Immune Flashcards

1
Q

inflammation is a part of the ________ immune system

A

Inflammation is our innate, or non-specific immunity

It does not result in future immunity to the same organism or injury

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2
Q

Antibody/Cell-mediated immunity is a part of the ________ immune system

A

adaptive

Also referred to as humoral immunity-Major cells in this process are B cells

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3
Q

What are b cells

A

These cells learn to make antibodies to specific antigens

Once they are sensitized to a specific antigen, they are imprinted and will only respond to that antigen

When these antigens come into the body, B cells then produce antibodies which attack the antigens and eliminate the threat

They also split and make memory B cells which allow the body to have a specific immune response to the same antigen if encountered in the future

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4
Q

What are t cells

A

conductors of the immune reaction, responsible for communication (helper t cells)

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5
Q

what are cytokines

A

messengers of the immune system

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6
Q

Describe Type I Hypersensitivity

A

Increased production of IgE antibodies (mast cells filled with histamine) in response to antigen leading to excessive release of histamine

Anaphylaxis
Allergic asthma
Exposure to allergens

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7
Q

Describe Type II Hypersensitivity

A

Body makes autoantibodies against self (Cytotoxic or cytolytic )

Transfusion reactions
Autoimmune hemolytic anemia
Myasthenia gravis

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8
Q

Describe Type III Hypersensitivity

A

Too many antigens attach to a structure, increased the molecular weight of the immune structure and causing it to block up small vessels, leading to ischemia and inflammation

Systemic lupus erythematosus.
Rheumatoid arthritis.

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9
Q

Describe Type IV Hypersensitivity

A

Delayed reactions that occur when T-cells recruit macrophages to attack hours to days after initial exposure.

Poison ivy
Graft rejection
Positive TB skin test
Sarcoidosis

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10
Q

What would the patient’s lab’s look like if they had an autoimmune disease

A

But rheumatoid factor is a specific thing that we can look at that can tell us if there’s an auto-immune disease.

Same for antinuclear antibodies. These are antibodies that attack the nucleus of cells, and so they are commonly seen in auto-immune diseases.

Complement is part of your system that is involved in your immune response. And so when we see the complement levels decrease, That’s means it’s being used. And so that helps us to understand that it’s likely an auto-immune disease.

They can do HLA testing, which a certain markers on the cells that make individuals at higher risk

sed rate, ESR, that will typically be increased when there’s general inflammation. Same for a CRP, C-reactive protein. those being elevated helps us know that the inflammatory response is going on in the body

elevated white count, especially with the innate immune response being involved.

We can see different types of anemias depending on what’s going on.

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11
Q

What drugs bind with part of the inflammatory process in order to decrease inflammatory/immune response

A

Biological Response Modifiers

Rule out TB or MS for these patients-can cause a flare

Etanercept
Infliximab
Adalimumab

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11
Q

What drug blocks certain enzymes in the immune response

A

Disease-Modifying Antirheumatic Drugs (DMARDs)

Methotrexate
Leflunomide
Hydroxychloroquine

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11
Q

How do you treat an autoimmune flare?

A

Glucocorticoids, side effect is immunosupression

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12
Q

What are two common, highly effective immunosuppressants used to treat autoimmune disorders?

A

Azathioprine
Cyclophosphamide

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13
Q

Describe some manifestations of Rheumatoid Arthritis

A

can deposit in pericardium, lungs,

MORNING STIFFNESS/GEL PHENOMENON (WAKE UP STIFF, IMPROVES WITH MOVEMENT)

GENERALLY BILATERAL INFLAMMATION,

FINGER DRIFTS TOWARD ULNA AT REST,

BAKERS CYSTS (INFLAMMATION BEHIND THE KNEE)

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14
Q

Autoimmune disorder patients often take high-doses of NSAIDs for pain management. What medication do they need to take with the NSAID to avoid GI complications?

A

H2 blockers

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15
Q

What labs indicate Rheumatoid Arthritis

A

ANA (Antinuclear Antibody) present
Anti-cyclic citrullinated peptide antibodies (Anti-ccp) present
Rheumatoid factor present
Serum complement LOW
Increased inflammation

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16
Q

What Dx test is best for rheumatoid arthritis

A

Arthrocentesis: where you get most dx info

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17
Q

How do you treat rheumatoid arthritis

A

DMARDs: disrupt enzymes of the autoimmune process
Methotrexate
Leflunomide
Hydroxychloroquine

NSAIDs w/ H2 blockers

Biological Response Modifiers—slows progression of RA
Make sure no TB/MS
Etanercept
Infliximab
Adalimumab

Glucocorticoids: for flares

Immunosuppressants:
Azathioprine
Cyclophosphamide

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18
Q

Rheumatoid arthritis s/s that need to be reported:

A

Fever, infection, pain on inspiration

19
Q

How do you treat a patient in rheumatoid crisis

A

Plasmapheresis: CRISIS TX take blood out, centrifuge to take out Rh factor, put back in

20
Q

How does RA cause Sjogren’s syndrome

A

Disease that causes decreased production of tears and saliva that can occur as a result of RA

