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Blood Vessels Flashcards

1
Q

Essential hypertension (cause unknown) accounts for 90-95% of all cases of hypertension. For the following systems which can cause secondary hypertension give three examples of relevant conditions:
1. Renal
2. Endocrine
3. Cardiovascular
4. Neurologic

A
  1. Acute glomerulonephritis, CKD, polycyclic disease
  2. Adrenocortical hyperfunction, exogenous hormones, acromegaly
  3. Coarctation of the aorta, polyarteritis nodosa, rigidity of aorta
  4. Psychogenic, sleep apnea, increased intracranial pressure
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2
Q

What blood diastolic and systolic pressure is considered clinically significant hypertension?

A

Above 120/80mmHg

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3
Q

Blood pressure is a function of cardiac output and peripheral vascular resistance. What in turn influences these factors?

A
  • Cardiac output is a function of stroke volume (preload most important effect) and heart rate (this and contractility(affects SV) regulated by alpha and beta adrenergic systems)
  • Peripheral resistance predominantly regulated at arterioles by neural (alpha constricts, beta dilates) and hormonal inputs, also autoregulation and tissue pH and hypoxia
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4
Q

What is released from myocardium (particularly atrial) in response to volume expansion and inhibits sodium resorption in the distal renal tubules as well as induces systemic vasodilation?

A

Myocardial natriuretic peptides

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5
Q

What sodium transporter is tightly regulated (unlike those responsible for 98% of sodium resorption) by the renin-angiotensin-aldosterone system?

A

The epithelial sodium channel (EnaC)

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6
Q

Fill in the blanks for the following walk through of the renin-angiotensin-aldosterone system:

Renin produced by XXXX. Released in response to XXXX, XXXX or XXXX (due to fall in glomerular filtration rate, eg with low CO, leading to increased sodium resorption in proximal tubules).
Renin cleaves plasma angiotensinogen (made in liver) to angiotensin I. XXXX (in many tissues) converts to angiotensin II.
Angiotensin II raises BP by XXXX, stimulating XXXX and increasing XXXX.
Aldosterone increases blood volume by increasing sodium resorption in the XXXX.

A

Renin produced by renal juxtaglomerular cells. Released in response to low BP in afferent arterioles, high catecholamines or low sodium in the distal convoluted tubules (due to fall in glomerular filtration rate, eg with low CO, leading to increased sodium resorption in proximal tubules).
Renin cleaves plasma angiotensinogen (made in liver) to angiotensin I. ACE (in many tissues) converts to angiotensin II.
Angiotensin II raises BP by inducing vascular contraction, stimulating aldosterone secretion from adrenal gland and increasing tubular sodium resorption.
Aldosterone increases blood volume by increasing sodium resorption in the distal convoluted tubules.

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7
Q

Hypertension is a major risk factor for atherosclerosis, congestive heart failure and renal failure. What are some other forms (other than atherosclerosis) of vascular pathology caused by hypertension?

A
  • Degenerative changes to large and medium artery walls that can lead to aortic dissection and cerebrovascular haemorrhage
  • Small vessels- hyaline arteriolosclerosis, hyperplastic arteriosclerosis (in severe hypertension) and changes in pulmonary hypertension such as fibrotic intimal thickening and medial hyperplasia.
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8
Q

What is arteriosclerosis?

A

Arterial wall thickening and loss of elasticity

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9
Q

Name the type of arteriosclerosis that fits the following definitions:
1. Characterised by calcifications of the medial walls of muscular arteries, typically starting along the internal elastic membrane. They do not usually encroach the vessel lumen and are usually not clinically significant. Over 50y/o most commonly affected.
2. Occurs in muscular arteries larger than arterioles. Driven by inflammation (e.g. transplant-associated arteriopathy) or by mechanical injury (e.g. stents) and can be considered a healing response. Affected vessels can become quite stenotic.
3. Affects small arteries and arterioles and may cause downstream ischemic injury. Often caused by hypertension.

A
  1. Mönckeberg medial sclerosis
  2. Fibromuscular intimal hyperplasia
  3. Arteriolosclerosis
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10
Q

What is atherosclerosis?

A

A disease affecting the intima of arteries where plaques typically consisting of a raised lesion with a soft grumous core of lipid covered by a fibrous cap are formed

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11
Q

What are the major 1. Non-modifiable and 2. Modifiable risk factors for artherosclerosis?

A
  1. Genetic abnormalities, family history, increasing age, male gender
  2. Hyperlipidemia, hypertension, cigarette smoking, diabetes, inflammation
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12
Q

In the “response to injury” hypothesis, what are the eight steps by which atherosclerosis progresses?

