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JMP Semester 1 > Week 9 "The Heart- Perfusion" > Flashcards

Week 9 "The Heart- Perfusion" Flashcards

1
Q

how do pH and CO2 regulate tissue perfusion?

A
  1. pH and CO2 are used to locally drive the perfusion of circulating O2 into the tissue as well as vasodilation.
  2. as well as systemically to central control centres to modify respiration.
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2
Q

What are some mechanical factors impacting coronary blood flow?

A
  1. contraction stops perfusion
  2. coronary flow = pressure gradient/coronary vascular resistance
  3. HEART IS PERFUSED DURING DISTOLE
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3
Q

what is the tissue most susceptible to low perfusion

A

sub endocardium

as it furthest from coronary arteries

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4
Q

Describe neural control mechanisms for coronary blood flow.

A
  1. Sympathetic control mainly with maybe minor parasympathetic control.
  2. sympathetic has opposite control compared to other body vasculature (vasodilation)
    - calibre increased
    - resistance reduced
    - flow increased
  3. NA (noradrenaline acts at a different receptor in coronary vascular beds compared to normal vasculature (b2-AR instead of a1-AR.
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5
Q

How does endothelial control modify vascular tone?

A

Endothelin pathway-
(endothelin receptor antagonists) (causing vasoconstriction)
Nitric oxide pathway:
Activates cGMP
- inhibits Ca entry into the cell, and decreases [Ca]in
- activates K-channels > hyperpolarization and relaxation
- directly stimulates relaxation.
Prostacyclin pathway:
activates cAMP
(vasodilation)

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6
Q

What medication can be given to have a similar effect to NO based vasodilation?

A

Nitroglicerin (GTN)

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7
Q

What is an example of metabolic autoregulation in the endothelial of cardiac myocytes?

A

In the presence of low pO2:

  1. ATP breaks down
  2. increases adenosine
  3. adenosine activates A2 receptors (on vascular smooth muscle
  4. activates K+ ATPase
  5. cells hyperpolarised
  6. Relaxation
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8
Q

Why is fast intervention required for an MI

A
  1. Reduce tissue death

2. Injured tissue losing adenosine will die if too much is lost

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9
Q

How is oxygen supply in the heart different from the body.

A

The heart extracts a high proportion of the pO2 compared to that of the body as it has high capillary density). Low pO2 conditions are first noticed by the heart.

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10
Q

Why is O2 so important to cardiac tissue

A

Cardiac tissue has high energy demands. ATP is the principle energy source and is produced by oxidative phosphorylation using O2 as a primary electron acceptor.

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11
Q

What is the primary use of ATP in cardiac tissue

A

60-70% muscle contraction

20-40% ion pumps.

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12
Q

How does O2 consumption by the heart muscle compare to the rest of the body?

A

The heart has a large O2 requirement (similar to skeletal muscles during exercise)

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13
Q

What are the primary sources of energy for the myocardium?

A
  1. Fatty acids - in healthy myocardium fatty acids provide 60-80% of energy production for cardiac cells (primary substrate) (preferred substrate)
  2. Glucose - relatively much less contribution compared to fatty acids
  3. Ketone bodies, lactate and amino acids - can also be used as energy substrate under certain circumstances to provide energy
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14
Q

Why are fatty acids favoured for energy extraction?

A
  1. Produces high amounts of ATP
  2. huge body reserves
  3. relatively simple pathway to ATP:
    B-oxidation–>krebs cycle–>oxidative phosphorylation
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15
Q

Why is glucose not as good as fatty acids for heart energy source?

A
  1. lower amount of ATP
  2. limited reserves
  3. extra pathway required (glycolysis)
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16
Q

What is glycolysis and what is its products?

A

the conversion of 1x glucose –> 2 pyruvate +2ATP (net) + 2NADH.
Requires 1x ATP to initiate (2 in total) but produces 4ATP.

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17
Q

What is the krebs cycle and what are its products?

A

conversion of pyruvate –> Acetyl CoA –> 2CO2 + 3NADH + 1FADH2 + 1ATP. (Not much ATP production but generates 4 multiple electron carries for use in oxidative phosphorylation) (N.B produces CO2)

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18
Q

What happens in aerobic glycolysis?

A

In presence of O2 there is not a build up of pyruvate and NADH as pyruvate can enter the Krebs cycle and NADH is used in the electron transport chain for oxidative phosphorylation.
36ATP produced

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19
Q

What happens in anaerobic glycolysis?

A
  1. No O2 causes build up of pyruvate and NADH as they are not used in ETC.
  2. pyruvate is instead converted into lactate.
    (this process only gains ATP from glycolysis step)
    HENCE NET 2 ATP.
20
Q

How is lactate processed after synthesised by anaerobic glycolysis?

A
  1. travels to liver
  2. metabolised back to pyruvate
  3. pyruvate converted back to glucose (gluconeogenesis)
  4. glucose returns to body cells for further anaerobic glycolysis.
    CYCLE KNOWN AS CORI CYCLE
21
Q

What is primary hypertension?

A

The cause is unknown (90% of cases)

22
Q

What is secondary hypertension?

A

caused by known condition (10% of cases)

23
Q

What is some impacts on vasculature from hypertension?

