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Physiology and Pharmacology I > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

What are the tissue layers in the vascular system?

A

Adventitia - connective tissue

Smooth muscle

Endothelium

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2
Q

What are the tissue properties of arteries?

A

Thick elastic tissue layer

Some smooth muscle

Endothelium

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3
Q

What are the tissue properties of arterioles?

A

Less elastic tissue than arteries

More smooth muscle than arteries

Endothelium

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4
Q

What are the tissue properties of capillaries?

A

One cell thick endothelium

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5
Q

What are the tissue properties of veins?

A

Little smooth muscle

Walls slightly thicker than capillaries

Large lumen

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6
Q

How is blood transport carried out in capillaries.

A

Connect arterioles to venules.

Dilate to the diameter of 1 red blood cell.

Nutrients enter interstitial fluid.

Waste enters capillary.

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7
Q

How do different substances cross the capillary wall?

A

Lipid soluble molecules fuse with the plasma membrane

Lipid-insoluble molecules travel through endothelial pores

Large molecules endo/exocytose through the plasma membranes

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8
Q

Which part of the vascular system is impermeable to most substances?

A

Blood-brain barrier?

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9
Q

Where is the blood-brain barrier located?

A

Endothelium of cerebral capillaries and epithelium of choroid plexus.

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10
Q

How can the impermeability of the blood-brain barrier be shown experimentally?

A

Using tryptan blue dye. The brain/spinal cord will be the only part of the vascular system not affected by the dye.

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11
Q

Which substances can permeate the blood-brain barrier?

A

CO2

O2

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12
Q

What is the function of the blood-brain barrier?

A

Maintaining a constant extracellular environment around neurones.

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13
Q

How are fluids exchanged between capillaries and lymphatics?

A

Interstitial fluid drains into the lymphatic system.

Periodic swelling of lymph nodes.

Valves open when swelling too high.

Lymph drains into subclavian/jugular veins.

Lymph removes bacteria via lymphocytes.

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14
Q

What effect does oedema have on the lymphatic system and the body?

A

Blocks lymph flow by a build up of protein from capillaries in interstitial spaces.

Promotes water retention.

Causes injury, inflammation, and infection.

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15
Q

What function do valves perform in veins and lymphatic system?

A

Ensure single direction of flow.

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16
Q

What could cause reversed flow of blood?

A

Muscle contraction

Valve tissue damage

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17
Q

What is systolic blood pressure?

A

Pressure caused by force of the heart

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18
Q

What is diastolic blood pressure?

A

Basal blood pressure in the system

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19
Q

What is a normal blood pressure reading for a healthy adult?

A

120/70

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20
Q

What are the units for measuring blood pressure?

A

Millimeters of Mercury (mm Hg)

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21
Q

What happens to blood pressure with age?

A

Rises slowly to 130/80

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22
Q

Describe how blood pressure is measured and the changes in bloodflow that occur during measurement.

A

Cuff is inflated to >120mm Hg - Stops arterial blood flow.

Cuff slowly deflates. 120-80mm Hg - Blood starts to surge in korotkaft sounds.

Cuff deflated to <80mm Hg - silent bloodflow.

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23
Q

What is cardiac Output?

A

Blood flow at any level of circulation.

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24
Q

How is flow calculated?

A

Pressure/Resistance

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25
Q

How is the relationship between vessel and resistance?

A

Resistance proportional to 1/r^4 where r is the radius of the lumen.

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26
Q

How is blood velocity calculated?

A

Flow rate/cross sectional area of vessel.

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27
Q

How is hypertension defined?

A

Diastolic blood pressure exceeding 90mm Hg.

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28
Q

What are the possible effects of hypertension?

A

Heart attack

Stroke (myocardial infarction)

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29
Q

What is primary hypertension? What are the associated risk factors?

A

Hypertension with no apparent cause. Risk factors include alcohol, obesity and genetic predisposition.

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30
Q

What can secondary hypertension caused by?

A

Renovascular disease

Endocrine disease

Adrenal tumour

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31
Q

How does an adrenal tumour induce hypertension?

