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N935 Advanced Pathophysiology II > Immune > Flashcards

Immune Flashcards

1
Q

antibiotic resistance

A
  • occurs when germs (i.e., bacteria, fungi) develop the ability to defeat the drugs designed to kill them)
  • does NOT mean the body is becoming resistant to antibiotics
  • the bacteria have become resistant to the antibiotics designed to kill them
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2
Q

history of penicillin

A
  • first discovered in 1928, first commercialized antibiotic effective against staph and strep
  • natural product of penicillium mold
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3
Q

what kind of antibiotic is penicillin?

A

beta-lactam (due to the beta lactam ring)

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4
Q

penicillin G

A
  • given IV

- destroyed by stomach acid

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5
Q

penicillin V

A
  • given PO

- semi-synthetic

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6
Q

how frequently do TRUE penicillin allergies occur?

A

<1%

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7
Q

which group of antibiotics has a crossover in allergy with penicillins?

A
  • cephalosporins, contain benzylpenicillin causing the side chain reaction
  • estimated cross reactivity with ancef (1st generation) is 1.9-7.9%
  • NOTE –> potentially inconsistent definitions of allergic reactions resulting in overestimation of cross-reactivity
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8
Q

Surgical Site Infections (SSIs)

A
  • infections that occur within 30 days of surgery or within 1 year of a prosthetic implant or organ
  • costly
  • increase M & M
  • occur frequently
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9
Q

SSI Prevention includes…

A
  • preoperative antibiotics [timed so that the concentration is established in serum and tissues before incision is made]
  • glycemic control [<180-200 mg/dL]
  • maintain normothermia
  • optimize oxygenation
  • usage of antimicrobial soap before surgery
  • intraop skin prep with alcohol based antiseptic
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10
Q

what is the predominant cause of nosocomial blood-stream infections?

A

CVCs

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11
Q

CLABSI

A
  • catheter associated blood stream infection
  • bacteremia or fungemia in patient with an IV catheter and at least one positive blood culture obtained form a peripheral vein
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12
Q

CLABSI prevention

A
  • full barrier precautions when placing a CVC
  • handwash/scrub
  • clean skin with CHG
  • antimicrobial impregnated catheters
  • avoid fem site if possible
  • sterility when accessing ports/med admin
  • remove line as soon as no longer needed
  • avoid parenteral dextrose/nutrition when no longer needed
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13
Q

what is clostridium difficicle?

A
  • Clostridium difficile colitis results from disruption of normal healthy bacteria in the colon, often from antibiotics
  • spore forming bacterium
  • can cause antibiotic associated diarrhea and pseudomembranous colitis (or inflamed megacolon) due to the production of toxins A and B
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14
Q

what are the potential detrimental effects of C. Diff?

A
  • toxic megacolon
  • antibiotic associated diarrhea
  • may lead to subtotal colectomy
  • ileostomy
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15
Q

what is the treatment for C. Diff?

A
  • removal of causative antibiotic

- administer oral antibiotics [metronidazole or vancomycin]

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16
Q

anesthetic implications of C. Diff

A
  • hemodynamic instability is likely if these patients go to surgery
  • contact/isolation precautions are essential to prevent spread
  • must use handwashing to remove spores
  • must use bleach germicidal wipes on equipment/room
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17
Q

types of necrotizing soft tissue infections

A
  • gas gangrene
  • toxic shock syndrome
  • fournier’s gangrene (occurs in the genital/perineal area; level 1 emergency)
  • severe cellulitis
  • flesh-eating infection
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18
Q

presentation of those with necrotizing soft tissue infections

A
  • general infection
  • AMS
  • pain (hard to get adequate pain control)
  • infection begins in DEEP tissue planes
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19
Q

anesthetic management of necrotizing soft tissue infections

A
  • resuscitation often necessary (septic picture with fluid shifts)
  • do NOT delay surgical debridement
  • hemodynamic instability common due to release of cytokines/inflammatory mediators
  • make sure you have good IV access, and a-line, and potentially a CVC
  • high risk for multiorgan failure –> ICU post surgery
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20
Q

Tetanus

A
  • disease produced by the neurotoxin tetanospasmin which is prodcued by clostridium tetani
  • suppresses inhibitory neurons in the spinal cord resulting in generalized sustained muscle contractions
  • trismus (or lock jaw) and neck rigidity are early S/S
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21
Q

tetanus treatment

A
  • control of skeletal muscle spasm with benzos or muscle relaxants
  • neutralize exotoxin with human anti-tetanus immunoglobulin
  • PCN
  • immunization!!
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22
Q

what are the different types of pneumonia

A
  • community-acquired
  • aspiration
  • postoperative
  • ventilator-associated
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23
Q

community acquired pneumonia

A
  • streptococcus pneumoniae is most common cause of bacterial pneumonia in adults
  • can also be caused by viruses (RSV, COVID-19, flu) or fungi (pneumocystis, histoplasmosis, cryptococcus)
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24
Q

aspiration pneumonia

A
  • clinical manifestations depend on the nature and volume of aspirated material
  • arterial hypoxemia
  • airway obstruction
  • atelectasis
  • pneumonia
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25
Q

