1
Q
What is the function of the immune system?
A
To protect the host against micro-organisms
2
Q
What are the 2 categories of the immune system? Briefly describe them
A
- Innate immunity: baseline immunity
- Adaptive/acquired immunity: developed thru life
3
Q
Describe innate immunity (7)
A
- Rapid
- Non-specific
- Natural protective mechanisms
- Requires no prior exposure
- Not a long lasting immunity
- Has no memory
- Does NOT form antibodies
4
Q
T/F: Innate immunity always has an identical repsonse to pathogens
A
T
5
Q
What type of pathogens is innate immunity okay for?
A
Common pathogens
6
Q
Innate immunity is you ______ line of defense
A
1st
7
Q
Innate immunity consists of a structural component which is the _______ cell elements and the _______ cell elements. What does each component consist of? (3-4)
A
Non-immune:
1. Epithelial & mucous membranes
2. Complement proteins
3. Acute phase proteins
Active immune:
1. Neutrophils
2. Macrophages
3. Monocytes
4. Natural Killer cells (NK cells)
8
Q
What part of the immune system is the epithelial and mucous membranes? What is the purpose of them?
A
Structural portion of Non-immune cell elements
They are the surface layer to protect against harmful pathogens
9
Q
The fastest responding immune cell is _______
A
Neutrophils
10
Q
NK cell =
A
Natural killer cell
11
Q
The slowest responding immune cell is ______. What is special about this cell?
A
Macrophages
They have a sustained immune response that lasts longer
12
Q
Active immune cell elements stem off __________ cell
A
Hematopoietic stem cell
13
Q
Hematopoietic stem cell —> _________ –> NK cell
A
Common lymphoid prognitor
14
Q
Hematopoietic stem cell —> _________ –> __________ –> Neutrophil
A
Common myeloid progenitor
Granulocyte monocyte progenitor
15
Q
Hematopoietic stem cell —> _________ –> Granulocyte monocyte progenitor –> Monocyte –> ________
A
Common myeloid progenitor
Macrophage
16
Q
T/F: Compliment proteins only work in innate immunity
A
F
Works in both innate & adaptive
17
Q
Compliment proteins augments _________ (2) production. There are over _____ plasma & cell surface proteins in the compliment system. What else does the system do?
A
- Phagocytes
- Antibody
Over 30
Mark pathogens so antibodies can recognize them for permanent destruction
18
Q
Where are complement proteins produced? What are they activated by?
A
Produced in liver
Activated by C1 or C3 (compliment1 or compliment3)
19
Q
The most numerous WBC is __________. they rapidly migrate in ________ infections and release ____________. what does this do?
A
Neutrophils
Bacterial
Cytokines
Phagocytize bacterial cells (destroy them)
20
Q
What is the half life of Neutrophils? What causes this? What happens after this?
A
half life = 6.5 hrs
They breakdown dt sensitivity to acid environment of infection
They break down into purulent exudate (puss)
21
Q
The largest blood cell is _________. they circulate to Tissue specific areas and become _________.
A
Monocytes
Macrophages
22
Q
Macrophages tissue specific: epidermis
A
Langerhans
23
Q
Macrophages tissue specific: liver
A
Kupffer
24
Q
Macrophages tissue specific: lungs
A
Alveolar cells
25
Macrophages tissue specific: CNS
Microglia
26
When do Marcophages mobilize? Why? What do marcophages do? (2) Why is this important? (2)
After the activation of neutrophils
This is so they can provide a longer/sustained anti-inflammatory response
1. Cause a phagocytic destruction of bacteria
2. Produces NO & cytokines --> **vasodilation**
Importance:
1. Persist at site of **chronic infections**
2. Slow/sustained response, lasting for days
27
Which immune cells function specifically with hypersensitivity reactions involving the IgE antibodies? (2)
1. Basophils
2. Mast cells
28
The least common blood granulocyte is __________ & __________ reside in connective tissues close to blood vessels.
Basophils
Mast cells
29
Basophils & Mast cells cause massive release of ___________ (4). What does this do? What is pathos can this contribute to? (3)
1. Histamine
2. Leukotrienes
3. Cytokines
4. Prostaglandins
This stimulates smooth muscle contraction --> airway constriction & bronchospasm
Pathos:
1. Allergies
2. Asthma
3. Eczema
30
Eosinophils are heavily concentrated in the _______. What is this protect against? How?
