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3: MED1 Y3 - Cardiovascular [2] > [10] Hypertension > Flashcards

[10] Hypertension Flashcards

1
Q

What is the problem with defining a value for hypertension?

A

Because blood pressure has a skewed distribution within the population, it is difficult to definitively define a value for hypertension

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2
Q

How is the diagnostic value for hypertension determined>

A

It is the value where there is a significant risk, and obvious benefit of treatment

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3
Q

What value is the diagnostic threshold for hypertension?

A

135/85mmHg

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4
Q

What should a diagnosis of hypertension be made based on?

A

Not on a single reading, but rather an assessment of a period of time

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5
Q

What is the period of time of assessment before diagnosis of hypertension determined by?

A

The BP, and the presence of other factors or end organ damage

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6
Q

What is ambulatory blood pressure monitoring (ABPM)?

A

When your blood pressure is measured as you move around, living normal day-to-day life

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7
Q

What time period is ABPM normally carried out over?

A

24 hours

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8
Q

How is ABPM carried out?

A

Using a small digital blood pressure machine that is attached to a belt around the body, and connected to a cuff around the upper arm

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9
Q

Why is ABPM useful?

A

It can determine how blood pressure changes throughout the day, to determine the efficacy of medicine, and to see if blood pressure stays high at night

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10
Q

What is blood pressure a measure of?

A

How well the cardiovascular system is functioning

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11
Q

Why is it important blood pressure is controled to remain at a normal level?

A

Because blood pressure needs to be high enough to give organs enough blood and nutrients, but not so high that it damages vessels

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12
Q

What is short-term regulation of the blood pressure via?

A

The autonomic nervous system

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13
Q

How are short-term changes in blood pressure detected?

A

By baroreceptors located in the arch of the aorta and the carotid sinus

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14
Q

How does the autonomic nervous system know when arterial BP is increased?

A

Increased arterial BP stretches the walls of the blood vessel, triggering the baroreceptors. The baroreceptors then feedback to the autonomic nevous system

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15
Q

How does the autonomic nervous system respond when baroreceptors detect an increased arterial BP?

A

It reduces the heart rate and cardiac contractility via the efferent parasympathetic fibres (vagus nerve), thus reducing blood pressure

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16
Q

What happens when decreased arterial blood pressure is detected by baroreceptors?

A

A sympathetic response is triggered, which stimulates an increase in HR and cardiac contractility, leading to an increased blood pressure

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17
Q

Can baroreceptors regulate blood pressure long term?

A

No

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18
Q

Why can baroreceptors not regulate blood pressure long-term?

A

Because the mechanism triggering baroreceptors resets itself once a more adequate blood pressure is restored

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19
Q

What is involved in the long-term regulation of blood pressure?

A
  • Renin-angiotensin-aldosterone system
  • Anti-diuretic hormone
  • Natiuretic peptides
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20
Q

What is renin?

A

A peptide hormone

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21
Q

Where is renin released from?

A

The juxtaglomerular apparatus of the kidney

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22
Q

What is renin released in response to?

A

Sympathetic stimulation, reduced sodium-chloride delivery to the DCT, or decreased blood flow to the kidney

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23
Q

What is the role of renin?

A

It facilitates the conversion of angiontensinogen to angiotensin I

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24
Q

What happens to angiotensin I?

A

It is converted to angiontensin II using ACE

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25
Q

What is angiotensin II?

A

A potent vasoconstrictor

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26
Q

What does angiotensin II do?

A
  • Acts directly on the kidney to increase sodium reabsorption in the proximal convoluted tubule
  • Promotes the release of aldosterone
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27
Q

How is sodium reabsorbed in the proximal convulted tubule?

A

Via the sodium-hydrogen exchanger

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28
Q

In addition to the conversion of angiotensin I to II, what is the role of ACE?

A

It breaks down bradykinin, which is a potent vasodilator

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29
Q

What is the result of the breakdown of bradykinin by ACE?

A

It potentiates an overall constricting effect

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30
Q

What does aldosterone do?

A
  • Promotes salt and water retention by acting on the distal convoluted tubule to increase expression of epithelial sodium channels.
  • Increases activity of basolateral sodium-potassium ATP-ase, thus increasing the electrochemical gradient for the movement of sodium ions
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31
Q

What is the result of aldosterones effect on sodium?

