[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
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
3
Q
What value is the diagnostic threshold for hypertension?
A
135/85mmHg
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
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
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
7
Q
What time period is ABPM normally carried out over?
A
24 hours
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
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
10
Q
What is blood pressure a measure of?
A
How well the cardiovascular system is functioning
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
12
Q
What is short-term regulation of the blood pressure via?
A
The autonomic nervous system
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
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
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
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
17
Q
Can baroreceptors regulate blood pressure long term?
A
No
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
19
Q
What is involved in the long-term regulation of blood pressure?
A
- Renin-angiotensin-aldosterone system
- Anti-diuretic hormone
- Natiuretic peptides
20
Q
What is renin?
A
A peptide hormone
21
Q
Where is renin released from?
A
The juxtaglomerular apparatus of the kidney
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
23
Q
What is the role of renin?
A
It facilitates the conversion of angiontensinogen to angiotensin I
24
Q
What happens to angiotensin I?
A
It is converted to angiontensin II using ACE
25
What is angiotensin II?
A potent vasoconstrictor
26
What does angiotensin II do?
* Acts directly on the kidney to increase sodium reabsorption in the proximal convoluted tubule
* Promotes the release of aldosterone
27
How is sodium reabsorbed in the proximal convulted tubule?
Via the sodium-hydrogen exchanger
28
In addition to the conversion of angiotensin I to II, what is the role of ACE?
It breaks down bradykinin, which is a potent vasodilator
29
What is the result of the breakdown of bradykinin by ACE?
It potentiates an overall constricting effect
30
What does aldosterone do?
* 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
31
What is the result of aldosterones effect on sodium?
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
32
What are prostaglandins?
Local vasodilators
33
What is the role of prostaglandins in the kidney?
They increase GFR and reduce sodium reabsorption.
They also act to prevent excessive vasoconstriction triggered by SNS and RAAS systems.
34
Where is ADH released from?
The OVLT of the hypothalamus
35
What is ADH released in response to?
* Thirst
* Increased plasma osmolality
36
What does ADH do?
* 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
37
What is the result of the increased sodium reabsorption caused by ADH?
It increases water reabsorption, thus increasing plasma volume and decreasing osmolarity
38
Do naturiretic peptides regulate blood pressure in the short- or long-term?
Long term
39
Give two examples of natiuretic peptides?
* ANP
* Prostaglandins
40
Where is ANP synthesised and stored?
In cardiac myocytes
41
When is ANP released?
When the atria are stretched (indicating high blood pressure)
42
What effect does hypertension have on vessel walls?
It damages them, making them weaker
43
How does hypertension damage vessel walls?
The higher blood pressure causes increased arterial thickening through smooth muscle hypertrophy and accumulation of vascular matrix, leading to a loss of arterial compliance.
44
What does hypertension-mediated damage to vessel walls lead to?
A number of pathologies, including atherosclerosis, thromboembolism (progressing to MI or stroke), and aneurysms
45
How does hypertension damage the heart itself?
By increasing the afterload of the heart, meaning the heart is pumping against greater resistance, leading to left ventricular hypertrophy.
46
What can hypertension-mediated damage to the heart cause?
* It increases the risk of heart failure in the future
* It increases the hearts oxygen demands, predisposing to myocardial ischaemia and ultimately angina
47
What is the optimal blood pressure?
\<120/80mmHg
48
What is considered to be normal blood pressure?
\<130/85mmHg
49
What is considered to be grade 1 (mild) hypertension?
140-159 / 90-99mmHg
50
What is considered to be grade 2 (moderate) hypertension?
160-179 / 100-109mmHg
51
What is considered to be grade 3 (severe) hypertension?
\>180 / \>110mmHg
52
What is considered to be grade 1 isolated systolic hypertension?
140-159 / \<90mmHg
53
What is considered to be grade 2 isolated systolic hypertension?
\>160 / \<90mmHg
54
What are the different types of hypertension?
* Primary, or essential, hypertension
* Secondary hypertension
* White-coat hypertension
* Masked hypertension
* ‘Malignant’, or accelerated phase hypertension
55
What is white-coat hypertension?
