Fall24 PoA II > Immune Dysfunction pt2 > Flashcards

Immune Dysfunction pt2 Flashcards

(49 cards)

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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?

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

What is Graves disease? What causes it?

Study These Flashcards
A

Hyperthyroidism caused by Autoantibodies to TSH receptor

22
Q

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

Study These Flashcards
A

Autoimmune antibodies against:

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

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

Study These Flashcards
A

C1 Esterase inhibitor deficiency/dysfunction → excessive bradykinin production.

24
Q

What factors can cause C1 esterase problems? (5)

Study These Flashcards
A
  • Menses
  • Trauma
  • Infection
  • Stress
  • Oral contraceptives
25
What typically limits the production of excessive bradykinin?
C1 *C1 limits kallikrein and Factor XIIa*.
26
What occurs anatomically with **excessive bradykinin**? (2)
- Laryngeal swelling - potent Vasodilation
27
What dose of **antihistamine** should be used for hereditary angioedema?
Trick question. Hereditary Angioedema = excessive bradykinin and is **unaffected by antihistamines**.
28
What body parts are typically affected by hereditary angioedema? (4)
* Legs * hands * face * upper resp tract
29
What is the typical cause of acquired angioedema?
- ACE Inhibitors
30
What symptoms are conspicuously absent with acquired angioedema?
No Urticaria or Pruritus
31
What is responsible for the **breakdown of bradykinin**?
ACE *Thus ACE inhibitors = ↑ bradykinin = angioedema*.
32
What are the treatments for **Angioedema**? (6)
- Airway maintenance - FFP - C1 Inhibitor concentrate - Epinephrine - Antihistamines - Glucocorticoids?
33
What cells are destroyed by the **HIV virus**? (3)
Monocytes Macrophages T-cells
34
How long does **seroconversion** take after inoculation with the HIV virus?
2-3 weeks
35
What are the **initial signs and symptoms** of HIV conversion to AIDS? (2)
Weight loss and failure to thrive
36
How is HIV/AIDS diagnosed? (4)
- ELISA: 4-8 weeks after infection - Viral Load - CD4/Helper T lymphocytes < 200k - HAART agent sensitivity
37
Inhibition of the liver's ________ has huge implications for anesthetic delivery in HIV/AIDS patients.
CYP 450's
38
What s/s characterize scleroderma? (3)
- Inflammation - Vascular Sclerosis - Fibrosis of skin/viscera
39
At what age does scleroderma typically occur? What gender is typically affected?
- 20-40 - Females
40
What **GI symptoms** of scleroderma are particularly pertinent to anesthesia? (2)
- GI Tract Hypomotility - ↓ LES tone
41
______ fibrosis and ______ artery stenosis are prominent considerations for anesthesia in scleroderma patients.
**Pulmonary** fibrosis and **renal** artery stenosis
42
What are the overall anesthesia implications of **scleroderma**? (5)
- Arterial catheter issues - Contracted intravascular volume - Aspiration risk - Limited neck mobility - ↓ pulmonary compliance
43
What do inhalation agents do the immune system? (3)
- Suppress NK cells - Induce apoptosis of T-cells - Impair phagocytes *Unclear effects on tumor cells*.
44
This benzodiazepine, ________, **decreases the migration of neutrophils**.
Midazolam
45
This induction agent, _______, will **depress natural killer cell activity**.
Ketamine
46
This induction agent, ________, **decreases cytokines and promotes NK cells**.
Propofol
47
What **drug class** will suppress NK cells?
Opioids *Particularly morphine and fentanyl*.
48
What cell type plays the greatest role in chronic inflammation?
T-Cells
49
What cell type activates IgE and produces interleukins and interferons?
T-Cells
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