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Unit 9 > Week 1: circulatory pathology > Flashcards

Week 1: circulatory pathology Flashcards

1
Q

What are endothelial cells?

A

Cells that make up a continuous sheet lining the entire vascular tree
They regulate aspects of blood and blood vessel function.

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2
Q

What are some of the properties of blood vessels/blood that endothelial cells can regulate?

A

Permeability barrier
ECM
Anti-coagulant, anti-thrombotic and fibrinolytic regulators
Pro-thrombotic molecules
Blood flow and vascular reactivity
Inflammation and immunity
Cell growth
Oxidation of LDL

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3
Q

What maintains a normal basal state of endothelial cells and what is the result of this on endothelial cell properties?

A

Basal state is maintained by normotension, laminar flow and some growth factors (VEGFs)
This results in endothelial cells being non-ahdesive and non-thrombogenic.

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4
Q

What is meant by an endothelial cell in the activated state?

A

An endothelial cell that changes its function and properties due to pathological or physiological mechanisms.

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5
Q

What can trigger an endothelial cell to enter an activated state?

A

Pathological or physiological

Turbulent flow
Hypertension
Cyotkines
Complement
Pathogen products
Lipid products
Advanced glycation end-products
Hypoxia and acidosis
Cigarette smoke

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6
Q

What are some of the changes in endothelial cells properties and function in the activated state?

A

Increased pro-coagulants, adhesion molecules and proinflammatory factors
Altered chemokines, cytokines and growth factors.

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7
Q

What are the different properties of endothelial cells and what mediators do they use to express these properties?

A
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8
Q

What are the functions of vascular smooth muscle?

A

Can proliferate
Upregulate ECM collagen, elastin and proteoglycan production
Secrete growth factors and cytokines
Regulate vasoconstriction and vasodilation is response to physiologic or pharmacologic stimuli

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9
Q

What factors contribute to maintaining the quiescent state of Smooth muscle cells in the blood vessels?

A

Heparan sulphate
NO
Transforming Growth Factor TGF-beta

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10
Q

What factors contribute to a proliferative state of smooth muscle cells?

A

Platelet derived growth factor
Endothelin
Thrombin
Fibroblast Growth Factor
Inflammatory mediators (IFNy and IL-1)

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11
Q

How do you calculate blood pressure?

A

Cardiac output x peripheral resistance

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12
Q

What factors influence the cardiac output?

A

Heart rate
Contractility
Influences on blood volume - sodium, mineralcorticoid levels

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13
Q

What factors affect peripheral resistance?

A

Neural factors - constriction by alpha-adrenergic receptors, dilation by beta-adrenergic receptors
Humoral factors - constrictors (angiotensinogen, endothelin, thromboxane) and dilators (prostaglandin, kinins and NO)
Local factors - pH, hypoxia, autoregulation

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14
Q

How is angiotensin 2 produced in the RAAS system?

A

responsible for long term regulation of blood pressure
Low BP= low perfusion to kidney - production of renin from juxtaglomerular cells
Angiotensinogen produced by liver is converted to angiotensin 1 by renin.
Endothelium of lungs and kidneys contains ACE1 enzymes which convert angiotensin 1 to angiotensin 2.

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15
Q

What are the effects of angiotensin 2 in the RAAS system?

A

Binds to AT1 and AT2 receptors
Adrenal gland: increase aldosterone production, increase renal Na+ absorption
Hypothalamus: Increase ADH secretion, increase thirst signals and decrease sensitivity to baroreceptor responses
Systemic arterioles: vasoconstriction

Increases blood volume, greater venous return to heart leading to a greater cardiac output (Frank-Starling mechanism) leading to higher blood pressure.

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16
Q

What is hypertension as a pathological condition?

A

Persistent elevation of BP in systemic circulation, accelerates atherogenesis and degernerative changes in the walls of medium and large arteries.
Increase risk of aortic dissection and cerebrovascular haemorrhage

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17
Q

What are the two different types of arteriosclerosis and how are they different?

A

Hyperplastic arteriosclerosis
“onion skinning causing lumina obliteration”
Hyaline arteriosclerosis - hyalinized material to deposited thickening the wall

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18
Q

What condition is seen below?

A

Hyperplastic arteriosclerosis
“onion skinning causing lumina obliteration”

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19
Q

What condition is seen below?

A

Hyaline arteriosclerosis - hyalinized material to deposited thickening the wall

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20
Q

What is the aetiology of hypertension?

A

95% is essential ir idiopathic
5% secondary to renal disease, endocrine condition or neurological disease etc

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21
Q

What is the pathophysiology of essential hypertension?

A

Reduced renal sodium excretion
Increased vascular resistance
Genetic factors
Environmental factors

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22
Q

What are the renal causes of secondary HTN?

