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PHAR > PHAR6 - Hypertension > Flashcards

PHAR6 - Hypertension Flashcards

1
Q

Define hypertension.

A

High blood pressure.

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2
Q

When referring to blood pressure, which blood vessels are being considered?

A

Arteries.

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3
Q

Define blood pressure.

A

The pressure at which the blood within arteries pushes against the arterial walls.

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4
Q

What formula is commonly used to calculate blood pressure?

A

Blood pressure equals the force exerted by the blood, divided by the area of the arterial wall.

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5
Q

How does the area of the arterial wall vary within humans?

A

Larger elastic arteries have larger arterial wall areas comparative to smaller, less elastic arterioles.

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6
Q

Which artery is used for the measurement of blood pressure in clinical settings ?

A

Brachial artery.

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7
Q

What are the two distinct general stages of the cardiac cycle?

A

Relaxation and contraction.

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8
Q

Discuss the change in arterial blood pressure during a single cardiac cycle.

A

During cardiac systole, blood pressure rises to a maximum (systolic blood pressure). During cardiac diastole, blood pressure gradually decreases until a minimum is reached (diastolic blood pressure).

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9
Q

What is the approximate length of one cardiac cycle?

A

0.8 seconds.

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10
Q

What change in blood pressure is associated with the opening of the heart valve?

A

Rapid increase in blood pressure, giving rise to the systolic blood pressure (maximum).

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11
Q

What change in blood pressure is associated with closing of the valve?

A

Gradual decrease in blood pressure until lowest blood pressure is reached - diastolic blood pressure.

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12
Q

Define systolic blood pressure.

A

The maximum force exerted by the blood against the arterial wall, following full heart contraction.

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13
Q

Discuss the pathway by which blood goes from the heart to the brachial artery.

A

Blood is ejected from the left ventricle through the aorta, as the heart contracts forcefully. The aorta branches into the brachial artery.

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14
Q

Define systole.

A

Stage of the cardiac cycle when the ventricles are contracting and ejecting blood into the pulmonary arteries or aorta.

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15
Q

Define diastolic blood pressure.

A

Minimum force exerted by the blood against the wall of the artery.

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16
Q

When does diastolic blood pressure occur ?

A

When the ventricles of the heart are fully relaxed.

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17
Q

What is diastolic blood pressure?

A

The lowest possible blood pressure.

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18
Q

What is the main factor contributing to why diastolic blood pressure (within arteries) does not reduce to zero?

A

Elastic recoil of the arteries.

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19
Q

Why does ventricular blood pressure decrease to zero?

A

Ventricles do not contain elastic vessel walls therefore blood pressure will go down to zero.

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20
Q

Describe how the elastic recoil characteristic of the artery ensures that the blood pressure does not decrease to zero.

A

When blood is pumped into the arteries, the elastic arterial walls expand. When the heart relaxes (and no more blood is being pumped into the arteries) the arteries recoil to the original size and shape.

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21
Q

Define elastic recoil.

A

The ability of the arteries to change shape and size due to the presence of elastic fibres within the arterial walls.

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22
Q

What unit is used to measure blood pressure?

A

mmHg.

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23
Q

Why is the elastic recoil characteristic of the arteries vital?

A

Ensures that blood continues to flow around the circulatory system and never reaches a minimum state with no blood flow.

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24
Q

What is the name of the machine used to measure blood pressure and what does it consist of?

A

Sphygmomanometer- inflatable arm cuff, pump and pressure gauge. Stethoscope is usually used.

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25
Q

What is the purpose of the stethoscope when measuring blood pressure ?

A

Measure/observe the regions at which blood flow is disturbed.

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26
Q

Describe the general process of measuring blood pressure.

A

Pump is used to inflate the inflatable arm cuff to a sufficient pressure. The pressure causes a disruption to regular blood flow within the brachial artery. Pressure is slowly released menacing that the artery slowly widens (due to the elastic recoil ability) allowing blood to flow through the artery once more.

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27
Q

When measuring blood pressure, what does systolic pressure concern?

A

Maximum pressure that the heart is able to exert - point at which blood starts flowing through the brachial artery once the disruption (increased pressure) is removed.

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28
Q

When measuring blood pressure, what does diastolic pressure concern?

A

Concerns the point at which blood pressure within the brachial artery is at its lowest due to the being no tubule the flow.

