module c & d hematology & immunology test iii notes · page 2 of 50 hematology bone marrow...

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Module

C & D

Hematology & Immunology

Test III Notes

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Hematology

Bone Marrow – Hematopoiesis happens here. Highly vascular. Contains

primitive stem cells that will become RBC, WBC, or Platelet.

Yellow (adipose)

Red (hematopoietic) – in flat, irregular bones

5 – 6 liters of volume

7 – 10% of total body weight

Plasma – has proteins, electrolytes, wastes, nutrients. 90% is water. 10% is

plasma protein, clotting factors, nutrients, enzymes, waste products, gases. If

not allowed to clot, remaining fluid is serum.

Plasma proteins – albumin, globulins, and fibrinogen

Albumin – maintenance of fluid balance in vascular system.

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Globulins – Alpha, Beta, Gamma

o Gamma globulins – immunoglobulins or antibodies

o Alpha and Beta globulins – transport globulins and clotting

factors

o Clotting factors remain inactive in blood until activated by

clotting cascade.

Cellular Components

RBC (erythrocytes) – 175 billion

WBC (leukocytes) (Neutrophils) – 70 billion

Platelets – 175 billion

Stem Cells (pluripotent) – have ability to self-replicate.

Continuous supply of stem cells throughout lifetime

When stimulated, stem cells begin differentiation into either myeloid or

lymphoid stem cells.

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o Lymphoid – differentiate into T or B lymphocytes.

o Myeloid – differentiate into RBC, WBC, platelets

Leukocytes – protect the body from invasion by bacteria and foreign invaders.

WBC (leukocyte count 5,000 – 10,000)

Important for protection through inflammation & immunity.

Five Types:

o Granulocytes (Neutrophils, Eosinophils, Basophils)

o Agranulocytes (Lymphocytes, Monocytes)

Granulocytes – presence of granules in cytoplasm of cell

Basophils – contain heparin, serotonin, histamine. Produce and store

histamine.

Eosinophils – primary function is to engulf antigen – antibody

complexes during allergic reaction. Protection from parasites. Neutralize

histamine.

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Neutrophils – primary function is phagocytosis. Mature neutrophil

“seg.” Immature neutrophil “band” (↑ bands-known as left shift). Arrive

w/in 1 hour and go away fast.

Agranulocytes

Monocytes-potent in phagocytosis, migrate to tissues and become

macrophages (Kupffer cells in liver, also active in spleen, peritoneum,

alveoli, etc).

Lymphocytes – finish maturation in lymph nodes.

o T Cells – derived from thymus gland, cellular immunity. Kill

foreign invaders directly or byway of lymphokines. Responsible

for delayed allergic reactions, rejection of foreign tissue, and

destruction of tumor cells.

o B Cells – humoral immunity. Produce cells that aid in attacking

foreign material. Capable of differentiating into plasma cells.

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Plasma cells then produce antibodies called immunoglobulin

(Ig).

Mnemonic

Never Let Monkeys Eat Bananas

White blood cells (% of all WBCs)

Neutrophils (65%)

Lymphocytes (25%)

Monocytes (6%)

Eosinophils (3%)

Basophils (1%)

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Accessory Organs

Spleen – LUQ, tissues help balance blood cell production w/blood cell

destruction, help w/immunity.

Liver – produce prothrombin and most of clotting factors. Important in formin

Vitamin K in intestine.

Bone Marrow Biopsy

Aspiration and biopsy give information about what blood cells are being

formed in the marrow and can document infection or tumor w/in the

marrow.

In adults, bone marrow is aspirated from iliac crest and less often, the

sternum.

Aspirate – contains small sample of cells, aspirated out w/syringe and needle

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Biopsy – taken from posterior iliac crest, shows architecture of marrow +

cellularity. Bone marrow is cored out w/large bore needle.

Jamshidi Needle

Aseptic Technique used

Local skin anesthesia, bone CANNOT be anesthetized. Aspiration can be

painful.

Iliac crest common site – sterile procedure

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Leukemia

Origin: Blood Stem

Pathology: Overproduction of WBC’s. Leads to anemia, thrombocytopenia, leukopenia, and infection.

Leukemic cells invade spleen, liver, lymph, CNS. Usually die from infection or hemorrhage. Often thought

of as childhood disease, but adults is 10 times that of children.

Risk Factors: Idiopathic, but can be from ionizing radiation, viral infection, chemicals/drugs, bone

marrow hypoplasia, genetic factors, immunologic factors, interaction of many hosts/environmental

factors.