A

More sodium collects in the kidney tissue, then water follows by osmosis, resulting in decreased water excretion and therefore increased blood volume, thus increased blood pressure

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32
Q

What are prostaglandins?

A

Local vasodilators

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33
Q

What is the role of prostaglandins in the kidney?

A

They increase GFR and reduce sodium reabsorption.

They also act to prevent excessive vasoconstriction triggered by SNS and RAAS systems.

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34
Q

Where is ADH released from?

A

The OVLT of the hypothalamus

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35
Q

What is ADH released in response to?

A
  • Thirst
  • Increased plasma osmolality
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36
Q

What does ADH do?

A
  • Acts to increase the permeability of the collecting duct to water by inserting aquaporin channels (AQP2) into the apical membrane
  • Stimulates sodium reabsorption from the thick ascending limb of Henle
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37
Q

What is the result of the increased sodium reabsorption caused by ADH?

A

It increases water reabsorption, thus increasing plasma volume and decreasing osmolarity

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38
Q

Do naturiretic peptides regulate blood pressure in the short- or long-term?

A

Long term

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39
Q

Give two examples of natiuretic peptides?

A
  • ANP
  • Prostaglandins
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40
Q

Where is ANP synthesised and stored?

A

In cardiac myocytes

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41
Q

When is ANP released?

A

When the atria are stretched (indicating high blood pressure)

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42
Q

What effect does hypertension have on vessel walls?

A

It damages them, making them weaker

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43
Q

How does hypertension damage vessel walls?

A

The higher blood pressure causes increased arterial thickening through smooth muscle hypertrophy and accumulation of vascular matrix, leading to a loss of arterial compliance.

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44
Q

What does hypertension-mediated damage to vessel walls lead to?

A

A number of pathologies, including atherosclerosis, thromboembolism (progressing to MI or stroke), and aneurysms

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45
Q

How does hypertension damage the heart itself?

A

By increasing the afterload of the heart, meaning the heart is pumping against greater resistance, leading to left ventricular hypertrophy.

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46
Q

What can hypertension-mediated damage to the heart cause?

A
  • It increases the risk of heart failure in the future
  • It increases the hearts oxygen demands, predisposing to myocardial ischaemia and ultimately angina
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47
Q

What is the optimal blood pressure?

A

<120/80mmHg

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48
Q

What is considered to be normal blood pressure?

A

<130/85mmHg

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49
Q

What is considered to be grade 1 (mild) hypertension?

A

140-159 / 90-99mmHg

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50
Q

What is considered to be grade 2 (moderate) hypertension?

A

160-179 / 100-109mmHg

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51
Q

What is considered to be grade 3 (severe) hypertension?

A

>180 / >110mmHg

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52
Q

What is considered to be grade 1 isolated systolic hypertension?

A

140-159 / <90mmHg

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53
Q

What is considered to be grade 2 isolated systolic hypertension?

A

>160 / <90mmHg

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54
Q

What are the different types of hypertension?

A
  • Primary, or essential, hypertension
  • Secondary hypertension
  • White-coat hypertension
  • Masked hypertension
  • ‘Malignant’, or accelerated phase hypertension
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55
Q

What is white-coat hypertension?

A

An elevated clinic pressure, but normal ambulatory blood pressure monitoring

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56
Q

Do NICE recommend treatment for white-coat hypertension?

A

No

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57
Q

What is the clinical significance of white-coat hypertension?

A

More likely to develop hypertension in the future, and may have an increased risk of CVD

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58
Q

What is masked hypertension?

A

When BP is normal in clinic, but high on ABPM

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59
Q

What is primary hypertension?

A

Hypertension when there is no identifable cause

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60
Q

What % of hypertension cases are primary hypertension?

A

95%

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61
Q

What are the causes of secondary hypertension?

A
  • Renal disease
  • Endocrine disease
  • Coarction
  • Pregnancy
  • Liquorice
  • Drugs
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62
Q

What drugs can cause hypertension?

A
  • Steroids
  • MAOIs
  • Oral contraceptive pill
  • Cocaine
  • Amphetamines
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63
Q

What is the most common cause of secondary hypertension?

A

Renal disease

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64
Q

What are the most common renal causes of hypertension?

