PMO1 - cardiovascular Flashcards
what are the two types of necrosis and how do they differ?
Coagulative necrosis keeps sturctures in place despite cell death – you can still see the structures
liquefactive necrosis - tissue becomes liquid due to the action of enzymes
- formation of cysts or cavities within the tissue
- in the brain during strokes
- common in bacterial/fungal infections
- Histologically, the affected area appears as a fluid-filled cavity with cellular debris
how do you detect a myocardial infarction?
troponin biomarker
What would you see histologically after an acute myocardinal infarction?
Dense polymorphonuclear leukocytic infiltrate
what does cardiac tissue look like?
smooth muscle cells
striations
intercollated discs
(no striations in longitudinal sections)
attached to adipose tissue
how to you detect the intima histologically?
Hematoxylin and eosin (H&E) staining
- consists of endothelial cells forming a single layer lining the luminal surface
- thin layer of connective tissue, including elastic fibers.
In veins, the intima may appear less organized compared to arteries and may contain fewer elastic fibers.
Describe how vascular injury can lead to intimal thickening
- Damage to the endothelial layer of blood vessels exposes the underlying layers to circulating blood components
- initiates inflammation - monocytes and macrophages accumulate and release cytokines and GFs
- inflam activates smooth muscle cells within the vessel wall – migrate from the media (middle layer) to the intima (innermost layer). – facilitated by chemotactic factors released by inflammatory cells and endothelial cells.
- smooth muscle cells proliferate and secrete extracellular matrix proteins such as collagen and elastin in the intima
- intima thickens
- risk of atherosclerosis
what are some causes of intimal thickening?
hypertension, atherosclerosis, mechanical trauma, or inflammatory processes.
what is the difference between Hyaline arteriolosclerosis and Hyperplastic arteriolosclerosis
Hyaline arteriolosclerosis
- response to chronic hypertension or diabetes mellitus.
- hypertension/hyperglycaemia can damage the endothelial cells lining the arterioles.
- damage leads to leakage of plasma proteins into the vessel wall, which accumulate and form the hyaline material.
- common in kidneys = renal dysfunction
Hyperplastic arteriolosclerosis (more severe)
- severe hypertension.
- smooth muscle cells in the arteriolar walls proliferate
- thickening of the vessel walls and the formation of concentric layers.
- hypertensive encephalopathy, renal failure, and retinal hemorrhages
define atherosclerosis and how it is caused
chronic inflammation of the arterial wall in response to vascular injury
from hyperlipidemia,
- inflammation,
- smoking,
- LDL accumulation,
Monocyte adhesion to the endothelium (causing dysfunction of endothelium cell layer),
platelet adhesion
when does Hyaline arteriolosclerosis happen?
acute hypertension
when does Hyperplastic arteriolosclerosis happen?
chronic hypertension
what do monocytes differentiate into within tissue? why is this relevant for response to vascular injury?
monocytes differentiate into macrophages in tissue
- contribute to inflammation
- clearance of cellular debris
- tissue remodelling via phagocytosis of damaged cells
- secrete cytokines and growth factors to aid the immune response
can also form dendritic cells
- transport damaged antigens to T cells
describe the pathogenesis of atherosclerosis
- Endothelial dysfunction via smoking/hypertension/LDL accumulation
- adhesion molecules upregulated
- monocytes adhere to damaged endothelium and migrate to the intima
- differentiate into macrophages
- injest LDL to form foam cells
- accumulation of foam cells triggers inflammation within the arterial wall – release of cytokines, chemokines, and GFs
- Plaque growth
- Fibrous cap forms from proliferation of smooth muscle cells in the arterial wall
- Plaque rupture = myocardial infarction / stroke