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Introduction to Molecular Medicine > Molecular aspects of cardiovascular & brain-related disorders > Flashcards

Molecular aspects of cardiovascular & brain-related disorders Flashcards

1
Q

what is the cardiovascular system responsible for?

A

transport of oxygen, nutrients,, hormones, waste

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2
Q

pulmonary circulation

A

deoxygenated blood to the lungs

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3
Q

systemic circulation

A

highly oxygenated blood to the tissue

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4
Q

arteries

A

high pressure, away from the heart

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5
Q

veins

A

low pressure, to the heart

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6
Q

capillaries

A

exchange of O2, nutrients to the tissue

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7
Q

cardiovascular disease (CD)

A

any disease that affects the cardiovascular system

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8
Q

cerebrovascular disease

A

disruption of blood supply to the brain

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9
Q

aortic aneurism & dissection

A

dilatation/rupture of the aorta

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10
Q

peripheral arterial disease

A

of arteries supplying arms/legs

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11
Q

deep venous thrombosis & pulmonary embolism

A

blood clots in the leg veins which can dislodge and move to heart/lungs

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12
Q

coronary heart disease

A

of blood vessel supplying the heart muscles

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13
Q

rheumatic heart disease

A

damage to heart muscle and valves from rheumatic fever (caused by streptococcal infection)

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14
Q

congenital heart disease

A

malformations of heart structures existing at birth

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15
Q

non-modifiable risk factors for developing CVDs

A
  • advancing age
  • genetic predisposition
  • gender
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16
Q

modifiable risk factors for developing CVDs

A
  • tobacco smoking, physical inactivity, poor diet, excessive alcohol
  • high blood pressure/blood lipids (cholesterol), obesity
  • diabetes
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17
Q

describe the stages of atherosclerosis

A
  1. fatty streak formation
  2. plaque progression (adaption)
  3. plaque disruption (clinical manifestation)
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18
Q

stage 1 of atherosclerosis (fatty streak formation)

A
  • endothelial cell dysfunction
  • lipoprotein entry & modification
  • leukocyte recruitment & foam cell formation
  • > impaired trafficking, local accumulation of macrophages, failure to resolve inflammation
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19
Q

endothelial cell dysfunction

A

vasoconstriction, lipoprotein oxidation, pro-inflammatory genes, NO-catabolism

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20
Q

lipoprotein entry

A

LDL binds to proteoglycans and accumulates (adds cholesterol)

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21
Q

how can HDL protect against atherosclerosis?

A

removes excess cholesterol

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22
Q

LDL / HDL

A

low/high density lipoprotein

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23
Q

oxidises LDL

A

LDL + free radical: introduces tissue damage, stimulates endothelial cells to produce pro-inflammatory molecules
(inhibits production of NO by endothelial cells, promotes recruitment of leukocytes)

24
Q

leukocyte recruitment & foam cell formation

A

-phagocytic macrophages take up oxidized lipoproteins, forming foam cells

25
Q

diaptesis

A

passage of blood cells through intact vessel walls

26
Q

stage 2 of atherosclerosis (plaque progression /adaption)

A
  • smooth muscle cell migration (foam cells release PDGF)
  • extracellular matrix metabolism
  • > fibrotic plaque generation
27
Q

extracellular matrix metabolism

A

production of extracellular matrix molecules

28
Q

stage 3 of atherosclerosis (plaque disruption)

A

clinical manifestation: integrity of plaques, thrombogenic potential
->thinning of fibrous cap, prone to rapture

29
Q

how to inflammatory cells contribute to plaque disruption?

A

produce IFN-gamma (inibits matrix production), produce cytokines (stimulate foam cells to produce MMP)

30
Q

MMP

A

metalloproteinases (degrade matrix)

31
Q

integrity of plaques

A
  • apoptosis of foam cells/SMCs

- release of cellular content, absorbed to lipid core (plaque instability)

32
Q

factors for plaque rupture

A
  • size of inflammation area
  • size of lipid core
  • thickness of fibrous cap
  • disturbed balance of proteolytic enzymes
  • plaque calcification (mineral disposition)
  • hemorrhage in plaque (neovascularization)
33
Q

thrombogenic potential

A
  • components of necrotic core in direct contact with blood
  • tissue factor produced by endothelial cells & macrophages
  • initiates coagulation cascade by activation of platelet & clotting factors
  • block of blood supply
34
Q

how does advancing age contribute to CD?

A
  • risk 3x with each life decade

- cardiac/vascular aging (dysregulated signaling, endothelial dysfunction..)

35
Q

how does genetic predisposition contribute to CD?

A

-rare variants e.g. severe hypercholesterolemia, disturbed blood pressure

36
Q

how does gender contribute to CD?

A

2-5x more common in men (young age), major differences in body weight/fat distribution, protective effect of estrogen on blood vessels

37
Q

how does excessive alcohol consumption lead to disease?

A

high blood pressure, calories, increased triglyceride in blood

38
Q

how can moderate drinking reduce risk of CD

A

beneficial effects on HDL cholesterol

39
Q

how does inactivity influence CD?

A

-impairs endothelial function, blood pressure, lipid profile, weight gain

40
Q

how does a poor diet contribute to CD?

A

undesirable lipid profile, insulin resistance, obesity, blood pressure

41
Q

why is there a higher risk of cardiovascular event when having high blood pressure?

A

damage to endothelial cells, enlargement of heart, high levels of LDL accumulate and undergo oxidation

42
Q

why does diabetes increase the risk of CD?

A
  • increased blood glucose level -> uptake of cholesterol

- high prevalence of endothelial dysfunction among diabetes groups -> reduced NO, enhanced leukocyte adhesion

43
Q

myocardial infarction (MI)

A

sudden ischemic death of myocardial tissue (imbalanced oxygen supply/demand)

44
Q

what happens in the first seconds of MI?

A

aerobic metabolism & ATP production stop, lactic acid accumulates in toxic levels
-loss of myocardial contractility

45
Q

when is the iscemic period reversible

A

if blood flow is restored before 15-20 mins

46
Q

generally describe the cardiac repair after MI

A

very limited, lost cells replaced by fibrotic scar

  1. inflammatory phase
  2. reparative & proliferative phase
47
Q

cerebral ischemic stroke

A
  • mostly caused by compromised vascular supply to the brain

- brain tissue vulnerable to oxygen & glucose deprivation

48
Q

global ischemia

A

entire brain

49
Q

local ischemia

A

specific brain region

50
Q

what follows vascular occlusion in cerebral ischemia?

A

cerebral blood flow goes down, metabolism interrupted (no oxygen/glucose), energy failure, loss of ion homeostasis, acidosis, toxicity, disruption of blood-brain barrier, activation of glia cells

51
Q

panumbra

A

bordering region next to core region (immediate necrotic cell death), potential to recover

52
Q

excitotoxicology

A

process of neuronal damage by overreaction of receptors for the excitatory neurotransmitter glutamate (ion fluxes, cell death)

53
Q

neurogenesis

A

new neurons, birth of new cells, migration to injured sites

54
Q

fats are not water soluble. How are they transported in the body?

A

complex with different proteins called lipoproteins

55
Q

what is the major function of HDL?

A

transport cholesterol and triglycerides from peripheral tissues to liver

56
Q

why are LDL receptor mutations associated with increased risk of coronary heart disease?

A

the mutations inhibit cellular uptake and processing of cholesterol

Introduction to Molecular Medicine (12 decks)

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