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Kirstys Flashcards > CPT1: Vasodilators > Flashcards

CPT1: Vasodilators Flashcards

1
Q
  1. What direction does blood flow travel in?
  2. What is the equation to determine blood flow rate?
  3. What is the relationship between Resistance and arteriole radius?
A
  1. From areas of high pressure to areas with low pressure
  2. Flow = Pressure gradient/ Resistance
  3. Resistance is directly propotional to 1/ (radius of ateriole)4
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2
Q

Describe blood flow though veins

A
  • Carries blood to the heart
  • Valves to prevent back flow of blood and direct blood flow towards the heart
  • Veins offer very little resistance to blood flow
  • Skeletal muscle pumps the blood
  • Contain sympathetic nerves - a1 causes vasconstriction increasing venous return to heart and therefore increasing preload
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3
Q

What is the benefit of respiratory movements in terms of blood flow with veins?

A

Aids venous return

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4
Q

How is arterial blood pressure calculated?

A

Blood pressure (mmHg) = CO x TPR

(total peripheral resistance)

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5
Q

What is the calculation for CO?

A

CO (l/min) = HR x SV

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6
Q

Describe the control of arterial blood pressure

A
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7
Q
  1. What is the therapuetic overview of vasoconstriction?
  2. Disadvantages of vasodilators?
A
  1. VC is important in regulating blood pressure. The aim to is balance BP
  2. Vasodilators only provide sympathometic relief - don’t cure
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8
Q

What are the uses of vasoodilators?

A
  1. Surgery - reduce bleeding
  2. Peripheral vacular diseases - Increases blood flow to ischaemic areas
  3. Heart failure - increases CO, reduces O2 consumption
  4. Hypertension - decreases BP
  5. Coronary artery disease - increases blood flow to coronary artety and decreases O2 consumption
  6. Male impotence - increased erectile function
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9
Q

What is the steal phenomen

A

vasodilation is not selectove so targets all blood vessels. Therefore blood vessels in unadequtely perfused ischaemia areas will have increased blood flow and become adequetly perfused, however blood vessels in non-ischaemia areas already perfused will become over perfused. Blood is shunted away from ischaemic areas

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10
Q
  1. Where is smooth muscle found?
  2. What is contraction controlled by?
A
  1. Present in resistance (arteriole) vessels and capcitance (venules) vessel
  2. Humoral and neural mechanisms
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11
Q

How is smooth muscle contraction initiated? What are the steps involved?

A
  1. A rise in intracellular Ca2+
  2. INcrease in Ca-calmodulin complex, activation of MLCK which phosphorylates MLC
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12
Q

What ways do agents cause contraction?

A
  1. Release of Cai following receptor meditated IP3 formation
  2. Depolarisation of membrane (via Cl- efflux) allowing Ca2+ entery through Voltage operated channels (VOCs)
  3. Entery of Ca2+ through receptor-operated channels (ROCs) - sensitive to NA, ATP (ligand gated ion channels allowing Ca2+ influx)
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13
Q

How do relax agents cause relaxation

A
  1. –Inhibition of Ca2+ entry through VOC’s, either directly (e.g. calcium antagonists) or indirectly (K+ channel activators)
  2. –Increasing cGMP to oppose agonist-induced changes in [Ca2+]i (e.g. nitrates)
  3. –Increasing cAMP, to inactivate myosin light-chain-kinase (e.g. adenosine)
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14
Q

What is the function of ACE?

What does Ang II do?

A
  1. ACE converts angiontensin I into Angiotensin II
  2. ANG II
    1. Ang II is a potent vasoconstrictor (Gq linked)
    2. It is an anti diuretic and antinaturetic. It promotes aldosterone synthesis which causes the membrane insertino of eNAC in the collecting tubules. This causes Na+ to be retained therefore water therefore increased BV therefore increased BP.
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15
Q

Mechanism of action of ACEi

A
  • Inhibit RAAS
  • Inhibit Ang II formation therefore alodosterone
  • Diuretic activity - facilitate water and Na+ excretion
  • Sympatholytic activity
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16
Q

Side effects of ACEi and alternative drug. What is its mechanism?

Side effects and contraindications

A

Dry persistant cough

ANg II inhibitors can be used instead. This blocks AT1 receptor

Both result in hyperkalaemia

contraindicated in preg or breast feeding women

17
Q

What are example of Ca2+ channel blockers?

A
  • Benzothiazepine (e.g. Diltiazem)
  • Phenylalkylamine (verapamil)
  • dihydropiridines (e.g. nifedipine)
18
Q

What types of Ca2+ channels exist?

Which one is present in vascular smooth muscle?

A
  1. L -type, N-type, T-type
  2. L-type
19
Q

What happens when Ca2+ influxes through L-type channels?

A

Triggers Ca2+ release from intracellular stores e.g. sarcoplamic recticulum and inner surface of membranes

20
Q

Different binding sites of Ca Channel blockers result in different pharmacological effects. Where do each of the following bind:

  1. Nifedipine
  2. Verapamil
  3. Diltiazem
A
  • Use dependent binding tageting Cardiac cells: Verapamil and Diltiazem bind to the a1 subunit and display use dependent binding
  • Voltage-dependent binding targteing smooth muscle: Nifedipine bindsyoa different region of the a1 subunit and displays voltage depenident bindni
21
Q

Describe the effects of Verapamil

A
  • Decreased CO and HR due tp negative chronotropic and inotropic effects
  • Decreased Aterial blood pressure due to dcr CO
  • Centeral venous pressured decreased due to decreased cardiac function
  • Coronary blood flow moderately increased and peripheral resistance slightly decreased due to direct vasodilation effet
22
Q

Describe the effects of Nifedipine

A
  • Selective for smooth muscle
  • ABP reduced to arteriolar vasodilation (ie dcr PVR and afterload)
  • CVP reduced due to vasodilation (ie decreased PL)
  • Coronary blood flow increased due to dilation of coronary arteries
  • HR and CO increase as a reflex response to dcr ABP (baroreceptors)
23
Q

Describe the mechanism of angina relief

A
24
Q

Side effects of Ca2+ channel blockers

A
  • Flushing
  • Ankle odema
  • HEadache
  • Gum hyperplasma
25
Q

Contradindications

A
  • People with heart block
  • Digoxin or B-Blockers (both have negative) chronotropic effect)

Kirstys Flashcards (116 decks)

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