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Biomedical Sciences BS22001 > ❤️ > Flashcards

❤️ Flashcards

1
Q

adventitial layer

A

connective tissue

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2
Q

medial layer

A

smooth muscle tissue

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3
Q

intimal layer

A

endothelial cells

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4
Q

elastic artery (% composition)

A

arteries: ELective Can Surely Educate

elastic tissue > connective tissue > smooth muscle > endothelium

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5
Q

arteriole (% composition)

A

arterioles like to perform SCEEnes

smooth muscle > connective tissue > elastic tissue & endothelium [both 10%]

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6
Q

capillary (% composition)

A

95% endothelium

5% basal lamina (connective tissue)

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7
Q

venule (% composition)

A

Venules Can be like ENdangered blue Snakes🐍🐍🐍
connective tissue > endothelium & smooth muscle [both 20%]
NO elastic tissue [0%]

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8
Q

vascular tone (def.)

A

a state of partial constriction (displayed by arteriolar smooth muscle)

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9
Q

vascular tone is affected by:

A

myogenic activity

sympathetic activity

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10
Q

vascular tone is important because… [tonic]

A

tonic activity makes it possible to decrease / increase contractile activity (vasodilation/vasoconstriction)

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11
Q

flow rate depends on…

A

the pressure difference (ΔP)

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12
Q

resistance to blood flow depends upon 3 factors:

A

blood viscosity Ƞ
vessel length L
VESSEL RADIUS r

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13
Q

2-fold change in vessel radius will produce…

A

a 16-fold change in flow

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14
Q

a slight change in radius…

A

brings about a notable change in flow

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15
Q

🔼activity in the sympathetic nerves to the ❤️…

A

🔼 HR (tachycardia)

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16
Q

🔼activity in the parasympathetic nerves to the ❤️…

A

🔽HR (bradycardia)

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17
Q

🔼HR

A

tachycardia

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18
Q

🔽HR

A

bradycardia

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19
Q

PSNS (vagus nerve) releases…

A

acetylcholine (ACh; muscarinic receptors)

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20
Q

SNS releases…

A

noradrenaline (NorAd, US: norepinephrine; β1-adrenergic receptors)

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21
Q

ACh and NorAd alter the activity of the ________ in the innervated cardiac cells

A

cAMP 2nd messenger pathway

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22
Q

ACh is coupled to ___(1)___ G-protein that ___(2)___ activity of the cAMP pathway

A

(1) an inhibitory

(2) reduces

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23
Q

NorAd is coupled to ___(1)___ G-protein that ___(2)___ the cAMP pathway

A

(1) a stimulatory

(2) accelerates

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24
Q

PSNS 🔽 HR through 2 effects on pacemaker tissue:

A

1) Hyperpolarisation of the SA node membrane (takes longer to reach threshold)
2) 🔽 the rate of spontaneous depolarisation

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25
Q

ACh increases K+ permeability by…

A

slowing the closure of K+ channels

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26
Q

PS stimulation ________ (🔼/🔽) the AV node’s excitability which _________ (prolongs/shortens) transmission of impulses to the ventricles

A

🔽

prolongs

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27
Q

PS stimulation ________ (shortens/elongates) the plateau phase of the AP in atrial contractile cells, _________ (weakening/strengthening) atrial contraction

A

shortens

weakening

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28
Q

PS stimulation has _____ (no/little/big) effect on ventricular contraction

A

little

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29
Q

overall, PS stimulation causes:

  • _______ HR
  • _______ time between atrial and ventricular contraction
  • _______ (stronger/weaker) atrial contraction
A

🔽
🔼
weaker

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30
Q

SNS’s main effect on the ❤️ is to ______ (speed up/slow down) depolarisation, so threshold is reached more _______ (rapidly/slowly)

A

speed up

rapidly

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31
Q

NorAd auguments ____ and ____ channel activity

A

If (lower case ‘f’; funny current)

T-type

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32
Q

SNS stimulation of the AV node _____ (🔼/🔽) AV nodal delay by ______ (🔼/🔽) conduction velocity