An elevated clinic pressure, but normal ambulatory blood pressure monitoring
56
Do NICE recommend treatment for white-coat hypertension?
No
57
What is the clinical significance of white-coat hypertension?
More likely to develop hypertension in the future, and may have an increased risk of CVD
58
What is masked hypertension?
When BP is normal in clinic, but high on ABPM
59
What is primary hypertension?
Hypertension when there is no identifable cause
60
What % of hypertension cases are primary hypertension?
95%
61
What are the causes of secondary hypertension?
* Renal disease
* Endocrine disease
* Coarction
* Pregnancy
* Liquorice
* Drugs
62
What drugs can cause hypertension?
* Steroids
* MAOIs
* Oral contraceptive pill
* Cocaine
* Amphetamines
63
What is the most common cause of secondary hypertension?
Renal disease
64
What are the most common renal causes of hypertension?
* Intrinsic renal disease
* Renovascular disease
65
Give 5 intrinsic renal diseases that can cause hypertension
* Glomerulonephritis
* Polyarteritis nodosa
* Systemic sclerosis
* Chronic pyelonephritis
* Polycystic kidneys
66
What % of renal induced hypertension cases are due to intrinsic renal disease?
75%
67
What renovascular disease can cause hypertension?
Most frequently atheromatous renovascular disease, or rarely fibromuscular dysplasia
68
What % of renal disease induced hypertensin is due to renovascular disease?
25%
69
What endocrine diseases can cause hypertension?
* Cushing’s syndrome
* Conn’s syndrome
* Phaeochromocyoma
* Acromegaly
* Hyperparathyroidism
70
What are the modifiable risk factors for hypertension?
* Excess weight
* Excess dietary salt intake
* Lack of physical activity
* Excessive alcohol intake
* Stress
71
What are the non-modifiable risk factors for hypertension?
* Older age
* Family history
* Ethnicity
* Male gender before 65, female gender after 65
72
What are the symptoms of hypertension?
Usually asymptomatic, however can look for symptoms of an underlying cause
73
Give 4 examples of symptoms of an underlying cause you could look for in hypertension
* Renal bruits
* Radiofemoral delay
* Palpable kidneys
* Signs of Cushing's syndrome
74
How do you ensure you have the correct size cuff when measuring BP with a sphygmomanometer?
Check the cuff width is 40% of the arm circumference
75
What is the correct placement of a BP cuff?
The bladder of the cuff should be central over the brachial artery, and the cuff should be applied snuggly
76
What position should the arm be in when measuring BP with a sphygmomanometer?
The arm should be supported in a horizontal position at a mid-sternal level
77
How do you obtain an estimate of the systolic blood pressure when measuring BP with a sphygmomanometer?
You inflate the cuff whilst palpating the radial artery until the pulse disappears
78
Once you have obtained an estimate of the systolic blood pressure, how do you take an accurate reading when measuring BP with a sphygmomanometer?
You inflate the cuff until 30mmHg over the estimated systolic pressure, then place a stethoscope over the brachial artery, and deflate at 2mmHg/sec
79
What indicates the systolic pressure when measuring BP with a sphygmomanometer?
The appearance of sustained reptitive tapping sounds
80
What indicates the diastolic pressure when measuring BP with a sphygmomanometer?
The disappearance of sounds
81
How is hypertension investigated?
* 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
82
What is the purpose of ABPM or home monitoring in the investigation of hypertension?
To confirm the diagnosis
83
What is the purpose of fasting glucose and cholesterol in the investigation of hypertension?
To help quantify overall risk
84
What is the purpose of ECG, echo, and urine analysis in the investigation of hypertension?
To assess for end-organ damage
85
What is the purpose of U&Es and calcium levels in the investigation of hypertension?
To exclude secondary causes
86
What is the purpose of renal artery ultrasound or arteriography in the investigation of hypertension?
To look for renal artery stenosis
87
What is the purpose of an MRI of the aorta in the investigation of hypertension?
