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
2
Q
history of penicillin
A
- first discovered in 1928, first commercialized antibiotic effective against staph and strep
- natural product of penicillium mold
3
Q
what kind of antibiotic is penicillin?
A
beta-lactam (due to the beta lactam ring)
4
Q
penicillin G
A
- given IV
- destroyed by stomach acid
5
Q
penicillin V
A
- given PO
- semi-synthetic
6
Q
how frequently do TRUE penicillin allergies occur?
A
<1%
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
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
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
10
Q
what is the predominant cause of nosocomial blood-stream infections?
A
CVCs
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
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
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
14
Q
what are the potential detrimental effects of C. Diff?
A
- toxic megacolon
- antibiotic associated diarrhea
- may lead to subtotal colectomy
- ileostomy
15
Q
what is the treatment for C. Diff?
A
- removal of causative antibiotic
- administer oral antibiotics [metronidazole or vancomycin]
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
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
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
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
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
21
Q
tetanus treatment
A
- control of skeletal muscle spasm with benzos or muscle relaxants
- neutralize exotoxin with human anti-tetanus immunoglobulin
- PCN
- immunization!!
22
Q
what are the different types of pneumonia
A
- community-acquired
- aspiration
- postoperative
- ventilator-associated
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)
24
Q
aspiration pneumonia
A
- clinical manifestations depend on the nature and volume of aspirated material
- arterial hypoxemia
- airway obstruction
- atelectasis
- pneumonia
25
pneumonia clinical presentation
- 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
26
pneumonia prevention
- 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
27
pneumonia anesthesia management
- 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
28
severe acute respiratory viral illnesses
- Highly virulent with a high mortality
- H5N1 influenza A = bird flu
- coronavirus strains - MERS-CoV, SARS-CoV, SARS-CoV-2
29
S/S of acute respiratory viral illness
- nonspecific
- fever
- HA
- diarrhea
- respiratory distress
- hemoptysis
30
viral infections treatment
- 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
31
anesthetic management of acute viral infections
- 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
32
negative pressure rooms
- 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
33
provider PPE
- goggles
- face shield
- gown
- gloves
- masks
- shoe covers
34
UV Germicidal Irradiation
- 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
35
HEPA filters
- 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)
36
HMEF
consist of heat and moisture exchange medium together with an electrostatic filter medium
37
mycobacterium tuberculosis
obligate aerobe responsible for TB which survives most successfully in tissues with high oxygen concentrations
38
S/S TB
- cough
- anorexia
- weight loss
- night sweats
- chest pain
- CXR = apical or subapical infiltrates or bilateral upper lobe infiltration with the presence of cavitation
39
extrapulmonary TB
- Pott's disease is common manifestation
| - tuberculosis vertebral osteomyelitis or tuberculosis spondylitis
40
Mantoux's test
skin test for TB, most common test
41
TB Treatment
- 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
42
AIDS
- 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
43
AIDS diagnosis
- 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
44
AIDS anesthesia considerations
- 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
45
AIDS pre-op testing
- CBC
- BMP
- renal function studies
- LFTs
- coagulation panel
- CXR
- ECG
- NOTE - CD4 cell count and viral may not have utility
46
antiretroviral treatment
SIX major classes currently in use
47
Prions
- 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
48
types of spongiform encephalopathies caused by prions
- 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)
49
Standard precautions
- 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
50
contact precautions
- 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
51
enhanced barrier precautions
- 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
52
Droplet Precautions
- 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
53
airborne precautions
- known or suspected infection with pathogen transmitted by airborne route
- examples = TB, measles (rubeola), varicella-zoster, HSV, variola (smallpox), chickenpox
54
precautions in order of least to most PPE
standard < contact < special enteric < droplet < airborne < full barrier
55
innate immune system
- 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
56
components of innate immune system
- epithelial membrane
- mucous membrane
- complement factors
- neutrophils
- macrophages
- monocytes
57
principle cells of the innate immune system
myeloid cells which includes macrophages, neutrophils, and dendritic cells
58
adaptive immune system
- 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
59
principle cells of the adaptive immune system
lymphoid cells, which are T and B lymphocytes
60
two components of adaptive immunity