pneumonia clinical presentation

A
  • fever, chest pain, dyspnea, fatigue, rigors, cough, sputum production
  • patient history - travel, cave exploration, diving, contact with birds/sheep, immunocompromised
  • CXR with infiltrates
  • positive cultures (sputum)
  • increased WBC count
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26
Q

pneumonia prevention

A
  • vaccine available for pneumococcal pneumonia
  • CDC recommends for all adults 65 and older or adults 19-64 who smoke cigarettes or suffer from certain health conditions
  • pneumococcal pneumonia kills ~1 in 20 adults that get it
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27
Q

pneumonia anesthesia management

A
  • delay surgery if possible (esp during acute pneumonia)
  • avoid fluid overload
  • LPV, often PEEP dependent
  • consider same vent settings as ICU
  • LOWEST FiO2 possible
  • SUCTIONING
  • maintain antibiotic, antiviral or antifungal med schedule
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28
Q

severe acute respiratory viral illnesses

A
  • Highly virulent with a high mortality
  • H5N1 influenza A = bird flu
  • coronavirus strains - MERS-CoV, SARS-CoV, SARS-CoV-2
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29
Q

S/S of acute respiratory viral illness

A
  • nonspecific
  • fever
  • HA
  • diarrhea
  • respiratory distress
  • hemoptysis
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30
Q

viral infections treatment

A
  • prevention of spread is KEY
  • vaccinations when available
  • neuroaminidase inhibitors (zanamivir, peramivir, oseltamivir, baloxavir marboxil) may help with symptom management and decrease severity; only given in first 48hrs of symptoms
  • supportive care
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31
Q

anesthetic management of acute viral infections

A
  • LPV and symptom management
  • barrier precautions - full-body disposable suits, double glove, goggles, air-purifying respirators, filters, N95
  • filters placed on both limbs of breathing circuit to protect pt and ventilator
  • clean room with alcohol
  • if possible, wait 48 hrs until another case
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32
Q

negative pressure rooms

A
  • minimum recommendation is total of 15 air exchanges per hour with a min of 3 air changes of outdoor air per hour
  • isolation rooms need anteroom (negative to hallway, patient room is negative to hallway and anterooms
  • NOTE - ORs are positive pressure
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33
Q

provider PPE

A
  • goggles
  • face shield
  • gown
  • gloves
  • masks
  • shoe covers
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34
Q

UV Germicidal Irradiation

A
  • works against multiple organisms incl ebola, coronavirus, bacteria
  • different types of wavelengths - hospitals use UV-C or germicidal UV
  • can be installed into HVAC
  • needs direct line of sight to surface (blind spots are NOT sanitized)
  • can cause burns
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35
Q

HEPA filters

A
  • high-efficiency particulate air (HEPA) filters
  • can theoretically mechanically remove at least 99.97% of dust, pollen, mold, bacteria, and airborne particles with a size of 0.3 microns
  • in HVAC for isolation rooms
  • available for AGM breathing circuit to put on insp and exp limbs
  • portable devices filter air in a room when its not an isolation room (useful in positive pressure ORs)
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36
Q

HMEF

A

consist of heat and moisture exchange medium together with an electrostatic filter medium

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37
Q

mycobacterium tuberculosis

A

obligate aerobe responsible for TB which survives most successfully in tissues with high oxygen concentrations

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38
Q

S/S TB

A
  • cough
  • anorexia
  • weight loss
  • night sweats
  • chest pain
  • CXR = apical or subapical infiltrates or bilateral upper lobe infiltration with the presence of cavitation
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39
Q

extrapulmonary TB

A
  • Pott’s disease is common manifestation

- tuberculosis vertebral osteomyelitis or tuberculosis spondylitis

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40
Q

Mantoux’s test

A

skin test for TB, most common test

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41
Q

TB Treatment

A
  • can be resistant to second-line therapeutic agents
  • chemo with isoniazid
  • delay case until treatment if possible
  • negative pressure room (bc airborne)
  • patient and staff should wear N95
  • HEPA filter
  • caution to avoid spine injury during airway manipulation
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42
Q

AIDS

A
  • acquired immunodeficiency syndrome
  • acute seroconversion illness occurs with a high viral load soon after infection
  • several months –> decrease in viremia as patient’s immune response is stimulated
  • gradual involution of lymph nodes, concomitant decrease in T-cells (CD4 T cells) and increase in viral load
  • pneumocystis pneumonia occurs when CD4 < 200 cells/mL
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43
Q

AIDS diagnosis

A
  • nucleic acid testing of HIV RNA is most specific and sensitive test for HIV
  • diagnosis of aids in HIV positive patient established when ONE of the AIDS-defining diagnoses is present
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44
Q

AIDS anesthesia considerations

A
  • subject to metabolic complications (lipid/glucose) –> DM, CAD, and cerebrovascular disease can develop
  • focal neurologic lesions may increase ICP and preclude neuraxial
  • neurologic involvement may make succ dangerous
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45
Q

