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2a ILA's > anaphylaxis > Flashcards

anaphylaxis Flashcards

1
Q

Define anaphylaxis

A

acute allergic reaction to an allergen to which someone has become hypersensitive

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2
Q

Describe the sensitisation of the immune system in anaphylaxis

A

Antigen presenting cells process and display the antigens of the allergen on their cell surface. they then travel to lymph nodes where they present to the T-helper cells, these activate the B plasma cells via interleukin-21 . Interleukin-4 causes B cells to class switch into IgE. Mast cells have FC receptors, which bind to the heavy chain of IgE, which can also bind to basophils

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3
Q

Describe the subsequent immune response in anaphylaxis after the sensitisation of the immune system

A

In subsequent exposure the IgE on the mast cells cross links with the allergen, which causes degranulation (histamine released). This allows for extravasation. Hours later more mediators are released which leads to more symptoms of anaphylaxis

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4
Q

list the triggers of anaphylaxis that you may find in a hospital

A

1.food- nuts, milk, fish, shellfish
2. medicines- antibiotics, NSAIDS
3.genreal anaesthetic
4. contrast agents (dyes used in medical tests
5. latex

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5
Q

Name anaphylaxis triggers you may find outside of a clinical setting

A
  1. food- nuts, fish, shellfish, eggs, fruits
  2. insect stings
  3. latex
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6
Q

How do we describe anaphylaxis when the trigger is unknown?

A

idiopathic

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7
Q

Describe the CNS symptoms of anaphylaxis

A
  1. light-headedness
  2. loss of consciousness
  3. confusion
  4. headache
  5. anxiety
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8
Q

Describe the resp symptoms of anaphylaxis

A
  1. shortness of breath
    2.wheezes or stridor
  2. hoarseness
  3. pain swallowing
  4. cough
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9
Q

Describe the GI examples of anaphylaxis

A
  1. Crampy abdominal pain
  2. diarrhoea
  3. Vomiting
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10
Q

Describe the skin symptoms in anaphylaxis

A
  1. hives
  2. itchiness
  3. flushing
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11
Q

Describe the cardio symptoms of anaphylaxis

A
  1. tachy/ bardycardia
  2. hypotension
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12
Q

What other symptoms may you see in anaphylaxis?

A
  1. pelvic pain
  2. loss of bladder control
  3. swelling of oral cavity
    4.swelling of conjunctiva
  4. runny nose
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13
Q

How quick is the onset of anaphylaxis?

A

begins in minutes and lasts for 1-2 hours

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14
Q

What is a biphasic response?

A

where after the 1st reaction occurs a second reaction occurs without the allergen.

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15
Q

what pathophysiology occurs due to activation of H1 and H2 histamine receptors?

A
  1. vasodilation
  2. hypotension
  3. flushing
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16
Q

what pathophysiology occurs because of activation of the H1 receptors alone?

A

1.coronary vasoconstriction
2. tachycardia
3. vascular permeability
4. pruritus (itchy skin)
5.bronchospasm
6. rhinorrhoea( runny nose)

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17
Q

Outline the treatment for anaphylaxis

A
  1. Basic life support
  2. stop drug infusion
  3. IM adrenaline, 500 micrograms or 300 micrograms EpiPen
  4. IV fluids, aggressive resuscitation
  5. may require IV adrenaline if in anaphylactic shock
    6.antihistamines not first line of action but required for skin resolution
  6. corticosteroids no longer recommended
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18
Q

describe the action of adrenaline via alpha adrenergic receptors

A
  1. vasoconstriction
    This counteracts the vasodilation, increased vascular permeability which lead to the loss of intravascular fluid and subsequent hypotension
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19
Q

Describe the action of adrenaline through beta adrenergic receptors

A
  1. powerful bronchodilator effect
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20
Q

Describe the general effects of adrenaline in anaphylaxis treatment

A
  1. alleviates puritus( itchy skin)
  2. alleviates utricia ( hives)
  3. allevaites angioedema( swelling under skin)
  4. attenuates further release of mediators from mast cells or basophils by increasing intracellular cAMP
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21
Q

Describe the structure of a normal arterial vessel wall

A

lumen> vascular endothelial cells> basement membrane> intima> internal elastic lamina> media (smooth muscle layers, allows vessel to handle high pressure)> external elastic lamina> adventitia

22
Q

where do the T lymphocytes and macrophages gather in atherosclerosis?

A

intima

23
Q

Describe atherogenesis

A

damage to endothelial cells> endothelium secretes chemoattractant> leukocytes migrate to intima> foam cells/ macrophages/ T-lymphocytes form fatty streaks> foam cells rupture, releasing lipids and smooth muscle cells migrate from media to intima> dense fibrous cap with necrotic core formed.

