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Med Chem modules > Inflammation > Flashcards

Inflammation Flashcards

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1
Q

What is an antacoid?

A

Mediators of inflammation produced locally around the site of stimulus to inflammation

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2
Q

What are the conceptual challenges in developing new anti-inflammatory drugs?

A

Cost

Lack of oral availability

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3
Q

How do histamine a fulfil Dale’s criteria for a pharmacological mediator?

A 
Present in histaminergic neurones
Store in granules
Upon antigen-IgE cross-linking, granules are released
Effects shown at H receptors
Terminated by histaminase
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4
Q

How does histamine contribute to a local inflammatory response?

A

Causes vasodilation of the small arteriolar and precapillary sphincters
Causes the release of CGRP and other vasodilatory by anti-dromic impulses in sensory nerve fibres

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5
Q

How does histamine contribute to anaphylaxis?

A

Causes smooth muscle contraction in bronchi

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6
Q

Name 3 chemical mediators which regulate acid secretion from parietal cells

A

Histamine (+)
Gastric (+)
Prostaglandins E(2) and I(2) (-)

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7
Q

Describe ranitidine.

A

H(2) antagonist

Heals duodenal ulcers

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8
Q

Describe terfenidine.

A

H1 non sedative antagonist

No entry to CNS

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9
Q

Describe diphenhydramine.

A

H1 antagonist
Used to treat motion sickness
Can cross BBB

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10
Q

What is an eicosanoid?

A 
Locally produced lipids
Work in the 10(-12)M range
Small t(1/2) 
Metabolised into active prostaglandin
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11
Q

Describe the biosynthesis of PGE(2)

A

Phospholipid is converted into arichidonic acid by phospholipase A(2)
arichidonic acid is converted to PGG(2) by cyclooxygenase
PGG(2) converted to PGH(2) by cycloendoperoxides
PGH(2) converted to PGE(2) by PG isomerise reductase

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12
Q

How is the biosynthesis of PGE(2) targeted by anti-inflammatory drugs?

A

Lipocortin inhibits phospholipase A(2)

NSAIDS inhibit cyclooxygenase

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13
Q

What are the main side-effects of NSAIDs?

A

Gastro-intestinal bleeding

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14
Q

What is the biological mechanism behind NSAID gastrointestinal bleeding?

A

NSAIDs block cox-1, inhibiting PGE(2) production
Reducing PGE(2) increases acid production
Acid irritates gastrin mucosa increasing susceptibility to ulceration
They prolong bleeding by reducing the platelet stickiness

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15
Q

How do cox-2 inhibitors avoid gastrointestinal bleeding?

A

Cox-2 doesn’t affect platelet stickiness

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16
Q

Why is aspirin used for platelet inhibition and not other NSAIDs?

A

Aspirin is the only NSAID which irreversibly inhibits cyclooxygenase. This means much lower doses can be used and less frequently

17
Q

Uses of prostaglandin analogues.

A

Abortion
Labour induction
Postcoital contraception
Peptic ulcer treatment

18
Q

Main causative agents of peptic ulcer formation.

A

H. pylori
NSAIDs
Stress
Diet

19
Q

What is the HPA axis?

A

Hypothalamic- pituitary- adrenal axis
A complex set of direct feedback interactions among the 3 endocrine glands
Regulates glucocorticoids i.e cortisol

20
Q

How does the HPA axis contribute to the regulation of inflammation?

A

Glucocorticoids are anti-inflammatory
They suppress the production of antacoids
Inhibitor of induction and effector phases of immune response

21
Q

Omeprazole

A

Proton pump inhibitor
Treats peptic ulcers
Inhibits H/K ATPase of parietal cell
Decreases gastric acid secretion

22
Q

Aluminium hydroxide.

A

Antacid

Neutralises gastric acid

23
Q

Sucralfate.

A

Coating agent

Provides protection to GI epithelium

24
Q

Misoprostol.

A

Prostaglandin

Inhibits acid production

25
Q

Dicyclomine.

A

Anti cholinergic agent
mAChR inhibitor
Decrease acid secretion

26
Q

How do steroidal anti-inflammatory drugs affect prostaglandin production?

A

Inhibit the expression of cox-2, reducing the amount of PGE(2)

27
Q

How do NSAIDs affect prostaglandin production?

A

Inhibits cox-2, reducing the amount of PGE(2)

28
Q

List the 5 cardinal signs of inflammation

A 
Pain- dolor
Redness- rubor
Immobility- functo leasa
Swelling- tumor
Heat- calor
29
Q

Describe the mechanism of action of glucocorticoids.

A

Bind to intracellular receptors, causing them to dimerise and move to the nucleus
The complex inhibits the transcription of genes for cox-2 and NO synthase, cytokines, interleukins, and cell adhesion molecules

30
Q

What are the therapeutic affects of glucocorticoids?

A

Hydrocortisone:
Decreases egress of neutrophils from blood vessels and reduced activation of neutrophils, macrophages, and mast cells
Decreased activation of T(helper) cells

31
Q

What are the adverse effects of glucocorticoids?

A

Decreased fibroblast function, reduced healing and repair

Reduced activity of osteoblasts but increased activity of osteoclasts, develop osteoporosis

32
Q

What effects are encounter after administration of high doses and cessation of glucocorticoid treatment?

A 
Suppression of the response to infection
Osteoporosis
Hyperglycaemia 
Muscle wasting
Acute adrenal insufficiency
33
Q

List the pathological characteristics of asthma

A

Inflammation of airways
Bronchial hyperactivity
Reversible airways obstruction

34
Q

Give two symptomatic relievers

A

Salbutamol- beta 2 agonist- bronchodilation

Theophylline- activates PKC- bronchodilation

35
Q

Give two pathology modifying drugs

A

Cromoglycate

Nedocromil

36
Q

What is a biologic?

A

A medicinal preparation created by a biological process

37
Q

Discuss the use of therapeutic antibodies to treat inflammatory diseases.

A

Treats patients who do not respond to glucocorticoids
Do not need glucocorticoids, avoiding side effects
High cost
Requirement of long term administration
Has to be injected

38
Q

Compare infliximab with etanercept (TNF- alpha blockers)

A

Etanercept cannot neutralise receptor bound TNF when infliximab can
Infliximab can also lyse cells in the inflammatory process

Med Chem modules (8 decks)

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