wk 4 - haemodynamics Flashcards

1
Q

how can infarcts occur in the vascular system 2

A
  1. blockage of arterial system- ischaemia- necrosis - infarct
  2. blockage in venous system - congestion - haemorrhge - necrosis - infarct
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2
Q

define congestion

A

passive build up of blood in the vessel

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3
Q

define oedema

A

increased fluid in interstitial tissue

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4
Q

define effusion

A

increased fluid in body cavity

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5
Q

define exudate

A

high in plasma poteins- occurs in acute inflammation

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6
Q

define transudate

A

low in plasma proteins odema - usually occurs in most pathology

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7
Q

define ischaemia

A

lack of blood supply, partial or complete

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8
Q

define haemorrhage

A

damage to a vessel and release of all blood

accumulation of blood which if large it is referred to as haematoma

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9
Q

define thrombus

A

Blood clot attached to the wall (vessel/heart chamber)

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10
Q

define embolus

A

Undissolved mass travelling in the blood

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11
Q

define aneurysm

A

localised, abnormal ballooning out of an artery or ventricle of heart

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12
Q

define antheroma

A

sclerotic (hardening) plaque in an artery. referred to this when dead

lesion in the artery

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13
Q

define atherosclerosis

A

chronic inflammatory process within the wall of an artery. typically affects the intima of an artery.
-ongoing injury
-attempts to reparir
-hardening of lipids and calcium

referred to this when alive

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14
Q

define hypertension

A

raised blood pressure

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15
Q

define anaemia

A

decreased number or quality of RBCs

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16
Q

define stasis

A

lack of blood flow

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17
Q

define hypercoagulability

A

blood with a higher tendency of clotting

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18
Q

what are blood flow and blood pressure differences in the systemic, pulmonary and venous circuits

A

systemic - high blood pressure (hard to get congestion to occur)
pulmonary - low blood pressure
venous - low blood pressure (easy for congestion to occur)

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19
Q

what causes venous thrombi vs arterial thrombi

A

venous- stasis and coagulation
arterial- endothelial injury and atherosclerosis

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20
Q

compare superficial and deep vein thrombi

A

same risk factors but different in:

superficial-
pain, ulceration, oedema
rarely embolise.

deep-
asymptomatic often, maybe swelling
often embolise

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21
Q

list the 2 main risk factors for DVT and track their path if they embolise

A

stasis- lack of movement
hypercoagulation- promotes blood clotting

22
Q

list the 8 main risk factors for the development of atherosclerosis

A

age
male gender (oestrogen is protective)
Smoking
Diabetes (both)
Systemic Hypertension
Hyperlipidaemia (high LDL, low HDL)
/dyslipidaemia
Visceral adiposity

23
Q

how do the kidneys contribute to systemic hypertension

A

kidneys regulate blood volume and pressure and they activate the RAAS system

24
Q

what 3 vascular pathologies does atherosclerosis predispose towards

A
  1. thrombus
  2. embolus
  3. aneurysm
25
Q

what are consequences of having atherosclerosis in the abdominal aorta, coronary arteries carotid and cerebral arteries

A

abdominal aorta- embolise and infarct downstream. it could kill if you get an aneurysm and a haemorrhage

coronary- ischemic heart disease

cerebral - cerebral vascular disease

26
Q

infarction is

A

area of necrosis

27
Q

thrombus is

A

bloot clot attached to the wall of a vessel or heart chamber

28
Q

embolus

A

anything undissolved travelling in the blood

29
Q

aneurysm

A

localised abnormal ballooning out or dilation of part of a vessel/ventricle wall

30
Q

antheroma

A

sclerotic plaque which represents an area of chronic inflammation within the wall of an artery

31
Q

atherosclerosis is

A

the process of atheroma formation

32
Q

congestion is

A

passive build up of blood within a vessel, which increased hydrostatic pressure

33
Q

transudate

A

low protein oedematous fluid caused by increased hydrostatic pressure and/or reduced collodial osmotic pressure

34
Q

what is the main site for haemopoiesis in the adult

A

the red marrow in the axial skeleton- produces red blood cells in response to erythropoietin

35
Q

can you live without a spleen?

