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Physiology > Circulatory Pathology - Y2 > Flashcards

Circulatory Pathology - Y2 Flashcards

1
Q

General structure of blood vessel

A

Tunica intima = endothelium - inner
Tunica media = circ smooth musc + elastic tissue - middle
Tunica adventitia = CT + longitudinal smooth muscle = outer

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2
Q

Structure of artery

A

Thicker tunica media - most prominent
Thinner tunica adventitia than veins
Int elastic lamina - between intima & media = in musc arteries
Ext elastic lamina - between media & adventitia = in musc & medium ateries
Smaller lumen
Thicker walls
Elastic & smooth muscle concentric layers = in elastic arteries

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3
Q

Structure of vein

A

Tunica adventitia thickest - most prominent
Tunica media thinner than arteries
Large lumen
Thinner walls
Valves
No int or ext elastic lamina

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4
Q

Types of capillary

A

Continuous
Fenestrated
Sinusoidal

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5
Q

2 states of endo cells

A

Basal
Activated

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6
Q

What caused endo cells to be in basal state

A

Laminar blood flow
Growth factors - VEGF
Normotension - normal BP

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7
Q

Function of endo cells in basal state

A

Non-adhesive - doesn’t allow leukocyte extravasation/infiltration into ECM
Non-thrombogenic surface - prevents blood clotting

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8
Q

What causes endo cells to be in activated state

A

Turbulent flow
Hypertension
Cytokines
Bacterial products
Viruses
Hypoxia
Cigarette smoke
AGE (advanced glycation end products)

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9
Q

Function of endo cells in activated state

A

Inc expression of adhesive factors - E-selectin, ICAM
Inc expression of procoagulants = plasminogen activator inhibitor, Von Willebrand factor, tissue factor
Inc expression of pro-inflamm factors = IL-1, IL-6
Altered expression of chemokines, cytokines, GFs

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10
Q

Blood vessel which doesn’t have smooth muscle cells

A

Capillaries

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11
Q

Function of smooth muscle in blood vessels

A

Constrict & dilate
-> involved in vascular repair & in pathological processes - atherosclerosis

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12
Q

What activates smooth muscle cells

A

PDGF
Endothelin growth factors
Thrombin growth factors
Fibroblast growth factors
IFNy
IL-1

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13
Q

What keeps smooth muscle cells in inactive state

A

Heparan sulfate
NO
TGFB

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14
Q

How is hypertension physiologically responded to

A

RAAS inhibited
Barorec reflex
Vasodilation - parasymp NS

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15
Q

Barorec reflex

A

Inc Pa - stimulates barorecs (a type of mechanorec) - stretched more
Inc aff impulses from carotid sinus barorecs along glossopharyngeal nerve
Inc aff impulses from aortic arch barorecs along vagus nerve
-> both to nucleus tractus solitarus
Causes:
-Inc parasymp outflow to SAN via eff nerves = dec conduction velocity = dec HR & CO
-Dec symp outflow to heart via eff nerves = dec contractility = dec HR & CO
-Dec symp outflow to blood vs from vasoconstrictor centre -> so get vasodilation - epinephrine binds to B2 ad recs on blood vs = dec TPR
===» so overall dec Pa
Vasodilation also mediated by ANP & NO
-> ANP release by atria in heart failure - so when is high BP/hypertension

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16
Q

How is hypotension physiologically responded to

A

RAAS activation
Barorec reflex inhibited
Vasoconstriction

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17
Q

RAAS

A

Dec BP
Dec GFR
Activates macula densa in DCT - which monitor Na+ & H2O
Induced JG cells in walls of aff arteriole -> release renin
Renin enters blood
Renin converts angiotensingogen -> aniotensin I
Angiotensin I sent to lungs
In lungs angiotensin I converted to angiotensin II by ACE
Angiotensin II causes:
- Aldosterone release from adrenal cortex - stimulates ENaC insertion into CD & stimulates aquaprotin insertion too - due to ADH
- Vasoconstrction of peripheral blood vs = inc blood flow - inc glom hydrostatic pressure = inc GFR
=> all inc Pa

