Scc Third Sem Mid Term

Front 1

tpn components

Back 1

3-8 % amino acids
10-20% glucose
multivit
electrolytes
supplaments can be added including fats; dont add if egg alergy

Front 2

tpn administration

Back 2

1-2 L over 24 hrs at a constant rate. if to d/c must be tapered off. must be refidgerated, expires in 12 hours. incompatable with most meds

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picc line

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o bp in picc side. no needle sicks near or above. avoid shoulder use, cover before water exposure, change if solied or wet, if breaks secure with tape call provider. if sudden cp or sob, clamb cathether have pt lay on l side, head down , call md.

Front 4

tpn side effects

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hyperosmolar coma, hyperglycemia, septicamia, thrombosis, sclorosis, air embolism, pneumo.

Front 5

RN care of site

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aseptic care, daily wt, i/o, blood glcose q 6, monitor chem 20 and electrolytes, monitor for complications, tpn at room temp..

Front 6

air embolus

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stat abg, cxr, ekg. aspirate air from catheter. left side head down. valsalva monover.

Front 7

type 2 dm

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1. absolute defecancy w. insulin r/t slow delayed responce of islets to release insulin or reduction of insulin receptors, or a postreceptor defect

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subjective dm assesment

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blurry vision, puritis, lathargy, polydipsia, impotence

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dm objective

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polyuria, glycosuria,

Front 10

lab data dm

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bs fasting>125
non fasting>200
hgba1c>7

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sulfonylureas

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diabenese, tolazamide, glipizide, glyburide,

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metformin

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increases body sensativity to insulin

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rapid acting

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lispo, aspart

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short acting

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humulin r

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intermediate acting

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lente and nph

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slow acting

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protamate zinc

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long extended acting

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ultralente

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long acting basal analog

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glargine

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dm diet

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50-60 protein
20fats
decrease cals if fat
limit refined sugars
ass vits

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teach

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room temp insulin, infection control, f/u appts, when to seek help s/s of complications

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nkhhs

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profound hypergly and coma. non insulin dependent dm. critically ill. mortality over 50%. hyperglycemia causes osmotic dyuresis

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nkhhs risk factors

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old, kidney failure, shock, hemorrage, diuretics, glucosteriods, tube feedings

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nkhhs care

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iv fluids, electrolytes and nacl. monitor i/o npo till stable, admin insulin

Front 24

lupus

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chronic inflammatory connective tissue disease. may effect organs. unk etilogy may be r/t virus, hormone, drugs,primarly women 18-35

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dle

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effects skinonly

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sle

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effects multible organs

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patho

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possible toxic effexcts from immune complexes deposited in tissue. necrosis of collagen in connective tissue. cell death obstruction of blood flow.

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lupus subjective

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joint pain, anorexia, photophobia, weakness n/v

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lupus objective

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fever, rash, lesions, oral ulcerations

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lupus labs

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increased le cells. decreased rbcs, wbcs and thrombocytes
urine; hematuria and protein.

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lupus rn care

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rest increase sleep, steriod cream, assist w/ rom. mouth care soft blan liquid diet to aid w/ mouth care. low sodium diet, low k diet low protein if renal pt.

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observe lupus for complications

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tachycardia, tachy resp, doe, orthopnea, d, abd pain and distension. decrease urine, increase weight, ataxia, malaise, weakness report immediatly

Front 33

lupus meds

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analgesics, antiinflam(pred, asa)immunosupressive drugs(imuran, cytoxan.
antimaliarials for skina nd joint manifistations.

Front 34

lupus teaching

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avoid sun, altering meds, pg, fatigue, stress, infx, increase excercise wear med alert braclet.

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hiv patho

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decrease cell metaeated immunity t lymphs, t helperand hyperactivity of humoral b cells.

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hiv lab data

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decreased cd7, hct, wbc, platlets

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rn goals

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reduce infx monitor s/s
protective isolation

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hiv diet

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high cal high protein low bulk. fav foods from home six small meals q day.

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protease inhibitors

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Protease inhibitors (PIs) block the protease enzyme. When protease is blocked, HIV makes copies of itself that can't infect new cells. Studies have shown that protease inhibitors can reduce the amount of virus in the blood and increase CD4 cell counts. In some cases these drugs have improved CD4 cell counts, even when they were very low or zero.

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protease side effects

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dm, body fat, liver tox,


end in vir

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natural immunity

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Definition of Natural immunity

Natural immunity: Immunity that is naturally existing, Natural immunity does not require prior sensitization to an antigen

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acquired immunity

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ACQUIRED IMMUNITY

Acquired immunity is immunity that develops with exposure to various antigens. Your immune system builds a defense that is specific to that antigen.

