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Principles of Anes II > Immune > Flashcards

Immune Flashcards

1
Q

Active vs Passive Immunity

Definition and Examples

A

ACTIVE
-Pathogen deliberately admin
-Repeat exposure…quicker response
-Ex: Vaccines

PASSIVE
-Receive antibodies from another
-Protection lasts few weeks to months
- Ex: Maternal IgA antibodies via breast milk

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2
Q

Types of Cells

1.) Neutrophils
2.) Monocyptes/ Macrophages
3.) Basophils/Mast
4.) Eosinophils

A
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3
Q

Neutrophils

-#
-How it works?
-How long it lasts?
-Works in what environ?

A

-Most numerous of WBC’s
-Migrate rapidly in bacterial infections

—-Release cytokines
–>phagocytize
–>Purulent exudate
—
½ life 6 hours

Sensitive to acid environments of infection

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4
Q

Monocytes and Macrophages

Size?
What tissues does it work on?
Skin, liver, lung, CNS

How does it work? (2)
Where does it usually work at?

A

Monocytes: largest blood cells
—
Circulate to tissue specific areas…macrophages

TO DIFFERENT LOCATIONS:
— Langerhans (epidermis)
— Kupffer (liver)
— Alveolar cells (lung)
— Microglia (CNS)
—
Mobilize just after neutrophils
-Phagocytic destruction
-Produce NO and cytokines
-NO DILATE = more BF for better response

-Persist at sites of chronic infection

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5
Q

Basophils and Mast

Common?
Where do they both reside in?

High affinity receptors for ___?
Functions? Releases (4)
Stimulates : ____
Plays major roles in: _____ (3 disease)

A

Basophils
=Least common blood granulocytes

Mast cells
–>Reside in connective tissue close to blood vessels

They BOTH:
-Express high affinity receptors for IgE
-Initiators of hypersensitivity
-Histamine, leukotrienes, cytokines, prostaglandins
-Stimulate smooth muscle contraction

-Play major role in allergies, asthma, eczema

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6
Q

Eosinophils

Heavily resides in _____
Helps protect against: _____
Function: _____

A

-Heavily concentrated in GI mucosa
-Protect against parasites (we get in GI)

-Degrade mast cell inflammation

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7
Q

Innate vs Adaptive Immunity

Type of memories?
Components?
Non-cellular elements
Type of cells? Humoral components of each?

A

INNATE:
 Rapid, non-specific and no antibodiy
 Requires no prior exposure
 No memory/ No long-lasting immunity
• response always identical

 Non-cellular elements
• Epithelial and mucous membranes
• Complement
• Acute phase proteins

• Neutrophils
• Macrophages
• Monocytes

ADAPTIVE
 Present only in vertebrates
 Delayed onset WITH memory and specific antigen response

 Derived from hematopoietic stem cells

Humoral component
• B cells= antibodies
• T cells (helper and cytotoxic)
o –>Originate in bone marrow; Mature in thymus
• Produce interferon, interleukin
• Role in chronic inflammation
• Respond to infection
• Activate IgE

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8
Q

Type 1 Allergic Response

AKA:______

What cells stimulated: !!
Ig__?

Second exposure response, what happens?? Whats released? (4)

Examples: (5)
Treatments??

A

aka: “immediate hypersensitivity”
(ADAPTIVE IMMUNITY)

T cells stimulate B cells
— IgE antibodies produced
— IgE =IMMEDIATE

On second exposur:
-Antigen releases calcium
-Release of histamine,heparin, inflammatory mediators

**Histamine triggers:
— Bronchoconstriction
— vascular permeability,
— Vasodilation
— Gastric acid

Example:
Anaphylaxis, asthma, angioedema, conjuctivitis, dermatitis

Treatment Type I:
Prevent histamine effects:
— Antihistamines
— Cromolyn sodium
— Bronchodilators
— COX pathway inhibitors
— Diagnostic tests
— Small doses of allergen to desensitize

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9
Q

Type 1 Allergic Response Treatment

Types of meds?
Types of Test?