- humoral immunity
| - cell mediated immunity
61
humoral immunity
- mediated by antibodies produced by B cells
| - antibodies neutralize microbes, opsonize them for phagocytosis and activate the complement system
62
Cell mediated immunity
- T cells activated by protein antigens from antigen presenting cells (APCs)
- requires repeat antigen stimulation to perform their functions
63
2 types of T cells
- CD4+ helper T cells
| - CD8+ helper T cells
64
CD4+ Helper T cells
secrete cytokines to activate macrophages, helps B cells make antibodies, stimulates inflammation
65
CD8+ Helper T cells
kill infected and transformed cells
66
examples of inadequate immune response
- neutropenia
- abnormal phagocytosis
- deficient in the complement system
- hyposplenism
67
examples of excessive immune response
- neutrophilia
- monocytosis
- asthma
68
example of misdirected immune response
angioedema
69
examples of adaptive immune dysfunction
- defective antibody production
- defect in T lymphocytes
- combined immune system defects (SCIDs)
- allergic reactions
- anaphylaxis
- autoimmune disorders
70
penia
lack of, poverty, deficiency
71
philia
affinity, attraction, fondness
72
allergy
reaction against normally harmless environmental antigen
73
autoimmune
reactions against self antigens
74
hypersensitivity
excessive immunologic reactions to microbes or environmental agents dominated by inflammation
75
atopy
propensity or genetic tendency to develop allergic reactions
76
antibody (Ab) or immunoglobulin (Ig)
large, Y-shaped protein used by the immune system to ID and neutralize foreign objects such as pathogenic bacteria and viruses
77
neutrophils
- 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
78
neutropenia
-neutrophil count <1500/mm3
79
types of neutropenia
- neonatal sepsis
- Kostmann syndrome (autosomal recessive)
- acquired defects (chemo, antiviral drugs)
- autoimmune (SLE, RA)
- infection (the rate of neutrophil consumption exceeds their production)
80
neutropenia treatments
- cessation of medication causes
- granulocyte colony stimulating factor (filgrastim), which stimulates the production of WBCs
- bone marrow transplant
81
anesthetic implications of neutropenia
maintain asepsis in the perioperative area
82
spleen
- 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
functions of the spleen
- 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
breakdown of hemoglobin
- globin --> broken down to amino acids
| - heme --> metabolized to bilirubin which is removed by the liver
85
asplenia
- 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
hyposplenism
reduced spleen function
87
sickle cell anemia and the spleen
can cause auto-infarction in the spleen resulting in vaso-occlusive disease
88
implications of dysfunctional spleen
- immunizations important (challenging in developing countries)
- travel restrictions, antibiotic prophylaxis even with minor procedures, and alert warning bracelets
89
leukocytosis
- 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
left upper shift
- increase in the ratio of immature to mature neutrophils
| - bone marrow is trying to make more
91
right shift
- decrease ratio of immature to mature neutrophils
| - shows bone marrow suppression (radiation sickness)
92
acute leukemia
immature WBCs in the peripheral blood
93
chronic leukemia
mature, non-functioning WBCs in peripheral blood
94
what can cause neutrophilia
- bacterial infection
- inflammation
- MI
- burns
95
what can cause eosinophilia
-allergic disorders (asthma, hay fever, drug allergy, allergic skin disease, parasitic infection, malignancy, Hodgkin's, some forms of lupus)
96
what can cause basophilia
myeloproliferative diseases like blood cancers
97
what can cause monocytosis
- chronic infections - TB, bacterial endocarditis, malaria
| - inflammatory disorders - RA, SLE, ulcerative colitis
98
what can cause lymphocytosis
-chronic infections - TB, CMV, hepatitis, pertussis
99
eosinophilic esophagitis
- 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
neutrophilia
- 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
leukostasis
- >100,000/mm3
- blood gets really thick and there is WBC clumping
- can lead to TIA or stroke
102
how many neutrophils in myeloproliferative disorder or hematologic malignancy
>50,000/mm3
103
asthma
exaggerated bronchoconstriction response to a stimulus
104
extrinsic asthma
- IgE production, allergens
- usually begins in childhood
- genetic component
- hypersensitivity to allergens
- increase IgE
105
intrinsic asthma
- 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
angioedema
- subcutaneous and submucosal edema formation
- usually involves face, extremities and GI tract
- can be hereditary or acquired
107
three types of bradykinin mediated angioedema
- autosomal dominant deficiency/dysfunction of C1 esterase inhibitor
- ACE inhibitors
- acquired
108
autosomal dominant deficiency/dysfunction of C1 esterase inhibitor
- 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
ACE inhibitor induced angioedema
drug-induced resulting from increased bradykinin availability secondary to ACE inhibitor mediated blockage of bradykinin catabolism
110
acquired angioedema
lymphoproliferative disorders acquire C1 esterase inhibitor deficiency secondary to antibody production
111
treatment of acute angioedema
- 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
are catecholamines and antihistamines a viable treatment option for bradykinin-mediated angioedema
NO!!!!!!!