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29
Q

What is the name of the sounds that are heard when measuring blood pressure?

A

Korotkoff sounds.

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30
Q

Why are Korotkoff sounds heard?

A

Rhythmic noises are made within the brachial artery due to turbulent blood flow within the partially compressed brachial artery.

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31
Q

When do Korotkoff sounds stop being heard when measuring blood pressure?

A

When the brachial artery is completely relaxed and there is no more turbulent flow within the artery. As the elastic recoil ability of the arteries causes the pressure to be slowly released.

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32
Q

What measurement is taken when Korotkoff sounds are no longer heard?

A

Diastolic blood pressure

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33
Q

What are the five factors influencing blood pressure?

A

Cardiac output. Total peripheral resistance. Volume of circulating blood. Blood viscosity. Elasticity of vessel walls.

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34
Q

What is the formula to calculate cardiac output?

A

Cardiac output is equal to stroke volume multiplied by heart rate.

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35
Q

Define cardiac output.

A

Volume of blood pumped through the circulatory system (out of the heart) in one minute.

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36
Q

Define stroke volume.

A

The volume of blood pumped out of the heat per beat.

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37
Q

Define heart rate.

A

The number of contractions that the heart undergoes within one minute.

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38
Q

Discuss the link between cardiac output and blood pressure.

A

Increased cardiac output means more blood is present within systemic circulation, resulting in a higher blood pressure.

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39
Q

What is the other name used for total peripheral resistance?

A

Systemic vascular resistance.

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40
Q

Define total peripheral resistance.

A

The total resistance that a blood vessel has to the flow of blood within it. Considered the total of all peripheral blood vessels.

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41
Q

Discuss the link between total peripheral resistance and blood pressure.

A

The greater the total peripheral resistance, the greater the blood pressure.

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42
Q

Discuss the link between volume of circulation blood and blood pressure

A

The higher the volume of circulating blood, the greater the the blood pressure.

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43
Q

What is circulating blood volume?

A

Volume of blood flowing within the blood vessels.

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44
Q

Discuss what blood viscosity is.

A

Blood viscosity refers to the thickness of the blood. Also can include stickiness.

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45
Q

Discuss the link between blood viscosity and blood pressure.

A

The greater the viscosity of the blood, the greater the blood pressure.

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46
Q

What two fibres are present within vessel walls to give them elasticity ?

A

Collagen. Elastic fibres.

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47
Q

Why do different blood vessels have differing elastic abilities?

A

Contain different amounts of collagen and elastic fibres within their walls.

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48
Q

Why is elasticity a useful characteristic for blood vessels - specifically arteries ?

A

Ensures that vessels are able to expand and recoil during periods of increased force within the vessel.

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49
Q

What are the two factors that influence blood pressure, that are controlled primarily by the autonomic nervous system?

A

Cardiac output. Total peripheral resistance.

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50
Q

What are the two factors that pharmacological intervention can alter to reduce blood pressure? How should they be altered?

A

Cardiac output - can be decreased by lowering heart rate.

Total peripheral resistance - can be decreased by inducing vasodilation to increase blood vessel diameter.

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51
Q

Which factors that influence blood pressure may not undergo pharmacological intervention to reduce blood pressure? Why?

A

Circulating blood volume, blood viscosity and vessel wall elasticity. Unable to be rapidly changed therefore would have none/little effect with pharmacological intervention.

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52
Q

What are the three main factors of a person that affect blood pressure? What additional variable could be considered?

A

Age, weight, height.

Gender plays a role within some of these categories.

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53
Q

Discuss the basic link between height and blood pressure, providing explanation.

A

Generally, the greater the height, the greater the blood pressure. Greater height means larger surface area for blood to perfuse to meaning higher blood pressure is required.

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54
Q

Give a scenario which serves as evidence for the link between blood pressure and height.

A

Children have lower blood pressures than adults.
Children - 100/60 mmHg
Adults - 120/80 mmHg

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55
Q

Give one piece of evidence that contradicts the relationship: increasing height, increases blood pressure.

A

Older adults - as height increases, a lower blood pressure is observed.

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56
Q

Discuss the link between weight and blood pressure, giving an explanation.

A

The greater the weight, the higher the blood pressure. Larger weight suggests larger surface area meaning greater surface area that the blood needs to perfuse to, so a higher blood pressure is required.

