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Cardioresp > 15 > Flashcards

15 Flashcards

1
Q

vascular endothelium main function

A

maintain vascular tone, controlling tissue blood flow and inflammatory responses and maintaining blood fluidity

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2
Q

what are the 4 main types of CVD

A
  1. coronary heart disease (angina)
  2. aortic disease
  3. peripheral arterial disease
  4. strokes and TIA
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3
Q

how many people suffer from CVD

A

422 million

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4
Q

cost of CVD

A

300 B dollar

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5
Q

goal of treatment

A

return to normal physiological ranges

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6
Q

is high BP a disease

A

no

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7
Q

how many people worldwide have high BP

A

1 in 3 worldwide have high BP

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8
Q

how many of those w high BP are unaware

A

half

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9
Q

hyperT is risk factor for

A

stroke and HR

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10
Q

number one cause of death worldwide

A

CVD

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11
Q

optimal systolic BP

systole

A

120

less than 80

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12
Q

risks of CVD increases with

A

medical history

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13
Q

optimal pressure

A

less 120
AND
less 80

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14
Q

normal pressure

A

120-129
AND
80-84

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15
Q

high normal

A

130-139
AND OR
85-89

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16
Q

grade 1 hypertension

A

140-159
AND OR
90-99

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17
Q

grade 2 hypertension

A

160-179
AND OR
100-109

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18
Q

grade 3 hypertension

A

over or equal 180
AND OR
over 110

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19
Q

lifestyle changes to help with HyperT

A

less salt

no smoking

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20
Q

what will drug choice depend on

A

race
age
severity

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21
Q

how would you treat high normal BP

A

lifestyle advice

consider drugs in high risk like Hx

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22
Q

how would you treat grade 1 BP

A

lifestyle advice
immediate drug treatment in high risk patients or all patients if BP not controlled with lifestyle changes after 3-6 months

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23
Q

how would you treat grade 2 BP

A

lifestyle advice
immediate drug treatment
AIM for BP control within 3 months

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24
Q

how would you treat grade 3 BP

A

lifestyle advice
immediate drug treatment
AIM for BP control within 3 months

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25
Q

firstline drug for patients age under 55

A

Angiotensin converting enzyme inhibitor ACE

young Rafa aces

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26
Q

firstline drug for patients age over 55 or black or African or carribean family

A

ca chanel blockers

carribean calcium…

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27
Q

does age or race affect drug choice more

A

race

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28
Q

if drug doesn’t help what happens

A

combination of drugs

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29
Q

second line

A

A and C

30
Q

third line

A

A and C and thiozide diuretic (D)

31
Q

fourth line

A

A C D and further diuretic or alpha and beta blockers

32
Q

processes that regulate BP

A

rening angiotensin aldosterone system (RAAS)

baroreceptor reflex (actue changes)

33
Q

how long does it take after you take steroids to see effects? why?

A

hours bc its affect is on gene expression

34
Q

what factors activate the RAAS system

A
  1. Sympathetic nerve activation (via β1-adrenoceptors)​
  2. Renal artery hypotension (e.g. systemic hypotension or renal artery stenosis)​
  3. ↓sodium delivery to the distal tubules of the kidney
35
Q

explain the RAAS system

A
  1. Activation of JG cells = cleaves prorenin to renin​
  2. Renin converts Angiotensinogen (liver) into angiotensin I​
  3. Angiotensin converting enzyme (ACE; Lungs & kidneys)​ converts Angiotensin I to Angiotensin II ​
  4. Angiotensin binds to Angiotensin II Type I & type II receptors ​
  5. Proximal tubule: Angiotensin II = ↑Na+ reabsorption = ↑blood flow bc water follows=​
    ↑BP​
  6. Adrenal cortex: Angiotensin II: ↑aldosterone= ↑Na+ reabsorption (at distal​
    tubule) = ↑blood flow=↑BP​
  7. Systemic arterioles: Angiotensin II binds to GPCR = arteriolar​ vasoconstriction=↑BP
    ​
  8. Brain: Angiotensin II stimulates release of antidiuretic
    hormone (ADH). ↑ ADH = ↑Na+ reabsorption
36
Q

affect of angiotensin II on systemic material

A

binds GPCR and leads to arteriole vasoconstriction and so increase in BP

37
Q

angiotensin and the brain

A

angiotensin II acts on hypothalamus (pituitary??) makes you thirsty so increase blood volume

