

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

Effects of Cholinomimetics on the lungs

A

Bronchoconstriction and increased secretions

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

Effects of Cholinomimetics on the GI

A

Increased motility and secretions.

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

Effects of Cholinomimetics on the Bladder

A

Increased bladder contraction and urination

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

Effects of Cholinomimetics on the Glands

A

Increased secretion (salivation, lacrimation, sweat).

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

Use of Cholinomimetics
o Open-Angle Glaucoma

A

(e.g., pilocarpine) help to increase aqueous humor outflow by contracting the ciliary muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Use of Cholinomimetics
o Angle-Closure Glaucoma

A

used less frequently but may help facilitate drainage before surgical intervention.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Organophosphate Insecticide Poisoning

A

 Symptoms: Excessive salivation, sweating, bronchoconstriction, miosis, bradycardia, diarrhea, convulsions, respiratory failure.
 Caused by inhibition of acetylcholinesterase, leading to acetylcholine buildup.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Acute Nicotine Toxicity:

A

 Symptoms: Nausea, vomiting, diarrhea, abdominal pain, tachycardia, hypertension, confusion, seizures, respiratory paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Enzyme that breaks down acetylcholine into acetate and choline, terminating its action at the synapse

A

o Acetylcholinesterase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

block acetylcholine breakdown, increasing its availability

A

AChE inhibitors (e.g., neostigmine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

After binding to AChE, they form an irreversible bond, making enzyme reactivation by antidotes (e.g., pralidoxime) ineffective.

A

o Organophosphate Aging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Effects of Atropine on eyes

A

Mydriasis (pupil dilation) and cycloplegia (paralysis of ciliary muscles).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Effects of Atropine on the heart

A

Increases heart rate (tachycardia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Effects of Atropine on the lungs

A

Bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Effects of Atropine on GI

A

Decreases motility (constipation).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Effects of Atropine on the glands

A

Reduces secretions (dry mouth, dry eyes, decreased sweating).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Atropine Overdose (s/s)

A

 Hyperthermia, dry mouth, blurred vision, photophobia, tachycardia, urinary retention, confusion, hallucinations.
 Mnemonic: “Hot as a hare, dry as a bone, blind as a bat, red as a beet, mad as a hatter.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Atropine Overdose, treatment

A

 Supportive care, benzodiazepines for seizures, physostigmine as an antidote (it crosses the blood-brain barrier and reverses central effects).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Cholinomimetic Use in Myasthenia Graves

A

Pyridostigmine and neostigmine improve muscle contraction by inhibiting AChE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Cholinomimetic Use in Glaucoma

A

Pilocarpine reduces intraocular pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Cholinomimetic Use in Post-Operative Ileus and Urinary Retention

A

Bethanechol stimulates smooth muscle contraction in the GI and urinary systems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Indications for Muscarinic Antagonists (Atropine)

A

 Bradycardia, organophosphate poisoning, preoperative to reduce secretions, eye exams (to induce mydriasis), asthma (bronchodilation).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Contraindications for Muscarinic Antagonists (Atropine)

A

 Narrow-angle glaucoma, urinary retention, tachycardia, obstructive GI disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Block nicotinic receptors at autonomic ganglia (e.g., hexamethonium), causing global autonomic disruption (e.g., decreased blood pressure).

A
  1. Ganglionic Blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Block nicotinic receptors at the NMJ, inhibiting muscle contraction (e.g., succinylcholine, pancuronium).

A
  1. Neuromuscular Blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

(e.g., succinylcholine) cause initial depolarization of the muscle (fasciculations) followed by paralysis.

A
  1. Depolarizing Muscle Relaxants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

(e.g., rocuronium, vecuronium) competitively block acetylcholine at the NMJ without causing depolarization.

A
  1. Non-Depolarizing Muscle Relaxants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

binds to nicotinic receptors, causing continuous depolarization and preventing repolarization, leading to paralysis.

