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!!!!! BRS YR2 !!!!! > Cardio - Ischaemic Heart Disease > Flashcards

Cardio - Ischaemic Heart Disease Flashcards

1
Q

What are the 2 types of Coronary Heart Disease?

A

Ischaemic Heart Disease

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2
Q

What is Ischaemic Heart Disease?

A

CHD affecting coronary arteries

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3
Q

What is cerebrovascular disease?

A

CHD affecting carotid arteries

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4
Q

What are the modifiable risk factors?

A 
→ smoking
→ lipids intake
→ blood pressure
→ diabetes
→ obesity
→ sedentary lifestyle
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5
Q

What are the non-modifiable factors?

A

→ age
→ sex
→ genetic background

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6
Q

What is the treatment for lipids intake?

A

→ statins
→ anti-hyperlipidemic agents
→ antibodies against PCSK9

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7
Q

What is the treatment protocol for BP?

A

→ ACE inhibitors
→ beta blockers
→ conducting enzyme inhibitors
→ diuretics

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8
Q

What is risk factor multiplication?

A

when multiple risk factors multiply your chances of getting a disease

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9
Q

What are the changes in epidemiology?

A

→ reduced hyperlipidaemia (statin treatment)
→ reduced hypertension (antihypertensive treatment)
→ increased obesity => increased diabetes
→ new improvements in diabetes treatment have doubtful effect on macrovascular disease
→ changing pathology of coronary thrombosis possibly related to altered risk factors
→ SGLT-2 inhibitors can reduce CVD effects +

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10
Q

Where do plaques commonly occur?

A

→ bifurcations in arteries

→ areas of turbulent flow

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11
Q

Where does LDL deposition occur?

A

in the sub-intimal space and binds to matrix proteoglycans

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12
Q

What do LDLs bind to?

A

matrix proteoglycans

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13
Q

What is the Type II lesion of atherosclerosis?

A

macrophage foam cells

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14
Q

What is the Type III lesion of atherosclerosis?

A

→ preatheroma

→ small pools of extracellular

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15
Q

What is the Type IV of atherosclerosis?

A

→ atheroma

→ core of extracellular lipid

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16
Q

What is the Type V of atherosclerosis?

A

→ fibroatheroma

→ fibrous thickening

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17
Q

What is the Type VI of atherosclerosis?

A

→ thrombus

→ fissure + hematoma

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18
Q

What can be done as primary prevention?

A

→ life-style changes

→ risk factors management

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19
Q

What can be done as clinical intervention?

A

→ secondary prevention
→ catheter based interventions
→ revascularisation surgery
→ treatment of heart failure

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20
Q

What are the main cells involved?

A 
→ vascular endothelial cells
→ platelets
→ monocyte-macrophages
→ vascular smooth muscle cells
→ T lymphocytes
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21
Q

What is the role of vascular endothelial cells?

A

→ barrier function (e.g. to lipoproteins)

→ leukocyte recruitment

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22
Q

What are the roles of platelets?

A

→ thrombus generation

→ cytokine + growth factor release

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23
Q

What are the roles of monocyte-macrophages?

A

→ foam cell formation
→ cytokine + growth factor release
→ major source of free radicals
→ metalloproteinases

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24
Q

What are the roles of vascular smooth muscle cells?

A

→ migration and proliferation
→ collagen synthesis
→ remodelling + fibrous cap formation

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25
Q

What is the role of T lymphocytes?

A

→ macrophage activation

26
Q

What is a huge basis in atherosclerosis?

A

inflammation

27
Q

What was given to high risk atherosclerosis patients in a trial? Why?

A

→ Interleukin-1

→ to understand how important inflammation is in atherosclerosis

28
Q

What was the result of the trial?

A

→ Fewer major adverse cardiovascular events (MACE) mostly stroke and heart attacks in treated patients
→ Multiple mechanisms including cholesterol crystal formation connect lipids and inflammation in atherosclerosis

29
Q

How did IL-1 help?

A

x

30
Q

What are the 2 main classes of macrophages?

A

→ Inflammatory macrophages

→ Resident macrophages

31
Q

What is the purpose of inflammatory macrophages?

A

adapted to kill microorganisms (germs)

32
Q

What is the purpose of resident macrophages?

A

→ normally homeostatic - suppress inflammatory activity
→ alveolar resident macrophages - surfactant lipid homeostasis
→ osteoclasts - calcium + phosphate homeostasis
→ splenic red pulp macrophages - iron homeostasis

33
Q

What are LDLs?

A

→ ‘Bad’ cholesterol
→ Synthesised in liver.
→ Carries cholesterol from liver to rest of the body including arteries

34
Q

What are the structural points of LDLs?

A

→ docking molecule “molecular addresses for fat delivery”
→ lipid monolayer (like cell membrane) but one molecule thick
→ cargo fat for fuel

35
Q

What are HDLs?

A

→ ‘Good’ cholesterol

→ Carries cholesterol from ‘peripheral tissues’ including arteries back to liver (=“reverse cholesterol transport”)

36
Q

What are oxidised LDLs?