AIDS pre-op testing

A
  • CBC
  • BMP
  • renal function studies
  • LFTs
  • coagulation panel
  • CXR
  • ECG
  • NOTE - CD4 cell count and viral may not have utility
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46
Q

antiretroviral treatment

A

SIX major classes currently in use

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47
Q

Prions

A
  • proteinaceous infective particles are infectious proteins without (known) nucleic acid genomes
  • preferentially target neurologic tissue causing spongiform encephalopathies
  • universally LETHAL
  • transmission seems to require direct inoculation of the brain or nervous system with infectious tissue
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48
Q

types of spongiform encephalopathies caused by prions

A
  • Cruetzfeldt Jakob Disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and kuru in humans
  • scrapie in sheep
  • bovine spongiform encephalopathy (BSE) in cows (i.e., mad cow disease)
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49
Q

Standard precautions

A
  • applies to care of ALL patients, regardless of suspected or confirmed infection/colonization status
  • hand hygiene, safe injection practices, respiratory hygiene and cough etiquette, environmental cleaning + disinfection, and reprocessing of reusable medical equipment
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50
Q

contact precautions

A
  • known or suspected infection that are of increased risk of contact transmission
  • prevents transmission of infectious agents like MDROs (MRSA, VRE, norovirus, C. diff, scabies, MSSA)
  • glove + gown
  • dedicated equipment
  • private room when possible OR cohort with like infection
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51
Q

enhanced barrier precautions

A
  • expand use of PPE beyond situations in which exposure to blood and body fluids is anticipated
  • care activities requiring gown and glove = toilet, airway care, wound care
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52
Q

Droplet Precautions

A
  • pathogens transmitted by respiratory droplets that are generated by a patient who is coughing, sneezing, or coughing
  • examples = meningitis, TB, petechiae with fiver, RSV, adenovirus, influenza, SARS-CoV, avian flu
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53
Q

airborne precautions

A
  • known or suspected infection with pathogen transmitted by airborne route
  • examples = TB, measles (rubeola), varicella-zoster, HSV, variola (smallpox), chickenpox
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54
Q

precautions in order of least to most PPE

A

standard < contact < special enteric < droplet < airborne < full barrier

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55
Q

innate immune system

A
  • non-specific response that targets many common pathogens
  • rapid response
  • mediated by cells and plasma proteins that are always present
  • not pathogen specific, limited diversity
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56
Q

components of innate immune system

A
  • epithelial membrane
  • mucous membrane
  • complement factors
  • neutrophils
  • macrophages
  • monocytes
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57
Q

principle cells of the innate immune system

A

myeloid cells which includes macrophages, neutrophils, and dendritic cells

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58
Q

adaptive immune system

A
  • developed individually
  • delayed response
  • develops a memory toward a specific antigen
  • the receptors are created by rearrangements of antigen-receptor genes that occur during the maturation of the lymphocytes
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59
Q

principle cells of the adaptive immune system

A

lymphoid cells, which are T and B lymphocytes

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60
Q

two components of adaptive immunity

A
  • humoral immunity

- cell mediated immunity

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61
Q

humoral immunity

A
  • mediated by antibodies produced by B cells

- antibodies neutralize microbes, opsonize them for phagocytosis and activate the complement system

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62
Q

Cell mediated immunity

A
  • T cells activated by protein antigens from antigen presenting cells (APCs)
  • requires repeat antigen stimulation to perform their functions
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63
Q

2 types of T cells

A
  • CD4+ helper T cells

- CD8+ helper T cells

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64
Q

CD4+ Helper T cells

A

secrete cytokines to activate macrophages, helps B cells make antibodies, stimulates inflammation

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65
Q

CD8+ Helper T cells

A

kill infected and transformed cells

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66
Q

examples of inadequate immune response

A
  • neutropenia
  • abnormal phagocytosis
  • deficient in the complement system
  • hyposplenism
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67
Q

examples of excessive immune response

A
  • neutrophilia
  • monocytosis
  • asthma
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68
Q

example of misdirected immune response

A

angioedema

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69
Q

examples of adaptive immune dysfunction

A
  • defective antibody production
  • defect in T lymphocytes
  • combined immune system defects (SCIDs)
  • allergic reactions
  • anaphylaxis
  • autoimmune disorders
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70
Q

penia

A

lack of, poverty, deficiency

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71
Q

philia

A

affinity, attraction, fondness

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72
Q

allergy

A

reaction against normally harmless environmental antigen

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73
Q

autoimmune

A

reactions against self antigens

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74
Q

hypersensitivity

A

excessive immunologic reactions to microbes or environmental agents dominated by inflammation

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75
Q

atopy

A

propensity or genetic tendency to develop allergic reactions

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76
Q

antibody (Ab) or immunoglobulin (Ig)

A

large, Y-shaped protein used by the immune system to ID and neutralize foreign objects such as pathogenic bacteria and viruses