A
  • Intrinsic renal disease
  • Renovascular disease
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65
Q

Give 5 intrinsic renal diseases that can cause hypertension

A
  • Glomerulonephritis
  • Polyarteritis nodosa
  • Systemic sclerosis
  • Chronic pyelonephritis
  • Polycystic kidneys
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66
Q

What % of renal induced hypertension cases are due to intrinsic renal disease?

A

75%

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67
Q

What renovascular disease can cause hypertension?

A

Most frequently atheromatous renovascular disease, or rarely fibromuscular dysplasia

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68
Q

What % of renal disease induced hypertensin is due to renovascular disease?

A

25%

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69
Q

What endocrine diseases can cause hypertension?

A
  • Cushing’s syndrome
  • Conn’s syndrome
  • Phaeochromocyoma
  • Acromegaly
  • Hyperparathyroidism
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70
Q

What are the modifiable risk factors for hypertension?

A
  • Excess weight
  • Excess dietary salt intake
  • Lack of physical activity
  • Excessive alcohol intake
  • Stress
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71
Q

What are the non-modifiable risk factors for hypertension?

A
  • Older age
  • Family history
  • Ethnicity
  • Male gender before 65, female gender after 65
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72
Q

What are the symptoms of hypertension?

A

Usually asymptomatic, however can look for symptoms of an underlying cause

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73
Q

Give 4 examples of symptoms of an underlying cause you could look for in hypertension

A
  • Renal bruits
  • Radiofemoral delay
  • Palpable kidneys
  • Signs of Cushing’s syndrome
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74
Q

How do you ensure you have the correct size cuff when measuring BP with a sphygmomanometer?

A

Check the cuff width is 40% of the arm circumference

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75
Q

What is the correct placement of a BP cuff?

A

The bladder of the cuff should be central over the brachial artery, and the cuff should be applied snuggly

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76
Q

What position should the arm be in when measuring BP with a sphygmomanometer?

A

The arm should be supported in a horizontal position at a mid-sternal level

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77
Q

How do you obtain an estimate of the systolic blood pressure when measuring BP with a sphygmomanometer?

A

You inflate the cuff whilst palpating the radial artery until the pulse disappears

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78
Q

Once you have obtained an estimate of the systolic blood pressure, how do you take an accurate reading when measuring BP with a sphygmomanometer?

A

You inflate the cuff until 30mmHg over the estimated systolic pressure, then place a stethoscope over the brachial artery, and deflate at 2mmHg/sec

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79
Q

What indicates the systolic pressure when measuring BP with a sphygmomanometer?

A

The appearance of sustained reptitive tapping sounds

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80
Q

What indicates the diastolic pressure when measuring BP with a sphygmomanometer?

A

The disappearance of sounds

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81
Q

How is hypertension investigated?

A
  • ABPM or home monitoring
  • Fasting glucose and cholesterol
  • ECG or echo
  • Urine analysis for protein or blood
  • U&Es and calcium levels
  • Renal artery ultrasound or arteriography
  • MRI of aorta
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82
Q

What is the purpose of ABPM or home monitoring in the investigation of hypertension?

A

To confirm the diagnosis

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83
Q

What is the purpose of fasting glucose and cholesterol in the investigation of hypertension?

A

To help quantify overall risk

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84
Q

What is the purpose of ECG, echo, and urine analysis in the investigation of hypertension?

A

To assess for end-organ damage

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85
Q

What is the purpose of U&Es and calcium levels in the investigation of hypertension?

A

To exclude secondary causes

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86
Q

What is the purpose of renal artery ultrasound or arteriography in the investigation of hypertension?

A

To look for renal artery stenosis

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87
Q

What is the purpose of an MRI of the aorta in the investigation of hypertension?

A

To check for coarction

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88
Q

What is the treatment goal for hypertension?

A

<140/90mmHg

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89
Q

What is the treatment goal for hypertension in diabetes?

A

<130/90

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90
Q

What is the treatment goal for hypertension if over the age of 80?

A

<150/90

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91
Q

Why is it important to slowly reduce blood pressure in hypertension?

A

As rapid reduction can be fatal, especially in the context of an acute stroke

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92
Q

What are the approaches in the management of hypertension?

A
  • Look for and treat underlying causes
  • Lifestyle changes
  • Drugs
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93
Q

When are lifestyle changes alone sufficient in the management of hypertension?

