Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Unit 9 > Week 1: circulatory pathology > Flashcards

Week 1: circulatory pathology Flashcards

(96 cards)

Start Studying
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you calculate blood pressure?

A

Cardiac output x peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What factors influence the cardiac output?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What condition is seen below?

A

Hyperplastic arteriosclerosis
“onion skinning causing lumina obliteration”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What condition is seen below?

A

Hyaline arteriosclerosis - hyalinized material to deposited thickening the wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the pathophysiology of essential hypertension?

A

Reduced renal sodium excretion
Increased vascular resistance
Genetic factors
Environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the endocrine causes of secondary HTN?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What are the neurological causes of secondary HTN?
Psychogenic Increased intracranial pressure Sleep apnoea Acute stress, including surgery
26
What is the vascular response to injury?
****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
27
What is Virchow's triad in relation to thrombosis?
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.
28
What is the result of endothelial injury in relation to thrombus formation?
Promotes platelet adhesion and aggregation Causes the production of pro-coagulant factors
29
What are some pathological examples of endothelial injury?
Over ulcerates plaques in atherosclerosis Endocardial injury in MI - mural thrombus Traumatic or inflammatory vascular injury - vasculitis
30
How does an abnormal blood flow lead to thrombus formation? Examples?
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
31
What are the primary causes of a hypercoagulable state?
Leiden factor 5 mutation Deficiency of antithrombin 111 Protein C and S (liver proteins)
32
What are the secondary causes of a hypercoagulable state?
Typically: increased concentration of fibrinogen and prothrombin Immobilisation, MI, neoplasia, tissue damage, prosthetic valves, heparin induced thrombocytopenia syndrome, antiphospholipid syndrome
33
What are the two different types of thrombus?
Arterial thrombus Venous thrombus
34
What are the features of an arterial thrombus?
Typically caused Secondary to atheroma or endothelial injury Consist of platelets Commonly found in the brain (MCA) and coronary arteries Termed 'white thrombus'
35
What are the features of a venous thrombus?
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
36
What are the pathological features below?
Aortic thrombus from an aortic aneurysm Shows lins of zahn, lines of fibrin and platelets.
37
What is shown in the image below?
Portal vein thrombosis Note the gallbladder and IVC
38
What is shown in the image?
Renal vein thrombosis Note dark red/black colour
39
What are the different fates of a thrombus?
Lysis: due to thrmobolytic activity in blood Propagation (increase in size): anchor for further thrombosis Organisation Canalisation Embolisation
40
What is meant by organisation of a thrombus?
Invaded by connective tissue Causes to become white and greyish in appearance
41
What is meant by canalisation of a thrombus?
New lumens lined by endothelial cells form in an organised thrombus
42
What is meant by embolisation of a thrombus?
PArt or all of thrombus becomes disloadged. travels through circulation and lodges in a blood vessel some distance from thrombus formation.
43
What is shown in the image below?
Canalisation of a thrombus
44
What is shown in the image below?
Organisation of a thrombus The position of the internal elastic lamina notes the original position of the artery walls
45
What is an embolism?
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
What are some rare types of embolism?
Fat and bone marrow embolism - traumatic fracture to long bones Air embolism - deep sea divers Tumour embolism Amniotic fluid embolism
47
What is a pulmonary thromboembolism and what are their normal features?
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
What are the different outcomes of a pulmonary embolism?
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
Suggest why the damage from a pulmonary embolism is sometimes less than expected?
Dual blood supply to the lungs - collateral blood supply can temporarily meet demand to reduce damage
50
Why is a pulmonary infarct sometimes referred to as a red infarct?
Dual blood supply, causes area of heamorrhage (typically dur to higher pressure in the bronchial system) despite one blood supply being blocked
51
What is shown in the image below?
Blood clot in a pulmonary vessel
52
What is an arterial infarct?
Arterial occlusion leads to ischemic necrosis of tissue due to: Thrombosis Emboli Vasospam or compression of a vessel
53