S/S: Excessive bleeding episodes (gums, bruising, rectum, hematuria, epistaxis), Weakness/Fatigue

(H/A’s, lethargy, anorexia, weight loss), Heart murmurs, bruits, Pallor, coolness of skin, Petechiae, Bone

Marrow Failure: (Thrombocytopenia, Anemia), Weight loss, Abdomen tenderness, Bone/Back pain,

Pancytopenia, Dyspnea, ↓ BP, ↓ Cap Refill, ↓ appetite, Massive Wt. Loss, N/V, Dizzy, Hematomas –

Bleeding, ↓ O2, ↑ HR,↓ H/H, ↓ RBC, ↓ HgB, ↓ PLT, Coag normal, WBC may be low, norm, or

increased. High WBC w/many blast cells = poor prognosis.

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Myeloid Stem Cell Lymphoid Stem Cell

AML CML ALL CLL

Fast, Most common Adult type (15 – 39) Hyperplasia of bone

marrow/spleen Uncontrolled

proliferation of myeloblasts

(precursors of granulocytes)

Excessive amounts of mature neoplastic

granulocytes in bone marrow. Philadelphia

Chromosome (genetic abnormality)

Onset after 50 3 phases: chronic, accelerated, blast

Turns into AML

Increased leukocytes (lymphoblast –

immature) proliferate the bone

marrow. Most common in Pediatric

Onset < 15 years

Inactive, but long-lived, mature-

appearing lymphocytes

B Cell involved Lymph node enlargement

noticeable in entire body - ↑ incidence

of infection. Pain, paralysis from

enlarged lymph nodes causing

pressure

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Blood Stem

/ \

Myeloid Stem Cell Lymphoid Stem Cell

/ \ / │ \

AML CML ALL Lymphoblast CLL

/ \

B Cell T Cell

│

Plasma Cells

│

Myeloma

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Leukemia Treatments

Acute Leukemia Chronic Leukemia

Goal = Attain remission Chemotherapy TX regimen

3 Phases: Induction, Consolidation, Maintenance SEE

BELOW

CML – Oral Drug (Gleevec) = Targeted therapy, Prevents

activation of enzyme needed for cell growth; Interferon Alpha –

causes flu-like symptoms CLL – Delayed until symptoms,

does not cure; Standard Chemo

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Phases of Acute Leukemia TX

Induction Consolidation Maintenance

Very intense, attempt to induce or bring remission, seeks to

destroy leukemic cells in tissues, peripheral blood, bone marrow,

can become critically ill Chemo Combo – mainstay TX, 3

purposes = ↓ drug resistance/toxicity, interrupt cell growth at multiple points in cell

cycle Causes major bone marrow

suppression Neutropenic

Other SE: Alopecia; Stomatitis; Cardiac, kidney, and liver toxicity

Starts after remission achieved Can be same drugs as Induction,

but lower dosage or can be different drugs

Intent is to cure Purpose is to eliminate

remaining leukemic cells that may not be evident

Hematopoietic stem cell transplant may be considered

May be prescribed for months to years after successful

induction/consolidation therapies.

Maintain remission Not all leukemias respond to

maintenance therapy

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Leukemia & Infection

Treatment Protection Suspected?

AML – drug therapy best defense Antiviral Drugs (acyclovir) –

watch for oto/nephro toxicity Antifungal Drugs (amphotericin

B, Nizoral, Diflucan) – DX of fungal infection or neutropenic pt. has fever x 7 days after ABT

started ABT/Antibacterial Drugs –

Gentamycin, Tobramycin, PCN, Vancomycin if MRSA

Frequent thorough handwashing Mask for employees w/URI

Strict asepsis w/dsgs. Private Room

No standing H2O in vases, denture cups, or humidifiers

No Raw Foods HEPA filter in room

Fever/Pus indicators of infection CBC monitoring daily

Assess q 8 h: mouth, lungs, urine VS q 4 h: temp of 1° above

baseline = infection until proven otherwise

Set protocol Notify healthcare provider

Blood cultures for bacteria/fungal cultures from

peripheral/central IV catheters Urine specimen

Sputum specimen Wound specimen

IV antibiotics begun after all cultures collected

Skin care: daily bath Turn q 1 h, use skin lubricants

Pulmonary hygiene

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Leukemia: Bone Marrow/Stem Cell Transplant

Goal: Totally eliminate cancer cells from body using combo of chemo with or w/o

total body irradiation, need closely matched donor, need to be in temp remission

after induction therapy

Transplant:

5 phases = Stem cell obtainment, Conditioning regimen, Transplantation,

Engraftment, Post-transplantation recovery

Eradicates patient’s hematopoietic stem cells- either by more chemo and/or

total body irradiation. Lethal for bone marrow.