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passive immunity

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PASSIVE IMMUNITY

Passive immunity involves antibodies that are produced in a body other than your own. Infants have passive immunity because they are born with antibodies that are transferred through the placenta from the mother. These antibodies disappear between 6 and 12 months of age.

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innate immunity

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INNATE IMMUNITY

Innate immunity is immunity that you are born with. Innate immunity involves barriers that keep harmful materials from entering your body. These barriers form the first line of defense in the immune response. Examples include:

* Cough reflex
* Enzymes in tears and skin oils
* Mucus, which traps bacteria and small particles
* Skin
* Stomach acid

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inflammation

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NFLAMMATION

The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. The damaged tissue releases chemicals including histamine, bradykinin, and serotonin. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling. This helps isolate the foreign substance from further contact with body tissues.

The chemicals also attract white blood cells called phagocytes that "eat" microorganisms and dead or damaged cells. This process is called phagocytosis. Phagocytes eventually die. Pus is formed from a collection of dead tissue, dead bacteria, and live and dead phagocytes.

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immune responce

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Immune cells and foreign particles enter the lymph nodes via incoming lymphatic vessels or the lymph nodes’ tiny blood vessels. All lymphocytes exit lymph nodes through outgoing lymphatic vessels. Once in the bloodstream, they are transported to tissues throughout the body. They patrol everywhere for foreign antigens, then gradually drift back into the lymphatic system, to begin the cycle all over again.
The spleen is a flattened organ at the upper left of the abdomen. Like the lymph nodes, the spleen contains specialized compartments where immune cells gather and work, and serves as a meeting ground where immune defenses confront antigens.
Clumps of lymphoid tissue are found in many parts of the body, especially in the linings of the digestive tract and the airways and lungs—territories that serve as gateways to the body. These tissues include the tonsils, adenoids, and appendix.

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immune system againg

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Specifically, in old age, the number of CD8 T cells diminishes. CD8 T cells have two functions: to recognize and destroy abnormal or infected cells, and to suppress the activity of other white blood cells to protect normal tissue. The scientists believe that late in life a different kind of CD8 T cell is increasingly produced by the body. These cells, called T cell clonal expansions (TCE), are less effective in fighting disease They also have the ability to accumulate quickly as they have a prolonged lifespan and can avoid normal elimination in the organism.

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immune blood tests

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Rheumatoid factor (RF, Latex)
"This measures whether a certain amount of abnormal antibody called
rheumatoid factor is in the blood. The majority of people with
rheumatoid arthritis (a common disease of inflamed joints that can
cause joint alignment problems and loss of function) have a large
amount of rheumatoid factor in their blood."

* Antinuclear antibody tests (ANA)
"These detect a group of autoantibodies that are found in most people
with lupus and scleroderma and in a few people with rheumatoid
arthritis. These autoantibodies react with antigens in the nuclei of
cells. The antibodies suggest that an autoimmune illness may be
present, although many people test positive and have little evidence
of serious disease."

* Complement tests
"These tests measure the amount of complement proteins circulating in
the blood. Complement tests involve the reaction of antibodies with
antigens. These tests usually are reserved for diagnosing or
monitoring people with active lupus. Those people with lupus
frequently have lower-than-normal amounts of complement, especially if
the kidneys are affected."

* Human leukocyte antigen (HLA) tissue typing tests
"These tests detect the presence of certain "genetic markers" or
traits in the blood. For example, B-27 is a genetic marker that nearly
always is present in people with ankylosing spondylitis (a disease
involving inflammation of the spine and sacroiliac joint) and Reiter's
syndrome (a disease involving inflammation of the urethra, eyes, and
joints). This test also is positive in five to 10 percent of the
healthy population."

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immune disorders

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Immune system cells called T lymphocytes (T cells) use special receptors on their surfaces to identify foreign microbes, such as bacteria and viruses. Usually, T cells that react to the tissues of the body are destroyed by the thymus, an organ of the immune system located behind the breastbone. The 'self-attacking' T cells that escape destruction may be activated by a trigger. The exact triggers are unknown, but viral infections and hormones are among the suspects. The rogue T cells then instruct B lymphocytes (B cells) to make antibodies against the particular tissue, organ or system. Such antibodies are called 'autoantibodies'.

