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MVST1B MODA > Cardio renal L6 > Flashcards

Cardio renal L6 Flashcards

1
Q

the water-permeability of the collecting duct is under the control of …

A

the water-permeability of the collecting duct is under the control of ADH (antidiuretic hormone, otherwise known as vasopressin, arginine vasopressin or AVP).

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2
Q

with out ADH - describe the permeability of the collecting duct - and how this facilitates dilute urine?

A

lack of ADH makes collecting duct impermeable.

Na+ actively pumped out, without water following = dilute urine

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3
Q

Diuretics do what?

A

Diuretics cause an increase in urine output

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4
Q

how do diuretics increase urine output?

A

All diuretic drugs increase Na+ excretion (this phenomenon is called ‘natriuresis’), as Na+ enters the lumen of the renal tubule water follows to maintain osmotic equilibrium

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5
Q

bothdiuretics and drinking fack loads of water increase urinary output - whats the differnece?

A

drinking: urine = mainly water, solute excretion is not increased
diuretics: both solute and water excretion are increased

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6
Q

overall end effect of diuretics?

A

As diuretic therapy leads to loss of Na+ and water, their effect is to reduce the volume of the body’s extracellular fluid (ECF) compartment.

This results in alleviation of oedema, reduction of blood volume, and as a result these drugs are useful in the treatment of heart failure and/or hypertension.

They can also be useful in maintaining kidney function in various renal diseases.

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7
Q

The sites of action in the nephron of the different types of diuretic drugs

A
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8
Q

where do loop diuretics act?

A

the loop of henle

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9
Q

are loop diuretics powerful?

A

yes - called high ceiling diuretics as they can cause upto 4 litres per day of urine excretion

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10
Q

2 main loop diuretics?

A

The main drugs are furosemide and bumetanide - they are sulphonamides (like some antibacterial drugs)

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11
Q

how do loop diuretics work?

A

loop diuretics block Na+-K+-2Cl- co-transport in the apical (luminal) membrane of cells of the thick ascending limb

can cause 15-20% of filtrate to be excreted

very powerful

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12
Q

diuretics are mainly used to treat ?

why?

A

acute heart failure

as well as diuresis furosemide also causes venodilation and thus reduces atrial filling pressure. This venodilator mechanism also increases the effect of furosemide on the nephron by increasing renal blood flow without a change in GFR, i.e. by decreasing the fraction of the blood flow that is filtered at the glomer

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13
Q

give some problems with loop diuretics?

A
  • continued administration can lead to hypokalaemia
  • Concurrent metabolic alkalosis (as a result of increased H+ loss into filtrate partly as a result of enhanced Na+/H+ exchange and partly due to stimulated renal synthesis of NH3 and secretion as NH4+).
  • Ca2+ and Mg2+ loss increased
  • Uric acid excretion in urine is decreased - can lead to gout
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14
Q

which are the most common Thiazide diuretics

A

hydrochlorothiazide and bendroflumethiazide.

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15
Q

Like loop diuretics thiazides can produce some inhibition of ….

A

Like loop diuretics thiazides can produce some inhibition of carbonic anhydrase

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16
Q

thiazide diuretics compared to high cieling diuretics?

A

They have a lesser effect than high-ceiling loop diuretics, but can still result

in the loss of 10 to 15% of the filtered load

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17
Q

where do thiazide diuretics act?

A

act in the cortical segment of the thick ascending limb or in the distal tubule

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18
Q

how do thiazide loop diruetics work

A

location: cortical segment of the thick ascending limb or in the distal tubule.

early distal tubule: by blocking Na+-Cl- cotransport, probably by binding at the Cl- site

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19
Q

like loop diuretics, thiazides also have ______ effects.

A

like loop diuretics, thiazides also have vasodilator effects.

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20
Q

describe gout?

A

The symptoms of gout result from excessive production of purines leading to deposition of sodium urate crystals in the synovial tissue of joints.

The condition is treated with probenecid, which competes for the same carrier as uric acid in the proximal tubule and thereby inhibits uric acid reabsorption.

