cardio renal L7

Question 1

whats noraml BP?

Answer 1

120/80

Question 2

does BP rise gradually with age

Answer 2

yes

Question 3

Hypertension is commonly treated if diastolic pressure remains above…

Answer 3

Hypertension is commonly treated if diastolic pressure remains above 95 mm Hg, sometimes treated if it is above 90 mm Hg

Question 4

__% of the adult population suffer from hypertension

Answer 4

20% of the adult population suffer from hypertension

Question 5

waht is ‘Essential hypertension’

Answer 5

95% of hypertension is of unknown aetiology - ‘Essential hypertension’

Question 6

what is phaeochromocytoma

Answer 6

tumour of adrenal medulla chromaffin cells - secrete lots of adrenaline - hypertension

Question 7

how can renal artery sclerosis lead to hypertension?

Answer 7

1. drop in filtration pressure,
2. renin release
3. increase BP to increase GFR

Question 8

young adult mean arterial pressure?

Answer 8

96mmHg

Question 9

The following mechanisms are likely to be the most significant involved in development of essential hypertension: (6)

Answer 9

• Cardiac output
• Peripheral resistance
• The renin-angiotensin-aldosterone system and the kidney
• The autonomic nervous system
• The endothelium
• Vasoactive peptides

Question 10

bp equation

Answer 10

cardiac output x total peripheral resistance (CO x TPR)

Question 11

to reduce blood pressure ___ or ____ must be reduced.

Answer 11

to reduce blood pressure CO or TPR must be reduced.

Question 12

most patients with essential hypertension have a ___ CO and a ____ TPR (and TPR is mainly due to arteriolar resistance).

Answer 12

most patients with essential hypertension have a normal CO and a raised TPR (and TPR is mainly due to arteriolar resistance).

Question 13

Autonomic stimulation can cause of vessels to what?

Answer 13

Autonomic stimulation can cause both arteriolar constriction and dilatation

Question 14

T or F

There is little evidence to suggest that adrenaline and noradrenaline have any clear role in the aetiology of essential hypertension

Answer 14

T

Question 15

T or F

drugs that block the sympathetic nervous system do lower blood pressure and are in extensive use.

Answer 15

T

Question 16

describe how the vascular endothelium is important in cardiovascular regulation

Answer 16

produce a number of local vasoactive agents, including nitric oxide and endothelin.

Dysfunction of the endothelium has been implicated in human essential hypertension.

Question 17

what can happen to endothelial cells when atheroma developes/

Answer 17

NO production can be compromised

Question 18

describe endothelin

Answer 18

Endothelin, as well as being a vasoconstrictor, may produce a salt-sensitive rise in blood pressure and activate local renin-angiotensin systems

Question 19

is it suggested that endothelial dysfunction is irreversible

Answer 19

it would appear so

Question 20

describe how bradykinin is involve in BP

Answer 20

Bradykinin, which is inactivated by angiotensin converting enzyme, so ACE inhibitors may exert some of their effect by blocking bradykinin inactivation

vasoactive peptide - involved in renin angiotensin system

Question 21

describe ANP adn what it does

Answer 21

Atrial natriuretic peptide, increases Na+ and water excretion from the kidney. A defect in this system may cause fluid retention and hypertension

Question 22

T or F

Many hypertensive patients have low levels of renin and angiotensin II

Answer 22

T

which suggests: Circulating renin-angiotensin system is not thought to be directly responsible for the rise in blood pressure in essential hypertension

Question 23

are there local renin angiotensin systems too?

Answer 23

Non-circulating “local” paracrine renin-angiotensin systems also control blood pressure.

local systems (paracrine) may be important too.

Question 24

are there some genes which predispose to high BP?

Answer 24

yes- so called mendelian forms of BP. ## Footnote at least 8 genes that cause Mendelian forms of hypertension and 9 genes that cause hypotension in humans eg Liddles syndrome

Question 25

whats liddles syndrome?

Answer 25

high rate of Na+ reabsorption in the presence of very low aldosterone secretion. This results in severe hypertension caused by various mutations in the ß- and gamma -subunits of epithelial Na+ channels (ENaCs) in the late distal tubule The channels are both **over-expressed** and **open more frequently** than other channels

Question 26

All the mutated gene products that have been clearly demonstrated to cause hypertension act in the ....

