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AD2 > Anti-inflammatories > Flashcards

Anti-inflammatories Flashcards

1
Q

What are the main vascular responses of inflammation?

A
  • Vasodilation
  • Increased vascular permeability
  • Exudation
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2
Q

What occurs in exudation?

A
  • Fluid filters from the circulatory system into the surrounding tissue
  • carries leukocytes & components of proteolytic enzyme cascades e.g. complement, coagulation, fibrolytic & kinin systems
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3
Q

What are the general principles of autocoids/local hormones in an inflammatory reaction?

A
  • All act locally
  • Have a paracrine or autocrine effect
  • Are released from cells upon stimulation
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4
Q

How is histamine deactivated?

A

diamine oxidase
histamine-N-methyl-transferase

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5
Q

What are some of the different roles of histamine?

A
  • Tissue repair & inflammation
  • Control of local blood supply
  • Contributes to allergic & anaphylactic reactions
  • Neurotransmission in the CNS
  • Gastric acid secretion
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6
Q

Where in the body is histamine located?

A
  • Has a high concentration in areas of interface between the body & external environment e.g. lung, skin, GI tract
  • Brain
  • Present in mast cells & basophils
  • Also in neurones (brain) & enterochromaffin-like cells in the stomach
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7
Q

Where are mast cells produced and found?

A

Produced in bone marrow
Found beneath skin and throughout resp, digestive and urinary tract

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8
Q

What occurs in the priming of the mast cell?

A
  • Exposure to allergen creates IgE antibodies
  • IgE antibodies bind to mast cells
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9
Q

What occurs to the mast cell on the 2nd exposure to an allergen?

A
  • Allergen binds to the IgE on the mast cell surface
  • This activates the mast cell
  • Leads to degranulation and the release of histamine
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10
Q

How does degranulation occur in the mast cell?

A
  • Binding of IgE to Fc3R receptor increases the calcium concentration in the cell
  • Calcium release triggers the release of granules which fuse with the membrane & release histamine
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11
Q

What is another way that histamine can be released from mast cells?

A
  • Some neuropeptides
  • Complement 3a & 5a also activates mast cells to release granules by binding to other cell surface receptors
  • Some basic drugs can directly displace histamine from the granules in mast cells causing the release of histamine without activating cell surface receptors
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12
Q

How can histamine release be inhibited?

A

By an increase in cyclic AMP via B-adreno-receptor agonists

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13
Q

What type of receptors are histamine recpetors?

A

4

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14
Q

What are the effects of the histamine H1 receptor?

A

G-Protein coupled receptors

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15
Q

What are H1 receptor antagonists used for and where are they metabolized?

A
  • Systemic vasodilation
  • Increased vascular permeability
  • Itching
  • Bronchoconstriction
  • Ileum contraction
  • Effects on neuronal action potential firing
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16
Q

What is the average duration of the effects of H1 receptor antagonists?

A
  • Increased IP3 & DAG
  • Stimulates calcium release
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17
Q

What is the difference between 1st generation H1 receptor antagonists & H2 receptor antagonists?

A

1st generation cross the blood-brain-barrier - affects CNS
2nd generation can’t cross the BBB and have a longer duration

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18
Q

What is the duration of 2nd generation H1 receptor antagonists?

A

12-24 hours

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19
Q

What are 2nd generation H1 antagonists used for?

A
  • Allergy-induced asthma
  • Allergic skin disorders
  • Relief of itching
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20
Q

What can 1st generation H1 antagonists be used for?

A
  • Motion sickness
  • Mild sedation
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21
Q

What do H2 receptor antagonists do?

A

Inhibit gastric acid secretions - treatment for gastric ulcers

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22
Q

What does a type 1 hyper-sensitivity reaction immediately produce?

A
  • Smooth muscle contraction
  • Vasodilation
  • Increase in vascular permeability
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23
Q

What does a type 1 hypersensitivity reaction cause within 2 minutes?