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21
Q

describe Diazoxide

A

Diazoxide is a non-diuretic thiazide which has vasodilator action.

It acts by opening ATP-sensitive K+ channels and is used as an antihypertensive- but only in hypertensive emergency.

Opening of ATP-sensitive K+ channels in pancreatic ß cells produces hyperpolarisation and inhibition of insulin release leading to a rise in blood glucose.

Thiazides increase blood glucose levels and this may reflect their ability to open ATP-K+ channels.

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22
Q

Potential problems with thiazides?

A
  • Hypokalaemia and metabolic alkalosis (as for furosemide)
  • The average fall in plasma K+ is reported to be 0.7 mM. This is quite significant and would be a problem if thiazides were combined with cardiac glycosides in therapy for heart failure as described (under ‘ heart failure’) above, lower plasma K+ can potentiate action of cardiac glycosides, which compete with K+ for binding to the Na+/K+-pump
  • Thiazides increase Mg2+ excretion, but decrease that of Ca2+
  • Uric acid excretion is also decreased
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23
Q

Thiazides _______ Mg2+ excretion, but _______ that of Ca2+

A

Thiazides increase Mg2+ excretion, but decrease that of Ca2+

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24
Q

give the main drugs in Potassium-sparing diuretics

A

amiloride, triamterene and spironolactone

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25
Q

As their name implies Potassium sparing diuretics do not have the side-effect of ______ loss that occurs with loop diuretics and thiazides

A

As their name implies these drugs do not have the side-effect of potassium loss that occurs with loop diuretics and thiazides

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26
Q

potasssium sparing diuretics depend on the fact that …

A

t in the late distal tubule Na+ enters cells through a channel in the apical membrane, down the concentration gradient generated by the Na+-K+ ATPase pump in the basolateral membrane. K+ or H+ are drawn into the lumen by the potential gradient across the apical membrane (which in turn is created by Na+ movement). This is a major site of K+ loss into the urine.

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27
Q

how do Amiloride and triamterene work?

A

Amiloride and triamterene prevent Na+ reabsorption by blocking apical trimeric Na+ channels

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28
Q

how do

Spironolactone and canrenone work?

A

Spironolactone and canrenone act as antagonists of the action of aldosterone.

block aldosterone = decreased membrane sodium conductance

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29
Q

can Potassium-sparing diuretics be used with thiazides or loop diuretics to counteract hypokalaemia?

A

yep!

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30
Q

Spironolactone is metabolised to _______ in the liver.

A

Spironolactone is metabolised to canrenone in the liver.

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31
Q

how does aldosterone increase apical membrane sodium conductance?

A

The release of aldosterone is induced by angiotensin II (see below). Aldosterone migrates across the cell membrane into the cell and there combines with the cytoplasmic steroid receptor. The whole complex is translocated to the nucleus where it leads to synthesis of Na+ channels and Na+-K+ ATPase pumps.

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32
Q

The effect of spironolactone is only significant when distal tubule cells are under the influence of ______.

A

The effect of spironolactone is only significant when distal tubule cells are under the influence of aldosterone.

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33
Q

why is the rate of onset for spironolactone so slow?

A

Because the mechanism depends on the turnover of Na+ channels, the rate of onset of diuresis produced by spironolactone is slow.

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34
Q

Carbonic anhydrase inhibitors: give a major example

A

Acetazolamide

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35
Q

The carbonic anhydrase inhibitors were the first diuretics to be introduced but are now, to all intents and purposes ______.

A

The carbonic anhydrase inhibitors were the first diuretics to be introduced but are now, to all intents and purposes obsolete.

36
Q

how do carbonic anhydrase inhibitors work?

A
  • work only in proximal tubule
  • Carbonic anhydrase inhibitors decrease the availability H+ in the cell
  • This is because 33% of proximal tubule Na+ reabsorption occurs in exchange for H+ (through the Na+-H+ antiporter)
  • The urine pH rises as HCO3- content is increased (Na+ excreted as the major counterion)
37
Q

It is necessary to block more than ___% of carbonic anhydrase to produce an appreciable effect.