Risk factors
The exact causes of autoimmune disorders are not known. The risk factors seem to include:

* Genetics - a predisposition to autoimmune disorders seems to run in families. However, family members can be affected by different disorders; for example, one person may have diabetes, while another has rheumatoid arthritis. It seems that genetic susceptibility alone is not enough to trigger an autoimmune reaction, and other factors must contribute.
* Environmental factors - a family's susceptibility to autoimmune disorders may be linked to common environmental factors, perhaps working in conjunction with genetic factors.
* Gender - around three quarters of people with autoimmune disorders are women.
* Sex hormones - autoimmune disorders tend to strike during the childbearing years. Some disorders seem to be affected, for better or worse, by major hormonal changes such as pregnancy, childbirth and menopause.
* Infection - some disorders seem to be triggered or worsened by particular infections.

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immune disorder mangment

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* Anti-inflammatory drugs - to reduce inflammation and pain.
* Corticosteroids - to reduce inflammation. They are sometimes used to treat an acute flare of symptoms.
* Pain-killing medication - such as paracetamol and codeine.
* Immunosuppressant drugs - to inhibit the activity of the immune system.
* Physical therapy - to encourage mobility.
* Treatment for the deficiency - for example, insulin injections in the case of diabetes.
* Surgery - for example, to treat bowel blockage in the case of Crohn's disease.
* High dose immunosuppression - the use of immune system suppressing drugs (in the doses needed to treat cancer or to prevent the rejection of transplanted organs) have been tried recently, with promising results. Particularly when intervention is early, the chance of a cure with some of these conditions seems possible.

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nursing care of lupus

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Medications are important for managing many systemic lupus erythematosus (SLE) patients. An array of drug therapies is now available, and this has increased the potential for effective treatment and excellent patient outcomes. Once a person has been diagnosed with lupus, the doctor will develop a treatment plan based on the person’s age, health, symptoms, and lifestyle. It should be reevaluated regularly and revised as necessary to ensure that it is as effective as possible. The goals for treating a patient with lupus include:

* reducing tissue inflammation caused by the disease
* suppressing immune system abnormalities that are responsible for tissue inflammation
* preventing flares and treating them when they do occur
* easing symptoms such as joint pain and fatigue
* minimizing complications of the disease

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antimilarial drugs

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Types of Antimalarials

The drugs most often prescribed are hydroxychloroquine sulfate (Plaquenil®) and chloroquine (Aralen®).
Mechanism of Action and Use

The anti-inflammatory action of these drugs is not well understood. In some patients who take antimalarials, the total daily dose of corticosteroids can be reduced. Antimalarials also affect platelets to reduce the risk of blood clots and lower plasma lipid levels.
Side/Adverse Effects

Central Nervous System: headache, nervousness, irritability, dizziness, muscle weakness, and tinnitus

Gastrointestinal: nausea, vomiting, diarrhea, abdominal cramps, and loss of appetite

Ophthalmologic: Visual disturbances and retinal changes are manifested by blurring of vision and difficulty in focusing. A very serious potential side effect of antimalarial drugs is damage to the retina. Because of the relatively low doses used to treat SLE, the risk of retinal damage is quite small: about 1 in 5,000. However, patients should have a thorough eye examination before starting this treatment and yearly thereafter.

Dermatologic: dryness, pruritus, alopecia, skin and mucosal pigmentation, skin eruptions, and exfoliative dermatitis

Hematologic: blood dyscrasia and hemolysis in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency

Front 53

nsaids drugs

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ypes of NSAIDs

There are more than two dozen different NSAIDs on the market, and many new ones are in development. Some can be purchased as over-the-counter preparations, whereas larger doses of those drugs or other preparations are available only by prescription. For example, prescriptions are required for diclofenac sodium (Voltaren®), indomethacin (Indocin®), diflunisal (Dolobid®), and nabumetone (Relafen®).
Mechanism of Action and Use

The therapeutic effects of NSAIDs stem from their ability to inhibit the release of prostaglandins and leukotrienes, which are responsible for producing inflammation and pain. NSAIDs are very useful in treating joint pain and swelling, as well as muscle pain. They may also be used to treat pleuritic chest pain. An NSAID may be the only drug needed to treat a mild flare; more active disease may require additional medications.

Although all NSAIDs appear to work in the same way, not every one has the same effect on every person. In addition, patients may do well on one NSAID for a period of time, then, for some unknown reason, derive no benefit from it. Switching the patient to a different NSAID should produce the desired effects. Patients should use only one NSAID at any given time.
Side/Adverse Effects

Gastrointestinal (GI): dyspepsia, heartburn, epigastric distress, and nausea; less frequently, vomiting, anorexia, abdominal pain, GI bleeding, and mucosal lesions. Misoprostol (Cytotec®), a synthetic prostaglandin that inhibits gastric acid secretion, may be given to prevent GI intolerance. It prevents gastric ulcers and their associated GI bleeding in patients receiving NSAIDs. Another product, Arthrotec®, combines misoprostol with the NSAID diclofenac sodium in a single pill.