A

→ Due to action of free radicals on LDL. (see later)
→ Not one single substance.
→ Families of highly inflammatory and toxic forms of LDL found in vessel walls.

37
Q

How do LDLs become modified into oxLDLs?

A

→ LDLs leak through the endothelial barrier by uncertain mechanisms.
→ LDL is trapped by binding to sticky matrix carbs (proteoglycans) in the sub-endothelial layer and becomes susceptible to modification.
→ Best studied modification is oxidation - represents partial burning
→ LDL becomes oxidatively modified by free radicals.
→ Oxidised LDL is phagocytosed by macrophages and stimulates chronic inflammation

38
Q

How do oxLDLs promote foam cell formation?

A

→ LDLs become oxidised
→ phagocytosis by macrophages
→ macrophages now known as “foam cells”
→ goes back to chronic inflammation

39
Q

What is FH?

A

Familial Hyperlipidemia
→ Autosomal genetic disease (main form dominant with gene dosage)
→ Massively elevated cholesterol (>~20 mmol/L). (effective ‘normal’ ~1-5 mmol/L)
→ Failure to clear LDL from blood
→ Xanthomas and early atherosclerosis; if untreated fatal myocardial infarction before age 20

40
Q

What receptor do FH patients lack? What are the features of this receptor?

A

LDL receptor

- negatively regulated by intercellular cholesterol

41
Q

Why was a second LDL receptor deduced?

A

In LDLR-negative patients, macrophages accumulate cholesterol
- therefore there must be a second LDL receptor, not under negative feedback regulation so that macrophages can still ingest LDLs.

42
Q

What are the secondary LDL receptors called?

A

Macrophage scavenger receptors

43
Q

What are the 2 types of macrophage scavenger LDL receptors?

A

Macrophage scavenger receptor A = CD204

Macrophage scavenger receptor B = CD36

44
Q

What do CD204 do?

A

Binds to oxidised LDL
Binds to Gram-positive bacteria e.g. staph + strep
Bind to dead cells

45
Q

What do CD36 do?

A

Binds to oxLDLs
Binds to malaria parasites
Binds to dead cells

46
Q

What do macrophages in plaques do to worsen + propagate atherosclerosis?

A
  • generate free radicals to further oxidise LDLs
  • phagocytose modified LDLs + become foam cells
  • express cytokine mediators to recruit monocytes
  • express chemo-attractants + growth factors for VSMC
  • express proteinases that degrade tissue
47
Q

How do macrophages generate free radicals that further oxidise LDLs?

A

Macrophages have oxidative enzymes that modify LDLs

  • NAPDH oxidase
  • myeloperoxidase
48
Q

What cytokines do macrophages produce?

A
  • IL-1 upregulates vascular cell adhesion molecule VCAM-1

- VCAM-1 mediates tight monocyte binding

49
Q

What chemokines do macrophages produce?

A
  • monocyte chemotactic protein-1 (MCP-1)

- MCP-1 binds to monocyte G-protein coupled receptor CCR2

50
Q

Why is it a vicious cycle of inflammation ?

A

Positive feedback loop + vicious cycle that leads to self-perpetuating inflammation

51
Q

What chemo-attractants + growth factors do macrophages produce for VSMC? What do they promote?

A 
Platelet derived growth factor (PDGF)
- VSMC chemotaxis
- VSMC survival
- VSMC division
Transforming growth factor beta (TGF-b)
- increased collagen synthesis
- matrix deposition
52
Q

Why do macrophages release these growth factors in atherosclerosis?

A

“Wound healing” role of the macrophage in atherosclerosis - Macrophages release complementary protein growth factors that recruit VSMC and stimulate them to proliferate and deposit extracellular matrix

53
Q

What is the difference between atherosclerotic VSMCs compared to normal ones?

A
54
Q

What are metalloproteinases?

A

Family of 28 homologous enzymes
Activate each other in proteolysis
Degrade collagen
Catalytic mechanism based on zinc

55
Q

What is the effect of plaque erosion + rupture?

A

blood coagulation at site of rupture may lead to an occlusive thrombus + cessation of blood flow

56
Q

What are the characteristics of a vulnerable + unstable plaque?

A

→ large soft eccentric lipid rich necrotic core
→ increased VSMC apoptosis
→ reduced VSMC + collagen content
→ thin fibrous cap
→ infiltration of activated macrophages expressing MMPs

57
Q

What is the process of macrophage apoptosis?

A
58
Q

What is Nuclear Factor kappa B (NFkB)?

A

Transcription factor

Master regulator of inflammation

59
Q

What can NFkB be activated by?

A

Numerous inflammatory stimulation

  • scavenger receptors
  • toll-like receptors
  • cytokine receptors e.g. il-1
60
Q

What does NFkB do?

A

Switches on numerous inflammatory genes

  • matrix metalloproteinases
  • Inducible nitric oxide synthase
  • interleukin-1
61
Q

What is the positive feedback involved with NFkB?

A

Interleukin-1 activates it, it also causes release of IL-1

62
Q

What is a summary of atherosclerosis?

A

!!!!! BRS YR2 !!!!! (72 decks)

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