Cleaning of all leukemic cells

Replaced with those of an HLA-matched = sibling (allogeneic), volunteer,

identical twin (syngeneic), patient’s own stem cells removed before

(autologous)

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Conditioning regimen to “wipe out” bone marrow to prepare to take graft

and rid person of cancer cells (chemo/radiation)

Transplantation – separate from conditioning by 2 days

Engraftment - ? How does it work; 8-12 days for peripheral blood stem cell

transplant; 12-28 days bone marrow stem cell transplant.

Peripheral Blood Stem Cell Harvesting

PBSC’s are stem cells that have been released from bone marrow and

circulate within the blood.

3 Phases: Mobilization – if autologous = chemo/growth factors given to pt., if

allogeneic = growth factors given to ↑ WBC’s and stem cells in peripheral

blood; Pheresis Collection – withdrawal of whole blood, filtering out of cellse

needed, then return plasma to pt. 1-5 pheresis procedures needed to get

enough: cells are frozen/stored until there is enough, monitor for catheter

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clotting, hypocalcemia, VS; Reinfusion – giving pheresed stem cells to patient

by infusion

BMT Prevention of Complications

Pancytopenia expected in beginning

Failure to engraft – die w/o another transplant

Graft-Versus-Host-Disease (GVHD) donated marrow starts to attack host

Veno-occlusive disease – occlusion of liver blood vessels

Nursing Management

SE of all types of stem cell transplant = Fever (give acetaminophen, steroids,

Benadryl before infusion), HTN (antihypertensives, diuretics), Red Urine

(hemolysis of infused cells)

Infection Risk – Neutropenia

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Bleeding Risk – Thrombocytopenia

o Monitor pt. blood levels

o Bleeding precautions

Assessment, Abd girth, body fluids for blood, gentle pt.

handling, No venipuncture/injections, small guage needles,

avoid trauma to mouth, nose, rectum

o Platelet infusions

o Neumega IV

Fatigue

o Nutritional therapy

Small, frequent meals

High protein and carbs

o Blood transfusions: PRBC’s

o Drug Therapy

Epogen/Procrit

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o Energy Management

Altered Nutrition

o Antiemetic meds, meds to soothe stomatitis, high calorie and high

protein, supplements, no raw foods, soft foods, favorite foods, TPN

Hematopoietic Growth Factors

CSF’s (Colony Stimulating Factors) – family of glycoproteins that stimulate

production, maturation, regulation, and activation of cells of hematologic

system

G-CSF – filgrastim (Neupogen) for neutropenia (also pegfilgrastime (Neulasta)

WBC’s

GM-CSF – sargramostim (Leukine, Prokine) for neutrophils, eosinophils,

monocytes

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IL-3 – stimulates neutrophils, monocytes, eosinophils, basophils, and platelets

Erythorpoietin (Epogen, Procrit) – mature RBC’s; long-acting; darbepoetin

(Aranesp) – HgB < 10

Oprelvekin (Neumega) – platelet growth factor

Types of Transfusions

Red blood cell- PRBC- 250 ml bags, compatibility must be checked carefully, ABO antigens, Rh antigens

Platelet-300 ml pooled or 200 ml single donor, Fragile, must be infused immediately, infuse over 15-30

min using a special transfusion set. Fever, chills are not sign of reaction. Vital signs before, 15 minutes

into, and at the end of transfusion.

Plasma-fresh frozen plasma (FFP) infuse immediately after thawing, ABO compatibility required, 200 ml,

infuse over 30-60 min through filter. Replaces clotting factors.

Cryoprecipitate-derived from plasma, clotting factors VIII and XIII, von Willebrand factor, and fibrinogen.

10-15 ml/unit, give IV push over 3 minutes, ABO compatibility required.

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Granulocyte (WBC) – controversial, may cause severe reaction, suspended in 400 ml plasma, give over

45-60 min.

Transfusion Responsibilities

Pretransfusion: Verify prescription, Test donor’s/recipient’s blood for compatibility

(T&CM), Examine blood bag for identification, Check expiration date, Inspect blood

for discoloration, gas bubbles, cloudiness, Identify blood and recipient with two

identifier and numbers!

Provide patient education

Assess vital signs

Begin transfusion slowly, stay with patient first 15 to 30 minutes

Ask patient to report unusual sensations (e.g., chills, shortness of breath, hives, itching) If any

occur STOP TRANSFUSION!