A

🔽

🔼

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33
Q

SNS _____ (speeds up/slows down) the spread of the AP throughout the specialised conduction pathway

A

speeds up

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34
Q

SNS _____ (🔼/🔽) contractile strength of the atrial and ventricular contractile cells (heart beats _______ (more/less forcefully) and squeezes out _____ (less/more) blood)

A

🔼
more forcefully
more

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35
Q

SNS _____ (🔼/🔽) Ca2+ permeability through prolonged opening of _________ channels

A

🔼

L-type Ca2+

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36
Q

SNS ________ (speeds up/slows down) relaxation

A

speeds up

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37
Q

The overall effect of SNS stimulation on the ❤️ is to improve its effectiveness as a pump by:
__ (🔼/🔽) HR
__ (🔼/🔽) the delay between atrial and ventricular contraction
__ (🔼/🔽) conduction time through the heart
__ (🔼/🔽) the force of contraction
__ (⏮/⏭) the relaxation process so that more
time is available for filling

A 
🔼 HR
🔽 the delay
🔽 conduction time
🔼 the force
⏭ (speeding up) the relaxation process
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38
Q

under resting conditions _____ (PS/S) discharge dominates = vagal tone (___ - ___ bpm)

A

PS (parasympathetic)

~70 - ~100 bpm

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39
Q

HR can be altered by shifting the balance of AN stimulation:

  • HR 🔼 by simultaneously 🔼 ___ and 🔽 ___ activity
  • HR 🔽 by simultaneously 🔼 ___ and 🔽 ___ activity
A

S; PS

PS; S

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40
Q

Activity of the autonomic nervous system is co-ordinated by the ________________, located in the brain stem

A

cardiovascular control centre

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41
Q

The hormone ___________ also exerts an important influence in HR regulation

A

adrenaline (epinephrine)

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42
Q

Adrenaline is released into blood in response to ____________

A

sympathetic stimulation

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43
Q

Hormone adrenaline and noradrenaline (______) 🔼 HR (_______) and force of myocardial contraction (_______)

A

catecholamines
chronotropic action
inotropic action

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44
Q

Adr acts on ❤️ in a ______ (different/similar) manner to NorAd to ____ (🔼/🔽) HR

A

similar

🔼

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45
Q

Adrenaline ______ (lessens/reinforces) the direct effect of the sympathetic nervous system

A

reinforces

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46
Q

The pacemaker potential is regulated by a depolarizing current the ‘funny current’ (If) mediated by channels that are activated by:

(i) ________ and
(ii) ________

A

hyperpolarization

cyclic AMP

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47
Q

cyclic AMP are also known as HCN channels

what does the HCN channel stand for?

A

Hyperpolarization-activated Cyclic Nucleotide gated channel

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48
Q

Hyperpolarization following the action potential activates ___ channels in the ___ node causing a ____ (fast/slow) depolarization aka the pacemaker potential

A

HCN
SA
slow

for full text see p. 83

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49
Q

Block of HCN channels ______ (🔼/🔽) the slope of the pacemaker potential and ______ (🔼/🔽) heart rate

A

🔽 [decreases]

🔽 [reduces]

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50
Q

________ is a selective blocker of HCN channels that is used to _____ (🔼/🔽) heart rate in angina
_____ (🔼/🔽) rate ______ (🔼/🔽) O2 consumption

A

Ivabradine
🔽
🔽
🔽

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51
Q

angina

A

a condition in which coronary artery disease reduces the blood supply to cardiac muscle

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52
Q

β-adenoreceptor agonists (3)

A

Dobutamine, adrenaline and noradrenaline (catecholamines)

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53
Q

Pharmacodynamic effects of β-adenoreceptor agonists on ❤️:
___ (🔼/🔽) force, rate and cardiac output (i.e. HR x SV) and O2 consumption
___ (🔼/🔽) cardiac efficiency (O2 consumption___ (🔼/🔽) more than cardiac work)
____ (✅/❌) cause disturbances in cardiac rhythm (arrhythmias)