A

Acute glomerulonephritis
Chronic renal disease
Polycystic disease
Renal artery stenosis
Renal vasculitis
Renin-producing tumour

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23
Q

What are the endocrine causes of secondary HTN?

A

Adrenocortical hyperfunction
Exogenous hormones
Pheochromocytoma
Acromegaly
Hypo/hyperthyroidism
Pregnancy induced (pre-eclampsia)

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24
Q

What are the cardiovascular causes of secondary HTN?

A

Coarcttion of the aorta
Polyarteritis nodosa
Increased intravascular volume.
Increased cardiac output
Rigidity of the aorta

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25
Q

What are the neurological causes of secondary HTN?

A

Psychogenic
Increased intracranial pressure
Sleep apnoea
Acute stress, including surgery

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26
Q

What is the vascular response to injury?

A

Intimal Thickening*

Endothelial cells become dysfunctional, stimulating SMC growth and ECM synthesis resulting in thickening of the wall
In order to heal the vessel, SMC migrate to the intima. SMC proliferate and synthesise ECM, forming a neointima covered by an intact EC layer

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27
Q

What is Virchow’s triad in relation to thrombosis?

A

Three factors that all contribute the thrombosis formation.
Endothelial injury, hypercoagulability and abnormal blood flow.
Endothelial injury and abnormal blood flow have a positive feedback effect on each other, they both also increase hypercoagulability.

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28
Q

What is the result of endothelial injury in relation to thrombus formation?

A

Promotes platelet adhesion and aggregation
Causes the production of pro-coagulant factors

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29
Q

What are some pathological examples of endothelial injury?

A

Over ulcerates plaques in atherosclerosis
Endocardial injury in MI - mural thrombus
Traumatic or inflammatory vascular injury - vasculitis

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30
Q

How does an abnormal blood flow lead to thrombus formation? Examples?

A

Prevents the activation of blood diluting activated clotting factors
Stasis - as caused by venous thrombosis - platelets encounter endothelium and slow washout of activated clotting factors
Turbulence - (arterial, near valves) - can cause physical trauma to endothelial cells or can cause counter currents and pockets of stasis

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31
Q

What are the primary causes of a hypercoagulable state?

A

Leiden factor 5 mutation
Deficiency of antithrombin 111
Protein C and S (liver proteins)

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32
Q

What are the secondary causes of a hypercoagulable state?

A

Typically: increased concentration of fibrinogen and prothrombin
Immobilisation, MI, neoplasia, tissue damage, prosthetic valves, heparin induced thrombocytopenia syndrome, antiphospholipid syndrome

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33
Q

What are the two different types of thrombus?

A

Arterial thrombus
Venous thrombus

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34
Q

What are the features of an arterial thrombus?

A

Typically caused Secondary to atheroma or endothelial injury
Consist of platelets
Commonly found in the brain (MCA) and coronary arteries
Termed ‘white thrombus’

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35
Q

What are the features of a venous thrombus?

A

Typically caused by slow blood flow, stasis or low BP
Consist of rbcs, platelets and fibrin
Typically found in deep calf veins (can embolise to lungs) and hepatic portal vein.
‘red thrombus’
Endothelial walls express increased adhesion factors

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36
Q

What are the pathological features below?

A

Aortic thrombus from an aortic aneurysm
Shows lins of zahn, lines of fibrin and platelets.

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37
Q

What is shown in the image below?

A

Portal vein thrombosis
Note the gallbladder and IVC

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38
Q

What is shown in the image?

A

Renal vein thrombosis
Note dark red/black colour

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39
Q

What are the different fates of a thrombus?

A

Lysis: due to thrmobolytic activity in blood
Propagation (increase in size): anchor for further thrombosis
Organisation
Canalisation
Embolisation

40
Q

What is meant by organisation of a thrombus?

A

Invaded by connective tissue
Causes to become white and greyish in appearance

41
Q

What is meant by canalisation of a thrombus?

A

New lumens lined by endothelial cells form in an organised thrombus

42
Q

What is meant by embolisation of a thrombus?

A

PArt or all of thrombus becomes disloadged. travels through circulation and lodges in a blood vessel some distance from thrombus formation.

43
Q

What is shown in the image below?

A

Canalisation of a thrombus

44
Q

What is shown in the image below?

A

Organisation of a thrombus
The position of the internal elastic lamina notes the original position of the artery walls

45
Q

What is an embolism?

A

When detached fragments from a solid (thrombus), liquid (amniotic fluid) or gas (nitrogen) are carried by blood to a distant site.
Most common thromboembolism

46
Q

What are some rare types of embolism?

A

Fat and bone marrow embolism - traumatic fracture to long bones
Air embolism - deep sea divers
Tumour embolism
Amniotic fluid embolism

47
Q

What is a pulmonary thromboembolism and what are their normal features?