A

o Depolarizing: Succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

compete with acetylcholine for nicotinic receptors, preventing muscle depolarization and contraction.

A

o Non-Depolarizing: Drugs like rocuronium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

 What is the structure of Catecholamines?

A

These molecules consist of a catechol nucleus (a benzene ring with two hydroxyl groups at positions 3 and 4) and an amine group. Examples include dopamine, norepinephrine, and epinephrine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

increases susceptibility to degradation by catechol-O-methyltransferase (COMT).

A

 Hydroxyl group at the 3,4 position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

affect interaction with monoamine oxidase (MAO) and receptor selectivity (e.g., adding bulky groups increases beta receptor affinity).

A

 Modifying the amine group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

These directly bind to and activate adrenergic receptors (e.g., epinephrine acts on both alpha and beta receptors).

A

 Direct-Acting Catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

These increase the availability of endogenous catecholamines by promoting release (e.g., amphetamines) or inhibiting reuptake (e.g., cocaine) or degradation (e.g., MAO inhibitors).

A

 Indirect-Acting Catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Types and Subtypes of Adrenergic Receptors

A

 α1 Receptors
 α2 Receptors
 β1 Receptors
 β2 Receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Gq-protein coupled → activates phospholipase C → IP3 and DAG → increases intracellular calcium → smooth muscle contraction (vasoconstriction).

A

 α1 Receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Type of adrenergic receptor:

Gi-protein coupled → inhibits adenylyl cyclase → decreases cAMP → inhibits norepinephrine release (negative feedback). Vasodilation

A

 α2 Receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Gs-protein coupled → activates adenylyl cyclase → increases cAMP → increases heart rate (chronotropy) and contractility (inotropy).

A

 β1 Receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Gs-protein coupled → increases cAMP → smooth muscle relaxation (bronchodilation, vasodilation).

A

 β2 Receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

drugs that increase blood pressure, by causing vasoconstriction or increasing cardiac output (e.g., norepinephrine or phenylephrine)

A

A pressor agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

 (α1 agonist) cause Vasoconstriction, increasing systemic vascular resistance (SVR) and blood pressure. Reflex bradycardia may occur.

A

phenylephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Ex. of a drug that cause…
 β1 activation: Increases heart rate and contractility.
 β2 activation: Vasodilation in skeletal muscle, bronchodilation, lowering peripheral resistance.

A

isoproterenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Mixed agonist
 At low doses: β2 effects predominate (vasodilation).
 At higher doses: α1 effects predominate (vasoconstriction), increasing blood pressure.

A

epinephrine

112
Q

 Nonselective α agonist (drug)

A

Oxymetazoline (acts on both α1 and α2).

113
Q

 Selective α2 agonist (drug)

A

Clonidine

114
Q

 Nonselective β agonist: drug

A

Isoproterenol (acts on β1 and β2).

115
Q

 Selective β1 agonist; drug

A

Dobutamine

116
Q

 Selective β2 agonist

A

Albuterol, Salmeterol

117
Q

Receptor:
 Vascular smooth muscle (vasoconstriction).
 Pupillary dilator muscle (mydriasis).
 Prostate and bladder sphincter (urinary retention).

A

 α1 Receptors

118
Q

Receptor:
 Presynaptic adrenergic nerve terminals (inhibits norepinephrine release).
 Pancreatic islet cells (inhibits insulin release).
 CNS (sedation, decreased sympathetic outflow).

A

 α2 Receptors

119
Q

Receptor
 Heart (increases heart rate and contractility).
 Kidney (renin release).

A

 β1 Receptors

120
Q

Receptor
 Bronchial smooth muscle (bronchodilation).
 Vascular smooth muscle in skeletal muscle (vasodilation).
 Liver (glycogenolysis, gluconeogenesis).

A

 β2 Receptors

121
Q

treatment for Anaphylaxis, cardiac arrest, asthma

A

 Epinephrine

122
Q

treatment for Acute hypotension, septic shock

A

 Norepinephrine

123
Q

treatment for Heart failure (increases cardiac output).

