Brainscape's Knowledge GenomeTM

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


See full index

Cardiovascular System > Session 5 > Flashcards

Session 5 Flashcards

1
Q

What physiological functions does the autonomic nervous system regulate?

A
  • Heart rate
  • Blood pressure
  • Body temperature
  • Response to exercise and stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does the autonomic nervous system exert control over in the body?

A
  • Vascular smooth muscle
  • Visceral smooth muscle
  • Rate of heart contraction
  • Force of heart contraction
  • Exocrine secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two divisions of the autonomic nervous system and how are they defined?

A
  • Parasympathetic (craniosacral)

- Sympathetic (thoracolumbar)

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

What is the ‘third’ division of the autonomic nervous system and how is it controlled?

A

ENTERIC SYSTEM

  • Neurones surrounding GI tract
  • Controlled via sympathetic and parasympathetic fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How are sympathetic pre and post ganglionic fibres arranged?

A
  • Pre ganglionic neurone is short and has the cell body in the CNS.
  • Synapse at a ganglion.
  • Post ganglionic neurone is very long and originates from sympathetic trunk to the target tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are parasympathetic pre and post ganglionic fibres arranged?

A
  • Pre ganglionic neurones long.
  • Synapse at a ganglion.
  • Post ganglionic neurones are very short, often in the tissue that is being innervated.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When is sympathetic activity dominant?

A

Under stress (eg. fight or flight response)

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

When is parasympathetic activity dominant?

A

Under basal/resting conditions

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

What happens when both parasympathetic and sympathetic divisions innervate a tissue?

A

They have opposite effects and work together to maintain a balance most of the time.

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

What are some examples of ANS control and how are they controlled under parasympathetic and sympathetic innervation? *

A
  • Eye - contraction and dilation
  • Airways - contraction and relaxation
  • Heart - increased force of contraction and rate, and reduced rate ONLY
  • Sweat glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What receptors are in the parasympathetic system and what neurotransmitter do they use?

A
  • Muscarinic (M1, M2, M3)

- Acetylcholine

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

What receptors are in the sympathetic system and what neurotransmitters do they use?

A
  • Alpha-1, Alpha-2, Beta-1, Beta-2

- Noradrenaline + circulating adrenaline

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

What does it mean if the sympathetic activity to the tissues is independently regulated?

A

Activity can be increased to one system (eg. heart) without affecting the other (eg. GI)

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

What does the ANS control in the cardiovascular system?

A
  • Heart rate
  • Force of contraction
  • Peripheral resistance of blood vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does the ANS N O T control?

A
  • Does not initiate electrical activity in the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What influence is the heart under?

A

Vagus nerve (parasympathetic dominant)

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

What happens when the heart is denervated?

A

Will still beat but at a faster rate (about 100bpm)

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

What is the parasympathetic input to the heart?

A

VAGUS NERVE

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

Where do the preganglionic fibres synapse?

A

On epicardial surface/within the walls of the heart at AVN or SAN.

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

Why can the parasympathetic system not change the force of contraction?

A

There is not much innervation of the myocardium (heart muscle)

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

What receptors does the acetylcholine released by the postganglionic fibres in the PNS act on and what are the effects?

A

M2 receptors (Gi)

  • Negative chronotropy
  • Reduced AVN conduction velocity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the sympathetic input to the heart?

A

Post ganglionic fibres from the sympathetic trunk.

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

What do the postganglionic fibres innervate and what transmitter do they release?

A
  • SAN, AVN and myocardium

- Release noradrenaline

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

What receptors does noradrenaline mainly act on, and what is the effect?

A
  • Beta-1 adrenoceptors (main in heart)
    Effects:
  • Positive chronotropy
  • Negative inotropy (contraction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What other receptors are present in the heart aside from beta-1?

A

Beta-2 and beta-3.

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

Look at the diagram showing ANS input to heart!*

A

OK :)

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

How do the SAN cells initiate an action potential?

A
  • Steadily depolarise toward threshold (pacemaker potential)
  • Slow Na+ conductance is turned on (funny current, slow inward movement of Na+)
  • Opening of Ca2+ channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the action potential firing in SAN responsible for?

A

Setting rhythm of heart

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

How are action potentials in SAN initiated?*

A
  • HCN channels open, allowing Na+ in and slow depolarisation
  • Opening of fast Ca2+ channels (upstroke of AP)
  • Closing of Ca2+ channels and opening of K+ channels to allow repolarisation (efflux of K+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What effect does sympathetic activity have on the pacemaker potential?