A

If the blood pressure is consistently above 140/90mmHg, but the risk of other problems is low

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94
Q

When should medication be given in addition to lifestyle changes in the management of hypertension?

A
  • When the blood pressure is consistently above 140/90mmHg, and the risk of other problems is high
  • If the blood pressure is consistently above 160/100mmHg
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95
Q

What lifestyle changes can be made in the management of hypertension?

A
  • Reduction in salt intake to under 6g/day
  • Eating a low-fat, balanced diet
  • Being active
  • Cutting down on alcohol
  • Loosing weight
  • Drinking less caffeine
  • Stopping smoking
  • Getting at least 6 hours of sleep/night
96
Q

What is the first choice drug in the mangement of hypertension in patients who are 55 years or older, or in black patients of any age?

A

Calcium channel antagonists, or thiazides

97
Q

What is the first choice drug in the management of hypertension in patients who are aged under 55 years?

A

ACE inhibitors

98
Q

What is given if a person is intolerant to ACE inhibitors?

A

Angiotension-receptor blockers

99
Q

Why are beta-blockers not first line in hypertension?

A

Due to their reduced effectiveness in reducing major cardiovascular events, particularly stroke, and their increased risk of new onset diabetes

100
Q

Who can beta-blockers be considered for in the management of hypertension?

A

Younger people, particularly if they are intolerant or contraindcated to ACE inhibitors or ARBs, or are a woman of childbearing age

101
Q

Which drugs can be used in conjunction with one another in hypertension?

A

ACE inhibitors, Ca channel antagonists, and diuretics (thiazide recommended)

102
Q

What should be done if hypertension is still uncontrolled on adequate doses of 3 drugs?

A

Consider adding spironolactone, or a higher dose thiazide. Alternatively, add a ß-blocker or selective alpha blocker.

In this situation, check drug compliance

103
Q

How can drug compliance be checked in hypertension?

A

Using urinary drug screen or observed prescription

104
Q

Do calcium channel blockers have good oral absorption?

A

Yes

105
Q

What % of calcium channel blockers are protein bound?

A

>90%

106
Q

What organ metabolises calcium channel blockers?

A

Liver

107
Q

What is the half-life of calcium channel blockers after oral administration?

A

Most have short half-lives (3-8 hours)

108
Q

Is once daily dosing possible with calcium channel blockers?

A

Yes, sustained release preparations are available which allow this

109
Q

What is the exception to calcium channel blockers having short half-lives?

A

Amlodipine, which has a very long half-life and does not require a sustained release preparation

110
Q

What can the calcium channel blockers be divided into?

A

3 chemical classes, each with different pharmacokinetic properties and clinical indications

111
Q

What are the different classes of calcium channel antagonists?

A
  • Phenylalkyamines
  • Benzothiazepines
  • Dihydropyridines
112
Q

What is the only member of the phenylalkyamine class?

A

Verapamil

113
Q

How does verapamil compare to other calcium channel blockers in terms of selectivity?

A

It is the least selective of any calcium channel blocker, and has significant effects on both cardiac and vascular smooth muscle cells

114
Q

What is the result of verapamils action on cardiac and vascular smooth muscle cells?

A

It causes peripheral vasodilation and a reduction in cardiac preload and myocardial contractility

115
Q

What are the adverse effects of verapamil?

A
  • Constipation
  • Risk of bradycardia
    *
116
Q

Who should verapamil be avoided in?

A

Patients with congestive heart failure or AV block

117
Q

Why should verapamil be avoided in patients with congestive heart failure or AV block?

A

Due to it’s negative inotopic and dromotopic (velocity of conduction) effect

118
Q

What are the therapeutic uses of verapamil?

A
  • Angina
  • Supraventricular tachyarrhythmias
  • Prevention of migraine and cluster headaches
119
Q

What is the only member of the benzothiazepine class?

A

Diltiazem

120
Q

What kind of smooth muscle does diltiazem act on?

A

Cardiac and vascular

121
Q

How does diltiazem compare to verapamil?

A

It has a less pronounced negative inotopic effect on the heart compared to verapamil

It has a favourable side effect profile

122
Q

What are the adverse effects of benzothiazepines?

A

Risk of bradycardia

123
Q

Is diltiazem safe in heart failure?

