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Pharmacology PED1003 > Antihistamines > Flashcards

Antihistamines Flashcards

1
Q

Autocoid =

A

‘self-remedy’

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2
Q

Local hormone =

A

Chemical messenger formed by tissues on which it acts.

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3
Q

Where is histamine found?

A

High concentration in lungs, skin and smooth muscle (blood vessels)
Stored in basophils and mast cells
In granuoles
Rapidly inactivated by amine oxidase if not stored

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4
Q

Histamine in the stomach

A

Histamine found un histaminocytes

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5
Q

Histamine in the CNS

A

Histamine found in histaminergic neurones

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6
Q

Histamine in venom

A

Histamine found in toxics of venom

EG Insect stings and plant stings

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7
Q

Synthesis of Histamine

A

Synthesised from histidine (amino acid)

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8
Q

Release of Histamine from Mast cells: Acute inflammatory response

A

One of several mediators released in response to a pathogen. EG Bacteria or toxin.
Complement components -> C3a and C5a receptors -> Mast cell.
Pathogen -> Pathogen pattern receptors -> Mast cell

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9
Q

Release of Histamine from Mast cells: Hypersensitivity

A 
Allergic immune system reaction to typical harmless substances.
Harmless antigen (EG Pollen) -> Immunoglobulin (Ig) E Cell fixed antibody -> Mast cell
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10
Q

Release of Histamine from Mast cells: Physical destruction

A

Mast cell

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11
Q

Release of Histamine from CNS: Arousal pathways

A

Histaminergic neurones in TMN.

Spontaneously active and release histamine during wakefulness.

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12
Q

Release of Histamine from CNS: Emetic centre

A

Histaminergic neurones in TMN also receive input from vestibular centre in inner ear (spatial orientation) and other sensory inputs.
If mismatch between inputs = Activate histaminergic neurones = Activate emetic (Vomiting) centre in medulla.

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13
Q

Histamine receptors

A

G-protein coupled receptors
H1: Myosin phosphorylation, vascular permeability, NFkB activation. Inside Ca2+ increases. H1 coupled to phospholipase C
H2: Proton pump function, gastric acid secretion. Increase in inside cAMP. Coupled to adenylate cyclase.
H3/H4: Proton pump function, gastric acid secretion. decrease in inside cAMP. Coupled to adenylate cyclase.

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14
Q

Histamine receptor functions (H1)

A 
CNS neuronal activation
Nasal and bronchial mucus secretion
Smooth muscle contraction
Sensory nerve endings
Proinflammatory cytokine secretion
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15
Q

Histamine receptor functions (H2)

A

Stimulation of gastric acid secretion

Cardiac stimulation - Chronotropic (time change), increase HR

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16
Q

Histamine receptor functions (H1 and H2)

A

Capillary permeability and dilation

Cardiac stimulation - Inotropic (time change), increase heart contraction

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17
Q

Histamine receptor functions - Pathologies

A 
Allergic reaction: mild to severe.
Immune system hypersensitive response to typically harmless substance in environment.
EG Pollen or food
Release of histamine from mast cells
Can be localised
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18
Q

Allergic rhinitis

A 
Inflammation inside nose in response to allergen
EG Pollen or dust
Very common (1 in 5)
Can be localised immune response
Sneezing, itchiness, runny nose
Sensory nerve ending stimulation
Increase nasal secretions
Capillary permeability and dilation
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19
Q

Urticaria (hives)

A 
Skin rash in response to allergen or toxic substance.
EG Nettle sting, latex
Itchy, raised bump, redness, pain
Sensory nerve ending stimulation
Capillary permeability and dilation
Can be localised response
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20
Q

Moderate allergic reaction to allergen. EG food

A 
1. Rhinitis conjunctivitis
Sensory nerve ending stimulation
Increase secretion
Capillary permeability and dilation
2. Hives
Sensory nerve ending stimualtion
Capillary permeability and dilation
3. Tummy pain/diarrhoea
Intestinal muscle contraction
4. Wheezing/chest tightness/shortness of breath
Bronchiole contraction
21
Q

Severe allergic reactions (Anaphylaxis)

A

Reapid onset
Breathing difficulties
Rapid HR
Loss of conciousness

22
Q

Motion sickness

A

Sensory input (visual)
Spatial orientation (vestibular system in inner ear)
Input mismatch at Tuberomamillary nucleus
Histamine released to Emetic centre
Contraction of stomach muscles
Motion sickness

23
Q

Antihistamines: 1st generation - Prophylaxis

A

Much more effective if given before histamine receptor stimulation to prevent development of symptoms

24
Q

Antihistamines: 1st generation - Receptors

A

Typically H1 receptor antagonists
Can be muscarinic cholinergic receptor antagonists
Particularly diphenhydramine and promethazine
Can be α1-adrenoceptor antagonists
Particularly promethazine