A
  • Nausea
  • Abdominal pain
  • Palpitation
  • Urticaria
  • Difficulty breathing
  • Hypotension
  • Inadequate circulation
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24
Q

What does a type 1 hypersensitivity reaction cause within 2 more minutes?

A

Circulatory shock

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25
Q

What is the immediate drug treatment for anaphylaxis?

A

Epineprine - subcut and iv administration to maintain intravascular volume

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26
Q

What other drugs are given for the treatment of anaphylaxis?

A
  • A H1 receptor antagonist
  • Glucocorticoids- suppress slow-onset of urticaria, bronchospasm, laryngeal oedema & hypotension
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27
Q

What are the 4 main sub-groups of cytokines?

A
  • Interleukins
  • Interferons
  • Chemokines
  • Colony stimulating factors
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28
Q

What can arachidonic acid be used to produce?

A
  • Prostaglandins
  • Thromboxanes
  • Leukotrienes
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29
Q

What activates phospholipase A2?

A
  • Bradykinin
  • Antigen-antibody binding on mast cells
  • Thrombin
  • Complement C5a
  • Cell damage
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30
Q

Which prostaglandins are key in the inflammatory response?

A

PGE2 and PGI2

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31
Q

How can arachidonic acid be converted into prostaglandins?

A
  • Arachidonic acid is converted to PGG2 by cycloooxygenase, which also coverts PGG2 into PGH2, both of which are unstable & have no effect
  • PGH2 is rapidly converted into the end products (PGI2, PGF2-alpha, PGD2 & PGE2) by different enzymes
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32
Q

How are thromboxanes produced?

A

PGH2 is converted to thromboxane A2 by TXA2 synthetase

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33
Q

What are the effects of PGD2?

A
  • Relaxation (& constriction at a high concentration) of vascular smooth muscle
  • Constriction of bronchial muscle
  • Relaxation of the GI & uterine muscle
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34
Q

Where is COX1 and 2 expressed?

A

COX-1 - constitutvely expressed in most cells
COX-2 - not normally produced, expression induced by inflammatory mediators

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35
Q

What are the effects of PGE2?

A
  • Relaxation of vascular smooth muscle
  • Dilation of bronchial muscle
  • Hyper-algesia: lower nociceptor (pain) threshold, & sensitises receptors on afferent nerves to agents not causing pain
  • Produces fever
  • Promotes platelet aggregation
  • Inhibits gastric acid secretion & increases gastric mucus
36
Q

What are the effects of PGF2-alpha?

A
  • Constriction of vascular smooth muscle
  • Constriction of bronchial muscle in dogs & cats
  • Luteolysis in some species
  • Uterus contraction
37
Q

What are the effects of PGI2?

A
  • Potent vascular smooth muscle relaxation
  • Hyper-algesia
  • Inhibits platelet aggregation
  • Modulates kidney function
38
Q

What are the effects of thromboxane A2?

A
  • Vasoconstriction
  • Bronchoconstriction
  • Induces platelet aggregation
  • TXA2 is mainly found in platelets
39
Q

Where are leukotrienes produced?

A

In leukocytes, lungs, mast cells & platelets

40
Q

What does LTB4 cause?

A

Causes activation & targeting of leukocytes & cytokines production

41
Q

What does cysteinyl-LTs cause?

A

Bronchoconstriction & vasodilation

42
Q

What is the main effect of histamine in inflammation?

A

Vasodilation, increased vascular permeability

43
Q

What is the main effect of prostaglandins in inflammation?

A

Vasodilation, pain, fever

44
Q

What is the main effect of leukotrienes in inflammation?

A

Increased vascular permeability, leukocyte activation & chemotaxis

45
Q

What is the main effect of thromboxanes in inflammation?

A

Platelet aggregation, vasoconstriction

46
Q

What is the name for the outer layer of the adrenal cortex and what is secreted?

A

Zona Glomerulosa

47
Q

What is the name for the middle layer of the adrenal cortex and what is secreted?

A

Zona fasiculata

48
Q

What is the main glucocorticoid in animals?