A

No, it can worsen heart failure

124
Q

Give two examples of calcium channel blockers in the dihydropyridine class

A
  • Nifedipine
  • Amlodipine
125
Q

How do dihydropyridines differ from the other classes of calcium channel blockers?

A

In pharmacokinetics, approved uses, and drug interactions

126
Q

Why are dihydropyridines particularly good in treating hypertension?

A

Because they all have a much greater affinity for vascular calcium channels than for calcium channels in the heart

127
Q

What is the advantage of dihydropyridines, in terms of drug interactions?

A

They show little interaction with other cardiovascular drugs such as digoxin and warfarin, which are often used alonside calcium channel blockers

128
Q

What are the adverse effects of dihydropyridines?

A
  • Sympathetic nervous system activation, causing tachycardia and palpitations.
  • Flushing
  • Sweating
  • Thobbing headache
  • Oedema
  • Gingival hyperplasia
129
Q

Give an example of a loop diuretic

A

Furosemide

130
Q

Where does furosemide have its major action?

A

In the ascending limb of the loop of Henle

131
Q

How do loop diuretics compare to all other types of diuretic?

A

They have the highest efficacy in mobilising sodium and chloride from the body, and produce copious amounts of urine

132
Q

What is the mechanism of action of loop diuretics?

A

it it inhibits the co-transport of Na/K/Cl in the luminal membrane of the ascending limb of Henle, and so reabsorption of these ions is decreased

133
Q

Why are loop diuretics the most efficaious of the diuretic drugs?

A

Because the ascending limb accounts for 25-30% of filtered NaCl, and downstream sites are not able to compensate for this increased Na load

134
Q

What are the adverse effects of loop diuretics?

A
  • Ototoxicity
  • Hyperuricaemia
  • Acute hypovolaemia
  • Potassium depletion
135
Q

When in particular can hearing be adversely affected by loop diuretics?

A

When used in conjunction wtih aminoglycoside antibiotics

136
Q

Is hearing damage caused by loop diuretics pernament?

A

It can be with continued treatment

137
Q

How does furosemide cause hyperuricaemia?

A

It competes with uric acid for the renal and biliary secretory systems, thus blocking its secretion and causing or excerbating gouty attacks

138
Q

What might acute hypovolaemia caused by loop diuretics lead to?

A

Hypotension, shock, and cardiac arrhythmias

Hypercalcaemia may also occur under these conditions

139
Q

How can loop diuretics can potassium depletion?

A

The heavy load of sodium in the collecting tubule results in an increased exchange of tubular sodium for potassium, with the possibility of inducing hypokalaemia

140
Q

How can potassium depletion caused by loop diuretics be averted?

A
  • Using potassium-sparing diuretic
  • Dietary potassium supplementation
141
Q

How are loop diuretics administered?

A

Orally or parenterally

142
Q

What is the duration of action of loop diuretics?

A

2-4 hours

143
Q

How are loop diuretics removed from the body?

A

They are excreted into urine

144
Q

What kind of diuretic is bumetanide?

A

Loop diuretic

145
Q

How does bumetanide compare to furosemide?

A

It is much more potent than furosemide

146
Q

In what respects is bumetanide the same as furosemide?

A

The mechanism of action, pharmacokinetics, and adverse effects are the same as for furosemide, except it doesn’t cause hyperuricaemia

147
Q

What kind of diuretic is bendroflumethiazide?

A

A thiazide

148
Q

What is the clinical use of bendroflumethiazide?

A

It can be added to a loop diuretic in heart failure if addition diuresis is required

149
Q

Where does bendroflumethiazide act?

A

Mainly in the cortical region of the ascending loop of Henle and distal convoluted tubule. They also have a lesser effect in the proximal tubule

150
Q

What is the mechanism of action of bendroflumethiazide?

A

It decreases the reabsorption of sodium by the inhibition of the Na/K cotransporter on the luminal membrane of the tubules. As a result, there is an increase in concentration of Na and Cl in the tubular fluid, and water follows causing increased fluid loss

151
Q

What are the adverse effects of bendroflumethiazide?

A
  • Potassium depletion
  • Hyponatraemia
  • Hyperuricaemia
  • Volume depletion
  • Hypercalcaemia
  • Hyperglycaemia
  • Hyperlipidaemia
152
Q

What is the most frequent adverse effects with thiazide diuretics?