A

 Dobutamine

124
Q

treatment for Asthma and COPD (bronchodilation).

A

 Albuterol

125
Q

treatment for Hypertension, ADHD (central α2 agonist).

A

 Clonidine

126
Q

 Low dose: Activates D1 receptors → vasodilation, increased renal perfusion.
 Moderate dose: Activates β1 receptors → increased heart rate and contractility.
 High dose: Activates α1 receptors → vasoconstriction, increased blood pressure.

A

Dopamine

127
Q

 For bronchodilation: Select β2 agonist

A

albuterol

128
Q

 For cardiogenic shock: Use β1 agonist

A

dobutamine

129
Q

 For hypotension: Use α1 agonist

A

phenylephrine or mixed agonist norepinephrine

130
Q

Common Toxicities Associated with Sympathomimetics

A

 Cardiovascular: Hypertension, tachycardia, arrhythmias.
 CNS: Anxiety, tremors, headache, insomnia.
 Metabolic: Hyperglycemia (β2 effects on the liver).
 Excessive vasoconstriction: Can lead to ischemia, especially in peripheral tissues.

131
Q

Effects of an (α Blocker) on Blood Pressure

A

Alpha blockers (e.g., prazosin) block α1-adrenergic receptors in vascular smooth muscle, leading to vasodilation and lowering blood pressure. This reduces peripheral vascular resistance (PVR).

132
Q

Risk effects of an (α Blocker) on Heart Rate?

A

As blood pressure drops due to vasodilation, the baroreceptor reflex may induce a reflex tachycardia(an increase in heart rate) as a compensatory mechanism. This happens because the body tries to restore blood pressure by increasing heart rate.

133
Q

a Blocker (phentolamine) in the Presence of an Agonist

A

If a drug (e.g., epinephrine) that stimulates adrenergic receptors is present, an alpha blocker (e.g., phentolamine) will prevent the agonist from binding to α1 receptors, leading to vasodilation and counteracting the agonist’s vasoconstrictive effects.

134
Q

Effects of a Blocker in the Absence of an Agonist

A

Without an agonist, the primary action of the alpha blocker is to inhibit baseline sympathetic tone. Primarily cause vasodilation and a drop in blood pressure.

135
Q

 Prazosin (a blocker)

A

Used for hypertension and benign prostatic hyperplasia (BPH) by relaxing vascular smooth muscle and the prostate/bladder sphincter.

136
Q

 Phentolamine (a blocker)

A

Used in pheochromocytoma (adrenal tumor) and for treating hypertensive emergencies caused by catecholamine excess.

137
Q

 Tamsulosin (a blocker)

A

Used for BPH to improve urinary flow without much effect on blood pressure.

138
Q

 Propranolol (non-selective): b blocker used to treat ____

A

hypertension, angina, arrhythmias, migraines, and anxiety.

139
Q

 Atenolol (β1 selective): mainly used for

A

Used for hypertension and angina, particularly when selective β1 blockade (heart-specific) is desired.

140
Q

 Metoprolol (β1 selective): used for

A

Used for hypertension, heart failure, and post-myocardial infarction (reduces mortality).

141
Q

 Carvedilol (non-selective with α-blocking properties): B blocker used for

A

Used for heart failure and hypertension

142
Q

 Labetalol (non-selective β and α1 blocker): used for…..

A

Used in hypertensive emergencies and pregnancy-related hypertension.

143
Q

Explain Phentolamine

A

non-selective alpha blocker. When epinephrine is administered, it normally acts on both alpha and beta receptors, causing vasoconstriction (via α1) and vasodilation (via β2) with an overall pressor effect (decreased blood pressure).