24
Q

How can a plaque lead to ischaemia?

A

it can partially occlude lumen leading to restricted blood flow and ischaemia

25
Q

How can a plaque lead to infarction?

A

The plaque can rupture forming a thrombus, this can fully occlude a lumen and lead to infarction.

26
Q

define pharmacokinetics

A

what the body does with a drug

27
Q

describe pharmacokinetics

A

Absorption- through the gut or parenteral
Distribution- affected by blood flow, molecular size/ weight, how lipophilic or lipophobic a drug is, the blood-brain barrier or blood-testicular barrier
Metabolism- 1st pass metabolism happens in the liver, parenteral administration doesn’t do this
Excretion- usually renal, however can be via urine, bile, sweat, saliva, tears, milk and stool

28
Q

define pharmacodynamics

A

what the drug does to the body

29
Q

describe pharmacodynamics

A

Affinity- how well the drug binds to the target site
Efficacy- how well the drug works at the target site once it has bonded, the maximum effect the drug can have on the body
Potency- how much of te drug is required to elicit a response from the body

30
Q

what is the role of an intravenous induction agent?

A

They cause a rapid loss of consciousness, they induce anesthesia so that other drugs may be administered to maintain anesthesia

31
Q

describe drugs that will induce anesthesia the quickest

A

unbound lipid soluble, unionized molecules as they cross the blood-brain barrier the quickest.

32
Q

Why is a second anesthetic required after the induction?

A

After the drug enters the CNS and other well-vascularised tissues, the drug diffuses into less blood-rich tissues, this secondary uptake is mainly done by skeletal tissues. It causes the plasma concentration of the drug to drop, which changes the concentration gradient and allows the drug to diffuse out of the CNS, which leads to rapid re-awakening if another dosage of anesthesia isn’t administered

33
Q

which drugs are given to maintain anesthesia

A

volatile drugs

34
Q

define agonist

A

A substance that initiates a physiological response when combined with a receptor

35
Q

Give 3 examples of agonists

A

morphine, opium, heroin

36
Q

define antagonist

A

stops a receptor from eliciting a response, which can be primary or at another site.

37
Q

give 3 examples of antagonists

A

naloxone, cassipa and depade

38
Q

Who’s the best snack?`

A

You.

39
Q

give an example of a competitive antagonist

A

naloxone, against all opioid receptors

40
Q

give an example of a non-competitive antagonist

A

ketamine, at the NMDA glutamate receptor, blocks other things from sitting at the site of action and may attach to a different part of the receptor, causing its shape to change

41
Q

receptors are the main targets of drugs, and what are the three other sites of action?

A

ion channels, enzymes, transporter proteins

42
Q

Give an example of a drug that affects ion channels

A

amlodipine causes vasodilation and widening, which lowers BP, and calcium channel blocker, which only acts on smooth vascular muscle, inhibits calcium influx in vascular and cardiac muscle.

43
Q

Give an example of a drug that acts on enzymes

A

erythromycin, antibiotic, bacteriostatic drug, inhibits protein synthesis in ribosomes by binding to the 23s of the 50s subunit

44
Q

Give an example of a drug that affects membrane transporters

A

heparin, used for venous thrombosis and prophylaxis( preventative treatment), inactivates antithrombin 3, inactivating factors 11a and 10a

45
Q

define bioavailability

A

the amount of drugs that makes it to systemic circulation to elicit its effect

46
Q

describe first-pass metabolism

A

drugs taken orally enter the hepatic circulation and are metabolized by the liver in phase one and phase 2 reactions. phase 1 reactions involve using CYP45 enzymes to make a drug more hydrophilic, and phase 2 reactions involve conjugation, including glucuronidation

47
Q

Give 3 examples of parenteral administration

A
  1. topical treatments
  2. Intravenous
  3. intramuscularly
48
Q

what is the bioavailability of parenteral administration

A

100%

49
Q

describe the bioavailability of morphine when administered orally and parenterally

A

50% orally and 80-100% paraneterally

50
Q

Why can morphine be dangerous to prescribe to someone with renal impairment?

A

Toxic accumulation of metabolites in the kidney, morphine-6 beta glucuronide can’t be excreted and is between 80 and 650-fold more potent than morphine, which can lead to opioid overdose and respiratory depression

51
Q

describe the mechanism of action by propanol

A

beta-adrenergic receptor antagonist, it is used when treating hypertension and AF, it causes vasoconstriction

2a ILA's (1 decks)

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