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57
Q

What medical condition concerning weight behaves as a high blood pressure risk factor? Explain.

A

Obesity. Various pathophysiological processes are affected, in addition to the larger surface area for blood to perfuse to, resulting in an increased risk of high blood pressure.

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58
Q

Discuss the link between age and blood pressure, giving an explanation.

A

Increasing age is associated with increasing blood pressure. Due to loss of elasticity within arterial walls.

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59
Q

Name one potential condition that can develop with age, that increases the risk of high blood pressure.

A

Atherosclerosis. Refers to build up of fatty acids and substances on arterial walls. Constricts the lumen meaning blood pressure increases.

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60
Q

What is the standard blood pressure?

A

120/80 mmHg.

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61
Q

What are the six categories of blood pressure ?

A

Hypotensive, Normal, elevated, hypertensive stage 1, hypertensive stage 2, hypertensive crisis.

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62
Q

What blood pressure is considered as hypertensive ?

A

Above 130/80 mmHg.

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63
Q

What is the threshold for blood pressure to be considered hypertensive crisis?

A

Above 180/120mmHg

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64
Q

What is the threshold for blood pressure to be considered elevated ?

A

Above 120/80.

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65
Q

Why is hypertension referred to as the silent killer?

A

No symptoms are shown.

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66
Q

What factors affect the treatment of hypertension?

A

Condition severity. Age. Risk of CVD. Target organ damage. Underlying medical conditions.

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67
Q

If symptoms are not apparent for hypertension, how can it be monitored?

A

Monitor blood pressure regularly.

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68
Q

What are the two types of hypertension ?

A

Primary and secondary.

Can also be considered as stage I, stage II and crisis when considering levels of hypertension.

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69
Q

What is primary hypertension?

A

Hypertension that is not caused by any underlying medical condition.

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70
Q

What is secondary hypertension?

A

Hypertension caused by a known underlying medical condition.

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71
Q

Give examples of underlying medical conditions that can contribute to secondary hypertension.

A

Chronic kidney disease. Diabetes.

.

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72
Q

Which organs/systems, when adversely affected, provide higher risk of hypertension development ?

A

Kidneys, heart, arteries and endocrine system.

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73
Q

What two categories are risk factors categorised into?

A

Modifiable - lifestyle related.

Non-modifiable - hereditary and physical attributes.

74
Q

What are the three non modifiable risk factors for hypertension?

A

Race, family history and gender.

75
Q

What are seven modifiable risk factors for hypertension?

A 
Unhealthy diet (excess sodium)
Obesity
Excess alcohol consumption
Stress
Physical activity
Smoking
High cholesterol
76
Q

Discuss the link between race and risk of developing hypertension.

A

Some races are thought to be at higher risk of developing hypertension. Thought to be due to differences in genes involved in salt sensitivity, or medication effectivity.

77
Q

Discuss the link between family history and risk of developing hypertension.

A

Some families are at greater risk of developing hypertension due to presence of specific genetic variants. If previous family members have hypertension, one may also be at higher risk of it. Lifestyle choices/modifiable risk factors, are likely to be similar within families also e.g. excess salt in diet.

78
Q

Which race is at a higher risk of developing hypertension?

A

African-Americans.

79
Q

How does gender affect risk of developing hypertension?

A

Under 65 years of age, men are at higher risk of developing hypertension.
Over 65 years of age, women are at higher risk of developing hypertension.

80
Q

Discuss link between testosterone levels and risk of hypertension.

A

Within men, lower testosterone levels are thought to contribute to higher risk of hypertension.

81
Q

Why are women associated with a higher risk of hypertension, after 65 years of age?

A

Thought to be associated with hormonal changes of menopause. Systolic blood pressure becomes increased.

82
Q

Why is a diet high in salt considered a risk factor for hypertension development?

A

Kidney is unable to excrete excess salt. Salt remains in blood, and means more water is in blood also. Circulating blood volume is increased. Venous return to heart is increased. Cardiac output increases. Blood pressure increases.

83
Q

What is the link between diet and family history, for risk of developing hypertension?

A

Diet (modifiable risk factor) is likely to be similar within families (non modifiable risk factor), which can contribute to the risk of developing hypertension.

84
Q

Why is obesity considered a risk factor for high blood pressure?