A

🔼
🔽
✅

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54
Q

clinical uses of adrenaline (3)

A
  • cardiac arrest
  • emergency treatment of asthma
  • anaphylactic shock
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55
Q

clinical uses of dobutamine (1)

A

(selective for 1-adrenoceptors)

acute, but potentially reversible, heart failure (e.g. following cardiac surgery, or cardiogenic shock)

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56
Q

cardiac arrest

A

sudden loss of pumping function

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57
Q

anaphylactic shock

A

life threatening respiratory distress and often vascular collapse

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58
Q

Pharmacodynamic effects of β-adenoreceptor antagonists on ❤️ depend upon the degree to which ___ is activated

A

the SNS

59
Q

Antagonists may block β-adrenoceptors __________ [how?] in a competitive manner

A

non-selectively or selectively (e.g. β1)

60
Q

Antagonists may possess…

A

partial AGONIST activity😱

61
Q

Pharmacodynamic effects of propranolol:

  • At rest (normal subjects) - _____ (no/little/big) effect on rate, force, CO or MABP
  • During exercise, or stress, rate, force and CO are significantly _______ (going up/depressed) - _______ (increase/reduction) in maximal exercise tolerance
  • Coronary vessel diameter marginally _______ (increased/reduced) (β2-adrenoceptors mediate vasodilatation in small coronary vessels, but !myocardial O2 requirement falls even further!, thus _____(worse/better) oxygenation of the myocardium)
A 
little
depressed
reduction
reduced
better
62
Q

propranolol [features,e.g. agonist/antagonist, what channel affected?]

A

non-selective β-blocker, antagonist of β1 and β2

63
Q

metoprolol [features,e.g. agonist/antagonist, what channel affected?]

A

selective β1-blocker

64
Q

atenolol [features,e.g. agonist/antagonist, what channel affected?]

A

selective β1-blocker

65
Q

metoprolol and atenolol

Have advantages because ______ is/are little affected

A

β2-adrenoceptors

66
Q

Excessive sympathetic activity associated with stress or disease (e.g. heart failure, myocardial infarction) can lead to… (2)

β-blockers ____ (🔼/🔽) excessive sympathetic drive and help restore normal sinus rhythm (i.e. rhythm driven by the ___ node)

A
  • tachycardia
  • spontaneous activation of ‘latent cardiac pacemakers’ outside nodal tissue

🔽

SA

67
Q

disturbances of cardiac rhythm are collectively all called…

A

dysrhythmias

68
Q

β-adrenoceptor agonists can help in treatment of (3):

A
  • hypertension (HT)
  • angina
  • ❤️ failure
69
Q

Atropine [features,e.g. selective/non-selective, what channel affected?]

A

non-selective muscarinic receptor antagonist

70
Q

Pharmacodynamic effects of atropine:

  • _____ (no/little/big) increase in HR (_______ bradycardia/normal/tachycardia) in normal subjects – more pronounced effect in highly trained athletes (who have increased vagal tone)
  • ______ (no/little/big) effect upon arterial BP (resistance vessels lack a parasympathetic innervation)
  • ______ (no/little/big) effect upon the response to exercise
A

little
no
no

71
Q

Clinical uses of atropine (3):

A
  • reverse bradycardia after MI (MI - vagal tone 🔼)
  • as an addition to anaesthesia
  • in anticholinesterase poisoning (to 🔽 excessive PSNS activity)
72
Q

digoxin

A

a cardiac glycoside that 🔼 contractility of the ❤️

73
Q

heart failure (def.)

