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Molecules and cells in human disease > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

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Organic Chemistry 101 flashcards
1
Q

name 3 important conditions caused/ propogated by chronic inflammation

A
  • rheumatoid arthritis
  • gout
  • atherosclerosis
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2
Q

what is the predominant feature of inflammatory athritis?

A

synovial inflammation

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3
Q

what’s the synovial joint?

A

where 2 bones separated by space e.g. knee joint

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4
Q

what does synovial fluid contain?

A

albumin

hyaluronic acid

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5
Q

what is the purpose of albumin and hylaluronic acid in synovial joints?

A

nourish articular cartilage

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6
Q

what important role do macrophages play in synovial joint?

A

clear up debris from wear and tear of cartilage

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7
Q

what do cartilage and synovial fluid allow in the joint?

A

friction- free movement

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8
Q

what occurs in the synovial joint in rheumatoid arthritis?

A
  • there’s a loss of space between bones- increased friction
  • synovial tissue releases lymphocytes- inflammation
  • destruction of articular cartilage
  • anyklosis of joints (stiffening due to bone fusion)
  • increased permeability- oedema- swelling
  • neutrophils die and release PADA which changes AA arginine to citrilline- alters proteins- attacked by immune system
  • osteoplasts break-down bone
  • loss of movement
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9
Q

what are the 2 overall causes of rheumatoid arthritis?

A

genetic suseptibility
environmental factors
(overall a suseptible host exposed to arthrogenic pathogen)- inflammatory response

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10
Q

which 3 cytokines are involved in rheumatoid arthritis?

A

TNF-a, IL-1B, IL-6

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11
Q

which TLRs are involved in rheumatoid arthritis?

A

2,3,4,7,8

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12
Q

which DAMP is key in rheumatoid arthritis?

A

Tenascin-C

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13
Q

give evidence that Tenascin-C plays an important role in RA

A

KO mice who were given inflammation inducing chemical had reduced inflammation and enhanced recovery
reduced immune cell infiltration
no chronic inflammation

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14
Q

what disease is gout a type of?

A

arthritis

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15
Q

what causes gout?

A

build up of uric acid, which form crystals in joints

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16
Q

what are the risk-factors that lead to gout?

A

diet- high alcohol/purine rich food

genetic predisposition

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17
Q

how is purine broken down?

A

to guanine and hypoxanthine to allow uric acid secretion - if not, it can’t be excreted and builds up in joints

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18
Q

what inflammasome is activated in gout?

A

NLRP3

19
Q

how quickly is gout resolved if caused by diet- with simple diet changes?

A

days- weeks

20
Q

what wider branch of disease is atherosclerosis a form of?

A

arteriosclerosis

21
Q

what is arteriosclerosis?

A

thickening and hardening of arterial wall

22
Q

what component is specific to atherosclerosis?

A

formation of a plaque

23
Q

what, overall is a plaque?

A

lesion with a core of lipid covered by a white fibrous cap

24
Q

what further complication can a plaque lead to?

A

blocking blood flow

causing rupture- thrombosis/ haemorrhage or aneurysm

25
Q

what’s the most common cause of atherosclerosis?

A

high fat and cholesterol diet

26
Q

where do we get cholesterol from?

A

diet and liver

27
Q

what are chylomicrons?

A

a class of lipoproteins that transport dietary cholesterol after meals from small intestine to tissues for degradation

28
Q

what removes remnant chylomicrons?

A

liver

29
Q

how is cholesterol made in the liver?

A

conversion of HMG-CoA to melvalonic acid by the enzyme HMG-CoA reductase

30
Q

what are generally, the 3 main steps of atherosclerosis?

A

1- endothetial damage/dysfunction
2- Vascular muscle cell proliferation and platelet aggregation
3- foam cell formation

31
Q

what causes the endothelial damage? (4)

A
  • high lipid levels
  • hypertension
  • chemicals from smoking tobacco
  • pathogens
32
Q

what does endothelial damage lead to?

A

an inflammatory response
increased permeability of chemical mediators and immune cells
neutrophils trigger recruitment of macrophages which internalise LDL
- T-cells recruited and release further cytokines

33
Q

what causes the proliferation of Vascular Smooth Muscle cells?

A

they are recruited by PDGF, TGF and FGF

cause VSM prolieration and growth to produce ECM, like collagen to stabilise plaque

34
Q

what are the earliest lesions in atherosclerosis?

A

fatty streaks

35
Q

what are fatty streaks made of?

A

foam cells

36
Q

what are foam cells?

A

macrophages which have ingested and oxidised LDL- foam-like appearance

37
Q

give 3 non-pharmacological treatments of atherosclerosis

A
  • diet change- reduce cholesterol and lipid intake
  • quit smoking- reduces damage
  • exercise
38
Q

give the 3 main families of lipid-lowering drugs used to treat atherosclerosis

A
  • fibric acid (fibrates)
  • statins
  • bile acid binding resins
39
Q

what do fibrates do?

A

promote metabolism and reduce levels of VLDLs and triglycerides

40
Q

what do statins do?

A

lower LDL levels and are anti-inflammatory

41
Q

what do bile acid binding resins do?

A

inhibit cholesterol absorption

42
Q

what are 2 possible drug targets for atherosclerosis?

A

Inhibitors of IL-1

PPAR agonists

43
Q

what would inhibitors of IL-1 do to treat atherosclerosis?

A

reduce adhesion molecles so reduce migration of monocytes into tunica intima (usually cause by high BP)

44
Q

what would PPAR agonists do to treat atherosclerosis?

A

PPARs are nuclear receptors

binding of ligands to these receptors reduces expression of pro-inflammatory molecules

Molecules and cells in human disease (7 decks)

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