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Patho > Patho- Cardiovascular disorders > Flashcards

Patho- Cardiovascular disorders Flashcards

1
Q

what is hyperlipidemia ?

A
  • elevated lipid content in blood
  • elevated cholesterol, phospholipids, triglycerides in blood
  • Apoproteins transport lipids
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2
Q

lipid + apoprotein = ?

A

lipoprotein

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3
Q

explain the density of lipoprotein

A

they can very in density

LDL, HDL, VLDL

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4
Q

atheros?

A

soft paste

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5
Q

sclerosis?

A

hardening

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6
Q

what is an atherosclerosis ?

A

when an atheroma ( fibrofatty lesion) forms in intimate of larger arteries

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7
Q

what does atherosclerosis cause?

A

affects perfusion–> ischemia ( restrictive blood flow because of some obstruction in the blood vessel at the local level)

—>schema can cause stroke, MI or PVD

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8
Q

what is infarction?

A

tissue death due to ischemia

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9
Q

what is hypercholesterolemia ?

A

excessive cholesterol in the blood

40 percent of Canadians experience this

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10
Q

pathogenesis of atherosclerosis

A

insidious origin–> subtle endothelial injury from risk factors (inflam)

  • -> monocytes and other inflam cells bind to endothelium
  • -> monocytes enter intimate–> become macrophages—>
  • –> 1. release free radicals by oxidizing lipids ( unstable damaged reactive cells)
    2. engulf the lipids, are now foam called foam cells
    3. release growth factors which cause proliferation of smooth muscle cells

All of this requires space so an atheroma forms which pushes into the lumen.

NOTE; centre is called necrotic core, blood goes inside and is a clot which can be dislodged to a thrombus

highest incidence of atherosclerosis are in the abdominal and iliac arteries

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11
Q

what are the three lesion stages of atherosclerosis ?

A

fatty streak-
fibrinous atheromatous plaque– > clinical lesion, smooth muscle cells in intimate
complicated lesion—> changes inside the lumen

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12
Q

is HDL good or bad?

A

HDL is good, 50 % carrier high density

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13
Q

is LDL good or bad?

A

LDL is lousy because it contains 50 % cholesterol

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14
Q

atherosclerosis facts

A

32 % of all deaths (1.3 of all Canadian deaths)

72000 deaths per year

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15
Q

hypertension range?

A

when you can’t bring bp back to normal and its elevated all the time ( 140/90)
classified by type, cause and severity

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16
Q

BP = ? x ?

A

BP = CO x PR

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17
Q

systole?

diastole?

A 
systole= pumping
diastole= filling
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18
Q

what are the four major control systems of hypertension ?

A
  1. arterial baroreceptors (aorta and wall of ventricles)
  2. renin- angiotensin system
  3. regulation of fluid volume ( by kidney with ADH and aldosterone)
  4. vascular auto regulation ( ability to dilate and constrict)
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19
Q

how much blood in a person?

A

5-6 L

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20
Q

what is normal bp?

A
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21
Q

what is high normal BP ?

A

120- 139 over 80- 89

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22
Q

Hypertension, what are the stages?

A

stage 1: mild
stage 2: moderate
stage 3: severe

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23
Q

stage 1: mild hypertension?

A

140-159 over 90-99

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24
Q

stage 2; moderate hypertension?

A

160-179 over 100-109

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25
Q

stage 3: severe hypertension?

A

> 180 over >110

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26
Q

primary hypertension ?

A 
idiopathic (unknown cause)
90 of cases
multifactorial aetiology (kidney involved but isn't due to kidney failure )
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27
Q

secondary hypertension ?

A 
identifiable causes ( renal disease/ failure)
10 percent of cases
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28
Q

white coat hypertension?

A

hypertension in health care setting ( may develop to primary hyper tension

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29
Q

Systolic hypertension?

A

jut systolic pressure elevated > 140
mostly after age 50 due to; tissues changes, vessel compliance, dec elasticity
heart is pumping harder during systole but normal during diastole (filling)

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30
Q

Malignant hypertension?

A 
same as persistent hypertension or resistant hypertension
sudden, quick, severe increase in bp
diastolic > 120
emergency
tiny vessels damaged causing shock
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31
Q

gestational hypertension ?

A

develops in pregnant women
most become normal after, some develop hypertension

problems with visual disturbances

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32
Q

Manifestations of hypertension?

A
  • silent killer
  • no early signs except bp
  • later systemic manifestations, non specific; fatigue, palpitations, am headaches( bp highest in am due to circadian rhythms), blurred vision, dizziness
  • progressive problems; organ damage to heart, kidneys, eyes and smaller blood vessels
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33
Q

treatment of hypertension

A
  1. life style moderation (diet and exercise)

1st line- diuretic( excessive loss of fluid at the kidneys, loss of electrolytes)

2nd line- ACE inhibitor;blocks conversion of angiotensin1 to angiotensin2 –> will not form angiotensin2 and thus will stop potent vasoconstrictor, inc prod aldosterone, inc secretion of ADH

Angiotensin2 receptor blocker- blocks receptor of angiotensin2 , same results as ACE inhibitor

CA channel blocker; blocks channel where ca goes into cell calcium in heart and muscles –> decreased contraction of the heart causes decreased pressure

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34
Q

What is PVD

A

peripheral vascular disease

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35
Q

what does peripheral mean?

A

vessels away from heart (limbs, legs)

36
Q

what does vascular mean?

A 
any vessel ( arteries, veins, lymphatic vessels)
mostly refers to peripheral arteries
similar to changes in coronary arteries
37
Q

acute arterial occlusion?

