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CVS > 5-ANS And Hypertension > Flashcards

5-ANS And Hypertension Flashcards

1
Q

Name the causes of secondary hypertension

A
  • Reno-vascular
  • Reno-parenchymal
  • Adrenal causes
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2
Q

Describe how Reno-vascular disease can lead to secondary hypertension

A 
Renal artery stenosis 
Reduced perfusion pressure 
Increased renin production 
Activation of RAAS
Vasoconstriction and increased Na absorption at other kidney
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3
Q

Describe how renal-parenchymal disease can lead to secondary hypertension

A 
Loss of local vasodilators
Poor glomerular filtration 
Water and Na retention 
Increased plasma volume 
Kidney scars and shrinks
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4
Q

Describe how adrenal causes can lead to secondary hypertension

A

-Conns syndrome: Aldosterone secreting tumour in adrenal gland, activating RAAS, causing hypokalemia

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5
Q

What are the consequences of hypertension?

A
  • Increased after load: LV hypertrophy-heart failure, increased o2 demand-myocardial ischaemia and MI
  • Arterial damage - atherosclerosis: Stroke, renal failure, retinopathy and aneurysm
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6
Q

What are the pharmacological ways to treat hypertension?

A
  • Beta blockers to reduce sympathetic stimulation of renin release and vasoconstriction (but negative inotropy and chronotropy)
  • Renin inhibitors prevent renin release from JGA
  • ACE inhibitors prevent ANG 2 forming
  • Aldosterone antagonist, prevents water and Na retention at kidneys
  • Thiazide diuretics, inhibit Na/Cl co-transporter, reduces circulating volume
  • Vasodilators: alpha 1 antagonists and l type calcium channel blockers, both relax vascular smooth muscle
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7
Q

Name the 4 neurohumoral pathways that control long term blood pressure

A
  • Renin-angiotensin-aldosterone-system (RAAS)
  • Sympathetic nervous system
  • Antidiuretic hormone (ADH)
  • Atrial Natriuretic Peptide (ANP)
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8
Q

Where is renin released from?

A

The granular cells of the juxtaglomerular apparatus in the afferent arteriole

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9
Q

What factors (in the kidney) contribute to renin release?

A
  • Macula densa detected lower NaCl concentration
  • Juxtaglomerular apparatus detect sympathetic stimulation
  • Baroreceptors detect lower renal perfusion pressure
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10
Q

What effects does ANG II have on the body?

A
  • Vasoconstriction
  • Breaks down vasodilator bradykinin
  • Stimulates adrenal gland to produce aldosterone
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11
Q

What effects does aldosterone have on the kidneys?

A
  • Increases water retention
  • Increases Na absorption by activating apical Na and K channels
  • Raises blood pressure
  • Also increases basolateral Na extrusion
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12
Q

What does the liver produce in RAAS?

A

The precursor angiotensinogen

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13
Q

What is found in lungs for RAAS?

A

ACE - angiotensin converting enzyme

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14
Q

How does the sympathetic nervous system reduce renal blood flow?

A
  • Vasoconstriction of arterioles

- Decreased glomerular filtration rate therefore decreased Na excretion

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15
Q

What effect does the sympathetic nervous system have on the proximal tubule?

A
  • Activates apical Na/H exchanger in proximal tubule

- Activates basolateral Na/K/ATPase

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16
Q

Which of the neurohumoral pathways stimulates renin release?

A
  • Sympathetic nervous system

- RAAS

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17
Q

What is the formula for mean arterial blood pressure?

A

Mean arterial blood pressure = CO X TPR

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18
Q

What stimulates the release of ADH?

A 
Increased plasma osmolarity
Severe hypovolaemia (reduced blood volume)
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19
Q

What are the effects of ADH?

A
  • Increases water retention in distal nephron to form concentrated urine, controlling plasma osmolarity
  • Vasoconstriction
  • Stimulates apical Na/K/Cl co-transporter, increasing Na reabsorption
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20
Q

What are the effects of ANP?

A
  • Vasodilation of the afferent arteriole, which increases glomerular filtration rate
  • Inhibition of Na reabsorption along nephron, causing natriuresis
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21
Q

Where is ANP synthesised and stored?

A

Atrial myocytes

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22
Q

How is ANP inhibited?

A

Reduced filling of heart
Less stretch
Less ANP released

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23
Q

Define hypertension

A

A sustained increase in blood pressure

24
Q

What is the function of prostaglandins?

A
  • Vasodilation to increase glomerular filtration rate
  • Reduce Na reabsorption
  • Buffer to excessive vasoconstriction by RAAS/SNS/high ANG II
25
Q

What is the effect of dopamine on the kidneys?

A
  • Vasodilation, increasing blood flow

- Inhibits Na/H exchanger and Na/K/ATPase reducing reabsorption of NaCl

26
Q

Where is dopamine formed and what is it formed from?

A

In the kidneys, formed from circulating L-Dopa

27
Q

What does the ANS control in the CVS?