113
DiGeorge Syndrome
- 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
treatment of DiGeorge
thymus transplant or infusion of T cells
115
anesthetic considerations for DiGeorge
- SBE prophylaxis
- calcium supplementation (if hypoparathyroidism)
- strict asepsis due to infection risk
116
SCIDs
- 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
SCIDs patho
- 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
SCIDs treatment
bone marrow or stem-cell transplant, gene therapy, or enzyme replacement
119
anaphylaxis
- fall in BP (shock) caused by vascular dilation
| - airway obstruction due to laryngeal edema
120
bronchial asthma
- airway obstruction caused by bronchial smooth muscle hyperactivity
- inflammation and tissue injury caused by late-phase reaction
121
allergic rhinitis, sinusitis (hay fever)
- increased mucus secretion
| - inflammation of upper airways and sinuses
122
food allergies
-increased peristalsis due to contraction of intestinal muscles, resulting in vomiting and diarrhea
123
allergic reactions
- immune mediated
| - overreaction of the immune system
124
types of allergic reactions (4)
- type I - IgE; anaphylaxis
- type II - IgG, IgM; myasthenia gravis, Graves
- type III - immune complex; SLE
- type IV - T lymphocytes; RA, MS
125
Type I
- 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
Type II
- 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
Type III
- 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
Type IV
- 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
anaphylaxis
- life threatening
- causes CV collapse (tachycardia, hypovolemia)
- interstitial edema, urticaria
- bronchospasm, laryngeal edema
130
immune mediated anaphylaxis
- previous exposure to antigens in drugs evokes production of antigen-specific IgE antibodies
- subsequent exposure results in marked mast and basophil degranulation
131
non-immune mediated anaphylaxis
- IgE or IgM
- less common
- direct release of histamine from mast cells or basophils
132
histamine
- vasoactive amine
- stored in mast cells
- released upon mast cell degranulation
- causes rapid vasodilation, increases vascular permeability and smooth muscle contraction
133
prostaglandins and leukotrienes
- 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
TNF and chemokines
- cytokines
| - recruit, activate leukocytes, amplify
135
anesthesia and anaphylaxis
- 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
clinical manifestations of anaphylaxis
- tachycardia
- bronchospasm
- laryngeal edema
- cutaneous rash
137
diagnosis of anaphylaxis
- plasma tryptase concentration (indicative of mast cell activation)
- plasma histamine concentration (not as specific)
- skin testing
138
management of perioperative anaphylaxis
- 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
antihistamines for anaphylaxis
- 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
epinephrine for anaphylaxis
- 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
what meds can you give if anaphylaxis is unresponsive to epi?
- vasopressin
- glucagon
- norepinephrine
142
B2 agonists for anaphylaxis
- albuterol
- metered dose inhaler or nebulizer
- helpful in treatment of bronchospasm
143
corticosteroids for anaphylaxis
- 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
drug allergies and anesthesia
- 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
common drugs associated with perioperative anaphylaxis
- muscle relaxants
- antibiotics
- latex
146
muscle relaxants + perioperative anaphylaxis
- 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
antibiotics + periop anaphylaxis
- 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
two allergenic components of PCN
- beta lactam ring
| - r group side chain
149
latex allergy OR
- produced by rubber tree hevea brasiliensis which has proteins that can cause IgE-mediated antibody response
- peaked in 1990s
- now latex free ORs
150
distinguishing feature of latex induced allergy
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
patients at risk for latex allergy
- spina bifida
- multiple previous operations
- history of fruit allergy
- healthcare worker
152
propofol allergy
- 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
ASA and NSAID allergy
- 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
radiocontrast media allergy
- 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
other sources of allergy in OR
- Local anesthetics (esters > amides)
- halothane
- dyes
- CHG
- synthetic volume expanders (dextran, hespan, albumin)
- blood products
156
autoimmune
- 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
rejection
- 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
allograft
graft exchanged between nonidentical individuals of the same species
159
histocompatibility
determines if the tissue graft (histo=tissue) will be accepted (compatible) by the receiving individual
160
MHC
major histocompatibility complex; polymorphic genes that differ among individuals; function to recognize t cells
161
treatment of graft rejection
-immunosuppression needed to prolong graft survival --> corticosteroids, anti- T cell antibodies, drugs that inhibit T cell function
162
GVHD
- 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
tumor lysis syndrome
- 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
what is Lupus?