GI tract
Ingested pathogens & parasites
They are degraded through mast cell inflammatory mediators: histamine, LT, cytokines, prostaglandins
31
Who is adaptive immunity present in?
Higher level beings with vertebraes
32
Describe adaptive immunity (4)
1. Delayed onset of activation
2. Requires prior exposure
3. Capable of memory & specific antigen response
4. Generate antibodies
33
Vaccines are considered what type of immunity? What types are there? (3)
Adaptive/aquired immunity
1. Live
2. Inactivated
3. Recombinant (lab made)
34
Adaptive immunity is derived from _________ cells. What are they? (3)
Hematopoietic stem cells
Lymphoid proginator -->
1. T cells
2. B cells
3. NK cells
35
What are the 2 components of adaptive immunity? What type of cell does each involve?
1. Humoral -- B cells
2. Cellular -- T cells (helper T cells & cytotoxic)
36
B cells are a part of the ______ component of adaptive immunity. They produce ________ (3) antibodies that bind to foreign proteins of __________ (3). What is their purpose?
Humoral component
Antibodies: (MAE)
1. IgE
2. IgA
3. IgM
Proteins of:
1. bacteria
2. Viruses
3. Tumors
They help form immunity against pathogens & cancers
37
T cells, which can also be ________ (2), are a part of the __________ component of adaptive immunity. They originate in __________ and mature in the __________. They produce ___________ (2). What is their purpose?
1. Helper T cells
2. Cytotoxic
Cellular component
Bone marrow
Thymus
produce:
1. Interferon
2. Interleukin
They play a role in chronic inflammation they respond to infection and **activate IgE**
38
What is active immunity? Why is it relevant?
Environmental pathogen exposure to induce antibody formation
The more exposures you have = the immune quicker response
39
What is passive immunity? Ex? Why is it relevant?
Receiving antibodies from another individual
Ex. baby receiving antibodies from mother's breastmilk
--IVIG
Protection last few weeks to a month, but it's not long-term
40
Can you get a bloodbourne pathogen from IVIG? Why?
Yes
Antibodies pulled from 1000s donor. There's a risk even through processing
41
What are the different types of immune responses? (3) Briefly described them
1. Immunocompromised (inadequate)
-neutropenia (low WBC)
2. Exaggerated/excessive
-hypersensitivity
-asthma, hives, anaphylaxis
3. Misdirected
-autoimmune disorders
42
What happens during an autoimmune disorder?
Antibodies form against natural receptors/ligands
43
What is the definition of hypersensitivity? What are the most common drugs associated with this? (4)
Reaction to a foreign antigen, that requires a prior exposure/sensitization, that causes altered T-cell & antibody response
Drugs:
1. NMB
2. Abx
3. NSAIDs
4. PPIs
44
There are ____ types of allergic responses
4
45
Type I allergic response is also called _________. It is mediated by ______ which stimulate _____. What does this cause?
Immediate hypersensitivity
T cells
B cells
This causes IgE antibodies to be produced immediately
46
With type I allergic response, on 2nd exposure antigen releases _______ & there is a release of ________ (3). What symptoms does this cause? (4)
Calcium
1. Histamine
2. Heparin
3. Inflammatory mediators
s/s:
1. Bronchoconstriction
2. Vascular permeability
3. Vasodilation
4. Gastric acid secretion
47
What are examples of Type I allergic responses? (5)
(immediate hypersensitivity)
1. Anaphylaxis
2. Asthma
3. Angioedema
4. Conjuctivitis
5. Dermatitis
48
What are the Tx of Type I allergic response? (3)
1. Remove trigger
2. Prevent histamine response
--antihistamines, cromolyn sodium, bronchodilators, cox-inhibitors
3. Ongoing tx
--Dx tests, small doses of allergens to desensitize
49
Type II allergic response is also called _________. It is mediated by ______ (3) which activate _____ that produce ________ formed against antigens on cells & tissues.