A

Hypokalaemia

153
Q

Why does potassium depletion occur with thiazide diuretics?

A

Because thiazides increase sodium arriving at the distal tubule, which is exchange for ptoassium, resulting in continual loss of potassium from the body

Furthermore, thiazides decrease the intravascular volume, resulting in activation of the RAAS system, increasing aldosterone and therefore increasing urinary potassium losses

154
Q

What can potassium depletion predispose to in patients also taking digoxin?

A

Ventricular arrhythmias

155
Q

How can potassium depletion caused by thiazide diuretics be managed?

A

Often, it can be supplemented by dietary measures, however sometimes clinical supplementation is necessary

Low sodium diets blunt the potassium depletion caused by thiazide diuretics

156
Q

What factors contribute to hyponatraemia caused by thiazide diuretics?

A
  • Loss of sodium
  • Elevation of ADH as a result of hypovolaemia
  • Diminished diluting capacity of the kidney
  • Increased thirst
157
Q

What can prevent hyponatraemia with thiazide use?

A
  • Limiting water intake
  • Lowering diuretic dose
158
Q

How do thiazides cause hyperuricaemia?

A

They increase serum uric acid by reducing its secretion

159
Q

What is the clinical relevance of hyperuricaemia?

A

Uric acid is insoluble, and so it deposits in the joints and precipitates a gouty attack in prediposed individuals

160
Q

Who should thiazides be used with caution in due to their potential for causing hyperuricaemia?

A

People with gout, or high levels of uric acid

161
Q

What can volume depletion caused by thiazides lead to?

A
  • Orthrostatic hypotension
  • Light-headedness
162
Q

How do thiazides cause hypercalcaemia?

A

They inhibit the secretion of calcium

163
Q

How do thiazides lead to hyperglycaemia?

A

They lead to glucose intolerance, possibly due to impairment release of insulin and reduced uptake of glucose into tissues

164
Q

What is the clinical relevance of hyperglycaemia caused by thiazides?

A

It can cause diabetic patients taking thiazides to become hyperglycaemia, and cause difficulty in maintaining appropriate blood sugar levels

165
Q

What effect might thiazides have on serum lipids?

A

They can cause a 5-15% increase in serum cholesterol, as well as increased serum LDLs.

166
Q

How does the hyperlipidaemia adverse effect of thiazides change with time?

A

It may resolve with long-term therapy

167
Q

What kind of drug is indapamide?

A

A thiazide-line analog

168
Q

What is meant by a ‘thiazide-like analogue’?

A

It lacks the thiazide structure, but has the same mechanism of action

169
Q

What is good about indapamide?

A

It has a long duration of action, and shows significant antihypertensive effects even at low doses

170
Q

How is indapamide removed from the body?

A

It is metabolised and excreted by the gastrointestinal tract and kidneys

171
Q

What kind of diuretic is amiloride?

A

A potassium sparing diuretic

172
Q

What is the mechansim of action of amiloride?

A

It acts in the collecting tubule to inhibit sodium reabsorption and potassium excretion

173
Q

What is it very important to ensure happens when a patient is taking amiloride?

A

Careful monitoring of potassium levels

174
Q

What is the clinical use of amiloride?

A

Amiloride is not a very efficacious diuretic, and so is commonly used in combination with other diuretics for it’s potassium sparing properties

175
Q

What is the mechanism of action of amiloride?

A

It blocks sodium channels, resulting in a decrease in Na/K exchange

176
Q

What are the common side effects of amiloride?

A
  • Hyperkalaemia
  • Vomiting
  • Loss of appetite
  • Rash
  • Headache
177
Q

In whom is the risk of hyperkalaemia with amiloride greater?

A

Those with kidney problems, diabetes, and the elderly

178
Q

What is spironolactone?

A

A synthetic steroid

179
Q

What does spironolactone do?

A

Antagonises aldosterone at intracellular cytoplasmic receptor sites, inactivating it

180
Q

What is the result of the inactivation of aldosterone by spironolactone?

A

It prevents the translocation of the receptor complex into the nucleus of the target cell, and therefore it cannot bind to DNA to produce proteins that are normally synthesised in response to aldosterone

181
Q

What is the result of spironolactone stopping the synthesis of mediator proteins normally made in response to aldosterone?

