CV Pathology Quiz Flashcards
- The following features are present in the affected myocardium 24 h after a heart attack:
a. heavy infiltrate of neutrophils to the peri-infarct zone
b. global coagulative necrosis of the myocardium
c. infiltrate of macrophage cells to the peri-infarct zone
d. a heart murmur
a. heavy infiltrate of neutrophils to the peri-infarct zone
- What is the earliest event in the mechanisms of atherogenesis?
a. lesion formation
b. endothelial dysfunction
c. both of the above
d. none of the above
b. endothelial dysfunction
- Describe the 5 layers of the arterial wall.
3 main layers, separated by elastic laminae.
- Innermost - INTIMA - contains endothelium monolayer + minimal subendothelial space
- Internal Elastic Lamina - fenestrated for diffusion
- MEDIA - layers of vascular SMC’s, defined by external & internal elastic lamina.
- External elastic lamina
- ADVENTITIA - protects the vascular wall from external shock, contains fat cells, fibroblasts, blood vessels, nerve fibres etc.
- Which is FALSE regarding endothelial cells?
a. Polygonal, elongated, containing many pinocytotic vesicles
b. form junctional complexes with their neighbours
c. are leaky to allow the diffusion of nutrients into ECM
d. line the entire vascular system (arteries, capillaries, veins, heart, lymphatics) in a monolayer of single cells
c. are leaky to allow the diffusion of nutrients into ECM.
Junctions bw cells in the monolayer are TIGHT, brought about by specific interactions between the proteins of the cells. They do not leak (in most cases), and act as a very tight barrier to blood-borne components.
- Name 7 functions of endothelial cells.
- semi-permeable membrane
- non-thrombogenic blood-tissue interface
- modulate vascular tone (blood flow) through action of NO (stimulates smc relaxation; helps allow blood from heart to pump through entire vasculature)
- metabolise hormones
- regulate immune & inflammatory reactions (important in wound healing)
- modify lipoproteins in arterial wall
- regulate growth of other cell types eg VSMCs
ALSO: critically involved in atherosclerosis & hypertension
- Describe a pathology of vascular smooth muscle cells (VSMCs)
Normal physiology: primarily to maintain vascular tone and assist in circulating blood.
But (in response to injury) they may become involved in aiding vascular repair by formation of neointima - expression of potent growth factors and oxidants can stimulate uncontrolled cellular proliferation into the vascular lumen (hindering blood flow).
ATHEROSCLEROSIS constitutes an exaggerated healing response by VSMCs, resulting in uncontrolled neointima formation that impacts on luminal blood flow.
- What are the two phenotypes of VSMCs?
CONTRACTILE (normal) - in media that contract to maintain vascular tone
PROLIFERATIVE/synthetic (pathogenic) - de-differentiated VSMC that lose the capacity to contract, but gain the ability to DIVIDE (proliferate), synthesise ECM, migrate to the intima.
- What happens to monocytes as a result of endothelial dysfunction?
a) adhesion via adhesion molecules, extravasation & maturation into macrophages within the sub-endothelial space
b) oxidise LDL to become foam cells
c) proliferate to occlude the vessel
d) synthesise ECM and migrate to the intima
a) adhesion via adhesion molecules, extravasation & maturation into macrophages within the sub-endothelial space.
As macrophages, they then engulf lipid (oxidised LDL mostly), to become foam cells. b) is incorrect; neither monocytes nor macrophages themselves oxidise LDL c & d) refer to the synthetic (pathogenic) phenotype of VSMCs that de-differentiate and lose the capacity to contract, instead gaining the ability to divide, synthesise ECM and migrate to the intima.
- What happens to macrophages once they ingest oxidised LDL?
They become “foam cells”. These foamy macrophages become immobilised, and attract further monocytes, further promoting a cycle of EC dysfunction through the generation of toxic oxygen-centred free radicals (that further oxidse LDL).
- Which of the following is a non-modifiable risk factor for atherosclerosis?
a) hyperlipidemia
b) genetics
c) hypertension
d) smoking
CORRECT: b) genetics (but could influence diabetes and hyperlipidemia)
a) hyperlipidemia alone can be modifiable: - monitor LDL intake (diet) - increase HDLs (exercise, moderate alcohol intake)
c) hypertension - can somewhat be monitored and influenced by diet (e.g. sodium)
d) smoking obviously - 1 pack/day x 3 years increases risk 4 fold (although risk can reverse over time with cessation)
- True or false? Atherosclerosis is an acute inflammatory response of the vascular wall to a variety of events that are initiated early in life.
False - CHRONIC (not acute)
- Multiple mechanisms contribute to plaque formation and progression. List 6.
- endothelial dysfunction
- monocyte adhesion and filtration
- lipid accumulation & oxidation in the sub-endothelial space
- smooth muscle proliferation
- ECM deposition
- thrombosis
- Pathology of Atherogenesis: 1. The normal artery has a) ____ layers, the _____, _____ and _______. b) ______ injury is the initiating factor in atherogenesis.
- The c) _____ streak is formed by accumulation & oxidation of d)__________ (mainly _______) and the initiation of e) __________ adhesion & f) __________.
- g)________ adhere to the wall and migrate to the h) __________ _______ where they become mature i)__________. T cells also invade the intima (immune response) and j)______ migrate from the media to the intima. k)________ continue to accumulate and undergo oxidation.
- After migration to the intimal layer, VSMCs l)__________ and become activated. More lipid accumulates and some is engulfed by m)______ & ______ the latter which become n)__________.
- Advanced lesions are characterised by continued localisation of o)_______, ____, ____ & _____ and the formation of the p) n_______ c___ & q) f______ c__.
a) three, intima, media, adventitia
b) Endothelial
c) fatty
d) lipoproteins (mainly LDL)
e) monocyte
f) migration
g) Monocytes
h) subendothelial space
i) macrophages
j) VSMCs
k) Lipids
l) proliferate
m) VSMCs & macrophages
n) foam cells
o) macrophages, VSMCs, T cells & lipids
p) necrotic core
q) fibrous cap
- What are the macro and micro features of a myocardial infarction at the following time points?
a) 0-4 hours
b) 4-24 hours
c) 1-7 days
d) 7-14 days
e) 2-8 weeks
f) 2 months
MACRO
a) 0-4 hours - None
b) 4-24 hours - Dark mottling
c) 1-7 days - Tan infarct centre
d) 7-14 days - Hyperaemic border, tan centre
e) 2-8 weeks - Grey/white collagenous scar forms
f) 2 months - Scarring complete
MICRO
a) 0-4 hours - Practically none
b) 4-24 hours - Coagulation necrosis, pyknosis of nuclei
c) 1-7 days - Neutrophil infiltrate
d) 7-14 days - Macrophages, granulation tissue forms
e) 2-8 weeks - Collagen deposition
f) 2 months - Dense collagenous scar
- Very briefly summarise the process of Myocardial Repair.
The process taking weeks to months, involves deposition of ELASTIC COLLAGEN (fibrosis) to replace NECROTIC CELLS removed by the action of infiltrating MACROPHAGES.