A

a CO insufficient to provide adequate tissue perfusion

74
Q

heart failure (causes, treatment)

A
  • many causes, ultimately the ventricular function curve is depressed
  • inotropic drugs (e.g. digoxin, dobutamine) enhance contractility
75
Q 
presence of digoxin v. cell membrane:
Na+/K+ATPase \_\_\_\_\_\_ (opened/blocked)
\_\_\_ (🔼/🔽)[Na]i and \_\_\_ (🔼/🔽) Vm
\_\_\_ (🔼/🔽)Na+/Ca2+ exchange and \_\_\_ (🔼/🔽) [Ca2+]i
\_\_\_ (🔼/🔽)storage of Ca2+ in SR
\_\_\_ (🔼/🔽) of CICR and contractility
A 
blocked
🔼 and 🔽
🔽 and 🔼
🔼
🔼
76
Q

Digoxin binds to the ______ of Na+/K+ ATPase in competition with K+ - effects can be !dangerously! enhanced by low plasma [K+] (hypokalaemia). Particularly important because digoxin has a low T.R. [WHAT’s TR?]

A

α-subunit

77
Q

Digoxin has complex direct and indirect actions on electrical activity

DIRECT

  • ___ (🔼/🔽) the length of AP and refractory period in atrial and ventricular myocytes
  • toxic concentration cause membrane (hyperpolarisation/depolarization/repolarisation) and !oscillatory afterpotentials!
A

🔽

depolarization

78
Q

Digoxin has complex direct and indirect actions on electrical activity

INDIRECT: increased vagal activity (CNS?)
______ (🐢/🐇) SA node discharge
______ (🐢/🐇) AV node conduction
______ (🔼/🔽) refractory period

A

🐢 (slows)
🐢 (slows)
🔼

79
Q

SUMMARY of PS stimulation (PSNS)

  • SA node ______ (🔼/🔽)
  • AV node (nodal delay) 🔼/🔽 nodal delay
  • ventricular conduction pathway (no effect/conduction speed up)
  • atrial muscle - contractility & strength 🔼/🔽?
  • ventricular muscle - contractility & strength 🔼/ no effect
  • veins & venous return
  • adrenal medulla (releasing adrenaline)
A
  • 🔽
  • 🔼
  • no effect
  • contractility & strength 🔽
  • no effect
  • no effect
  • no effect
80
Q

SUMMARY of S stimulation (SNS)

  • SA node ______ (🔼/🔽)
  • AV node (nodal delay) 🔼/🔽 nodal delay
  • ventricular conduction pathway (no effect/conduction speed up)
  • atrial muscle - contractility & strength 🔼/🔽?
  • ventricular muscle - contractility & strength 🔼/ no effect
  • veins & venous return
  • adrenal medulla (releasing adrenaline)
A
  • 🔼
  • 🔽
  • conduction speed up
  • contractility & strength 🔼
  • contractility & strength 🔼
  • reduces capacitance hence increasing venous return
  • 🔼adrenaline release & thus augment effect of symp NS action
81
Q

cardiac cycle

A

the sequence of pressure and volume changes that takes place during cardiac activity

82
Q

mechanical events of the cardiac cycle are caused by…

A

rhythmic changes in cardiac electrical activity

83
Q

SYSTOLE

A

contraction and emptying

84
Q

DIASTOLE

A

relaxation and filling

85
Q

atria and ventricles go through ____ (separate/same) cycles of systole and diastole

A

separate

86
Q

At rest, _____ (systole/diastole) is longer in duration, and accounts for ____ of cardiac cycle

A

diastole

~65% or 2/3

87
Q

at rest 70 ppm
SYSTOLE ____ s
DIASTOLE ___ s

A
  1. 3

0. 55

88
Q

at 200 bpm
SYSTOLE ____ s
DIASTOLE ___ s

A
  1. 15

0. 15

89
Q

formula for max HR

A

max. heart rate = 220 bpm – age in years

90
Q

the valve opens when…

A

the pressure is greater behind it

91
Q

the valve closes when…

A

the pressure is greater in front of the valve

92
Q

a ____________ is the valve that won’t open in the opposite direction even if the the pressure is greater in front of it

A

one-way valve

93
Q

ECG

A

a record of the overall spread of the electrical activity through the ❤️

94
Q

P wave

A

atrial depolarisation

95
Q

PR segment

A

AV nodal delay

96
Q

QRS segment

A

ventricular depolarisation (atria repolarising simultaneously)

