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Pharmacology > inflammation > Flashcards

inflammation Flashcards

1
Q

what enzymes do NSAIDs inhibit? and what are the functions of those enzymes?

A

COX-1 constitutive enzyme

COX-2 induced at the site of inflammation

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2
Q

which enzyme is NSAID toxicity associated with?

A

COX-1 inhibition

this is can lead to gastric ulceration and massive GI bleeding

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3
Q

how does the anti-pyretic effect of NSAIDs work?

A

they prevent the formation of PGE in the anterior hypothalamus, PGE formation by endogenous pyrogens in the anterior hypothalamus resets the body’s thermostate

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4
Q

what inflammatory mediators are associated with pyretic effects?

A

TNF-A and IL-1

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5
Q

how is the analgesic effect of NSAIDs mediated?

A

PGE formation at the site of inflammation sensitises sensory nerves, lowering pain threshold.

by inhibiting PGE formation, neuronal sensitisation is reduced

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6
Q

how is the anti-inflammatory effect of NSAIDs mediated?

A

PGE,PDG and PGI are vasodilators and promote oedema

NSAIDs inhibit the formation of those prostanoids and reduce the signs of inflammation by this

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7
Q

how is NSAID toxicity minised?

A

by making drugs which are more selective for COX-2

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8
Q

when and how is anti-TNF-a therapy used?

A

used for chronic inflammatory disease

TNF-a antibody or binding protein are used to prevent the molecule from binding to its receptor

humanised antibodies: Infliximab or adalimumab used

soluble TNF-a receptors (E.g. etanercept)

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9
Q

what are the key features of asthma?

A
  • REVERSIBLE bronchonconstriction and airway obstruction
  • non-specific airway hyper-reactivity
  • inflammation of bronchial mucosa
  • loss of bronchial epithelium
  • mucus plugging of the airway
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10
Q

what is the main feature of allergic asthma?

A

its a type I hypersentivity to its allergen binding to IgE - causing histamine release

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11
Q

what is salbutamol?

A

a short - acting B2 agonist

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12
Q

what is salmeterol?

A

a long acting B2 agonist

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13
Q

give examples of the bronchodilators used in asthma

A

B2 agonists

  • salbutamol
  • salmeterol (long acting)

methylxanthines:

  • theopylline
  • PDE 4 inhibitor

muscuranic receptor antagonist
- ipratropium bromide

leukotriene receptor antagonists:
- montelukast

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14
Q

what are the anti-inflammatory agents used in asthma?

A

glucocorticoids:

  • beclamethazone (inhaled)
  • prednisolone (oral)

anti-allergic:
-cromoglycate

leukotriene receptor antagonists:
- montelukast

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15
Q

what is chromogylcate?

A

this is an anti-allergic drug

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16
Q

what is prednisolone?

A

this is a glucocorticoid

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17
Q

what is the mechanism of action of chromoglycate and nedocromil?

what is the difference between them?

A

those drugs are used as prophylaxis, they cannot prevent an already established attack

  1. inhibition of the release of inflammatory mediators (from cells involved in asthma: mast cells, eosinophils and neutrophils)
  2. inhibition of sensory nerve activation
    (those activations are involved in reflexes that mediate bronchoconstriction and neurogenic inflammation of the airways)

chromoglycate - given via inhaler
nedocromil: orally active

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18
Q

what is the difference between chromoglycate and nedocromil?

A

nedocromil is orally active while chromoglycate is not orally active so much be given via an inhaler

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19
Q

how do B2 agonists work?

A

relax smooth muscle by increasing cAMP

they also prevent the release of mediators from mast cells

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20
Q

what is the difference between salbutamol and salmeterol?

A

salbutamol is short acting (4hrs)
- can be given iV/orally or via inhalation

salmeterol:

  • long acting (12 hours)
  • given via inhalation
  • very useful for nocturnal asthma
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21
Q

when are muscarnic antagonists given in asthma?

how do they work? what type of asthma is it not effective against?

how is it administered, why?

A

they’re given, or most effective where reflex bronchoconstriction predominates (this is Ach mediated)

  • does not affect histamine mediated bronchoconstriciton

ipratropium is given by inhalation (oral or parenteral administration avoided) this is to avoid extensive side effects associated with muscuranic blockade

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22
Q

what are caffeine, theobromine and theophylline examples of?

A

methylxanthines

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23
Q

how do methylxanthines work in the cell?

A
  • at high concentrations can release calcium from intracellular pools
  • inhibition of cAMP and cGMP phosphodiesterases
  • this increases intracellular rise in cAMP mediated by other drugs (E.g. the B2 agonists)
  • competitive antagonism of adenosine at the adenosine receptors
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24
Q

what are the overall effects of methylxanthines

A
  • bronchodilation
  • relaxation of vascular smooth muscle (although it causes cerebral artery contraction)
  • diuresis (weak effect, may inhibit sodium resorption)
  • positive ionotropic and chronotropic effect on the heart (causing potential toxicity) narrow TI
  • increased GI secretions causing diarrhoea
  • CNS stimulant
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25
Q

apart from the use in severe asthma what can methylxanthines be used for? and what is the specific drug?

