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biomedical pharmacology > Block A - hypertension > Flashcards

Block A - hypertension Flashcards

1
Q

role of arteries ?

A

carrying oxygenated blood Away from the heart are Arteries

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2
Q

largest artery ?

A

Aorta

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3
Q

role of veins ?

A

Vessels carrying deoxygenated blood from organs/tissues back to the heart for oxygenation are Veins.

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4
Q

pulmonary system ?

A

The pulmonary system contains a pulmonary vein returning oxygenated blood from the lungs to the heart and a pulmonary artery which sends deoxygenated blood from the heart to the lungs to be oxygenated.

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5
Q

Bronchial circulation ?

A

Bronchial circulation – complementary to pulmonary circulation, supplying lung cells with oxygen and nutrients.

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6
Q

Blood pressure in arteries vs veins ?

A

arteriole system carries blood at a much higher pressure, while the blood in the venous system is at a lower pressure

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7
Q

muscle thickness arteries vs veins ?

A

In arteries there is a much thicker muscular wall, to help withstand the increased pressure along with elasticity in the body.

In the veins, there is a much thinner muscular wall, as the thicker layer is not needed as the blood is at a lower pressure when compared to the arteriole system.

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8
Q

valves arteries vs veins ?

A

presence of valves in the venous system , which prevents any backflow of blood.

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9
Q

both arteries and veins contain an innermost layer of endothelial cells , why ?

A

endothelial cells which acts as a barrier between the blood and the vessel. However, it can secrete multiple factors that are chemical mediators which can affect the muscle layer of the vessel which is adjacent to the endothelial layer.

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10
Q

Blood pressure depends upon two factors , what are they ?

A

Blood pressure depends upon 2 factors: total peripheral resistance (TPR) and cardiac output (CO). BP = CO x TPR.

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11
Q

Cardiac output defined as and formula ?

A

Cardiac output is defined as the amount of blood ejected by the heart in a minute. CO is influenced by HR x Stroke volume

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12
Q

what is TPR ?

A

The TPR is the diameter of the arterioles which determines resistance to flow

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13
Q

low TPR ?

A

dilated this causes low resistance to flow, therefore low peripheral vascular resistance and as a consequence low blood pressure

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14
Q

increase TPR how and effect on BP ?

A

reduce the size of the lumen this will cause an increase in resistance and as a consequence the BP will increase

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15
Q

what are some factors affecting BP ?

A

cardiac output

Stroke volume

Heart rate

Peripheral resistance

Elastic vessels

Blood volume

Ventricular ejection

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16
Q

factors affecting systemic BP ?

A

Autonomic nervous system has an immediate effect to Blood pressure

Renin-angiotensin system has a slower effect to blood pressure

Local chemical mediators released from vascular endothelium to affect smooth muscle in the vessel to alter constriction or dilation.

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17
Q

effect of heart on systemic blood pressure ?

A

Sympathetic Nervous System acts mainly via noradrenaline acting on b1-adrenoceptors on heart to increase cardiac contractility and HR resulting in increased CO and BP.

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18
Q

effect of arteries and veins on systemic blood pressure ?

A

SNS produces vasoconstriction (more resistance) by stimulation of a1 adrenoceptors found in the vascular system. This increases BP and afterload on the heart. In a healthy heart CO is maintained via b1 stimulation and increased contractility for example in exercise.

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19
Q

effect of noradrenaline / adrenaline on adrenoreceptors ?

A

agonist at a and b adrenoceptors

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20
Q

isoprenaline ?

A

non selective b agonist

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21
Q

phenylephrine ?

A

a1 agonist

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22
Q

non selective beta blockers such as propranolol ?

A

non selective beta blockers

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23
Q

metoprolol ?

A

selective beta one blocker

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24
Q

phentolamine ?

A

non selective alpha blocker

25
Q

prazosin ?

A

selective alpha one blocker

26
Q

generally how are beta blockers used ?

A

for their cardio depressant effect

27
Q

generally why are alpha blockers used ?

A

for their vasodilatory effects

28
Q

why is the Renin Angiotensin system used ?

A

as a longer term control of Blood pressure

29
Q

how is the RAAS system kicked into action and the stages ?

A

by sodium ion depletion and sympathetic nerve stimulation causes the enzyme renin to be released from the kidneys. This acts on angiotensinogen which is produced constitutively form the liver and converts it into angiotensin I. Angiotensin I is converted into angiotensin II by the angiotensin converting enzyme (ACE) present in the lungs. Angiotensin II is one of the most potent vasoconstrictors produced in the body. Angiotensin II can lead to aldosterone release which results in sodium ion retention.

30
Q

what do endothelium derived factors have an effect on ?

A

modulating the vascular smooth muscle and therefore vessel diameter.

31
Q

nitric oxide ?

A

Nitric oxide is perhaps the most important EDRF, with its physiological antagonist being endothelin-1.

32
Q

what are nitrix oxide , prostacyclin and hyperpolarising factors and effects ?

A

EDRF’s ( relaxants)

33
Q

what are endothelin (ET-1) and thromboxane A2 ( TxA2) and effects ?

A

EDCF’s ( contractile )

34
Q

systolic pressure ?

A

Systolic pressure (SP): the maximum arterial pressure reached during peak ventricular ejection

35
Q

diastolic pressure ?