97
Q

ST segment

A

time during which ventricles are contracting and emptying

98
Q

T wave

A

ventricular repolarisation

99
Q

TP interval

A

time during which ventricles are relaxing and filling

100
Q

the 5 phases of the cardiac cycle are:

A
  1. passive filling [during ventricular and atrial diastole]
  2. atrial contraction
  3. isovolumetric ventricular contraction
  4. ejection
  5. isovolumetric ventricular relaxation
101
Q

❤️ sounds are generated by…

A

❤️ action

102
Q

❤️ sounds can be detected using a…

A

phonocardiogram

103
Q

LUB sound is produced by… and coincides with the begging of…

A
  • closure of the AV valves

* systole

104
Q

DUB sound is produced by… and begins with the onset of…

A
  • closure of the aortic and pulmonary valves aka semilunar valves
  • diastole
105
Q

what happens during: MID-DIASTOLE
Atrial and ventricular pressures (high/low)
Ventricles contain ___% of final filled volume
Aortic and pulmonary valves ____ (open/closed)
Aortic pressure _____ (low/high)

A

low
~80%
closed
high

106
Q

what happens during: LATE DIASTOLE
___a___ of ECG occurs
Towards end of ___a.___ atria ______ (contract/relax), ______(🔼/🔽) atrial pressure - most of the blood in the atria is propelled into ventricles - adds ______% to ventricular
filling - accompanied by ____ (no/small/big) increase in ventricular pressure

Volume in each ventricle at end of diastole is:
____ ml - standing
____ ml - lying

A 
a. P wave
contract
🔼
~20%
small
~130 ml
~160 ml
107
Q

what happens during: END OF DIASTOLE/EARLY SYSTOLE
____✩____ of ECG begins = start of ventricular ___________ (depolarisation/repolarisation/hyperpolarisation)
ventricles contract at end of ____✩____ = early systole
_____ (slow/rapid) ______ (increase/decrease) in ventricular pressure
AV valves _____ (open up/snap shut), resulting in ________
Ventricles contract but both ____ and _____ are _____ - ____ (all/no) blood can enter or leave
“Isovolumetric or Isometric Phase”

A 
✩ QRS complex
depolarisation
rapid increase
snap shut
first heart sound
AV and aortic valves 
shut
no
108
Q

what happens during: EJECTION PERIOD
Ventricular pressure exceeds arterial pressure aortic and ______ valves open
Blood is ejected into the
_____ and ___❅___
Aortic pressure ____(🔽/🔼) from diastolic minimum of ____ mmHg to systolic peak of ____ mmHg
Corresponding pressures in ___❅____ are ___ mmHg diastolic and
___ mmHg systolic

A 
pulmonary
aorta and pulmonary artery
🔼
80  mmHg
120 mmHg
8 mmHg
25 mmHg
109
Q

what happens during: END OF VENTRICULAR SYSTOLE
_____ of ECG signals ventricular _____ (depolarisation/repolarisation/hyperpolarisation)
ventricles start to ____ (contract/relax) - ventricular pressure ____ (rises above/falls below) aortic pressure - aortic valve ____ (opens/shuts) - second heart sound, and Dicrotic notch (incisura) on aortic pressure record
_____ valves also shut - no blood can enter or leave
“Isometric Ventricular Relaxation”

A 
T wave 
repolarisation
relax
falls below
shuts 
AV
110
Q

what happens during: FILLING PERIOD
Ventricular pressure ____ (rises above/falls below) atrial pressure
AV valves ____ (open/shut)
Major part of ventricular filling
Blood which entered atria during ventricular systole is released into ventricles by opening of ______
Atrial and ventricular pressures ____ (rise/fall) sharply and ventricular volume (🔼/🔽) rapidly

A 
falls below
open
AV valves
Atrial and ventricular pressures fall sharply and ventricular volume increases rapidly
fall
🔼
111
Q

baroreceptors are activated by…

A

stretch, not pressure

112
Q

carotid sinus afferents travel via ____ and later _____ to the cardiovascular centre in the _______