A
  1. vessel wall inflammation
  2. smooth muscle hypertrophy
  3. loss of vessel integrity
24
Q

What is atherosclerosis?

A

is a chronic inflammatory and healing response of the arterial wall to the injury of the endothelial - leads to occlusion of the affected vessels

25
Q

What is atheroma?

A

artery wall degeneration - fatty deposits and scar tissue, leading to restricted circulation and risk of thrombosis.

26
Q

What is a thrombus?

A

An abnormal intravascular clot attached to the vessel wall.

27
Q

What is an embolism

A

is a detached intravascular mass (solid, liquid or gaseous) that is carried by blood to a distant sit where it causes dysfunction or infarct.
(usually a detached thrombus)

28
Q

What is an aneurism?

A

excessive localised enlargement of an artery caused by weakness of the arterial wall.

29
Q

Describe how ischemia causes pain

A
  1. Ischemia –>
  2. lack of oxygen –>
  3. lack of oxidative phosphorylation –>
  4. less ATP synthesis –>
  5. ADP degrades into Adenosine –>
  6. adenosine goes out of the deprived cell
  7. binds to a1 receptors to trigger pain.
30
Q

what receptor causes localised adenosine induced vasodilation?

A

a2

31
Q

What is ischemia

A

reduced blood flow

32
Q

what is an infarction?

A

localised cell death due to obstruction of blood flow

33
Q

What are the stages of atheroma formation?

A

1) endothelial dysfunction,
2) formation of lipid layer or fatty streak within the intima,
3) migration of leukocytes and smooth muscle cells into the vessel wall,
4) foam cell formation and
5) degradation of extracellular matrix.

34
Q

What are type A adverse drug reactions?

A

relate to the mechanism of action (i.e.the known pharmacology) of the medication, and are associated with high morbidity and low mortality.

35
Q

What are type B adverse drug reactions?

A

are idiosyncratic and cannot be predicted from the known pharmacology of a drug. These reactions are associated with low morbidity and high mortality.

36
Q

What impact does athersclerotic plaque build up have on endogenous Nitric oxide (NO) action?

A

The plaque prevents the action of the Nitric Oxide as it cannot reach the smooth muscle. hence no NO induced vasodilation.

37
Q

What is the mechanism of Organic nitrates? (eg GTN)

A
  1. Provides a source of NO
  2. Activates guanylate cyclase (GuCy) in vascular smooth muscle
    - An enzyme similar to adenylate cyclase (AdCy)
  3. Causes an increase in cGMP levels
    - Inhibits Ca++ channels
    - Activates protein kinase G (PKG) to prevent action of myosin light chain
    Combination causes vascular relaxion = dilation!
38
Q

What are some clinical effects of organic nitrates?

A
  1. Fast action
  2. small decrease in venous return (smaller preload= reduced afterload=reduced work by the heart.
  3. small decrease in afterload-through relaxation of elastic and large muscular arteries.
  4. otimises ejection-more time to ensure adequate blood flow without increasing heart work
39
Q

What are the issues in regards to organic nitrate clinical uses?

A
  1. Exact mechanism unknown
  2. there is a rapid drug tolerance developed by patients
  3. Side effects:
    vasodilation mediated BP decrease can cause headache dizzy oedema etc.
40
Q

What are drugs options to treat angina?

A
  1. Beta blockers (adrenergic antagonists)

2. calcium channel blockers

41
Q

How does adrenergic antagonists (Beta blockers) help with angina?
specifically at the Sinoatrial node.

A

SA:

  1. decreases AdCy activation–>less cAMP–>less PKA activation
  2. Reduced activation of voltage gated Ca++ channels by PKA.
  3. lower Ca++ influx–>delays depolarisation–>Longer AP–>reduces HR
  4. THUS reduces cardiac work and optimises filling time.
42
Q

How does adrenergic antagonists (Beta blockers) help with angina?
specifically at the cardiomyocytes

A
  1. decreases AdCy activation–>less cAMP–>less PKA activation
  2. Reduced activation of Ca++ channels by PKA.
  3. reduces contractile force –>less work +ejection optimisation
43
Q

What are the two ways calcium channel blockers can act to relieve angina?

A
  1. vascular selective

2. cardio selective

44
Q

How does vascular selective calcium channel blockers relieve angina?

A
  • Blocks voltage gated Ca++ channels in vascular structures (arteries)
  • Decreases Ca++ influx into vascular smooth muscle
  • Reduce Ca++ liberation from SR
  • Reduces smooth muscle contraction = vasodilation
  • Reduces force required to overcome diastolic BP and eject SV
  • Reduces cardiac work and demand and increases supply of blood to the heart.
45
Q

How does cardio selective calcium channel blockers relieve angina

A
  • blocks voltage gated Ca++ channels
  • decrease Ca++ influx into SA node
  • Delays rapid depolarisation to prolong AP duration
  • Results in reduced HR
  • Decreases heart work and optimises filling time and ejection fraction.
46
Q

Why cant cardio-selective Ca++ channel blockers be used alongside a beta blocker.

A

Essentially the same mechanism- where they both reduce calcium influx in SA node cells. this may induce fatal bradycardia.

JMP Semester 1 (12 decks)

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