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APEX/BOARD STUDY > UNIT 2 - ANS > Flashcards

UNIT 2 - ANS Flashcards

1
Q

What is homeostasis?

A

A steady state condition that requires energy to maintain the system

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2
Q

What are the four functions a control system must perform?

A
  • SENSE the vital parameter
  • COMPARE the input signal with a set point
  • MULTIPLY the error signal by a proportionality factor
  • ADJUST the vital parameter by activating an effector system
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3
Q

What is negative feedback?

A

Reverses a disturbance in some factors and leads to stability

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4
Q

What is positive feedback?

A

A change in some factors produces an enhanced change in the same direction

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5
Q

What is cell signaling?

A

The intracellular response to extracellular signals that allows cells to communicate

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6
Q

What is signal transduction?

A

The conversion of information into a chemical change, a universal property of living cells

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7
Q

What are the three main methods of intercellular communication?

A
  • Endocrine
  • Paracrine
  • Autocrine
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8
Q

What is specificity in signal transduction?

A

Cell specific receptors and bonds

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9
Q

What is amplification in signal transduction?

A

An enzyme cascade where one enzyme activates multiple others

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10
Q

What is integration in signal transduction?

A

The ability to receive multiple signals and produce an appropriate response

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11
Q

What is desensitization in signal transduction?

A

When a signal is present continuously, resulting in reduced receptor sensitivity

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12
Q

What are the six processes in a signal transduction sequence?

A
  • Recognition
  • Transduction
  • Transmission
  • Modulation
  • Response
  • Termination
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13
Q

What are the four categories of receptor-based signal transducers?

A
  • Transmembrane G protein-coupled receptors (GPCRs)
  • Transmembrane gated ion channels
  • Transmembrane enzyme linked receptors
  • Soluble nuclear receptors
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14
Q

What are the four categories of chemical signaling molecules?

A
  • Small hydrophilic molecules
  • Lipophilic molecules
  • Peptides and proteins
  • Others (nucleotides, gases, endocannabinoids)
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15
Q

What is the primary neurotransmitter of the peripheral efferent neural pathways?

A

Acetylcholine (ACh)

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16
Q

What are the two types of synapses?

A
  • Electrical
  • Chemical
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17
Q

What distinguishes ionotropic receptors from metabotropic receptors?

A

Ionotropic receptors are ion channels, while metabotropic receptors activate enzymes and trigger cascades

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18
Q

What neurotransmitter is synthesized from tryptophan?

A

Serotonin

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19
Q

What is the role of dopamine in the brain?

A

It is involved in reward, motivation, and motor control

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20
Q

What is excitotoxicity?

A

Neuronal injury initiated by excessive glutamate receptor activity

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21
Q

True or False: GABA is the primary excitatory neurotransmitter in the brain.

A

False

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22
Q

Fill in the blank: The end product of catecholamine metabolism is _______.

A

Vanillylmandelic acid (VMA)

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23
Q

What is the rate-limiting step in catecholamine biosynthesis?

A

Tyrosine hydroxylase

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24
Q

What neurotransmitter receptors are primarily metabotropic G protein-coupled receptors?

A

Biogenic amine neurotransmitter receptors

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25
Q

What is the function of calmodulin (CaM) in signaling events?

A

It modulates downstream signaling events mediated by calcium

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26
Q

What are biogenic amine neurotransmitters removed from the synaptic cleft by?

A

Reuptake into the presynaptic terminal, reuptake into non-neuronal cells & glands, or diffuse into circulation to be metabolized

Examples include norepinephrine (NE), epinephrine (EPI), and dopamine.

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27
Q

What type of receptors do biogenic amine neurotransmitters primarily use?

A

Metabotropic G protein-coupled receptors, with the exception of the ionotropic 5-HT3 serotonin receptor.

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28
Q

List the adrenergic receptor subtypes and their associated pathways.

A
  • α1 – Gq → PLC
  • α2 – Gi → inhibits AC → reduces cAMP
  • β – Gs → activated AC → increases cAMP
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29
Q

Where are the largest dopaminergic neurons located?