A

It is necessary to block more than 99% of the enzyme to produce an appreciable effect.

38
Q

carbonic anhydrases are still used to treat what?

A
  1. glaucoma is a result of raised intraocular pressure which can lead to blindness. The carbonic anhydrase inhibitors suppress HCO3- secretion, which is part of the process of formation of aqueous humour in the eye.
  2. Acetazolamide can be used to help acclimatisation to high altitudes and can guard against mountain sickness and help to alleviate sleep apnoea that can occur at high altitudes.
39
Q

T o rF

he actions of carbonic anhydrase inhibitors are self-limiting because excess HCO3- loss results in metabolic acidosis.

A

True

40
Q

classic example of osmotic diuretics?

A

mannitol

41
Q

are osmotic diuretics the simplest?

A

in their action, yes

42
Q

how do osmotic diuretics work

A
  1. Low molecular weight substances filtered at the glomerulus, but not reabsorbed
  2. They retain their osmotic equivalent of water and so increase urine volume.
  3. They decrease Na+ reabsorption in the proximal tubule as concentration is lowered
  4. Acutely mannitol rapidly reduces intracranial and intraocular pressure and so is useful in cerebral oedema
43
Q

does mannitol cross the BBB?

A

no

44
Q

why are diuretics useful for treating hypertension?

A

Their effectiveness in hypertension is because blood pressure is a function of the cardiac output and the total peripheral resistance. If either of these factors is altered, the blood pressure changes in the same direction. A reduction in circulating fluid volume reduces blood pressure.

45
Q

lebel the control of BP diagrma:

A
46
Q

BP diagram label

A
47
Q

Aldosterone is secreted from the ….

A

Aldosterone is secreted from the zona glomerulosa of the adrenal cortex.

48
Q

Renin release is induced by ….

A

Renin release is induced by a reduction in perfusion pressure to the kidneys and by sympathetic nerve stimulation

49
Q

Renin is released from cells of the ….

A

Renin is released from cells of the juxtaglomerular apparatus as a result of the rise in intracellular cAMP

50
Q

Sympathetic stimulation of the juxtaglomerula apparatus causes….

A

Sympathetic stimulation causes a rise in cAMP and of renin release

51
Q

Renin release is reduced by….

A

Renin release is reduced by adenosine, atrial natriuretic peptide (ANP) and by negative feedback by angiotensin II

52
Q
A
53
Q

describe ACE inhibitors

A

Antagonism of the renin-angiotensin system is mainly achieved by ACE inhibitors.

54
Q

ACE inhibitor exmaples?

A

common examples

are ramipril, followed by lisinopril and perindopril (the latter a pro-drug)

55
Q

Saralasin - what does it do?

A

Saralasin is an angiotensin II partial agonist , but it is a peptide and so not suitable for oral administration and so is not really competitive with other antihypertensive drugs.

56
Q

T or F

Some people cannot tolerate ACE inhibitors

A

T

57
Q

what losartan?

A

Non-peptide angiotensin II antagonists

which works on the AT1 angiotensin II

receptor)

58
Q

descibe what AT2 receptors do?

A

Activation of AT2 receptors causes vasodilatation by generation of nitric oxide with a subsequent increase in cGMP, and binding of angiotensin II to AT2 receptors inhibits, in certain cells, proliferation, mediates differentiation in neural tissue, and can induce apoptosis.

59
Q

ACE inhibitors are almost always combined with ….

A

ACE inhibitors are almost always combined with diuretics.

60
Q

cardiovascular role of AT2 receptors?

A

insifnificant

61
Q

ACE inhibitors are used for ….

A

ACE inhibitors are used for hypertension and congestive heart failure

62
Q

Theoretically ACE inhibitors should be of most benefit in heart failure associated with ____ renin levels.

A

Theoretically they should be of most benefit in heart failure associated with high renin levels.