A

Obesity can result in inflammation to specific organs which are involved in blood pressure regulation - means that blood pressure is at risk of increasing.

Organs include kidney, heart and vasculature.

Also, larger surface area for blood to perfuse to meaning cardiac output needs to be higher so blood pressure can increase.

85
Q

Discuss the link between excess alcohol consumption and risk of developing high blood pressure.

A

The higher the alcohol consumption, the greater the risk of developing hypertension.

86
Q

Explain why excess alcohol consumption is associated with a higher risk of hypertension.

A

Alcohol increases activity of sympathetic nervous system. Thought to stimulate renin-angiotensin-aldosterone system which acts to increase blood pressure. Also, cortisol increase due to alcohol which also contributes to high risk of hypertension.

87
Q

Discuss the link between stress and the risk of developing hypertension.

A

Increased stress causes the release of cortisol, the stress hormone. Cortisol results in the detainment of sodium. This results in increased water retention. Together, they cause an increase to circulating blood volume, via the mineralocorticoid activity. Blood pressure becomes increased as a result.

88
Q

What is the link between stress, nitric oxide and hypertension?

A

Stress release cortisol hormone. Cortisol hormones inhibits nitric oxide from causing vasodilation. This, alongside cortisols own mechanisms, results in increased hypertension risk.

89
Q

Discuss the link between physical inactivity and risk of hypertension.

A

Lack of physical activity means that the cardiovascular system is not as healthy. Resting heart rate is likely to be higher, as is cardiac output, which generally contributes to a higher risk of high blood pressure.

90
Q

What are the two stimulants commonly inhaled via smoking?

A

Nicotine and tobacco.

91
Q

What is the link between nicotine and risk of hypertension?

A

Nicotine activates sympathetic nervous system activity. Increased heart rate and vasoconstriction which leads to increased blood pressure.

92
Q

What is the link between tobacco and risk of hypertension?

A

Tobacco is associated with damage to arterial walls. Blood vessels become narrower. Blood pressure increased.

93
Q

Discuss the link between cholesterol and hypertension risk.

A

High cholesterol results in the build up of plaque and fatty acids on the arterial walls. Reduction in arterial diameter and loss of elasticity. Total peripheral resistance increases, increased blood pressure also.

94
Q

What is the most severe risk associated with high cholesterol? Explain.

A

Cholesterol causes artery to become clogged with fatty acids and plaque. If this occurs in the coronary arteries, blood supply to heart is restricted. Lack of blood to heart causes myocardial infarction/stroke.

95
Q

What are the three main classes of anti hypertensive medication ?

A

ACE inhibitors/angiotensin II receptor blockers.
Calcium channel blockers.
Thiazide like diuretics.

96
Q

What type of system is the renin-angiotensin system?

A

Endocrine system.

97
Q

What are the two factors that influence blood pressure that are targeted by the renin angiotensin system?

A

Peripheral vascular resistance and circulating loos volume.

98
Q

How does the kidney detect changes in blood pressure?

A

Baroreceptors are located in the kidney afferent arterioles. Detect differences to renal perfusion.

99
Q

How does the kidney detect changes to sodium levels?

A

Macula densa cells of the distal convoluted tubule detect changes to sodium ion concentration in the kidney filtrate.

100
Q

Why is it the detection of sodium ion conc. changes important in blood pressure regulation?

A

Increased sodium in blood means increased water in blood so increased circulating blood volume which eventually causes increased blood pressure.

101
Q

What factors cause the release of renin?

A

Low blood pressure detected by baroreceptors of afferent arterioles of the kidney.
Increased sodium concentration in kidney filtrate detected by macula densa cells of distal convoluted tubule.

102
Q

Where is renin released from?

A

Juxtaglomerular apparatus within the kidney.

103
Q

Where is renin released to?

A

Systemic circulation.

104
Q

Where is angiotensin produced?

A

Angiotensin precursor molecule is produced by the liver and enters circulation.

105
Q

Discuss the life cycle of angiotensin.

A

Angiotensin precursor protein (released by liver) is cleaved into angiotensin I by renin (released by kidney), within circulation. Angiotensin converting enzyme (ACE) from the liver converts angiotensin I into angiotensin II. Some angiotensin II is converged into angiotensin III and IV by the removal of a single amino acid by amino peptidase enzymes.