A

These proteins normally stimulate the Na/K exchange sites of the collecting tubule, so lack of these proteins prevents Na reabsorption, and therefore K and H secretion

182
Q

How does the efficacy of spironolactone for mobilising sodium from the body compare to other drugs?

A

It has a low efficacy compared to other drugs

183
Q

What useful property does spironolactone have?

A

It causes the retention of potassium

184
Q

What is the clinical use of spironolactone?

A

It is often given in conjunction with a thiazide diuretic or loop diuretic to prevent the potassium excretion that would otherwise occur with these drugs

185
Q

What are the adverse effects of spironolactone?

A
  • Gastric upsets and peptic ulcers
  • Gynaecomastia
  • Menstrual irregularites
  • Hyperkalaemia
  • Nausea
  • Lethargy
  • Mental confusion
186
Q

Is spironolactone completely absorbed orally?

A

Yes

187
Q

Is spironolatone bound to plasma proteins?

A

Yes, strongly

188
Q

What happens to spironolactone in the body?

A

It is rapidly converted to an active metabolite, canrenone

189
Q

What is the importance of canrenone?

A

The action of spironolactone is largely due to the action of canrenone, which has a mineralocorticoid blocking activity

190
Q

Does spironolactone affect the hepatic cytochrome P450 system?

A

Yes, it induces it

191
Q

How do ß-blockers reduce the blood pressure?

A

Primarily by decreasing the cardiac output, but they may also decrease sympathetic outflow from the CNS and inhibit the release of renin from the kidneys, thus decreasing the formation of angiotensin II and the secretion of aldosterone

192
Q

What is the mechanism of action of beta blockers?

A

They are copmetitive antagonists that block the receptor sites for the endogenous catecholamines adrenaline and noradrenaline in the SNS, which mediates the fight-or-flight response

193
Q

What are the known types of ß-receptors?

A

ß1, ß2, and ß2

194
Q

Are ß-blockers selective for specific ß receptors?

A

Some block the activation of all types of ß-receptors, and others are selective

195
Q

Where are ß1 receptors located?

A

Mainly in the heart and kidneys

196
Q

Where are ß2 receptors located?

A
  • Lungs
  • GI tract
  • Liver
  • Uterus
  • Vascular smooth muscle
  • Skeletal muscle
197
Q

Where are ß3 receptors located?

A

Fat cells

198
Q

Give three examples of non-selective ß-blockers, which shown ß1 and ß2 antagonism

A
  • Propanolol
  • Carvedilol
  • Sotalol
199
Q

What are ß1 selective ß-blockers also known as?

A

Cardioselective ß-blockers

200
Q

Give 3 examples of cardioselective ß-blockers

A
  • Bisoprolol
  • Metoprolo
  • Atenolol
201
Q

Give an example of a ß2 selective agent

A

Butaxamine

202
Q

How does the side effect profile of cardioselective ß-blockers compare to non-selective?

A

Adverse effects associated with ß2 receptor antagonism, including bronchospasm, peripheral vasoconstriction, and alteration of glucose and lipid metabolism, are less common with cardioselective agents, but receptor selectivity diminishes at higher doses

203
Q

Are ß-blockers orally active?

A

Yes

204
Q

How long do ß-blockers take to develop their full effects?

A

May take several weeks

205
Q

What are the adverse effects of ß-blockers?

A
  • Hypotension
  • Bradycardia
  • Fatigue
  • Insomnia
  • Sexual dysfunction – decreased libido and impotence
  • Disturb lipid metabolism, decreasing HDL and increasing plasma triglycerides
  • Impaired glucose tolerance
  • Raynauds
206
Q

What might abrupt withdrawal of ß-blockers cause in patients with IHD?

A
  • Angina
  • MI
  • Sudden death
207
Q

How are adverse effects associated with abrupt withdrawal of ß-blockers avoided?

A

The dose of drugs must be tapered over 2-3 weeks in patients with hypertension and ischaemic heart disease

208
Q

How does the effectiveness of ß-blockers vary?

A

They are more useful in some patients than others, for exampel they are more effective in treating hypertension in white than black patients, and in young than old patients

209
Q

What conditions discourage the use of ß-blockers?

A
  • COPD
  • Chronic CHF
  • Severe symptomatic PVD
210
Q

Who are the conditions that discourage the use of ß-blockers more commonly found in?