A

acute interruption to perfusion; almost always due to thrombus or embolus

38
Q

Atherosclerotic occlusive disease

A

causes pain, pooling of blood (venous statius)
hydrostatic pressure increases causing edema
venous or lymphatic stasis
severe inc waster and fluid accumulation causing ischemia causing tissue damage

39
Q

claudification

A

pain from ischemia

40
Q

how does your body compensate for PVD?

A 
vasodilation
collateralization ( creation of new vessels that bypass block, takes time thus long term process )

anaerobic metabolism

41
Q

complications from PVD

A

ulceration, gangrene–> amputation

42
Q

what is an aneurysm?

A

localized dilation of artery d/t degeneration of vessel wall

43
Q

is an aneurysm permanent?

A

yes

44
Q

risks/ causes of aneurysms?

A

atherosclerosis, hypertension, trauma, infection, congenital defects

45
Q

three types of aneurysms?

A
  1. fusiform
  2. saccular
  3. dissecting
46
Q

shape of a fusiform aneurysm ?

A

both sides of vessel

47
Q

shape of a saccular aneurysm ?

A

sac or pouch on one side

48
Q

shape of dissecting aneurysm?

A

blood flows into and directs the layers of the wall, often at bends or divides

49
Q

common sites for aneurysms?

A

thoracic and abdominal aorta, iliac, femoral, popliteal

50
Q

complications from aneurysms?

A

rupture, blood slows, pools, blood clots develops—> thrombosis, distal embolization, applying pressure on surrounding areas

51
Q

what is infarction?

A

necrosis d/t ischemia

52
Q

stable angina?

A

fixed plaque
impedes perfusion
brief pain

53
Q

unstable angina?

A

unfixed plaque–> may break off
can become embolisms
if disrupted platelet aggregation, thrombosis, de granulate and release prostaglandin –. constriction of vessels
plaque collects fibrin, platlets and cellular debris
pain; severe longer

54
Q

variant angina

A

d/t spasm in arteries, can happen anytime

55
Q

treatments of angina?

A

nitro glycerin (vaso dilator- reduces chest pain )

56
Q

what is angina an manifestations of?

A

coronary artery disease

57
Q

myocaridal infarction is caused by?

A

atherosclerosis, coronary artery spasm, hemorrhage

58
Q

extent of infarction based on ?

A

proximal or diastal occlusion( close or far away), duration of ischemia,
if other blood vessels were supplying the same area

59
Q

What is a transmural infarction?

A

involves all three layers of the heart

proximal occlusion

60
Q

what is a subendochardial occlusion?

A

inner 1/3 to 1/2 of ventricular wall

distal occlusion

61
Q

diagnostics used in MIs?

A 
echocardiogram
angiogram
serum markers
troponin 1 & T
CKmb
myoglobin
62
Q

when is myoglobin present in the blood?

A

1 hr post MI

non specific marker

63
Q

when is troponin 1 & T present in the blood?

A

elevated 3-10 hours after MI

64
Q

when is CK mb present in the blood?

A

4-8 hours after MI

65
Q

how do you treat an MI?

A 
o2
pain control
anticolagulants
antiarrhythmics 
thrombolytics
angioplasty (stient) 
bypass
66
Q

what is cardiomyopathy?

A

idiopathic muscle disorder in the heart myocardium

67
Q

what is hypertrophic cardiomyopathy?

A

when cell are excessively larger
ventricles hypertrophy

as ventricles get larger they grow inwards and the intra ventricular septum thickens

genetic

68
Q

what is dilated congestive cardiomyopathy ?

A

cardiomyopathy d/t decreased elasticity in heart wall –> congested, pooling of blood because heart can’t dilate

decreased ejection fraction

69
Q

what is restrictive cardiomyopathy?

A

walls or heart become rigid
loose elasticity –> don’t fill enough—> don’t empty enough
incomplete ventricular filling –> dec CO
leads to CHF

70
Q

what is the normal bpm ?

A

70 bpm

71
Q

what is arrhythmias?

A

abnormal heart rhythms that affect cardiac cycle –> cardiac filling and perfusion

72
Q

atrial flutter?

A

regular, fast rate atrial tachycardia ( 300 bpm)

regular inc ventricular rate ( 150 bpm)

73
Q

atrial fibrillation

A

uncoordinated spontaneous muscle contractions ( 400- 600 bpm)

causes irregular ventricle rapid ventricular rate ( 80 -180 bpm)

74
Q

Heart block?

A

block in the impulse from atria to ventricles

signal can’t pass from atria to ventricles

75
Q

what is 1st degree heart block?

A

delayed av conduction, regular rhythms

76
Q

what is 2nd degree heart block ?

A

only some signals go through

77
Q

what is 3rd degree heart block ?

A

loss of av conduction

independent atria and ventricle contractions

78
Q

what is ventricular fibrillation ?

A

ventricular quivering but no contractions

fatal within minutes–> needs defibrillation

79
Q

treatment of arrhythmias ?

A

electrical ( defib, pacemakers)
ablation
drugs

80
Q

what is valvular disease?

A

valves are damaged- allow for regurgitation or impeded slow ( stiff valve stenosis) due to damage

81
Q

etiology of valvular disease?

A 
congenital defects
trauma
infarction/ ischemic damage
tissue deterioration  with age 
inflammation causing valves falling back or scar tissue causing hardening of valves
82
Q

stenosis?

A

stiffening–> narrow opening–>obstructed flow

83
Q

incompetent valve

A

floppy/ distorted –> closing problems—> improper shutting of valves—> regurgitation

84
Q

hemodynamic

A

changes of pressure related to movement of blood from valves

85
Q

treatment of valvular disease?

A

some drugs– force blood through valve

surgery ( repair of replace valve)

Patho (2 decks)

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