- 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
lupus genetic predisposition and environmental exposures
- 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
diagnosis of SLE
- CBC
- antibody tests (ANA and anti-dsDNA antibody)
- complement test
- blood clotting tests
- urine test
- biopsies
167
criteria for classification
- 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
4 types of lupus
- systemic lupus erythematosus
- drug-induced lupus erythematosus
- cutaneous lupus erythematosus
- neonatal lupus
169
clinical presentation of SLE
- 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
drug-induced lupus erythematosus
- lupus like disease that mimics lupus
- S/S usually disappear 6 months after drugs stopped
- men>women
- common drugs - hydralazine, procainamide, isoniazid
171
cutaneous lupus erythematosus
- 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
neonatal lupus
- 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
lupus treatment
- tylenol
- NSAIDs
- immunosuppressants
- corticosteroids
- antimalarial
- anticoagulants
- monoclonal antibodies
- respiratory corticotropin injections
174
anesthetic implications of lupus
- pre-op testing --> PFTs, ECHO, EKG, renal function, labs
- continue SLE meds
- airway involvement - laryngeal function, cricoarytenoid arthritis (hoarseness)
175
incidence of RA
- onset 22-55 years
- 1.3-1.5 million people with RA
- prevalence 2-3x more in women
176
etiology of RA
- environment
- heredity
- viral/bacterial infection
- rheumatoid factors
177
osteoarthritis vs. RA
- 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
RA patho
- 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
clinical manifestations of RA
- joint involvement
- nerve entrapment (carpel tunnel)
- TMJ
180
joint inflammation in RA
- inflammation of synovial joint membrane
- rapid division and growth of cells in the joint
- release of osteolytic enzymes, collagenases, and proteases
181
alantoaxial instability
- C1-C2 involvement
| - erosion and collapse of bone from destruction of supporting cervical ligaments
182
alanto odontoid separation
odontoid to impinge on the spinal cord potentially leading to neurologic damage
183
alantoaxial subluxation
- 66% of spine disorders r/t RA
| - exert pressure and impair BF through the vertebral arteries
184
cricoarytenoid joint in RA
- 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
systemic involvement of RA
- 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
primary treatment
- 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
two types of DMARDS
- 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
anesthetic considerations RA
- 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
Scleroderma
- 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
scleroderma etiology
- unknown
- collagen vascular disease with autoimmune characteristics
- onset 20-40 years
- women more
- accelerated by pregnancy
191
CREST syndrome
- 2-3 to be diagnosed with scleroderma
- calcinoses (Ca2+ deposits)
- raynauds phenomenon
- esophageal hypomotility
- sclerodactyly (thickened/tight skin)
- telangiectasia (dilated capillaries
192
scleroderma skin + MSK clinical manifestations
- skin thickened
- diffuse edema
- contractures
- skeletal muscle myopathy
- arthritis and limited joint mobility
- avascular necrosis
193
scleroderma nervous system clinical manifestations
- peripheral and central neuropathies due to nerve compression by thickened connective tissue
- trigeminal neuralgia
- dry eyes
194
slceroderma CV manifestations
- 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
slceroderma respiratory manifestations
- diffuse interstitial pulmonary fibrosis
- arterial hypoxemia secondary to decreased diffusion capacity
- decreased pulmonary compliance
196
scleroderma renal manifestation
- renal artery stenosis due to arteriolar intimal proliferation
- decreased renal blood flow
- HTN
197
scleroderma GI manifestation
- dry oral mucosa
- progressive fibrosis of GI tract
- dysphagia
- hypomotility
- decrease lower esophageal sphincter tone
- malabsorption - vitamin K deficiency (coagulopathies)
198
scleroderma anesthetic implications
- 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
flashcards
Decks in class (16)
# Cards
-
Immune198
-
Hepatic 1166
-
Hepatic 277
-
Hematologic Anemias73
-
Hemoglobin Disorders41
-
Coagulation Disorders42
-
Neuromuscular Disorders83
-
Renal Pathophysiology100
-
Endocrine Pituitary Gland66
-
Adrenal Disease53
-
Endocrine55
-
Thyroid Pathophysiology65
-
Parathyroid Pathophysiology39
-
Peds Advanced Patho92
-
Anesthesia Considerations for Premie, Neonate, and Peds57
-
Peds Congenital Hearts and Things106