A

Diastolic pressure (DP): the minimum arterial pressure just before ventricular ejection begins

36
Q

pulse pressure ?

A

Pulse pressure (PP): the difference between SP and DP

37
Q

mean arterial pressure ?

A

Mean arterial pressure (MAP): the average pressure across the Cardiac cycle

38
Q

sphymomanometer ?

A

A sphygmomanometer is used to estimate systolic and diastolic pressures, pressure is released from an inflatable cuff on the upper arm while listening via a stethoscope (placed over the brachial artery) as blood flow returns to the lower arm. The cuff is inflated so that it stops blood flowing, it is occluded, then it is gradually released to allow blood flow to return.

When the blood flow returns this is monitored through the stethoscope, this is just below peak systolic pressure. As the cuff is released the sounds become more continuous and louder, then when the artery is completely open there will be no sound , at this point it is diastolic pressure.

39
Q

normal blood pressure ?

A

A normal blood pressure is 120/80 mmHg ( systolic/diastolic) mm of mercury

40
Q

pre hypertension ?

A

Pre hypertension range is about 140/90 mmHg

41
Q

hypertension stage one ?

A

Once the BP rises above 140/90 this is classified as hypertension stage one

42
Q

hypertension stage two ?

A

Once the BP rises above 160/100 this is classified as hypertension stage two

43
Q

systemic hypertension ?

A

Systemic hypertension is concerningly usually asymptomatic and often diagnosed when patient presents with another condition maybe unrelated. Therefore BP needs to be carefully monitored.

44
Q

pulmonary hypertension /

A

Pulmonary hypertension is less common than systemic Hyper tension. It is commonly found in patients with COPD where the pulmonary vasculature has been affected leading to increased vascular resistance. Patients present with shortness of breath and sometimes chest pain. The sustained increase in pulmonary vascular resistance leads to a progressive effect on the right side of the heart , which pumps blood to the lungs for oxygenation.

45
Q

primary risk factors ?

A

Primary Risk factors include:

obesity

lack of exercise

alcohol

non insulin-dependent diabetes ( type 2 )

Age

The primary risk factors can be managed to help reverse the hypertension to some extent.

46
Q

secondary risk factors ?

A

Secondary – initiated by other diseases

Aortic coarctation

Renal disease

Mineralocorticoid excess

Thyroid disease

Eclampsia

47
Q

effects of hypertension on vasculature ?

A

Progressive structural changes in vasculature such as thickening and narrowing of lumen of arteries.

48
Q

hypertension of atherscelosis

A

HT will lead to acceleration of atherosclerosis and this increases vascular resistance.

development of small aneurysms (localised dilation) in cerebral arteries to increase risk of stroke

49
Q

atherclerosis on left ventricle of heart ?

A

left ventricular ( thickest wall of heart) hypertrophy is thickening of the wall’s heart to accommodate the increased resistance which is already thick is a risk factor for ischaemic heart disease and heart failure as causes poor pumping action.

50
Q

what do HT patients have an increase of ?

A

Hypertension patients, have an increase in muscle proliferation, as well as a proliferation of cells in the adventia such as fibroblasts , inflammatory cells and macrophages. Ultimately the lumen of the vessel is smaller, and this is restrictive for blood flow which creates problems for the heart.

51
Q

name anti hypertensive drugs that act on sympathetic nervous system ?

A

beta and alpha blockers

52
Q

beta blockers such atenolol and propranolol ?

A

Decrease Cardiac Output which feeds into BP , reduce renin production which in turn reduces vasoconstrictor AngII production, can indirectly cause vasodilation of peripheral arteries as we have beta 2 receptors on the vascular , when activated promote vasodilation. Predominate effect is on the heart and reduce AngII.

53
Q

alpha blockers such as prazosin?

A

Block post-synaptic a1 adrenoceptors leading to blocking the vasoconstriction will lead to dilation of arteriolar resistance vessels and lower peripheral resistance. Also dilate venous capacitance vessels, reducing venous return and therefore CO.

54
Q

drugs acting on RAAS system ?

A

ACE inhibitors and Ang IIR antagonists ,

55
Q

ACE inhibitors such as captopril ?

A

Act by reducing AngII levels which decreases vasoconstriction and as a result the BP will decrease.(N.B. AngII is implicated in the development of Left Ventricular Hypertrophy in hypertension).

56
Q

Ang IIR blockers such as losartan ?

A

These drugs selectively block AT1 receptors which mediate the vasoconstrictive effects of AngII , by reducing this we reduce BP. They don’t reduce the circulating effects of AngII , but they block the effects the levels can have.

57
Q

vasodilators ?

A

duiretics , calcium channel blockers

58
Q

diuretics such as thiazide ?

A

Act at varying sites in the kidney to increase Na+ and water depletion leading to a hypotensive effect. Prevents water retention which is associated with high BP and hypertension in patients.

59
Q

calcium channel blockers suc as amlodipine ?

A

Block calcium entry into vascular smooth muscle cells and/or cardiac muscle cells. This promotes relaxation of the muscle and vasodilation. Calcium is important in mediating cardiac muscle cell contraction and smooth muscle cell contraction , so by decreasing the intracellular levels of calcium in these cells , this will reduce the capacity for contraction and promote vasodilation and relaxation

biomedical pharmacology (15 decks)

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