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Anatomy > Cardiovascular pathophysiology W8 > Flashcards

Cardiovascular pathophysiology W8 Flashcards

1
Q

What is the Australian Classification of clinical hypertension

A

Sustained systolic >140mmHg
OR
Sustained diastolic >90mmHg

High blood pressure!

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2
Q

What are the risk factors that lead to hypertension

A

Combination of genetics and environmental factors
- Hereditary
- Diet: High intake of NaCl, cholesterol, fats
- Obesity
- Age
- Diabetes Mellitus
- Stress
- Smoking: Nicotine -> vasoconstriction & chemicals damage blood vessels -> narrowing of arteries

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3
Q

Describe the pharmacoloical treatments for hypertension

A
  • ACE inhibitors (Angiotensin converting enzyme inhibitors)
  • Angiotensin (2) receptor blockers
  • Beta blockers
  • Calcium channel blockers
  • Diuretics
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4
Q

What is hypertension a risk factor for?

A

CVD - cardiovascular disease

(as well as stroke, kidney disease, heart failure, coronary heart disease, acellerated atherosclerosis)

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5
Q

Why is hypertension called ‘the silent killer’

A

Asymptomatic for 10-20 years
Creates greater after load -> myocardium hyperthropy -> weakened heart
Accelerates process of atherosclerosis
Affects cardiac output and perfusion to tissues

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6
Q

Why is afterload, and therefore cardiac output, effected with hypertension

A

If pressure in Aorta is 100 (hypertension) the minimum pressure the ventricle has to generate is 150, to generate that higher pressure you need a greater contraction and therefore more effort is required -> strain -> Valves get stiffer, muscle hyperthropy
= cardiac output drops and less blood to tissues

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7
Q

What are the two types of Hypertension

A
  • Primary (90%)
    No underlying cause
    Lifestyle factors? - Physical activity and weight loss -> treatment
  • Secondary
    Underlying cause ie. kidney disease
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8
Q

Are the hormones estrogen and testosterone good or bad in the prevention of hypertension

A

Estrogen = supple = protective
Testosterone = hardens arteries (less compliant) = risk

Post-menopausal = higher risk ie. loose protective factor
Men at older age = lower risk ie. loose risk factor

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9
Q

Why is obestity a risk factor for hypertension

A

Mechanical stress from high level of fat tissue (needs blood so heart works harder)

Atherosclerosis due to poor diet

Physical stress on vascular (fat) -> impedes venous return

Impaired kidney function

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10
Q

What is the action of aldosterone

A

Controls the level of Na+ (main extracellular cation - salt) –> Osmolarity of blood –> how much fluid you retain

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11
Q

What is the action of Angiotensin

A

POTENT VASOCONSTRICTOR

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12
Q

Briefly describe the control system for managing Na+ levels

A

Renin-Angiotensin-Aldosterone System (cascase)

  • Kidneys (pressure sensors) get less blood -> release RENIN
  • Liver pro-hormone (ANGIOTENSINOGIN) is converted to ANGIOTENSIN 1 by RENIN
  • ACE in lungs convert ANGIOTENSIN 1 to ANGIOTENSIN 2
  • ANGIOTENSIN 2 acts on B.V -> vasocontriction AND acts on to adrenal gland stimulating release of ALDOSTERONE
  • ALDOSTERONE acts on kidneys causing more reabsorbtion of Na+ (ie. increased water reabsorbtion to) = higher blood volume = higher blood pressure
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13
Q

What are the three hormones involved in the control system for managing Na+ levels

A

-Aldosterone
-Angiotensin
-Renin

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14
Q

Describe the effects of Angiotensin 2

A

B.V -> vasocontriction
acts on to adrenal gland stimulating release of ALDOSTERONE A-> reabsorbtion of Na+ by kidneys = increased B.V

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15
Q

Describe the mechanism of action of ACE inhibitors (Captopril, perindopril ect.)

A

Blocks angiotensin converting enzyme (NO angiotensin 1 converted to angiotensin 2 in lungs)

= reduced constriction of arteries
&
= reduced Na+ and water retenion by kidneys (= lower blood volume)

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16
Q

What does ACE 2 do?