A

In the brain’s substantia nigra.

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30
Q

What roles do serotonergic neurons play?

A
  • Sleep & wakefulness
  • Emotions
  • Cognition
  • Cardiovascular, respiratory, & intestinal activities
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31
Q

True or False: Derangement of serotonergic pathways can contribute to anxiety and depression.

A

True

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32
Q

What is the target receptor for Zofran?

A

The ionotropic 5-HT3 serotonin receptor.

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33
Q

What role does histamine play in the body?

A
  • Arousal & attention
  • Memory, learning, & mood
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34
Q

Fill in the blank: Nonconventional neurotransmitters cannot be stored in vesicles and must be synthesized and released on _______.

A

demand

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35
Q

What are the main purinergic neurotransmitters?

A
  • ATP
  • ADP
  • Adenosine
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36
Q

What enzyme converts ATP to adenosine in the synaptic cleft?

A

Ectonucleotidase.

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37
Q

What are the two major pathways that initiate apoptosis?

A
  • The intrinsic (mitochondrial) pathway
  • The extrinsic (cell receptor-initiated) pathway
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38
Q

What is the function of Nitric Oxide (NO) in cell signaling?

A

Acts as a universal intracellular messenger, involved in autocrine & paracrine signaling.

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39
Q

What is the role of receptor guanylyl cyclases?

A

Turn GTP to cGMP.

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40
Q

What do receptor tyrosine kinases (RTKs) primarily bind to?

A
  • Insulin
  • Growth factors
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41
Q

What is the JAK-STAT system associated with?

A

Tyrosine kinase-associated receptors.

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42
Q

What are the two families of intracellular (nuclear) receptors?

A
  • Steroid hormones
  • Prostaglandins, vitamin D, thyroid hormones, & retinoic acid
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43
Q

What is the difference between necrosis and apoptosis?

A

Necrosis is uncontrolled cell death with inflammation; apoptosis is programmed cell death without inflammation.

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44
Q

What type of signaling do β1-adrenoreceptors primarily mediate in cardiac myocytes?

A

Chronotropic, inotropic, dromotropic, & lusitropic effects.

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45
Q

What is the role of phosphodiesterases (PDE) in cyclic nucleotide signaling?

A

Terminate cyclic nucleotide signals.

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46
Q

What is the significance of cyclic nucleotide phosphodiesterase 3 (PDE3)?

A

It metabolizes cAMP to 5’-AMP.

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47
Q

What is the primary function of the autonomic nervous system (ANS)?

A

Ensure the physiological integrity of cells, tissues, & organs.

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48
Q

What are the three major divisions of the autonomic nervous system?

A
  • Sympathetic nervous system (SNS)
  • Parasympathetic nervous system (PNS)
  • Enteric nervous system (ENS)
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49
Q

What type of receptors are primarily involved in signal transduction through GPCRs?

A

G-protein-coupled receptors.

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50
Q

What are the five second messengers you should know?

A
  • cAMP
  • cGMP
  • IP3
  • DAG
  • Calcium ion (Ca++)
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51
Q

True or False: SNS stimulation of most arterial vessels causes vasodilation.

A

False

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52
Q

What is the effect of α2 receptors in the CNS?

A

Stimulation leads to sedation, MAC reduction, bradycardia, & vasodilation.

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53
Q

What does stimulation of postsynaptic alpha-2 receptors lead to?

A

Acute vasocontraction & hypertension.

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54
Q

What is the effect of increased cAMP in the heart?

A

It ↑ intracellular Ca++ & the force of contraction, but also ↑ the rate of relaxation by accelerating the return of Ca++ to the SR

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55
Q

What happens to vascular smooth muscle when cAMP levels increase?

A

Increased cAMP inhibits light chain kinase, causing vasodilation and decreased systemic vascular resistance (SVR)

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56
Q

In which situations are PDE inhibitors helpful?

A

Beta-blocker-induced myocardial depression, acute heart failure unresponsive to IV catecholamines, anytime increased inotropy & reduced afterload are desirable

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57
Q

What is the prototype nonselective PDE inhibitor?