106
Q

Is angiotensin I active or inactive?

A

Angiotensin I is inactive.

107
Q

How does angiotensin I become activated?

A

Converted into angiotensin II by angiotensin concerting enzymea (ACE).

108
Q

Which aminopeptidase enzymes are involved in the conversion of angiotensin II to angiotensin III or IV?

A

Aminopeptidase A and N.

109
Q

What is the main role of angiotensin II?

A

Acts on the adrenal gland to stimulate the release of aldosterone.

110
Q

What is the main role of angiotensin III?

A

Act on the adrenal gland to stimulate release of aldosterone. (Does not have as big of an effect as angiotensin III)

111
Q

What is the main role of angiotensin IV?

A

Involved in blood clot breakdown by release of plasminogen activator inhibitor 1

112
Q

What are the receptors that mainly interact with angiotensin II?

A

Angiotensin II type 1 receptor (AT1) and angiotensin II type 2 receptor (AT2).

113
Q

What G protein is AT1 coupled to?

A

Gq protein.

114
Q

What G protein is AT2 receptor coupled to?

A

Coupled to Gq and Gi.

115
Q

How does angiotensin increase blood pressure via interaction of the AT1 receptor?

A

Activation of AT1 receptor by binding to angiotensin II.
AT1 receptor activates couple G protein - Gq protein.
Gq protein activates phospholipase C enzymes.
Phospholipase enzymes produce inositol triphosphate (IP3).
IP3 triggers calcium release.
Calcium allows muscle contraction causing vasoconstriction.

116
Q

Where are AT2 receptors expresses?

A

Specific regions in the brain, in addition to during foetal development.

117
Q

What is the effect of activation of AT1 receptors within the kidney, by angiotensin II?

A

Increased reabsorption of water and sodium ions meaning increase to circulating blood volume and resultant blood pressure increase.

118
Q

How do AT1 receptors increase sodium and water reabsorption within the kidney?

A

Alter action of the sodium-proton exchange pump.

119
Q

What is the main release following activation of AT1 receptors within the posterior pituitary gland?

A

Release of vasopressin/ADH.

120
Q

How do AT1 receptors within the posterior pituitary act to increase blood pressure?

A

Release vasopressin which activates vasopressin 2 receptor (V2R). This increases the expression of aquaporins within collecting tubules via adenyl cyclase enzyme activation. More aquaporins means more water is reabsorbed. Increased circulating blood volume and blood pressure.
Can also cause vasoconstriction, which increases peripheral resistance which increases blood pressure.

121
Q

Which enzyme is activated to increase the expression of aquaporins within collecting ducts due to vasopressin released by AT1?

A

Adenyl cyclase

122
Q

What are the four locations of AT1 receptors?

A

Vascular smooth muscle. Posterior pituitary gland. Adrenal cortex. Kidney.

123
Q

What are the affects of AT1 receptors within the adrenal cortex becomes activated by angiotensin II?

A

Release of aldosterone. Aldosterone activates cytosolic receptors in epithelial cells of kidney collecting ducts. Increased sodium reabsorption due to upregulation of transcription of proteins within sodium potassium ATPase pump or sodium-proton exchange. Water also increase reabsorption. Increased circulating blood volume. Increased blood pressure.

124
Q

What is aldosterone?

A

Mineralocorticosteroid hormone released by adrenal cortex upon activation of AT1 receptors by angiotensin II.

125
Q

What are the two drug types that can target the renin-angiotensin system?

A

ACE inhibitors and angiotensin II type receptor blockers.

126
Q

Which individuals are not administered ARBs and ACE inhibitors?

A

Over 55 years of age or of black-African or African-Caribbean origin.

127
Q

Why are ACE inhibitors and ARBs not used within some individuals, for hypertension treatment?

A

Due to the medication not having the desired effect plus having unwanted, and potentially lethal, side effects.

128
Q

Discuss one potential side effect of the use of ACE inhibitors or ARBs within those of African origin.

A

Angioedema (swelling of lower skin and tissue layers) abounds lips and eyes.

129
Q

What is the common side effect of the use of ACE inhibitors or ARBs within older individuals?

A

Allergic reactions are common .

130
Q

When are ACE inhibitors commonly administered?

A

In hypertensive individuals with increased renin release.

131
Q

Which type of individual has minimal effects when administered ACE inhibitors?