Genitourinary: fluid retention, reduction in creatinine clearance, and acute tubular necrosis with renal failure.

Hepatic: acute reversible hepatotoxicity

Cardiovascular: hypertension and moderate to severe noncardiogenic pulmonary edema. All NSAIDS now carry a warning that they may increase the risk of myocardial infarction.

Hematologic: altered hemostasis through effects on platelet function

Other: skin eruption, sensitivity reactions, tinnitus, and hearing loss

Pregnancy and Lactation

NSAIDs should be avoided after the first trimester. NSAIDs appear in breast milk and should be used cautiously by breast-feeding mothers.

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corticosteriods

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Corticosteroids

Corticosteroids are hormones secreted by the cortex of the adrenal gland. SLE patients with symptoms that do not improve or who are not expected to respond to NSAIDs or antimalarials may be given a corticosteroid. Although corticosteroids have potentially serious side effects, they are highly effective in reducing inflammation, relieving muscle and joint pain and fatigue, and suppressing the immune system. They are also useful in controlling major organ involvement associated with SLE. These drugs are given in much higher doses than the body produces and act as potent therapeutic agents. The decision to use corticosteroids is highly individualized and is dependent upon the patient’s condition.

Once the symptoms of lupus have responded to treatment, the dose is usually tapered until the lowest possible dose that controls disease activity is achieved. Patients must be monitored carefully during this time for flares or recurrence of joint and muscle pain, fever, and fatigue that can result when the dosage is lowered. Some patients may require corticosteroids only during active stages of the disease; those with severe disease or more serious organ involvement may need long-term treatment.

Treatment with corticosteroids must not be stopped suddenly if they have been taken for more than 4 weeks. Administration of corticosteroids causes the body’s own production of adrenal hormones to slow down or stop, and adrenal insufficiency will result if the drug is stopped suddenly. Tapering the dose allows the body’s adrenal glands to recover and resume production of the natural hormones. The longer a patient has been on corticosteroids, the more difficult it is to lower the dose or discontinue use of the drug.

Types of Corticosteroids

Prednisone (Orasone®, Meticorten®, Deltasone®, Cortan®, Sterapred®), a synthetic corticosteroid, is most often used to treat lupus. Others include hydrocortisone (Cortef®, Hydrocortone®), methylprednisolone (Medrol®), and dexamethasone (Decadron®). Corticosteroids are available as a topical cream or ointment for skin rashes, as tablets, and in injectable form for intramuscular or intravenous administration.
Mechanism of Action and Use

The frequently prescribed corticosteroids are highly effective in reducing inflammation and suppressing the immune response. These drugs may be used to control exacerbation of symptoms and are used to control severe forms of the disease. These drugs are usually administered orally. During periods of serious illness or prior to surgery, they may be administered intravenously; once the patient has been stabilized (or patient is able to have oral fluids after surgery), oral administration should be resumed.
Side/Adverse Effects

Central Nervous System: depression, mood swings, and psychosis

Cardiovascular: congestive heart failure (CHF) and hypertension*

Endocrine: Cushing’s syndrome, menstrual irregularities, and hyperglycemia

Gastrointestinal: GI irritation, peptic ulcer, and weight gain

Dermatologic: thin skin, petechiae, ecchymoses, facial erythema, poor wound healing, hirsutism,* urticaria, and acne

Musculoskeletal: muscle weakness, loss of muscle mass, and osteoporosis*

Ophthalmologic: increased intraocular pressure, glaucoma, exophthalmos, and cataracts*

Other: immunosuppression and increased susceptibility to infection

* long-term effects

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immunospressive drugs

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Immunosuppressives

Immunosuppressive agents are generally used to reduce rejection of transplanted organs. They are also used in serious, systemic cases of lupus in which major organs such as the kidneys are affected or in which there is severe muscle inflammation or intractable arthritis. Because of their steroid-sparing effect, immunosuppressives may also be used to reduce or sometimes eliminate the need for corticosteroids, thereby sparing the patient from undesirable side effects of corticosteroid therapy.

Immunosuppressives can have serious side effects. Patients need to understand, however, that side effects are dose-dependent and are generally reversible by reducing the dose or stopping the medication.