63
Q

For treatment of heart failure ACE inhibitors _______ pre- and afterload

A

For treatment of heart failure ACE inhibitors decrease pre- and afterload

64
Q

T or F

the failing heart leads to activation of renin-angiotensin system

A

T

65
Q

ACE inhibitors are almost always combined with …..

A

ACE inhibitors are almost always combined with diuretics.

The reduction in aldosterone should, in principle, help to avoid hypokalaemia

66
Q

why is hypotension dangerous wiht any ACE inhibitor?

A

Hypotension is dangerous with any ACE inhibitor, since the risk of renal failure is increased by the blockade of glomerular efferent arteriolar constriction which is normally mediated by angiotensin II.

67
Q

net result for ACE inhibitors

A

The net result is a reduction in vascular resistance, not blood pressure (a compensating increase in cardiac output tends to maintain blood pressure)

68
Q

Aliskiren…. does hwat>

A

Aliskiren is a renin inhibitor

69
Q

Angiotensin II and angiotensin III exhibit_______ affinity(s) for type 1 and type 2 angiotensin II receptors (AT1 and AT2)

A

Angiotensin II and angiotensin III exhibit the same affinity for type 1 and type 2 angiotensin II receptors (AT1 and AT2)

70
Q

Intracerebroventricular injection of either Angiotensin II or III causes ….

A

Intracerebroventricular injection of either peptide causes a similar increase in vasopressin release and blood pressure

71
Q

In vivo, angiotensin II is converted to angiotensin III (by the action of ….

A

In vivo, angiotensin II is converted to angiotensin III (by the action of brain aminopeptidase A)

72
Q

Angiotensin IV acts in the….

A

Angiotensin IV acts in the brain, where it seems to be involved in learning, memory and long-term potentiation

73
Q

where are AT4 receptors located?

A

AT4 receptors are located widely, not just in the brain and their activation has been proposed as a strategy for memory enhancement, particularly in Alzheimer’s disease.

74
Q

describe Bradykinin

A

Bradykinin is a short peptide released from various cells

Bradykinin is a potent natriuretic agent and a renal vasodilator

Bradykinin is degraded by angiotensin converting enzyme

75
Q

If very high Na+ reaches the distal tubule, then ________ is released, bradykinin is formed from kinogen and Na+ reabsorption inhibited

A

If very high Na+ reaches the distal tubule, then kallikrein is released, bradykinin is formed from kinogen and Na+ reabsorption inhibited

76
Q

Under normal physiological conditions the role of the kallikrein-kinin system may be _______,

A

Under normal physiological conditions the role of the kallikrein-kinin system may be minimal,

77
Q

Bradykinin - other effects?

A

Bradykinin is an inflammatory mediator and nociceptive agent

most pain inducing agent known

78
Q

might bradykinin be the cause of ACE inhibitors bad side effects?

A

It may be that cause of the ‘dry cough’ seen with some ACE inhibitors

79
Q

do ACE inhibitors lead to bradykinin buildup?

A

yes

80
Q

ANP is released from ______ in response to ….

A

ANP is released from heart in response to atrial stretch

81
Q

ANP acts via?

A

It acts via a membrane-bound guanylate cyclase (GC-A) receptor to form cGMP

82
Q

Responses to ANP are directed towards?

A

Responses are directed towards a reduction of blood pressure and blood volume (i.e. the reverse of those of the renin-angiotensin system

83
Q

t or F

ANP is a directly-acting vasodilator, and it also reduces release of noradrenaline.

A

T

84
Q

ANP stimulates diuresis and natriuresis by increasing GFR and inhibition of Na+ absorption in the collecting duct.

A

T

85
Q

does ANP inhibit renin releasE?

A

yep

86
Q

drugs influencing ANP?

A

There are no useful drugs acting to influence ANP (or its receptors) and there is no clear evidence that a defect of this system is involved in any form of hypertension, but mice lacking the GC-A gene are hypertensive (which is not made worse by a high-salt diet).

87
Q

fat

A

mamba

MVST1B MODA (22 decks)

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