A

Causes excessive adrenaline secretion.

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32
Q

What are the factors regulating blood pressure?

A

Changes in cardiac output

Peripheral control of blood flow

Drugs acting on sympathetic NS or muscle contraction

Endothelium regulation

Renin angiotensin system

Changes in blood volume

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33
Q

How is blood pressure detected in the body?

A

Baroreceptors.

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34
Q

Where are baroreceptors located?

A

Aortic arch

Carotid sinus

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35
Q

What effect would an increase in pressure have on baroreceptors?

A

Increase in baroreceptor output.

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36
Q

What effect to baroreceptors have on the sympathetic nervous system?

A

Increased baroreceptor output causes decreased sympathetic activity and vice versa.

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37
Q

Describe the pathway by which baroreceptors affect sympathetic activity.

A

Input from baroreceptor leads into the brain.

Signal relayed onto sympathetic system in the vasimotor centre via an inhibitory neuron.

Sympathetic nerve contains a sympathetic ganglion. Relays the signal onto the artery.

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38
Q

How do sympathetic neurons relay the signal onto arteries?

A

Via depolarisation-stimulated NA release from varicosities. NA activates GqPCRs on the artery. Causes formation of IP3 that leads to muscle contraction.

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39
Q

What are the 3 ways via which arterial contraction can be blocked?

A

NA release

Adrenoceptor antagonists

Effects on calcium (secondary messenger pathway)

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40
Q

Give 2 examples of adrenergic neuron blockers that can be used to inhibit arterial contraction.

A

Reserpine

Guanethidine

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41
Q

How does reserpine affect arterial contraction?

A

Taken up into axon via uptake 1

Affects storage of NA

Binds to NA vesicles and stops them concentrating NA

Decreases amount of NA stored

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42
Q

What are the side effects associated with reserpine use?

A

Depression

Peripheral (non-CNS) action

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43
Q

How does guanethidine affect arterial contraction?

A

Taken up into axon via uptake 1

Competes with NA for storage in vesicles - has higher affinity at the pump than noradrenaline

Decreases amount of NA stored

Also blocks AP propagation.

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44
Q

Why is guanethidine effective as a false substrate?

A

Has higher affinity at the vesicle pump than NA.

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45
Q

What is a common side effect of adrenergic neuron blockers?

A

Postural hypertension

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46
Q

What is postural hypertension?

A

Bloods falls down upon standing up. Muscles don’t contract in time to stop this.

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47
Q

Where in the cardiovascular system are Alpha1-adrenoceptors located?

A

Artery Smooth muscle

48
Q

What causes cardiovascular shock?

A

Inadequate perfusion with blood caused by hypovolemia or cardiac failure.

49
Q

What is hypovolemia?

A

Loss of blood volume due to dehydration or blood loss.

50
Q

Give examples of pharmaceuticals that can be used to treat cardiovascular shock.

A

Alpha1-adrenoceptor agonists:

Methoxamine

Phenylephrine

51
Q

How do Alpha1-adrenoceptor agonists work to treat cardiovascular shock?

A

Increase BP through activation of smooth muscle via alpha1-adrenoceptors.

52
Q

What type of pharmaceutical can be used to treat hypertension? Give an example.

A

Alpha1-adrenoceptor antagonists e.g.: Prazosin

53
Q

How do Alpha1-adrenoceptor antagonists work to treat hypertension?

A

Blocks NA-induced vasoconstriction

54
Q

Where in the cardiovascular system are the Alpha2-adrenoceptors present?

A

Nerve terminals

55
Q

What effect do Alpha2 agonists have on neurones? Outline central and peripheral effects.

A

Inhibit NT release presynaptically

Central (vasimotor centre) - Decreases sympathetic output

Peripheral (artery) - Decreases NA release from varicosities

56
Q

Give an example of an alpha2 antagonist and it’s effect on the cardiovascular system.

A

Yohimbine.

Blocks presynaptic alpha2-adrenoceptors.

Promotes NT release from terminals

57
Q

Describe the mechanism of calcium induced artery contraction.