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77
Q

neutrophils

A
  • WBCs formed by stem cells in the bone marrow
  • make up 40-70% of all WBCs in humans
  • phagocytes and found in blood stream
  • first responders to inflammation (especially bacterial)
  • predominant cells in pus
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78
Q

neutropenia

A

-neutrophil count <1500/mm3

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79
Q

types of neutropenia

A
  • neonatal sepsis
  • Kostmann syndrome (autosomal recessive)
  • acquired defects (chemo, antiviral drugs)
  • autoimmune (SLE, RA)
  • infection (the rate of neutrophil consumption exceeds their production)
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80
Q

neutropenia treatments

A
  • cessation of medication causes
  • granulocyte colony stimulating factor (filgrastim), which stimulates the production of WBCs
  • bone marrow transplant
81
Q

anesthetic implications of neutropenia

A

maintain asepsis in the perioperative area

82
Q

spleen

A
  • organ that is part of the lymphatic system
  • located in the left part of the diaphragm
  • adult = 2.8 in by 5.5 in and 1-8 oz.
  • like a LARGE lymph node
  • primary filter of our blood
  • primary creator of RBCs in fetal life and up to 5 months
83
Q

functions of the spleen

A
  • remove old RBCs
  • blood reservoir (~250 mL)
  • recycling of iron
  • metabolizes hemoglobin
  • stores 1/4 of circulating lymphocytes
  • stores and clears platelets
  • synthesizes antibodies in the white pulp
  • removes antibody-coated bacteria
84
Q

breakdown of hemoglobin

A
  • globin –> broken down to amino acids

- heme –> metabolized to bilirubin which is removed by the liver

85
Q

asplenia

A
  • absence of normal spleen function (either due to trauma, sickle cell or removal)
  • type of immuno-dysfunction
  • increases sepsis risk 350 fold (WHOA) due to inability to clear bacteria from the blood
86
Q

hyposplenism

A

reduced spleen function

87
Q

sickle cell anemia and the spleen

A

can cause auto-infarction in the spleen resulting in vaso-occlusive disease

88
Q

implications of dysfunctional spleen

A
  • immunizations important (challenging in developing countries)
  • travel restrictions, antibiotic prophylaxis even with minor procedures, and alert warning bracelets
89
Q

leukocytosis

A
  • when WBC count is above normal range
  • normal reaction to an inflammatory response
  • can also be from tumors/leukemias, stress, pregnancy, convulsions, and meds
90
Q

left upper shift

A
  • increase in the ratio of immature to mature neutrophils

- bone marrow is trying to make more

91
Q

right shift

A
  • decrease ratio of immature to mature neutrophils

- shows bone marrow suppression (radiation sickness)

92
Q

acute leukemia

A

immature WBCs in the peripheral blood

93
Q

chronic leukemia

A

mature, non-functioning WBCs in peripheral blood

94
Q

what can cause neutrophilia

A
  • bacterial infection
  • inflammation
  • MI
  • burns
95
Q

what can cause eosinophilia

A

-allergic disorders (asthma, hay fever, drug allergy, allergic skin disease, parasitic infection, malignancy, Hodgkin’s, some forms of lupus)

96
Q

what can cause basophilia

A

myeloproliferative diseases like blood cancers

97
Q

what can cause monocytosis

A
  • chronic infections - TB, bacterial endocarditis, malaria

- inflammatory disorders - RA, SLE, ulcerative colitis

98
Q

what can cause lymphocytosis

A

-chronic infections - TB, CMV, hepatitis, pertussis

99
Q

eosinophilic esophagitis

A
  • chronic immune system disease in which a type of WBC (eosinophil) builds up in the lining of the esophagus
  • usually reaction to foods, allergen or acid reflux
  • can inflame or injure esophageal tissue
  • can lead to difficulty swallowing or cause food to be stuck
100
Q

neutrophilia

A
  • considered >7000/mm3
  • within hours of infection, granulocytes increase 2-3 fold; mobilization of stored and new produced from bone marrow to fight infection
101
Q

leukostasis

A
  • > 100,000/mm3
  • blood gets really thick and there is WBC clumping
  • can lead to TIA or stroke
102
Q

how many neutrophils in myeloproliferative disorder or hematologic malignancy

A

> 50,000/mm3

103
Q

asthma

A

exaggerated bronchoconstriction response to a stimulus

104
Q

extrinsic asthma

A
  • IgE production, allergens
  • usually begins in childhood
  • genetic component
  • hypersensitivity to allergens
  • increase IgE
105
Q

intrinsic asthma

A
  • triggers unrelated to the immune system (i.e., stress, ETT placement, cold, exercise, inhaled irritants)
  • develops in adulthood
  • no family hx
  • no recognizable allergens
  • normie IgE
  • symptoms come on after trigger (listed above)
106
Q

angioedema

A
  • subcutaneous and submucosal edema formation
  • usually involves face, extremities and GI tract
  • can be hereditary or acquired
107
Q

three types of bradykinin mediated angioedema

A
  • autosomal dominant deficiency/dysfunction of C1 esterase inhibitor
  • ACE inhibitors
  • acquired
108
Q

autosomal dominant deficiency/dysfunction of C1 esterase inhibitor

A
  • leads to release of vasoactive mediators that increase vascular permeability and produce edema by bradykinin
  • repeated bouts of facial/laryngeal edema lasting 24-72 hrs
109
Q