Administer blood product per protocol

Assess for hyperkalemia

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Transfusion Reactions

Febrile transfusion reactions

Hemolytic transfusion reactions - deadly

Allergic transfusion reactions

Bacterial transfusion reactions

Circulatory overload

Transfusion-associated graft-versus-host disease

Autologous Blood Transfusion

Collection and infusion of patient’s own blood

Eliminates compatibility problems; reduces risk for transmission of bloodborne disease

Types: Preoperative, Acute normovolemic hemodilution, Intraoperative autologous

transfusion, Postoperative blood salvage

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The Older Adult & Blood Transfusions

Assess circulatory, kidney, and fluid status before initiating transfusion.

Use no larger than 19 gauge needle.

Try to use blood that is less than 1 week old.

Check vital signs q15minutes throughout the transfusion.

Administer blood slowly taking 2-4 hours for each transfusion.

Avoid concurrent fluid transfusion into any other IV site.

If possible, wait two hours between multiple transfusions.

Watch carefully for transfusion reaction:

Rapid, thready pulse; Hypotension, Increased pallor, cyanosis

Watch carefully for fluid overload:

Rapid bounding pulse, HTN, Swollen superficial veins

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Lymphomas

Definition: Malignant neoplasms originating in the bone marrow and lymphatic

structures, resulting in the proliferation of lymphocytes

Abnormal overgrowth of committed lymphocytes rather than stem cells

Two major types of lymphomas

1.Hodgkin’s disease

2.Non-Hodgkin’s lymphoma (NHL)

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Non-Hodgkin’s Hodgkin’s

Types: 90% B-cells (bone marrow), 10%

T-cells (thymus)

Cause: Unknown, but can be from

autoimmune conditions, immune

suppression (organ transplants, HIV),

Chronic infection (H. Pylori, Epstein Barr),

Gene damage (inherited), Chemical

exposure (pesticides, insecticides, and

dust)

S/S: abdominal cramping, constipation,

pain, anorexia, weight loss, ascites, and

obstruction w/vomiting, can go to CNS =

AMS & Seizures

Interventions: Chemo, Family Support

Patho: insidious onset, enlargement of

cervical, axillary, or inguinal lymph nodes

S/S: unexplained fevers, weight loss, night

sweats, painless firm movable adenopathy

in cervical and supraclavicular region,

spleen pain, B-Symptoms (worse

prognosis) = Fever, Night sweats, Wt. loss,

Alcohol-induced pain, pruritis w/o lesions,

jaundice, mediastinal node involvement

(cough, dyspnea, stridor, dysphagia); 4

stages: Stage 1 & 2 above Diaphragm,

Stage 3 above diaphragm & 4 above/below

diaphragm; DX: + Reed-Sternberg cells on

biopsy

Interventions: Most treatable, radiation,

chemo; 95% of stage ½ cured w/4-6 weeks

of radiation – pediatrics has to use chemo.

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Multiple Myeloma

Patho: Overgrowth of B-lymphocyte plasma cells, invade the bone marrow, develop

into tumors, and destroy bone

Overproduction of aberrant antibodies

Abnormal, excessive amounts of immunoglobulins & cytokines

Changes in immunoglobulin structure

Incidence 4/100,000

Usually two year survival if untreated

Usually develops after 40 years of age (average age 65 years)

Cause: Unknown, but can be from radiation, chemical exposure, HIV

No Cure

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Mnemonic

C-R-A-B

C – Calcium elevated

R – Renal Involvement

A – Anemia

B – Bone Lesions

S/S: Develops slowly & insidiously; Often no symptoms until the disease is advanced.

Fatigue, easy bruising, bone pain; Skeletal pain triggered by movement is the major

manifestation (swiss cheese bones); Loss of bone integrity can lead to pathological

fractures; May see proteins in urine called Bence-Jones protein. Calcium lost from

bones can lead to hypercalcemia with polyuria, anorexia, confusion, seizures, coma &

cardiac problems, High protein levels can lead to renal failure, Also concerned with

anemia, thrombocytopenia & granulocytopenia

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DX: Labs – CBC, CMP, Serum protein levels, UA; Radiology – X-rays, MRI’s,

Myelogram; Bone Marrow Aspiration/Biopsy

TX: Watchful waiting, Radiation, Chemotherapy, Biologic therapy, Stem cell

transplantation, Pain control, Adequate hydration up to 3-4L/ day to keep urine

output 1.5-2L/day, Weight bearing to help bones reabsorb some circulating calcium,

Hyperuricemia treatment with adequate hydration and allopurinol to prevent renal

damage, Radiation, Corticosteroid therapy, Plasmapheresis, Prolonged hemodialysis,

Bleeding precautions, Infection control

Problems from TX:

Myelosuppression

Happens as a result of chemotherapy/radiation

Monitor lab work 24-48 hours prior to each dose of chemo

NADIR . . . The lowest point that blood count falls after each chemo admin.

