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SBT > Local hormones > Flashcards

Local hormones Flashcards

1
Q

What are the signs of inflammation?

A
  • Calor (heat - increased blood flow)
  • Rubor (redness - increased blood flow)
  • Dolor (pain - sensitisation of sensory nerves)
  • Tumor (swelling - increased post-capillary venule/capillary bed permeability)
  • Functio laesa (loss of function - pain/injury)
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2
Q

What are the 5 Rs?

A
  • Recognition of the injurious agent
  • Recruitment of leukocytes
  • Removal of the agent
  • Regulation of response
  • Resolution
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3
Q

What is the time scale of acute inflammation?

A
  • Mins, hrs to about 3-5 days
  • Mediator release whole time
  • Microvascular changes - first 24hrs
  • Cell accumulation and activation - 12 hrs-4th day
  • Systemic effects - 12hrs-4th day
  • Repair/healing - 3rd-5th day
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4
Q

What vascular changes are there?

A
  • Mediators disrupt the endothelium and allow it to become more leaky
  • The immune cells such as neutrophils and eosinophils, can then get to the infected areas and deal with the pathogens
  • This reduces blood volume and therefore blood pressure
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5
Q

What are the benefits of systemic effects?

A
  • Entry of antibodies
  • Fibrin formation
  • Stimulation of immune response
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6
Q

What are the harmful effects of immune response?

A
  • Destruction of normal tissues
  • Swelling
  • Inappropriate inflammatory response
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7
Q

Give 6 examples of local hormones

A
  • Gastrin
  • CCK
  • Glucagon
  • VIP
  • Substance P
  • Motilin
  • NA
  • DA
  • 5-HT
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8
Q

Give a brief overview of basic chemical signalling

A
  • Reception - binding of signal with a cellular protein
  • Transduction - binding triggers a series of cellular changes
  • Response - transduced signal elicits context-driven specific cellular responses
  • Receptors are either membrane bound or nuclear receptors
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9
Q

What is Histamine synthesised from?

A

Histidine by histidine decarboxylase

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10
Q

What is Histamine metabolised by?

A

Imidazole-N-methyltransferase (INMT) and diamine oxidase

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11
Q

Where is Histamine synthesised and stored?

A
  • Mast cells
  • Basophils
  • Neurones
  • Enterochromaffin-like cells (ECL)
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12
Q

What causes the release of Histamine?

A
  • IgE mediated release (allergic reaction)
  • Production of complement agents C3a and C5a -> act on receptors on mast cells
  • Insect stings
  • Trauma
  • Stimulation of b2 adrenoceptors
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13
Q

What are the actions of mast cells in normal conditions?

A
  • TNFa release -> neutrophil recruitment to kill pathogens
  • TGFb and FGF release -> go to site of injury and start wound healing and fibrosis
  • Histamine, PGD2 and proteases will be released -> act on nerve cells and SMCs -> neuroimmune interactions, peristalsis, bronchoconstriction and pain
  • IL-5,9,13 will cause the recruitment of other immune cells (eosinophils, b cells, Treg)
  • Histamine, LTC4 and others will act on the blood-vessel endothelium, causing changes in blood flow, vascular permeability and coagulation -> recruitment of immune cells
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14
Q

What are the different histamine receptors?

A
  • H1 = Gq (PLC) - smooth muscle, endothelium, CNS
  • H2 = Gs (increased cAMP) - parietal cells to increase acid secretion, heart
  • H3 = Gi (decreased cAMP) - neuronal presynapstic terminals
  • H4 = Gi (decreased cAMP) - basophils, bone marrow, gut
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15
Q

How are mast cells activated by IgE?

A
  • Allergen enters
  • Mast cell priming - IL-4 from basophils and Th2 acts on mast cells
  • Th2 and basophils release IL-4 and 13 to act on B cells -> release of specific IgE
  • IgE binds to Fc receptors on mast cells and cross-link
  • Now when allergen enters and binds to antibodies on mast cell, it will release its granules
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16
Q

What specific effects does the H1 receptor have?