A

Breaks down angiotensin 2
ie. Constriction only lasts a little bit of time

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17
Q

What is the side effects of a ACE inhibitor

A

Promotes production of Bradykinin (inflammation)
= COUGH a lot

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18
Q

What is the mechanism of action for Angiotensin 2 receptor blockers

A

Inhibit action of angiotensin 2
= vasodilation of arteries
= reduces Na+ and water retention by kidneys = lower B.V

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19
Q

ACE inhibitors are the most common hypertensive drug as it is cheap and effective.
In what situations are Angiotensin 2 receptor blockers more commonly used?

A

More commonly used for heart failure, hypertrophy of the left ventricle, history of myocardial infarction or renal disease due to diabetes mellitus

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20
Q

What are the mechanism of action of calcium channel blocker (in general)

A

Calcium channel blockers block movement of calcium into cell and therefore reduce contraction likihood

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21
Q

What are the mechanism of action of calcium channel blocker - DIHYDROPYRIDINES Most common

A

Smooth muscle req. calcium to enter cell for contraction (Ca2+ binds to troponin - troponin removes tropomyosin - exposed myosin binding site for actin)

DIHYDROPYRIDINES effect smooth muscle in blood vessels - not the heart!
= no contraction = vasodilation

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22
Q

What are the mechanism of action calcium channel blocker - NON-DIHYDROPYRIDINES Less common

A

NON-DIHYDROPYRIDINES the heart!

Pacemaker AP depolarisation due to Ca2+ influx
Therefore block Ca2+ entry

= Less AP’s generated
= Reduced heart rate and force of contraction

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23
Q

What is the mechanism of action for Beta Blockers

A

Reduce the effect of noradrenaline
ie. Block site of action (Beta 1 receptors) ie. reduced Ca2+ influx

= Reduced HR and cardiac output

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24
Q

In which situations are Beta Blockers most commonly used

A

Myocardial infarction, angia, heart, failure, arrthymia

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25
Q

What is the difference between B1 and B2 receptors (adrenergic receptors)

A

B1 = Increases contraction - stimulatory action
- Adrenalines binds and incerases Ca2+ influx
- Mostly on the heart

B2 = dilates B.V’s - inhibitory action (no contraction)
- Mostly on B.V’s

general rule odd numbers stimulate

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26
Q

What is the mechanism of action for diuretics with regard to Hypertension

A
  • Reduce water retention
  • Reduce sodium retention
  • Decreases blood volume
    = reduced cardiac output = reduced BP

Ex. Loop diuretics - increases loss of Na+ (and water)

Usually used in combination with another drug

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27
Q

Which of the five antihypertensive drug classes cause vasodilation

A
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28
Q

Which of the five antihypertensive drug classes reduce cardiac output

A
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29
Q

Which of the five antihypertensive drug classes reduces blood volume

A

ACE inhibitors
Angiotensin 2 receptor blockers
Diuretics

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30
Q

What is considered to be ‘good clinical practice’ for dental profressionals in relation to blood pressure.

A

Routinely assess their patients blood pressure as a part of their overall assessment - especially when these patients might not be routinely assessed.
Also, anti-hypertensive drugs can interact with other drugs used in the dental clinic.

31
Q

How can hypertension lead to heart failure

A
32
Q

Describe the process of atherosclerosis

A

When the endothelium is damaged (tunica intima) it progresses to tunica media. Most of the time blood particles move in and out of the hole but sometimes lipids (droplets of cholestrol - LDL) gets stuck -> accumulates.
Macrophages try to remove LDL by endocytosis -> can’t process LDL = foam cell (in tunica media).
Accumulate and protrude into lumen of blood vessel = narrowing of artery = reduced blood flow

33
Q

Why are the artieries of the heart most affected by atherosclerosis

A

As they are the smalled arteries in the body

34
Q

Why does smoking increase atheroscerosis risk

A

Because smoking releases toxis = more nicks and damage to the B.V’s

35
Q

Describe the different layers of B.V’s

A

Inside = Tunica intima (epithelial tissue) <- layer that gets damaged
Tunica media = muscle layer
Outside = Tunica adventitia = connective tissue