A

Elderly and diabetic patients

211
Q

What conditions that may co-exist with hypertension are ß-blockers useful in treating?

A
  • Supraventricular tachycardia
  • Previous MI
  • Angina
  • Chronic heart failure
212
Q

What kind of drug is doxazosin?

A

Alpha blocker

213
Q

What is the mechanism of action of alpha-blockers?

A

They produce a competitive block of alpha1 adrenoceptors, decreasing peripheral vascular resistance and lowering arterial blood pressure by causing relaxation of both arterial and venous smooth muscle

214
Q

What effect do alpha blockers have on cardiac output, renal blood flow, and glomerular filtration rate?

A

They only cause a minimal change

215
Q

What are almost universal adverse effects of alpha-blockers?

A
  • Reflex tachycardia
  • First dose syncope
216
Q

What may be necessary to blunt the short-term effect of reflex tachycardia caused by alpha blockers?

A

Concomitant use of a beta blocker

217
Q

What are the other adverse effects of alpha blockers?

A
  • Postural hypotension
  • Dizziness
  • Headache and fatigue
  • Oedema
218
Q

What is malignant hypertension?

A

An extremely high blood pressure that develops rapidly, and causes organ damge

219
Q

What must the blood pressure be to be considered malignant hypertension?

A

180/120mmHg or above

220
Q

What are the causes of malignant hypertension?

A
  • In most cases, high blood pressure
  • Missing doses of blood pressure medications
  • Collagen vascular disease, such as scleroderma
  • Kidney disease
  • Spinal cord injuries
  • Tumour of the adrenal gland
  • Use of certain medications, including birth control pill and MAOIs
  • Use of illegal drugs, such as cocaine.
221
Q

What groups are at increased risk of malignant hypertension?

A
  • Male
  • Young
  • Black
  • Lower economic status
  • Poor access to health care
222
Q

What are the symptoms of malignant hypertension?

A
  • Rapidly increasing blood pressure, and signs of organ damage to kidneys or eyes
  • Bleeding and swelling of retinal vessels
  • Blurred vision
  • Angina
  • Shortness of breath
  • Dizziness
  • Numbness of arms, legs, and face
  • Severe headache
223
Q

What investigations are done in malignant hypertension?

A
  • Measurement of blood pressure
  • Check for signs of organ damage, including CVS and respiratory examination
  • Check eyes
  • Blood and urine testing
  • Other imaging tests to evaulate kidneys and their arteries
224
Q

What should be checked for in the eyes in malignant hypertension?

A
  • Damage to blood vessels of retina
  • Papilloedema
225
Q

What investigations should be done if there is suspected heart failure in malignant hypertension?

A

ECG and echo

226
Q

What investigations should be done if there is suspected respiratory failure in malignant hypertension?

A

CXR

227
Q

What blood tests should be done in malignant hypertension?

A
  • Blood urea, nitrogen, and creatinine levels
  • Blood clotting tests
  • Glucose levels
  • FBC
  • Sodium and potassium
228
Q

Why are blood urea, nitrogen, and creatinine levels done in malignant hypertension?

A

To determine kidney damage

229
Q

What should be checked for on urinalysis in malignant hypertension?

A

Blood, protein, or abnormal hormone levels

230
Q

How is malignant hypertension managed?

A
  • Use oral therapy unless encephalopathy or cardiac failure
  • Ensure bed rest
231
Q

What anti-hypertensive should be used in malignant hypertension?

A

There is no ideal antihypertensive, but atenolol or a long-acting calcium blocker are good optoins

232
Q

What is the aim of treatment in malignant hypertension?

A

Controlled reduction of BP over days, not hours

233
Q

Why should sudden drops in BP be avoided in malignant hypertension?

A

Because cerebral autoregulation is poor, and this can lead to an increased stroke risk

234
Q

What are the complications of malignant hypertension?

A
  • Death
  • Hypertensive encephalopathy
  • Sudden kidney failure
  • Aortic dissection
  • Coma
  • Pulmonary oedema
  • Heart attack
  • Heart failure
  • Stroke
235
Q

What are the symptoms of hypertensive encephalopathy?

A
  • Blindness
  • Changes in mental status and confusion
  • Coma
  • Headache that progresses
  • Nausea and vomiting
  • Seizures

3: MED1 Y3 - Cardiovascular [2] (19 decks)

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