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Anti-inflammatories Flashcards

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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
What is the immediate drug treatment for anaphylaxis?
Epineprine - subcut and iv administration to maintain intravascular volume
26
What other drugs are given for the treatment of anaphylaxis?
- A H1 receptor antagonist - Glucocorticoids- suppress slow-onset of urticaria, bronchospasm, laryngeal oedema & hypotension
27
What are the 4 main sub-groups of cytokines?
- Interleukins - Interferons - Chemokines - Colony stimulating factors
28
What can arachidonic acid be used to produce?
- Prostaglandins - Thromboxanes - Leukotrienes
29
What activates phospholipase A2?
- Bradykinin - Antigen-antibody binding on mast cells - Thrombin - Complement C5a - Cell damage
30
Which prostaglandins are key in the inflammatory response?
PGE2 and PGI2
31
How can arachidonic acid be converted into prostaglandins?
- 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
32
How are thromboxanes produced?
PGH2 is converted to thromboxane A2 by TXA2 synthetase
33
What are the effects of PGD2?
- Relaxation (& constriction at a high concentration) of vascular smooth muscle - Constriction of bronchial muscle - Relaxation of the GI & uterine muscle
34
Where is COX1 and 2 expressed?
COX-1 - constitutvely expressed in most cells COX-2 - not normally produced, expression induced by inflammatory mediators
35
What are the effects of PGE2?
- 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
What are the effects of PGF2-alpha?
- Constriction of vascular smooth muscle - Constriction of bronchial muscle in dogs & cats - Luteolysis in some species - Uterus contraction
37
What are the effects of PGI2?
- Potent vascular smooth muscle relaxation - Hyper-algesia - Inhibits platelet aggregation - Modulates kidney function
38
What are the effects of thromboxane A2?
- Vasoconstriction - Bronchoconstriction - Induces platelet aggregation - TXA2 is mainly found in platelets
39
Where are leukotrienes produced?
In leukocytes, lungs, mast cells & platelets
40
What does LTB4 cause?
Causes activation & targeting of leukocytes & cytokines production
41
What does cysteinyl-LTs cause?
Bronchoconstriction & vasodilation
42
What is the main effect of histamine in inflammation?
Vasodilation, increased vascular permeability
43
What is the main effect of prostaglandins in inflammation?
Vasodilation, pain, fever
44
What is the main effect of leukotrienes in inflammation?
Increased vascular permeability, leukocyte activation & chemotaxis
45
What is the main effect of thromboxanes in inflammation?
Platelet aggregation, vasoconstriction
46
What is the name for the outer layer of the adrenal cortex and what is secreted?
Zona Glomerulosa
47
What is the name for the middle layer of the adrenal cortex and what is secreted?
Zona fasiculata
48
What is the main glucocorticoid in animals?
corticosterone
49
Describe the hypothalamic-pituitary-adrenal gland secretion pathway of glucocorticoid production
- 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
What is the negative feedback system in the secretion of glucocorticoids?
- Glucocorticoids have a long negative feedback loop on the hypothalamus - ACTH has a short negative feedback loop on the hypothalamus
51
What is the mode of glucocorticoid secretion?
Stimulated by ADH activating CRF & the anterior pituitary - increased ACTH production and therefore more glucocorticoid production
52
How is secretion of glucocorticoids stimulated?
Pulsitile in a circadian rhythm
53
What are the metabolic effects of glucocorticoids?
- 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
What can a loss of corticosteroids cause?
- Muscle weakness - Hypotension - Hypoglycaemia - Weight loss
55
What is Addison's disease?
auto-immune condition or caused by the destruction of adrenal glands by chronic inflammation
56
What is Cushing's disease?
excess of corticosteroids. Can be caused by prolonged glucocorticoid administration or excessive activity of the adrenal glands
57
What are the signs of Cushing's disease in dogs?
- Increased appetite - Distended abdomen/pot belly - Coat issues e.g. baldness, hair thinning, discolouration - Polyuria/polydipsia
58
What can the causes of Cushing's disease be?
- Exogenous glucocorticoids - Pituitary gland tumour which can lead to increased ACTH (can also cause decreased ACTH) - Increase in ACTH due to lung tumours
59
What are the main anti-inflammatory effects of glucocorticoids?
- Decreased cyclooxygenase-2 expression - Increased lipocortin (annexin) which acts to inhibit phospholipase-2
60
What are glucocorticoids used for in the treatment of inflammation?
- They inhibit the early inflammation response - done by decreasing the production of prostaglandins
61
How are glucocorticoids used clinically?
- 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
Which types of glucocorticoids have the highest potency and last the longest?
- Dexamethasone - Betamethosone
63
What disorders can be treated with glucocorticoids?
- Asthma - Recurrent airway obstruction - Eczema, rhinitis, allergic conjunctivitis - Hypersensitivity states - To suppress graft rejection - Acute spinal injury
64
What is the effect of glucocorticoids on the immune response?
- Suppress IL2 gene transcription
65
What are chondroprotective drugs?
Used in osteoporosis & other joint diseases to protect cartilage
66
What is the action of NSAIDs?
inhibits cyclooxygenase - decreases prostaglandin and thhromboxane synthesis
67
What are the effects of NSAIDs?
anti-inflammatory, analgesic, antipyretic
68
What are the roles of COX-1?
- House-keeping role - Gastric protection - Blood clotting - Renal blood regulation
69
What is the function of COX-2?
Produces prostanoids mediating inflammation
70
Can COX-1 inhibitors inhibit COX-2 and vice versa?
COX-1 inhibitors can inhibit COX-2 but COX-2 inhibitors cannot inhibit COX-1
71
What is the action of paracetalmol?
- Inhibits cyclooxygenase - Can be used for analgesia & is anti-pyretic but has no anti-inflammatory effects
72
Which NSAIDs are COX-2 selective?
- Firocoxib & meloxicam (widely selective) - Carprofen (Slightly COX-2 selective) - Phenylbutazone (Very slightly COX-2 selective)
73
What are the consequences of COX-1 inhibition?
- 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
What is the effect of COX-1 inhibitors on platelet activation?
Inhibit platelet aggregation so can cause persistent bleeding
75
What is the effect of COX-2 inhibition in the kidney?
- Can cause sodium retention - Leads to hypertension - Can decrease the effectiveness of some diuretics
76
What are other NSAID side effects
- 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
Why is phenylbutazone not allowed for animals entering the food chain?
Decreases white blood cell count in humans
78
When are NSAIDs used in dogs, cats & horses?
- Acute & chronic pain management - Trauma - Peri-operative pain - Management of pain associated with osteoarthritis and other chronic pain conditions
79
What are the benefits of administering NSAIDs pre-operatively?
- Prevents secondary hyperalgesia - Some evidence in dogs that giving an NSAID pre-operatively is beneficial
80
What are the risks of administering NSAIDs pre-operatively?
- 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
What are the side effects of using NSAIDs in dogs & cats?
- 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
When are NSAIDs used in horses?
- Chronic/acute pain management - For anti-endotoxaemic effects
83
What are the side effects of NSAIDs in horses?
- Renal side effects appear less problematic - GI ulceration does occur
84
When are NSAIDs used in farm animals?
- 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
How can you choose/discriminate between different NSAIDs?
- COX-selectivity - Formulation (tablet/injectable/liquid) - Licensed indication (acute/chronic pain/both) - Duration of action - Cost - Switching between NSAIDs can improve efficacy & tolerability

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