A
  • Heart rate
  • Force of contraction
  • Peripheral resistance of blood vessels
  • Amount of vasoconstriction
28
Q

What is the electrical activity of the heart controlled by?

A

The vagus nerve

29
Q

What is the preganglionic input to the heart?

A

Vagus nerve

30
Q

What do the postganglionic fibres of the parasympathetic system release?

A

Acetyl choline

31
Q

What receptors does acetyl choline bind to and what effect does this have on the heart?

A

Ach binds to M2 receptors
Negative chronotropic effect
Reduces AVN conduction velocity

32
Q

What do the postganglionic fibres of the sympathetic system release?

A

Noradrenaline

33
Q

What does noradrenaline bind to and what effect does this have on the heart?

A

Act on b1 adrenoreceptors
Positive chronotropic effect
Positive inotropic effect

34
Q

How does noradrenaline increase the force of contraction?

A
  • Act on b1 adrenoreceptors in myocardium to increase cAMP
  • Activates PKA
  • Phosphorylation of calcium channels increases influx during action potential plateau
  • increased calcium uptake in the sER
  • increased sensitivity of contractile machinery to calcium therefore increased force of contraction
35
Q

Describe the stages of an action potential in the SAN

A

1) opening of fast L type calcium channel (upwards stroke)
2) closing of calcium channels and opening of potassium channels (downwards stroke)
3) Slow depolarisation of pacemaker potential (aka funny current) (slow increase)

36
Q

What effect does sympathetic input have on pacemaker potential?

A

Speeds up pacemaker potential - increases heart rate

37
Q

What effect does parasympathetic input have on pacemaker potential?

A

Slowed down pacemaker potential, decreased heart rate

38
Q

What does increased sympathetic output do to vascular smooth muscle?

A

Binds to a1 receptors, causing vasoconstriction

39
Q

What does decreased sympathetic input do to vascular smooth muscle?

A

Binds to a1 receptors, causing vasodilation

40
Q

What does circulating adrenaline bind to preferentially and at high concentrations?

A

Preferentially binds to B2 receptors

At high concentrations will bind to a1 receptors

41
Q

Describe how activating B2 receptors leads to vasodilation of vascular smooth muscle

A 
Increased cAMP
Activation of PKA
Opening of potassium channels and inhibition of MLCK
No actin cross bridges form 
Vasodilation
42
Q

Describe how activation of a1 receptors leads to vasoconstriction of vascular smooth muscle

A

Increased IP3 production
Extracellular calcium influx, intracellular calcium released from stores
Causing contraction of muscle

43
Q

What effect does increased metabolite concentration have on vascular smooth muscle

A

Strong vasodilator effect

44
Q

What are the three classes of drug that act on the ANS?

A

Sympathomimetics
Adrenoreceptor antagonists
Cholinergics

45
Q

What triggers the baroreceptor reflex?

A

Increased arterial pressure causing stretching

46
Q

What response does the baroreceptor reflex promote?

A

Bradycardia

Vasodilation

47
Q

Why isn’t the baroreceptor reflex triggered in hypertension?

A

Persistent increases in blood pressure reset the baroreceptor reflex to a higher threshold

48
Q

What kind of drug is salbutamol and what does it treat?

A

Sympathomimetic, B2 agonist

Treats asthma as it relaxes airway

49
Q

What kind of drug is dobutamine and what does it treat?

A

Sympathomimetic, B1 agonist

Treats caridogenic shock (pump failure), as it has a positive chronotropic effect and increases cardiac output

50
Q

What kind of drug is adrenaline and what does it treat?

A

Sympathomimetic, non selective agonist

Treats cardiac arrest and anaphylactic shock

51
Q

What kind of drug is miodrine and what does it treat?

A

Sympathomimetic, a1 agonist

Treats postural hypotension

52
Q

What kind of drug is prazosin and what does it treat?

A

Adrenoreceptor antagonist, a1 antagonist

Treats hypertension as it inhibits noradrenaline on smooth muscle, preventing vasoconstriction

53
Q

What kind of drug is propanolol and what does it do?

A

Adrenoreceptor antagonist, B antagonist
Negative inotropy and chronotropy (B1)
BUT
Bronchoconstriction (B2)

54
Q

Why is atenolol used preferentially to propanolol?

A

Atenolol is selective B1 antagonist so less risk of bronchoconstriction

55
Q

What kind of drug is pilocarpine and what does it treat?

A

Cholinergic, muscarinic agonist

Treats glaucoma as it activates constrictor pupillae muscle

56
Q

What kind of drug is atropine and what does it do?

A

Cholinergic, muscurinic antagonist
Positive chronotropic effect
Bronchial dilation
Pupil dilation- used in eye exams

57
Q

Which afferent nerve receptors detect high pressure changes and which low pressure changes?

A

Baroreceptors detect high pressure changes

Atrial receptors detect low pressure changes

CVS (10 decks)

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