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MedSurg Test 1 Study Guide
Hematology: The study of blood and blood forming tissues including the blood cells
(erythrocytes, leukocytes, and platelets), the bone marrow, the spleen, and the lymph
system.
Bone marrow is the home of stem cells from which the blood cells are formed.
The best place for a bone marrow aspirate is the iliac crest. After a bone
marrow aspirate we want to lay the patient on the affected side and apply pressure
for 5-10 minutes after procedure. Bleeding is our priority after a bone marrow
aspiration!
Hematopoiesis- blood cell production that occurs within bone marrow of the flat
and irregular bones.
Stem-cell- an immature blood cell that is able to self-renew and differentiate into
hematopoietic progenitor cells
Plasma- 55% of the blood; composed of water, proteins, electrolytes, gases,
nutrients, and waste.
Serum- blood plasma minus the clotting factors!
Erythropoiesis- RBC production that is regulated by cellular oxygen requirements
and general metabolic activity. This is stimulated by hypoxia and regulated by
erythropoietin, which is grown and released by the kidney. (Critical thinking: this
is why kidney problems lead to anemia, due to decreased erythropoietin. Also
when there is a high demand for O2 their will be increased production of RBCs.)
Essential nutrients required for erythropoiesis: protein, iron, folic acid,
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cobalamine, riboflavin, pyridoxine, pantothenic acid, niacin, ascorbic acid, and
vitamin e. (Deficiencies of some of these lead to anemia!)
Hemolysis- the destruction of RBC’s which occurs by monocytes and
macrophages.
Lab Values to Know
RBC: 4-6 (Think red is a little boy’s favorite color. Little boys are 4-6 years old)
Hgb: 12-17 this is the oxygen binding capacity of the cell. (This is the age most teenagers want
to travel the globe= hemo-globe-in)
Hematocrit: 35-50: This is the percentage of RBC’s in relationship to the total blood volume.
(This is a critical age in a persons life to have kids and live life)
WBC: 5,000-10,000 (This is the amount of $$ I make each year with a part time job)
Platelets: 150,000- 400,000 (What I would love my income to be!!)
<50,000 low critical value (I would not want less than 50,000 a year!)
>1 million high critical value (It would be unrealistic to make more than 1 million $
$!)
MCV- volume or size of single RBC (Normal value: 80-100- the way I remember that is that
some patients from 80-100 have either a very large size or a very small size) (Critical thinking:
if RBC production is decreased, the RBC’s will be larger to compensate, this is termed
macrocytic. If RBC production is sufficient, they will be smaller because there are plenty of
them. When we get to anemia remember that macrocytic anemia is associated with decreased
RBC production!!)
MCH- the weight of the hemoglobin within an RBC (Normal: 27-34- the way I remember is
because this is the best age to have kids, and during pregnancy you gain weight)
MCHC- the % of hemoglobin within a single cell (Normal: 32-36%- the way I remember is
because if you are a generous person you will leave that percent tip at a restaurant.)
What is your best representative of blood volume loss?? Hematocrit! We always
get an H&H if our patient is bleeding.
Luekocytes: Remember WBC count is between 5,000 and 10,000 (What I make in
a year with a part time job)! Neutrophils are WBC’s that are involved in the early
phase of inflammation. A normal level is 2,500-8,000 (This is the amount of
money that I pay each semester to go to LU). When WBC’s drop below 4,000 or
neutrophils drop below 1,000 my patient is immunologically compromised!!
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For immunologically compromised patients that meet the criteria above, we often
place them on neutropenic precautions: (The priority with these patients is
prevention of infection!)
oFrequent hand washing (staff and ALL visitors)
oPrivate room (we don’t want them with an infected patient! Put on isolation
precautions! If hospital is overcrowded put with an ortho patient or someone
who will not spread an infection! )
oLimit/screen visitors- children and sick people are a bad idea!!
oRemove fresh flowers and plants from the room- you don’t know what
bacteria may be present. Same for fresh fruits or veggies. They may only have
produce from nutritionist.
oFrequently monitor temp and look for s/s of infection!
Shift to the left: A high WBC count with lots of immature counts. May be result
of rapid reproduction during an infection. It got the term “shift to the left” because
the usual lab procedure is to report WBC’s in order of maturity with the less
mature types written on the left of the repot. It is possible for the WBC to remain
essentially normal despite a marked change in one type of leukocyte.
Shift to the right: Low WBC count usually caused by a disease or cancer.
Hemostasis- The bodies attempt to stop bleeding
There are 4 components of the normal clotting mechanism:
1) Vascular response: vasoconstriction (lasts about 20-30 minutes)
2) Platelet plug formation: agglutination or aggregation
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3) The development of the fibrin plug on the platelet plug by the plasma clotting
factors
4) The ultimate lysis of the clot
Thrombocytes: Initiate the clotting process. They work as “plugs” to close any
openings in the capillary wall. They originate from stem-cells which mature into
megakaryocytes, which fragment into platelets. This is regulated by
thrombopoetien, which is a growth factor that stimulates the bone marrow.
Thrombocytosis: Excessive amount of platelets, can occur with inflammation and
some malignant disorders.
Thrombocytopenia: Too few platelets resulting in hemorrhaging or bleeding.
The formation of a clot requires the activation of thrombin which then activites
fibrin. This activation requires several additional factors: (Important to know in
relation to hemophilia!)
Disseminated intravascular coagulation (DIC): A serious bleeding and thrombotic
disorder that results from abnormally initiated and accelerated clotting, decreased
clotting factors and platelets occur in the rest of the blood as a result, leading to
uncontrollable hemorrhage. This is always caused by an underlying condition!
You want to treat the underlying condition and stabilize both the bleeding and
clotting. (Also a term mentioned several times in OB!)
oVon Willibran Factor: forms an adhesive bridge between the platelets and
vascular subendothelial structures. It acts as a carrier for factor VIII.
oFactor VIII- “Antihemophillic factor” - works with factor IX and calcium to
activate factor X.
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oFactor IX (Christmas factor): together with factor VIII activates factor X.
If our patients platelet count falls below 50,000 (the critical value) they are at risk
for bleeding out!!
Functions of the Spleen: Filters out old RBC’s and takes the hemoglobin from
hemolysis and catobolizes the iron. Contains lots of lymphocytes and
monocytes, as well as storing immunoglobulins. The spleen sequesters 30% of
the platelets.
So if out patient has a splenectomy what is our priority?? INFECTION (the body
just lost lots of lymphocytes and monocytes!!) Monitor the patients temperature.
The immune response is now our main priority! Think neutropenic precautions!!
But what about the platelet count, will the patient bleed out??? Well the platelet
count actually goes up a bit because the spleen is know longer calling them.
Bleeding is not our concern!
When the patient comes into the hospital, what should we assess for?? Past
medical history, current medications, previous surgeries, family history,
nutritional history, signs of bleeding, activity level, reproductive pattern, and lab
values. Lots of hematologic problems have a strong genetic link such as sickle-
cell anemia, hemophilia, thalassemia, and hemochromatosis. When asking about
medications be sure to ask about herbal therapy as it can interfere with clotting!
Petachiae, ecchymosis, and spider nevus may indicate bleeding disorders.
Erythrocyte sedimentation rate: The rate at which RBC’s settle in saline over a
specified period. This is a nonspecific measure of inflammatory conditions- the
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more inflammation that is present the longer it will take for them to settle. Normal
range (Male- 15, Female-20)
Iron and ferritin (major iron storage protein) increase/decrease together, while
total iron binding capacity (TIBC) and transferrin (largest protein that binds with
iron) increase/decrease together. Think of it as a dance.
PT- 11-16 seconds, measures the effectiveness of warfarin/ INR- 2-3 sec more
commonly used!
PTT- 25-35 seconds- measures the effectiveness of heparin
Hemophilia is a genetic condition more common in med. Three types to know:
1) A type Classic hemophilia results from factor VIII deficiency
2) B type Christmas disease- results from factor IX deficiency. (Only treated
with factor IX!)
3) Von Williebrand disease- deficiency of Von Willebrand coagulation protein
What is our biggest concern with a hemophiliac?? BRAIN BLEED!!! We are also
concerned with joint bleeds. We want to rest joints, use ice packs, no aspirin, use
ROM to mobilize joints as soon as bleeding stops. Assess for airway obstruction from
neck hemorrhage.
Cryoprecipitate- retrieved from blood plasma. Contains factor VIII and fibrinogen,
frozen, slowly thawed, and administered. Used for minor bleeds for 72 hours, or
surgery for 10-14 days. Factors are short lived so patients will need continuous
infusion.
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DDAVP- a synthetic analog of vasopressin, may be used to stimulate an increase in
factor VIII and von williebrand factor thus increasing their concentration. Used to
treat minor bleeding for 72 hours.
Anemia: Deficiency in the # of erythrocytes, the quantity of Hgb, and/or the volume
of packed RBC’s. Many diverse causes!
oIron deficiency anemia- This is a microcytic, hypochromic anemia that is
caused by poor diets, alcoholism, poor absorption, GI bleed, and
menstruation. S/S includes pallor, glossitis, burning of the tongue, chellitis,
headache, paresthesia. Patient will take a little green pill PO that smells bad,
educate patients not to tae this with food and to be careful because this may
stain the teeth! Diet changes such as red meats, leafy greens, whole grains,
enriched cereals, and potatoes may be encouraged.
oThalassemia: This is an unusual genetic condition that results in empty
RBC’s, which are microcytic, and hypochromic. It is caused by an inadequate
production of hemoglobin. S/S include pallor, thickening of the cranium and
maxillary cavity, hyperplasia of the bone marrow, growth, retardation,
splenomegaly, and ultimately death. Look out for jaundice d/t the hemolysis
of RBC’s, which increases the serum bilirubin. Goal is to keep hemoglobin at
a therapeutic level of at least 10 with palliative transfusions and IV desferal or
ferriprox.
oCobalamin (B12) Deficiency (also called pernicious anemia): This is a
macrocytic, normochromic anemia that occurs because of an insufficient
amount of intrinsic factor (pernicious anemia) or a deficiency of B12
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(cobalamine deficiency anemia) in the diet. Intrinsic factor is in the gut and
helps absorb B12 so these are very closely related, but not the exact same.
Chronic alcoholism, GI surgery, Chrohn’s disease, Ileitis, and Diverticuli are
the most common causes. S/S are very similar to an iron deficiency anemia,
but also include neurological symptoms, paraesthesia, ataxia, weakness,
confusion, or dementia. This is treated with a vit B12 IM injections once a day
for 2 weeks and then every week until HCT is normal, and then months. The
injections allow it to go straight into the blood since there is an absorption
issue! For patients who are just B12 deficient it may benefit them to add red
meats, eggs, enriched grain products, milk, dairy foods, and fish. Vegans and
vegetarians are at a high risk for this because of their lack of dietary B12. Be
sure to ask your patients about nutrition!
oFolic Acid Deficiency- Macrocytic, normochromic anemia caused by poor
diet, malabsorption disorders, oral contraceptive use, patient’s on antiseizure
drugs, alcohol abuse, anorexia, and hemodialysis patients. This is most
commonly found in pregnant women! These patients will need to take a little
yellow pill PO to replace folic acid. This pill can NOT be crushed. Must use a
liquid form if patient cant swallow. In the diet they can increase leafy greens,
liver, meat, fish, legumes, whole grains, OJ, and peanuts.
oAnemia of Chronic Disease: normocytic, normochromic anemia caused by
an underlying inflammatory, autoimmune, infectious, or malignant disease.
Treat underlying disease and get blood products on board! This is very
common in chemotherapy patients.
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oAplastic Anemia: LIFE THREATENING! Stem cell disorder where there is
no production of stem cells and results in pancytopenia (a deficiency of ALL
blood cells- patient will be at risk for poor oxygenation, infections, and
bleeding out). These patients need lots of blood until the problem is resolved!
Also place them on neutropenic precautions.
oSickle cell anemia: This is a genetic mutation. With an increased O2 demand
the cells take on a sickle shape and clump, this causes lots of pain for these
patients and leads to vascular occlusion! A vascular occlusion left untreated
will lead to tissue DEATH. These people cant handle things that increase O2
demand such as disease, high altitudes, dehydration, caffeine, and activity. In
the case of a crisis O2 is the priority followed by narcotics.
oHint: An anemia is macrocytic (large RBC) if it is the result of a decreased
factor in RBC production such as folic acid or B12, because the body is not
producing enough RBC’s so it must compensate by producing larger RBC’s.
Conditions such as Thalassemia or iron deficiency anemia are microcytic
(small RBC) because they have adequate quantity production, but the quality
of the blood cells is inadequate so they produce more and more deficient
blood cells to try to compensate.
When a patient has anemia there are many compensatory mechanisms. There is a shift
of oxygen from the tissues to the blood, and the blood is shunted away from the
tissues that don’t need it as much (this is similar to the stress response!) We see an
increased cardiac output, heart rate, and stroke volume (this is too compensate, since
there is not as much oxygen rich blood the body must circulate the blood more
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quickly to meet the oxygen demand. We want to get those previously mentioned labs
to diagnose anemia!
Cancer: a group of more than 200 diseases characterized by uncontrolled and
unregulated growth of cells. This is an “orderly process” that occurs over time and has
several stages.
Differentiation: how well the cell matures. This has nothing to do with appearance
and DNA. Poorly differentiated= immature, good differentiation= mature! If a
questions says “differentiation” look for the words mature/immature in the answer!
Appearance: how the cell looks.
How does cancer develop?
1) Initiation phase: Mutation occurs either inherited or acquired. The host is exposed
through a carcinogen that is environmental, physical, or biological. This is
nonreversible and once this occurs it cannot be undone!! “placing the key in the
lock”
2) Promotion phase: characterized by reversible proliferation of the cell. “turning on the
ignition”. This includes a latent phase which occurs from mutation until actial clinical
evidence of disease. The length of the latent phase is based on cellular division rate
and environmental factors. Lifestyle changes can be effective in preventing
promotion. When the cell becomes detectable, around 1 cm (referred to as the critical
mass).
Immunological escape: mutated cells take on the appearance of normal cells to
escape the immune response.
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Oncofetal antigens- cells coded themselves with certain proteins to hide them
from natural killer cells. The are markers to track tumor presence and
development.
3) Progression phase: characterized by an increased growth rate, increased invasiveness,
and metastasis (where it spreads from one organ to another). This is usually spread
via blood or lymph and can be spread by physical manipulation.
Histologic Grading of Tumors:
Grade 1: Well differentiated, slightly different from normal cells in appearance.
Grade 2: Moderately differentiated, moderate dysplasia
Grade 3: Poorly differentiated severe dysplasia, very abnormal
Grade 4: Undifferentiated anaplasia, immature, primitive cells, difficult to
determine the cells of origin, most difficult to treat, and poorest response rate.
Clinical Staging: This is different than grading, it represents how much the tumor has
grown
Stage O: Cancer is in situ (self contained entity)
Stage 1: Tumor limited to tissue of origin
Stage 2: Limited local spread
Stage 3: Extensive local and reginal spread
Stage 4: Metastasis
Tumor Nodes Metastasis Classification > Be able to read a description and classify!!
What are the primary goals of cancer treatment?
Cure the cancer- get rid of it.
Control- shrink or remove as much as we can.
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Palliative care- there is nothing we can do but we make what life the patient has left
enjoyable.
We always do chemotherapy through a central line and monitor the IV site for
extravasations. We will discontinue for swelling.
Care of the radiation patient (and teaching points for them!)
Gently cleanse skin with mild soap, tepid water, a soft cloth, and gentle patting
motion. Rinse thoroughly and pat dry.
Apply non medicated, non perfumed lotion or cream to moisturize
Rinse the area w/saline solution
Expose to air as much as possible
Wear lose clothing- light weight/cotton
Use gentle detergents for laundry
Avoid direct sun exposure
Avoid extreme temperatures: hot/cold
No irritants: perfumes, adhesives, razors
We are concerned with nausea and vomiting with both chemo and radiation: give
antiemetics!
Bone marrow suppression may lead to immunosuppression so place patients on
neutropenic precautions.
Harvested marrow is transfused into the recipient
Leukemia: The general term used to describe a group of malignant disorders affecting
the blood and blood-forming tissues of the bone marrow and the spleen. It results in an
accumulation of dysfunctional cells because of loss of regulation in cell division.
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TYPES OF LEUKEMIA: AML (found in 60-70 year olds, sounds like “AMF” and the
elderly bowl together), ALL (most common in ALL the little children), CML (Common
in Middle-age Lads/Ladies- this can change to AML during a blast crisis- think they can
get old and start to bowl!), and CLL (more common in men 50-70 years old- think of C.
“L”. Lewis). There may be mixed presentations of all of these.
Chronic is characterized by involving more mature forms of WBS and having a
more gradual development
Acute is characterized by the proliferation of immature cells. The become
defective past the myeloblasts or the lymphohoblasts stage so that the blood does
not have mature cells.
Lymphomas: Cancer originating in the bone marrow and lymphatic system resulting in
the proliferation of lymphocytes: Know which one is curable and which one spreads!
Hodgkin’s: a malignant condition characterized by the proliferation of
giant, multinucleated cells called Reed-Sternberg cells in the lymph
nodes. This is very treatable and has a good prognosis!!
Non-Hodgkin’s: (Think “non” Hodgkin’s means “not” good!)
Heterogeneous group of malignant neoplasms (means there are multiple
presentations of varying cancer cells). No Reed-Sternberg cells. This can
metastasize. Poor prognosis for these patients.
Lymph Node Biopsy: This is done to assess the progress of a tumor. Needle biopsy
ONLY indicates that the site aspirated does or does not have cancer cells, may need to
check multiple nodes for accurate result. Hold pressure on the area to avoid excessive
bleeding after procedure and observe for infection!
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Multiple Myeloma: “Ow!! My large bones hurt!!” This is a plasma cell cancer that
invades the marrow and destroys bone. Twice as common in men than in women. S/S
generally only present when the disease has progressed and most commonly are pain in
ribs, spine, and pelvis. Ultimately the bone is getting decalcified which leads to there
being lots of calcium in the blood stream! HYDRATION IS KEY!! This decreases the
viscosity of calcium in the blood stream. We want to see a urinary output of 1.5-2 liters
per day. This patient is on fracture precautions, which means that they walk frequently
with assistance
Immunology
Immunity is an organized series of actions by the body in order to protect itself
against a pathological organism resulting in destruction or neutralization of the
organism
oAlso a state of responsiveness to foreign substances such as microorganisms
and tumor proteins
oFunctions of the Immune System include
Homeostasis: excretion of by products; maintain balance w/i body
Defense: protection (NK cells, CD8 T cells, phagocytes)
Surveillance: finding cancer cells or invading antigens w/i the body
oImmunity follows this progression: Inflammatory Response (general) to
Cytokine Response (determines cellular or humoral) to Immune Response
(Cellular or Humoral action)
Foreign Substances/Antigens (Problem Makers)
oBacteria, Virus, Fungi, Prions (parts/pieces of disease; chronic), Parasites
Haptens vs. Antigens
Haptens are very small particles, but combine w/ substances to
form an antigen in the body (ex. pt. is given penicillin,
normally would be okay but if they have haptens for penicillin
then their body will have an allergic reaction to the antibiotic
b/c the haptens will bind to penicillin in the body and create an
antigen)
Properties of Immune Response
oSpecificity: when foreign substance enters body, cellular changes occur; form
antibodies on lymphocytes
oMemory: allows for quicker response to antigen from subsequent exposure
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oSelf-recognition: Immune system’s ability to recognize self vs. non-self; if
body unable to recognize self then results in antibodies against self and tissue
destruction
oSelf-limitation: once antigen is removed the response decr. to prevent damage
to body’s own cells
oSpecialization: different organisms and foreign material are attacked in the
correct way to stop them (refers to cell & humoral mediated immunity; both
have specific jobs)
Cells Involved w/ Immune System (Major players)
oMononuclear Phagocytes
oLymphocytes
B lymphocytes: humoral immunity & originate from bursa cells in
bones; produce antibodies/immunoglobulins
T lymphocytes: cell mediated immunity & originate from thymus;
responsible for destroying invading pathogens (particularly fungi,
virus, cancer cells)
T cytotoxic cells CD8: inject toxin upon coming into contact
w/ marked pathogen
Helper T cells CD4: sensitize CD8 cells to specific pathogen
through cell markers
Natural Killer cells
oDendritic Cells: lookout cell
oCytokines: determines whether humoral or cell mediated responds
Types of Immunity
oInnate (Natural) Immunity
Born with; non-specific (mucous membranes, skin, etc.)
Exists w/o former contact w/ antigen
Involves inflammatory response
Limited in extent of response; anything that is foreign is attacked
oAcquired Immunity: as a person goes through life they acquire immunity to
different pathogens that they encounter
Active Acquired Immunity
Occurs when body RESPONDS to presence of pathologic
organism and produces antibodies against them
Comes following an invasion and results in a sensitized
reaction
When reinvaded by organism response is faster
Can take a while to develop but lasts a long time
Ex. Body produces antibodies b/c of vaccine targeted
immunization (any vaccine is active immunity)
Passive Acquired Immunity
Temporary b/c person RECIEVES antibodies passively instead
of making them
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Is quick but doesn’t last long; temporary because there are no
memory cells specific to infecting antigen
Ex. immunoglobulin from mother to fetus (IgG)
Ex. injection of gamma-globulins (serum antibodies)
Types of Immune Responses: each has unique properties & actions based on the
antigens involved
oHumoral Immunity: comes from bursa cells and responsible for development
of IgM, IgG, IgE, IgA, IgD; slow response
The antigen that invades causes B cells to divide and become plasma
cells (differentiated B cells) which produce antibodies
(immunoglobulins) that travel to the bloodstream to communicate w/
other cells
“Humor”=Latin word for liquid
Primary immune response takes 4-8 days after initial exposure
Secondary exposure response takes 1-3 days; quicker, stronger, longer
lasting (faster b/c of IgG sensitivity to antigen)
Look at Fig. 14-5 pg. 208
oCell-Mediated Immunity: comes from thymus and responsible for killing
invading pathogen
T cells recognize antigen and start immune response (CD8 & CD4)
CD8 injects lethal toxins into antigen to kill them
CD4 sensitized CD8 to antigen
Production of sensitized T lymphocytes to kill and destroy pathologic
organisms
Primary protection against cancer cells (unless immunological escape
occurs), virus infected cells, and fungal infections
Responsible for rejection of transplanted tissue if rejection occurs
Responsible for contact hypersensitivity reaction
Humoral Cellular
Cell Involved B lymphocytes T lymphocytes
Macrophages
Products Antibodies
(Immunoglobulins)
Sensitized T cells
Cytokines
Memory Cells Present Present
Protection Bacteria, Extracellular virus
(attached to outer cell
membrane), Respiratory/ GI
pathogens (have knobs that
are recognized by
immunoglobulins)
Fungus, Intracellular virus
(HIV), Chronic infectious
agents (prions), Tumor cells
(cancer)
Immunological Effects on Aging: related to decr. stem cells at 30yrs & 65yrs; impacts
cellular & humoral immunity
oDecr. immune system function
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oIncr. susceptibility to infection
oIncr. incidence in tumors
oImmunity b/c of vaccines may not be as strong (Still ensure elderly receive
vaccinations)
Altered Immune Response
oUnder Responsive Immune System
Severe infection
Immunodeficiency diseases
Malignancies
oOveracting Immune Response
Hypersensitivity disorders
Allergies
Autoimmune diseases
Over reactive against antigens; no self-limitation
4 classifications
Type I: IgE Mediated
Type II: Cytotoxic Reaction
Type III: Immune-Complex Reaction
Type IV: Delayed Hypersensitivity Reaction
Type I: IgE Mediated Reaction
oChemical mediators are released from mast cells
Histamine, serotonin, leukotriene, eosinophil chemotactic factor,
kinins, bradykinin
oSymptoms assoc. w/
Incr. mucosal secretion, itching, incr. vascular permeability, smooth
muscle contraction
oMild (not an issue): mild vasodilation, mild bronchoconstriction, incr. mucous
production, sneezing (histamine)=allergies
Ragweed attaches to bursa cells, responds by producing lots of IgE
that then attach to mast cells and grab any other ragweed in body. This
activates IgE which causes the mast to release (possibly rupture) and
release cellular mediators that result is symptoms assoc. w/ allergies
oSevere (Deadly): results is severe reaction incr. HR, tachypnea, decr. CO
(anaphylactic reaction)
Medical Emergency b/c shock can occur; proceed in the following way
airway, IV, drugs
Treatment: maintain/secure airway, high flow O2, maintain circulatory
volume, IV access (large bore), epinephrine (1st) then albuterol,
diphenhydramine, corticosteroids
Type II Cytotoxic (IgG or IgM) Reaction
oTarget cells are usually red/white cells and platelets
oCommonly antigens involved are assoc. with mismatched blood (ABO blood
groups), Rh factors (+ve/-ve), and drugs
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oIf pt. is transfused w/ incompatible blood then:
Antibodies immediately coat the foreign RBC’s
RBC’s then agglutinate (clump together)
Life threatening situation
Cellular lysis and possibly renal failure secondary to hemaglobinuria
o1st thing to do is STOP the transfusion
oThen get large bore IV and replace fluids
Type III Immune-Complex Reaction
oOccurs secondary to antigen-antibody complexes
Soluble antigens combine w/ IgG & IgM immunoglobulins and form
complexes that are too small to by removed by the mononuclear
phagocyte system
These complexes then deposit in the vessels & tissues and trigger the
complement system---release of chemotactic factors---inflammation---
destruction of involved tissue
oCan occur locally or systemically and can be immediate or delayed
oClinical manifestations depend on where it occurs and number of complexes
oCommon sites of occurrence are: kidneys, skin, joints, blood vessels, lungs
oSevere type III reactions are assoc. w/ autoimmune disorders (systemic lupus
erythematosus, acute glomerulonephritis, rheumatoid arthritis)
Type IV Delayed Hypersensitivity Reaction (Cell Mediated Immune Response)
oType of IV reaction; usually cell-mediated responses are protective in nature
but tissue damage occurs in delayed hypersensitivity reactions
oDoes not occur the presence of antibodies or complement, but is rather due to
sensitized T cells attacking antigens or releasing cytokines
Some of the released cytokines attract macrophages into the area
The presence of the macrophages and the enzymes released by them
are what cause the tissue damage
oTakes 24-48hrs. to occur
oS&S: dermatitis, hypersensitivity reaction to bacterial-fungal-viral infections,
transplant reactions, some drug sensitivity reactions
oEx. Allergic Contact Dermatitis & Microbial Hypersensitivity Reactions
(Tubercle bacillus)
Collaborative Care of Hypersensitivity Reactions
oAfter allergy is diagnosed
AVOID triggers, allergens (simplest and best solution)
Treat symptoms
If needed desensitization through immunotherapy
oDocument allergies
oImplement drug therapy if needed
Drug Therapy for Chronic Allergies
oAntihistamines
oSympathomimetic/Decongestant Drugs
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Epinephrine (Adrenalin)
Pseudoephedrine (Sudafed)
oCorticosteroids
Most common; given nasally
oTopical Antipruritic Drugs
Calamine Lotion
oMast Cells (Stabilizing Drugs): coats cell to keep them from rupturing; must
take 1-2 weeks before allergy season starts
Cromolyn (Intal, Nasalcrom, Rynacrom)
Nedocromil (Tilade)
Both available as nasal spray or inhalant nebulizer solution
Latex Allergies
oThe longer one uses latex the likelihood of getting latex allergy increases
oTwo types of latex allergies can occur
Type I (Immediate Response)
Occurs w/i minutes
Type IV (Delayed Response)
Contact dermatitis; delayed reaction that can occur b/t 6-48hrs
after exposure to latex
Symptoms for both types include: skin rash, hives, flushing, itching,
nasal-eye-sinus symptoms, asthma, and/or shock
oCommon allergy in nurses b/c of frequent use of latex
oBe sure to ask pt. about latex allergy; protect them from allergic reaction
Autoimmunity (look at slide for examples of autoimmune diseases)
oImmune response attacks itself b/c it cannot tell self from non-self (absence of
self-recognition)
oCause is unknown; classified by organ/system of disease
oTreatment: apheresis- procedure where blood components are separated then 1
of those components are removed (ex. plasmapheresis); monitor for
hypotension and citrate toxicity
Immunodeficiency Disorders (refresh on 1st week immunocompromised precautions)
oOccurs when immune system does not provide adequate protection to the
body
oOne or more immune mechanism is impaired
oPrimary Immunodeficiency Disorder: improperly developed/absent immune
cells
oSecondary Immunodeficiency Disorder: caused by illness/treatment (ex.
chemotherapy or radiation); look at slide for causes of 2nd immunodeficiency
oLeukopenia <4000 or Neutropenia <1000; incr. risk for infection so pt. on
neutropenic precautions
Frequent hand washing (staff and family)
Private Room (isolation precautions)
Limit/Screen Visitors
Nurse 301
Remove Fresh Flowers & plants from room
NO fresh fruits or veggies in diet
Closely monitor temp. and for S&S of infection
Adult Immunizations
o30,000 deaths yr. due to diseases preventable through vaccination
oHow do vaccines work?
Contain small amounts of pathogenic organism (altered so that it
doesn’t cause disease; inert=not alive)
Pt. produces antibodies against that pathogen so that it can recognize it
in the future
Later when pt. is exposed to pathogen the body can get rid of it before
it can advance into disease; therefore pt. protected from disease w/o
actually ever contracting the disease
oPrecaution/Contraindication for Adult Vaccinations
History of anaphylactic reaction (ask and if yes find out to what)
Immunocompromised state (refers to live vaccines)
Patients w/ febrile illness (temp 105<; do not administer vaccine)
Allergy to eggs (some developed in egg cultures so beware of egg
allergy ex. influenza, pneumococcal, meningococcal vaccines)
oAdult Immunizations
Tetanus & Diptheria (booster dose q10yrs.)
Influenza Vaccine (Annually)
Pneumococcal Vaccine (dose w/ 1 time revaccination after 5yrs.)
Hep B (3 doses-1st then 2nd in one-two mon. then 3rd in four-six mon.)
Varicella (recommended for people who don’t demonstrate immunity
to varicella)
oVaccinations to be wary of for prego, women who could become prego, &
immunocompromised pts: Varicella, Zoster, MMR b/c vaccination injects live
virus and this group of people has an increased risk of actually getting sick
Nursing Responsibilities
oAssess for contraindications, history of reaction, allergies to components of
vaccine
oEducate on side effects like soreness at injection site (rub, ice, warmth), low
grade fever (no greater then 101), myalgia, general malaise (1-2 days)
oMonitor for local/systemic reactions, anaphylactic reactions, and
report/document any reactions
oALWAYS WASH HANDS UPON ENTERING AND LEAVING ROOM!!!
Human Immunodeficiency Virus
HIV is not synonymous w/ AIDS b/c AIDS is specific to certain determinants and is
characterized by advanced immunosuppression
Classification of HIV
oType I: prevalent in US, Canada, and Europe (most responsive to drugs)
oType II: more prevalent in 3rd world countries (more resistant to drugs)
Nurse 301
oImportant to know which type dealing w/ to know pt. expected response to
ART
Mode of Transmission
oSexual (anal, oral, vaginal)
oBlood product transmission
oPerinatal transmission (during pregnancy, birth, while breastfeeding)
HIV +ve mom will only give their baby virus ¼ of the time=75% of
babies born to HIV +ve moms are HIV free
oBlood, vaginal secretions, and semen are the only body fluids that transmit
HIV virus
Incidence of HIV
o33mill worldwide
oOver 1mill people in U.S. live w/ HIV
oApprox. 56,000 newly infected each year
oUp from 40,000-50,000 reported in early 2000’s
o70% are men (reason is due to participation in homosexual activity; #1 cause
of HIV transmission)
oDecr. # of HIV cases each year but over-all number of HIV infected people
incr. b/c of more effective therapy=infected people live longer
How does HIV work?
oRetrovirus: has RNA, no DNA therefore needs host cell to replicate and uses
reverse transcriptase to do so
oVirus attaches its gp 120 knobs to human CD4 receptor (T helper cell;
cornerstone of cell mediated response)
Infected CD4 cells last only a few days, usually last 120 days
oVirus then injects RNA which then hijacks CD4 DNA genome and proceeds to
replicate through budding (creation of new viruses; multiple buds come from
1 CD4)
Once inside then what?
oThe RNA makes viral DNA w/ reverse transcriptase
oViral DNA enters the cell’s DNA and alters the cell’s genome
oThe infected immune cell makes HIV viral copies
Phases of HIV
oAcute infection: duration of 1-2 weeks
Develop HIV specific antibodies
Characterized by headache, body ache, diarrhea, pharyngitis,
lymphadenopathy, photophobia, &/or rash; some have meningitis or
Guillian-Barre
Occurs 1-3 weeks after infection
CD4 count drops sharply temporarily and then returns to baseline
Viral load rises quickly
oChronic Infection
Asymptomatic Infection (Latent Phase)
Nurse 301
Duration 1-8mons. to 8yrs
Viral load b/t 200-500 (if pt. not infected viral load=0)
CD4 count maintains above 500 cells/ul
oLevel is adequate enough to fight off invading
pathogens; norm. range is 800-1200 cells/ul
Intense disease proliferation
Characterized by fatigue, headaches, low grade fever, night
sweats, and generalized lymphadenopathy
Early Symptomatic Infection
Duration 8-10yrs.
CD4 T cells b/t 200-500 cells/ul
Significant elevation of viral load
Characterized by night sweats, fever, chronic diarrhea,
headaches, fatigue, propensity to infection, lymphadenopathy,
neurological symptoms
Late Symptomatic Infection
Worsening of symptoms, persistent night sweats and fever
Candidiasis (thrush; opportunistic fungal infection)
Kaposi Sarcoma (common cancer seen in HIV pts.)
Oral Hairy Leukoplakia: caused by Epstein Barr virus infection
(signs of disease progression)
CD4 low significantly lowered and affects cell mediated
immunity; tumors are often problem for these pts.
Acquired Immunodeficiency Syndrome (AIDS)
Occurs 10+ years (untreated maybe)
CD4 count below 200 (must have this & will more than likely
have 1 or more of the following opportunistic infections)
Opportunistic infections
oPneumocystis jiroveci (pneumonia)
oCryptococcal meningitis
oCytomegalovirus retinitis
Opportunistic cancers (Kaposi Sarcoma)
Wasting syndrome (affects muscles)
Dementia (AIDS dementia complex)
Rapid Screening for HIV
oOraSure testing (uses gum line)
oOraQuick (uses drop of blood)
Both are 20min. screens
If either screen is +ve MUST follow up w/ actual test (EIA or ELISA)
Testing for HIV
oBased on Risk factors
oEIA or ElISA: repeat if +ve and confirm w/ Western Blot (only after previous
tests were repeated)
Nurse 301
oIf –ve but suspect repeat EIA in 3-6mons.
oIf consistently inconclusive perform polymerase chain or a viral culture
Testing for HIV progression
oMeasure CD4 counts and viral loads (ALWAYS!!!)
oCD4 norm value 800-1200 cell/ul (w/o disease)
oViral load b/t 200-500 means early chronic phase is stable
oHigh viral load b/t 5,000-10,000 means disease is progressing
Viral load is undetectable or –ve if pt. isn’t infected
Drug Therapy
oAntiretroviral Agents (ART’s)
NRTI’s: Nucleoside Reverse Transcriptase Inhibitors
NNRTI’s: Non-Nucleoside Reverse Transcriptase Inhibitors
Both of these drugs prevent the transcription of viral RNA in
CD4
Protease Inhibitor: prevent cleaving of RNA proteins for bud
production in CD4
Fusion Inhibitor: prevent attachment of virus to CD4
oDrugs to treat opportunistic infection
oGoals: decr. viral load, maintain/raise CD4 count, delay the development of
HIV related symptoms and opportunistic diseases (many cancer related)
Nursing Management/Assessment
oAsk at risk pts.
Received blood transfusion/clotting factors before 1985 (mostly not
applicable b/c most people that received the virus this way are dead)
Shared needles, syringes, or other injection equipment w/ another
person?
Had sexual experience w/ penis, vagina, rectum, or mouth contact w/
these areas of another person? (homosexual; HIV infected person)
Had sexually transmitted disease (STD)? (need to be screened for HIV
at the very least)
oManagement dependent on stage but always: prevention, treating ongoing
infection, and preparation for death
oMain Goals of Planning: KEEP viral load low, maintain immune function,
improve quality of life, prevent opportunistic disease/new infections, reduce
disability
oPlanning Interventions: ***adhere to drug regimen (make sure liver & renal
functions are optimal through diagnostic tests)***, promote healthy lifestyle,
prevent transmission to others, have supportive relationships, maintain
productive activity, explore spirituality, come to terms w/ living w/ disease-
disability-death, cope w/ symptoms/treatments
oEthical Issues: can you decide to treat or not treat HIV infected person?
NOOOO!!!
Nurse 301
The Rehabilitation Act and the Americans w/ Disabilities Act both
include language that prohibits discrimination or the withholding of
treatment for these pts.
Use standard precautions and care for as anyone else
Case Study pg. 244; several charts in powerpoint dealing w/ HIV progression
reference these
Test 4066 4:00 Cardio-36, Immunology-8, and HIV-6