To check for coarction
88
What is the treatment goal for hypertension?
\<140/90mmHg
89
What is the treatment goal for hypertension in diabetes?
\<130/90
90
What is the treatment goal for hypertension if over the age of 80?
\<150/90
91
Why is it important to slowly reduce blood pressure in hypertension?
As rapid reduction can be fatal, especially in the context of an acute stroke
92
What are the approaches in the management of hypertension?
* Look for and treat underlying causes
* Lifestyle changes
* Drugs
93
When are lifestyle changes alone sufficient in the management of hypertension?
If the blood pressure is consistently above 140/90mmHg, but the risk of other problems is low
94
When should medication be given in addition to lifestyle changes in the management of hypertension?
* 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
95
What lifestyle changes can be made in the management of hypertension?
* 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
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?
Calcium channel antagonists, or thiazides
97
What is the first choice drug in the management of hypertension in patients who are aged under 55 years?
ACE inhibitors
98
What is given if a person is intolerant to ACE inhibitors?
Angiotension-receptor blockers
99
Why are beta-blockers not first line in hypertension?
Due to their reduced effectiveness in reducing major cardiovascular events, particularly stroke, and their increased risk of new onset diabetes
100
Who can beta-blockers be considered for in the management of hypertension?
Younger people, particularly if they are intolerant or contraindcated to ACE inhibitors or ARBs, or are a woman of childbearing age
101
Which drugs can be used in conjunction with one another in hypertension?
ACE inhibitors, Ca channel antagonists, and diuretics (thiazide recommended)
102
What should be done if hypertension is still uncontrolled on adequate doses of 3 drugs?
Consider adding spironolactone, or a higher dose thiazide. Alternatively, add a ß-blocker or selective alpha blocker.
In this situation, check drug compliance
103
How can drug compliance be checked in hypertension?
Using urinary drug screen or observed prescription
104
Do calcium channel blockers have good oral absorption?
Yes
105
What % of calcium channel blockers are protein bound?
\>90%
106
What organ metabolises calcium channel blockers?
Liver
107
What is the half-life of calcium channel blockers after oral administration?
Most have short half-lives (3-8 hours)
108
Is once daily dosing possible with calcium channel blockers?
Yes, sustained release preparations are available which allow this
109
What is the exception to calcium channel blockers having short half-lives?
Amlodipine, which has a very long half-life and does not require a sustained release preparation
110
What can the calcium channel blockers be divided into?
3 chemical classes, each with different pharmacokinetic properties and clinical indications
111
What are the different classes of calcium channel antagonists?
* Phenylalkyamines
* Benzothiazepines
* Dihydropyridines
112
What is the only member of the phenylalkyamine class?
Verapamil
113
How does verapamil compare to other calcium channel blockers in terms of selectivity?
It is the least selective of any calcium channel blocker, and has significant effects on both cardiac and vascular smooth muscle cells
114
What is the result of verapamils action on cardiac and vascular smooth muscle cells?
It causes peripheral vasodilation and a reduction in cardiac preload and myocardial contractility
115
What are the adverse effects of verapamil?
* Constipation
* Risk of bradycardia
*
116
Who should verapamil be avoided in?
Patients with congestive heart failure or AV block
117
Why should verapamil be avoided in patients with congestive heart failure or AV block?
Due to it's negative inotopic and dromotopic (velocity of conduction) effect
118
What are the therapeutic uses of verapamil?
* Angina
* Supraventricular tachyarrhythmias
* Prevention of migraine and cluster headaches
119
What is the only member of the benzothiazepine class?
Diltiazem
120
What kind of smooth muscle does diltiazem act on?
Cardiac and vascular
121
How does diltiazem compare to verapamil?
It has a less pronounced negative inotopic effect on the heart compared to verapamil
It has a favourable side effect profile
122
What are the adverse effects of benzothiazepines?
Risk of bradycardia
123
Is diltiazem safe in heart failure?
No, it can worsen heart failure
124
Give two examples of calcium channel blockers in the dihydropyridine class
* Nifedipine
* Amlodipine
125
How do dihydropyridines differ from the other classes of calcium channel blockers?
