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Drugs > Lectures 12-16 > Flashcards

Lectures 12-16 Flashcards

1
Q

what is the normal blood pressure?

A

120/80

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2
Q

what is systolic pressure?

A

pressure while the heart is contracting. (maximum)

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3
Q

what is diastolic pressure?

A

pressure while the heart is filling. (minimum)

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4
Q

what is the pulse pressure?

A

difference between systolic and diastolic

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5
Q

what is hypertension?

A

increased diastolic, systolic and pulse pressure

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6
Q

what is hypo tension?

A

decreased blood pressure

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7
Q

what is severe, moderate and mild bp?

A 
diastolic:
severe >120 mm Hg (mm of mercury)
moderate 105-120
mild 90-105
"normal" 80

no real symptoms

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8
Q

what are the types of hypertension?

A

primary/essential/idiopathic - cause unknown.

secondary - identified cause

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9
Q

what is stenosis?

A

narrowing of a vessel.

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10
Q

what are the consequences of hypertension?

A

coronary artery disease (myocardial infarction)

stroke (cerebral haemorrhage, thrombosis (blood clot in arteries)).

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11
Q

how can you try to control hypertension?

A

lifestyle interventions, education, monitoring.

antihypertensive drug treatments.

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12
Q

what is blood pressure?

A

cardiac output x peripheral resistance.

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13
Q

describe resistance arterioles.

A

A major determinant of blood pressure is the diameter of the peripheral resistance vessels. These are arterioles that can relax and contract in response to sympathetic input.

noradrenaline from sympathetic neuromuscular junction causes Ca2+ to make smooth muscle contract.

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14
Q

describe how noradrenaline acts and affects L type calcium channels.

A 
When noradrenaline (norepinephrine) is released at the sympathetic  nerve terminals at resistance arterioles, it binds to alpha1 adrenoceptors to cause constriction, and hence blood pressure goes up. 
This causes the activation of the phospholipase C pathway, and causes production of InsP3 (inositol triphosphate).
This causes the release of calcium in the cell from intracellular sources.

ca sensitive cl- channels open, cl- efflux and the membrane depolarises.

the depolarisation causes L type (voltage sensitive) ca channels.

ca2+ influx and contraction.

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15
Q

what can you target to lower blood pressure?

A

L type calcium channels.

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16
Q

structure of NT and precursors?

A

slides from lecture 8?

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17
Q

describe the ASCOT trial

A

compared amlodipine (L type calcium channel inhibitor) with atenolol (beta adrena receptor antagonist) - old drug.

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18
Q

benefits of amlodipine?

A

BP controlled.
reduced incidence of associated CV disease.

proved calcium antagonists should replace older treatments.

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19
Q

what is a diuretic?

A

osmotic diuretics - ie mannitol
loop diuretics - ie frusemide, bumetanide
thiazide diuretics - ie bendroflumethiazide, chlortalidone

increases urine output.

increase excretion of Na+, Cl- and water.
the pattern of electrolyte excretion varies.
effects can be additive or synergistic.

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20
Q

what are the benefits of diuretics?

A

intracellular salt and water loss
arterial dilation –? decrease BP
can treat oedema (fluid build up) in the lungs (pulmonary oedema).

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21
Q

how do osmotic diuretics work?

A

ie mannitol. given IV (direct to bloodsteam)
filtered at the glomerulus but not reabsorbed.
ends up in urine, can’t be taken out.
exerts high osmotic pressure, helps water be retained in the urine, less water reabsorption.

only diuretic to act outside nephron.
3 toilets

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22
Q

what is a synergistic effect?

A

the two effects accentuate each other to be larger than each of them individually

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23
Q

benefits of mannitol?

A

treatment of renal failure.

reduces intracranial, intraoccular (eyes) pressure.

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24
Q

describe loop diuretics.

A

ie. frusemide/furosemide, bumetanide

act by inhibiting Na+/K+/2Cl- cotransporters in the ascending loop of henle.
salt is retained in the urine, water stays with it.
water not absorbed from the descending loop.

5 toilets

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25
Q

what are the benefits of loop diuretics?

A

heart failure.
pulmonary oedema
renal failure

all involve salt and water overload.

hypertension with renal failure??

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26
Q

describe thiazide diuretics.

A

ie. bendroflumethiazide, chloralidone.

act by inhibiting Na+/Cl- cotransport in distal convoluted tubule.