Types of Immunosuppressives

A variety of immunosuppressive drugs is available to treat lupus. Although they have different mechanisms of action, each type functions to decrease or prevent an immune response. The immunosuppressives most frequently used with SLE patients are:

* azathioprine (Imuran®). Azathioprine, one of the most widely used immunosuppressives for lupus, is an antimetabolite. Antimetabolites work by blocking metabolic steps within immune cells and then interfering with immune function. Used to control the underlying disease process, azathioprine has fewer serious side-effect risks than some other drugs used to control lupus.
* cyclophosphamide (Cytoxan®). An alkylating agent and strong immunosuppressive, cyclophosphamide is reserved for treating lupus with kidney disease or other internal organ involvement. It works by targeting and damaging autoantibody-producing cells, thereby suppressing the hyperactive immune response and reducing disease activity. It has the potential for severe side effects, including risk of serious infection.
* methotrexate (Rheumatrex®). Originally developed as a cancer treatment and later approved for rheumatoid arthritis, methotrexate, like azathioprine, is an antimetabolite. It is predominantly used for lupus arthritis. It requires monitoring of the CBC and liver function tests. To reduce toxicity, daily folic acid is prescribed.
* cyclosporine (Neoral®). Originally developed to prevent the body from rejecting transplanted organs, cyclosporine is now commonly used to treat rheumatic diseases, including lupus. Cyclosporine is an antimetabolite.
* mycophenolate mofetil (CellCept®). A strong immunosuppressive drug developed to prevent the rejection of transplanted organs, mycophenolate is sometimes used as an alternative to cyclophosphamide for lupus with kidney involvement. Mycophenolate works by keeping T and B lymphocytes from replicating.

There are many serious risks associated with the use of immunosuppressives. They include immunosuppression (resulting in increased susceptibility to infection), bone marrow suppression (resulting in decreased numbers of RBCs, WBCs, and platelets), and development of malignancies.
Side/Adverse Effects

Dermatologic: alopecia (cyclophosphamide and methotrexate)

Gastrointestinal: nausea, vomiting, stomatitis, esophagitis, and hepatotoxicity

Genitourinary: hemorrhagic cystitis, hematuria, amenorrhea,* impotence,* and gonadal suppression (cyclophosphamide only) **

Hematologic: thrombocytopenia, leukopenia, pancytopenia, anemia, and myelosuppression

Respiratory: pulmonary fibrosis***

Other: increased risk of serious infections or malignancies

* temporary or reversible once drug therapy is discontinued

** recovery of function after drug is discontinued is unpredictable

*** with high doses

Front 56

iv immunoglobulins

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Intravenous Immunoglobulins (IVIGs)

IVIGs may be used to control SLE with organ involvement or vasculitis. Although the mechanism by which these products help is not well-understood, it is thought that they reduce antibody production or promote the clearance of immune complexes from the body.

Risks

Although an IVIG, like any drug, can cause potentially dangerous side effects, it doesn’t suppress the immune system the way immunosuppressives and corticosteroids do. Thus, the risk of serious infections with these drugs is less.
Side/Adverse Effects

Dermatologic: rash, mild skin reaction at injection site

Gastrointestinal: abdominal cramps, nausea, vomiting

Musculoskeletal: chest, back or hip pain; muscle pain; joint pain

Neurologic: anxiety, chills, dizziness, fever, headache

Other: chest tightness, difficulty breathing, burning sensation in the head

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multiple myloma

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Multiple Myeloma

Also called: Plasma-cell myeloma

Multiple myeloma is a cancer that begins in plasma cells, a type of white blood cell. These cells are part of your immune system, which helps protect the body from germs and other harmful substances. In time, myeloma cells collect in the bone marrow and in the solid parts of bone.

No one knows the exact causes of multiple myeloma, but it is more common in older people and African-Americans. Early symptoms may include
# Bone pain, often in the back or ribs
# Broken bones
# Weakness or fatigue
# Weight loss
# Repeated infections

Myeloma is hard to cure. Treatment may help control symptoms and complications. Options include chemotherapy, stem cell transplantation and radiation.

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mm tx

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transplantation. Peripheral stem cell transplantation involves the use of high-dose chemotherapy or radiation therapy and the transfusion of previously collected immature, or "young," blood cells to replace diseased or damaged marrow. chemo, radiation.