A

aminophylline orally can be used for left ventricular failure with pulmonary oedema:
- because of it cardiovascular
respiratory and diuretic effects

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26
Q

what are some of the side-effects of methylxanthines?

A

tachycardia with dysrhythmias
diarrohea
tremor
wakefullness

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27
Q

why are glucocorticoids not used?

when are they used?

A

oral use of GC is not used because of major unwanted side-effects

  • potent oral GC reserved for severe asthma
  • inhaled GC are preferred (E.g. beclomethasone)
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28
Q

what is the use of cetirizine in asthma?

A

cetirizine is a H1 antagonist

  • of no value in asthma
  • will partially reduce acute airway obstruction
29
Q

where does montelukast act?

what is its effect?

A

this acts on LTD4 receptors (antagonise them)

  • has bronchodilation and anti-inflammatory effect because LT cause bronchonstriciton and airway inflammation
30
Q

what is the use of omalizumab in asthma?

A

this is an anti - IgE antibody

31
Q

what are the compounds used in cough medicine?

A

codeine, dexomethorphan and pholcodine

those are narcotic analgesics, they’re only effective. cough medication which has no narcotic analgesics has no real effect

32
Q

give an example of a respiratory stimulant. when is it used?
how does it work?
when is it not used?

A

doxapram

  • used to bring patients with COPD out of crisis (but has no long term use)
  • stimulates the carotid chemoreceptors and respiratory centre in the medulla
  • not used in asthma or respiratory depression due drug overdose or CNS disease
33
Q

what is the naturally occurring GC?

why are synthetic GC better?

A
  • hydrocortisone is a naturally occurring GC

- synthetic ones are better because they’ve greater selectivity for anti-inflammatory over MC action

34
Q

what determines the duration of action of a GC?

give long acting GCs and short acting GCs

A

duration of action:

  • fraction bound to plasma protein =
  • affinity for 11-b HSD-2
  • lipophilicity
  • affinity for GCR

long acting:

  • dexamethosone
  • betamethasone

short acting:
- cortisol

intermediate acting:
- prednisolone

35
Q

what is the mechanise of action of

A

they’re both anti-inflammatory and immunosuppressive

GC are lipid soluble, so easily cross the cell membrane and bind to cystosolic GCs.

dissociation of hsp complex and dimeresis and moves into cells binding to GRE (GC regulatory element)

  • those activate gene transcription of anti-inflammatory proteins
  • those negatively regulate pro-inflammatory gene transcription
36
Q

what are the unwanted side effects of GCs?

short term?
long term?

A

suppression of hypothalamic function

iatrogenic cushing’s

long term:
- obesity 
- increased appetite 
- immunosupressive 
- MC effect 
-- salt and water retention
- glaucoma 
- increased BO 
- oedema 
- diabetogenic (because reduces glucose uptake and use, but increases gluconeogenesis) 
- oesteoprosis (Reduces OB activation) 
- redistribution of body fat around abdomen, back of the neck and face 
increased protein catabolism and reduced protein synthesis (this causes skin that is easily bruised)
37
Q

why cannot we not stop the using GCs immediately/

A

patient must be weaned off
exogenous GCs suppress CRH/ACTH (this causes adrenal cortex atrophy and a risk of iatrogenic addison’s)

  • drugs must be first given to return adrenal glands to normal size
38
Q

why cannot we not stop the using GCs immediately/

A

patient must be weaned off
exogenous GCs suppress CRH/ACTH (this causes adrenal cortex atrophy and a risk of iatrogenic addison’s)

  • drugs must be first given to return adrenal glands to normal size
39
Q

what is the Triple Lewis Response?

A

this is when the reaction induced when the skin is stroked heavily r pricked: it is caused by histamine release

  • red spot (Capillary dilation)
  • flair (arteriolar dilation)
  • exudate (caused by vascular permeability in venues
40
Q

How is histamine associated with pain?

A

C-fibres have H1 receptors, their binding causes peripheral sensitisation of the nerve fibre

41
Q

how is histamine released?

- what factors increase or decrease histamine release?

A

• Histamine release is dependant on calcium influx. Antigen binding to IgE causes cross-linking and this increases membrane permeability to calcium. Which encourages granule exocytosis
o It is stored as complex with heparin in the granules
• Drugs which increase cAMP (e.g. b2 agonists) reduce histamine release by reducing membrane permeability to calcium
• tubocarine and morphine increase histamine release and are associated with idiosyncratic allergic reactions
• complement components C5a and C3a increase histamine release
• Substance p AND VIP increase histamine release

42
Q

how does histamine effect the heart?

