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APA II > Immune system > Flashcards

Immune system Flashcards

1
Q

what is most common opportunistic infection in HIV patients

A

pneumocystic carini

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2
Q

what is most common adverse reaction to a blood transfusion

A

a febrile reaction

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3
Q

the appearance of hives on a person getting a blood transfusion indicates what

A

an allergic reaction

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4
Q

what are the signs of a hemolytic reaction in the anesthetized patient

A

1) first sign is HGB in urine
2) bleeding in surgical field
3) unexplained tachycardia and hypotension
4) rise in temperature

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5
Q

what are the signs of a hemolytic transfusion reaction in awake patient

A

fever chills chest and flank pain, nausea

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6
Q

what immunoglobulin are latex allergies mediated by

A
  • some might be contact dermatitis (type IV)

- serious reactions to latex are type I mediated IgE reactions to polypeptides in latex

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7
Q

name 2 common protocols used for latex allergies

A

1) schedule for first case of the day to prevent exposure of latex particles in the air from other cases in room
2) removal of rubber stoppers from drug vials

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8
Q

what 3 factors are associated with risk for developing a latex allergy

A

1) spinal bifida
2) multiple procedures on urogenital tract
3) spinal cord injury

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9
Q

what food allergies are associated with latex allergies

A

tropical fruit allergies such as bananas, mangoes, peaches, avocados kiwi, passion fruit, celery, buckwheat, papa, and chestnuts

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10
Q

how long after exposure to latex will a latex sensitive person develop an allergic reaction

A

onset of symptoms to latex allergy do not genuine until after 30 minutes of exposure compared to 5-10 minutes with other allergies

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11
Q

what family of viruses are HIV a part of

A

retroviruses

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12
Q

what type of lymphocyte does HIV destroy

A

T helper cells (CD4 cells)

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13
Q

what are odds of seroconversion after exposure from open bore needle infected with HIV

A

0.3-0.4%

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14
Q

what are respiratory complications from pneumocystis carinii pneumonia

A

breathlessness, nigh sweats, bacterial lung abscesses, tuberculosis, fungal infections, pneumothorax, pulmonary kaposi’s sarcoma, and respirator failure. pulmonary adenopathy can be so severe that it results in tracheobroncial and pulmonary vessel compression. Kaposis sarcoma in lungs can cause massive hemoptysis. HIV can also lead to emphysematous destruction to alveolar tissue

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15
Q

How does CXR in a patient with HIV infected with pneumocystis carinii appear

A

often normal, or with a ground glass appearance and pneumothoracies

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16
Q

what does a positive acid fast bacilli test indicate in a patient with HIV

A

tuberculosis

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17
Q

what are potential cardiac complications in a person with HIV/AIDS

A
  • abnormal echo in 50% of patients
  • pericardial effusions
  • myocarditis with ventricular dilation resulting from infection with cryptococcus, coxsackie B virus, CMV, toxoplasmosis, and aspergillus
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18
Q

what does the HAART acronym stand for

A

Highly active antiretroviral therapy -prevents advancement of HIV infection to AIDS

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19
Q

An HIV patient takes non-nucleoside reverse transcriptase inhibitor-how might this effect your anesthetic plan

A

prolong the half life and effects of drugs such as diazepam, midazolam, fentanyl, and meperidine

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20
Q

what are the five major classes of antiretroviral dugs used in treatment of HIV

A

-nucleoside analogue reverse transcriptase inhibitors, non nucleoside reverse transcriptase inhibitors, protease inhibitors, entry inhibitors, and integrate inhibitors

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21
Q

what is zidovudine and what is its principle side effect

A

nucleoside analogue reverse transcriptase inhibitor use to that HIV, side effect is bone marrow suppression

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22
Q

what is underlying pathology of joints in patients with rheumatoid arthritis

A

cellular hyperplasia occurs in the synovium with progressive infiltration by lymphocytes, plasma cells, and fibroblasts, which destroy articular cartilage

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23
Q

name symptoms of RA

A
  • symmetric polyarthropathy effecting weight bearing joints and proximal interphalangeal and metacarpophalangeal joints
  • symptoms worse in the AM
  • every joint may be effected except lumbar and sacral spine
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24
Q

what are treatment options for RA

A

palliative medial therapy such as corticosteroids(surpression of inflammatory symptoms)

  • anticytokine agents such as etanercept, adimumab, and infiximab interfere with cytokine growth known as tumor necrosis factor (slow progression of the disease)
  • methotrexate(reduces symptoms)
  • immunosuppressive drugs (cyclophosphamide and cyclosporine)
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25
Q

Name major anesthetic considerations for patients with RA

A
  • laryngeal, tempomandibular, and cervical joint issues
  • perform careful evaluation
  • use of cyclophosphamide can inhibit plasma cholinesterase and prolong duration of action for succinylcholine
  • use of long term corticosteroid therapy will warrant extra steroid coverage
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26
Q

what is most common hematologic abnormality in RA patients

A

anemia

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27
Q

what is the most common pulmonary complication os RA

A

pleural effusion

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28
Q

what cardiac complications may be present in the patient with RA

A
  • pericardial thickening with effusion in 1/3 of patients
  • pericarditis, myocaridits, and coronary artery arteritis
  • aortitis may produce dilation of the aortic root and cause aortic regurgitation
  • cardiac conduction system issues from rheumatoid nodules
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29
Q

what are airway management concerns in patient with RA

A

tempomandibular joint and restricted mouth opening

  • joints of larynx and cause edema and laryngeal swelling
  • cervical spine instability
  • atlantoaxial subluxation can push the odontoid process into the foramen magnum during laryngoscopy
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30
Q

what is primary focus of PMNs

A

phagocytosis of pathogens, recognize self verses non self via pathogen associated molecular patters present on surface of pathogens

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31
Q

what is an interferon

A

cytokines with anti viral activity-interfere with viral replication

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32
Q

natural killer cells

A

kill virally infected “self”cells, important for killing cancer cells, release interferon gamma

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33
Q

what is passive immunity

A

lasts hours to weeks
produced by administering preformed antibody to provide protection against an invasive pathogen or toxin-examples botulism, diphtheria, snake bite-pre-formed antibodies from humans or animals

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34
Q

What type of immunity are B lymphs responsible for

A

formed in bone marrow-provide humoral immunity via soluble antibody production directed against a specific antigen

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35
Q

what type of immunity are T lymphocytes responsible for

A

formed in thymus-cell mediated immunity directed against a particular antigen
-most common type are CD4 and CD 8

36
Q

describe vaccination

A

type of acquired immunity in which specific diseases by deliberate exposure to a pathogenic antigen. can administer dead organisms
-toxoid vaccines=chemical modifications
attenuated=mutated pathogens that do not cause disease, but produce immunity when exposed via vaccine

37
Q

mononuclear cells

A

injection and destruction of damaged and neoplastic cells and bacteria

38
Q

PMNs

A

ingestion of phagocytosis, killing microorganisms, facilitation of bodily clearance of dead cells

39
Q

Eosinophils

A

phagocytosis of parasites, defense in allergic reponses

40
Q

neutrophils

A

phagocytosis, cytokine release, secretion of hydrolytic enzymes, secretion of reactive oxygen species

41
Q

basophils/mast cells

A

sources of histamine and heparin, increase vascular permeability, smooth muscle contractility, inflammatory response

42
Q

platelets

A

facilitation of coagulation, influence of reactivity of tissue to injury

43
Q

B cells

A

humoral immunity, plasma cell transformation, produce antibodies and imunoglobulines, active in circulatory system, cytokine release

44
Q

T cells

A

recognition and reaction to foreign material inside fixed tissues and to harmful organisms such as neoplastic and tuberculosis cells, important in transplant rejection, cytokine release