A

Prevent histamine effects:
— -Antihistamines
— -Cromolyn sodium
— -Bronchodilators
— -COX pathway inhibitors

-Diagnostic tests
-Small doses of allergen to desensitize

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10
Q

Type II Allergic Response (DELAYED)
AKA:

Ig__
Ig__

What type of cell activated? Antibodies or no?

Examples? (3)

Treatment? (2)

A

Aka: cytotoxic hypersensitivity

-IgG, IgM, and complement mediated
-Activate B cells to produce antibodies

Presentation and severity vary (DELAYED)
–>Reaction time: minutes-hours

Examples:
hemolytic anemia, myasthenia gravis, transfusion reactions

Treatment:
— Anti-inflammatories
— Immunosuppressives

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11
Q

Type 3 Allergic Response

AKA:

Works when:

Complexes deposits in:
(4)

Mediated by/ Immediate or Delayed?? How long does it take?
Ig__
Ig___

Examples: (2)

Treatment (2)
What class of meds?

A

Aka: immune complex hypersensitivity

-Failure of the immune system to eliminate antibody-antigen complex
—
Complexes deposited in
-Joints, kidneys, skin, eyes

Also mediated by IgG and IgM (DELAYED)
–>Take hours-weeks to develop

Examples:
* Systemic lupus erythematosus (SLE), rheumatoid arthritis

Treatment:
— Anti-inflammatories
— Maybe immunosuppressives

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12
Q

Type 4 Allergic Response

What types of cells mediated? (3)

Does it involve any anti-bodies?

What types of symptoms? Examples?? (3)

Treatment: (2)
What types of meds classes?

A

Mediated by:
-T lymphocyte
-Monocyte
-macrophage

Does NOT involve antibodies

Cutaneous symptoms most common
Examples:
* Contact dermatitis
* Tuberculosis
* Stevens-Johnson syndrome (ASA/Tylenol)

Treatment:
— Anti-inflammatories
— Immuosuppressives

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13
Q

Hypersensitivity:

What type of response?

Prior sensitization?
Examples?

Response to what common drugs? (3)

A

-Causes altered T-cell and antibody response

-Requires prior sensitization to foreign antigen
–>Grass, latex, gluten, nuts,

Most common: drugs
–>NSAIDS, antibiotics, PPI’s

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14
Q

Complements

Role of immune cells: innate vs adaptive

How many plasma and cell surface proteins? Most produced in the ____.

Activated by ____ or ____ pathways

A

Both innate and adaptive

-Augments phagocytes and antibodies
-Marks pathogens for permanent destruction

Over 30 plasma and cell surface proteins –>Most elements produced in LIVER

—LIVER FAILURE = WORSE IMMUNE SYSTEM

Activated by C1 or alternately C3

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15
Q

Anaphylaxis

Occus within ____ mins of exposure

Symptoms?? <3 and resp?

Risk factors?? (4)

A

5-10 mins exposure

—-Systemic vasodilation
—-Hypotension
—-Extravasation of protein& fluid
—-Bronchospasm
—-Untreated…PEA

  1. Longer duration of anesthesia
  2. Females (Not in teen years)
  3. Multiple past surgeries
  4. Presence of other allergic conditions (ex: Asthma, Type 2/3)
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16
Q

Bi phasic anaphylaxis?

occurs in % pt?
occurs in ___ hours later?

Risk factors (2):

A

“Biphasic” anaphylaxis
-Occurs in 4-5% of patients
Secondary anaphylactic episode
-Occurs following an asymptomatic period

—Without second exposure
—Occurs 8-72 hours later
—
Risk factors
-Severe initial response
-Initial response required multi doses of epi

17
Q

Diagnosis of Anaphylaxis:

Plasma tryptase concentration
-Within__ hrs
-To check for what?

Plasma histamine concentration
-to get a baseline within ___ mins?

-What kind of testing?
-How long to test after rx?

A

¢ Compromised by
— Communication issues
— Covered by surgical drapes

Plasma tryptase concentration
—-1-2 hours
—-Verifies mast cell activation & release

Plasma histamine concentration
-Baseline within 60 minutes of treatment

Skin testing
— -6 weeks after reaction
— -Wheal and flare response

18
Q

Primary Treatment for anaphylaxis?
–> Epi doses for adult
–> Epi doses for peds?
–> Backup?