A

Rise in intracellular calcium.

Calcium binds to calmodulin which forms a complex.

Complex stimulates MAPK to phosphorylate myosin.

Phosphorylation causes contraction.

58
Q

By which receptor pathway does arterial contraction occur?

A

Activation of GqPCRs.

59
Q

Where are N-type calcium channels located an what is their function?

A

On neurones

Involved in depolarisation/NT release

60
Q

Where are T-type calcium channels located an what are their properties?

A

Heart and brain

Transient-opening channels

61
Q

Where are L-type calcium channels located an what are their properties?

A

On smooth muscle

Long-lasting opening

62
Q

Which molecules can be used as L-type channel blockers? Give examples.

A

Dihydropyridines (DHPs) e.g.: Nifedipine

Phenethylalkalmines e.g.: Verapamil

Benzotiazepines e.g.: Diltiazem

63
Q

Which DHP acts as an L-type channel opener rather than a blocker?

A

BayK8644

64
Q

Describe the 3 modes of L-type channel opening.

A

Mode 0 - Cannot open on depolarisation

Mode 1 - Low probability of opening on depolarisation

Mode 2 - High probability of opening on depolarisation

65
Q

What is the effect of BayK8644 on opening of L-type calcium channels compared to Nifedipine?

A

BayK8644 increases calcium currents causing the opening to change from mode 1 to mode 2. Nifedipine changes the mode of opening from 1 to 0.

66
Q

What are the common side effects of using DHPs?

A

Headache

Heart palpitations

Sweating

Flushing

Effect on other smooth muscle

67
Q

What is the site of action of Nifedipine?

A

L-type calcium channels of the smooth muscle.

68
Q

What is the site of action of Verapamil?

A

L-type calcium channels of the heart.

69
Q

What is the site of action of Diltiazem?

A

L-type calcium channels of the smooth muscle and the heart.

70
Q

What are endothelins?

A

Vasoconstrictors produced in endothelium.

71
Q

How are ET-1 endothelins produced?

A

Produced at level of transcription.

Precursor “Pre-proET” processed.

Forms big WT-1. Cleaved by endothelin converting enzyme.

Forms ET-1.

72
Q

Where are ET-1 located?

A

Endothelial cells of various tissues.

73
Q

Where are ET-2 located?

A

Kidney.

74
Q

Where are ET-3 located?

A

Brain

Lung

Adrenal gland

75
Q

What are the 2 types of endothelin receptors?

A

ETA

ETB

76
Q

What effect does activation of ETA receptors have on the body?

A

Causes vasoconstriction via GqPCR pathway

77
Q

What is the function of endothelins?

A

Paracrine (local) or autocrine vasoconstrictors

May play a role in pregnancy

78
Q

Which vasodilators may revert the effect of endothelins?

A

Prostacyclin

Endothelium derived relaxing factors (EDRF)Nitrovasodilators

79
Q

How do EDRFs work?

A

Nitric oxide biosynthesis by the synthase enzyme (NOS) in endothelium.

NO diffuses into smooth muscle.NO stimulates guanylate cyclase.

Promotes production of cGMP.

cGMP stimulates PKG which causes relaxation.

80
Q

How is NOS activity controlled?

A

NOS activity controlled by calcium/calmodulin. Rise in Ca-calmodulin activates NOS.

81
Q

What are nitrovasodilators used to treat? Give examples.

A

Heart failure.

Sodium nitroprusside.

82
Q

How does sodium nitroprusside work to treat heart failure?

A

Reduces blood pressure by breaking down into NO in the smooth muscle. NO causes muscle relaxation which lowers the blood pressure.

83
Q

What is renin?

A

An enzyme that catalyses conversion of angiotensinogen to angiotensin in the plasma.

84
Q

Where is renin synthesised stored and secreted?

A

Granular juxtaglomerular cells of the kidneys.

85
Q

What is angiotensin?

A

Vasoactive substance used in control of blood volume by the renin-angiotensin system.

86
Q

How are angiotensin I and II different?