A

sinus nerve
glossopharyngeal (cranial IX) nerve
medulla

113
Q

aortic arch afferents travel in _____

A

vagus (cranial X) nerve

114
Q

Baroreceptors are the terminals of _______ and ________ sensory fibres that express ______-selective ion channels activated by ______. When opened, these generate a graded receptor potential that causes AP generation which has both ______ and _____ components

A 
myelinated
unmyelinated
cation
stretch
dynamic
static
115
Q

Blood pressure is measured using _____________

A

a sphygmomanometer

116
Q

Korotkoff sounds begin when…

A

cuff pressure is just below systolic pressure

117
Q

Korotkoff sounds fade when…

A

cuff pressure is close to diastolic pressure

118
Q

systolic blood pressure at rest (20 y.o. person) [values]

A

100-140 mmHg

119
Q

diastolic blood pressure [values]

A

50-90 mmHg

120
Q

systolic pressure is mainly affected by…

A

STROKE VOLUME and in particular EJECTION VELOCITY

121
Q

diastolic pressure is mainly affected by… (2)

A

TOTAL PERIPHERAL RESISTANCE and the time allowed for blood to flow out of the arteries– depends on HR

122
Q

typical venous pressure in a limb vein on a ❤️ level… (mmHg)

A

8-10 mmHg

123
Q

central venous pressure (pressure in venae cavae) is… (mmHg)

A

0-7 mmHg

124
Q

typical venous pressure in a foot vein while standing is… (mmHg)

A

90 mmHg

125
Q

minimum value for CO in untrained adults…

A

~5.6 (l/min)

126
Q

maximum value for CO in untrained adults…

A

21.5 (l/min)

127
Q

minimum value for CO in trained adults…

A

~5.3 (l/min)

128
Q

maximum value for CO in trained adults…

A

~30.0 (l/min)

129
Q

major drug classes used in the treatment of heart failure (5):

A 
venodilators
vasodilators
positive ionotropes
ACE inhibitors
diuretics
130
Q

venodilators [mechanism of action in ❤️ failure + effects]

A

dilate veins
reduce increased central venous pressure (pressure in venae cavae)
reduce preload (extent of filling)

131
Q

vasodilators [mechanism of action in ❤️ failure + effects]

A

dilates blood vessels
decreases afterload (arterial BP)
increases tissue perfusion

132
Q

positive ionotropes [mechanism of action in ❤️ failure + effects]

A

🔼 [Ca2+ intra] or 🔼 the sensitivity of receptor proteins to Ca2+ => 🔼 myocardial contractility
[bind to TRANSMITTER-GATED ION CHANNELS aka Ionotropic Receptors]
increase CO

133
Q

ACE inhibitors [mechanism of action in ❤️ failure + effects]

A

prevent conversion of Angiotensin I into Angiotensin II (RAAS)
stop the chain reaction leading to oedema, 🔼 central venous pressure & 🔼 preload

134
Q

diuretics [mechanism of action in ❤️ failure + effects]

A

makes you pee
additional indirect venodilator action (before diuresis) that is beneficial in pulmonary oedema caused by heart failure
prevents/reduces extent of oedema

135
Q

afterload [def.]

A

arterial BP

workload imposed on the ❤️ after contraction has begun

136
Q

DIURETICS

Inhibit ____, _____, and _____ reabsorption in the thick _________________________ [location]
by blocking the ________________
Cause up to_______ of filtered Na+ to be excreted along with H20 producing a ‘_______’ diuresis

______(🔼/🔽) the tonicity of the interstitium of the medulla
______(🔼/🔽) the load of Na+ delivered to distal regions of the nephron (causing K+ loss)
______(🔼/🔽) excretion of Ca2+ and Mg2+

Possess an additional, indirect, venodilator action (before diuresis) that is beneficial in pulmonary oedema caused by heart failure– possibly results from:

