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1Fall24 PoA II > Immune Dysfunction pt2 > Flashcards

Immune Dysfunction pt2 Flashcards

1
Q

What rhythm occurs with untreated anaphylaxis?

A

PEA/arrest

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2
Q

What causes the hypotension noted with anaphylaxis?

A

Vasodilation from NO release with subsequent extravasation of protein and fluid

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3
Q

What is the pathophysiology of anaphylaxis?

A
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4
Q

What is Biphasic anaphylaxis?

A

Secondary anaphylactic episode occurring 8 - 72 hours later after an asymptomatic period.

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5
Q

What are risk factors for a secondary anaphylactic episode?

A
  • Severe initial response
  • Initial response requiring multiple epi doses
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6
Q

What are risk factors for perioperative anaphylaxis? (5)

A
  • Asthma
  • Female
  • Prolonged Anesthetic
  • Multiple past surgeries
  • Presence of other allergic conditions
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7
Q

What lab can verify mast cell activation and release?

A

Plasma Tryptase

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8
Q

Plasma histamine concentration should be at baseline within _____ minutes of treatment.

A

within 60 minutes of treatment

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9
Q

When is anaphylactic response skin testing typically done after an episode?

A

Wheal and flare response 6 weeks after initial reaction.

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10
Q

What is the primary treatment for anaphylaxis? (5)

A
  • Call for help
  • Stop blood, drugs, colloids
  • 100% O₂
  • Epi
  • Fluids
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11
Q

What is the epinephrine dose for adult anaphylaxis?

A

10 mcg - 1000mcg (1mg) IVP q1-2 min

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12
Q

What is the epinephrine dose for child anaphylaxis?

A

1-10 mcg/kg IVP q1-2 min

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13
Q

If a patient experiencing anaphylaxis is resistant to epi, what should be given? Why?

A

Vasopressin or Methylene blue

These will inhibit NO production and thus counteract vasodilation.

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14
Q

What is the crystalloid dosage for anaphylaxis?

A

NS 10 - 25 mL/kg over 20 min PRN

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15
Q

What is the colloid dosage for anaphylaxis?

A

10 mL/kg over 20 min PRN

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16
Q

Why is epinephrine the drug of choice for anaphylaxis?

A
  • ↓ degranulation of mast cells & basophils → reduced vasodilation
  • α1 = supports blood pressure (vasoconstriction)
  • β1 = Inotropy & chronotropy
  • β2 = Bronchodilation
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17
Q

What drug classes are secondary treatments for anaphylaxis? (3)

A
  • Bronchodilators
  • Antihistamines
  • Corticosteroids
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18
Q

What are the antihistamines (and dosages) typically used as secondary treatments for anaphylaxis? (2)

A
  • H1 → Diphenhydramine 0.5-1 mg/kg IV
  • H2 → Ranitidine 50 mg IV
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19
Q

What are the corticosteroids (and dosages) used as secondary treatments for adult anaphylaxis?

A
  • Hydrocortisone 250 mg IV
  • Methylprednisolone 80 mg IV
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20
Q

What are the corticosteroids (and dosages) used as secondary treatments for pediatric anaphylaxis?

A
  • Hydrocortisone 50-100 mg IV
  • Methylprednisolone 2 mg/kg IV
21
Q

What is Graves disease? What causes it?

A

Hyperthyroidism caused by Autoantibodies to TSH receptor

22
Q

What is affected by the immune response characteristic of SLE? (5)

A

Autoimmune antibodies against:

  • RBCs
  • WBCs
  • nucleic acids
  • platelets
  • coag proteins
23
Q

What is/are the cause(s) of hereditary angioedema?

A

C1 Esterase inhibitor deficiency/dysfunction → excessive bradykinin production.

24
Q

What factors can cause C1 esterase problems? (5)

A
  • Menses
  • Trauma
  • Infection
  • Stress
  • Oral contraceptives
25
Q

What typically limits the production of excessive bradykinin?

A

C1

C1 limits kallikrein and Factor XIIa.

26
Q

What occurs anatomically with excessive bradykinin? (2)

A
  • Laryngeal swelling
  • potent Vasodilation
27
Q

What dose of antihistamine should be used for hereditary angioedema?

A

Trick question. Hereditary Angioedema = excessive bradykinin and is unaffected by antihistamines.

28
Q

What body parts are typically affected by hereditary angioedema? (4)

A
  • Legs
  • hands
  • face
  • upper resp tract
29
Q

What is the typical cause of acquired angioedema?

A
  • ACE Inhibitors
30
Q

What symptoms are conspicuously absent with acquired angioedema?

A

No Urticaria or Pruritus

31
Q

What is responsible for the breakdown of bradykinin?

A

ACE

Thus ACE inhibitors = ↑ bradykinin = angioedema.

32
Q

What are the treatments for Angioedema? (6)

A
  • Airway maintenance
  • FFP
  • C1 Inhibitor concentrate
  • Epinephrine
  • Antihistamines
  • Glucocorticoids?
33
Q

What cells are destroyed by the HIV virus? (3)

A

Monocytes
Macrophages
T-cells

34
Q

How long does seroconversion take after inoculation with the HIV virus?

A

2-3 weeks

35
Q

What are the initial signs and symptoms of HIV conversion to AIDS? (2)

A

Weight loss and failure to thrive

36
Q

How is HIV/AIDS diagnosed? (4)

A
  • ELISA: 4-8 weeks after infection
  • Viral Load
  • CD4/Helper T lymphocytes < 200k
  • HAART agent sensitivity
37
Q

Inhibition of the liver’s ________ has huge implications for anesthetic delivery in HIV/AIDS patients.

A

CYP 450’s

38
Q

What s/s characterize scleroderma? (3)

A
  • Inflammation
  • Vascular Sclerosis
  • Fibrosis of skin/viscera
39
Q

At what age does scleroderma typically occur?
What gender is typically affected?

A
  • 20-40
  • Females
40
Q

What GI symptoms of scleroderma are particularly pertinent to anesthesia? (2)

A
  • GI Tract Hypomotility
  • ↓ LES tone
41
Q

______ fibrosis and ______ artery stenosis are prominent considerations for anesthesia in scleroderma patients.

A

Pulmonary fibrosis and renal artery stenosis

42
Q

What are the overall anesthesia implications of scleroderma? (5)

A
  • Arterial catheter issues
  • Contracted intravascular volume
  • Aspiration risk
  • Limited neck mobility
  • ↓ pulmonary compliance
43
Q

What do inhalation agents do the immune system? (3)

A
  • Suppress NK cells
  • Induce apoptosis of T-cells
  • Impair phagocytes

Unclear effects on tumor cells.

44
Q

This benzodiazepine, ________, decreases the migration of neutrophils.

A

Midazolam

45
Q

This induction agent, _______, will depress natural killer cell activity.

A

Ketamine

46
Q

This induction agent, ________, decreases cytokines and promotes NK cells.

A

Propofol

47
Q

What drug class will suppress NK cells?

A

Opioids

Particularly morphine and fentanyl.

48
Q

What cell type plays the greatest role in chronic inflammation?

A

T-Cells

49
Q

What cell type activates IgE and produces interleukins and interferons?

A

T-Cells

1Fall24 PoA II (34 decks)

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