Fluid Therapy
Crystalloid dose:
Colloid dose:

Secondary Treatment for anaphylaxis? What types of meds?

A

Primary:
1.) STOP drugs, blood, colloids
2.) 100% O2
3.) Epi
Adult: 10mcg-1mg IVP q 1-2 mins
Peds: 1-10 mcg/kg IV q 1-2 mins

Vasopression/Methylene Blue
-use if resistent to epi
-Inhibits NO production

Fluid Therapy:
-Crystalloid dose: NS 10-25 ml/kg over 20 mins PRN

-Colloid dose: 10 ml/kg over 20 mins PRN

Secondary Treatment:
-Blood sample/ allergy testing
-Bronchodilators
-Antihistamines
-Corticosteroids

19
Q

Secondary Treatment for anaphylasis:

Diphenhydramine dose:
Ranitidine dose:

ADULT
Hydrocortisone dose: ___ mg
OR
Methylpredinosolone dose: ____ mg

PEDS
Hydrocortisone dose: ___ mg
OR
Methylpredinosolone dose: ___ mg/kg

A

Diphenhydramine dose: 0.5-1 mg/kg IV
Ranitidine dose: 50 mgIV

ADULT
Hydrocortisone: 250 mg IV
OR
Methylpredinosolone:80 mg IV

PEDS
Hydrocortison: 50-100 mg IV
Methylpredinosolone: : 2 mg/kg IV

20
Q

EPINEPHRINE

How does it work??

Alpha1:
Beta1:
Beta2:

A

-Decreases degranulation of mast cells and basophils
-↓ effect of degranulation….vasodilation

-Alpha1: supports BP
-Beta 1: inotropic and chronotropic effects
-Beta 2: bronchodilation

21
Q

CAUSES IN ANGIOEDEMA

Hereditary Angio-edema
Deficient in: ______
Causes:
Excess in: _____ (causes?)
Symptoms??

Acquired Angio-edema
What meds cause?
Degradation of: ____
L> Symptoms

What if the patient is itching???

A

C1 esterase inhibitor deficiency/dysfunction
— Menses (period)
— oral-contraceptives
— trauma
— infection
— stress

Excessive production of bradykinin
—-Usually limited by C1 inhibiting kallikrein and factor XIIa

-Laryngeal swelling, potent vasodilator
—-Not responsive to antihistamines
Involves legs, hands, face, upper respiratory tract

Acquired
–> ACE INHIBITORS (responsible for degradation of bradykinin
–> L> Lip, tongue, face swelling
**NO urticaria and itching –> Itching = anaphylactic

22
Q

Treatment for Angio-edema (3)
TYPE ___ SENSITIVITY

Airway maintenance:

DRUGS?

A

Airway maintenance
— -Tracheal intubation/Tracheostomy
—
Drugs
-FFP
-C1 inhibitor concentrate

-Epinephrine
-Antihistamines, glucocorticoids? (wont really work for angioedema)

23
Q

Specific Immune Responses

Transfusion reactions Rx to:

Transplant rejection Rx to:
—
Graves disease causes:
—
Multiple sclerosis causes what:
(destroys ___)
—
Rheumatoid arthritis
(abnormal production of: )
—
SLE

A

Transfusion Rx:
-Response to surface antigen on donor RBC
— A, B, and Rh

Transplant rejction:
-Response to antigens on donor organ
-Due to preexisting antibodies
-Acute or chronic

Graves Disease
-Most common cause of hyperthyroidism
-Caused by autoantibodies to the TSH receptor

Multiple sclerosis:
-Immune mediated inflammation
-Destroys myelin and underlying nerve fibers

Rheumatoid arthritis
-Abnormal production of proinflammatory factors
-Infection thought to play a role

SLE
-Autoimmune, inflammatory
Antibodies against RBC, lymphocytes nucleic acids, platelets, coagulation proteins
Affects multiple organ systems

24
Q

HIV

One of the most common forms of acquired immune deficiency

How does HIV work?
Destroys ____ (3) cells

How to diagnosis?
CD4/ helper T Lymphocytes: <_____
How long after infection?