144
Q

Explanation: Phentolamine Converts a Pressor (Epinephrine) into a Depressor

A

 When phentolamine is administered, it blocks α1 receptors, preventing vasoconstriction. This leaves the β2-mediated vasodilation unopposed, causing vasodilation and a drop in blood pressure, thus converting epinephrine’s pressor (blood pressure-increasing) effect into a depressor (blood pressure-lowering) effect.

145
Q

 Selective Beta-Blockers good for Pt’s with asthma/COPD, why?
 Example: Atenolol, Metoprolol

A

Primarily block β1 receptors (found mostly in the heart). They have fewer effects on β2 receptors (found in the lungs and vasculature), making them safer in patients with asthma or chronic obstructive pulmonary disease (COPD).

146
Q

 Non-Selective Beta-Blockers
 Example: Propranolol, Timolol
Not good for asthma/COPD Pt’s because…

A

Block both β1 and β2 receptors. They affect the heart (β1) and can cause bronchoconstriction by blocking β2 receptors, making them less desirable in patients with respiratory conditions.

147
Q

 α Blockers:
 Indications:

A

 Hypertension (especially resistant cases).
 Benign prostatic hyperplasia (BPH) to ease urination.
 Pheochromocytoma (to control catecholamine excess).

148
Q

 α Blockers:
 Toxicities:

A

 Orthostatic hypotension: Sudden drop in blood pressure upon standing.
 Reflex tachycardia: Due to reduced vascular resistance and baroreceptor-mediated compensation.
 Nasal congestion, dizziness, and fatigue.

149
Q

 β Blockers:
 Indications:

A

 Hypertension (especially with ischemic heart disease).
 Angina, heart failure, post-myocardial infarction (cardioprotective).
 Arrhythmias (to reduce heart rate).
 Migraine prophylaxis and anxiety.

150
Q

 β Blockers:
 Toxicities

A

 Bradycardia: Excessive slowing of the heart rate.
 Heart failure exacerbation: In patients with severe heart failure.
 Bronchoconstriction (with non-selective β blockers, problematic in asthmatic patients).
 Fatigue, depression, and sexual dysfunction.

151
Q

Blood Pressure Evaluation

A

 Blood pressure (BP) is measured using a sphygmomanometer and stethoscope or an automated BP cuff. The cuff is inflated above systolic pressure and deflated slowly, while listening for Korotkoff sounds. The first sound indicates systolic BP, and the disappearance of sounds indicates diastolic BP.

152
Q

 MAP (Mean Arterial Pressure):

A

 reflects average pressure in arteries during one cardiac cycle.
 MAP = 2 (DBP)+ (SBP)/3

153
Q

Different levels of BP acuities

A

 Normal: <120/80 mmHg
 Elevated: 120–129/<80 mmHg
 Hypertension Stage 1: 130–139/80–89 mmHg
 Hypertension Stage 2: ≥140/90 mmHg

154
Q

 Cardiac Output (CO):

A

 CO = Heart Rate (HR) × Stroke Volume (SV). Increased CO raises blood pressure.

155
Q

 Peripheral Vascular Resistance (PVR):

A

 Resistance in the arteries; increased PVR leads to higher BP.
 Regulated by the diameter of arterioles and influenced by autonomic nervous system, hormones (angiotensin II), and local factors (e.g., nitric oxide).

156
Q

Anatomic Control Sites for Blood Pressure

A

 Baroreceptors: In the carotid sinus and aortic arch; sense BP changes and modulate autonomic responses.
 Renal System: Controls blood volume via the renin-angiotensin-aldosterone system (RAAS).
 Vascular Smooth Muscle: Responds to sympathetic stimulation and vasoactive agents (e.g., angiotensin II).

157
Q

Non-Pharmacologic Interventions for Elevated Blood Pressure

A

 Weight loss.
 Sodium restriction.
 Regular physical activity.
 DASH diet (Dietary Approaches to Stop Hypertension).
 Alcohol moderation.
 Smoking cessation.