A
  • Endothelial injury and dysfunction
  • Accumulation of lipoproteins in the vessel wall
  • Monocyte adhesion to the endothelium and migration to the intima
  • Platelet adhesion
  • SMC recruitment via factor release
  • SMC proliferation, ECM production and recruitment of T-cells
  • Lipid accumulation (extracellular, macrophages and SMCs)
  • Calcification of the ECM and necrotic debris
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13
Q

What transcription factor is upregulated when blood flow is laminar and non-turbulent, or by statins, that turns off inflammatory gene transcription and turns on atheroprotective genes?

A

Krüppel-like factor-2 (KLF2)

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14
Q

What are three important forms of dyslipoprotrinemias in hypercholesterolemia in relation to artherosclerosis?

A

Increased LDL levels, decreased HDL levels, increased levels of the abnormal lipoprotein a (Lp(a))

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15
Q

In descending order list the six most extensively involved vessels in artherosclerosis

A
  • Lower abdominal aorta
  • Iliac arteries
  • Coronary arteries
  • Popliteal arteries
  • Internal carotid arteries
  • Vessels of the circle of Willis
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16
Q

What are four secondary changes that artherosclerotic plaques can undergo, having further pathological impact?

A
  • Rupture, ulceration or erosion (leading to thrombosis)
  • Haemorrhage into a plaque (expanding size or causing rupture)
  • Atheroembolism
  • Aneurysm formation (from pressure or ischemic atrophy of underlying media)
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17
Q

What are the three major clinical consequences of atherosclerosis?

A

Myocardial infarction, cerebral infarction and peripheral vascular disease

18
Q

In atherosclerotic stenosis at approximately what percentage does 1. the inner diameter begin to narrow (as the outward remodelling of vessel media is no longer able to compensate? and 2. critical stenosis occur (when sufficiently severe to cause tissue ischemia)?

A
  1. 40%
  2. 70-75%
19
Q

Define the following:
1. True aneurysms saccular and fusiform
2. False aneurysm
3. Arterial Dissection

A
  1. Involve all the layers of an intact, but attenuated arterial or ventricular wall. Saccular involve an outpouching of a section of the wall while fusiform are circumferential
  2. Defect in a vascular wall leading to an extravascular haematoma that freely communicates with the intravascular space
  3. When blood enters a defect in the arterial wall and tunnels through the medial or medial-adventitial planes. Often, but not always, aneurysmal
20
Q

What are four defects that contribute to the pathobiology of both heritable aneurysmal diseases as well as sporadic forms of aneurysms?

A
  • The intrinsic quality of the vascular wall connective tissue is poor e.g. due to defective type III collagen synthesis in the vascular form of Ehlers-Danlos syndrome
  • Abnormal TGF-B signalling (excessive diminishes ECM content and integrity) e.g. defective fibrillin in Marfan syndrome means TGF-B is not appropriately sequestered
  • Balance of collagen degradation and synthesis is altered by inflammation and associated processes.
  • Vascular wall is weakened through loss of SMCs (e.g. by infarct) or the inappropriate synthesis of noncollagenous or nonelastic ECM
21
Q

The two most important causes of aortic aneurysms are atherosclerosis (esp for AAAs) and hypertension (esp for ascending aortic aneurysms). What are six other risk factors?

A
  • Advanced age
  • Smoking
  • Trauma
  • Vasculitis
  • Congenital defects
  • Infections (mycotic aneurysms)
22
Q

AAAs generally grow at a rate of 0.2-0.3cm/year. At what size does the yearly risk of rupture become 11% and is when they are large enough to warrant aggressive management?

A

5cm

23
Q

What is the major risk factor for aortic dissection?

A

Hypertension (causes medial degenerative changes with SMC loss and altered ECM content).
Note atherosclerosis is protective

24
Q

What are the two types of aortic dissections?

A
  • Type A - proximal lesions involving either both the ascending and descending aorta (DeBakey I) or the ascending aorta only (DeBakey II). More common and more dangerous
  • Type B - distal lesions not involving the ascending aorta and usually beginning distal to the subclavian artery (DeBakey III)
25
Q

Define vasculitis

A

Vessel wall inflammation with protean manifestations depending on the vascular bed affected

26
Q

Physical and chemical injury can cause vasculitis, but what are the two main pathogenic mechanisms?

A

Immune mediated inflammation and direct invasion of vascular walls by infectious pathogens

27
Q

In what two vasculitides is immune complex deposition implicated?