A
  • Increases the slope and speeds up the action potential
  • Mediated by B1 receptors
  • Increased cAMP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What effect does parasympathetic activity have on the pacemaker potential?

A
  • Decreases the slope and therefore slows down the action potential
  • Beta-gamma subunit directly increases potassium conductance
  • Decreased cAMP
  • Mediated by M2 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does adrenaline increase the force of contraction?

A
  • Acts on B1 receptors, increases cAMP and activates PKA
  • PKA phosphorylates Ca2+ channels and increases Ca2+ entry
  • Increased uptake of Ca2+ in SR
  • Increased force
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What kind of innervation do most vessels receive, and what are exceptions?

A 
Sympathetic innervation 
(exception is erectile tissue - parasympathetic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What receptors do most arteries and veins have?

A

Alpha-1

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

What additional receptors to a1 do coronary and skeletal muscle vessels have?

A

B2 receptors

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

What is the vasomotor tone?

A

A basal level of activity that permits both vasodilatation and vasoconstriction.

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

How does the sympathetic output initiate vasodilation and why?

A
  • Less NAd, less sympathetic output
  • Reduces blood pressure
  • Allows more blood flow to tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does the sympathetic output initiate vasoconstriction?

A
  • Increased sympathetic output
  • Restricts blood flow to tissue
  • Increases blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Which blood vessels have B2 AND a1 adrenoceptors?

A

Vascular smooth muscle of the vessels in skeletal muscle, liver and myocardium.

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

What is the effect of noradrenaline on a1 receptors?

A
  • Causes vasoconstriction

- Controls arterial blood pressure

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

What is the effect of circulating adrenaline on B2 receptors?

A

Relaxation of vascular smooth muscle.

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

What is the affinity of adrenaline and how does it change?

A
  • Circulating adrenaline has a higher affinity for B2 receptors than for a1
  • If at higher concentrations than physiological, adrenaline will also activate a1 receptors which can cause vasoconstriction.
43
Q

How does activating B2 adrenoceptors affect vascular smooth muscle?

A

VASODILATION (Gs)

  • Affected by circulating adrenaline
  • Increased cAMP
  • Activated PKA
  • Open K+ channels and inhibited MLCK (can’t phosphorylate)
  • Relaxation of smooth muscle
44
Q

How does activating a1 receptors affect vascular smooth muscle?

A

VASOCONSTRICTION (Gq)
- Stimulates IP3 production
- Increased intracellular calcium from stores and influx of extracellular Ca2+
= Contraction
- DAG activates PKC which inhibits MLCP and promotes the active conformation

45
Q

Look at the excitation contraction coupling diagram!*

A

Ok :D

46
Q

What is the role of local metabolites and how are they important?

A
  • Ensure adequate perfusion of skeletal + coronary muscle
  • Local increases have strong vasodilator effect
  • More metabolites produced by active tissue (eg. K+, H+, more CO2)
47
Q

How are the changes in the state of the cardiovascular system communicated to the brain?

A

Afferent nerves

  • Baroreceptors (aortic arch/carotid sinus) - high pressure
  • Atrial receptors - low pressure
48
Q

What is the effect of the changes that are being communicated?*

A

Altered activity of efferent nerves.

49
Q

Where are baroreceptors located and what are they?*

A
  • Nerve endings sensitive to STRETCH (stretched by increased arterial pressure).
50
Q

How does the information from the carotid sinus travel to control centre?

A

Glossopharyngeal nerve.

51
Q

How does the information from the aortic arch travel to control centre?

A

Vagus nerve.

52
Q

Describe the baroreceptor reflex. *

A
  • Increase in MABP
  • Stretch detected by baroreceptors, which send the information to the coordinating centre in the medulla (oblongata)
  • Increased parasympathetic and reduced sympathetic activity
  • Reduced heart rate and vasodilation occur to reduce BP.
53
Q

Why is the baroreceptor reflex important?

A

Compensates for short term changes in BP

54
Q

What is the issue with the baroreceptor reflex?

A

Baroreceptors can reset to higher levels with persistent increases in BP

55
Q

What are sympathomimetics?

A

Agonist drugs that mimic the action of the sympathetic nervous system.

56
Q

What are cardiovascular uses of sympathomimetics?

A
  • Adrenaline to restore heart function in cardiac arrest by vasoconstriction
  • Dobutamine B1 agonist - given in cardiogenic shock
  • Adrenaline given for anaphylactic shock, allows more a1 to be activated to prevent blood pressure from falling and allows vasoconstiction.
  • Redirects blood to vital organs
57
Q

What are non-cardiovascular uses of sympathomimetics?