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18
Q

What substance causes vasoconstriction primarily

A

Norepinephrine - from symp NS

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19
Q

What is hypertension

A

High BP in systemic arterial circ over long period of time

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20
Q

Impacts of hypertension

A

-Accelerates atherogenesis = formation of fatty deposits in arteries
-Hyperplastic arteriolosclerosis = type of arteriosclerosis = artery wall thickens due to abnormal concentric prolif/growth of smooth muscle cells - occludes lumen - common in kidney arteries - will impair renal blood flow/supply
-Hyaline arteriolosclerosis = type of arteriosclerosis = often in kidney arteries in pats with diabetes & hypertension - arteriolar wall is hyalanised by deposition of amphorous proteinaceous material = narrows lymen
-Arteriosclerosis = general term - which includes atherosclerosis, arteriolosclerosis, Monckeberg medial calcific sclerosis

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21
Q

2 types of hypertension

A

Idiopathic = 95%
Secondary = 5%

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22
Q

What is iodopathic hypertension

A

High BP not caused by another medical condition - so cause is unknown - so treat symptoms
-> vasodilators for vascular origin
-> diuretics for blood vol origin

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23
Q

What is secondary hypertension

A

High BP caused by anther medical condition - so treat underlying cause

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24
Q

What can hypertension lead to - x2

A

Aortic dissection
Cerebrovascular haemorrhage

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25
Q

How to smooth muscle cells respond to vascular injury

A
  1. Vascular injury causes = infection, inflamm, imm injury, physical trauma, toxic exposure,
  2. Endo cell loss or dysfunction
  3. SMCs activated & recruited into intima
  4. SMCs prolif = forms neointima (intimal thickening)
  5. Intimal thickening narrows lumen - causes turbulent blood flow - due to compromised blood flow
  6. Activates endo cells
  7. Actuvated endo cells express: adhesive factors, pro-coag factors, pro-inflamm factors & have altered expression of chemokines, cytokines & GFs
  8. Pro-coag factors - tissue factor, Von Willebrand act on endo cells causing pro-thrombotic state
    Also get production of factors (vasoconstrictors) which cause SM contraction - vasoconstriction
    And get production of factors for ECM synthesis
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26
Q

What layer of blood vessel is endothelium in

A

Tunica intima - inner

27
Q

3 causes of thrombosis - Virchow’s triad

A

Endo injury
Hypercoaguability
Abnormal blood flow

28
Q

How does endo injury cause thrombosis

A

Inflamm (damage) = endo injury = activates endo cells
Activated endo cells downreg anti-thrombotic, anti-coag factors = thrombomodulin
& upreg pro-thrombotic factors = von willebrand factor, plasminogen activating factor, tissue factor
& production of endothelin & ACE**
& production of pro-coag factors = thrombin
Thrombin activates platelets
So platelets aggregate & adhere - ‘stick’ together
Endothelin & ACE -> activate SM cells**
-> Causes SM contraction (vasoconstriction)
-> disrupts laminar blood flow (abnormal blood flow = part of V triad)
-> acts to further activate endo cells (more pro-thrmobotic factors…)
Leads to arterial thrombus forming

Causes of endo injury:
- Cuts
- Ulcerated plaques in atherosclerosis
- Endocardial injury in MI
- Traumatic or inflamm vascular injury (vasculitis)

29
Q

Type of thrombus in endo injury

A

Arterial thrombi

30
Q

How does abnormal blood flow cause thrombosis

A

Abnormal blood flow (not laminar - i.e., stasis or turbulence):

Stasis:
Blood flows slower (loss of laminar flow) - so…
Platelets make more contact with endothelium
(activating endo cells) & slows removal of:
-Pro-thrombotic (von willebrand, tissue factor, plasminogen activator factor)
-ACE, endothelin (vasoconstrictors)
-Pro-coag factors (thrombin)
= all produced by activated endo cells due to loss of laminar flow
Thrombin causes platelet aggregation & adhesion
Endothelin & ACE -> activate SM cells
-> causes SM vasoconstriction
So ultimately end up with venous thrombi forming

Turbulence:
Blood flows faster (loss of laminar flow) - so…
Activates endo cells - as is more endo injury - preg of:
-Pro-thrombotic factors (von willebrand, tissue factor, plasminogen activator factor)
-Adhesion factors (E-selectin & ICAM)
((And more))
-> These factors cause leukocyte adhesion
Also local pockets of stasis form - causing countercurrents = disrupts laminar flow
This brings platelets into contact with endothelium
= pro-thrombotic & pro-coag factors

31
Q

Type of thrombus in stasis (abnormal blood flow)

A

Venous thrombi

32
Q

Types of thrombus in turbulence (abnormal blood flow)