What is a venous infarct?
Venous occlusion leading to ischemic necrosis of tissue due to: Strangulated bowel hernia Bowel volvulus, torsion testiticular
54
What is the histological characteristic of infarction in most tissue?
Coagulative necrosis Except in the brain - liquefactive necrosis
55
What typically results in a red (haemorrhagic) infarct?
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
What typically results in white (Anaemic) infarcts?
Arterial occlusions Solid organs End arterial circulation organs (heart, spleen, kidney) Dense tissues
57
What is a septic infarct?
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
What is shown in the image below?
White infarcts in the spleen
59
What is shown in the image below?
Red infarction in the small bowel
60
What is shown in the image below?
Red infarct in the lungs
61
What is shown in the image below?
White infarct in the kidney
62
What factors influence infarct development?
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
What is gangrene?
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
What are the key symptoms to differentiate between wet and dry gangrene?
Wet: foul smelling discharge, signs of infection, wet may also have loss of digits
65
What is arteriosclerosis?
Thickening of the blood vessel walls. Are three main divisions: 1. atherosclerosis 2. arteriolosclerosis 3. Monckeberg medial calcific sclerosis
66
What are the features of atherosclerosis?
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
What are the features of arteriolosclerosis?
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
What are the features of monckeberg anteriosclerosis?
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
Define atheromas
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
What is atherosclerosis?
When intimal lesions called atheromas (atherosclerotic plaques) impinge on vascular lumen and can rupture to cause sudden occlusion Large and medium sized arteries
71
What are the major non-modifiable risk factors for atherosclerosis?
Genetic Family history Age Sex
72
What are the major modifiable risk factors for atherosclerosis?
Hyperlipidaemia HTN Smoking Inflammation Diabetes mellitus
73
What is the pathogenesis (process by which an atherosclerosis forms)?
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
What can be seen in the image?
Fatty streaks within the intima - sign of atherosclerosis
75
What can be seen in the image?
Athersclerotic plaque
76
What is an endarterectomy?
A surgical procedure to remove plaque build up from narrowed or blocked arteries Used to treat atherosclerosis
77
Describe the histological features of an atherosclerosis plaque?
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
What can be seen in the image?
narrowed or obliterated artery lumen Fibrosis plaque (stained like collagen often blue or yellow) Lipid (mainly necrotic centre) staining white Indicates atherosclerotic plaque
79
What features of an atherosclerotic plaque can be seen in the image?
Calcification - arrow heads Neurovascularisation - arrows
80
How does atherosclerotic plaque lead to a thrombus formation?
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
What is shown in the image?
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
What are the potential outcomes of atherosclerotic plaque?
1. Thrombus formation 2. Hemorrhage into a plaque (may result in plaque expansion or rupture) 3. Atheroembolism 4. Aneurysm formation
83
What is a haematoma?
A pooling of blood
84
How can atherosclerosis lead to an aneurysm?
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
What is the difference between a vulnerable and a stable atherosclerotic plaque?
Vulnerable - small fibrous cap Stable - large fibrous cap Stable is less likely to rupture
86
What are the pre-clinical stages of an atherosclerotic plaque?
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
What are the clinical phases of a atherosclerotic plaque?
Aneurysm and rupture Occlusion by thrombus Critical stenosis (blood flow into ischemic zone)
88
What is an aneurysm?
Congenital or acquired dilation of blood vessels or the heart
89
What are the two main predisposing factors for an aneurysm?
Athersclerosis Hypertension
90
What are the different types of aneurysm?
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
What is an aortic dissection?
When there is a tear in the intima, blood collects between the intima and the media.
92
What is shown in the image below?
An AAA White arrow shows point of rupture Inside shows layered thrombus
93
What is shown in the image?
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
What is shown in the image?
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
What are the three different classifications of dissections?
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
What is shown in the image?
Dry gangrene

Unit 9 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions