Module C & D Hematology & Immunology Test III Notes · Page 2 of 50 Hematology Bone Marrow –...
Transcript of 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.