A

Theophylline

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58
Q

What is the primary neurotransmitter of the sympathetic nervous system?

A

Norepinephrine (NE)

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59
Q

What is the rate-limiting step in catecholamine synthesis?

A

Tyrosine hydroxylase activity

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60
Q

How can cells generate tyrosine if the supply is low?

A

Cells can generate tyrosine from phenylalanine

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61
Q

What enzyme converts L-DOPA to dopamine?

A

Aromatic L-amino acid decarboxylase

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62
Q

What is the role of dopamine in the synthesis of norepinephrine?

A

Dopamine is converted into NE by the enzyme dopamine-β-hydroxylase

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63
Q

How is norepinephrine released from presynaptic nerve terminals?

A

An action potential depolarizes the nerve terminal, opening voltage-gated Ca++ channels, leading to exocytosis of NE

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64
Q

What mechanism primarily removes catecholamines from the synaptic cleft?

A

Reuptake into the presynaptic nerve (~80%)

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65
Q

Which drugs block norepinephrine reuptake?

A

Tricyclic antidepressants & cocaine

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66
Q

What are the two main enzymes involved in catecholamine metabolism?

A

Monoamine oxidase (MAO) & Catechol-O-methyltransferase (COMT)

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67
Q

What is vanillylmandelic acid (VMA) in relation to catecholamines?

A

It is the end-product of catecholamine metabolism eliminated through urine

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68
Q

What is the primary neurotransmitter in the parasympathetic nervous system?

A

Acetylcholine (ACh)

69
Q

What are the three types of receptors that acetylcholine stimulates?

A
  • Nicotinic type N (NN)
  • Nicotinic type M (MN)
  • Muscarinic (M1-5)
70
Q

What is the rate-limiting factor for acetylcholine synthesis?

A

Availability of substrates, choline & acetyl-CoA

71
Q

What enzyme is responsible for the synthesis of acetylcholine?

A

Choline acetyltransferase

72
Q

How is acetylcholine released from the presynaptic nerve terminals?

A

An action potential causes voltage-gated Ca++ channels to open, leading to exocytosis

73
Q

What role does acetylcholinesterase (AChE) play in neurotransmission?

A

It hydrolyzes ACh after it unbinds from receptors

74
Q

What are the two complementary pathways of the autonomic nervous system?

A
  • Sympathetic nervous system (SNS)
  • Parasympathetic nervous system (PaNS)
75
Q

What is the main exception in the efferent architecture of the ANS?

A

The adrenal medulla has no postganglionic neuron; chromaffin cells secrete EPI & NE into circulation

76
Q

What is a ganglion in the context of the autonomic nervous system?

A

A peripheral collection of nerve cell bodies where preganglionic & postganglionic neurons synapse

77
Q

What is the stellate ganglion and its significance?

A

It is a confluence of the inferior cervical ganglion & T1 ganglion, providing SNS innervation to the ipsilateral head, neck, & upper extremity

78
Q

What syndrome results from blockade of the stellate ganglion?

A

Horner’s syndrome

79
Q

Fill in the blank: The sympathetic preganglionic neurons arise from _______.

80
Q

What are the two key areas of the adrenal gland?

A

Medulla and Cortex

Medulla secretes catecholamines; Cortex secretes glucocorticoids, mineralocorticoids, and androgens.

81
Q

What type of fibers travel directly to the adrenal medulla?

A

Preganglionic sympathetic B fibers

These fibers arise from T5-T9 and there are no postganglionic sympathetic fibers in this pathway.

82
Q

What neurotransmitter do preganglionic sympathetic B fibers release onto chromaffin cells?

A

ACh (Acetylcholine)

This stimulates NN ACh receptors on chromaffin cells.

83
Q

What is the typical secretion ratio of EPI to NE at rest from the adrenal medulla?

A

80% EPI and 20% NE

EPI is secreted at 0.2 mcg/kg/min and NE at 0.05 mcg/kg/min.

84
Q

What is pheochromocytoma?

A

A catecholamine-secreting tumor, mostly NE

It usually originates in the chromaffin tissue of the adrenal gland.