Increased NaCl passed to more distal segments.
Less difference in osmolality between urine and plasma.
Lesser ability to reabsorb water in more distal portions.

2 toilets

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27
Q

what are uses for thiazide diuretics?

A

Oedema due to heart failure
Hypertension (lower doses)
Initial effects due to diuresis
Later, get vascular effect

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28
Q

what is hypokalaemia?

A

One of the major unwanted effects of the loop diuretics and the thiazides is potassium loss. This happens because much more Na+ is passed to distal parts of the nephron. In the principal cells, this Na+ is reabsorbed, leading to a more negative potential in the lumen. This will cause the movement of K+ into the lumen, which will quickly be flushed away by the higher volume of urine. Hypokalemia is potentially fatal, and can also increase the effects and side effects of many drugs (some of which are commonly used in patients with cardiac disorders).

Increased NaCl passed on to collecting duct increases transport across PRINCIPAL cells.
Increases lumen –ve potential leading to K+ loss.
Increased volume of urine: increased flushing of K+.

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29
Q

how can you counter hypokalaemia?

A

potassium sparing diuretics.
stop Na+ movement across principal cells.
decreases the flushing effect.

very weak, 1 toilet. used in combo with other diuretics.
ie spironolactone, amiloride, triaterene

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30
Q

what is aldosterone?

A

aldosterone - steroid produced by the adrenal cortex.

increases sodium absorption/potassium loss by increasing no of Na+ channels.

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31
Q

describe spironolactone.

A

aldosterone antagonist.

less potassium lost

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32
Q

describe amiloride and triamterene

A

block sodium channels in lumenal membrane.

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33
Q

describe the slow compensatory system.

A

seperate to para and sympathetic.
works through angiotensin and aldosterone. together increase blood pressure.
works through the kidneys and vasculature.

34
Q

describe aldosterone

A

salt and water balance.

35
Q

describe angiotensin

A

heart and vasoconstriction, also creates aldosterone.

36
Q

what is renin?

A

controls adosterone and angiotensin, enzyme. produced near the kidneys.

37
Q

describe the physiological role of aldosterone.

A

Acts on specific receptors in collecting duct/tubule.
Aldosterone (mineralocorticoid) increases sodium absorption by

genomic effects

  • increasing number of Na+/K+ ATPases
  • increasing number of Na+ channels

non-genomic effects
-stimulating Na+ channels via protein mediator

lose potassium and salt, increased salt in the blood so blood pressure goes up.

38
Q

what is the pre cursor to angiotensin?

A

angiotensinogen, plasma globulin (found in the blood).

tail is cleaved off by renin

39
Q

Describe the renin angiotensin system.

A

Renin itself is a protease that cleaves the precursor of angiotensin, angiotensinogen to produce angiotensin I. This decameric peptide is inactive, but is further acted upon by the enzyme angiotensin converting enzyme (ACE) to produce the active octomer, angiotensin II. Angiotensin II binds to two main receptors (we will talk more about these later). The most important one is the AT receptor type 1 (AT1R). This receptor stimulates aldosterone release from the adrenal cortex and causes vasoconstriction.

Angiotensin II and III bind to AT1R (GPCR, angioyensin II type 1 receptor). present in adrenal cortex, releases aldosterone and causes vasoconstriction.

40
Q

what are the ways to interfere with the renin angiotensin system?

A

aldosterone
blocking renin
blocking ACE
antagonising the AT1R receptor

41
Q

where is renin secreted from?

A 
juxtaglomerular apparatus (cells next to the glomerulus) (kidney)
secreted into circulation.
42
Q

Describe the tissue distribution of ACE.

A

found in many tissues, local production of angiotensins.

43
Q

What is renin stimulated by?

A

Its release can be stimulated by adrenaline, other hormones, prostacyclins, decreased blood pressure in the kidney and decreased Na+ in the distal convoluted tubule.

44
Q

describe Renin inhibitors.

A

Aliskiren, if Renin is shut off we don’t get angiotensin made, this reduces secretion of aldosterone and reduce vasoconstriction - lower bp.

45
Q

describe ACE inhibitors.

A

angiotensin I cannot be converted to angiotensin II, ATI is inactive.

catopril, enalapril, ramipril.

46
Q

what are the side effects of ACE inhibitors?

A

cough caused by bradykinin (peptide hormone broken down by ACE, causes vasodilation so beneficial to remove, but also causes cough).