Cytotoxic hypersensitivity
1. IgG
2. IgG
3. Complement proteins
B cells
antibodies
50
Describe Type II allergic response presentation, severity, & reaction time
Presentation & severity: vary
Reaction time: vary widely -- can be mins-hrs or weeks-months later
51
What examples of Type II allergic response? (4)
1. Hemolytic anemia
2. Myasthenia gravis
3. Autoimmune diseases
4. Transfusion reactions
52
What is the Tx for Type II allergic response? (2)
1. Anti-inflammatories
2. Immunosuppressants
53
Type III allergic response is also called _________. It is mediated by ______ (2). What causes this type of reaction? Where is this reaction seen at? (4)
Immune-complex hypersensitivity
1. IgG
2. IgM
Failure of the immune system to eliminate antibody-antigen complex
The complex complexes are deposited in and seen in:
1. Joints
2. Kidneys
3. Skin
4. Eyes
54
It takes _______ for Type III allergic response to develop. What are examples of this? (2) What is the Tx for this? (2)
Hours-weeks
examples:
1. Lupus
2. Rheumatoid arthritis
Tx:
1. Anti-inflammatories
2. Immunosuppressants
55
Type IV allergic response is mediated by ______ (3) and does not involve _________. Describe this response
1. T lymphocytes
2. Monocytes
3. Macrophages
antibodies
This response is more superficial and cutaneous symptoms are most common
56
What are Type IV allergic response examples? (3) What is the Tx? (2)
ex:
1. Dermatitis
2. Tuberculosis
3. Stevens-Johnson syndrome
Tx:
1. Anti-inflammatories
2. Immunosuppressants
57
Anaphylaxis is a life-threatening condition that occurs in _______ to _______ anesthetics within ________ mins of an exposure to an antigen
1/5,000
1/20,000
5-10 mins
58
What are symptoms of anaphylaxis? (5)
1. Systemic vasodilation
2. Hypotension
3. Vessel permeability --> extravasation of protein/fluid
4. Bronchospasm
5. PEA/cardiac arrest
59
Describe the pathology of anaphylaxis
Preview exposure creates IgE antibodies --> subsequent exposure to antigen --> antigen-antibody reaction --> mast cells & basophils the granulate --> release histamine, leukotrienes, prostaglandins, eosinophils, neutrophils, chemotactic factors, platelet-activating factors --> **symptoms of anaphylaxis** --> up to 50% of intravascular fluid extravasates
60
With anaphylaxis there's a lifetime prevalence of ___% and ____% of intravascular fluid extravasates
5%
50%
61
____% of pts experience Biphasic anaphylaxis. What is this?
4-5%
This is a 2nd anaphylactic episode follwing an asymptomatic period w/o a second exposure.
62
Biphasic anaphylaxis occurs _______ after the initial event. What are the risk factors for this? (2)
8 - 72hrs
1. Severe initial response
2. Initial response required multiple doses of Epi
63
What are risk factors for periop anaphylaxis? (6)
1. Asthma
2. Long duration of anesthesia
3. Drug redosing
4. Female -- not in teen yrs
5. Multiple past sx
6. Presence of other allergies
64
How do you Dx anaphylaxis? (3)
1. Plasma tryptase
-Verifies mast cell activation/degranulation
-Spikes 1-2hrs post
2. Plamsa histamine
-Baseline w/i 60 mins of Tx
3. Skin testing
-Wheal & flare response
-6 weeks post
65
What are reasons why anaphylaxis may go unnoticed? (4)
1. Lack of Recognition
2. Communication issues
3. Monitor malfunction
4. Physical symptoms unseen dt dark room or covered by surgical drapes
66
What is the primary Tx of anaphylaxis? (4)
CALL FOR HELP!
1. Stop administration of causative agent
2. 100% O2
3. Epi/Pressors
4. Fluid therapy
67
Drug Dose: Anaphylaxis Epi (Adults/Peds)
Adult: 10mcgs - 1mg IVP q1-2mins
Peds: 1-10mcg/kg IVP q1-2mins
68
With Tx of anaphylaxis, what other medication's can you use in place of epi if your pt is resistant to it? (2) What does it do?