A

Relatively healthy individuals with normal salt levels.

132
Q

Give examples of ACE inhibitors.

A

Enalapril. Lisinopril. Perindopril. Ramipril.

133
Q

What is the main job of ACE inhibitors?

A

ACE inhibitors prevent the function of ACE meaning that angiotensin I is not converted into angiotensin II.

134
Q

What is the link between ACE inhibitors and bradykinin?

A

ACE inhibitors prevent ACE from breaking down bradykinin. Bradykinin is an inflammatory peptide which accumulate and can cause inflammation in the respiratory tract. Additionally, prostaglandin is released which is another inflammatory mediator.

135
Q

What is the side effect associated with ACE inhibitors due to bradykinin accumulation?

A

Inflammation in respiratory tract which results in irritating dry cough. Not observed in all patients so is debated.

136
Q

Provide common side effects associated with the use of ACE inhibitors.

A

Kidney complications, hyperkalaemia and hypotension.

137
Q

Why are ARBs preferential to ACE inhibitors?

A

Do not cause unwanted respiratory complications.

138
Q

Give examples of ARBs.

A

Candesartan. Losartan. Telmisartan. Valsartan.

139
Q

What is the effect of ARBs, in order to decrease blood pressure?

A

Reduction in the reabsorption of sodium and water - lower circulation blood volume - lower blood pressure.

Inhibition of vasoconstriction - lower blood pressure.

140
Q

What is the common side effect associated with ARBs?

A

Hyperkaelaemia - due to increased activity of sodium potassium ATPase pump within kidney collecting ducts.

141
Q

Give examples of calcium channel blockers.

A

Amlodipine. Felodipine. Nifedipine.

142
Q

How many types of calcium channel blockers are there? What are the different types?

A

Five types.

L, P, N, R, T

143
Q

How do calcium channels become opened?

A

Voltage gated therefore require membrane depolarisation.

144
Q

What is the type of calcium channel targeted by calcium channel blockers?

A

L type

145
Q

Where are L type calcium channels located?

A

Heart, vascular smooth muscle, skeletal muscle

146
Q

How does contraction occur in cardiac muscle?

A

Calcium channel opens. Influx of calcium. Release of calcium from intracellular store is initiated. This calcium results in contraction.

147
Q

How does contraction occur in vascular smooth muscle?

A

Calcium channel opens. Calcium influx. Muscle contraction.

148
Q

How do calcium channel blockers reduce blood pressure, when acting on vascular smooth muscle ?

A

Prevents contraction of muscle resulting in vasodilation. Total peripheral resistance decreases. Blood pressure decreases.

149
Q

Define ventricular afterload.

A

Force against which the heart must push to eject blood out of the ventricles and into the arteries.

150
Q

What is the effect on ventricular afterload by calcium channel blockers, and subsequent effects ?

A

Vasodilation causes ventricular afterload to decrease. Myocardial oxygen demand is also decreased. Further decrease in blood pressure (in addition to the decrease caused by the vasodilation).

151
Q

Name one calcium channel blocker that is targeted to vascular smooth muscle calcium channels.

A

Amlodipine.

152
Q

How is blood pressure decreased when calcium channel blockers act on calcium channels within cardiac myocytes?

A

Blocking of cardiac calcium channels means no release of intracellular calcium. Prevents contraction of cardio myocytes so less forceful contraction so decreased stroke volume which decreases blood pressure.

Also - SA and AV node activity reduced (fewer electrical impulses) so fewer contractions, lower heart rate, further decrease to cardiac output, decreased blood pressure.

153
Q

Give two specific calcium channel blockers that target cardiac myocyte calcium channels.

A

Verapamil and diltiazem.

154
Q

How can calcium channel blockers be used in the treatment of angina pectoris?

A

Calcium channel blockers can decrease heart rate which decreases myocardial oxygen demand which can relieve associated chest pains.

155
Q

What are the two overall effects of calcium channel blockers on the heart?

A

Decreased contractility and heart rate.

156
Q

What are the three overall effects of calcium channel blockers on blood vessels?

A

Increased vasodilation. Decreased ventricular afterload. Decreased myocardial oxygen demand.

157
Q

What do diuretics do generally?

A

Increase urine production.

158
Q

What is the overview as to why increased urine results in decreased blood pressure?