In pharmacokinetics, approved uses, and drug interactions
126
Why are dihydropyridines particularly good in treating hypertension?
Because they all have a much greater affinity for vascular calcium channels than for calcium channels in the heart
127
What is the advantage of dihydropyridines, in terms of drug interactions?
They show little interaction with other cardiovascular drugs such as digoxin and warfarin, which are often used alonside calcium channel blockers
128
What are the adverse effects of dihydropyridines?
* Sympathetic nervous system activation, causing tachycardia and palpitations.
* Flushing
* Sweating
* Thobbing headache
* Oedema
* Gingival hyperplasia
129
Give an example of a loop diuretic
Furosemide
130
Where does furosemide have its major action?
In the ascending limb of the loop of Henle
131
How do loop diuretics compare to all other types of diuretic?
They have the highest efficacy in mobilising sodium and chloride from the body, and produce copious amounts of urine
132
What is the mechanism of action of loop diuretics?
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
Why are loop diuretics the most efficaious of the diuretic drugs?
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
What are the adverse effects of loop diuretics?
* Ototoxicity
* Hyperuricaemia
* Acute hypovolaemia
* Potassium depletion
135
When in particular can hearing be adversely affected by loop diuretics?
When used in conjunction wtih aminoglycoside antibiotics
136
Is hearing damage caused by loop diuretics pernament?
It can be with continued treatment
137
How does furosemide cause hyperuricaemia?
It competes with uric acid for the renal and biliary secretory systems, thus blocking its secretion and causing or excerbating gouty attacks
138
What might acute hypovolaemia caused by loop diuretics lead to?
Hypotension, shock, and cardiac arrhythmias
Hypercalcaemia may also occur under these conditions
139
How can loop diuretics can potassium depletion?
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
How can potassium depletion caused by loop diuretics be averted?
* Using potassium-sparing diuretic
* Dietary potassium supplementation
141
How are loop diuretics administered?
Orally or parenterally
142
What is the duration of action of loop diuretics?
2-4 hours
143
How are loop diuretics removed from the body?
They are excreted into urine
144
What kind of diuretic is bumetanide?
Loop diuretic
145
How does bumetanide compare to furosemide?
It is much more potent than furosemide
146
In what respects is bumetanide the same as furosemide?
The mechanism of action, pharmacokinetics, and adverse effects are the same as for furosemide, *except it doesn't cause hyperuricaemia*
147
What kind of diuretic is bendroflumethiazide?
A thiazide
148
What is the clinical use of bendroflumethiazide?
It can be added to a loop diuretic in heart failure if addition diuresis is required
149
Where does bendroflumethiazide act?
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
What is the mechanism of action of bendroflumethiazide?
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
What are the adverse effects of bendroflumethiazide?
* Potassium depletion
* Hyponatraemia
* Hyperuricaemia
* Volume depletion
* Hypercalcaemia
* Hyperglycaemia
* Hyperlipidaemia
152
What is the most frequent adverse effects with thiazide diuretics?
Hypokalaemia
153
Why does potassium depletion occur with thiazide diuretics?
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
What can potassium depletion predispose to in patients also taking digoxin?
Ventricular arrhythmias
155
How can potassium depletion caused by thiazide diuretics be managed?
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
What factors contribute to hyponatraemia caused by thiazide diuretics?
* Loss of sodium
* Elevation of ADH as a result of hypovolaemia
* Diminished diluting capacity of the kidney
* Increased thirst
157
What can prevent hyponatraemia with thiazide use?
* Limiting water intake
* Lowering diuretic dose
158
How do thiazides cause hyperuricaemia?
They increase serum uric acid by reducing its secretion
159
What is the clinical relevance of hyperuricaemia?
Uric acid is insoluble, and so it deposits in the joints and precipitates a gouty attack in prediposed individuals
160
Who should thiazides be used with caution in due to their potential for causing hyperuricaemia?
People with gout, or high levels of uric acid
161
What can volume depletion caused by thiazides lead to?