1) ______(🔼/🔽) formation of vasodilating prostaglandins
2) ______(🔼/🔽) responsiveness to angiotensin II and noradrenalin
3) ______(opening/closing) of K+ channels in resistance vessels

A 
Na+, K+ and Cl- 
ascending limb of the loop of Henle
Na/K/2Cl- co-transporter
 15-25%
'high ceiling'

🔽
🔼
🔼

🔼
🔽
opening

137
Q

DIURETICS

Inhibit ____, _____, and _____ reabsorption in the thick _________________________ [location]
by blocking the ________________
Cause up to_______ of filtered Na+ to be excreted along with H20 producing a ‘_______’ diuresis

______(🔼/🔽) the tonicity of the interstitium of the medulla
______(🔼/🔽) the load of Na+ delivered to distal regions of the nephron (causing K+ loss)
______(🔼/🔽) excretion of Ca2+ and Mg2+

Possess an additional, indirect, venodilator action (before diuresis) that is beneficial in pulmonary oedema caused by heart failure– possibly results from:

1) ______(🔼/🔽) formation of vasodilating prostaglandins
2) ______(🔼/🔽) responsiveness to angiotensin II and noradrenalin
3) ______(opening/closing) of K+ channels in resistance vessels

A 
Na+, K+ and Cl- 
ascending limb of the loop of Henle
Na/K/2Cl- co-transporter
 15-25%
'high ceiling'

🔽
🔼
🔼

🔼
🔽
opening

138
Q

DIURETICS – adverse effects

K+ loss producing low serum K+ levels (__________) – corrected by the accompanying use of ____________ or ____________ (note 🔼 toxicity of digoxin and Class III antidysrhythmic drugs)

Shift in acid-base towards ______ side (__________) – caused by increased _____ secretion from intercalated cells in collecting tubule

______(🔼/🔽) volume of circulating fluid (________) and _______ (particularly in the elderly)

Depletion of ______ and _____ [ions]

______(🔼/🔽) plasma uric acid (_______) – partially explained by competition between uric acid and loop agents for the organic acid secretory mechanism in the proximal tubule

A

hypokalaemia
potassium sparing diuretics or potassium supplements

alkaline
metabolic alkalosis
H+

🔽
hypovolaemia
hypotension

Ca2+ and Mg2+

🔼
hyperuricaemia

139
Q

Spironolactone - example of Aldosterone Receptor Antagonist (K+-sparing diuretic)

Has ______(an unlimited/a limited) diuretic action (modulated by aldosterone levels)

Competitively antagonises the action of aldosterone at cytoplasmic aldosterone receptors, gains access to cytoplasm via the _________ [structure]

______(🔼/🔽) excretion of Na+
______(🔼/🔽) excretion of K+

______(poorly/well) absorbed from the G.I. tract and rapidly metabolised to_______ (which accounts for most of the action of the drug)

A

a limited
basolateral membrane
🔼
🔽

well
canrenone

140
Q

Clinical indications for the use of Spironolactone [Aldosterone Receptor Antagonist (K+-sparing diuretic)]

The major use of potassium sparing diuretics is in…
Given alone, they cause______

A

conjunction with other agents that cause potassium loss

hyperkalaemia

141
Q

Aldosterone antagonists are used in the treatment of (4):

A
  • Heart failure
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Resistant essential hypertension
  • Secondary hyperaldosteronism (due to hepatic cirrhosis with ascites)
142
Q

diuretic drugs in the treatment of hypertension and heart failure (3):

A

Ionotropic Drugs Other than Digoxin
Calcium-sensitizers
Levosimendan

143
Q

Levosimendan

  • Binds to _______ [protein] in cardiac muscle sensitizing it to the action of Ca2+
  • ______ (Opens/Closes) KATP channels in vascular smooth muscle causing _________ (vasoconstriction/vasodilation)
  • Relatively new agent, used in treatment of ______ ______ heart failure
A

troponin C
Opens
vasodilation
acute decompensated

Biomedical Sciences BS22001 (4 decks)

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