1. Vasopressin
2. Methylene Blue
Inhibits NO production --> decreases vasodilation
69
What are the 2 types of fluids to be given during anaphylaxis? What are the rates?
1. Crystalloids: NS 10-25ml/kg over 20mins -- PRN
2. Colloids: 10ml/kg over 20mins -- PRN
70
Why is epinephrine the 1st line drug in anaphylaxis? (4)
1. Decreases degranulation of mast cells and basophils --> decreases vasodilation (as well as other effects)
2. Alpha-1 -- vasoconstriction (increases SVR)
3. Beta-1 -- Increases COP (increases inotrop/chrono)
4. Beta-2 -- bronchodilation
71
What is considered secondary treatment for anaphylaxis? (5)
1. Bronchodilators
2. Antihistamines
3. Corticosteroids
4. Observed for relapse/biphasic anaphylactic
5. Blood sample/allergy testing
72
Drug dose: Anaphylaxis Diphenhydramine
0.5 - 1mg/kg IV
(H1)
73
Drug dose: Anaphylaxis Ranitidine
50mg IV
(H2)
74
Drug dose: Anaphylaxis hydrocortisone (adult/peds)
Adult: 250mg IV
Peds: 50 - 100mg IV
75
Drug dose: Anaphylaxis methylprednisolone (adult/peds)
Adult: 80 mg IV
Peds: 2mg/kg IV
76
What are your common antigen reactions? (6)
1. Transfusion reactions
2. Transplant rejection of an organ
3. Graves disease
4. Multiple sclerosis
5. Rheumatoid arthritis
6. Lupus
77
Transfusion reactions are response to surface antigens on donor ______. What type of antigens cause this? (3)
RBC
1. Type A
2. Type B
3. Rh antigens
78
Transplant rejection happens due to a response to ______ on the donor organ dt pre-existing ______. is this acute or chronic?
Antigens
antibodies
It can be acute or chronic
79
_________ is the most common cause of hyperthyroidism. It is caused by auto antibodies to the ________ receptor.
Graves disease
TSH receptor
80
_________ forms antibodies against myelination proteins. What does it cause?
Multiple sclerosis
It causes immune mediated in inflammation and destroys myelin and underlining nerve fibers
81
__________ is an abnormal production of pro-inflammatory factors. ________ plays a role in this disorder.
Rheumatoid arthritis
Infection
82
Lupus forms antibodies against _________ (5) & affects __________ systems
1. RBC's
2. Lymphocytes
3. Nucleic acids
4. Platelets
5. Coagulation protein proteins
Multiple organ
83
T/F: There is always a reason for angioedema
F
It can be idiopathic
84
Angiodema is profound swelling in the ________ (3) and is usually seen with ________.
1. Facial
2. Tissue
3. Airway
Severe anaphylaxis
85
Hereditary angioedema is a ________ disorder that is caused by ___________ deficiency/dysfunction. What is it triggered by? (5)
Rare genetic
C1 esterase inhibitor
1. Menses
2. Trauma
3. Infection
4. Stress
5. PO birth control
86
What does decreased C1 esterase inhibitor cause?
1. Excessive production of Bradykinin --> vasodilation & swelling (potent vasodilation & laryngeal swelling in angioedema)
87
T/F: Tx for hereditary angioedema is antihistamines
F
This is not responsive to antihistamines
88
What areas of the body are affected in hereditary angioedema? (4)
1. Legs
2. Hands
3. Face
4. Upper respiratory tract
(REMEMBER THIS IS NOT REGULAR ANGIOEDEMA)
89
Acquired angioedema can be the result of __________. Why does this happen?
ACE-inhibitors
It blocks the degradation of bradykinin --> affects vascular permeability --> **stimulates substance P** --> vasodilation & fluid extravasation
90
How does acquired angioedema present?
Swelling in the lip, tongue, face only
No rash/itching
(Not a histamine reaction--again, antihistamines won't work)
91
What is the treatment of angioedema? (4)
1. Airway maintenance
-intubation --> trach
2. FFP
-reestablish intravascular volume
3. C1 esterase inhibitor concentrate
4. Epi
92
What type of blood can be given to anyone? Why?
Type O -
It has no antigens and both antibodies
93
What type of blood can receive any type of blood? Why?