A

Arterial & cardiac thrombosis - near heart valves

33
Q

How does hypercoagubility cause thrombosis

A

= inc tendency for blood to clot
-> due to alterations to coag factors

34
Q

Type of thrombus in hypercoagubility

A

Venous thrombus
Then divided into primary (genetic) & secondary (acquired) disorders
-Primary = genetic mutation to factor V (factor V leiden) = clotting factor -> this mutation makes it harder/impossible to cleave factor V so protein C cannot activate factor V
-Secondary = acquired disorders inc conc of pro-thrombin & fibrinogen = clotting factors

35
Q

Clotting vs thrombosis vs coagulation

A

Clotting of blood forms thrombus (a blood clot)
-> so pro-thrombotic factors promote clotting
-> & clotting factors promote clotting (produced by liver)
Coagulation aka clotting = process where blood changes from liquid to solid state

So clotting/coagulation causes thrombosis (thrombus formation)
-> upreg of pro-thrombotic factors by activation of endo cells = von willebrand factor, tissue factor, plasminogen activator factor
-> upreg of pro-coag factors activation by endo cells = thrombin
-> downreg of anti-thrombotic/anti-coag factors by activation of endo cells = thrombomodulin
-> upreg of vasoconstrictors by activation of endo cells = ACE, endothelin
-> downreg of vasodilators by activation of endo cells = NO, prostacyclin
**DON’T WORRY ABOUT VASOCON/DIL!!! - think this is incorrect as either could be produced?
-> upreg of adhesion factors by activation of endo cells = ICAM, E-selectin

36
Q

Coagulation process

A

Coagulation cascade activated:
- Release clotting factors
- These form a clot - converting prothrombin to thrombin & then thrombin converts fibrinogen (soluble) into fibrin (insoluble) = pro-coagulant state
- Fibrin strands adhere to platelet plug - forms insoluble clot

37
Q

Arterial vs venous thrombus

A

Arterial
-> due to endo injury
-> occurs secondary to atheroma
-> made of platelets = so white colour
-> where? - brain middle cerebral artery, coronary arteries = common

Venous
-> due to stasis (abnormal blood flow)
-> so slow blood flow & pressure
-> made of RBCs, platelets, fibrin = so red colour
-> where? - deep calf veins (can embolise to lung = pulmonary embolism), hepatic portal veins

38
Q

5 fates of thrombi

A

Lysis
Propagation
Organisation
Canalisation
Embolisation

39
Q

Lysis

A

Thrombolytic activity of blood breaks down (lyses) thrombus - action of plasmin

40
Q

Propagation

A

= inc size
-> thrombus accumulates more platelets & fibrin

41
Q

Organisation & canalisation

A

O = Invasion/ingrowth of thrombi by CT (endo cells, SMCs, fibroblasts) -> thrombus becomes firm & grey colour => occludes lumen fully
C = lumen reforms by forming hole in thrombus - continued C causes thrombus to become smaller - incorporates thrombus into vessel wall

42
Q

Embolisation

A

Thromboembolism
-> part/all thrombus dislodges & travels in circulation = now called embolus - to other sites in vasulature
-> becomes lodged in new vessel = embolism
Locations of embolisms vary in significance -> some can cause strokes & others heart attacks & even death

43
Q

What is an embolus

A

Detached fragments from:
Solids - thrombi
Liquids - amniotic fluid
Gases - N2
=> carried by blood to distant site where can cause dysfunction or infarction of local tissue

44
Q

Types of emboli (x5 examples)

A

*Thromboemboli -> (process above) causes infarction of tissue distal to blood supply
*Fat & bone marrow embolism - a common cause is traumatic fracture to long bone
*Air embolism - if inject air or are deep sea diver
*Tumour embolism - metastasis of tumour can occlude vessel
*Amniotic fluid embolism - in pregnancy

45
Q

What is a pulmonary embolism (PE)

A

Where an embolus (of any type) travels in circulation & occludes pulmonary venous circulation

46
Q

Common causes of PE (x2)

A

DVT - deep vein thrombosis = 95%
-> so this is a thromboembolism example - where thrombus formed in deep veins of leg undergo embolism as its fate -> travel in circ through right side of heart & then to lungs - blocks pulmonary arteries

Pelvic vein thrombosis = 5%
-> again is an example of thromboembolism but here thrombus formed in pelvic veins travels -> travels in circ to right side of heart & then to lungs - blocks pulmonary arteries