Answer 26

All the mutated gene products that have been clearly demonstrated to cause hypertension act in the kidney, altering net renal salt reabsorption

Question 27

cool info

Answer 27

Cross-transplantation experiments with kidneys of hypertensive rats transferred to normotensive animals, and vice versa, indicate that hypertension has its origins in the kidneys

Question 28

is hypertension a consideration for transplants?\>

Answer 28

Human evidence from renal transplant recipients shows that they are more likely to develop hypertension if the donors’ relatives are hypertensive

Question 29

7 types of antihypertensive drugs?

Answer 29

1. Diuretics 2. ACE Inhibitors 3. ß adrenoceptor antagonists 4. α1 adrenoceptor antagonists 5. Ca2+-channel antagonists 6. K+-channel openers 7. Centrally-acting α₂/I₁-agonists

Question 30

Diuretics as antihypertensive drugs?

Answer 30

In the initial phase they decrease blood volume, in the later phase they produce vasodilatation The full hypertensive effect can take up to 12 weeks to develop.

Question 31

Answer 31

Question 32

ACE inhibitors as antihypertensive drugs?

Answer 32

* lead to decreased circulating angiotensin II and hence decreased aldosterone secretion, thus increasing Na+ excretion. * Decreased bradykinin metabolism may be a minor component. The side-effects are minimal but the commonest one is a ‘dry cough’, which can be severe * The effect increased by combination with a diuretic. *

Question 33

\_\_\_\_\_ can be used in patients who are intolerant of ACE inhibitors2.

Answer 33

ARBs can be used in patients who are intolerant of ACE inhibitors2.

Question 34

It is logical to use ACE inhibitors when ....

Answer 34

It is logical to use ACE inhibitors when plasma renin is high and 50-75% mild-moderate hypertensives respond to ACE inhibitors.

Question 35

ß-adrenoceptor antagonists (ß-blockers) use in hypertension

Answer 35

ß1-specific antagonists like atenolol and bisoprolol ■ Probably work by a combination of actions 1. Decreased cardiac output 2. Decreased plasma renin 3. CNS action (for some) starting to be eclipsed by new drugs with fewer side effects (CNS based - depression and insomnia)

Question 36

a1 adrenoceptor antagonists as antihypertensives

Answer 36

* not first line, but still used * dilate all arterial vessels. There is no tachycardia (probably due to lack of block of presynaptic α2 receptors) * eg: doxazosin, prazosin * modulate baroreceptor function (Blockade of CNS a1- receptors modulates baroreceptor reflex mechanisms, decreasing sympathetic discharge)

Question 37

what is labetalol?

Answer 37

Labetalol is an unusual drug being an á1, ß1 and ß2 antagonist (But more so ß than á). can be used for hypertension in pregnancy

Question 38

Ca2+-channel antagonists as antihypertensives?

Answer 38

* Act on L-type Ca2+ channels * They have a mild diuretic effect and may inhibit aldosterone release which is stimulated by angiotensin II * dihydropyridines can be combined with beta blockers to combat reflex tachycardia * Original dihydropyridine was nifedipine (newer ones like amlodipine are more common today though)

Question 39

K+-channel openers use in treating hypertension

Answer 39

* Important drug is minoxidil (also nicorandil) * They act on ATP-sensitive K+ channels in vascular smooth muscle, resulting in hyperpolarisation and relaxation * They can produce a rise in blood glucose through their inhibition of insulin release * KCOs are seldom used alone for hypertension. *

Question 40

The KCO, minoxidil is marketed as a...

Answer 40

The KCO, minoxidil is marketed as a hair-restorer

Question 41

Centrally-acting a2/I1-agonists as treatments for hypertension

Answer 41

* classic drugs: clonidine and guanfacine * clonidine is an a2 agonist * Clonidine causes vasoconstriction if it is applied to the periphery (e.g. in shaving cream), but vasodilatation if it is taken systemically * This dilatation effect was originally thought to be by decreasing noradrenaline release via an action on presynaptic α2 receptors in the CNS - but now thought to be through imidazoline receptors I1.

Question 42

which is a more potent a2 agonsit: clonidine or guanfacine\>

Answer 42

Guanfacine is a more potent á2 agonist than is clonidine, but it has a low efficacy as an antihypertensive agent.

Question 43

describe the mechanism of action for presynaptic a2 receptors for lowering BP

Answer 43

thorugh reduced NA release

Question 45

describe how á-methyldopa can be used as an antihypertensive

Answer 45

* Converted in the vesicles of adrenergic neurones into α-methylnoradrenaline * This is a false transmitter * α-methylnoradrenaline is less potent than noradrenaline on α1 receptors, but more potent on α2 and so acts centrally on presynaptic receptors

Question 46

fat

Answer 46

mamba