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disease of cardio system Flashcards

1
Q

atherosclerosis

A

fibrofatty legions in artery wall
hardening of artery wall
oxidaion occurs causing fatty streaks or plaque build up

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2
Q

non modifiable risk factors of atherosclerosis

A

age- older
sex- males more likely

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3
Q

modifiable risk factors of atherosclerosis

A

chronic infection, lifestyle, diet high in salt

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4
Q

progression of plaque in atherosclerosis

A

endothelial dysfunction and an increase in inflammatory cell recruitment

atherosclerosis- endothelial injury then activates endothelial cells and inflammatory response occurs

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5
Q

foam cell production in atherosclerosis

A

macrophages engul oxidised LDL- foam cell
leads to chronic inflammatory loop
necrotic core

leads to fatty streaks

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6
Q

plaque progression and fibrious cap atherosclerosis

A

smooth muscle cells migrate- proliferate and produce extracellular matrix of collageb and elastin= fibrous cap
decrease strength of protective layer/ destabilise plaque

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7
Q

plaque rupture in atherosclerosis

A

platlet activation and coagulation cascade/ thrombus causes rupture

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8
Q

vascular age effects excaerbating atherosclerosis

A

chronic low grade inflammation
endothelial dysfunction
intimital thickening of artery walls

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9
Q

ateriosclerosis

A

elastin replaced with stiff collagen in vessels
shift from normal to promote fibrosis/ calcyfying
increase glycation end products

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10
Q

glycation products

A

heterozygous group of compounds that become non-enzymatic, glycated and oxidised

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11
Q

peripheral artery disease

A

thrombus affecting superfical artery

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12
Q

thrombus

A

local formation of a blood clot

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13
Q

embolus

A

artrial fibrilation- travels around blood

it is an obstructive piece/ plaque

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14
Q

acute arterial occulsion

A

sudden loss of limb perfusion
it is an emergency

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15
Q

acute arterial occulsion
anerobic metablosim and acidolosis

A

lactic acid accumulates decrease PH
disrupts enzyme and damages tissue
oxidative stress cause athersclerosis

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16
Q

acute aterial occulsion
atp depletion and ion pump failure

A

swollen cells disrupt the tissue structure and function

excessive ca 2PLUS activates destructive enzymes

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17
Q

acute aterial occulsion
enzymes that are necrotic

A

protease- muscle protein
phospholipase- membrane
endonuclease- DNA irreversible

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18
Q

cellular components that indicate problems

A

K- heart arrythmia
phosphate- electrolyte imbalance
creatine- muscle damage
myoglobin- clog kidney

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19
Q

vasculitis

A

inflammation of vessels

weak/altered circulation or dizziness

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20
Q

aneurysm

A

enlargement of artery resulting in larger diameter

due to gentic, degenerative, inflammation, hemodynamic factors

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21
Q

risk factors of aneurysm

A

connective tissue disorder
atheroscleorsis
vasculitis
lifestyle

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22
Q

types of aneurysm

A

aortic
cerebral
peripheral

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23
Q

aortic aneurysm

A

loss of vascular smooth muscle cells due to chronic inflammation, oxidative stress, mechanical strain