A

B2 agonist salbutamol - causes relaxation of bronchial smooth muscle

58
Q

What are adrenoceptor antagonists?

A

Drugs that reduce the actions of adrenaline

59
Q

What are alpha adrenoceptor antagonists?

A

eg. prazosin

- Inhibits noradrenaline acting on a1 receptors to cause vasodilation

60
Q

What are beta adrenoceptor antagonists?

A
  • Propranolol - nonselective B1/2, slows heart rate and reduces force of contraction
  • Atenolol - cardioselective B1 antagonist
61
Q

Why is atenolol better than propranolol?

A
  • Propranolol not selective - can also cause bronchoconstriction by acting on bronchial smooth muscle
  • Atenolol specific so reduces risk of bronchoconstriction and side effects
62
Q

What are muscarinic agonists?

A

Pilocarpine

  • Treating glaucoma
  • Activates constrictor pupillae muscle
63
Q

What are muscarinic antagonists?

A

Atropine

  • Increases heart rate and bronchial dilation
  • Dilation of pupils for eye examination
64
Q

What is hypertension?*

A

A sustained increase in blood pressure (mmHg). Normal blood pressure is 90/60 mmHg - 120/80 mmHg
(anything above 140/90 mmHg is hypertension)

65
Q

What is the difference between primary and secondary hypertension?

A
  • Primary: from an unknown cause (95% cases)

- Secondary: hyperaldosteronism, Cushing’s syndrome, renal and renovascular disease (must treat the cause)

66
Q

What are the effects of hypertension?

A

LARGE RISK FACTOR FOR PREMATURE DEATH

Can damage heart and vasculature as well as lead to heart failure, MI, strokes, renal failure and retinopathies

67
Q

What can contribute to hypertension?*

A
  • All vascular diseases

- e.g. aortic aneurysm, heart failure, MIs

68
Q

What can hypertension increase?*

A
  • Afterload higher as heart must pump under a higher pressure to pump blood across in systole
  • Can lead to LV hypertrophy and increased O2 demand, which can lead to heart failure and ischaemia respectively
  • Can cause arterial damage, which leads to atherosclerosis and weakened vessels
  • Can contribute to retinopathies and strokes
69
Q

What target organs can be damaged by cardiovascular disease?*

A
  • Brain
  • Heart
  • Eyes
  • Kidneys
  • Arteries
70
Q

What can reducing blood pressure do?

A

Reduce risks of coronary heart disease, stroke, heart failure and mortality in general

71
Q

How is blood pressure regulated in the short term?

A

Baroreceptor reflex - adjusting the sympathetic and parasympathetic inputs to the heart to alter the cardiac output, as well as adjust sympathetic input to vessels to alter TPR

72
Q

What is the baroreceptor reflex?*

A

Baroreceptors/nerve endings found in carotid sinus and aortic arch which are sensitive to stretch.

  • Will be stretched with increased pressure
  • Signal will be send to the coordinating centre in the medulla via the afferent pathways
73
Q

Why can’t baroreceptors control blood pressure long-term?

A

The threshold for baroreceptor firing resets

74
Q

How is long-term control of blood pressure mediated and what are the 4 pathways?

A

Neurohumoral responses controlling sodium balance

  • Renin-angiotensin-aldosterone system
  • Sympathetic nervous system
  • Anti-diuretic hormone
  • Atrial natriuretic peptide
75
Q

Where is renin released from?*

A

Granular cells of the JUXTAGLOMERULAR APPARATUS in response to reduced perfusion pressure detected by baroreceptors (so low circulating volume)

76
Q

What stimulates renin release?*

A
  • Reduced NaCl in distal tubule
  • Reduced perfusion pressure in kidney
  • Sympathetic stimulation of JGA
77
Q

What is the function of renin?*

A
  • Stimulates cleavage of angiotensinogen to angiotensin I

- Angiotensin converting enzyme (ACE) then converts angiotensin I to the biologically active angiotensin II

78
Q

What are the effects of angiotensin?

A
  • Stimulating aldosterone release
  • Stimulating Na+ absorption
  • Vasoconstriction
79
Q

What and where are the angiotensin receptors?*

A

AT1 and AT2 (main AT1) - GPCR

- In arterioles, kidney, SNS, adrenal cortex and hypothalamus

80
Q

What is the function of aldosterone that is released from the adrenal cortex?

