cardio renal L7 Flashcards

1
Q

whats noraml BP?

A

120/80

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1
Q
A
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2
Q

does BP rise gradually with age

A

yes

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3
Q

Hypertension is commonly treated if diastolic pressure remains above…

A

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

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4
Q

__% of the adult population suffer from hypertension

A

20% of the adult population suffer from hypertension

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5
Q

waht is ‘Essential hypertension’

A

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

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6
Q

what is phaeochromocytoma

A

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

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7
Q

how can renal artery sclerosis lead to hypertension?

A
  1. drop in filtration pressure,
  2. renin release
  3. increase BP to increase GFR
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8
Q

young adult mean arterial pressure?

A

96mmHg

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9
Q

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

A
  • Cardiac output
  • Peripheral resistance
  • The renin-angiotensin-aldosterone system and the kidney
  • The autonomic nervous system
  • The endothelium
  • Vasoactive peptides
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10
Q

bp equation

A

cardiac output x total peripheral resistance (CO x TPR)

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11
Q

to reduce blood pressure ___ or ____ must be reduced.

A

to reduce blood pressure CO or TPR must be reduced.

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12
Q

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

A

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

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13
Q

Autonomic stimulation can cause of vessels to what?

A

Autonomic stimulation can cause both arteriolar constriction and dilatation

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14
Q

T or F

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

A

T

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15
Q

T or F

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

A

T

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16
Q

describe how the vascular endothelium is important in cardiovascular regulation

A

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

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

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17
Q

what can happen to endothelial cells when atheroma developes/

A

NO production can be compromised

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18
Q

describe endothelin

A

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

19
Q

is it suggested that endothelial dysfunction is irreversible

A

it would appear so

20
Q

describe how bradykinin is involve in BP

A

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

21
Q

describe ANP adn what it does

A

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

22
Q

T or F

Many hypertensive patients have low levels of renin and angiotensin II

A

T

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

23
Q

are there local renin angiotensin systems too?

A

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

local systems (paracrine) may be important too.

24
Q

are there some genes which predispose to high BP?

A

yes- so called mendelian forms of BP.

at least 8 genes that cause Mendelian forms of hypertension and 9 genes that cause hypotension in humans

eg Liddles syndrome

25
Q

whats liddles syndrome?

A

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

26
Q

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

A

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

27
Q

cool info

A

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

28
Q

is hypertension a consideration for transplants?>

A

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

29
Q

7 types of antihypertensive drugs?

A
  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
30
Q

Diuretics as antihypertensive drugs?

A

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.

31
Q
A
32
Q

ACE inhibitors as antihypertensive drugs?

A
  • 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.

*

33
Q

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

A

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

34
Q

It is logical to use ACE inhibitors when ….

A

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

35
Q

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

A

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)

36
Q

a1 adrenoceptor antagonists as antihypertensives

A
  • 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)
37
Q

what is labetalol?

A

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

38
Q

Ca2+-channel antagonists as antihypertensives?

A
  • 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)
39
Q

K+-channel openers use in treating hypertension

A
  • 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.

*

40
Q

The KCO, minoxidil is marketed as a…

A

The KCO, minoxidil is marketed as a hair-restorer

41
Q

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

A
  • 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.
42
Q

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

A

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

43
Q

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

A

thorugh reduced NA release

44
Q
A
45
Q

describe how á-methyldopa can be used as an antihypertensive

A
  • 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
46
Q

fat

A

mamba