25
Antihistamines: 1st generation - Examples
Hydroxyzine Promethazine Diphenhydramine
26
Antihistamines: 1st generation - Pros
Inexpensive and effective. Decrease allergy / inflammation Cross the BBB so can prevent motion sickness (Block H1 receptors in Emetic centre) Cross the BBB so can cause sedation (Block H1 receptors in arousal pathway/cerebral cortex) Not very H1 selective = extra unwanted effects
27
Antihistamines: 1st generation - Cons
Cross the BBB = Unwanted sedation (BLock H1 receptors in arousal pathway/cerebral cortex) May potentiate other CNS depressants ? Paradoxical hyperactivity in children (diphenhydramine) Not very H1 selective = Unwanted adverse effects
28
Antihistamines: 1st generation - Parasympathetic activation
``` Pupils constrict Lens of eye readjust for closer vision HR decrease Salivary secretions normalise Bladder contraction ```
29
Antihistamines: 1st generation - Effect of muscarinic antagonists
Pupils dilate (relaxation of constrictor pupillary muscle - blurred vision) Increased cardiac output (rate and force) Decreased exocrine gland secretion (dry mouth) Decreased bladder contraction (urinary retention) But muscarinic receptor antagonism therapeutic value = Antiemetic effects
30
Antihistamines: 1st generation - Can exacerbate anticholinergic adverse effects other drugs, Example.
EG Monoamine oxidase inhibitors or decrease effectiveness of cholinergic drugs. EG Rivastigmine in Alzheimers.
31
Antihistamines: 1st generation - Sympathetic activation
Vasoconstriction (α1-adrenoreceptor)
32
Antihistamine: 1st generation - Effect of α1-adrenoreceptor antagonist
Vasodilation (hypotension, dizziness)
33
Antihistamine: 1st generation - Diphenhydramine also affects 5-HT neurotransmission
``` 1960's discovered inhibited 5-HT reuptake. Search for antidepressants with similar structure but fewer side effects. SSRI Fluoxetine (Prozac) formed. ```
34
Antihistamine: 2nd generation - Examples
Cetirizine (partially sedating) Loratidine (non-sedating) Fexofenadine (non-sedating)
35
Antihistamine: 2nd generation - Features
Add carboxyl groups = More polar Do not cross BBB as easily Less unwanted sedation Less anticholinergic effects
36
Antihistamine - H1 Pharmacokinetics
``` Absorption -> Oral Cmax 1-2 hours Distribution -> 1st gen = All tissues 2nd gen = All tissues except CNS Metabolism -> 1st gen = cytochrome P450s 2nd gen = most cytochrome P450s, not cetirizine Elimination -> Average half life 4-6 hours ```
37
Antihistamines H1 receptor antagonist summary - Theraputic uses
Decreases allergy and inflammatory response Decrease motion sickness / nausea Increase sedation
38
Antihistamines H1 receptor antagonist summary - Adverse effects
Sedation (1st gen) Dry mouth, urinary retention, blurred vision (anticholinergic) Hypotension, dizziness (antiadrenergic)
39
Antihistamines H1 receptor antagonist summary - Not used to treat asthma
Additional chemical mediators involved in bronchial contraction
40
Antihistamines H1 receptor antagonist summary - Not used to treat anaphylaxis
Adrenaline used Activation of β2-adrenoceptors = bronchiole muscle relaxation Activation of β1-adrenoceptors = increase cardiac rate and force Activation of α1-adrenoceptors = vasoconstriction
41
Antihistamines: H2 receptor antagonist - Gastric acid secretion
``` Stomach -> Gastric gland -> Parietal cell -> Chloride co-transported (Cl- goes out of cell, into lumen), Proton pump H+K+ATPase (H+ goes out, into lumen) -> Release HCL (pH <1) ```
42
Antihistamines: H2 receptor antagonist - Peptic ulcers and GERD
Promote peptic ulcer healing Peptic ulcers = Perforation in the lining of the small intestine or stomach Infection with gram-negative Heliobacter pylori Use of NSAIDs (COX2 flashback) Reduce gastropharengeal reflux disease (heartburn)
43
Antihistamines: H2 receptor antagonist - Antimicrobials eradicate H.pylori
Treatment to reduce gastric secretion H2 antagonists competitively block histamine binding (fully reversible) Reduced gastric acid secretion by up to 70% Cimetidine and Ranitidine Also, Nizatidine and Famotidine
44
Antihistamines: H2 adverse effects - Pros
All 4 effective for H. Pylori peptic ulcers Effective for heartburn Inexpensive Relatively safe
45
Antihistamine: H2 adverse effects - Cons
Peptic ulcer reoccurence common in H.pylori is present and not treated. Not as effective treating and preventing NSAID induced peptic ulcers. Heartburn onset of action in 45mins. They can reduce efficacy of drugs requiring acidic environment for absorption. Cimetidine affects metabolism of other drugs.
46
Antihistamines - H2 receptor antagonists alternates
Proton pump inhibitors (PPIs) Decrease H+ secretion Dexlansoprazole omeprazole
47
Prodrug
``` Acid resistant coating Coating removed in duodenum Absorbed and transported to parietal cell Metabolised to activate drug there Binds to H+K+ATPase Gastric acid secretion decreases 18 hours to resynthesise ```
48
Prodrug - Pros
Higly effective | Long duration
49
Prodrug - Cons
Delayed onset of action Increased risk of gut infection (C.defficile) Gut pH substantially above physiological level

Pharmacology PED1003 (18 decks)

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