A

Increased urine means that excess water and sodium are removed from the body and do not remain in the blood. Circulating blood volume is lowered. Blood pressure is decreased.

159
Q

Diuretics are used to treat hypertension. What other conditions can they be used to treat?

A

Heart or renal failure.

160
Q

Give an overview as to how the kidney produces urine.

A

Blood enters kidney through afferent arterioles. Moves to glomerulus. Filtered into the bowmans capsule to form the glomerular filtrate. The filtrate moves along the PCT, loop of Henle and DCT, with ions and water being reabsorbed into the bloodstream. Anything not reabsorption forms the urine which leaves the kidney via the collecting duct, ureter and urethra.

161
Q

What are the inner and outer layers of the kidney called?

A

Cortex - outer layer.

Medulla - inner layer.

162
Q

What is the functional unit of the kidney?

A

Nephron

163
Q

What is the role of the kidney in drug metabolism?

A

Plays large role in the elimination of drugs and drug metabolites.

164
Q

How does urine produced in the kidney, leave the body?

A

From the collecting duct, urine travels to the renal pelvis where it connects to the ureter. Urine flows along the ureter to the urethra, where urine is eliminated from.

165
Q

What are transporter systems and what is their main role?

A

Protein systems that transport ions across cell membranes. Vital for maintaining ion balance between capillary networks and renal tubules. Governs urine production.

166
Q

How many transporter systems are present within a nephron and where are they located specifically?

A

4 systems present.
Proximal tubule.
Loop of Henle - thick ascending limb.
Distal tubule - contains 2.

167
Q

Which transporter system controls the majority of the sodium reabsorption?

A

Proximal tubule sodium and organic solutes/phosphates transporter systems. Moves 70% of sodium.

168
Q

Which transporter system controls the least proportion of sodium reabsorption?

A

Distal tubule sodium and potassium transporter system. Only 1-2% max.

169
Q

How do diuretics work to increase urine production?

A

Target transport systems to reduce the reabsorption of sodium. More sodium remains in the glomerular filtrate, as does water, so more urine produced.

170
Q

What are the two main categories of diuretics?

A

Thiazide diuretics or thiazide like diuretics.

171
Q

Which transporter system is targeted by diuretics and why is it not the other ones?

A

Sodium chloride co transporter system within the distal convoluted tubule which controls 5% of sodium reabsorption.

Other transporter systems either transporter too much or too little sodium.

Too much - excess urine production.
Too little - not a significant enough decrease in blood pressure.

172
Q

Give examples of thiazide diuretics.

A

Hydrochlorothiazide.

Bendroflumethiazide.

173
Q

Give examples of thiazide like diuretics.

A

Chlorothalidone, indapamide and metolazone

174
Q

What are the side effects associated with excess urine production?

A

Hypovolemia - low extracellular fluid.
Hypotension - low blood pressure.
Hypokalaemia- low plasma potassium levels.
Metabolic alkalosis - ph of tissues are alkaline

175
Q

When are thiazide like diuretics prescribed in the treatment of hypertension?

A

Following the use of ACE inhibitors or ARBs. It is used as a secondary treatment if the initial treatment fails.

176
Q

Explain how thiazide like diuretics work, to decrease blood pressure.

A

Diuretics target the sodium chloride co transporter pump. Binds to the chloride preventing chloride from binding. If chloride is unable to bind, then sodium is unable to be reabsorbed as the chloride must ebe reabsorbed alongside it. Reduced sodium reabsorption means reduced water reabsorption. More water and sodium removed via urine. Reduced sodium and water in blood so lower circulating blood volume. Lower blood pressure.

Also, lower circulating blood volume means lower venous return which reduced heart contractility, cardiac output and lowers blood pressure further.

177
Q

What is the main problem associated with the use of diuretics for hypertension treatment ?

A

Low blood pressure detected by baroreceptors in afferent arterioles. Release of renin from juxtaglomerular apparatus released. This acts to increase blood pressure. This may result in drug tolerance.

178
Q

What other general effect are diuretics thought to be associated with ?

A

Vasodilation.

179
Q

What does drug adherence refer to?

A

Refers to whether the patient is taking the drug that has been prescribed to them.

180
Q

Give one reason as to why drug adherence may be low within a patient.

A

Side effects.

PHAR (9 decks)

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