85
Q

What are common symptoms of pheochromocytoma?

A

HA, diaphoresis, tachycardia

HA stands for headache.

86
Q

What must be done before beta blocking in pheochromocytoma treatment?

A

Alpha block

This is crucial to prevent complications.

87
Q

What are the consequences of removing a pheochromocytoma?

A

Hypotension and hypoglycemia

88
Q

What factors influence the distribution of K+ across cell membranes?

A

SNS activity and insulin

Medications like digoxin, ACEi, ARBs, and BB can increase extracellular K+.

89
Q

What is the short-term effect of sympathetic stimulation on serum K+ levels?

A

Initial rise in serum [K+]

This effect is very short-lived.

90
Q

What is the long-term effect of EPI binding to Beta-2 receptors on skeletal muscle?

A

Decrease in serum [K+]

This is due to the activation of the Na+/K+ pump, shifting K+ into the cells.

91
Q

List some situations that promote transcellular K+ shifts.

A
  • Acidosis (Efflux)
  • Destruction of cell membrane (Efflux)
  • Succinylcholine (Efflux)
  • Hyperosmolarity (Efflux)
  • Alkalosis (Influx)
  • Methylxanthines (Theophylline) (Influx)
  • Beta-2 agonists (Influx)
  • Insulin (Influx)
92
Q

What is the role of the ANS in maintaining physiological parameters?

A

It uses reflexes and feedback loops.

93
Q

What are the components of biological feedback loops?

A
  • Sensor (Detector)
  • Afferent pathways
  • Control center
  • Efferent pathway
  • Effector organ or tissue
94
Q

Which tissues does the ANS influence?

A

All tissues except skeletal muscle.

95
Q

What are some key points of integration between the ANS and endocrine system?

A
  • Renin-Angiotensin-Aldosterone System (RAAS)
  • Vasopressin
  • Glucocorticoids
  • Insulin
96
Q

What are the two types of mechanisms that maintain blood pressure?

A
  • Neuronal (Short term)
  • Hormonal (Long term)
97
Q

What does the baroreceptor reflex primarily help maintain?

A

Arterial blood pressure

It operates as a negative feedback loop.

98
Q

What happens to HR and contractility when blood pressure increases?

A

Decreased HR and contractility

99
Q

What is a typical adaptation time for baroreceptor setpoint changes?

100
Q

What are the names of the surgeries that can affect the baroreceptor reflex?

A
  • Carotid Endartectomy
  • Mediastinoscopy
101
Q

Name two drugs that impair the baroreceptor reflex.

A
  • VA (Volatile Anesthetics)
  • NE (Norepinephrine)
102
Q

What is the Bainbridge reflex?

A

Prevents blood sludging in veins and atria due to right atrial stretch.

103
Q

What characterizes the Bezold-Jarisch reflex?

A

Triad of bradycardia, hypotension, and coronary artery dilation.

104
Q

What is the main cause of the vasovagal reflex?

A

Physiological stress

105
Q

What does the oculocardiac reflex involve?

A

Afferent CN5 and efferent CN10

Known as the ‘5 & dime’ reflex.

106
Q

What is the CNS ischemic response?

A

Massive activation of the SNS due to cerebral ischemia.

107
Q

What triad does Cushing’s Reflex consist of?

A
  • Hypertension
  • Bradycardia
  • Irregular respirations
108
Q

What is the primary neurotransmitter for the ANS?

A

ACh (Acetylcholine) and NE (Norepinephrine)

109
Q

What are the three alpha selective adrenergic agonists?

A
  • Phenylephrine
  • Clonidine
  • Dexmedetomidine
110
Q

What is a characteristic of Phenylephrine?

A

A pure alpha 1 stimulant

Causes venous and arterial vasocontraction.

111
Q

What is the primary effect of Clonidine?

A

Inhibits NE release causing vasodilation.

112
Q

What is the action of Dexmedetomidine?

A

Stimulates alpha 2 R leading to inhibition of neuronal firing.

113
Q

What are the effects of beta 2 selective agonists?

A

Bronchodilation and vasodilation.