38
Q

Brazilian pit viper nemo,

A

ACE inhibitor

39
Q

mechanism of ACE inhibitor

A

Inhibit Angiotensin II (potent vasoconstrictor)​
= vasodilation of small resistance arteries, ​
↓SVR & ↓BP ​

40
Q

where do diuretics act

A

nephron

41
Q

long term effect of antidiuretic

A

reduce vascular resistance

42
Q

where do loop diuretics act

A

loop of hence

43
Q

where do thiazides act

A

distal convoluted tubule

ti amo de loi (distal)

44
Q

mode of action of loop direuctics

A

Loop diuretics inhibit the luminal Na/K/2Cl co-transporter in the thick ascending limb of the loop of Henle​
Increased delivery of Na to the distal tubule enhances K secretion into the urine​

45
Q

which leads to more vasodilation, loop diuretics or thiazide

A

thiazide

46
Q

problems of diuretics

A

loss of K (hypokalaemia metabolic alkalosis)

loss of Ca

47
Q

name of a thiazide often used

A

indapamide

48
Q

thiazide mode of action

A

vasodilator by reducing systemic vascular resistance

decrease intravascular volume
sodium and water loss
reduce CO

49
Q

calcium channel blockers mode of action

A

block ca entry to vascular smooth muscle

so reduce contraction –> vasodilator

50
Q

what are the two types of calcium channels blockers

A

dihydropyridine (amlopidine)
vasodilation mainly
reduce systemic vascular resistance

non dihydropyridine (diltiazem)
reduce HR
negative ionotropes andchronotrops so may worsen heart failure

51
Q

angina

A

blockage of coronary artery

52
Q

diagnostic tool for determining wether to give drugs for prevention of angina

A

cholesterol plus que 200mg dL then you give preventative drugs

53
Q

first line preventative therapy of angina

A 
lipid lowering (statins)
lower BP
lifestyle changes
54
Q

what are statins

A

lipid lowering drugs

55
Q

common drugs to manage angina

A 
nitrates (vasodilator)
calcium blockers (vasodilator AND cardiac depressants)
beta blockers (cardiac depressants)
56
Q

is nitrate short or long response

A

quick short

57
Q

mode of action of nitrates

A

nitroglycerine converted to NO which is a major physiological molecule that leads to vasodilation.

NO activates GTP tp cGMP which leads to realxation of coronary arteries or veins

58
Q

mode of action of beta blockers

A

antagonist of b1 receptor

reduce HR and BP and myocardial oxygen demand

59
Q

Heart failure symptoms

A

Symptoms (e.g. breathlessness, ankle swelling and fatigue)

60
Q

heart failure sings

A

signs (e.g. elevated jugular venous pressure, pulmonary crackles and peripheral oedema bilateral ankle deem heart murmur)

61
Q

cause of Heart failure

A

Structural and/or functional cardiac abnormality, resulting in a ↓ cardiac output +/- ↑ intracardiac pressures at rest/stress

62
Q

ejection fraction

A

measurement of the percentage of blood leaving your heart each time it contracts

about of blood pumped out/amount of blood in chamber

63
Q

normal ejection fraction

A

50-70%

64
Q

below ejection fraction

A

heart failure

65
Q

chemical to diagnose heart failure

A

naturiuretic peptides

66
Q

drugs used in heart failure

A

positive inotropic drugs
vasodilators
miscellaneous drugs for chronic failure

67
Q

mrEF

pEF:

A

mrEF: mid-range ejection fraction​
pEF: Preserved ejection fraction​

68
Q

Heart Failure with preserved/mid-range ejection fraction​ recommendations

A

diuretics for congested patients to relieve symptoms

screen for comorbidities

69
Q

Heart Failure with reduced ejection fraction​

A

Ace and beta blockers plus MRA if still symptomatic

70
Q

problem of giving non dihydropyridine (diltiazem)

A

can worsen heart failure because it acts as a negative inotrop

71
Q

invasive treatment of angina

A

angioplasty and stent

72
Q

heart failure dx tool

A

natriuretic peptides and echocardiogram

Cardioresp (23 decks)

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