158
Q

Ex. Diuretics

A

Hydrochlorothiazide, furosemide

159
Q

Ex. ACE inhibitors

A

Lisinopril, enalapril

160
Q

Ex. B-Blockers

A

Metoprolol, atenolol

161
Q

Ex. Calcium Channel Blockers

A

Amlodipine, diltiazem

162
Q

Ex. Renin Inhibitor

A

Aliskiren

163
Q

Centrally Acting Sympathoplegic: Clonidine and Methyldopa

A

 Target: α2-adrenergic receptors in the CNS (brainstem).
 Mechanism: Decrease sympathetic outflow, reducing heart rate, and vascular resistance.
 Effects: Lower BP.
 Indications: Hypertension, especially in pregnancy (methyldopa).
 Side Effects: Sedation, dry mouth, rebound hypertension (if clonidine is abruptly withdrawn).

164
Q

 ex. Of Beta Blockers: Heart and kidneys (reduce HR and renin release).

A

Propranolol, metoprolol

165
Q

 Alpha Blockers: Vascular smooth muscle (cause vasodilation).

A

Prazosin, doxazosin (osin’s)

166
Q

Doses for Metoprolol, Atenolol, and Esmolol

A

 Metoprolol: 50-100 mg/day (divided into doses).
 Atenolol: 25-100 mg/day.
 Esmolol: 0.5-1 mg/kg bolus followed by 50-300 mcg/kg/min infusion (short-acting, used in emergencies).

167
Q

Mechanisms of Action of Vasodilators

A

Relax smooth muscle in blood vessels

168
Q
  1. Calcium Channel Blockers mechanism
A

Reduce calcium entry into smooth muscle (e.g., amlodipine).

169
Q
  1. Nitric Oxide Donors mechanism
A

Increase NO, leading to vasodilation (e.g., nitroglycerin).

170
Q
  1. Potassium Channel Openers
A

Hyperpolarize cells, causing relaxation (e.g., minoxidil).

171
Q
  1. Alpha Blockers mechanism
A

Block α1 receptors, reducing vasoconstriction (e.g., prazosin).

172
Q

Compensatory Responses to Vasodilators

A

 Reflex Tachycardia: Lower blood pressure triggers baroreceptors, increasing sympathetic output to raise heart rate.
 Fluid Retention: Reduced BP leads to activation of RAAS, increasing sodium and water retention.

173
Q

 Hydralazine indication

A

Arteriolar vasodilator, used in resistant hypertension

174
Q

 Nitroprusside indication

A

Arteriolar and venous vasodilator, used in hypertensive emergencies.

175
Q

Concerns for nitroprusside use

A

 Cyanide toxicity with prolonged use or high doses.
 Start at 0.3 mcg/kg/min, titrate up to 10 mcg/kg/min (short-term use only).

176
Q

Three Classes of Calcium Channel Blockers (CCBs)

A

 Dihydropyridines (Target vascular smooth muscle): Amlodipine, nifedipine.
 Non-Dihydropyridines (Target heart and vascular smooth muscle): Verapamil, diltiazem.
 Phenylalkylamines: Primarily affect the heart, reducing contractility.

177
Q

Renin-Angiotensin-Aldosterone Pathway

A

 Pathway:
Renin (kidneys) converts angiotensinogen to angiotensin I, which is converted to angiotensin II by ACE. Angiotensin II causes vasoconstriction and aldosterone release, leading to water and sodium retention to increase BP

178
Q

lisinopril

A

 ACE Inhibitors: Block conversion of angiotensin I to II

179
Q

losartan

A

 ARBs (Angiotensin II Receptor Blockers): Block angiotensin II receptors

180
Q

aliskiren

A

 Direct Renin Inhibitors: Inhibit renin directly

181
Q

Two Types of Angiotensin Antagonists

A

 ACE Inhibitors
 ARBs (Angiotensin Receptor Blockers)

182
Q

Pulmonary Hypertension Therapeutic effects
 Prostacyclin Analogs

A

Vasodilate pulmonary arteries (e.g., epoprostenol).