36
Q

Describe the progression of cholestrol accumulating in blood vessels ie. stages

A

Damaged endothelium = cholesrol droplets (LDL) accumulate
= Fatty streak
= Fibrous plauqe
= large plaque obstructing artery

37
Q

What do macrophages turn into when they consume LDL

A

Foam Cell

38
Q

Describe atherosclerosis briefly

A

Narrowing arteries due to fat accumulation at a site of damage

39
Q

What are the risk factors for atherosclerosis

A

Toxins (ie. smoking) -> damages B.V’s
High cholestrol (LDL) -> gets stuck in B.V’s

40
Q

What are LDL’s

A

‘Bad cholestrol’
- Accumulate in B.V’s
- Macrophage consumption (foam cells) -> Plaque accumulation -> atherosclerosis

41
Q

Is HDL considered to be good or bad cholestrol

A

HDL = good cholestrol <- binds cholestrol and takes it to the liver.

42
Q

What are the protective/risk factors between men and women

A

Testosterone = risk factor - promotes production of LDL
Oestrogens = protective factor - promote the production of HDL’s
As you age protective factors and risk factors change

43
Q

/What are the two ways cholestrol can be reovoed from the blood

A
  1. Statins (most popular)
  2. Eztimibe
44
Q

What is the mechanism of action for statins

A

Statins stop liver from producing cholestrol (75% of cholestrol production)

45
Q

What is the mechanism of action for Eztimibe

A

Stops intestines absorbing cholestrol

46
Q

Describe the difference between stable and unstable atherosclerotic plaque

A

Stable: smooth muscle in tunica media grows over plaque
- Usually in slow build up

Unstable: smooth muscle over plaque is very thin -> risk of rupture
- Usually present when build up is fast or build up progresses/grows

47
Q

Desribe stable plaque

A

Vessel is narrowed (restricts B.F and O2 to heart) but remains stable ie. muscle covering is thick blood can flow past without rupture

48
Q

Describe unstable plaque

A

When blood moves past thin muscle layered plaque might rupture, especially when cardiac output is high (high B.P)

48
Q

What can happen when unstable plaque ruptures

A

Result = Thrombus (blood clot) -> myocardial infarction (Heart attack)
Compromised even at rest.

49
Q

What can result from stable plaque

A

Coronary syndrome: Angina (especially during exertion due to anaerobic metabolism acid build up), silent myocardial ischaemia (restricted blood flow) and variant or vasopastic angina. No angina at rest.

50
Q

What is the difference between stable, unstable and varient angina

A

Stable: plaque constricts B.V. Adequate BF at rest, angina during exertion
Unstable: plaque -> thrombus -> lots of constriction. Compromised (angina) at rest!
Varient: unexplaind spasms constricting B.F. Angina occurs at any time

51
Q

What is another name for stable angina

A

Chronic coronary syndrome

52
Q

Describe the 3 subcategories of acute coronary syndrome

A

Unstable Angina: BV ruptures and clotting but resolves - no permanent damage
NSTEMI:
STEMI:

53
Q

Describe the lifestyle modifications that can decrease your risk of ischemic heart disease

A
  • Stop smoking
  • Stress reduction (decrease sympathetic stimulation)
  • Regular exercise (to increase cardiovascular fitness - heart and B.V;s more responsive to N.T’s = dilation more efficient.
  • Limit dietary intake of cholestrol and saturated fats
  • Weight reduction
  • Avoid cold and other physical stress
54
Q

What do you do when someone is having a heart attack

A

Immediate cessation of activity - sit or stand quietly (do not lie down)

55
Q

What is the common drug routinely used in managment of angina? ie. administered during attack to provide immediate relief

A

Glycrol Trinitrate (GTN)
- Potent vasodilator
Prevents Ca2+ influx
= decreases preload, increases venous capactiy, reduces ventricular filling pressure and BP, helps open constricted BV’s ie. improving cononary blood flow!
Administered sublingually and dissolved straight into the blood

56
Q

Long term, GTN is not a great treatment. What are some other long term common drugs used to treat atheroscerlosis?