* Orthrostatic hypotension
* Light-headedness
162
How do thiazides cause hypercalcaemia?
They inhibit the secretion of calcium
163
How do thiazides lead to hyperglycaemia?
They lead to glucose intolerance, possibly due to impairment release of insulin and reduced uptake of glucose into tissues
164
What is the clinical relevance of hyperglycaemia caused by thiazides?
It can cause diabetic patients taking thiazides to become hyperglycaemia, and cause difficulty in maintaining appropriate blood sugar levels
165
What effect might thiazides have on serum lipids?
They can cause a 5-15% increase in serum cholesterol, as well as increased serum LDLs.
166
How does the hyperlipidaemia adverse effect of thiazides change with time?
It may resolve with long-term therapy
167
What kind of drug is indapamide?
A thiazide-line analog
168
What is meant by a 'thiazide-like analogue'?
It lacks the thiazide structure, but has the same mechanism of action
169
What is good about indapamide?
It has a long duration of action, and shows significant antihypertensive effects even at low doses
170
How is indapamide removed from the body?
It is metabolised and excreted by the gastrointestinal tract and kidneys
171
What kind of diuretic is amiloride?
A potassium sparing diuretic
172
What is the mechansim of action of amiloride?
It acts in the collecting tubule to inhibit sodium reabsorption and potassium excretion
173
What is it very important to ensure happens when a patient is taking amiloride?
Careful monitoring of potassium levels
174
What is the clinical use of amiloride?
Amiloride is not a very efficacious diuretic, and so is commonly used in combination with other diuretics for it's potassium sparing properties
175
What is the mechanism of action of amiloride?
It blocks sodium channels, resulting in a decrease in Na/K exchange
176
What are the common side effects of amiloride?
* Hyperkalaemia
* Vomiting
* Loss of appetite
* Rash
* Headache
177
In whom is the risk of hyperkalaemia with amiloride greater?
Those with kidney problems, diabetes, and the elderly
178
What is spironolactone?
A synthetic steroid
179
What does spironolactone do?
Antagonises aldosterone at intracellular cytoplasmic receptor sites, inactivating it
180
What is the result of the inactivation of aldosterone by spironolactone?
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
What is the result of spironolactone stopping the synthesis of mediator proteins normally made in response to aldosterone?
*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
How does the efficacy of spironolactone for mobilising sodium from the body compare to other drugs?
It has a low efficacy compared to other drugs
183
What useful property does spironolactone have?
It causes the retention of potassium
184
What is the clinical use of spironolactone?
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
What are the adverse effects of spironolactone?
* Gastric upsets and peptic ulcers
* Gynaecomastia
* Menstrual irregularites
* Hyperkalaemia
* Nausea
* Lethargy
* Mental confusion
186
Is spironolactone completely absorbed orally?
Yes
187
Is spironolatone bound to plasma proteins?
Yes, strongly
188
What happens to spironolactone in the body?
It is rapidly converted to an active metabolite, canrenone
189
What is the importance of canrenone?
The action of spironolactone is largely due to the action of canrenone, which has a mineralocorticoid blocking activity
190
Does spironolactone affect the hepatic cytochrome P450 system?
Yes, it induces it
191
How do ß-blockers reduce the blood pressure?
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
What is the mechanism of action of beta blockers?
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
What are the known types of ß-receptors?
ß1, ß2, and ß2
194
Are ß-blockers selective for specific ß receptors?
Some block the activation of all types of ß-receptors, and others are selective
195
Where are ß1 receptors located?
Mainly in the heart and kidneys
196
Where are ß2 receptors located?
* Lungs
* GI tract
* Liver
* Uterus
* Vascular smooth muscle
* Skeletal muscle
197
Where are ß3 receptors located?
Fat cells
198
Give three examples of non-selective ß-blockers, which shown ß1 and ß2 antagonism
* Propanolol
* Carvedilol
* Sotalol
199
What are ß1 selective ß-blockers also known as?