183
Q

Pulmonary Hypertension Therapeutics
 Endothelin Receptor Antagonists

A

Block endothelin-induced vasoconstriction (e.g., bosentan).

184
Q

Pulmonary Hypertension Therapeutics
 Phosphodiesterase-5 Inhibitors

A

Increase cGMP, leading to vasodilation (e.g., sildenafil).

185
Q

 Hypertensive Urgency

A

BP ≥180/120 mmHg without end-organ damage

186
Q

 Hypertensive Crisis

A

BP ≥180/120 mmHg with end-organ damage (e.g., stroke, myocardial infarction).

187
Q

Treatments for Mild Hypertension

A

Lifestyle modifications, thiazide diuretics

188
Q

Treatments for Moderate Hypertension

A

ACE inhibitors, CCBs, beta blockers

189
Q

Treatments for Severe (emergent) Hypertension

A

IV medications (e.g., nitroprusside, labetalol, hydralazine).

190
Q

 Arterial Tone is regulated by

A

Regulated by smooth muscle and response to sympathetic activity and vasoconstrictors like angiotensin II

191
Q

 Describe Capillary Tone

A

Minimal; capillaries lack smooth muscle

192
Q

 Venous Tone

A

Veins are more compliant, but sympathetic stimulation can constrict veins to increase venous return

193
Q

 Describe, Effort Angina

A

Caused by increased myocardial oxygen demand during exertion. Determinants include heart rate, contractility, and wall tension.

194
Q

 Vasospastic Angina is due to…..

A

Caused by coronary artery spasms, reducing blood flow

195
Q

Coronary blood flow occurs mainly during

A

diastole;
when the heart muscle relaxes and perfusion to the coronary arteries increases.

196
Q

Why do you use of beta blockers or calcium channel blockers for angina?

A

 To reduce Oxygen Demand

197
Q

Use of nitrates to dilate coronary vessels in angina also does what?

A

 Increase Oxygen Supply

198
Q

 Nitric Oxide (NO) Pathway

A

NO activates guanylyl cyclase, increasing cGMP and leading to vasodilation. Drugs like nitroglycerin target this pathway.

199
Q

 Nitrates/Nitrites ex.

A

Nitroglycerin, isosorbide dinitrate
- Donate NO, increasing cGMP for vasodilation

200
Q

Concerns with Overexposure to Nitrates/Nitrites

A

 Tolerance: Continuous use can lead to decreased efficacy.
 Methemoglobinemia: Overexposure can cause abnormal hemoglobin formation.

201
Q

Epicardial arteries contain which receptors

A

alpha (vasoconstrictive) and beta (vasodilatory) receptors.

202
Q

 pFOX Inhibitors

A

Inhibit fatty acid oxidation, shifting metabolism to glucose, reducing oxygen consumption.

203
Q

 Ranolazine

A

Modulates late sodium currents, improving myocardial efficiency, decrease FOX and uses glucose for atp (not a pFOX inhibitor).

204
Q

Therapeutic and Adverse Effects of Nitrates,

A

Vasodilation, but can cause headaches and hypotension

205
Q

Therapeutic and Adverse Effects of Beta Blockers

A

Reduce heart rate, but can cause fatigue and bradycardia

206
Q

Therapeutic and Adverse Effects of CCBs

A

Vasodilation, but may cause edema and reflex tachycardia

207
Q

Nitrate with Beta Blocker or CCB

A

can reduce compensatory mechanisms like reflex tachycardia, providing better angina control.

208
Q

Medical Therapy for Angina

A

Focuses on reducing oxygen demand and increasing supply (e.g., drugs like nitrates, beta blockers).