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*Time varies for each drug & individual

*Nadir determines the next TX.

*Nadir determines risk of infection/bleed

Neutropenia

Decrease in Neutrophil count

Count < 1000 - 1500

Great risk of infection

Normal phagocytic activity impaired (no pus in wounds or on chest xrays)

Low-grade fever is of great significance

Appearance of any ulcers, sore throat, diarrhea, shortness of breath & cough is

significant

Patient’s own flora contribute significantly to life-threatening infections

Etiology - Overgrowth of B-lymphocyte plasma cells, invade the bone

marrow, develop into tumors, and destroy bone, Overproduction of aberrant

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antibodies, Abnormal, excessive amounts of immunoglobulins & cytokines,

Changes in immunoglobulin structure

Teaching - Wash hands, Notify HCP of temperature > 100.4, chills, redness,

cough, sore throat, Avoid crowds and sick persons, Avoid raw foods, Bathe

daily, No gardening or clean up after pets, No potted plants, No raw

fruits/vegetables

Neutropenic Precautions - PPE (formerly known as reverse isolation, now

Neutropenic Precautions), Aseptic techniques, Isolation/private room,

Reporting of problems, Rapid response,

Other - Delegation of duties, ANC < 1500 Possible Precautions,

NEUTROPENIC diet, Check temperature q2-4h, Blood cultures if temperature

spike > 101 degrees, Private room, no visitors, no flowers, Limit health care

workers

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Hemochromatosis

Patho - Disease characterized by increased intestinal iron absorption

Result - increase in tissue iron deposition, Excess iron accumulates in liver, Causes liver

enlargement (hepatomegaly), Eventually cirrhosis

Incidence

Most common genetic disorder among whites (persons of European ancestry)

Affects 1 in 100-500 whites of European ancestry

Genetics - Autosomal recessive disease

Total body iron level may be >50g

May occur secondary to other diseases (immune system) - Thalassemia & Sideroblastosis

May be caused by multiple blood transfusions

S/S: Excess iron accumulates in the liver, Hepatomegaly, Splenomegaly, Heart enlargement,

Skin bronzing, Liver and spleen enlargement, Skin pigment changes, Diabetes, Cardiac

changes, Arthritis, Testicular Atrophy

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DX: Labs - Iron level increased, Total iron binding capacity (TIBC); Exam - Enlarged liver and

spleen, Enlarged cardiac muscle, Skin discolored, Liver biopsy - Increased iron content, iron

deposits

Genetic Testing - Recommended for all first-degree relatives of people with disease

Useful other tests include: inc. serum iron concentration, dec. total-iron binding capacity, inc.

serum ferritin, inc. percentage of transferrin saturation

TX: If untreated, progressive iron deposits can lead to multiple organ failure. NO Iron

Supplements, NO High Iron Foods, NO Alcohol

Goal of TX: Remove excess blood from the body, Remove 500 mL each week for 2-3 years until

iron stores are depleting, Less frequent removal of blood is needed to maintain iron levels

within normal limits, Manage organ involvement, Decrease dietary iron

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Splenomegaly

Patho: When spleen enlarges, its normal filtering & sequestering capacity increases

Often a reduction in number of circulating blood cells

Patient may complain of abdominal discomfort & early satiety

Use CT scan, ultrasound & Tc-colloid liver-spleen scan

Causes: Hereditary, Hemolytic Anemias, Sickle cell disease, Thalassemia

Autoimmune Cytopenias - Acquired hemolytic anemias, Immune thrombocytopenia

Infections and Inflammations - Infectious mononucleosis, Systemic lupus erythematosus, HIV,

Viral hepatitis, Infiltrative Diseases

Acute and chronic leukemia – Lymphomas, Congestion - Cirrhosis of liver, CHF

Splenectomy

Meticulous post-op care with attention to potential hemorrhage which could lead to shock

and abdominal distention, Immunologic deficiencies may develop , IgM levels are reduced,

Have a lifelong risk for infection, Especially at risk for pneumococcus,Risk reduced with

immunization by pneumococcal vaccine (Pneumovax).

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Immune System

WBC (5 – 10,000) Inflammatory NK Killers Allergies

↑ ↑ / \

55 – 70% 5 – 6% 30 – 40% 1 – 2%

Neutrophils Monocytes Lymphocytes Eosinophils Basophils

↓ ↓ │ \ / Segmentals “seniors” Macrophages / \ “Eww Baso Allergies”

Baby Bands Phagocytes B Cells (Humoral) T Cells (cell mediator)

Left Shift Eat Bacteria / │

Severe Infection Plasma Cell / \

CD4 CD8

/ \ \

HIV 1.) In Charge Binds directly to Antigen (+ cyto kill)

2.) Summon B Cells (antibody), NK (Can), Macrophages

3.) Plan for Direct Attack “Thymus” = Final stage of development or Boot Camp. Spleen = Barracks/Graveyard. They store HgB, Platelets.