A
  • Acting on collecting duct cells to stimulate Na+ reabsorption and therefore water reabsorption
  • Activates apical Na+ and K+ channels (ENaC, epithelial Na+ channel)
  • Increases Na+ extrusion via Na/K ATPase
81
Q

What is the other function of angiotensin converting enzyme?

A

Breaking down bradykinin, which is a vasodilator, into peptide fragments

82
Q

What is an example of an ACE inhibitor?

A

Captopril, Lisinopril

83
Q

Why do high levels of sympathetic stimulation reduce renal blood flow?

A
  • Arterioles vasoconstrict so reduced delivery of blood

- Decrease of glomerular filtration rate so less Na+ removed

84
Q

What are the other functions of the sympathetic nervous system in regulating BP?*

A
  • ++ apical Na/H exchanger and basolateral Na/K ATPase in PCT
  • Stimulating renin release which eventually causes increased Na+ reabsorption
85
Q

What is the main function of antidiuretic hormone?

A

Formation of concentrated urine by retaining water to control plasma osmolarity (reabsorption in distal nephron via aquaporin 2)

  • Stimulating Na+ reabsorption
  • Vasoconstriction
86
Q

What stimulates ADH release?

A
  • Increase in plasma osmolarity

- Severe hypovolaemia

87
Q

What is atrial natriuretic peptide and how is it released?

A
  • A compound synthesised and stored in atrial myocytes - Released in response to stretch by recognition from low pressure volume sensors in atria
  • Less ANP with reduced filling
88
Q

What are the actions of ANP?

A
  • Vasodilation of afferent arteriole
  • Increased blood flow form vasodilation (+ GFR)
  • Inhibition of Na+ reabsorption
  • Natriuresis (loss of sodium into urine)
89
Q

What are prostaglandins?

A

Physiologically active lipid compounds that have diverse hormone-like effects

90
Q

What are the functions of prostaglandins?

A
  • Clinically important vasodilators
  • Enhance glomerular filtration and reduce Na+ reabsorption
  • Act when AngII levels high to prevent vasoconstriction further
91
Q

What is dopamine and how is it formed?

A
  • Neurotransmitter

- Formed in the kidney from circulating L-DOPA

92
Q

Where are dopamine receptors found?

A

Renal blood vessels and cells in the proximal convoluted tubule

93
Q

How does dopamine act?

A
  • Causes vasodilation so more renal blood flow

- Reduces reabsorption of NaCl by inhibiting NHX + Na/K ATPase

94
Q

How does renovascular disease cause hypertension?

A
  • Occlusion of renal artery and therefore less perfusion pressure
  • Increased renin production
  • Renin-angiotensin-aldosterone
  • Vasoconstriction and Na+ retention
95
Q

How does renal parenchymal disease cause hypertension?

A
  • Loss of vasodilators

- Na+ and water retention = poor filtration

96
Q

What are the adrenal causes of hypertension?

A
  • Conn’s syndrome (aldosterone-secreting adenoma)
  • Cushing’s syndrome (excess cortisol)
  • Phaerochromocytoma (AG tumour), secretes Ad + NAd
97
Q

How can the targets for treating hypertension be worked out?

A 
BP = CO X TPR so
BP = SV X HR X TPR
98
Q

What are non-pharmacological approaches to treating hypertension?

A
  • Diet and exercise
  • Reduced sodium intake
  • Reeduced alcohol
99
Q

How do ACE inhibitors and AngII receptor antagonists work?

A

ACEi: Prevent AngII production so prevents vasoconstriction and NaCl + water retention
- Will also reduce bradykinin breakdown so more vasodilation

AngII receptor antagonists: prevent angiotensin II binding to receptor

100
Q

What vasodilators are used to treat hypertension?

A
  • L-type Ca2+ channel blockers (verapamil) - reduce Ca2+ entry so relax muscle
  • Alpha 1 receptor blockers (doxazosin) - relaxation of vascular smooth muscle
101
Q

What diuretics are used to treat hypertension and how do they work?

A

Thiazide diuretics that reduce volume

- Will inhibit Na/Cl co-transporter on apical membrane of distal tubule cells

102
Q

When are beta-blockers used in treating hypertension?

A

Used when there are other indications along with hypertension, such as previous MI (reduce sympathetic output)

103
Q

What are the targets of drugs?*

A

SLIDE 48

ALSO LOOK AT NICE GUIDELINES

Cardiovascular System (11 decks)

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