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PY352 > Autocoids & Inflammation > Flashcards

Autocoids & Inflammation Flashcards

1
Q

What are autocoids?

A

Biological factors that act like local hormones. They have a brief duration and act near the site of synthesis

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2
Q

How is a normal hormone e.g. testosterone different to a local hormone e.g. histamine, kinins or ecosanoids?

A

Local hormones act near the site of synthesis, where as normal hormones e.g. testosterone, is made in the testes but travels to the brain and acts there.

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3
Q

Give three types of local hormones

A
  • histamines
  • kinins
  • ecosanoids
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4
Q

What are some examples of ecosanoids?

A

Prostaglandins, leukotreines and PAF (platelet activating factor)

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5
Q

Econasoids can cause the signs of ________.
The cardinal signs of inflammation include:
-
-
-
-
-

A 
inflammation
rubor
tumor
calor
dolor
functio laesa
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6
Q 
What do the following mean
functio laesa
calor
tumor
rubor
dolor
A 
loss of function
heat
inflammation/ swelling
redness
pain
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7
Q

Does inflammation always involve immunity?

A

NO

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8
Q

Does inflammation always involve immunity? What else could it be due to?

A

NO. Trauma: heat, radiation

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9
Q

What are the two reasons for inflammation

A

Trauma - heat, radiation

Immunity

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10
Q

What are the 4 types of immunological reactions?

A

Type 1 - anaphylaxis or allergy e.g. hay-fever
Type 2 - Antibody dependent cytotoxicity
Type 3 - complex mediated hypersensitivity e.g rheumatoid arthritis
Type 4 - cell mediated hypersensitivity e.g. T cell mediated (when you get checked for TB)

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11
Q 
What is histamine made from?
What is it important for?
Where is it stored?
Where can it be made on demand?
What is it caused to be released by?
A 
Histidine which is a basic amino acid.
Inflammation
Stored in structures called granules in either mast cells (found in tissues) or basophils (found in blood.
Gastric mucosa
It is released by allergens
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12
Q

Mast cells are found where in the body?
It contains dense structures called ______.
Granules are packed full of _____ coupled to _____

A

Tissues, especially in epithelium e.g gut wall, nasal epithelium
granules
histamine
heparin

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13
Q

When allergen comes into contact with mast cell, mast cell instantly breaks and histamine and heparin are released from the granules, If too much histamine or heparin (causes bruising) is released due to an ALLERGY (e.g anaphylactic shock), what will happen to blood pressure? Which organs does this affect

A

blood pressure falls dramatically.
brain
heart
kidney

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14
Q

After anaphylactic shock, how do you increase blood pressure?

A

Inject adrenaline/epinephrine

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15
Q

Which antibody coats the mast cell for it to detect the allergen?

A

IgE

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16
Q

In order for a histamin+heparin reaction to occur, what must happen?

A

the allergen MUST cross link with the IgE antibody

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17
Q

What causes histamines to be released?

A
  • Allergen cross linking with IgE antibody
  • Trauma
  • Side effect of drugs such as morphine, 48/80 and D-tubocurarine
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18
Q

People with respiratory problems e.g asthma/COPD are not usually given drugs (with histamine release occurring as a side effect) during surgery as it will aggravate

A

their respiratory conditions (vasodilation)

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19
Q

What do mast cells release?

A 
histamines
kallikrein
leukotreines
prostaglandin D2
PAF
TNF alpha
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20
Q

Treatment of allergy include:

Give an example of each

A
  • Antihistamines (H1 receptor blockers) e.g. mepyramine

- Mast cell stabilisers e.g. disodium cromoglycate or ketotifen

21
Q

How do antihistamines work?

A

By blocking the H1 receptor ( 7TM G protein coupled receptor)

22
Q

What ares some sedating antihistamines

A

promethazine

mepyramine

23
Q

What is a non sedating antihistamine? Why is it non sedating?