ACE inhibitor induced angioedema

A

drug-induced resulting from increased bradykinin availability secondary to ACE inhibitor mediated blockage of bradykinin catabolism

110
Q

acquired angioedema

A

lymphoproliferative disorders acquire C1 esterase inhibitor deficiency secondary to antibody production

111
Q

treatment of acute angioedema

A
  • androgens (increase hepatic synthesis of C1 esterase inhibitor)
  • antifibrinolytic therapy (inhibit plasmin activation so reduces inflammatory cascade)
  • C1 inhibitor concentrate
  • synthetic bradykinin receptor antagonist
  • recombinant plasma kallikrein inhibitor (blocks conversion of kininogen to bradykinin)
  • FFP (replaces deficient enzyme)
112
Q

are catecholamines and antihistamines a viable treatment option for bradykinin-mediated angioedema

A

NO!!!!!!!

113
Q

DiGeorge Syndrome

A
  • thymic, thyroid, and parathyroid hypoplasia
  • due to 22q11.2 gene deletion (decreased T cells)
  • may also include cardiac malformations and facial dysmorphisms (Truncus, TOF, cleft palate)
  • degree of immunocompromise related to amount of thymic tissue present
  • complete absence = SCIDs
114
Q

treatment of DiGeorge

A

thymus transplant or infusion of T cells

115
Q

anesthetic considerations for DiGeorge

A
  • SBE prophylaxis
  • calcium supplementation (if hypoparathyroidism)
  • strict asepsis due to infection risk
116
Q

SCIDs

A
  • severe combined immunodeficiency syndromes
  • genetic mutations that affect T, B, and NK cell function/maturation
  • X-linked form (1 in 58,000 in US)
  • appear healthy at birth but susceptible to severe infections
  • added to newborn screening
117
Q

SCIDs patho

A
  • gene mutation that encodes for interleukin receptors

- lack of receptor –> lack of interleukin signaling –> lack of NK, B and T cell differentiation and maturation

118
Q

SCIDs treatment

A

bone marrow or stem-cell transplant, gene therapy, or enzyme replacement

119
Q

anaphylaxis

A
  • fall in BP (shock) caused by vascular dilation

- airway obstruction due to laryngeal edema

120
Q

bronchial asthma

A
  • airway obstruction caused by bronchial smooth muscle hyperactivity
  • inflammation and tissue injury caused by late-phase reaction
121
Q

allergic rhinitis, sinusitis (hay fever)

A
  • increased mucus secretion

- inflammation of upper airways and sinuses

122
Q

food allergies

A

-increased peristalsis due to contraction of intestinal muscles, resulting in vomiting and diarrhea

123
Q

allergic reactions

A
  • immune mediated

- overreaction of the immune system

124
Q

types of allergic reactions (4)

A
  • type I - IgE; anaphylaxis
  • type II - IgG, IgM; myasthenia gravis, Graves
  • type III - immune complex; SLE
  • type IV - T lymphocytes; RA, MS
125
Q

Type I

A
  • production of IgE antibody
  • immediate release of histamine and other inflammatory mediators from mast cells
  • later recruitment of inflammatory cells
  • causes vascular dilation, edema, smooth muscle contraction, mucus production, tissue injury, inflammation
126
Q

Type II

A
  • production of IgG, IgM
  • binds to antigen on target cell or tissue
  • phagocytosis or lysis of target cell by activated complement or Fc receptors
  • recruitment of leukocytes
127
Q

Type III

A
  • deposition of antigen-antibody complexes
  • activation of complement system
  • recruitment of leukocytes by complement products and Fc receptors
  • release of enzymes and other toxic molecules
  • causes inflammation and necrotizing vasculitis
128
Q

Type IV

A
  • activated T lymphocytes leads to release of cytokines, inflammation, activation of macrophages, and T cell mediated cytotoxicity
  • causes perivascular cellular infiltrates, edema, granuloma formation, cell destruction
129
Q

anaphylaxis

A
  • life threatening
  • causes CV collapse (tachycardia, hypovolemia)
  • interstitial edema, urticaria
  • bronchospasm, laryngeal edema
130
Q

immune mediated anaphylaxis

A
  • previous exposure to antigens in drugs evokes production of antigen-specific IgE antibodies
  • subsequent exposure results in marked mast and basophil degranulation
131
Q

non-immune mediated anaphylaxis

A
  • IgE or IgM
  • less common
  • direct release of histamine from mast cells or basophils
132
Q

histamine

A
  • vasoactive amine
  • stored in mast cells
  • released upon mast cell degranulation
  • causes rapid vasodilation, increases vascular permeability and smooth muscle contraction
133
Q

prostaglandins and leukotrienes

A
  • lipid mediators
  • prostaglandin D2 is the most abundant mediator generated by cyclooxygenase pathway in mast cells–>causes intense bronchospasm
  • leukotrienes are the most potent vasoactive and spasmogenic agents known
134
Q

TNF and chemokines

A
  • cytokines

- recruit, activate leukocytes, amplify

135
Q

anesthesia and anaphylaxis

A
  • 1 in 3500-20,000 cases
  • mortality of perioperative anaphylaxis 3-9%
  • risk factors = asthma, atopy, multiple past exposures to latex, hereditary conditions (angioedema)
136
Q

clinical manifestations of anaphylaxis

A
  • tachycardia
  • bronchospasm
  • laryngeal edema
  • cutaneous rash
137
Q

diagnosis of anaphylaxis

A
  • plasma tryptase concentration (indicative of mast cell activation)
  • plasma histamine concentration (not as specific)
  • skin testing
138
Q

management of perioperative anaphylaxis

A
  • remove agent if possible
  • reverse hypotension (EPI) and hypoxemia
  • replace intravascular fluid
  • inhibit further degranulation
  • inhibit release of vasoactive mediators
  • treat inflammation
  • relieve bronchospasm
139
Q

antihistamines for anaphylaxis

A
  • H1 antagonist - diphenhydramine competes with histamine for membrane receptor sites
  • H2 antagonist - ranitidine
  • helps to decrease pruritis and bronchospasm
  • not as effective when vasoactive substances of anaphylaxis have already been released
140
Q

epinephrine for anaphylaxis

A
  • 1-10 mcg/kg IV bolus, repeat Q1-2 min PRN
  • increases intracellular cAMP, restores membrane permeability, and decreases release of vasoactive mediators
  • beta-agonist effect - relax bronchial smooth muscle
141
Q

what meds can you give if anaphylaxis is unresponsive to epi?

A
  • vasopressin
  • glucagon
  • norepinephrine
142
Q

B2 agonists for anaphylaxis

A
  • albuterol
  • metered dose inhaler or nebulizer
  • helpful in treatment of bronchospasm
143
Q

corticosteroids for anaphylaxis

A
  • no known effect on degranulation
  • takes hours for effect
  • may enhance beta agonist effects of other drugs or inhibition of release of arachidonic acid responsible for the production of leukotrienes and prostaglandins
144
Q

drug allergies and anesthesia

A
  • not predictable
  • patients with allergies at increase risk
  • previous uneventful exposure does not eliminate possibility of allergic/anaphylactic reaction on second exposure
  • can occur on first exposure due to cross-reactivity with other allergens
145
Q

common drugs associated with perioperative anaphylaxis

A
  • muscle relaxants
  • antibiotics
  • latex
146
Q

muscle relaxants + perioperative anaphylaxis

A
  • rocuronium and succinylcholine are most common
  • cross sensitivity among classes
  • OTC cosmetics contain ammonium ions and are capable of sensitizing patients to developing IgE antibodies to quarternary and tertiary ammonium ions
  • atracurium histamine release non-immune mediated
147
Q

antibiotics + periop anaphylaxis

A
  • PCN most common
  • IgE antibodies can wane over time (may have reaction as child but then fine as adult
  • sulfonamide second most common; stevens johnson syndrome
  • vancomycin also common (usually not IgE but direct histamine release; red mans)
148
Q

two allergenic components of PCN

A
  • beta lactam ring

- r group side chain

149
Q

latex allergy OR

A
  • produced by rubber tree hevea brasiliensis which has proteins that can cause IgE-mediated antibody response
  • peaked in 1990s
  • now latex free ORs
150
Q

distinguishing feature of latex induced allergy

A

delayed onset, typically 30 min after exposure or longer; antigen from gloves absorbed across mucous membranes into system circulation; can also be inhaled (gloves with powder)

151
Q

patients at risk for latex allergy

A
  • spina bifida
  • multiple previous operations
  • history of fruit allergy
  • healthcare worker
152
Q

propofol allergy

A
  • contains lecithin (derived from egg yolk) and soybean oil as emulsifying agents
  • formerly advised that propofol used with caution in those with history of egg, soy or peanut allergy
  • also contains preservatives, now thought that allergy is IgE mediated with preservatives
153
Q

ASA and NSAID allergy

A
  • rhinorrhea, bronchospasm, and angioedema can occur in at risk individuals
  • not IgE mediated rather due to inhibition of COX-1 that promotes synthesis of leukotrienes and subsequent release of mediators from basophils and mast cells
154
Q

radiocontrast media allergy

A
  • reactions in about 0.1-3% of patients
  • more common with ionic, high osmolar contrast agents (higher the iodine the higher the risk of adverse reaction)
  • often immune mediated so can pretreat with corticosteroids and histamine antagonists
155
Q

other sources of allergy in OR

A
  • Local anesthetics (esters > amides)
  • halothane
  • dyes
  • CHG
  • synthetic volume expanders (dextran, hespan, albumin)
  • blood products
156
Q

autoimmune

A
  • misdirected adaptive immunity
  • type of hypersensitivity to self-antigens; antibodies inappropriately mark self-components as foreign
  • may have genetic predisposition
  • affects 1-5% of Western population
  • immune complexes and autoantibodies
157
Q

rejection

A
  • due to the face that the graft donor and recipient host are genetically different
  • differences recognized by immune system and responsible for the immune destruction of the graft
  • if graft donor expresses MHC molecules that differ from those in the recipient, the graft is recognized as foreign by the recipient’s T cells (recipients CD4+ and CD8+ cells migrate back into the transplant and cause rejection)
158
Q

allograft

A

graft exchanged between nonidentical individuals of the same species

159
Q

histocompatibility

A

determines if the tissue graft (histo=tissue) will be accepted (compatible) by the receiving individual