114
Q

What is the main effect of Epi at lower doses?

A

Favors beta stimulation, increasing CO, HR, and inotropy.

115
Q

What happens at high doses of NE?

A

Favors B1 and alpha effects, causing systemic vasoconstriction.

116
Q

What is the effect of low-dose dopamine?

A

Stimulates D1R, resulting in vasodilation and increased renal blood flow.

117
Q

What is the significance of dopamine in renal function?

A

Increases renal blood flow and urine output at low doses.

118
Q

What is comorbidity?

A

The presence of one or more additional conditions co-occurring with a primary condition.

119
Q

Why must dopamine be administered as an infusion?

A

Due to its rapid metabolism.

120
Q

What effect does low-dose dopamine infusion (<3 ug/kg/min) have on renal blood flow?

A

Increases renal blood flow and urine output.

121
Q

Which receptors are stimulated by low-dose dopamine to increase renal blood flow?

A

D1 receptors.

122
Q

What is the conclusion regarding dopamine’s effectiveness in preventing acute kidney injury?

A

Dopamine does not prevent or reverse acute kidney injury or failure.

123
Q

What complications can low-dose dopamine be associated with?

A

CV, pulmonary, GI, immune, and endocrine complications.

124
Q

What is the recommendation regarding the administration of dopamine to protect the kidneys?

A

It should be abandoned due to unlikely benefits and potential detrimental effects.

125
Q

What is isoproterenol derived from?

126
Q

What are the receptor activities of isoproterenol?

A

B1 and B2 activity with no alpha activity.

127
Q

What is the main clinical use of isoproterenol?

A

Historically used to increase heart rate in patients with heart block, but now has limited clinical use.

128
Q

What adverse effects are associated with isoproterenol?

A

Precipitation of supraventricular and ventricular arrhythmias.

129
Q

What is dobutamine’s primary pharmacological activity?

A

Enhances myocardial contractility and reduces vascular tone.

130
Q

What type of agonist is dobutamine?

A

Selective B1 agonist with mild B2 effects.

131
Q

What is a potential adverse event associated with dobutamine?

A

May extend cardiac muscle infarction and increase AV conduction.

132
Q

What is ephedrine’s primary action on adrenoreceptors?

A

Exerts both direct and indirect actions with predominant indirect actions.

133
Q

What mechanism allows ephedrine to provoke the release of norepinephrine?

A

Endocytosis into adrenergic presynaptic terminals, displacing norepinephrine.

134
Q

What is tachyphylaxis in the context of ephedrine use?

A

Depletion of presynaptic norepinephrine leading to reduced efficacy with repeated use.

135
Q

What are the two classifications of selective B2 agonists based on their duration of action?

A

Short acting and long acting.

136
Q

Name three short-acting B2 agonists.

A
  • Albuterol
  • Terbutaline
  • Levalbuterol
137
Q

What are the side effects of B2 stimulation?

A

Tremor, anxiety, and restlessness.

138
Q

What is a significant risk associated with long-acting B2-selective agents?

A

Asthma-related death due to severe asthma exacerbations.

139
Q

What is the prototype for nonselective alpha antagonists?

A

Phenoxybenzamine.

140
Q

How does phenoxybenzamine affect blood pressure?

A

Reduces arterial BP but can trigger reflex tachycardia and orthostatic hypotension.

141
Q

What is the best treatment for hypotension induced by phenoxybenzamine?

A

Vasopressin and fluids.

142
Q

What is phentolamine used for?

A

As a competitive nonselective alpha-R antagonist.

143
Q

What are the selective alpha1 antagonists mentioned?

A
  • Prazosin
  • Terazosin
  • Doxazosin
  • Tamsulosin
144
Q

What is yohimbine primarily marketed for?

A

ED, athletic performance, weight loss, HTN, diabetic neuropathy.

145
Q

What is the prototype beta-adrenergic antagonist?

A

Propranolol.

146
Q

What effects can nonselective beta antagonists produce?

A

Bronchoconstriction, hypoglycemia, and peripheral vascular constriction.

147
Q

Name a selective beta-adrenergic antagonist.

A

Metoprolol.

148
Q

What is the primary use of esmolol?

A

Rapid control of heart rate and blood pressure.

149
Q

What are the three main classes of calcium channel blockers?

A
  • Dihydropyridines
  • Benzothiazepines
  • Phenylalkylamines
150
Q

What is the primary therapeutic use of calcium channel blockers?

A

Treatment of HTN, arrhythmias, PVD, cerebral vasospasm, and angina.

151
Q

What is the action of muscarinic antagonists?

A

Competitive inhibitors of ACh at parasympathetic muscarinic receptors.

152
Q

What are the symptoms of toxicity from muscarinic antagonists?

A

Excitation, restlessness, sedation, confusion, hallucination, coma.

153
Q

How can muscarinic antagonist toxicity be treated?

A

Administering physostigmine.

154
Q

What are the main classes of calcium channel blockers (CCBs)?

A
  • Dihydropyridines
  • Benzothiazepines
  • Phenylalkylamines

Dihydropyridines include drugs like Nicardipine and Clevidipine; Benzothiazepines include Diltiazem; Phenylalkylamines include Verapamil.

155
Q

Which CCB is known for its ability to reduce morbidity and mortality from cerebral vasospasm?

A

Nimodipine

Nimodipine is specifically indicated for this purpose.

156
Q

What is the impairment on contractility of CCBs from lowest to highest?

A
  • Nicardipine
  • Diltiazem
  • Nifedipine
  • Verapamil

This ranking indicates the relative contractility effects of these CCBs.

157
Q

What are the negative effects of Verapamil and Diltiazem as class 4 antiarrhythmics?

A
  • Negative chronotropic effects
  • Negative dromotropic effects

These effects relate to the depression of electrical impulses in the SA and AV nodes.

158
Q

True or False: Verapamil is often used to treat angina due to its greatest myocardial depression.

A

True

Verapamil is known for its significant myocardial depression effects.

159
Q

Fill in the blank: Direct-acting vasodilators exert an arterial relaxing effect without interfering with _______.

A

[systemic or local constrictor mechanisms]

This characteristic differentiates them from other vasodilators.

160
Q

What is the mechanism of action for Nitroglycerin (NTG)?

A

Liberation of nitric oxide

This mechanism leads to its vasodilatory effects.

161
Q

What are the side effects associated with ACE inhibitors?

A
  • Dry cough
  • Angioedema
  • Profound hypotension

These side effects are due to the inhibition of bradykinin degradation and other mechanisms.

162
Q

What are the primary receptors targeted by inhalational anesthetics?

A

GABAA receptors

These receptors are involved in the effects of anesthetics on the CNS.

163
Q

What is the effect of vasopressin in vasodilatory states?

A

It can be administered for those resistant or refractory to catecholamine & fluid therapy

This highlights vasopressin’s role in managing specific shock states.

164
Q

What condition is characterized by degradation and dysfunction of diverse CNS structures and includes symptoms like orthostatic hypotension?

A

Multiple system atrophy (MSA)

MSA was formerly known as Shy-Drager syndrome.

165
Q

What is the primary action of phosphodiesterase inhibitors (PDEi)?

A

Causing smooth muscle relaxation by reducing PDE breakdown of cAMP and cGMP

This leads to increased levels of these cyclic nucleotides.

166
Q

Fill in the blank: The transplanted heart is severed from ______ influences.

A

[autonomic]

This results in a heart rate that is determined solely by the intrinsic rate of the SA node.

167
Q

Which CCB is devoid of chronotropic effects and is ideally suited for IV infusion?

A

Clevidipine

Clevidipine’s properties make it suitable for this administration route.

168
Q

What is a potential risk when using nitroprusside (SNP) in myocardial infarction?

A

Induction of ‘coronary steal’

This occurs when blood flow from maximally dilated vessels in ischemic areas is diverted to nonischemic tissue.

169
Q

Which class of drugs is known to prevent platelet aggregation for thrombosis prophylaxis?

A

PDE3 inhibitors

Examples include Milrinone and Cilostazol.

APEX/BOARD STUDY (5 decks)

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