47
Q

Describe Captopril

A

first ACE inhibitor.
Found from snake.
brazillian pit fighter venom decreases blood pressure, captopril is a synthetic version of that venom.

used in HIV research ??

48
Q

how does ACE work?

A

AT1R is GPCR, binds angiotensin II which causes vasoconstriction effects.

49
Q

Describe Angiotensin II antagonists.

A

Iosartan, valsartan, candesartan.

hypotension but no cough.

50
Q

what is AT2R involved with?

A

growth and development, GPCR

51
Q

How are adrenoceptors divided?

A

alpha and beta.

A1 - vasoconstriction/increase BP. contract visceral smooth muscle.
relax GI tract.

A2 - releases insulin.

B1 - controls blood pressure.

B2 - controls diameter of bronchioles.
vasodilation/decrease BP.

B3 - stimulates breakdown of fat.

52
Q

learn the agonists and antagonists for Alpha and beta adrenoceptors.

A

slides lecture 13

53
Q

what is the main use of phentolamine?

A

Alpha adrenoceptor antagonist, used to treat phaeochromocytoma (tumours of the adrenal medulla) until surgery can occur.

phenoxygenzamine also used during surgery.

54
Q

Describe how phentolamine can cause reflex tachycardia.

compare this to prazosin

A

Both alpha 1 and alpha two receptors are involved in the control of blood pressure. Alpha 1 are present on blood vessels and activating these lead to vasoconstriction, so inhibiting them will produce clinically useful vasodilation. As we have heard, the fall in blood pressure that results will lead to a reflex attempt by the body to increase the heart rate: reflex tachycardia. This effect is mediated by beta1 adrenoceptors in the heart. Alpha 2 receptors are also present at these cardiac synapses where they act as inhibitory AUTORECEPTORS. They regulate the amount of noradrenaline released at synapses. Inhibiting these receptors with phentolamine (which acts on alpha 1 and alpha 2) will allow too much noradrenaline to be released, and this in turn will activate a large number of beta 1 receptors in the heart leading to unacceptable reflex tachycardia.

Prazosin on the other hand, does not act at the alpha 2 receptors so the regulatory mechanism for noradrenaline release remains intact. This keeps the reflex tachycardia to an acceptable level.

55
Q

describe prazosin

A

Dilates arterioles and veins by blocking alpha1 -adrenoceptors.

Used where other therapy has proved ineffective or
unacceptable.

can cause urinary incontinence and retrograde ejaculation.

56
Q

what is a beta blocker?

A

competitive antagonist at beta adrenoceptors.
propranolol, atenolol, metaprolol.

Beta1 adrenoceptors are present in many tissues and inhibiting them can affect blood pressure in different ways. The two most important are in the heart and kidney. Only lipid soluble drugs will act on the central mechanisms. In the heart, beta blockers will reduce both the heart rate and stroke volume, resulting in a decrease in cardiac output. This will, of course, reduce the blood pressure. We will come back to these actions in the heart in our lectures on antidysrhythmic drugs and antianginal drugs. In the kidney beta1 receptors regulate renin release.. Beta blockers can also reduce some of the symptoms of acute anxiety: primarily those due to increased heart rate. They are sometimes prescribed for this purpose and sometimes abused for it by medical professionals (before that “big presentation”!)

57
Q

describe propranolol

A

competetive antagonist.

It does not select between beta 1 and beta 2 which can cause problems. It is able to penetrate the CNS since it’s lipid soluble it can act on central blood vessel control as well as in the periphery. However, it can also cause CNS disturbances.

58
Q

describe atenolol and metoprolol.

A

Atenolol is a newer drug that is more selective for beta1 receptors. It does not penetrate the CNS well. Metoprolol has the selectivity of atenolol but is lipophilic like propranolol (can penetrate CNS)

59
Q

What are side effects of beta blockers?

A 
Bronchoconstriction.
cardiac failure
hypoglycaemia (blood sugar low)
cold extremities - Raynaud's phenomenon. fingers turn white.
vivid dreams.
60
Q

What are side effects of beta blockers?

A 
Bronchoconstriction.
cardiac failure
hypoglycaemia (blood sugar low)
cold extremities - Raynaud's phenomenon. fingers turn white.
vivid dreams. not for atenolol.
61
Q

What are side effects of beta blockers?