160
Q

MHC

A

major histocompatibility complex; polymorphic genes that differ among individuals; function to recognize t cells

161
Q

treatment of graft rejection

A

-immunosuppression needed to prolong graft survival –> corticosteroids, anti- T cell antibodies, drugs that inhibit T cell function

162
Q

GVHD

A
  • graft vs. host disease
  • syndrome commonly associated with bone marrow and stem cell transplants
  • donor’s WBCs. which remain with the donated tissue (graft) recognize the recipient (host) as foreign
  • donor’s immune system rejects the recipient
  • treatment is to suppress T cells with steroids and calcineurin inhibitors (cyclosporine and tacrolimus)
163
Q

tumor lysis syndrome

A
  • rare and potentially lethal
  • massive lysis of tumor cells which results in the release of intracellular substances into the blood stream (potassium, phosphate, uric acid)
  • causes - after chemo/radiation; steroids
164
Q

what is Lupus?

A
  • complex, multisystemic autoimmune disease characterized by presence of autoreactive B and T cells and the production of a broad heterogenous group of autoantibodies
  • antinuclear (anti DNA) antibody production most characteristic
165
Q

lupus genetic predisposition and environmental exposures

A
  • women age 15-44
  • African American, Asian American, Hispanic/Latinos, Native American, or Pacific Islanders
  • 50 genes associated with SLE
  • UV light, infection, virus, stress
  • maybe something to do with estrogen
166
Q

diagnosis of SLE

A
  • CBC
  • antibody tests (ANA and anti-dsDNA antibody)
  • complement test
  • blood clotting tests
  • urine test
  • biopsies
167
Q

criteria for classification

A
  • malar rash
  • photosensitivity
  • oral or nasopharyngeal ulcers
  • discoid rash
  • renal disorder
  • serositis
  • neurologic disorder
  • hematologic disorders
  • nonerosive arthritis of at least 2 peripheral joints
  • presence of antinuclear antibody (ANA)
  • serial or simultaneous presence of at least four of these indicates the individual has SLE
168
Q

4 types of lupus

A
  • systemic lupus erythematosus
  • drug-induced lupus erythematosus
  • cutaneous lupus erythematosus
  • neonatal lupus
169
Q

clinical presentation of SLE

A
  • CNS - vasculitis, anxiety, depression, psychosis, seizures, stroke
  • blood - thrombocytopenia, anemia, leukopenia, antiphospholipid syndrome
  • heart - pericarditis, pericardial effusion, CHF, HTN
  • joints - arthritis, avascular necrosis
  • kidneys - nephritis, proteinuria, hypoalbuminemia, hematuria, renal failure
  • lungs - pleural effusions, restrictive disease, atelectasis
  • airway - mucosal ulceration, cricoarytenoid arthritis, recurrent laryngeal nerve palsy
170
Q

drug-induced lupus erythematosus

A
  • lupus like disease that mimics lupus
  • S/S usually disappear 6 months after drugs stopped
  • men>women
  • common drugs - hydralazine, procainamide, isoniazid
171
Q

cutaneous lupus erythematosus

A
  • affected by sunlight and fluorescent
  • causes rashes and discolored lesions - face, arms, neck, shoulders, trunk; pigment change, hair loss due to lesions
  • raynaud occurs in some
  • 10% develop SLE
172
Q

neonatal lupus

A
  • pregnancy - pre-eclampsia, flare, pre-term delivery, miscarriages, intrauterine growth restrictions
  • affects infants in womb in women with lupus
  • caused by mom antibodies
  • born with skin rash, liver problems, low blood counts
  • disappear after some months
  • congenital heart block also possible (pacer)
173
Q

lupus treatment

A
  • tylenol
  • NSAIDs
  • immunosuppressants
  • corticosteroids
  • antimalarial
  • anticoagulants
  • monoclonal antibodies
  • respiratory corticotropin injections
174
Q

anesthetic implications of lupus

A
  • pre-op testing –> PFTs, ECHO, EKG, renal function, labs
  • continue SLE meds
  • airway involvement - laryngeal function, cricoarytenoid arthritis (hoarseness)
175
Q

incidence of RA

A
  • onset 22-55 years
  • 1.3-1.5 million people with RA
  • prevalence 2-3x more in women
176
Q

etiology of RA

A
  • environment
  • heredity
  • viral/bacterial infection
  • rheumatoid factors
177
Q

osteoarthritis vs. RA

A
  • osteoarthritis - degenerative disease, morning stiffness lasting less than 30 min, asymmetrical, cartilage loss
  • RA - autoimmune, morning stiffness lasting more than 30 min, symmetrical, inflamed synovium
178
Q