47
Q

Types of PE

A

Depends on size of embolus

Small emboli = 60-80%
-> clinically silent - as are small will be organised & canalised into blood v = fibrous web remains - but will inc pulmonary arterial pressure = pulmonary hypertension

Large emboli = 20-40%
-> sudden death - as these fully occlude the main pulmonary artery OR located between bifirc of pulmonary artery = low/no perfusion to ventilated areas = ‘dead space’ effect = dyspnoea, possible pulmonary infarct = chest pain & haemoptysis (cough up blood)

So size of PE determines outcome (i.e., severity)

48
Q

What is infarction

A

Area of ischaemic necrosis
Caused by either:
- Occlusion of arterial supply = arterial occlusion/infarct
- Occlusion of venous drainage = venous occlusion/infarct

49
Q

Histology of infarcts - necrosis type seen

A

Ischaemic coagulative necrosis
(except brain = liquifactive necrosis)

50
Q

What does arterial occlusion/infarct cause

A

Thrombosis
Embolism
Vasospasm or compressed vessel

51
Q

Effects of venous occlusion/infarct cause

A

Strangulated bowel - hernia

52
Q

2 types of infarct

A

Red/haemorrhagic
White/anaemic

53
Q

Red/haemorrhagic infarct

A

Venous occlusion = happens due to the inability of blood to exit the infarcted area - so area becomes congested - accumulation of blood around site
-> i.e., congested organs - organs previously affected by poor venous circulation
-> so appear red as blood (RBCs) accumulate in organ

OR

In organs with dual blood supply - arterial occlusion (main & collateral blood supply) - where a thrombus has embolises & lead to infarction (ischaemic necrosis of tissue - which is red due to dual blood supply)
-> lungs = pulmonary & bronchial arteries
-> hand & forearm = radial & ulnar arteries
-> SI = jejunal & ileal arteries from SMA
So appear red because the organ still has some blood supply to it (not all blood supply is compromised)

54
Q

White/anaemic infarct

A

Occurs in arterial occlusion
-> in solid organs supplied by terminal arterial vessels (being end arteries means is only single blood supply)
(end circulation organs) = kidney, liver, heart
-> are white in colour due to lack of hemorrhaging & limited RBC accumulation - so thes organs have only single blood supply - no alternative when this one is occluded
-> are often wedge shaped in an organ

55
Q

3 factors influencing infarct development

A

*Anatomy of vascular supply -> availability of alternative blood supply? - does the organ have single/terminal arterial supply or dual circ?
*Rate of occlusion -> slow then inf is less likely as gives time for collateral pathways to perfuse (e.g., heart coronary arteries)
*Tissue vulnerability to hypoxia -> does the organ have high O2 demands - if so = more vulnerable to hypoxia

56
Q

What is gangrene

A

Whole areas of limb or region of gut have arterial supply cut off (ischaemia) = death of large amounts of tissue (necrosis)

So is necrosis of tissue due to ischaemia
= ischemic necrosis

OR

tissue damage due to infection

***Infarct = tissue damage secondary to infection, ischemia, or both

57
Q

What condition is gangrene common in & why

A

Diabetes
-> do not feel when harm feet due to impaired circ & desensitised nerve endings (neuropathy)

58
Q

2 types of gangrene

A

Dry
Wet

59
Q

Dry gangrene

A

Tissue dies & is mummified
Healing occurs over top by coagulative necrosis
So is a sterile process - no infection
INFARCT DUE TO TISSUE DAMAGE

So coag necrosis which develops in ischaemic tissue

60
Q

Wet gangrene

A

Bacterial infection in gangrene (not sterile)
Leads to liquifactive necrosis
Leads to sepsis
INFARCT DUE TO INFECTION

61
Q

Arteriosclerosis

A

General term - which includes atherosclerosis, arteriolosclerosis, Monckeberg medial calcific sclerosis

So literally means hard arteries caused by thickening of blood vessel wall

62
Q

Atherosclerosis

A

Atheroma (intimal lesions) which narrow the lumen of a vessel & can rupture - causing sudden vessel occlusion

Atheroma = atheromatous plaque/atherosclerotic plaque

63
Q

Atheroma structure

A

Soft lipid (mainly cholesterol - LDL)
Necrotic core (foam cells)

Physiology (10 decks)

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