45
Q

plasma cells

A

active ein protein synthesis for the formation of immunoglobulins

46
Q

inflammation

A

involves innate and acquired immunity

  • vasodilation, blood flow, capillary permeability, extraversion of plasma proteins (key coag factors, complement)
  • erythemia, edema, pain
47
Q

allergies

A

antibodies attach to mast cells and basophils
release histamines and other substances, lead to abnormal response
clinically-urticaria, hay fever like symptoms, asthma, and anaphylaxis

48
Q

describe histamine

A

stored in granules of basophils and mast cells, released when antigen reacts with IgE or when complement components C3a and C5a interact with specific membrane receptors=vasodilation(h1), increased capillary permeability(h1), contraction of smooth muscle(h1), cardiac stimulation(h2), stimulation of gastric secretion (H2)

49
Q

describe “triple response”

A

erythema from local vasodilation
wheal from increased vascular permeability and protein and fluid extravasation,
flare from axon reflex in sensory never release a peptide mediator

50
Q

type I hypersensitivity

A

IgE mediated
tryptase is a marker for allergic reactions (>25mcg/L) indicates an allergic mechanism
-tissue mast cells, peripheral basophils
-pruitis, urticaria, angioedema, hypotension, wheezing, bronchospasm, nausea, vomiting, abdominal pain, diarrhea, uterine contractions, cardiac events, arrhythmia
50% fluid shift

51
Q

type II hypersensitivity

A

antibodies specific to antigen attach to cell surface

transfusion reactions, auto immune hemolytic anemia, myasthenia graves, good pastures syndrome

52
Q

anaphylactoid

A

non-IgE-may occur with first exposure, identical response to anaphylaxis
example-protamine reaction

53
Q

type III hypersensitivity

A

immune complex disease in which antigen antibody complexes deposit in tissues and cause injury=activation of complement, recruitment of phagocytes
-SLE, RA, glomerulonephritis

54
Q

type IV hypersensitivity

A

delayed, at least 12 hours after contact with antigen
migration of specific CD4 lymphocytes to reaction site followed by cytokine release and local inflammatory response
-contact dermatitis, granulomatous hypersensitivity (TB, sarcoidosis, Crohns disease)

55
Q

which type of local anesthetic is most likely to cause a drug reaction? what additives cause allergic reactions in LA

A

-ester anesthetics more likely to cause reaction because of PABA
-methylbaraben preservatives, and propylparaben. sulfite components
adverse reactions from accidental intravascular injection

56
Q

what does atopic mean

A

people with increased allergic tendencies hay fever asthma food/drug allergies

57
Q

in the atopic patient, what are anesthetic implications

A

60-70% cross reactivity among muscle relaxant allergies
avoid histamine releasing drugs (morphine, etc.)
-give H1 an dH2 blocker before

58
Q

treating allergic reaction

A

O2, airway patency maintained, IV epic, fluids, antihistamines, glucocorticoids (decrease protracted anaphylaxis)

59
Q

which commonly given agents induce reactions

A

rocuronium (NMB)>latex>abx>opioids>local anesthetics

60
Q

what does Epi do in an allergic reaction

A

increases cAMP which restores normal capillary permeability and relaxes smooth muscle
if on beta blocker may get poor response-give fluids and glucagon

61
Q

IgA deficiency

A

susceptible to pyogenic infections, type III sensitivity reactions, strep penumo and haemophilus influenzae

62
Q

SCID

A

low levels of circulating lymphocytes, need bone marrow transplant

63
Q

diGeorge syndrome

A

abnormal development of parathyroid gland and thymus gland

64
Q

Hereditary angioneurtonic edema

A

caused by absence of C1-inhibits Complement system=angioedema upper airway obstruction

65
Q

chronic granulamatomus disease

A

defective PMNs, ingested pathogens trigger cell mediated immune response and formation of granulomas

66
Q

glucocorticosteriods

A

cause 2ndary immunodeficiency syndrome, reduce monocytes and lymphocytes one dose only for 24 hours

