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'.
Test Bank for Robbins Basic Pathology 11th Edition by Vinay Kumar,AbulmK.Abba Chapters 1-24
TEST BANK FOR ROBBINS’ BASIC PATHOLOGY 10th EDITION BY KYMAR ABBAS TEST BANK ALL CHAPTERS INCLUDED 2024/2025
TEST BANK FOR ROBBINS’ BASIC PATHOLOGY 10th EDITION BY KYMAR ABBAS TEST BANK ALL CHAPTERS INCLUDED 2024/20254
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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)
, - 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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