Lymphatic System/Blood Stream = Highway Patrol.

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Immune Response

Purpose: neutralize, eliminate or destroy internal invading organisms

Major Histocompatibility Complex (MHC) – codes identifying genetic info

Human Leukocyte Antigen (HLA) – personal product code, cellular fingerprint

5 Cardinal Features of Immune System – 1.) Self/not self tolerance -

Discrimination of healthy self cells vs. foreign, cancerous, or infected self-cells (T-cells)

2.) Self-regulation - If needed, can carry out functions w/o other body systems

(nervous system or other controls) 3.) Specificity - Ability to target single specific

antigen or cell 4.) Diversity - Ability to develop indefinite # of responses

5.) Memory -Stores memories throughout the lifespan

Organization of Immune System

Hematopoiesis – bone marrow produces undifferentiated stem cell

Immune System Cell – committed to becoming WBC

Inflammation – Defensive response, short term, non-specific. Does not always mean

infection.

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5 Cardinal Signs of Inflammation (Stage 1) – 1.) Warmth 2.) Redness 3.) Swelling 4.)

Pain 5.) Decreased Function

Macrophages = cause Arteriole dilation, ↑ Blood Flow (warmth/redness), ↑

Hydrostatic Pressure (swelling) which leads to capillary leak (↓ function).

Cell Types (Stage 2 – cellular exudate (pus))

Neutrophils (1,000 – 1,500)– granules inside destroy invaders by

phagocytosis, 1st line defender. Segs – mature, Bands – less mature; life span

12-18 hrs. numerous mature neutrophils released daily. Only 1 episode

phagocytosis possible. # of circulating segs can measure pt’s risk of infection.

More bands than segs = shift to left.

Macrophages (Monocytes) – liver & spleen. Assist to stimulate longer-lasting

immune response. Function: phagocytosis.

Basophils/Eosinophils – Protect mucosal surfaces, many chemical substances

(heparin, histamine, etc.), role against parasitic infections, regulate against

hypersensitivity reactions (allergic reactions).

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Mast Cells – contain histamine, etc. Substances that support immune

response. Similar to basophils.

WBC’s/Leukocytes/Granulocytes – Neutrophils; left shift if increased, if

increased bands.

Lymphocytes – Active in Immune Response; B Cells = produce antibodies, T

Cells = mediate immunologic responses.

o B Cells – originate in bone marrow; mature there or some other place

Activate Humoral Immunity (AMI) In 4 body humors–

bacterial; recognized by helper T cells through antigen

presentation this activates the B cells specific to that antigen.

Divide into 2 cells

Plasma Cells – specific immunoglobulin (antibody) –

activate and secrete antibody.

Memory Cells – stockpile specific clones – stand by

for future activation.

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Specific Immunoglobulins (antibody)

IgG – most common; across placental barrier; passive

immune response

IgA – outside protector – saliva, sweat, etc.

IgM – primary immune response

IgD – elevated in chronic infections

IgE – releasing histamine (type 1 allergy); allergic S/S

o T Cells – Originate in bone marrow, mature in thymus

Cell-Mediated Immunity (CMI) – make direct contact

w/antigen & bind specifically (distinct receptors)

Long Lived; Long term immunity.

Divide to clone/orchestrate other cells.

Critically Important = CD4 – Helper/Inducer. Activates

specific immune response. CD8 – Suppressor. Reduces

humoral response. Cytotoxic/Cytolytic – direct lysis

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Natural Killer Cells – undifferentiated T cells. Spontaneously

react. Effective against cancer.

Types of Immunity – Humoral (Natural, Adaptive, Active, Passive Immunity) = B Cells;

Cell Mediator = T Cells

Natural Immunity – cannot be developed or transferred. Natural feature of

person.

Adaptive Immunity – made or received.

Active Immunity – body takes part

Natural Active Immunity – enters the body w/o human assistance. Most

effective. Longest lasting.

Artificial Active Immunity – vaccination or immunization.

Passive Immunity – in a person’s body but weren’t created there.