this produce free radicals able to block vessels

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24
Q

cerebral aneurysm

A

smaller/ low pressure vessels so easier to burst
unique shear and stress forces

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25
peripheral aneurysm
higher atherosclerosis of lower limb
26
venous pump
muscle contractions aid venous return drive blood superfical to deep vein
27
venous valves
bicuspid and prevent back flow
28
chronic vnous disease
venous hypertension/ structural obstruction
29
anatomical changes to veins
valvular incompetence- valve failure
30
symptoms of chronic venous disease
pain/ leg heaviness/ aches/ swelling/ skin dry/ serve deep pain/ dilated vein
31
types of venous thromboembolisim
DVT/ pulmonary embolisim cause- venous stasis/ hypercoagulation/ endothelial surgeries
32
DVT
unilateral leg swell, warmth, redness, calf tendernous
33
PE
chest pain, tachtponeia, cyanosis
34
risk factors venous thromboembolsiim
prolonged immobilisation cancer surgery
35
treatment to thromboembolisim
anticoagulation compression therapy
36
phlebitis
inflammation if a vein
37
2 types of phlebitis
superficial- no clot superficial thrombophlebitis- with a clot
38
treatment for phlebitis
NSAIDS WARM COMPRESSION COMPRESSION THERAPY
39
hypertension
High BP due to fluid imbalance, blood vessel resistance
40
Renal cause of high BP
kidney removes NA through urine will decrease BP RAAS- retain sodium to increase BP so overactive casues high Bp kidney vessel damaged decrease blood flow
41
vascular cause of hypertension
small arteries- widden/ stif/ narrow control BP nitric oxide- relax and widden vessels if endothelial damaged decrease NO3 large arteries stiffen- decrease in central diastolic BP INCREASE IN SYSTOLIC BP
42
RAAS overactivation
excess angiostinum 2, aldosterone- chronic vasoconstriction- increase BP
43
SNS/ Catecholamines
increase norepipherin and epipherin= increase hr and vessel constriction
44
aldosterone
increase ssodium retention- increase Bp
45
ADH
increase water retention
46
secondary hypertension
identifiable underlying cause has caused it
47
hypotension
low blood pressure
48
risk factors of hypotension
decrease cardiac output/ decrease stroke volume heart failure/ arrythmia/ myocardial infarction hemorrage/ dehydration septic shock hypothyroidisim prolonged bed rest
49
coronary heart disease risk factors
non modifiable- age, gender, genetics modifiable- hypertension/ dyslipidemia- increase LDL tobaco/ diabetes obesity inflammation
50
angina
discomfort in chest
51
stable angina
atherosclerosis lipid plaque/ decrease blood flow/ pain on exertion
52
unstable angina
plaque ruptue and thromboembolisim recent onset chest discomfort occurs at rest last longer then 20 minutes
53
how does unstable angina occur
clot formation- artiral fibrilation/ endocarditits = plaque rupture sudden coronary artery dissection tear in coronary artery creates false lumen= obstruct flow coronary vasospasm- sudden spasm reduces blood flow
54
pathophysiology of angina
myocardial ischeamia reduced O2 supply increase o2 demand
55
result of angina
decrease ATP production- Ion pump reduced increase lactic production- cellular acidosis increase ischemic metabolisites
56
bradykine
stimulate pain receptor
57
histamine
arterial spasm
58
3 types of acute coronary syndrome
unstable angina non ST eleavation MI ST elevation MI
59
ahterosclerotic plaque rupture
plaque rupture- thrombus formation/ STEMI ANGIOGRAPHY shows thrombus ECG- increase T/ ST waves
60
coronary vasospasm
transient coronary artery spasm decreases blood flow ST elevation
61
myocardial infarction
microvascular dysfunction/ embolisim x significant signs
62
aortic dissection
aortic tear extends into coronary artery serve tearing chest pain
63
inflammatory vasculitis
inflammation and endothelial dysfunction cause thrombus
64
ACS diagnostic criteria
UA- ischaemic symptoms with no elevate trophin levels NSTEMI- elevate trophin levels STEMI- elevated trophin need ECG
65
MYOCARDIAL INFARCTION
caused by myocardial ischeamia cell death measured by cardiac measure STEMI- complete onclussion - full muscle death NSTEMI- still has cell death partial cardiac muscle
66
troponins
proteins that regulate cardiac contraction tropnin T released from damged cells 1- peak early 2- peak continued because leakage
67
complication
mechanical- necrosis of conduction system rupture of left ventricle free wall
68
acute pericarditis causes
infectious- bacterial, virus, fungal autoimmune disease post caridac injury radiation
69
acute pericarditis
increase pericardial fluid decrease pericardial fluid drain rapid accumulation- cardiac tamponade
70
cardiac tamponade
rapid accumulation of pericardial effusion from trauma pericardial pressure exceeds R atrial/ ventricle diastole pressure Impaired cardiac filling leads to decrease stroke volume and CO
71
tachycardia
rapid firing before atrial and ventricle fill fast heart beat fibrilation- myocytes contract indepndently instead of coordinated
72
bradycardia
condcution block
73
re-entry tachycardia
tempoary block- decrease ionic current- no impulse conduction is slow re-entry loop- SA node new initiate another depolarisation re-entry cricut- extra beats
74
bradycardia degrees
1st- every impulse is recived but slow 2nd- indicates heart disease same as top 3rd- no impulses from atria recived
75
congenital AV block
immune mediated- disrupt calcium metabolisim
76
acquired av block
fibrosis or sclerosis irregular pulse
77
LBBB
RIGHT VENTRICLE ACTIVATES FIRST L IS DELAYED
78
RBBB
right ventricle depolarise late and L is normal

Pathophysiology (16 decks)

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