A

corticosterone

49
Q

Describe the hypothalamic-pituitary-adrenal gland secretion pathway of glucocorticoid production

A
  • Hypothalamus secretes corticotrophin-releasing factor which acts on the anterior pituitary gland to secrete adrenocorticotropic hormone (ACTH)
  • ACTH acts on the adrenal gland to secrete glucocorticoids & mineralocorticoids
50
Q

What is the negative feedback system in the secretion of glucocorticoids?

A
  • Glucocorticoids have a long negative feedback loop on the hypothalamus
  • ACTH has a short negative feedback loop on the hypothalamus
51
Q

What is the mode of glucocorticoid secretion?

A

Stimulated by ADH activating CRF & the anterior pituitary
- increased ACTH production and therefore more glucocorticoid production

52
Q

How is secretion of glucocorticoids stimulated?

A

Pulsitile in a circadian rhythm

53
Q

What are the metabolic effects of glucocorticoids?

A
  • Decrease glucose uptake & utilisation/Increase gluconeogenesis
  • Decrease protein synthesis/ increase protein catabolism
  • Cause a redistribution of fat
  • Increase calcium excretion from the kidney/Decrease calcium absorption in the GI tract
54
Q

What can a loss of corticosteroids cause?

A
  • Muscle weakness
  • Hypotension
  • Hypoglycaemia
  • Weight loss
55
Q

What is Addison’s disease?

A

auto-immune condition or caused by the destruction of adrenal glands by chronic inflammation

56
Q

What is Cushing’s disease?

A

excess of corticosteroids. Can be caused by prolonged glucocorticoid administration or excessive activity of the adrenal glands

57
Q

What are the signs of Cushing’s disease in dogs?

A
  • Increased appetite
  • Distended abdomen/pot belly
  • Coat issues e.g. baldness, hair thinning, discolouration
  • Polyuria/polydipsia
58
Q

What can the causes of Cushing’s disease be?

A
  • Exogenous glucocorticoids
  • Pituitary gland tumour which can lead to increased ACTH (can also cause decreased ACTH)
  • Increase in ACTH due to lung tumours
59
Q

What are the main anti-inflammatory effects of glucocorticoids?

A
  • Decreased cyclooxygenase-2 expression
  • Increased lipocortin (annexin) which acts to inhibit phospholipase-2
60
Q

What are glucocorticoids used for in the treatment of inflammation?

A
  • They inhibit the early inflammation response
  • done by decreasing the production of prostaglandins
61
Q

How are glucocorticoids used clinically?

A
  • Used as treatment of inflammatory, immune or tumour-related diseases
  • Also used in the emergency treatment of anaphylaxis, shock, asthma & trauma to the CNS
62
Q

Which types of glucocorticoids have the highest potency and last the longest?

A
  • Dexamethasone
  • Betamethosone
63
Q

What disorders can be treated with glucocorticoids?

A
  • Asthma
  • Recurrent airway obstruction
  • Eczema, rhinitis, allergic conjunctivitis
  • Hypersensitivity states
  • To suppress graft rejection
  • Acute spinal injury
64
Q

What is the effect of glucocorticoids on the immune response?

A
  • Suppress IL2 gene transcription
65
Q

What are chondroprotective drugs?

A

Used in osteoporosis & other joint diseases to protect cartilage

66
Q

What is the action of NSAIDs?

A

inhibits cyclooxygenase
- decreases prostaglandin and thhromboxane synthesis

67
Q

What are the effects of NSAIDs?

A

anti-inflammatory, analgesic, antipyretic

68
Q

What are the roles of COX-1?

A
  • House-keeping role
  • Gastric protection
  • Blood clotting
  • Renal blood regulation
69
Q

What is the function of COX-2?

A

Produces prostanoids mediating inflammation

70
Q

Can COX-1 inhibitors inhibit COX-2 and vice versa?

A

COX-1 inhibitors can inhibit COX-2 but COX-2 inhibitors cannot inhibit COX-1

71
Q

What is the action of paracetalmol?