AB
It has both antigens and no antibodies so it wont have a reaction
94
_____ is one of the most common forms of acquired immune deficiency. Describe its patho
HIV/AIDS
Patho:
Works through reverse transcription --> makes a double helix DNA with all viral genetic material --> change the amino acid sequence --> new version not recognized --> destroys immune cells
95
The HIV Seroconversion period is ________ after inoculation. _______ symptoms are associated with this period. What are they? (6)
2-3 weeks
Flu-like
1. Fever
2. Fatigue
3. Night sweats
4. Pharyngitis
5. Myalgias
6. Arthralgias
96
When does HIV convert to AIDS? What are the symptoms for this? (2) How is this Dx? (4)
When there is a higher basal level of the virus --> more rapid conversion to AIDS
1. Weight loss
2. Failure to thrive
Dx:
1. ELISA: 4-8 weeks after infection
2. Viral load level
3. CD4 T lymphocytes <200,000
4. HAART agent sensitivity test
97
T/F: there are multiple infections associated with AIDS
T
98
What is the main focus as anesthesia providers with a pt w/ HIV/AIDS?
**Detecting co-existing diseases**
-cardiovascular abnormalities
-neurological decline
-pulmonary dysfunction
-endocrine
-hematologic
-renal
99
AIDS pts can appear to be _________. What considerations should we have with this?
malnourished
Careful with positioning/pad dt abnormal fat redistribution
100
HIV/AIDS pts may have inhibition of ________ which may cause prolongation in __________ (5).
Cytochrome P-450
1. Hormone synthesis
2. Cholesterol synthesis
3. Vitamin D metabolism
4. Drug metabolism
5. BiliRubin metabolism --> hyperbilirubinemia
101
Systemic sclerosis, also called __________, is mostly affected by _____ gender from the ages of ________yo. What is a characterized by? (3) describe the spread of this?
Scleroderma
female
20-40 years
1. Inflammation
2. Vascular sclerosis
3. Fibrosis of skin & viscera
The spread can be localized/limited or diffuse/widespread
102
T/F: the cure for scleroderma is IVIG
F
There is no cure
103
What are the symptoms of scleroderma? (8)
1. Decreased mobility of fingers
2. Facial pain
3. raynauds
4. Hypomotility of GI
5. LES tome decreased
6. Cardiac dysrhythmia/conduction abnormalities
7. Pulmonary fibrosis
8. Renal artery stenosis
104
What are preop labs needed for scleroderma? (6)
1. EKG
2. BUN
3. Creatinine
4. CBC/platelets
5. CXR
6. PFT
105
What are anesthesia implication for scleroderma? (6)
1. Organ system dysfunction
2. Arterial catheter concerns -- difficult A-line placement
-**continue CCB for tissue perfusion**
3. Contracted intravascular volume
4. Aspiration risk
5. Limited neck mobility
6. Reduce pulmonary compliance
106
Anesthesia effects on the immune system: Inhalation agents/VA (5)
1. Suppress NK cells
2. Induce apoptosis of T cells
3. Impaire phagocytes
4. Sevo stimulates renal cell carcinoma
5. Sevo inhibits non-small cell carcinoma
107
Anesthesia effects on the immune system: induction (4)
1. Versed decrease his migration of neutrophils
2. Ketamine depresses NK cell activity
3. Propofol decreases cytokines
4. Propofol promotes NK cells
108
Anesthesia effects on the immune system: opioids
1. Suppress NK cells -- esp. Morphine & fentanyl
109
Anesthesia effects on the immune system: NSAIDs
1. Inhibit prostaglandin synthesis
Principles 2 Fall 2025
flashcards
Decks in class (17)
# Cards
-
OR Communication51
-
Burns127
-
Hospital Acquired Infections & Abx132
-
Anesthesia Implications for Obesity99
-
Geriatrics37
-
Positioning82
-
SCIP24
-
ERAS96
-
PACU122
-
Acute pain138
-
OFA33
-
Immune Dysfunction109
-
General & Laproscopic Sx96
-
GU Procedures88
-
Postop NV60
-
Oncology/Chemo136
-
Common Anesthesia Meds (Pharm ppt)133