A

Cetirizine

Crosses the BBB less

24
Q

kinins are peptide mediators that are synthesised by _____ and metabolised by _____

A

kininogen

kinases

25
Q

Describe the kinin diagram…
_____ (a substance that mast cells release) is activated by three factors
______, ____ ___ _______ and ______ surfaces.
This activated kallikrein, converts _______ to _______. This is then inactivated by _____1 and _____ 2 (ACE)

A 
Kallikrein
coagulation
uric acid crystals
bacteria surfaces
kininogen
bradykinin
kinases
kinase
26
Q

kinins are _____ mediators whereas ecosanoids are _____ mediators

A

peptide

lipid

27
Q

Actions of kinin involve:

This occurs via a ______ receptor which releases _____ such as prostaglandins

A 
Pain
Swelling
Redness
bradykinin
Eicosanoids
28
Q

What does PAF do?

A
  • Activates platelets
  • Bronchospasms
  • Chemotactic for WBC
  • Hyperalgesia (dolor)
  • Oedema (tumor)
29
Q

Prostanoid synthesis pathway

A

Arachidonic acid
COX 1 and COX 2
forms PGE2, PGD2, PGF2alpha, Prostacyclin, Thromboxane

30
Q

PAF causes dolor (hyperalgesia) and tumor (oedema) whereas prostaglandins cause

A

inflammation which dilate arterioles, constrict venues, increase capillary permeability + leakiness: calor, rubor, tumor

hyperalgesia (dolor)

31
Q

PAF causes dolor (hyperalgesia) and tumor (oedema) whereas prostaglandins cause

A
  • inflammation; which dilate arterioles, constrict venues, increase capillary permeability + leakiness: calor, rubor, tumor
  • hyperalgesia (dolor)
32
Q

During inflammation, arterioles ______, venules ______ and capillaries become ______ and so increase ________.

A

dilate
constrict
leaky
permeabiltiy

33
Q

During inflammation, arterioles ______, venules ______ and capillaries become ______ and so increase ________.

A

dilate
constrict
leaky
permeability

34
Q

What is the function of prostaglandins in the stomach?

A
  • Decrease acid secretion

- Increase mucus secretion (gastroprotective)

35
Q

What is the role of prostaglandins in the kidney?

A
  • Increase blood flow

- Increase Water + Sodium excretion (diuretic)

36
Q

Role of PG on smooth muscle? (side) effects on the following:

  • Gut
  • Uterus
  • Bronchioles
A

constrict smooth muscle
diarrhoea
labor
bronchoconstriction

37
Q

CNS effects of PGE2?

A

Pyrogen - Leukocyte - IL 1 - Hypothalamus - PGE2 - Increase body temp (fever)

38
Q

What are the vascular effects of PG?

A
  • vasodilate

- inhibit platelet aggregation

39
Q

What are some therapeutic uses of PGs?

A
  • Labor
  • Postpartum haemorrhage
  • Gastric ulcers
  • Vasodilator
  • Glaucoma
40
Q

Give three 3 properties of NSAIDS and give three examples

A

ANTI INFLAMMATORY
ANALGESIC
ANTIPYRETIC

Aspirin, Diclofenac, Ibuprofen

41
Q

Side effects of NSAIDS

A
  • Peptic ulcers (due to inhibition of gastric protection by PG)
  • Renal damage
  • Delays labour
42
Q

COX 1 reacts to _______ stimuli whereas COX 2 reacts to ______ stimuli. Constitutive sites for COX 1 include s____, k_____, i_____ and e_______. COX 2 inflammatory sites include m_______. PGE2, TXA1, PGI2 are formed by COX _, whereas inflammatory PGs, proteases and oxygen are formed by COX _.

A 
physiological
inflammatory
stomach
kidney
intestine
endothelium
macrophages
1
2
43
Q

COX _ inhibitors is less likely to have the side effects of NSAIDS

A

2

44
Q

NSAIDS mainly affect COX _

A

1

45
Q

Name two leukotrienes and what they cause

A

LTC4 - bronchoconstriction

LTB4 - chemotactic, hyperalgesia (dolor)

46
Q

Name a leukotriene antagonist (used second line for asthma)

A

montelukast

47
Q

Glucocorticoids targets COX __ expression

A

2

48
Q

Side effects of glucocorticoids?

A
  • increased infection
  • slow down healing
  • hyperglycaemia
  • increase osteoporosis
  • slow down growth
  • increase gastric ulceration

PY352 (25 decks)

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