ILA Flashcards
Define anaphylaxis
Potentially life threatening Type 1 hypersensitivity reaction, usually allergic reaction to a trigger
Signs/symptoms of anaphylaxis
Difficulty breathing/swallowing
Wheezing
Clammy skin
Confusion/anxiety
Angiooedema
Hypotension
Tachycardia
Loss of consciousness
Skin specific signs of anaphylaxis
Hives
Widespread flushing
Angiooedema
Pathology of anaphylaxis
Allergen reacts to IgE antibodies on mast cells and basophils, causing rapid release of:
Histamine, proteases, platelet activating factor, leukotrienes, prostaglandins.
This causes vasodilation, increased vascular permeability, smooth muscle spasm in resp tracts, mucus secretion.
Common triggers of anaphylaxis
Peanuts, fish, eggs, milk, bee/wasp stings, antibiotics, opioids, NSAIDs.
Treatment of anaphylaxis
Clear airway, remove obstruction
- Adrenaline IM, anterolateral aspect of thigh - Beta adrenergic receptor agonist
- Chlorphenamine - H1 receptor blocker
MoA of Adrenaline
Stimulates B1 receptor - increases SA and AV node firing, increasing heart rate and contractility, increasing stroke volume and output.
Stimulates B2 receptor - Smooth muscle relaxation, dilates bronchi, reduces oedema
Structure of athersclerotic plaque
Lipids, necrotic core, connective tissue, fibrous cap
Pathology of plaque formation
- High LDL causes them to deposit and oxidise in tunica intima, activating endothelial cells which present leukocyte adhesion molecules.
- Leukocytes move into intima and attract monocytes (macrophages/T helper cells)
- Macrophages take up oxidised LDL and form foam cells, which release IGF-1 causing smooth muscle to migrate to intima from media.
- Smooth muscle proliferation forms fibrous cap.
- As foam cells die they release lipid content, growing plaque, which eventually ruptures.
How risk factors promote atherosclerosis
(smoking, HTN, DM, high LDL, male)
Smoking - releases free radicals, CO, nicotine, into blood, damaging epithelium
Diabetes - increased free radicals so oxidation of LDL / Less Nitric Oxide - which normally relaxes vessel / increased platelet aggregation
High LDL - can get into endothelial wall in excess
Age - longer exposure
Male - oestrogen decreases LDL cholesterol and reduces leukocyte adhesion molecules
Why should protein binding be low in a drug?
Protein binding lowers free concentration of drug. Low enables high plasma concentration
How is extrinsic started
Damage to endothelial tissue exposes tissue factor (3), activating it.
How is intrinsic started
Collagen exposure activates 12 to 12a
Action of warfarin
Inhibits vitamin K - factors 10,9,7,8
Action of heparin
Activates antithrombin - inhibits thrombin and 10a