209
Q

Surgical Therapy for Angina

A

Coronary interventions like angioplasty or bypass surgery improve coronary blood flow mechanically

210
Q

Define  Heart Failure (HF):

A

clinical syndrome where the heart cannot pump blood sufficiently to meet the body’s needs. It results from structural or functional cardiac disorders that impair the filling (diastolic dysfunction) or pumping (systolic dysfunction) of blood

211
Q

 Neurohormonal activation (RAAS, sympathetic nervous system) worsens HF

A

by increasing afterload, fluid retention, and remodeling

212
Q

 Preload in HF

A

Increased in HF due to fluid retention (via RAAS).

213
Q

 Afterload in HF

A

Increased due to systemic vascular resistance (vasoconstriction).

214
Q

 Contractility in Systolic HF

A

Reduced in systolic HF, leading to decreased stroke volume and ejection fraction.

215
Q

 Heart Rate in HF

A

Often increased as a compensatory mechanism to maintain cardiac output but can worsen HF if persistent

216
Q

Starling’s Law

A

the strength of ventricular contraction increases with an increase in the volume of blood filling the heart

217
Q

Starling’s Law in HF

A

This mechanism is impaired in HF as the heart cannot contract forcefully despite increased preload.

218
Q

 End-Systolic Volume (ESV):

A

volume remaining in the ventricles after systole. In heart failure, ESV is elevated due to reduced contractility

219
Q

 Passive Filling

A

Blood flows into the ventricles during diastole, contributing to EDV.

220
Q

 Atrial Contraction

A

Contributes about 20% of ventricular filling, especially important in conditions with impaired ventricular compliance (e.g., diastolic HF).

221
Q

 Aldosterone antagonists

A

Spironolactone (K sparing)

222
Q

Drug ex.
 ARNI (angiotensin receptor-neprilysin inhibitor)

A

Sacubitril/valsartan

223
Q

Term for…
(during the plateau phase of the action potential triggers calcium release from the sarcoplasmic reticulum, which binds to troponin C, leading to actin-myosin interaction and muscle contraction).

A

 Calcium influx

224
Q

Digitalis mechanism

A

Inhibits the Na+/K+ ATPase, increasing intracellular sodium, which reduces the activity of the Na+/Ca2+ exchanger. This increases intracellular calcium, enhancing contractility

225
Q

Digitalis effects

A

Positive inotropy, reduced heart rate (via increased vagal tone).

226
Q

Toxic Effects of Digitalis on the Heart

A

Increased intracellular calcium can lead to arrhythmias, including ventricular tachycardia, AV block, and digitalis-induced bradycardia.

227
Q

causes increased automaticity and delayed depolarizations due to calcium and sodium overload.

A

Digitalis toxicity

228
Q

Drug ex. ____
Beta-1 agonist, increases contractility

A

 Dobutamine

229
Q

Phosphodiesterase-3 inhibitor, increases cAMP, enhancing contractility and vasodilation.

A

 Milrinone

230
Q

Mechanism of diuretics in Heart Failure:

A

Reduce preload and alleviate fluid overload.

231
Q

Mechanism of vasodilators in HF

A

Decrease afterload

232
Q

 ACE Inhibitors in HF

A

Reduce RAAS activity, decreasing afterload and preload, and preventing remodeling.

233
Q

 Beta Blockers in HF

A

Reduce sympathetic overactivity, slow heart rate, improve ejection fraction over time and prevent remodeling.

234
Q

Non-Pharmaceutical Interventions for Heart Failure

A

 Lifestyle modifications: Low-sodium diet, fluid restriction.
 Exercise: Cardiac rehabilitation.
 Surgical interventions: Pacemaker, ventricular assist devices, heart transplant.

235
Q

 Atrial arrhythmias

A

Atrial fibrillation, atrial flutter

236
Q

 Ventricular arrhythmias

A

Ventricular tachycardia, ventricular fibrillation

237
Q

 Bradyarrhythmias

A

Sinus bradycardia, heart block

238
Q

 Conduction System

A

SA node → AV node → Bundle of His → Right and left bundle branches → Purkinje fibers → ventrical contraction

239
Q

 P wave:

A

Atrial depolarization

240
Q

 QRS complex:

A

Ventricular depolarization.

