Lecture 20 - Control Of Blood Pressure : Pharmacology And The Role Of The Kidney Flashcards

1
Q

What is the cause of 90% of hypertension cases

A

It is unknown

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2
Q

If the cause of hypertension is unknown what type of hypertension is it

A

Primary/essential hypertension

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3
Q

Hypertension that can be traced to a known condition is usually associated with

A

Renal disease or endocrine disturbances

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4
Q

Hypertension that can be traced to a condition is known as what type of hypertension

A

Secondary hypertension

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5
Q

What are the consequences of chronic hypertension

A

Abnormal thickening of the left wall of the ventricle and narrowing of the lumen in resistance vessels

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6
Q

What is chronic hypertension a risk factor for

A

Heart failure, stroke, renal failure and myocardial infarction

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7
Q

How can hypertension be managed

A

Through lifestyle modification

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8
Q

What lifestyle modifications can be made to manage hypertension

A

The loss of additional weight, increase aerobic exercise, reduced alcohol intake, low salt diet and no smoking

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9
Q

What drugs are used in the treatment of hypertension

A

ACE inhibitors or AT1 receptor blockers (ARBs), beta-blockers, calcium channel blockers and diuretics

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10
Q

What is the stepwise treatment for hypertension in under 55 and non-black

A

Step 1 - ACE inhibitors
Step 2 - ACE inhibitors and calcium channel blockers
Step 3 - ACE inhibitors, calcium channel blockers and diuretics
Step 4 - Consider adding alpha-blockers, beta-blockers or spironolactone or additional diuretics

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11
Q

What is the stepwise treatment for hypertension for over 55 and black

A

Step 1 - Calcium channel blockers
Step 2 - ACE inhibitors and calcium channel blockers
Step 3 - ACE inhibitors, calcium channel blockers and diuretics
Step 4 - Consider adding alpha-blockers, beta-blockers or spironolactone or additional diuretics

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12
Q

What do B-blockers act as

A

Competitive antagonists of B-adrenoceptors

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13
Q

What effects do B-blockers have

A

A reduced cardiac output, reduced MABP, reduced renin release from the kidneys and a CNS action that reduces sympathetic activity

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14
Q

In what patients are B-blockers useful

A

Patients with angina or following a myocardial infarction

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15
Q

What are the adverse effects of B-blockers

A

Bronchospasm, aggravation of cardiac failure, bradycardia, hypoglycaemia, fatigue and cold extremities

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16
Q

What does the RAAS system play a major role in

A

The regulation of sodium excretion and vascular tone

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17
Q

What activates the RAAS

A

A drop in blood pressure

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18
Q

Describe the RAAS

A

A drop in blood pressure is detected by the kidneys which causes the stimulation of the granular cells to release renin. Renin interacts with angiotensinogen, produced by the liver, and converts it to angiotensin I. Ang I then travels to the lungs where angiotensin converting enzyme (ACE) converts it to angiotensin II. Ang II travels to the adrenal gland and causes the release of aldosterone. Aldosterone travels to the kidney and causes an increase in sodium chloride and water retention which causes an increase in blood pressure

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19
Q

What cells are found within the juxaglomerular apparatus

A

Macula densa, granular cells and mesanglial cells

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20
Q

What is the function of macula densa

A

To detect the sodium chloride concentration in the blood

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21
Q

What is the function of granular cells

A

To produce renin

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22
Q

What innervates the granular cells

A

The sympathetic nervous system

23
Q

What effect does RAAS have on congestive heart failure

A

A failing heart has a decreased CO and BP, the lowered BP causes the stimulation of RAAS and this increases the salt and water retention which causes the heart to fail

24
Q

Where are ACE-membrane bound enzymes found

A

On the surface of endothelial cells

25
Q

What is the function of the ACE-membrane bound enzymes

A

To convert inactive angiotensin I to angiotensin II

26
Q

What does angiotensin II inactivate

A

Bradykin

27
Q

Function of ACE inhibitors

A

They block the conversion of angiotensin I to angiotensin II

28
Q

Example of an ACE inhibitor

A

Lisinopril

29
Q

What is the function of AT1 receptor antagonists

A

To block the agonist action of angiotensin II at AT1 receptors in a competitive manner

30
Q

What do ACE inhibitors cause

A

Venous dilation so reduced preload, arteriolar dilation so reduced after load and TPR, which decreases the arterial blood pressure and cardiac load

31
Q

What do ACE inhibitors reduce the release of

A

Aldosterone

32
Q

What does a reduction in the production of aldosterone cause

A

An increase in the loss of Na+ and H2O

33
Q

What are the adverse effects of ACE inhibitors

A

A dry cough and can also cause hypotension

34
Q

What are the properties of ARBs

A

Similar to ACE inhibitors

35
Q

What conditions should ACE inhibitors and ARBs contraindicated in

A

Pregnancy and bilateral renal artery stenosis

36
Q

What are the clinical uses of ACE inhibitors and ARBs

A

Hypertension, cardiac failure and following a myocardial infarction

37
Q

What is the benefit of using ACE inhibitors and ARBs in hypertension

A

Reduced TRP and MABP and the possible suppression of proliferation of smooth muscle cells in the media of resistance vessels

38
Q

What is cardiac failure associated with

A

The inappropriate activation of the RAAS

39
Q

What do ACE inhibitors do

A

They decrease vascular resistance improving perfusion, increase secretion of Na+ and H2O and cause regression of left ventricular hypertrophy

40
Q

What do diuretics act on

A

The kidneys

41
Q

What is the function of diuretics

A

To increase excretion of Na, Cl and H2O and exert additional indirect relaxant effects on the vasculature

42
Q

What are the major classes of diuretics

A

Thiazides and loop agents

43
Q

Thiazides

A

Inhibit NaCl reabsorption in the distal tubule by blocking the Na+/Cl- co-transporter

44
Q

Example of a thiazide

A

Bendroflumethiazide

45
Q

What are thiazides widely used in

A

Heart failure, hypertension and additionally in severe resistant oedema

46
Q

What do thiazides reduce

A

MABP

47
Q

What does the loss of Na+ and H2O cause

A

Contracts blood volume and initially reduces the cardiac output

48
Q

Loop agents

A

They inhibit the the NaCl reabsorption in the thick ascending loop of henle by blocking the Na+/Cl-/K+ co-transporter

49
Q

What do thiazides and loop agents cause an undesirable loss of

A

K+

50
Q

How is the loss of K+ corrected

A

By co-administering a potassium sparing diuretic or K+ supplements

51
Q

Example of loop agent

A

Furosemide

52
Q

Loop agents are used to reduce the salt and water overload associated with

A

Acute pulmonary oedema and chronic heart failure

53
Q

How is the salt and water overload corrected

A

As a result of an absorption of extracellular fluid contributing to oedema in capillaries as a consequence of diuretic-induced reduction of blood volume