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rn care mm

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ovision of relevant, high-quality, up-to-date information, in a variety of formats, at all stages of their disease
* Expert pain assessment and control
* Education of patients about the need for adequate hydration
* Prompt recognition of the signs of hypercalcaemia, spinal cord compression and sepsis
* Recognition and management of fatigue
* Prevention or management of constipation
* Recognition and management of side effects, such as peripheral neuropathy, that occur with existing and new treatments
* Provision of psychological and social support for patients and their families

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sx of mm

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Plasma Cell Growth In Bone Marrow
and Skeletal Disease pain.
immunologic Abnormalities= increase infections
Effect of Abnormal Paraprotein effects blood viscosity and circulation.
renal failure

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type 1 hypersensetivity rxn

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Hypersensitivity type 1: Immediate hypersensitivity reaction - type I reaction, involves immunoglobulin E (IgE)-mediated release of chemical mediators from mast cells and basophils. Th2 cells produce IL-4 and IL-13, which then act on B cells to promote the production of antigen-specific IgE. Reexposure to the antigen can then result in the antigen binding to and cross-linking the bound IgE antibodies on the mast cells and basophils. This causes the release of preformed mediators (histamine, tryptase, tryptase, chemotactic factors), newly synthesized mediators (leukotrienes, prostaglandin, thromboxane, platelet-activating factor, adenosine, bradykinin), and cytokines from these cells that results in structural and functional changes to the affected tissue.

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type 1 hypersensativity rxn

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ype 1: Immediate Hypersensitivity Reaction

1. Mediated by IgE antibody to specific antigens
1. Mast cells stimulated and release histamine
2. Reaction within one hour of exposure
3. Examples
1. Anaphylaxis (e.g. Penicillin)
2. Urticaria
3. Angioedema
4. Atopic Allergy

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anaphaltic

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Etiology: allergic reaction to substance - massive vasodilation, increased cap permeability
S/S: sudden onset, hypotension, wheezing, stridor, swelling of lips and tongue, flusing, pruritus, urticarisa, feeling of impending doom

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anaphlatic interventions

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airway, remove causitve agent, epi 1;1000 0.2-0.5ml repeat q 20 for mild 0.5 iv 5-10 minute iterval severe. high flow o2, recombant, elevate legs, keep warm, benadryl im or iv, climidine tagament h2 blocker, monitor bpwith fluid volume expanders, vasopressor, dopamine nor epi. continue to monitor vs, resp effort, 02 stat, loc heart rhythm, anticipate intubation or trach.

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hiv drugs

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There are currently five categories of HIV antiviral drugs available that have FDA approval. These categories are:

* nucleoside reverse transcriptase inhibitors (NRTIs)

* nucleotide reverse transcriptase inhibitors (NtRTIs)

* non-nucleoside reverse transcriptase inhibitors (NNRTIs)

* protease inhibitors (PIs)

* fusion inhibitors

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nnrti

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combine with transcriptase enzyme to block hiv rna from becoming hiv dna.

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nrti

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insert a bit of protein into hiv dna blocking furthur development

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pi

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prevent protease enzymes from cutting hiv proteins

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fusion inhibitors
entry inhibitors

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prevent binding of hiv to cells

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hiv manifestations

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Early symptomatic HIV disease
At this stage symptoms including fever, unexplained weight loss, recurrent diarrhea, fatigue and headache. Cutaneous manifestations like seborrheic dermatitis, folliculitis, recurrent herpes simplex infections oral hairy leukoplakia may occur. During this period the CD4 T-cells count continues to come down. Usually anti retroviral therapy is started at this stage.

Opportunistic Infections are important part of the HIV disease process. It is common to find AIDS patients with multiple OIs. These OIs result in more rapid decline in CD4 T-cell count than the decline resulting from HIV disease itself. Thus effective therapy is required to treat and prevent these infection. The incidence and type of OIs in HIV patients is directly related to the CD4 count in that individual.

Common OIs are Tuberculosis both pulmonary and extra-pulmonary , Oropharyngeal candidiasis, Herpes zoster, Herpes simplex, Toxoplasmosis, Cryptococcal Meningitis, Pneumocystitis carini pneumonia, Cytomegalovirus retinitis, Cryptosporidial diarrhea.

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nnrti s/e

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rash

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nrtis

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ha latic acidosis

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pi

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gi upset hepatitis

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dm 1

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Type 1 diabetes
Results from the body's failure to produce insulin, the hormone that "unlocks" the cells of the body, allowing glucose to enter and fuel them. It is estimated that 5-10% of Americans who are diagnosed with diabetes have type 1 diabetes.

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dm2

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Type 2 diabetes
Results from insulin resistance (a condition in which the body fails to properly use insulin), combined with relative insulin deficiency. Most Americans who are diagnosed with diabetes have type 2 diabetes.