Natural Passive Immunity – given to baby

Artificial Passive Immunity – injected

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Terms

Autoimmunity – when self-destruction occurs. Lupus & Rheumatoid Arthritis

Cytokines – chemical messengers

Antigens – proteins capable of stimulating immune response (non-self)

Stages of Acute Infection

Infection – Entry of organism in body

Incubation – time between entry and appearance of symptoms

Prodromal – appearance of vague symptoms like fever

Acute – clinical S/S

Convalescence – organism destroyed

Types of Infection

Primary Acute – relatively short

Nosocomial – develop after admission to hospital

Drug Resistant Nosocomial – include MRSA, ORSA, & VRE

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Opportunistic – organisms normally controlled by immune system

Chronic, Latent, Secondary

Chain of Infection – All must be present: Agent (pathogenic organism), Reservoir

(environment), Portal of Exit (means of escape), Transmission mode, Portal of entry

(means of entry), Host susceptibility (many factors). Change in any one variable

changes entire infectious disease process.

Transmission Based Precautions

Droplet (lg. particles) Airborne (sm. particles) Contact (direct/indirect)

PIMP Pertussis (whooping cough) Influenza Meningitis (contact too) Pneumonia

“Iso Room; mask” Travel 3 ft. or less

MTV MMR (Measles, Mumps, Rubeola) TB Varicella (chicken Pox, C Too) – Contact too

“Iso Room; N95 Mask”

MRS. WEE MRSA Respiratory Infec. Skin Infec. Wound Infec. Enteric (C. Diff) Ebola/eye Infec. (conjunctivitis)

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Hospital-Acquired Infections

2 Types: Endogenous – from client’s own normal flora; Exogenous – from outside

client (hands of workers)

Adult Autoimmune Diseases – body fails to recognize self vs non-self & antibodies

produced to target own tissues (SLE ,Rheumatic fever, rheumatoid arthritis). More

common on females. Can predispose pt. to develop another.

Systemic Lupus Erythematosus

Patho: Autoimmune; Chronic Multisystem Inflammatory Disease; Affects skin, joints,

renal, hematologic, and neurologic systems. Antibody Response R/T to B/T cell

Hyperactivity. Affects women 9:1.

Causes: Idiopathic, but most commonly gentic, hormones, environmental, some

meds.

S/S: Butterfly rash, photosensitivity, vascular lesions, oral/nasopharyngeal ulcers,

alopecia, polyarthralgia, arthritis, Swan-neck fingers, ulnar deviation, tachypnea,

pleurisy, arrhythmias, abd. Pain, esophagitis, ulcers, fever (serious), fatigue, anorexia,

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vasculitis, nephritis, proteinuria, glomerulonephritis, generalized/focal seizures,

peripheral neuropathy, organic brain syndrome (disoriented, memory deficits, psych

symptoms).

Diagnostic Testing – No specific one test. Primarily from pt. hx, PE, and lab findings.

Classified w/SLE if 4 or more criteria present. Serially or simultaneously during any

interval observation. ANA, Anti-Ro (SSA), Anti-La (SSB), Anti-SM (Smith) antibody,

Anti-DNA, RF, Serum protein electrophoresis, CBC, Electrolytes, Renal function,

cardiac/liver enzymes, ESR, Skin biopsy

Interventions – Monitor wt. and I/O daily, VS q 4 h while in hospital, collect 24 hr.

urine, Assess neurological status, explain nature of disease, provide support. Educate

infertility can result from SLE regimen, neonatal LE may occur in infants born to

women w/SLE; counsel against pregnancy in women w/serious SLE. Meds: NSAIDS,

Acetaminophen, Antimalarial drugs, Steroid-sparing drugs, Corticosteroids,

Immunosuppressive drugs, Cyclophosphamide (Cytoxan), and Hydroxychloroquine

(Plaquenil) → Frequent eye exams.

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Allergies

The immune response to an antigen called an allergen that causes a hypersensitive

(excessive) or allergic reaction.

Hypersensitivity or Allergy – Excessive Humoral response to an external stimulus

(antigen or allergen). Overreaction, triggers B-cells.

Classified into 5 types – Type I, II, III, IV, V

o Type I – immediate; most common; caused by increased IgE. IgE

causes release of histamine. Examples: anaphylaxis, allergic, asthma,

allergies like hayfever, latex, bee sting, peanut. ASSESS: LOC, tongue

clicking, runny nose, skin lesions, UO, bronchospasms, etc. DX Tests:

excess eosinophils (>5% of WBC’s), RAST – determines specific

allergen, Nasal smear – excess eosinophils, Serum IgE, Skin Testing.

