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Block 2.1 Circulation and Lungs Summary
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  • Course
  • Block 2.1 Circulation and Lungs
  • Institution
  • Maastricht University (UM)
  • Book
  • Robbins Basic Pathology

This document includes all the cases, lecture notes and skills labs from block 2.1 (from 2016). It is extensive and includes all the details you need to go from a general overview to a precise picture. Written by someone who passed with a 'good'.

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Document information

  • No
  • Circulation and lungs
  • October 8, 2017
  • 106
  • 2016/2017
  • Summary

Subjects

  • medicine
  • circulation and lungs
  • summaries
  • lectures
  • cases
  • skillslabs
  • practicals
  • 21

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  • Block 2.1 Circulation and Lungs
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Fiche de Revision - Circulation and Respiration

Case 1: Atherosclerosis

I. Clinical Presentation of Atherosclerosis

1. Pathogenesis

- response to injury:
- injuries: endothelial dysfunction, hemodynamic disturbances, hypercholesterolemia, toxins,
inflammatory toxins
- LDL: impairs endothelial functions, increases ROS production, destroys NO
- location: areas of turbulent blood flow ; large/medium elastic and muscle arteries (coronary,
carotid, cerebral, aorta, major limb arteries)
-




development:

, - net effect of risk factors: inhibition of NO production ; stimulate production of adhesion
molecules, pro-inflammatory cytokines, chemotactic proteins, vasoconstriction
- steps:
- oxidized LDL
a) Fatty Streak
- endothelial binding of monocytes/T-cells
- migration of these to the subendothelial space
- initiation and perpetuation of local vascular inflammatory response
- lipids taken up/oxidised by the macrophages > results in foam cells

b) Atheroma
- macrophages produce cytokines which recruit smooth muscle cells ; increase ECM
- hypoxia in the plate causes cell death (worsening)
= subendothelial fibrous plaque w/ fibrous cap (intimal smooth muscle cells) surrounded by
connective tissue & intra/extracellular lipids + calcification w/i the plaque
- note: smooth muscle have receptors for LDL
- composition:
- lipid, lipid laden foam cells < inflammatory and smooth muscle cells < connective tissue
matrix (~ thrombi, Ca2+)
- types of atheromas:
- stable: collagen degradation/synthesis ratio in the smooth muscle cells (PDGF, FGF, TGDa)
- unstable: inflammatory cytokines, breakdown of ECM, high macrophage content, thick lipid
core, thin fibrous cap

2. Risk Factors

- 2 types:
- constitutional: genes, family, history, age, gender
- genetic: PCSK9 gene codes for LDL receptors for uptake from the blood
- gender: premenopausal women have a lower risk than men (estrogen protects)
- acquired: lifestyle choices, hyperlipidemia, hypertension, smoking, diabetes, obesity,
metabolic syndrome, etc…
- dyslipidemia: high total, high LDL/low HDL cholesterol

, - high LDL: oxidation, uptake causes increase of adhesion molecules, cytokines,
antigenic effect, T cell response, arterial wall inflammation
- normal HDL: reverse transport of LDL cholesterol; transport of antioxidant enzymes
- hypertension:
- vascular inflammation via angiotensin II mechanism
- angiotensin II stimulates endothelial cells/smooth muscle cells/macrophages to
produce atherogenic factors
- diabetes
- formation of AGEs ; increase of oxidative stress and ROS leading to endothelial injury
- smoking:
- nicotine/other chemicals toxic to the vascular endothelium
- increase in platelet reactivity (increase in thrombus formation risk)
- promotes vasoconstriction
- increases LDL, decreases HDL
- chronic inflammation: CRP production

3) Symptoms

- occur after the plaque has caused stenosis/acute plaque change = when blood flow is impeded
- typical signs:
- transient ischemia: angina pectoris, TIA (pre-stroke), intermittent claudication
- aneurysms, arterial dissection: pain, pulsatile mass, absent pulses, sudden death

4) Diagnosis

a) Symptomatic Patients
- basics: history/physical examination, fasting lipid profile, plasma glucose, glycosylated
hemoglobin levels
- systemic evaluation (despite localized symptoms)
- CT angiography w/ possibility of other imaging techniques

b) Asymptomatic Patients - Screening
- patients w/ risk factors but no symptoms
- blood tests: fasting lipid profiles
- urinary microalbuminuria (<30mg/24h)

II. Treatment and Management of Atherosclerosis

- goals: lower risk of clotting, widening/bypassing affected vessels, preventing complications
- basics:
- lifestyle: reduce obesity (BMI < 25), stop smoking, exercise, healthy diet

, - stabilize plaques
- antiplatelet, anticoagulants, antihypertensive medication
- diet: controlled BP and cholesterol, avoid diabetes 2
- no saturated fats, more omega 3, lots of soluble fibre
- surgery:
- angioplasty: procedure to open narrowed/blocked arteries ; can include stent placement
- bypass grafting: vessels from nearby body areas used to bypass the narrowed vessels
- endarterectomy: removal of plaque build up
- medications:
- commonly: anticoagulants, beta blockers, Ca channel inhibitors, niacin, statins,
thrombolytics, ACE inhibitors, diuretics, nitrates
- statins:
- lowers LDL cholesterol by reducing LDL production in the liver (1ry, 2ry prevention)
- mechanism: competitive inhibition of HMG-CoA reductase
- HMG-CoA reductase: first enzyme in cholesterol producing pathway mevalonate
- other effects: increase in LDL receptors to clear the LDL-cholesterol ; lowers blood
triglycerides
- nitrates (prodrug)
- vasodilator: donation of NO by reduction (w/ exception of certain forms where the nitrate is
in the correct state)
- mechanism: NO stimulates guanylate cyclase in vascular smooth muscle > GTP to cGMP >
protein kinase G activated > phosphorylation of proteins decreasing intracellular Ca2+ > muscle
relaxation > dilation
- acts primarily on veins = increases capacity of venous pool

III. Complications

- 2 major consequences:
- atherosclerotic stenosis: protrusion of the plaque into the lumen, leading to decrease of blood
flow
- acute plaque change: ruptured plaque causing thrombosis; erosion in the subendothelial
basement membrane; haemorrhage into the atheroma (can be caused by adrenergic
stimulation)
- physiology of acute plaque change:
- rupture: MTPs (metalloproteinases), cathepsins, collagenases, produced by plaque
macrophages
- these digest the fibrous cap causing thinning and rupture
- T cells secrete cytokines preventing smooth muscle recruitment
- 5 outcomes:
- thrombus organized/incorporated into a plaque leading to rapid plaque growth
- thrombus occludes vascular lumen, precipitates an ischemic events

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