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pre dm testing

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Doctors can use either the fasting plasma glucose test (FPG) or the oral glucose tolerance test (OGTT) to detect pre-diabetes. Both require a person to fast overnight. In the FPG test, a person's blood glucose is measured first thing in the morning before eating. In the OGTT, a person's blood glucose is checked after fasting and again 2 hours after drinking a glucose-rich drink

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ogtt test and dm

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Q: How does the OGTT define diabetes and pre-diabetes?

A: In the OGTT, a person's blood glucose is measured after a fast and 2 hours after drinking a glucose-rich beverage. Normal blood glucose is below 140 mg/dl 2 hours after the drink. In pre-diabetes, the 2-hour blood glucose is 140 to 199 mg/dl. If the 2-hour blood glucose rises to 200 mg/dl or above, a person has diabetes.

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rapid acting insulin

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Rapid-acting insulin, such as insulin lispro (Eli Lilly), insulin aspart (Novo Nordisk), or insulin glulisine (sanofi-aventis), begin to work about 5 minutes after injection, peak in about 1 hour, and continue to work for 2 to 4 hours.

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regular or short acting insulin

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Regular or Short-acting insulin (human) usually reaches the bloodstream within 30 minutes after injection, peaks anywhere from 2 to 3 hours after injection, and is effective for approximately 3 to 6 hours.

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intermed acting insulin

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Intermediate-acting insulin (human) generally reaches the bloodstream about 2 to 4 hours after injection, peaks 4 to 12 hours later and is effective for about 12 to 18 hours.

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long acting insulin

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Long-acting insulin (ultralente) reaches the bloodstream 6 to 10 hours after injection and is usually effective for 20 to 24 hours. There are also two long-acting insulin analogues, glargine and detemir. They both tend to lower glucose levels fairly evenly over a 24-hour period with less of a peak of action than ultralente.

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sulfonylureas

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Sulfonylureas. These diabetes pills lower blood glucose by stimulating the pancreas to release more insulin. The first drugs of this type that were developed -- Dymelor, Diabinese, Orinase and Tolinase -- are not as widely used since they tend to be less potent and shorter acting drugs than the newer sulfonylureas. They include Glucotrol, Glucotrol XL, DiaBeta, Micronase, Glynase PresTab and Amaryl. These drugs can cause a decrease in the hemoglobin A1c ( HbA1c) of up to 1%-2%

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biguanides

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biguanides. These diabetes pills improve insulin's ability to move glucose into cells especially into the muscle cells. They also prevent the liver from releasing stored glucose. Biguanides should not be used in people who have kidney damage or heart failure because of the risk of precipitating a severe build up of acid (called lactic acidosis) in these patients. Biguanides can decrease the HbA1c 1%-2%. Examples include metformin (Glucophage, Glucophage XR, Riomet, Fortamet and Glumetza).

Front 84

thiazolidinediones

Back 84

Thiazolidinediones. These diabetes pills improve insulin's effectiveness (improving insulin resistance) in muscle and in fat tissue. They lower the amount of glucose released by the liver and make fat cells more sensitive to the effects of insulin. Actos and Avandia are the two drugs of this class. A decrease in the HbA1c of 1%-2% can be seen with this class of oral diabetes medications. These drugs may take a few weeks before they have an effect in lowering blood glucose. They should be used with caution in people with heart failure. Your doctor will do periodic blood testing of your liver function when using this diabetes medicine.

Front 85

alpha glucoside inhibitors

Back 85

Alpha-glucosidase inhibitors, including Precose and Glyset. These drugs block enzymes that help digest starches, slowing the rise in blood glucose. These diabetes pills may cause diarrhea or gas. They can lower hemoglobin A1c by 0.5%-1%.

Front 86

meglitinides

Back 86

Meglitinides, including Prandin and Starlix. These diabetes medicines lower blood glucose by stimulating the pancreas to release more insulin. The effects of these oral diabetes medications depend on the level of glucose. They are said to be glucose dependent. High sugars make this class of diabetes medicines release insulin. This is unlike the sulfonylureas that cause an increase in insulin release, regardless of glucose levels, and can lead to hypoglycemia.

Front 87

combo meds for dm

Back 87

Combination therapy. There are several combination diabetes pills that combine two medications into one tablet. One example of this is Glucovance, which combines glyburide (a sulfonylurea) and metformin. Others include Metaglip, which combines glipizide (a sulfonylurea) and metformin, and Avandamet which utilizes both metformin and rosiglitazone (Avandia) in one pill

Front 88

normoglycemia

Back 88

fbs <110
2 hr pp 140

Front 89

dm lab

Back 89

fbs >126
2 hr pp >200

Front 90

other causes of dm

Back 90

pancreatic injury, tumors, cortsone, estrogen therapy, cushings syndrome, pg, hyperthyroid, infections.