REMEMBER – IgE leads to release of histamine.

o Type II – Cytotoxic; IgG or IgM – cell bound response (cell getting

killed); antibody reacts w/antigen causing cytolysis or phagocytosis

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against self cells. Examples: hemolytic transfusion reaction (wrong

blood), Goodpasture’s syndrome.

o Type III – Immune Complex – Mediated; IgG, IgM, IgA (systemic) –

antigen-antibody complexes form in the blood and cause

inflammatory reaction. Examples: RA, SLE, glomerulonephritis, &

serum sickness.

o Type IV – Delayed – T lymphocytes (no antibody). Examples: Graft vs.

host reactions, poison ivy, (+), TB skin test, contact dermatitis, local

response to insect stings, & sarcoidosis.

o Type V – Stimulated – Examples: Graves Disease, Myasthenia Gravis

Mneumonic

ACID

A (Type I) = Allergic, C (Type II) = Cytotoxic, I (Type III) = Immune Complex Deposition,

D (Type IV) = Delayed

Drug & Food Allergies - # 1 source of anaphylaxis in children.

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HIV

DX: Window Period – 2 to 4 weeks, can be 3 weeks to 3 years; High Viral Load w/Low

Antibodies(viremia); ARS = Antiretroviral Syndrome; May be HIV +, but it not show up

yet. May be DX’d w/Viral Meningitis or Flu d/t symptoms of fever, sweats, H/A, and

Muscle Aches. Retrovirus – replicates backwards: RNA to DNA instead of DNA to RNA.

Attacks and Destroys the Immune System.

12 Weeks – HIV +; Low Viral Load, High Antibodies

B Cells; Antibody; Lifelong Labels; T Cells mediate a cellular immune response to trap

virus in lymph nodes.

Tests:

#1 – ELISA

o False (-) – Low antibodies (window)

o False (+) – check mothers, check IV Drug users, Check Malaria HX

#2 – Western Blot (Confirmation Test)

o Detect serum HIV Antibodies

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o 2 of 4 “Specific” Antibodies “tags” = + test

#3 – Viral Load Test (Normally done during TX)

o HIV (RNA)

o Body (Antibodies)

o Very Expensive

HIV to AIDS

Compromised: CD4 < 200-499

Severe: CD4 (Normal = 800 – 1,000) is ↓ 200; 1.) Opportunistic Infection, 2.) Viral

Infection (Cytomegalovirus – Herpes), 3.) Kaposis Sarcoma (Raised purplish brown

raised skin lesions – nonpainful/nonpruritic)

Usually takes 10 + years to develop AIDS

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Education

Prevention = Abstinence, Be Faithful, Condoms

Body Fluids = Transmission: Highest = Semen, Blood; Lowest = Vaginal secretions,

Breast milk, saliva, amniotic fluid

3 ways transmitted = 1.) Sexual; 2.) Parenteral (IV Needles); 3.) Perinatal (8-25% risk)

Meds = HAART Therapy; H – Highly; A – Active; A – Anti; R – Retroviral; T – Therapy

Stop Replication, but DOES NOT kill virus

CAUTION – Drug Resistance can occur w/ Missed doses or < than

recommended

Nucleoside Analog Reverse Transcriptase Inhibitors (NRTI’s) – suppresses

viral replication in infected cells by inhibiting activity of reverse transcriptase;

Example: Retrovir. (Dine, Bine, Sine sound + Abacovir and Tenofovir)

Nonnucleoside Reverse Transcriptase Inhibitors (NNRTI’s) – combine

w/Reverse Transcriptase enzyme to block the process needed to convert HIV

RNA into HIV DNA; Example: Viramune, Rescriptor, Sustiva (VIR in the middle)

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Protease Inhibitors – stops the budding process of new HIV infected cells by

interfering with enzyme activity that cuts HIV proteins into proper lengths

needed to allow viable virons to assemble and bud out of the cell membrane

(budding leaves holes in the cell membranes allowing virus to spread).

Example: Viracept, Fortovase, Norvir, etc. (NAVIR sound)

Fusion Inhibitors – blocks fusion of HIV to host cells by blocking ability of

gp41 to fuse with the host cell’s CD4 receptor and prevents entry into cell;

Example: Fuzeon

Entry Inhibitors – blocks the CCR5 receptor on CD4+ T Cells; prevent cellular

infection w/HIV; must test pt. to see if their virus has the CCR5 (rather than

CXCR4 receptor – if not – med will not work; Example: Miraviroc (Selzentry)

Integrase Inhibitors – Prevents infection by blocking HIV integrase; newest

type of med., HIV integrase needed to insert the virus into the host cell, viral

proteins are not made and replication is inhibited; Example: Raltegravir

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(Isentress). (VIR at the end) → except for Abacovir and Tenofoavir which are

NRTI’s.

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