67
Q

mycophenylate mofetil

A

inhibits lymphocyte proliferation by blocking last step for purine synthesis and DNA replication

68
Q

cyclosporine, FK506 (tacrolimus) and rapamycin

A

inhibit t cell proliferation

69
Q

what is SLE

A

chronic inflammatory disease associated with production of antinuclear antiboides

70
Q

what are most common signs of SLE

A

polyarthritis, macular rash, renal disease (out common cause of death), risk of vasculitis, high risk of seizures, stroke, neuropathy, psychosis, pericardial effusion

71
Q

what drugs can exacerbate SLE

A

procainamide, hydralazine, catorpil, enalopril, isoniazid, d penicllamine, methyldopa

72
Q

pulmonary issues with SLE

A

pleural effusion, pneumonitis, alveolar hemorrhage, pulmonary hypertension

73
Q

airway issues with SLE

A

cricoarytenoid arthritis, RLN palsy

74
Q

if a patient with SLE takes corticosteroids and cyclophosphamide, how can this alter your anesthetic plan?

A

give more steroids during preoperative period because cyclophosphamide inhibits plasma cholinesterase, the effects of ester local anesthetic and succinylcholine may be prolonged

75
Q

what is scleroderma

A

collegen vascular disease characterized by inflammation, vascular sclerosis, and fibrosis of skin and organs

  • injury to vascular epithelium
  • vascular obliteration and leakage of proteins in interstitial space
  • tissue edema and lymphatic obstruction
  • tissue fibrosis
76
Q

anesthetic implications for scleroderma

A

positioning (may be difficult due to contractors)
fiberoptic intubation (decreased mandibular motion)
pharyngeal telangiectasis (bleeding due to airway manipulation)
chronic hypertension
hypotonia of LES (gerd)
avoid acidosis hypoxia can worsen pulmonary hypertension
*regional better because of peripheral vasodilation and improved post op analgesia
pulmonary fibrosis, avascular necrosis of femoral head, renal artery stenosis

77
Q

what airway complications in SLE

A

cricoid arthritis, RLN palsy

78
Q

symptoms of SLE may occur after administering which drugs

A

hydrazine, phenytoin, isoniazid (mild symptoms resolve in 4 weeks after discontinuation)

79
Q

patients with SLe have which type of respiratory deficit

A

restrictive deficit due to pleural effusion, pneumonitis, alveolar hemorrhage, and pulmonary hypertension

80
Q

which symptoms would you expect to see in a patient with SLE a)nephritis, b)thrombocytopenia, c)cognitive dysfunction, D)spinal arthralgia with limited ROM (select 3)

A

a, b, c
SLE is very likely if a patient exhibits three of the following characteristic manifestations: antinuclear antibodies, nephritis, serositis, thrombocytopenia, or a characteristic rash. SLE often results in symmetric arthralgias in the hands, wrists, knees, and ankles, but does not involve the spine. Cognitive dysfunction occurs in about 1/3 of patients with SLE.

81
Q

what is most common cause of death in SLE

A

renal disease

82
Q

all of the following pathologies are associated with sarcoidosis except a)cor pulmonae b)chronic extrinsic restrictive lung disease c)restrictive cardiomyopathy d)hypercalcemia

A

B)chronic extrinsic restrictive lung diseaseSarcoidosis is associated with diffuse granulomatous lesions resulting in intrinsic restrictive lung disease, cor pulmonale, and restrictive cardiomyopathy which may present as heart block and dysrhythmias. Other classic signs are hypercalcemia, hepatic granulomas, splenomegaly, and involvement of the parotid gland and facial and optic nerves.

83
Q

in regards to HIV drugs, what do NNRTIs do

A

induce the CYP450 system

84
Q

what is treatment for RA

A

corticosteroids, methotrexate, immunosuppressants, NSAIDS

85
Q

what is cyclophosphamide inhibit

A

plasma cholinesterase

ester LA, succinylcholine last longer

APA II (4 decks)

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