A

70% are small and clincally significant
95% originate from deep vein, 5% from pelvic veins
Passess through the heart into the lungs
May undergoe organisation and leave behind fibrous webs

48
Q

What are the different outcomes of a pulmonary embolism?

A

Smaller size - increase pulmonary arterial pressure
When areas are not supplied by blood - shortness of breath, infarction presents as chest pain and coughing up blood
Pulmonary hemorrhage - downstream capillaries rupture due to lack of oxygen, patient will cough up blood
Massive embolus - death

49
Q

Suggest why the damage from a pulmonary embolism is sometimes less than expected?

A

Dual blood supply to the lungs - collateral blood supply can temporarily meet demand to reduce damage

50
Q

Why is a pulmonary infarct sometimes referred to as a red infarct?

A

Dual blood supply, causes area of heamorrhage (typically dur to higher pressure in the bronchial system) despite one blood supply being blocked

51
Q

What is shown in the image below?

A

Blood clot in a pulmonary vessel

52
Q

What is an arterial infarct?

A

Arterial occlusion leads to ischemic necrosis of tissue due to:
Thrombosis
Emboli
Vasospam or compression of a vessel

53
Q

What is a venous infarct?

A

Venous occlusion leading to ischemic necrosis of tissue due to:
Strangulated bowel hernia
Bowel volvulus, torsion testiticular

54
Q

What is the histological characteristic of infarction in most tissue?

A

Coagulative necrosis
Except in the brain - liquefactive necrosis

55
Q

What typically results in a red (haemorrhagic) infarct?

A
  1. venous blockage
  2. loose tissue (lungs)
  3. Dual circulation (Small intestine)
  4. Congested organs
  5. Res-established blood flow in area of infarcted tissue
56
Q

What typically results in white (Anaemic) infarcts?

A

Arterial occlusions
Solid organs
End arterial circulation organs (heart, spleen, kidney)
Dense tissues

57
Q

What is a septic infarct?

A

When cardiac valve vegetations embolize or when microbes spread to necrotic tissue.
Infarct is converted to an abscess, triggers a greater inflammatory response and healing by organisation and fibrosis

58
Q

What is shown in the image below?

A

White infarcts in the spleen

59
Q

What is shown in the image below?

A

Red infarction in the small bowel

60
Q

What is shown in the image below?

A

Red infarct in the lungs

61
Q

What is shown in the image below?

A

White infarct in the kidney

62
Q

What factors influence infarct development?

A
  1. Anatomy of vascular supply - is there an alternative?
  2. Rate of occlusion - slow rates allow time for collateral blood supply to develop
  3. Tissue vulnerability to hypoxia - oxygen demand and metabolic rate
63
Q

What is gangrene?

A

When areas of a limb or region of gut have arterial supply cut off and large area of tissue die
Dry gangrene (Non-infectious): tissue mummifies and heals over
Wet gangrene: bacterial infections cause gangrene and sepsis
Typically in toes/fingers, becomes blackened and shrivelled in appearance

64
Q

What are the key symptoms to differentiate between wet and dry gangrene?

A

Wet: foul smelling discharge, signs of infection, wet may also have loss of digits

65
Q

What is arteriosclerosis?

A

Thickening of the blood vessel walls.
Are three main divisions:
1. atherosclerosis
2. arteriolosclerosis
3. Monckeberg medial calcific sclerosis

66
Q

What are the features of atherosclerosis?

A

Pathological process of Lipid accumulation
In large and medium sized vessels
Affects the intima and underlying smooth muscles
Results in plaque forming degenerative changes with some calcification
Decrease blood vessel diameter.

67
Q

What are the features of arteriolosclerosis?

A

Pathological process of protein accumulation and fibromuscular proliferation of the intima
Results in concentric media thickening of muscular arteries
Affects the media
Thickening of the media results in decreased vessel diameter with no calcification

68
Q

What are the features of monckeberg anteriosclerosis?

A

Can by pathological or physiological calcium deposition
Mainly affecting the internal elastic lamina
Seen as pathcy calcification of the intima
Has no effect on vessel dimension

69
Q

Define atheromas

A

Abnormal accumulation of abnormal tissue often fat or scar tissue in the intima of a vessel
Often have a soft lipid core with a necrotic centre and fibrous cap.

70
Q

What is atherosclerosis?

A

When intimal lesions called atheromas (atherosclerotic plaques) impinge on vascular lumen and can rupture to cause sudden occlusion
Large and medium sized arteries

71
Q

What are the major non-modifiable risk factors for atherosclerosis?

A

Genetic
Family history
Age
Sex

72
Q

What are the major modifiable risk factors for atherosclerosis?

A

Hyperlipidaemia
HTN
Smoking
Inflammation
Diabetes mellitus

73
Q

What is the pathogenesis (process by which an atherosclerosis forms)?

