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Pathology > Hypotension, Thrombosis, Embolism & Infarction > Flashcards

Hypotension, Thrombosis, Embolism & Infarction Flashcards

1
Q

what is systole

A

left vent cotract

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2
Q

what is diastole

A

left vent relax

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3
Q

BP is —-

A

CO x peripheral ritnce

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4
Q

Co consists of

A

heart rate
contractility
Blood vol

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5
Q

peripheral resist consist of

A

constrictor (angiotensin 2)

dilators ( Nitric oxide)

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6
Q

what is hypertension

A

disorder in which level od sustained arterial pressure i higher than expected for age, sex and race

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7
Q

high bp =

A

consistently >140/90 mmHg

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8
Q

when does BP inc

A

on standing on exercise and on expo to cold and emothion

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9
Q

indiv with larger than normal pressure rise in response to stimuli have inc risk of

A

permanent hypertension - labile hypertension

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10
Q

prevalence of hypertension UK

A

20%

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11
Q

what are the classficiatons of hyeprtension

A

primary
secondary

benign
malignant

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12
Q

95% cases hyperT =

A

no detectable cause
primary
essential

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13
Q

what’s primary hypertension induced by

A 
interplay genetics and enviro factors 
race 
stress
diet 
alcohol 
exercise
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14
Q

what is secondary hyperT

A

renal disease
endocrine disorders
aortic disease

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15
Q

what is coarctation of aorta

A

onental narrow of segments aorta

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16
Q

what are some endocrine causes of hyper T

A

adrenal gland tumour
conns syn - excess dlosterone
cashing syn - excess corticosteriod

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17
Q

prognosis of pt with hyperT dept on

A

height and rate of pressure rise

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18
Q

bening hyperT

A

prognosis measured in decades

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19
Q

malignant hyperT

A

accelerate from fatal within 2 years if untreat

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20
Q

benign causes of hyperT

A 
ischaemic heart disease
heart fail 
stroke
acceleration renal disease
malignant hyperT
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21
Q

does benign hyperT symptomatic

A

no

BP rises slowly over the years

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22
Q

what does benign hyperT have an affect

A

heart and arteries
taggert heart, brain and kidneys
ischeamic heart disease

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23
Q

how does benign hyperT affect CVD

A

inc pressure hypertrophy arteries and heart

resist in arteries - thicker walls more narrow
longstand hyperT aggravaties atherosclerosis = aneurysm and disscetions

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24
Q

how does benign hyperT affect the heart

A

left vent hypertrophy - diastole
inc muscle mass and intersistial fibrosis
poor canary artery perfusion
myocardial infart

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25
Q

how does benign hypertension affect the brain

A

micro aneurysm ina arteries supply baal gala and pons and cerebellum

rupture = hypertensive cerebral haemohhae

cerebral infarction - stroke

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26
Q

how does benign hyperT affect kinds

A

hyperT aggravates many renal diseases but only in severe cause = renal fail

27
Q

what are the definitive reading of benign hyper

A

every 10 mmHg diastole above 85 - double MI risk

every 8 mmHg diastole above 85 - inc stroke

28
Q

what is the basics of malignant hyperT

A

life threat

diastole >130 mmHg

29
Q

what can malgganat lead to

A 
retinal changes 
haemorrhages 
cerebral oedema 
heart fail acute
stroke
acute renal fail
blood vessels fibrinoid necrosis
30
Q

what does maligannayt dev from

A

benign ot secondary hyperT

31
Q

who is affected by malignant

A

30-40 yrs

needs urgent treat

32
Q

what is blood clotting

A

defence mech ag haemorrhage

solid mass blood external to vessel

33
Q

what is blood clot imp for

A

imp for trauma and surgery

34
Q

what is athormbus

A

solid mass IN the vessel

common found veins but sometimes in arteries

35
Q

what causes thrombus

A

rik inc by VIRCHOWS TRAID

36
Q

what is virchow train

A

injury to vessel walls
alter blood flow
alter blood constituents that in coagulability

37
Q

how is the vessel affected in virchows

A

loss end surface

inflam

38
Q

what is the flow affects in vrichow

A

stasis

turbulence

39
Q

what is constiunets affects in virchows

A

platelets
coat proteins
visc

40
Q

thowmus formation

A

platelets
coat cascade
fibrinolytic cascade

41
Q

what is the events of thrombus form

A 
rapid flow blood 
vasc injury 
for platelet rich thrombus 
build up 
\+ platelets and fibrin 
tick to end 
coat cascade = fibrin strands
42
Q

what does a thrombus do

A

occludes vessel

blood flow slow adhere to thrombus surface = RED THROMBUS

43
Q

what does red thrombus lead to

A

propagation of further affects

44
Q

what si the fate of thrombus

A

lysed into anticlht factors
larger thumb - infiltrate macrophages and ends cells - racanlise and restore blood flow

embolism

45
Q

what is an embolus

A

abnormal material carries in blood may cause block downstream - dept on site and nature of material

46
Q

what does a large emboli =

A

infarction of tissue

brain - stroke

47
Q

what are some examples of major types of embolism

A 
thromboembolism 
atheroembolism 
fat embolism 
air embolism 
tumour embolism 
septic embolism 
amniotic fluid
48
Q

if embolism on arterial side =

A

heart to brain nd kidney

49
Q

if embolism on venous side

A

pulmonar circ

50
Q

DVT =

A

deep vein thrombosis

51
Q

PTE =

A

pulmonary thromboembolism

52
Q

when can DVT occur

A

post op
bed bound
travel

53
Q

what can DVT cause

A

unilateral leg swell
oedema
pain

54
Q

what is pTE

A 
sudden onset 
life threat 
haemoptysis 
breathlessness
CVD collapse and shock 
cardiac arrest
55
Q

what is ana infarction

A

zonal necrosis due to sudden occulsion of blood supply

  • atheroma
  • embolism
56
Q

what si the nxrosis in an infarction due to

A

lack oxygen and nutrients

57
Q

what is the fate of an infarction

A

can be fatal
re perfusion injury
diff tissues have diff susceptibility

58
Q

what is an MI

A

death myocardial tissue caused by ischaemia
persistent ischaema - death myocytes
most due to thrombus over atherosclerotic plaque

59
Q

what is ischeamia

A

reduction or cessation of blood flow

60
Q

is ischaemia reveille

A

initially stable engine but if persist - death of myocytes

61
Q

what are some complications assc with MI

A 
atthythmias 
cariogenic shock 
caria rupture 
ventricular septal defects 
heart fail
62
Q

what is re-perfusion injury

A

result in injury to cells not prev afffetsd

63
Q

what is re-perfusion injury due to

A

due to toxic oxygen sp that over prod on restoration of blood supply

Pathology (13 decks)

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