A

-The virus (HIV) thru reverse transcription makes a double helix DNA with all viral genetic material

-Can change amino acid sequence; new version not recognized

Destroys monocytes, macrophages, Tcells

Diagnosis
-ELISA: 4-8 weeks after infection
-Viral load
-CD4/helper T lymphocytes <200,000
-HAART agent sensitivity

25
Q

HIV Seroconversion
happens ___ weeks after inoculation?

What symptoms?

What symptoms after AIDS? (2)

A

2-3 weeks after inoculation
Flu like symptoms
— Fever
— Fatigue
— Night sweats
— Pharyngitis
— Myalgias
— Arthralgias

AIDS
-Weight loss
-Failure to thrive

26
Q

Scleroderma

“Systemic Scleoreosis”

whos at risk?

Characterized by:
-Vascular
-Skin/viscera

LABS?

A

Characterized by:
-Inflammation
-Vascular sclerosis
-Fibrosis of skin and viscera
-Onset 20-40, mostly women
-no cure
-Localized, limited, diffuse……

LABS?
¢ ECG
¢ BUN/Creatinine
¢ CBC/Platelets
¢ CXR/PFT’s

26
Q

Scleoroderma symptoms:

Mobility:
GI:
Cardiac:
Resp:

A

¢ Decreasing mobility of fingers
¢ Facial pain
¢ Raynaud’s

¢ Hypo-motility of GI tract
¢ LES tone decreased

Cardiac dysrhythmias/conduction abnormalities

¢ Pulmonary fibrosis
¢ Renal artery stenosis

27
Q

Anesthesia implications of scleroderma

A

-Organ system dysfunction
-Arterial catheter concerns
— Continue preop calcium channel blockers –> to help w/ vasoconstriction

Contracted intravascular volume—theyre gonna be DRY

AIRWAY
¢ Aspiration risk
¢ Limited neck mobility/Pulmonary compliance

27
Q

Anesthesia Assessment:

Cardiac:
Neuro:
Pulmonary:
Endocrine/Hematologic:
Renal:

A

Cardiovascular
— Abnormal EKG
— LV dilation
— Pulmonary hypertension
— MI
— Pericardial effusions (25%)

Neurological
— Dementia
— Increased ICP
— Autonomic nervous dysfunction
— Peripheral neuropathy (35%)

Pulmonary
— Respiratory failure
— Pneumothorax
— COPD

Endocrine/Hematologic
— Adrenal insufficiency
— Glucose intolerance
— Anemia
— Bone marrow suppression
— Thrombocytopenia

Renal
— ATN
— ESRD

28
Q

Anesthesia affects on the immune system

Inhalation agents –> (3)
Sevo affect on renal cells?

Induction –>
Midazolam= decreases?
Ketamine= depresses?
Propofol = decrease? promotes?

Opioids –> suppress?

NSAIDS–> inhibs?

A

Inhalation agents
-Suppress NK cells, induce apoptosis of Tcells
-Impair phagocytes
-Unclear impact on tumor cells
¢ Sevo stimulates renal cell; inhibits non-small cell
¢ Cancer? Maybe not use VA and use TIVA

Induction
Midazolam :decreases migration of neutrophils

Ketamine depresses NK cell activity (BAD)

Propofol decreases cytokines, promotes NK cells

Opioids
Suppress NK (natural killer )cells (especially morphine and fentanyl)

NSAIDS
Inhibit prostaglandin synthesis :D

29
Q

Histamine effect on body:

Lungs:
Vascular:
GI:

A

**Histamine triggers:
— Bronchoconstriction
— vascular permeability,
— Vasodilation
— ^Gastric acid

30
Q

Causes for (5)
:C1 esterase inhibitor deficiency/dysfunction

C1= Decrease Bradykinin
C1 inhib deficient: Increase Bradykinin

A

— Menses (period)
— Oral-contraceptives
— Trauma
— Infection
— Stress

Think women and stress

Principles of Anes II (4 decks)

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