A

Response-to-injury-hypothesis
1. Dysfunctional endothelial cells and activated inflammatory response
2. Increased permeability allows monocytes, and leukocytes to adhere and migrate into the intima. Pro-coagulant factor release may result in thrombus formation.
3. Lipoproteins, mainly cholesterol and LDL, accumulate in the intima and are oxidised
4. Platelets adhere to the wall
5. Monocytes in the intima differentiate into macrophages and foam cells (phagocytose oxidised LDL)
6. Lipid accumulation with macrophage results in pro-inflammatory cytokine release and fatty streak formation as foam cells die spilling lipid content.
7. SMC are recruited by activated EC, platelets and M1, they proliferate and produce ECM.

74
Q

What can be seen in the image?

A

Fatty streaks within the intima - sign of atherosclerosis

75
Q

What can be seen in the image?

A

Athersclerotic plaque

76
Q

What is an endarterectomy?

A

A surgical procedure to remove plaque build up from narrowed or blocked arteries
Used to treat atherosclerosis

77
Q

Describe the histological features of an atherosclerosis plaque?

A

narrowed or obliterated artery lumen
Fibrosis plaque (stained like collagen often blue or yellow)
Lipid (mainly necrotic centre) staining white

In advanced plaques the tunica media, and the internal/external elastic lamine may also the thinned.

78
Q

What can be seen in the image?

A

narrowed or obliterated artery lumen
Fibrosis plaque (stained like collagen often blue or yellow)
Lipid (mainly necrotic centre) staining white

Indicates atherosclerotic plaque

79
Q

What features of an atherosclerotic plaque can be seen in the image?

A

Calcification - arrow heads
Neurovascularisation - arrows

80
Q

How does atherosclerotic plaque lead to a thrombus formation?

A

Erosion
Ulceration
RUpture
All of which can lead to thrombus formation
Is the patient survives thrombus formation, the thrombus is organised allowing the growth of a larger plaque

81
Q

What is shown in the image?

A

Blood vessel cross section
Arrow points to an area of fibrous cap rupture, B shows the thrombus formed in situ, A does not show the resulting thrombus.

82
Q

What are the potential outcomes of atherosclerotic plaque?

A
  1. Thrombus formation
  2. Hemorrhage into a plaque (may result in plaque expansion or rupture)
  3. Atheroembolism
  4. Aneurysm formation
83
Q

What is a haematoma?

A

A pooling of blood

84
Q

How can atherosclerosis lead to an aneurysm?

A

Pressure on the vessel wall from the atherosclerosis plaque
Ischemic atrophy of the underlying media
Combined with a loss of elastic tissue
structural weakening allow dilation and rupture of vessel walls.

85
Q

What is the difference between a vulnerable and a stable atherosclerotic plaque?

A

Vulnerable - small fibrous cap
Stable - large fibrous cap
Stable is less likely to rupture

86
Q

What are the pre-clinical stages of an atherosclerotic plaque?

A

Normal artery develops fatty streaks then becomes (or directly develops into) a fibrofatty plaque.
Inflammation, cell death and vascular processes such as plaque growth, organisation of thrombus and calcification lead to a vulnerable plaque.

87
Q

What are the clinical phases of a atherosclerotic plaque?

A

Aneurysm and rupture
Occlusion by thrombus
Critical stenosis (blood flow into ischemic zone)

88
Q

What is an aneurysm?

A

Congenital or acquired dilation of blood vessels or the heart

89
Q

What are the two main predisposing factors for an aneurysm?

A

Athersclerosis
Hypertension

90
Q

What are the different types of aneurysm?

A

True aneurysm - all layers of vessel wall dilate
Saccular - one side only
Falsiform - both sides

False aneurysm - penetrate the three blood vessel layers and blood pools in the surrounding extravascular connective tissue ( between tunica media and tunica adventicia)

91
Q

What is an aortic dissection?

A

When there is a tear in the intima, blood collects between the intima and the media.

92
Q

What is shown in the image below?

A

An AAA
White arrow shows point of rupture
Inside shows layered thrombus

93
Q

What is shown in the image?

A

An opened aorta
With a intimal tear shown by the probe
Allowing a intramural hematoma to form
Athersclerotic plaque (slightly yellowish) has stopped the progression of the dissection

94
Q

What is shown in the image?

A

Histological section of an aorta with a intramural hematoma
Astericks marks the lumen filled with red blood
Notice how the red blood continues through the concentric elastic rings of the tunica media

95
Q

What are the three different classifications of dissections?

A

DeBakey 1: dissection in proximal aorta but blood accumulates in an extensive way (typically past BCS)

DeBakey 2: dissection in proximal aorta but blood accumulates only locally (before BCS)

DeBaley 3: Dissection in distal aorta (past BCS)

96
Q

What is shown in the image?

A

Dry gangrene

Unit 9 (15 decks)

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