241
Q

 T wave

A

Ventricular repolarization

242
Q

Role in Cardiac Action Potential
 Potassium Channels:

A

Repolarization (Phase 3).

243
Q

Role in Cardiac Action Potential
 Calcium Channels:

A

Plateau phase (Phase 2).

244
Q

Role in Cardiac Action Potential
 Sodium Channels:

A

Rapid depolarization (Phase 0).

245
Q

 m gate:

A

Activation gate, opens during depolarization.

246
Q

 h gate:

A

Inactivation gate, closes during depolarization, reopens during repolarization.

247
Q
  1. Phase 0: in AP
A

Rapid depolarization (Na+ influx).

248
Q
  1. Phase 1: in AP
A

Initial repolarization (K+ efflux).

249
Q
  1. Phase 2: in AP
A

Plateau (Ca2+ influx).

250
Q
  1. Phase 3: in AP
A

Repolarization (K+ efflux).

251
Q
  1. Phase 4: in AP
A

Resting potential.

252
Q

 Impulse Formation

A

Abnormal automaticity (e.g., ectopic pacemakers)

253
Q

 Impulse Conduction

A

Re-entry circuits (e.g., AVNRT, WPW syndrome).

254
Q

 First-degree HB

A

Prolonged PR interval (>200 ms).

255
Q

 Second-degree (Type I) HB

A

Progressive PR lengthening until a beat is dropped.

256
Q

 Second-degree (Type II) HB

A

Sudden dropped beats without PR interval lengthening.

257
Q

 Third-degree HB

A

No relationship between P waves and QRS complexes.

258
Q

Antiarrhythmic drugs
 Class I

A

(Sodium channel blockers): Block sodium channels, slow depolarization.
 Ia: Quinidine.
 Ib: Lidocaine.
 Ic: Flecainide.

259
Q

Antiarrhythmic drugs
 Class II

A

(Beta blockers): Slow heart rate, reduce automaticity (e.g., Propranolol).

260
Q

Antiarrhythmic drugs
 Class III

A

(Potassium channel blockers): Prolong repolarization (e.g., Amiodarone).

261
Q

Antiarrhythmic drugs
 Class IV

A

(Calcium channel blockers): Slow AV conduction (e.g., Verapamil).

262
Q

 Class Ia: Quinidine (Toxicity) :

A

Torsades de Pointes

263
Q

 Class Ib: Lidocaine (Toxicity) :

A

CNS effects, seizures

264
Q

 Class Ic: Flecainide (Toxicity) :

A

Pro arrhythmia

265
Q

 Class II: Propranolol (Toxicity) :

A

Bradycardia, bronchospasm

266
Q

 Class III: Amiodarone (Toxicity) :

A

Pulmonary fibrosis, thyroid dysfunction

267
Q

 Class IV: Verapamil (Toxicity) :

A

Bradycardia, hypotension

268
Q

Effects of Adenosine on SVT

A

Temporarily blocks AV node conduction, rapidly terminating supraventricular tachycardia (SVT).

269
Q

Non-Pharmacological Therapy for Arrhythmias
 For Brady arrhythmia’s.

A

Pacemaker

270
Q

Non-Pharmacological Therapy for Arrhythmias
 For atrial fibrillation or flutter.

A

Cardioversion

271
Q

Non-Pharmacological Therapy for Arrhythmias
 For re-entry tachycardias.

A

Ablation

272
Q

Antiarrhythmic Drugs for ventricular arrhythmias

A

 Amiodarone

273
Q

Antiarrhythmic Drugs for SVT

A

 Adenosine

274
Q

Antiarrhythmic Drugs for rate control in atrial fibrillation

A

 Beta blockers

275
Q

Drugs for chronic suppression of arrhythmias

A

 Class Ic drugs

276
Q

Eg. Esters

A

ACh

277
Q

Eg. Esters

A

ACh

Pharm Dr. T (3 decks)

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