A

Bronchoconstriction.
cardiac failure
hypoglycaemia (blood sugar low)
cold extremities - Raynaud’s phenomenon. fingers turn white.
vivid dreams. not for atenolol. if lipid soluble can cross into brain.

62
Q

What are side effects of beta blockers?

A

Bronchoconstriction.
cardiac failure
hypoglycaemia (blood sugar low)
cold extremities - Raynaud’s phenomenon. fingers turn white.
vivid dreams. not for atenolol. if lipid soluble can cross into brain.

Beta blockers are not without unwanted effects, some of which can be very serious. The lipid solubility of propranolol can induce vivid dreams due to its penetration of the CNS. This does not happen with atenolol. Reduced cardiac output can reduce the blood supply to the legs causing pain in walking – claudication. This reduction in cardiac output can also induce heart failure in patients who already have compromised cardiac output - although it was traditional wisdom that beta blockers were detrimental for people with cardiac failure, it has been found that with some drugs ramping them in slowly can produce beneficial effects. Not all beta blockers are effective though. One beta blocker that is commonly used for this purpose is carvedilol. The reason why carvedilol (and not all beta blockers) works for heart failure is not entirely clear, but it is a relatively non-selective drug with actions at alpha adrenoceptors as well as beta adrenoceptors. It also has less inverse agonist activity at beta adrenoceptors than other beta blockers.
In the periphery, antagonist actions of non selective beta blockers e.g. propranolol at beta 2 adrenoceptors can cause Raynaud’s phenomenon: temporary vasospasm, resulting in cold, numb and discoloured fingers and toes (see picture). Raynaud’s phenomenon can be treated using vasodilating drugs such as ACE inhibitors, ATII antagonists or dihydropyridines.
In asthmatic patients or people with other lung diseases, the lack of selectivity of beta blockers can cause big problems. Beta2 receptors in the bronchial tract can become blocked, either precipitating an asthma attack or stopping the effects of salbutamol (used as a treatment for asthma).
Finally, diabetic patients often experience major sympathetic activation when they are becoming hypoglycaemic.

63
Q

what is a thrombosis?

A

a blood clot in an inappropriate place.

64
Q

what is deep vain thrombosis?

A

long haul flights.

65
Q

what is fibrin?

A

makes up blood clots with aggregated platelets and trapped RBCs.

66
Q

what are the effects of thrombois?

A

impede blood flow,
reduce perfusion of tissues,
can cause a heart attack

67
Q

what is a venous thrombosis?

A

in veins, coagulation has a major role.

68
Q

what is arterial thrombosis?

A

in arteries, platelet aggregation is more important than coagulation.

69
Q

what is coagulation?

A

formation of the fibrin network.

?

70
Q

what is an embolus?

A

fragment or whole thrombus detached from vessel wall, when it reaches a point that is too small to pass through it causes blockage. The point is called the embolus.

71
Q

what is a pulmonary embolism?

A

lungs from venous thrombus.

72
Q

what is an infarction?

A

tissue which is deprived of oxygen and thus damaged.

73
Q

why is inhibiting thrombus formation difficult?

A

don’t want to interfere with normal haemostasis.

don’t want patient to bleed to death.

74
Q

what are the targets for modifying coagulation and platelet aggregation?

A

coagulation - venous
platelet - arterial

if fails breakdown the thrombus.

75
Q

describe the clotting cascade.

A

coagulation.

damage to a blood vessel is detected.
this produces fibrin.

anticoagulants prevent the formation of fibrin from fibrinogen.

76
Q

describe fibrin

A

made from fibrinogen.

insoluble, forms a mesh work.

77
Q

describe fibrin

A

made from fibrinogen, enzyme thrombin.

insoluble, forms a mesh work.

78
Q

describe thrombin

A

prothrombin is precursor.

enzyme for fibrinogen –> fibrin.

79
Q

describe heparin

A 
suplhated mucopolysaccharides (ununiform).
has a high -ve charge.
present in the liver, lungs naturally.

3-40K molecular weight.
enoxoparin has low MW.

80
Q

describe heparin

A 
suplhated mucopolysaccharides (ununiform).
has a high -ve charge.
present in the liver, lungs naturally.

3-40K molecular weight.
enoxoparin has low MW.

inhibits action of thrombin.
requires antithrombin III (binds to thrombin) heparin aids antithrombin III.

81
Q

describe the action of heparin.

A

makes anti thrombin III and thrombin bind

82
Q

initial treatment for hypertension?

A

ACE inhibitors - losartan

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