A

Drug hypersensitivity vasculitis and vasculitis secondary to infections

28
Q

There is a close association between ANCA (antineutrophil cytoplasmic antibodies) titres and disease activity in vasculitis. What are the the two most important ANCAs whose antigen surface expression is thought to be upregulated with inflammatory stimulation (leading to injury or further activation by ANCA)?

A
  • Anti-proteinase-3 (PR3-ANCA). Shares homology with numerous microbial peptides
  • Anti-myeloperoxidase (MPO-ANCA). Induced by several therapeutic agents
29
Q

What are the four main immunologic mechanisms underlying noninfectious vasculitis?

A
  • Immune complex deposition
  • Antineutrophil cytoplasmic antibodies
  • Anti-endothelial cell antibodies
  • Autoreactive T cells
30
Q

Giant cell arteritis is a chronic, classically granulomatous and often focal vasculitis. It likely occurs as a result of a T cell mediated immune response to an as yet uncharacterised vessel wall antigen. Why is prompt diagnosis and treatment important?

A

It can involve the ophthalmic artery and can lead to sudden and permanent blindness

31
Q

Takayasu arteritis is a granulomatous vasculitis of medium and larger arteries characterised principally by occular disturbances and marked weakening of pulses in the upper extremities. The histology is essentially indistinguishable from giant cell arteritis. 1 What artery does it classically involve and 2.how is the distinction between this and giant cell arteritis typically made?

A
  1. Aortic arc
  2. Age - <50 designated as Takayasu aortitis, >50 Giant cell aortitis
32
Q

Polyarteritis Nodosa is associated with segmental transmural necrotising inflammation of small to medium sized arteries, often with superimposed aneurysms and/or thrombosis. During the acute phase, what is inflammation frequently accompanied by?

A

Fibrinoid necrosis and luminal thrombosis

33
Q

The majority of cases of polyarteritis nodosa are of unknown cause, what is believed to be the cause of a third of cases?

A

Immune complex mediated from chronic Hep B forming HBsAg-HBsAgAb complexes

34
Q

Untreated, polyarteritis nodosa is typically fatal after an episodic course (immunosuppression can remit or cure 90%). Name the organ involvement that is often a major cause of mortality and most frequent, followed by other organ involvement in order of descending order of frequency.

A

Kidney, heart, liver and GI tract

35
Q

Kawasaki disease is an acute, febrile, usually self-limited illness associated with large to medium sized vessel arteritis.
1. In what age group to 80% of cases fall?
2. How does it typically present?
3. What is likely pathogenesis?
4. What is the major clinical concern?

A
  1. <4 years old
  2. Conjunctival and oral erythema and blistering, oedema of hands and feet, erythema of palms and soles, desquamative rash and cervical lymph node enlargement
  3. Triggered by infection. Delayed type hypersensitivity to cross reactive or newly exposed antigens. Autoantibodies to ECs and SMCs
  4. Development of coronary aneurysms which risk rupture and MI
36
Q

Microscopic polyangiitis is a necrotising vasculitis that generally affects capillaries, small venules and arterioles. Necrotising glomerulonephritis and pulmonary capillaritis are particularly common. What is believed to be the pathogenesis?

A

Most cases associated with MPO-ANCA. Some also immune complex deposition. Triggers in some cases have been drugs, microorganisms, heterologous proteins and tumour proteins.

37
Q

Granulomatosis with polyangiitis (GPA) is a necrotising vasculitis likely representing a form of T cell mediated hypersensitivity to innocuous inhaled environmental agents (PR3 ANCA also present). Untreated 80% fatality in one year. What is the triad it is characterised by?

A
  • Acute necrotising granulomas of the upper and/or lower respiratory tract
  • Necrotising or granulomatous vasculitis affecting small to medium sized vessels
  • Focal necrotising, often crescentic, glomerulonephritis
38
Q

Churg-Strauss syndrome is a small vessel necrotising vasculitis classically associated with asthma and allergic rhinitis. How do the vascular lesions differ from that of PAN or microscopic polyangiitis?

A

Due to the presence of both granulomas and eosinophils

39
Q

What form of vasculitis occurs almost exclusively in heavy cigarette smokers, usually before the age of 35?

A

Thromboangiitis obliterans (particularly affects tibial and radial arteries)

40
Q

Arteritis can be caused by the direct invasion of infectious agents, usually bacteria or fungi, and in particular, what two species?

A

Aspergillus and Mucor

BPS (13 decks)

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