Brainscape's Knowledge GenomeTM

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


See full index

Medical Physiology > Exam #1: Physiology of the ANS II > Flashcards

Exam #1: Physiology of the ANS II Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

What muscarinic receptors are present in the heart? What nervous system are they associated with?

A
  • M2

- PNS

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

What type of G-protein is associated with the M2 receptor in the heart?

A

Gi/o= inhibitory G-protein

Decrease cAMP & PKA

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

What do M2 receptors inhibit in the heart?

A
  • SA node= negative chronotrope
  • AV node= decreased conduction velocity
  • Atrial muscle= decreased atrial contracion
  • Ventricular muscle= decreased ventricular contracion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of muscarinic receptor is present in the lungs?

A

M3

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

What is the effect of M3 activation in the lungs?

A
  • Contraction of the bonchi & bronchioles
  • Secretion from submucosal glands

*DO NOT use drugs in asthma patients that have PNS activity

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

What type of muscarinic receptor is present in the stomach? What is the effect of stimulation of these receptors?

A

M3, motility & cramps

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

What type of muscarinic receptor is present in the glands? What is the effect of stimulation of these receptors?

A

M1, secretion

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

What type of muscarinic receptor is present in the intestine? What is the effect of stimulation of these receptors?

A

M3, contraction–diarrhea & involuntary defecation

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

What is the general clinical picture of ACE inhibitor intoxication?

A

Voiding, urinary incontinence

V. wet

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

What is the difference between a coupled cell & an indirectly coupled cell?

A
  • Directly coupled= directly activated by a neurotransmitter released from a varicosity
  • Coupled= junction potentials spread from directly innervated cells
  • Indirectly coupled= a sufficient area of a muscle bundle is depolarized to propagate the action potential to the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does the innervation of the visceral smooth muscle differ from the vascular smooth muscle?

A

Visceral smooth muscle receives input from one source.

Vascular smooth muscle receives input from 2x sources:

1) Perivascular nerves
2) Endothelial input

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

What effects are mediated by perivascular nerves?

A
  • A number of neurotransmitters released from varicosities in the tunica adventita act on receptors in the media, leading to vasoconstriction.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What effects are mediated by endothelial input?

A
  • In response to shear stress or hypoxia, endothelial cells release factors that mediate vasodilation (Endothelium-Derived Relaxing Factors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the effect of damage to the endothelial cell layer?

A
  • When the Endothelium is damaged, activation of M3R on vascular smooth muscle causes vasocontriction (unopposed by EDRFs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Outline the pathway that underscores the effects of M3R activation in the blood vessels.

A

1) ACh binds to M3
2) Increase intracellular Ca++
3) Increase in Nitric Oxide Synthase
4) Increased NO production via the endothelial cell
5) Relaxation

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

Why is vasoconstriction the outcome if the endothelium has been damaged?

A

Ca++ increase leads to contraction of the smooth muscle, but there is not the opposing NO, ultimately resulting in vasoconstriction.

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

Describe the mechanism of M1 & M3 receptor activation.

A

1) Receptor activation
2) Gq (activation)
3) PLC
4) PIP2–>IP3 & DAG
5) Increase Ca++ & PKC

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

Describe the mechanism of M2 receptor activation.

A

1) Receptor activation
2) Gi
3) Adenylul Cyclase inhibited
4) Decrease cAMP
5) Decrease PKA

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

Name the three locations of nicotinic ACh receptors.

A

1) PNS ganglia
2) Targets of the somatic nervous system, skeletal muscle
3) Adrenal medulla

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

What type of nicotinic receptor is present in the adrenal medulla? What is the response to ACh binding?

A
  • Nn

- Secretion of Epi & NE

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

What type of nicotinic receptor is present in the autonomic ganglia? What is the response to ACh binding?

A
  • Nn
  • Stimulation

*Note that all autonomic ganglia have nicotinic AChR

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

What type of nicotinic receptor is present in the neuromuscular junction? What is the response to ACh binding?

A
  • Nm
  • Stimulation i.e. twitch & hyperactivity of skeletal muscle

Remember skeletal MUSCLE, N-M

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

How are catecholamines synthesized?

A

1) Tyrosine is converted to DOPA via Tyrosine Hydroxylase*
2) DOPA is converted to Dopamine
3) Dopamine is converted to Norepinephrine

Note that this is the rate-limiting step

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

What drug blocks tyrosine hydroxylase? What step of the catecholamine synthesis process does this drug block?

A
  • Metyrosine

- Conversion of Tyrosine to DOPA

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

What part of catecholamine synthesis only occurs in the adrenal medulla?

A

Norepinephrine is converted to Epinephrine

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

What is tyramine?

A

Tyramine is a naturally occurring monoamine compound, and a trace amine derived from the metabolism of tyrosine (alternative to DOPA)

27
Q

What causes an increase in Tyramine?

A

Ingested of naturally occurring fermented cheese

28
Q

What is Tyramine a precursor of?

A

Norephinephrine

29
Q

How are catecholamines stored?

A

Synthesized catecholamines are transported into vesicles for storage via the “Vesicular Monoamine Transporter (VMAT)”

*Note that the conversion of norephinephrine to epinephrine occurs in the vesicle, if the converting enzyme is available.

30
Q

What blocks VMAT? What is the mechanism of action?