A
  • Inhibits cyclooxygenase
  • Can be used for analgesia & is anti-pyretic but has no anti-inflammatory effects
72
Q

Which NSAIDs are COX-2 selective?

A
  • Firocoxib & meloxicam (widely selective)
  • Carprofen (Slightly COX-2 selective)
  • Phenylbutazone (Very slightly COX-2 selective)
73
Q

What are the consequences of COX-1 inhibition?

A
  • COX-1 will produce PGE2 & PGI2 which protect the gastric mucosa by increasing mucus & decreasing acid production
  • So COX-1 inhibitors lead to an increase in acid & decrease in mucus production which can lead to the formation of gastric ulcers
74
Q

What is the effect of COX-1 inhibitors on platelet activation?

A

Inhibit platelet aggregation so can cause persistent bleeding

75
Q

What is the effect of COX-2 inhibition in the kidney?

A
  • Can cause sodium retention
  • Leads to hypertension
  • Can decrease the effectiveness of some diuretics
76
Q

What are other NSAID side effects

A
  • Can cause renal toxicity if renal function is already decreased
  • Hepatotoxicity- in cats
  • Haematology & haemostasis- causing an increased risk of bleeding
  • Injury to articular cartilage: Chronic NSAID use leads to worsening of cartilage damage in osteoarthritis due to impaired proteoglycan synthesis
77
Q

Why is phenylbutazone not allowed for animals entering the food chain?

A

Decreases white blood cell count in humans

78
Q

When are NSAIDs used in dogs, cats & horses?

A
  • Acute & chronic pain management
  • Trauma
  • Peri-operative pain
  • Management of pain associated with osteoarthritis and other chronic pain conditions
79
Q

What are the benefits of administering NSAIDs pre-operatively?

A
  • Prevents secondary hyperalgesia
  • Some evidence in dogs that giving an NSAID pre-operatively is beneficial
80
Q

What are the risks of administering NSAIDs pre-operatively?

A
  • If the patient has concurrent disease that may make them more likely to become hypotensive
  • Long surgery
  • Can expect blood loss
  • May be an issue if the patient has CVS disease
  • May have renal damage if the patient becomes hypotensive
  • Geriatric
  • Surgery type may pre-dispose to CVS compromise
81
Q

What are the side effects of using NSAIDs in dogs & cats?

A
  • GI: gastric ulcers
  • Renal: PGI2 in the kidney is important in maintaining blood flow during periods of hypotension. Increased risk of renal ischaemia, cats can get chronic kidney disease
  • Hepatic: Hepatopathy more commonly reported in dogs, may cause an elevation in liver enzymes. Liver dysfunction may lead to the accumulation of drugs & side effects
  • CVS: Dullness & lethargy reported in cats
  • Blood clotting & platelet function: NSAIDs with COX-1 effects may block the synthesis of thromboxane A2 in platelets. NSAIDs with COX-2 effects may inhibit the production of prostacyclin (PGI2) which is responsible for vasodilation & limiting the clotting cascade. Can cause an increased risk of thrombosis.
82
Q

When are NSAIDs used in horses?

A
  • Chronic/acute pain management
  • For anti-endotoxaemic effects
83
Q

What are the side effects of NSAIDs in horses?

A
  • Renal side effects appear less problematic
  • GI ulceration does occur
84
Q

When are NSAIDs used in farm animals?

A
  • For their anti-inflammatory, anti-pyretic, anti-endotoxaemic effects
  • Calf pneumonia
  • Calf scour
  • Toxic metritis & mastitis
  • Peri-operatively for digit amputation, LDA, C-section
85
Q

How can you choose/discriminate between different NSAIDs?

A
  • COX-selectivity
  • Formulation (tablet/injectable/liquid)
  • Licensed indication (acute/chronic pain/both)
  • Duration of action
  • Cost
  • Switching between NSAIDs can improve efficacy & tolerability

AD2 (39 decks)

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