A

yes, in cases when theres trauma. however, because its role is to look for antigens and recycle RBC’s there is an increased risk of infection when removed

36
Q

how do the normal functions of the kidneys impact blood pressure and composition?

A
  1. kidneys produce EPO which stimulates RBCs
    2.renin angiotensin - aldosteron system (RAAS):
    aldosterone increases amount of water and salt reabsorbed and increases the blood volume as a result. through renin and angiotensin 2 causes vascular constriction increasing blood pressure.
  2. regulate ions and blood pH
37
Q

how do the normal functions of the liver impact blood composition?

A
  1. sythensis of plasma proteins which is responsible for increased collodial osmotic pressure and discouraging oedemea (transudate) occuring
  2. also has a role in RBCs formation
38
Q

in what ways do superficial and deep vein thrombi differ?

A

super- dont embolise, symptomatic
deep-embolise, asymptomatic

39
Q

what is the route of a deep vein thrombi that has embolised

A

femoral/iliac vein - inferior vena cava - right atria - right ventricle - pulmonary arteries - lungs

40
Q

what do aneurysms form in vessels and ventricles?

A

in arteries, they form in areas of atheroslcerosis (high pressure, weakened areas)

in heart ventricles, areas of scarring

41
Q

why do thrombi form on atherosclerotic lesions or within aneurysms?

A

atherosclerosis encourages turbulent blood flow where there is a bashing against the endothelial lining causing further injury. When endothelium is lost there are pro clotting factors released.

aneurysms the same reason applies because they form in areas of atherosclerosis but also because cells and proteins can get entrapped in them.

42
Q

an ebolus released from a thrombus in the addominal aorta can cause an infarction where

A

Anywhere downstream like lower limbs, bowels etc

43
Q

what is the difference between angina and a heart attack?

A

both caused by ischaemia but angina the blood is restored to the tissue before necrosis occurs

44
Q

what are the 4 ways atherosclerosis can cause death? -example of location as well

A
  1. BRAIN- aneurysm bursting or giving rise to thrombi/emboli (if it bursts in the brain it will lead to a haemorrhage stroke that increases intracranial pressure)
  2. CAROTID/BRAIN - thrombi/emboli leading to ischaemic strokes (in the carotid or cerebral arteries can be life threatening)
  3. HEART- atherosclerosis/thrombi can cause chronic ischaemia through blockage, if this is within the coronary arteries then it will cause a myocardial infarction
  4. ABDOMINAL AORTA- bursting of aneurysm causing hypovolemic shock
    cause myocardial infarctions
45
Q

what is the difference between a myocardial infarction and a brain infarction?

A

the heart undergoes coagulative necrosis where the dead tissue is walled off until inflammatory cells remove the dead tissue. Whereas the brain often encompasses a large area of necrosis and because of the difference in tissue like other organs, it turns into liquefaactive necrosis. mush.

46
Q

what are the scars in the brain formed from?

A

Glia, glial scars

47
Q

why are there symptoms to infarctions in the heart and brain compared to other organs?

A

they are both permanent therefore they must heal by scarring, meaning loss of functional tissue and because both work as a complete unit, this will cause symptoms to occur. compared to organs that have multiple functions and able to separate these functions, less symptomatic.

48
Q

atherosclerosis in what vessels could lead to a stroke?

A

cerebral or carotid arteries

49
Q

atherosclerosis in what vessels could lead to a myocardial infarct

A

coronary arteries

50
Q

atherosclerosis in what vessels could lead to ischaemic heart disease

A

coronary arteries

51
Q

atherosclerosis in what vessels could lead to cerebral atrophy?

A

cerbral or carotid arteries

52
Q

what is colloidal pressure governed by?

A

concentration of plasma proteins