A

Angiotensin II can be synthesised from I by cleaving 2aa off the C-terminal in angiotensin I. Cleaving catalysed by angiotensin converting enzyme.

87
Q

What inhibits conversion of angiotensin I to angiotensin II? Give an example

A

ACE inhibitors

e.g.: Captopril

88
Q

What are the two types of angiotensin II receptors?

A

AT1

AT2

89
Q

What type of receptors are AT1 and AT2?

A

GPCRs

90
Q

Where are AT1 receptors located?

A

Vascular tissue

Myocardial tissue

91
Q

Where are AT2 receptors located?

A

Adrenal medullaCNS

92
Q

What pathway does activation of AT1 lead to?

A

GqPCR pathway involving PLC-beta. Leads to contraction.

93
Q

Give an example of an AT1 receptor antagonist.

A

Losatran

94
Q

How does the renin-angiotensin system regulate blood volume?

A

Decrease in NaCl in the filtrate is sensed by macula densa cells of the distal tubule.

Stimulates renin release, via activation of beta-adrenoceptors, which is inversely proportional to the local blood pressure.

95
Q

What are Diuretics?

A

Drugs which increase rate urine flow.

96
Q

How do diuretics increase the rate of urin flow?

A

Some increase rate of excretion of sodium.Most reduce the volume of extracellular fluid by decreasing total body NaCl.

97
Q

Why does decreasing body NaCl reduce the extracellular fluid volume?

A

NaCl is the major determinant of extracellular fluid volume.

98
Q

What is the primary effect of diuretics?

A

Decrease in reabsorption of sodium and chloride.

99
Q

What is the secondary effect of diuretics?

A

Increase in water loss.

100
Q

What is the main filtering apparatus of the kidney?

A

The glomerulus of the nephron.

101
Q

What is the function of the tubular portion of the kidney?

A

Reabsorption of substances from the filtrate.

102
Q

How is the composition of filtrate different to the composition of blood plasma and why?

A

Filtrate lacks protein which can’t pass through the basement membrane of the glomerulus.

103
Q

Give an example of a diuretic that acts on the loop of Henle.

A

Frusemide.

104
Q

How does Frusemide perform its function in the kidney?

A

Causes 15-25% of sodium in the filtrate to be excreted.

Inhibits Na/-K/-Cl symporter which prevents reabsorption of NaCl in the ascending limb.

Indirect vasodilation by release of renal factor.

105
Q

What can loss of potassium cause?

A

Hypokalemia. Affects cardiac function.

106
Q

Give an example of a diuretic that acts on the distal tubule.

A

Bendrofluazide.

107
Q

How does Bendrofluazide perform its function in the kidney?

A

Inhibits the Na/Cl cotransporter.

108
Q

Why are DCT diuretics less effective than those affecting the loop of Henle?

A

90% of the filtrate is reabsorbed before it reaches DCT.

109
Q

How can DCT diuretics be used to treat hypertension?

A

Decrease BP due to decrease in blood volume.

Act indirectly on blood vessels to stimulate further BP drop.

110
Q

Give an example of a potassium sparing diuretic.

A

Amiloride.

111
Q

How does Amiloride perform its function in the kidney?

A

Block potassium excretion.

112
Q

How What are the benefits and issues with using Amiloride as a diuretic?

A

Unlike Frusemide it prevents hypokalemia however may cause cardiac disorders such as tachycardia.

113
Q

What is tachycardia and how may Amiloride cause it?

A

Abnormally high heart rate.

Caused by high potassium to sodium ratio in cardiac axons.

Causes more rapid repolarisation of neurons.

Lowers ventricular fibrillation which disrupts coordination of cardiac muscles.

114
Q

Give an example of an osmotic diuretic.

A

Mannitol.

115
Q

How does Mannitol perform it’s function in the kidney?

A

Mannitol increases the osmolarity of filtrate causing less water to be reabsorbed.

116
Q

What are the common combination treatments in diuresis?

A

Beta-antagonist + diuretic.

ACE inhibitor + diuretic.

Physiology and Pharmacology I (5 decks)

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