A

Reserprine, blocks VMAT & causes a depletion of catecholamine stores

Still used today for “resistant hypertension

31
Q

How are the catecholamines released?

A

Similar exocytosis mechanism as ACh

32
Q

What drug blocks VAMP?

A

Bretylium

33
Q

How is catecholamine transmission terminated?

A

1) Diffusion into the circulation & metabolized by liver COMT (catechol-O-methyl transferase)
2) Binding to an autoreceptor on the pre-synaptic nerve terminal
3) Neuronal Re-uptake via NET1 (NE transporter on the presynaptic nerve terminal), where:
- Repackaged in vesicles
- Metabolized by mitochondiral monoamine oxidase (MAO)
4) Extraneuronal uptake via extraneuronal transporters (ENT or NET2)

34
Q

What is the mechanism of action of cocaine & tricyclic antidepressants?

A

NET1 antagnoists that leads to an increase in NE in the synaptic cleft

35
Q

What is the effect of MAO antagonists? How are they related to Tyramine?

A

MAO is a mitochondrial enzyme that metabolizes catecholamines

  • Irreversible MAO antagonists enhance the availability of Tyramine
  • Can lead to hypertensive crisis
36
Q

Where are alpha-1 receptors located?

A

Vascular smooth muscle

37
Q

Describe the mechanism of alpha-1 receptor activation.

A

1) Catecholamine binding to alpha-1 receptors leads to simulation
2) Gq subunit activated
3) Gq activates PLC
4) PLC leds the the release of IP3 & DAG
5) IP3 stimulates the release of sequestered Ca++
6) Ca++ then activates Ca++ dependent protein kinases

38
Q

Describe the mechanism of B1 & B2 activation.

A

1) Catecholamine binding to B1 or B2 receptor leads to stimulation
2) Gs subunit activated
3) Activation of adenlyl cyclase
4) Increased cAMP
5) Increase PKA

39
Q

Describe the mechanism of alpha-2 activation.

A

1) Catecholamine binding to alpha-2 receptor
2) Gi subunit activated
3) Inactivation of adenlyl cyclase
4) Decrease cAMP
5) Decrease PKA

40
Q

Where are alpha 1 receptors located in the eye?

A

Radial (dilator muscle)

41
Q

Where are B1 receptors located in the eye?

A

Ciliary body epithelium

42
Q

Where are B2 receptors located in the eye?

A

Ciliary muscle

Ciliary body epithelium

43
Q

What is the effect of stimulating alpha 1 receptors in the eye?

A
  • Alpha-1 receptors are associated with the radial (dilator) muscle
  • Contraction of the muscle results in dilation/ mydriasis
44
Q

What is the effect of stimulating B1 receptors in the eye?

A
  • B1Rs are associated with the ciliary body epithelium

- Increased production of aqueous humor?

45
Q

What is the effect of stimulating B2 receptors in the eye?

A
  • B2Rs are associated with the ciliary body epithelium &ciliary muscle
  • Constriction & increased production of aqueus humor?
46
Q

What is the effect of stimulating alpha 1 receptors in the arterioles?

A

Contraction of the smooth muscle leading to an increase in total peripheral resistance, diastolic pressure, & afterload

47
Q

What is the effect of stimulating alpha 1 receptors in the veins?

A

Contraction of the smooth muscle leading to an increase in venous return & an increase in preload

48
Q

What is the effect of stimulating alpha 1 receptors in the liver?

A

An increase in glycogenolysis

49
Q

What is the effect of stimulating alpha 1 receptors in the male sex organs?

A

Ejaculation

50
Q

What is the effect of stimulating alpha 1 receptors in the bladder & internal sphincter?

A

Contraction & urinary retention

51
Q

What is the effect of stimulating alpha-2 receptors in the platelets?

A

Aggregation

52
Q

What is the effect of stimulating alpha-2 receptors in the pancreas?

A

Decreased insulin secretion

53
Q

Where are B1 receptors located?

A 
Heart 
- SA Node
- AV Node 
- Atrial & Ventricular Muscle
- His Purkinje 
Kidney
54
Q

What is the effect of B1 receptor activation in the heart?

A

SA Node= positive chronotrope
AV Node= positive dromotrope
Atrial & Ventricular M.= positive ionotrope

?

55
Q

What is the effect of B1 receptor activation in the kidney?

A

Increased renin release

56
Q

Where are B2 receptors located?

A 
Blood vessels
Uterus 
Bronchioles 
Skeletal Muscle 
Liver 
Pancreas
57
Q

What is the effect of B2 receptor activation in the blood vessels?

A

Vasodilation leading to a decrease in total peripheral resistance, diastolic blood pressure, & afterload

58
Q

What is the effect of B2 receptor activation in the uterus?

A

Relaxation

59
Q

What is the effect of B2 receptor activation in the bronchioles?

A

Dilation

60
Q

What is the effect of B2 receptor activation in the skeletal muscle?

A
  • Glycogenoylsis

- Contractility/ tremor

61
Q

What is the effect of B2 receptor activation in the liver?

A

Glycogenolysis

62
Q

What is the effect of B2 receptor activation in the pancreas?

A

Insulin secretion

63
Q

What is the rate-limiting step in catecholamine synthesis?

A

Conversion of Tyrosine to DOPA via Tyrosine Hydroxylase

Medical Physiology (74 decks)

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