21
Q

How does RA cause Felty syndrome

A

disease causes enlarged spleen and neutropenia (decreased WBCs)

22
Q

What is a sign of advanced RA

A

contractures

23
Q

How does RA cause Vasculitis

A

inflammation of the blood vessels normally due to deposition of immune complexes
Can cause infarction and necrosis of tissue

24
Q

Describe some physical manifestations of lupus

A

mouth/nose ulcers
butterfly rash on face
inflammation of small vessels (pericarditis, atherosclerosis)
clotting (stroke, dvt, pulm embolism)
HTN
joint pain without deformity,
photosensitivity (at risk for severe sunburn)
muscular atrophy,
Raynaud’s phenomenon (loss of circulation to fingers r/t late stage of vasculitis in smaller vasculature),
avascular necrosis of the femur,
tendon rupture

25
Q

Describe some lab manifestations of lupus

A

CBC-possible pancytopenia (if bone marrow isn’t getting blood)

Antinuclear antibody (ANA)
Other antibody panels
Rheumatoid factor

C3, C4 (Complement) (low)

CRP, ESR (elevated)

Labs consistent with organ damage (biomarkers)
Renal labs for example

26
Q

What is the first line drug for lupus

A

DMARDs-Hydroxychloroquine

27
Q

What labs should you pay attention to for a patient with lupus

A

monitor heart and renal labs
r/t:
Lupus nephritis
Pericarditis
Pleural effusion

28
Q

What is the Hardening of the skin and organs called

A

systemic sclerosis

Immune system attacks structures (skin, organs) This initiates the inflammatory process and causes the affected area(s) to become hardened (sclerosed) and fibrotic because of an overproduction of collagen

29
Q

Describe the clinical manifestations of systemic sclerosis

A

heart murmurs r/t fibrosis.

difficulty swallowing/GERD from esophageal hardening.

Calcinosis: calcium deposits in skin.

Sclerodactyly: skin tightened in hands and causes finger to lock in, can cause loss of circulation to fingers and become necrotic.

Telangiectasia: red spotting/botox like inability to move face muscles

CREST syndrome

30
Q

What labs do you expect for a patient with systemic sclerosis

A

Anticentromere antibodies
Antibodies to topoisomerase-1

31
Q

How do you treat ranon phenomenon caused by sclerosis

A

Calcium channel blockers

Ensure client does not get too cold, keep core warm, maybe use warm gloves

32
Q

How do you treat systemic sclerosis

A

Inflammation and Immune system control
NSAIDS
Corticosteroids
DMARDs
Immunosuppressants
Calcium channel blockers: to tx ranon phenomenon
ACE inhibitors: r/t kidney issues
H2 receptor antagonists and antacids if suffering GERD symptoms

33
Q

Nutrition for a patient with systemic sclerosis

A

Use antacids 45-60 minutes after each meal
Small, frequent meals
Sit upright for at least 2 hours after eating

34
Q

What body systems does systemic sclerosis affect

A

Fibrosis of myocardium
Fibrosis of lungs
Fibrosis of esophagus
Fibrosis of intestines
Fibrosis of the kidneys

35
Q

What kind of cells does HIV infect

A

CD4+ T-helper cells (help coordinate immune reaction)

36
Q

There is a period of normally ___months before HIV antibodies become detectable in the blood called the window period

A

1-3

This is a dangerous period because the individual can infect others at this time, but does not have serum markers that allow an HIV + identification

37
Q

How do you classify HIV

A

4 stages, the higher the more progressed the disease

Based on CD4 + cell count

38
Q

What type of secondary infection is a tell-tale sign of an HIV infection

A

fungal (pneumonia)
TB
Cytomegalovirus, normally found in infants w/ out immune system
HSV (herpes simplex virus) herpes in brain causes dementia
Kaposi’s sarcoma
Hodgkin’s lymphoma
Cervical cancer (HPV infection)

39
Q

T/F: HIV affects your endocrine system

A

True
Endocrine dysfunction: amenorrhea, gynecomastia
Lower testosterone
Irregular menstrual cycles
Loss of subcutaneous fat

40
Q

What labs would you expect for a HIV patient

A

HIV antibody/antigen testing
CBC
CD4: needs to be high, low mean dysfunctional immune system
Viral load testing: want to be low
Possible LFTs

41
Q

What is the gold standard diagnostic test for HIV

A

Lab testing

42
Q

What is an important thing you should educate your HIV patient on in regards to their antiretroviral medication?

A

ART (antiretroviral therapy)-must take combination of drugs correctly 90% of the time for this to be effective

43
Q

What is PrEP?

A

PrEP: reduce chance of getting HIV if exposed (prophylactic) so before intercourse, before IV drug use

44
Q

What is Immune Reconstitution Inflammatory Syndrome (IRIS)

A

SEPSIS LIKE STATE FOR IMMUNE OVERREACTION TO HIV VIRUS, SIDE EFFECT OF ANTIRETROVIRALS)

45
Q

What is a late Sx of an uncontrolled HIV infection

A

Fluid/Electrolyte imbalance