A

Anti-hypertensives ie. ACE inhibitors, angiotensin receptor blockers, Beta-blockers, Ca2+ channel blockers

57
Q

What arteries are affected in Myocardial infarction

A

Coronary circulation ie, blood vessels of the heart (braching striaght off aorta)
Big arteries lie on the top of the heart and on top of the muscles so they dont get squashed during contraction. Little artieries that desend into the heart do get squashed during contraction.**

58
Q

Which type of plaque is most likely to lead to myocardial infarction?

A

Unstable plaque

59
Q

Why would increased exercise potentially lead to angina in patients suffering from atherosclerosis

A

Increased cardiac output -> increases cardiac workload -> increasing cardiac muscle O2 requirement.

60
Q

What is meant by a NSTEMI event

A

Non-ST-elevation Myocardial infarction event
= T wave inversion and depression in ST segment
Minor blockage - not complete occlusion (thombus) -> damage to heart muscle in near the chamber (not all the way through the tissue to the walls). Inside parts of the part not depolarising at the right time, its dying (ectopic)

61
Q

What is meant by a STEMI event*

A

ST-elevation MI event
- elevated ST segment -> QRS and T wave combined.
Complete and presistent occlusion. Every bit of tissue the artery supplies is dying ie. entire thickness heart wall effected.

62
Q

What are the major risk factors for STEMI*

A

Dyslipidemia, diabetes mellitus, hypertension, smoking, family history of coronary artery disease

63
Q

What are the priorities for treatment for MI (STEMI)

A

Provide immediate O2 -? reperfuse ischaemic myocardium
Reduce cardiac workload
Resolve occlusion (at hospital) by thrombolytic agents
Relieve symptoms ie. pain by analgesia (decrease stress)
Aspirin
Nitrates

64
Q

What can you do to reduce the risk of thrombosis and a myocardial infarction

A
  • Anti-platelet agents ex. aspirin -> inactivate platelets by thromboxane ie. reduces aggregation
  • Anticoagulants ex. warfarin -> stops the liver making clotting cascade proteins

Take into account for dental surgery as patient could bleed alot!

64
Q

What can you do to reduce the risk of thrombosis and a myocardial infarction

A
  • Anti-platelet agents ex. aspirin -> inactivate platelets by thromboxane ie. reduces aggregation
  • Anticoagulants ex. warfarin -> stops the liver making clotting cascade proteins

Take into account for dental surgery as patient could bleed alot!

65
Q

What is the difference between coronary heart disease and heart failure

A

CHD: pathology in coronary blood vessels (low blood supply to muscle)

Heart failure: compromised heart muscle (either not relaxing properly or not contracting properly)

66
Q

What are the key differences between a STEMI and NSTEMI

A

STEMI: full thickness of heart wall & full occlusion of artery

NSTEMI: only part of heart wall effected (inner part) & partial clot of artery

67
Q

What are the principal pharacoloigal treamtent for infarction

A

Anticoagulants, vasodilators, maybe thombalitics?

68
Q

What are the various types of heart failure*

A
  1. Ejection fraction is preserved…thickened, fibrotic (unrelaxed) myocardium - can’t fill, doesnt get a lot of blood
  2. Ejection fraction is reduced (compromised)…over stretched muscle - weakened, thin myocardium ie. doesn’t contract
69
Q

What is the main result of heart failure

A

Redcued cardiac output due to hypertension, coronary artery disease, arryhtmias, valvular heart disease, excessive alcohol intake, hyperthyroidism.

70
Q

How do you treat heart failure with reduced ejection fraction

A

Reduce hypertension
• ACE inhibitors
• Angiotensin receptor blockers

Reduce cardiac workload
• Beta blocker

71
Q

How do you treat heart failure with preserved ejection fraction

A

Usually treat cause (commonly coronary artery disease, hypertension, vascular disease)
• Drugs for reduced ejection fraction not always useful forpreserved ejection fraction

Anatomy (13 decks)

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