RA patho

A
  • autoantibodies attack joints at synovium or where the bones articulate (most movable joints in body)
  • greater movement allowed by joint, the greater the risk of developing injury and greater impact by RA
179
Q

clinical manifestations of RA

A
  • joint involvement
  • nerve entrapment (carpel tunnel)
  • TMJ
180
Q

joint inflammation in RA

A
  • inflammation of synovial joint membrane
  • rapid division and growth of cells in the joint
  • release of osteolytic enzymes, collagenases, and proteases
181
Q

alantoaxial instability

A
  • C1-C2 involvement

- erosion and collapse of bone from destruction of supporting cervical ligaments

182
Q

alanto odontoid separation

A

odontoid to impinge on the spinal cord potentially leading to neurologic damage

183
Q

alantoaxial subluxation

A
  • 66% of spine disorders r/t RA

- exert pressure and impair BF through the vertebral arteries

184
Q

cricoarytenoid joint in RA

A
  • 26-86% of patients with severe RA have involvement here
  • vocal cord nodules or polyps
  • present without clinical symptoms
  • S/S – hoarseness, pain with swallowing, stridor, dyspnea
185
Q

systemic involvement of RA

A
  • Pulm - pleural effusion, pneumonitis, pulmonary nodules
  • CV - pericarditis, pericardial effusion, MVR, AVR, conduction defects
  • eyes - destruction of lacrimal and salivary duct
  • muscle - rheumatoid myositis
186
Q

primary treatment

A
  • DMARDS - disease modifying antirheumatic drugs
  • work to decrease the body’s overactive immune and/pr inflammatory processes that cause RA symptoms such as joint pain and swelling
187
Q

two types of DMARDS

A
  • non biologic - methotrexate; cornerstone of RA therapy; inhibits cells use of folate (which is necessary for cell survival)
  • biologic - proteins that are manufactured using recombinant DNA; block cells ability to cause inflammation; TNF inhibitors, interleukin-1 receptor agonists, anti-CD20 monoclonal antibodies
188
Q

anesthetic considerations RA

A
  • meds - NSAIDs and corticosteroids
  • airway - TMJ, cervical spine, cricoarytenoid joint
  • positioning - padding
  • spinal anesthesia - sensory (spread higher due to narrowing of subarachnoid space 1.5 dermatomes higher than normie), CSF decrease
189
Q

Scleroderma

A
  • inflammation, vascular sclerosis
  • fibrosis of skin and viscera
  • injury to vascular endothelium results in leakage of proteins into interstitial space
  • collagen production is not slowed down and gets deposited throughout the body
190
Q

scleroderma etiology

A
  • unknown
  • collagen vascular disease with autoimmune characteristics
  • onset 20-40 years
  • women more
  • accelerated by pregnancy
191
Q

CREST syndrome

A
  • 2-3 to be diagnosed with scleroderma
  • calcinoses (Ca2+ deposits)
  • raynauds phenomenon
  • esophageal hypomotility
  • sclerodactyly (thickened/tight skin)
  • telangiectasia (dilated capillaries
192
Q

scleroderma skin + MSK clinical manifestations

A
  • skin thickened
  • diffuse edema
  • contractures
  • skeletal muscle myopathy
  • arthritis and limited joint mobility
  • avascular necrosis
193
Q

scleroderma nervous system clinical manifestations

A
  • peripheral and central neuropathies due to nerve compression by thickened connective tissue
  • trigeminal neuralgia
  • dry eyes
194
Q

slceroderma CV manifestations

A
  • sclerosis of coronary arteries and conduction system
  • replacement of CV tissue with fibrous tissue
  • systemic and pulmonary HTN
  • pericarditis and pericardial effusion
  • peripherally - intermittent vasospasm (raynauds)
195
Q

slceroderma respiratory manifestations

A
  • diffuse interstitial pulmonary fibrosis
  • arterial hypoxemia secondary to decreased diffusion capacity
  • decreased pulmonary compliance
196
Q

scleroderma renal manifestation

A
  • renal artery stenosis due to arteriolar intimal proliferation
  • decreased renal blood flow
  • HTN
197
Q

scleroderma GI manifestation

A
  • dry oral mucosa
  • progressive fibrosis of GI tract
  • dysphagia
  • hypomotility
  • decrease lower esophageal sphincter tone
  • malabsorption - vitamin K deficiency (coagulopathies)
198
Q

scleroderma anesthetic implications

A
  • fibrosis = limited mouth opening and difficult intubation
  • dermal thickening = difficult IV access
  • pulmonary HTN
  • decreased pulmonary compliance and decreased oxygen diffusion
  • chronic systemic HTN
  • hypotonia of LES = risk for aspiration
  • sensitive to respiratory depressants
  • regional may be challenging with contractures and decreased joint mobility
  • protect eyes from corneal abrasion (esp bc already dry!!)
  • renal dysfunction and decreased drug elimination

N935 Advanced Pathophysiology II (16 decks)

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