A

H1+ H2 = positive ionotropic effects

H2: positive chronotropic effects

H1; reduces AV node conduction

can predispose to arryhtmias

43
Q

what are the effects of bradykinin?

A 
potent vasodilator 
venular permeability 
pain 
uterus contraction 
slow contraction of intestinal smooth muscle 
histamine release 
acts via B2 receptors
44
Q

what are the effects of bradykinin?

A 
potent vasodilator 
venular permeability 
pain 
uterus contraction 
slow contraction of intestinal smooth muscle 
histamine release 
acts via B2 receptors
45
Q

what is astemizole?

A

a selective H1 antagonist that does not cross the bob

46
Q

what is terfenadine?

A

a selective h1 ANTAGONIST that does not cross the bob

47
Q

give examples of selective H1 antagonists, that do not cross the BBB

A

loratidine, fexofenadine, astemizole, terfenadine

48
Q

give examples of selective H1 antagonists that cross the bBB?

A

chlorpheniramine

diphenyhydramine

49
Q

what drug can be used to treat narcolepsy?

A

selective H3 antagonist (reverse agonist) pitolisant

thioperamide

50
Q

what is icantibant

A

this is a B2, bradykinin inhibitor

51
Q

what is H1 coupled to? and what does it cause

A

coupled to Ga/q - causes an increase in calcium concentration

52
Q

what is H2 coupled to? what does it cause

A

Ga/s - causes an increase in cAMP

increases gastric acid secretion

53
Q

what is H3 coupled to?

A

Gai/o - inhibits cAMP

this is an auto-receptor

54
Q

what is H3 coupled to?

A

Gai/o - inhibits cAMP

this is an auto-receptor

55
Q

what were the old H1 antagonists used for?

A

mild hypnotics, anti-emetics and anti- hay fever because they crossed the blood brain barrier

56
Q

what are the neurotransmitter functions of histamine?

A
  • Histaminergic neurones are involved in the release of vasopressin from the posterior pituitary
  • They’re also involved in emesis, consciousness and temperature regulation
  • Cell bodies of histaminergic neurones in hypothalamus project to caudate, amygdala, hippocampus and central grey matter
  • Pre-synaptic H3 receptors also exist
57
Q

what causes hereditary angiodema?

A

a deficiency in C1 INHIBITORS

58
Q

what causes drug induced angiodema?

A

usually ACE inhibitors

59
Q

how does low dose aspirin work to prevent arterial thrombus?

A

low dose: 75mg per day

  • irreversible acetylation of cycle-oxygenase
  • platelets which produce TXA-2 are the most affected because of their absence of a nucleus
  • endothelial cells which produce PGI-2 (which is anti-aggreatory) affected also, but not as much because they have a nuclei, and usually just synthesize more enzyme
60
Q

what is aspirin combined with to prevent arterial thrombi?

A

used with dipyrimadole, which is a phosphodiesterase inhibitor. increasing cAMP inhibits platelet aggregation, and reduced the chance of thrombus further

61
Q

what are the actions of PGE-2?

A
  • gastric cyctoprotection
  • induce temperature rise in response to circulating pyrogenS (IL-1 production and rise in temperature is in anterior hypothalamus)
  • hyperalgesia
  • potentiates the effect of other mediators (Causes odema but not directly by increasing histamine release)
  • causes vasodilation
  • inhibits leucocytes

when produced by COX-2 from membrane it is a pro-inflammatory cytokine

62
Q

what are the effects of PGF-2?

A

smooth muscle contraction
bronchoconstriction
reproductive physiology

63
Q

what are the effects of PGI-2?

A

anti-platelet
vasodilation
hyperalgesai
renin secretion

most PG1-2 synthetase is found in endothelium

64
Q

what are the effects of TXA-2?

A

platelet aggregation

vasoconstriction

65
Q

explain how prostaglandins are formed? and their basic structure

A

20C molecule, with an OH group at C15 essential for their activity

– formed from arachnoid acid via two enzymes
COX-1 constitutive (cytoplasmic release)
COX-2 inflammatory (membrane release)

then from that via synthetases

66
Q

explain how prostaglandins are formed? and their basic structure

A

20C molecule, with an OH group at C15 essential for their activity

– formed from arachnoid acid via two enzymes
COX-1 constitutive (cytoplasmic release)
COX-2 inflammatory (membrane release)

then from that via synthetases

67
Q

why are diets in saturated fat bad?

A

because they’re associated with lipid perioxidation which inhibits PG1-2 formation. therefore, increases the risk of platelet aggregation and thrombus formation

68
Q

what is PGD TXA-3?

A

this is anti-aggregatory

Pharmacology (17 decks)

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