A
  • Dilates arterioles (decrease TPR)
  • Increased permability of post-capillary venules (decreased BP)
  • Contraction of smooth muscle (bronchoconstriction)
  • Pain, itching and sneezing from sensory nerves
17
Q

What specific effects does the H2 receptor have?

A
  • Increased HR

- Increased gastric acid secretion

18
Q

What are two main clinical roles of histamine?

A
  • ACUTE INFLAMMATION (H1)

- STIMULATING GASTRIC ACID SECRETION (H2)

19
Q

What are antidromic impulses?

A
  • Conduction along the nerve fibre in the opposite direction to normal
  • May be produced by electrical stimulation
  • Release neuropeptides which cause vasodilation distant from the site of irratation (flare)
20
Q

What causes the triple response?

A

Flare = vasoactive transmitters dilate arterioles, also cause degranulation of mast cells -> H1 receptors

Flush then wheal = Dilation of vessels and increased permeability by H1

21
Q

Exudate vs transudate

A
  • E = a mass of cells and fluid that has seeped out of blood vessels or an organ, especially in inflammation.
  • T = ↑ permeability to fluid, but not proteins
22
Q

What increases/ decreases gastric acid secretion?

A
  • Vagal innervation
  • Gastrin and Ach act on ECL cells -> histamine release -> H2 receptors on parietal cells -> increased acid production
  • Ach also directly acts on parietal cells to increase production
  • PGE2 dampens down the parietal cells acid production and increases the mucus production to protect the gut
23
Q

3 examples of 1st generation H1 antagonists

A

Mepyramine
Diphenhydramine
Promethazine

24
Q

Give an example of a 2nd/3rd generation H1 antagonist

A

Terfenadine

25
Q

What is a risk of Terfenadine?

A
  • potential cardiac arrhythmia actions in high conc

- increased with grapefruit juice consumption (inhibits CYP3A4)

26
Q

What are the effects of H1 antagonists?

A
  • Reduce minor inflammatory reactions
  • 1st gen are sedative
  • Some (e.g. promethazine) are anti-emetic
  • 1st gen also have muscarinic effects such as blurred-vision and constipation
27
Q

Give 2 examples of H2 antagonists

A
  • Cimetidine

- Ranitidine

28
Q

What are the effects of H2 antagonists?

A
  • Reduce gastric acid secretion (treatment for gastric and duodenal ulcers and Zollinger-Ellison syndrome)
  • Increases INMT activity so more breakdown of histamine
  • Mental confusion, dizziness, tiredness and diarrhoea
  • Cimitidine decreases CYP so potential for adverse reactions
29
Q

How is bradykinin synthesised?

A

PLASMA

  • Factor XIIa is activated (allowing its autoactivation)
  • It activates prekallikrein to kallikrein
  • Kallikrein is a protease that can act on HMWK (high MW kininogen) to produce bradykinin

TISSUE
- Prokallikrein –> tissue kallikrein HMWK –> Lysylbradikinin –> Bradykinin

30
Q

What is bradykinin activated and metabolised by?

A
  • Kininases activate it

- Metabolised by ACE, aminopeptidase and carboxy peptidase

31
Q

What are the pharmacological effects of bradykinin?

A
  • Vasoactive peptide
  • increases vascular permeability
  • Vasodilation
  • Pain
  • Contraction of gut and bronchus
  • Stimulation of Arachidonic acid metabolism
  • Chemotactic to leukocytes
  • Dry cough (ACE inhibitors inhibit bradykinin breakdown)
32
Q

How is 5-HT synthesised/ metabolised?

A
  • L-tryptophan + Tryptophan hydroxylase -> -> 5-HT

Metabolised by MAO

33
Q

Where is 5-HT distributed?

A
  • Platelets release 5-HT (and TXA2) -> platelet aggregation
  • mucosal cells in GIT - mediates gut movement and diarrhoea
  • Brain
  • Some tumours secrete excess 5-HT
34
Q

What are the inflammatory actions of 5-HT?

A
  • Promotes inflammation by increasing number of mast cells at site of injury
  • Mast cell adhesion and migration
  • Enhances inflammatory reactions of skin, lungs and gut
  • Synergises with TXA2 to cause platelet aggregation

SBT (8 decks)

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