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Scientific Basis of Theraputics > Local hormones: inflammation and anti-inflammatory agents > Flashcards

Local hormones: inflammation and anti-inflammatory agents Flashcards

1
Q

what is inflammation a reaction to

A
  1. invasion - by pathogens or allergens

2. Injury - heat, UV, chemical, physical trauma

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2
Q

what type of immune system does inflammation involve

A

innate and adaptive immune system

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3
Q

what are the 5 cardinal sins of inflammation

A
  • calor (warmth due to inc bf)
  • rubor (redness due to inc bf)
  • dolor (pain bc sensitisation of receptors
  • tumor (swelling due to inc. post-capillary venule permeabiliity)
  • functio laesa (loss of function (bc pain, swelling)
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4
Q

what are the 5 steps of acute inflammation

A

1 - recognition of injury (immediate microvascular changes and release of mediators)

  1. recruit leukocytes (cells accumulate at the site and get activated)
  2. removal of agent (engulf bacteria, remove allergens, remove debris)
  3. regulation of response (control/monitor the level of response. Systemic effects typically occur, resulting in things like fever)
  4. Resolution (repair damage done during inflammation)
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5
Q

when do microvascular changes occur and how long to they last

A

occur immediately and last for around 24hrs

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6
Q

what mediates the microvascular changes of inflammation

A

by local hormones like histamine and PGs and bradykinin

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7
Q

what microvascular changes occur in inflammation

A

inc. blood flow (histamine/PG)
histamine/bradykinin = inc endothelial permeability .’. in leakage of plasma (& immune cells) into interstitial space of tissue

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8
Q

characteristics of local hormones in inflammation

A
  • produced in response to wide range of stimuli
  • synthesised and released only when required
  • act locally ONLY
  • inactivated locally to prevent them from having systemic effects
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9
Q

what is histamine sythesised from

A

from the amino acid histidine by the enzyme histidine decarboxylase (histidine gets decarboxylated, loses CO2).

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10
Q

how is histamine broken down

A

by imidazole-N-methyltransferase (INMT) and diamine oxidase.

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11
Q

how is histamine released from mast cells

A

Synthesised and secreted from mast cells.
they express Fc receptors for IgE, C3a and C5a on their cell surface membrane.
When activated they mediate release of histamine.

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12
Q

where is histamine stored in mast cells

A

secretory granules within mast cells, which are degranulated when given signal
granules composed of hepain and acidic proteins

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13
Q

what cells can release histamine

A
  • mast cells
  • basophils
  • neurones in the brain
  • histaminergic cells in the gut
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14
Q

what happens when an allergen is present in the body

A

IgE binds to mast cell (or basophil) surface receptor
intracellular rise in Ca2+
degranulation and release of histamine

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15
Q

what is the effect of stimulating b-adrenoreceptors on mast/basophil cells

A

histamine release inhibited

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16
Q

what receptors do histamine work at

A

histamine receptors
H1, H2, H3 and H4
GPCR receptors

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17
Q

what GPCR is H1

A

Gq/11 -> linked to phospholiphase C -> PIP2->IP3+DAG

found in smooth muscle, endothelium, CNS

18
Q

what GPCR is H2

A

Gs -> adenylyl cyclase ->cAMP produces

found on parietal cells of the stomach to inc HCl secretion and on heart

19
Q

What GPCR is H3

A

Gi -> -vely linked to adenylyl cyclase -> decrease cAMP

located on presynaptic terminals

20
Q

what GPCR is H4

A

Gi -> -vely linked to adenylyl cyclase -> decrease cAMP

found in basophils, BM, gut

21
Q

which histamine receptors are involved in the inflammatory response

A

H1 & H2

22
Q

Cardiovascular effects of H1/2 stimulation

A
  • dilation of arterioles
    .’. decrease in TPR and BP
  • inc permeabilty of postcapillary venules .’. decreased plasma vol (H1)
  • inc in HR (try and maintain BP and stop it dropping too much) (H2)
23
Q

non vascular effects of H1/H2

A
  • nonvascular smooth muscle contraction (eg bronchoconstriction)
  • algesia
  • stimulates increase in H2 secretion
  • increased exocrine secretions due to inc blood flow to exocrine glands
24
Q

why does histamine cause algesia

A

histamine causes pain, itching and sneezing caused by sensitisation and stimulation of sensory nerves (H1)

25
Q

what are clinically most important roles of histamine

A
  • Acute inflammation (H1 effects)

- Stimulating gastric acid secretion (H2 effects)

26
Q

what characteristics of the triple response of lewis (cutaneous response to injury)

A
  • Reddening (due to local vasodilation)
  • Flare (due to surrounding vasodilation
  • Wheal (raised skin due to exudate of fluid
27
Q

what happens in the triple response of lewis

A
  1. trauma to the skin stimulates C-fibres that release histamine
  2. dilation of arterioles, increased permeability, stimulates nerves
  3. cfibres fire in antidromic manner, axon collaterals stimulate nearby histamine degranulation
28
Q

why is Terfenadine used no longer used in H1 antagonists

A

cause potential cardiac arrhythmias at high concentrations

29
Q

what is the therapeutic effect of H1 antagonists

A
  • reduce minor inflammatory reactions (no significant value in treating asthma)
    some can be antiemetic - used for things like motion sickness and nausea
30
Q

side effects of H1 agonists

A

1st gen -
sedative .’. cause drowsiness
antimuscarinic .’. blurred vision, constipation etc

31
Q

therpeutic effect of H2 antagonist

A

cimetidine and ranitidine block H2 receptors on parietal cells stop stimulation

  • reducing gastric acid secretion
  • treatment of duodenal and gastric ulcers
32
Q

sideeffects of H2 antagonist

A

mental confusion, dizziness, tiredness and diarrhoea

33
Q

contraindications of h2 antagonist

A
  • inc activity of INMT .’. more rapid breakdown of histamine .’.limited effects
  • decreases p450 activity .’. adverse drug reactions
34
Q

what is bradykinin

A

inflammatory mediator that induces vasodilation, increases vascular permeability and induces the sensation of pain

35
Q

how is bradykinin synthesised

A

synthesised by the Kinin-kallikrein system
-activation of hageman factor (HF) .’. prekallikrein cleaved to plasma kallikrein (an enzyme)
kallikrein cleaved HMWK to bradykinin

36
Q

what does bradykinin do

A

mediates pain, increased vascular permeability, vasodilation and has chemotactic function

37
Q

pharmacological effect of bradykinin

A
  • potent vasoactive peptide
  • inc vascular permeability
  • cause vasodilation .’. fall in BP
  • induces pain
  • contraction of smooth muscle in gut and bronchi
  • formation of arachidoinic acid
  • chemotactic to leukocytes
38
Q

what is 5HT

A

serotonin is a neurotransmitter derived from tryptophan (an amino acid)

39
Q

what metabolises bradykinin

A

metabolised by kininases, that include enzymes like ACE, aminopeptidase P and carboxypeptidase.

40
Q

what may release 5HT

A

platelets
ECL of gastrointestinal tract
brain neurones
tumours

41
Q

inflammatory effects of 5HT

A
  • stimulates mast cell adhesion and migration
  • enhance inflammatory reactions of skin, lungs, gut
  • promotes inflammation by inc the # of mast cells at the site of tissue injury
  • synergises with TXA2 to stimulate platelet activity and cause vasoconstriction

Scientific Basis of Theraputics (9 decks)

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