Cardioselective ß-blockers
200
Give 3 examples of cardioselective ß-blockers
* Bisoprolol
* Metoprolo
* Atenolol
201
Give an example of a ß2 selective agent
Butaxamine
202
How does the side effect profile of cardioselective ß-blockers compare to non-selective?
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
Are ß-blockers orally active?
Yes
204
How long do ß-blockers take to develop their full effects?
May take several weeks
205
What are the adverse effects of ß-blockers?
* Hypotension
* Bradycardia
* Fatigue
* Insomnia
* Sexual dysfunction – decreased libido and impotence
* Disturb lipid metabolism, decreasing HDL and increasing plasma triglycerides
* Impaired glucose tolerance
* Raynauds
206
What might abrupt withdrawal of ß-blockers cause in patients with IHD?
* Angina
* MI
* Sudden death
207
How are adverse effects associated with abrupt withdrawal of ß-blockers avoided?
The dose of drugs must be tapered over 2-3 weeks in patients with hypertension and ischaemic heart disease
208
How does the effectiveness of ß-blockers vary?
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
What conditions discourage the use of ß-blockers?
* COPD
* Chronic CHF
* Severe symptomatic PVD
210
Who are the conditions that discourage the use of ß-blockers more commonly found in?
Elderly and diabetic patients
211
What conditions that may co-exist with hypertension are ß-blockers useful in treating?
* Supraventricular tachycardia
* Previous MI
* Angina
* Chronic heart failure
212
What kind of drug is doxazosin?
Alpha blocker
213
What is the mechanism of action of alpha-blockers?
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
What effect do alpha blockers have on cardiac output, renal blood flow, and glomerular filtration rate?
They only cause a minimal change
215
What are almost universal adverse effects of alpha-blockers?
* Reflex tachycardia
* First dose syncope
216
What may be necessary to blunt the short-term effect of reflex tachycardia caused by alpha blockers?
Concomitant use of a beta blocker
217
What are the other adverse effects of alpha blockers?
* Postural hypotension
* Dizziness
* Headache and fatigue
* Oedema
218
What is malignant hypertension?
An extremely high blood pressure that develops rapidly, and causes organ damge
219
What must the blood pressure be to be considered malignant hypertension?
180/120mmHg or above
220
What are the causes of malignant hypertension?
* *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.
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What groups are at increased risk of malignant hypertension?
* Male
* Young
* Black
* Lower economic status
* Poor access to health care
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What are the symptoms of malignant hypertension?
* 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
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What investigations are done in malignant hypertension?
* 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
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What should be checked for in the eyes in malignant hypertension?
* Damage to blood vessels of retina
* Papilloedema
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What investigations should be done if there is suspected heart failure in malignant hypertension?
ECG and echo
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What investigations should be done if there is suspected respiratory failure in malignant hypertension?
CXR
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What blood tests should be done in malignant hypertension?
* Blood urea, nitrogen, and creatinine levels
* Blood clotting tests
* Glucose levels
* FBC
* Sodium and potassium
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Why are blood urea, nitrogen, and creatinine levels done in malignant hypertension?
To determine kidney damage
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What should be checked for on urinalysis in malignant hypertension?
Blood, protein, or abnormal hormone levels
230
How is malignant hypertension managed?
* Use oral therapy unless encephalopathy or cardiac failure
* Ensure bed rest
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What anti-hypertensive should be used in malignant hypertension?
There is no ideal antihypertensive, but atenolol or a long-acting calcium blocker are good optoins
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What is the aim of treatment in malignant hypertension?
Controlled reduction of BP over days, not hours
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Why should sudden drops in BP be avoided in malignant hypertension?
Because cerebral autoregulation is poor, and this can lead to an increased stroke risk
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What are the complications of malignant hypertension?
* Death
* Hypertensive encephalopathy
* Sudden kidney failure
* Aortic dissection
* Coma
* Pulmonary oedema
* Heart attack
* Heart failure
* Stroke
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What are the symptoms of hypertensive encephalopathy?
* Blindness
* Changes in mental status and confusion
* Coma
* Headache that progresses
* Nausea and vomiting
* Seizures