Front 91

hypoglycemic protocall concious pt

Back 91

bg,60
give 15 gm hco
order stat lab
recheck finger stick 15 min notify md
if bg <90 repeat
if bg >90 give snack
recheck bg 15 min
repeat till bg >90
call md for further orders

Front 92

hypoglcemic unconscious pt
npo or uncertin swallowing reflex

Back 92

bg<60
order stat lab call md 2nd nurse
check iv for patency give d 50 ivp
hang d10 at 100ml/hr check bg in 10 min

if no iv then give glucagon 1 mg sq or im
if pt able to swallow give 15 gm cho
start iv
recheck bg in 10 min

if bg,75 repeat d50 ivp
if greater then 75 order feed pt

check bg q 15 min until 90
call md for furrther orders.

Front 93

retinopathy

Back 93

Retinopathy is a general term that refers to some form of non-inflammatory damage to the retina of the eye. Most commonly it is a problem with the blood supply that is the cause for this condition. Frequently, retinopathy is an ocular manifestation of systemic disease.

Front 94

neuropathy

Back 94

Peripheral neuropathy is caused by damage to your body’s peripheral nerves.
This damage disrupts the body’s ability to communicate with its muscles, skin, joints, or internal organs. It is like the body’s wiring system breaking down. If ignored, neuropathy can lead to numbness, pain, weakness and incoordination. However, if it is diagnosed and treated early, peripheral neuropathy can often be controlled, slowing the disease’s progression.

Front 95

neuropathy meds

Back 95

Duloxetine hydrochloride (Cymbalta®) has been approved by the Food and Drug Administration (FDA) to treat diabetic peripheral neuropathy. Common side effects include constipation, diarrhea, dry mouth, and nausea. In some cases, Cymbalta® causes dizziness and hot flashes.

Although anticonvulsants such as gabapentin (Neurontin®) and topiramate (Topamax®) and antidepressants such as amitriptyline (Elavil®) are not approved by the FDA to treat neuropathy, they are often prescribed to treat this condition. Side effects of these drugs include drowsiness, dizziness, low blood pressure, and fatigue.

Other medications include anticonvulsants (e.g., carbamazepine [Tegretol®], lamotrigine [Lamictal®]), local anesthetics (e.g., lidocaine [Xylocaine®]), and antiarrhythmics (e.g., mexiletine [Mexitil®]). Anticonvulsants may cause low white blood cell counts, nausea, vomiting, and dizziness. Side effects of lidocaine and mexiletine include nervousness, lightheadedness, drowsiness, and double vision.

Topical treatment with capsaicin cream (Zostrix®) may be prescribed for patients with focal neuropathy. Capsaicin causes stinging upon application and is often combined with a local anesthetic to reduce this side effect. Axsain® (.25% capsaicin in Lidocare® vehicle) contains a higher dose of capsaicin in a cream that reduces stinging and burning. Lidoderm® (lidocaine patch 5%) has been shown to be helpful for localized areas of tingling or burning.

Pregabalin (Lyrica®) has been approved by the Food and Drug Administration (FDA) to treat post-herpetic neuralgia (shingles pain). Common side effects include drowsiness, dizziness, nausea, weight

Front 96

sulfonylurea s/e

Back 96

the side effects of Amaryl and the Sulfonylureas include:

* Low blood sugar (hypoglycemia)
* Weight gain
* Water retention
* Allergic reactions (usually only in those with an allergy to sulfa treatments)
* Cardiac (slight risk only).

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meglitinide side effects

Back 97

The side effects of Prandin or Starlix and the Meglitinides may include:

* Diarrhea
* Headache
* Cardiac (slight risk only).
* Low blood sugar (hypoglycemia)
* Upper respiratory infections, nasal and sinus inflammation, and bronchitis.
* Joint and back pain.
* Nausea
* Constipation

Front 98

biguanide s/e

Back 98

The side effects of Glucophage or Metformin may include:

* A metallic taste in the mouth.
* Nausea
* Diarrhea
* Flatulence
* Vitamin B12 deficiency
* Anemia
* Anorexia
* Lactic Acidosis

Front 99

thiazolidone s/e

Back 99

The side effects of Avandia and Actos may include:

* Headache
* Mild swelling of the legs and ankles
* Increased cholesterol
* Anemia

Front 100

alphaglucosidase s/e

Back 100

The side effects of Acarbose and Precose may include:

* Gas
* Bloating
* Abdominal Cramps
* Diarrhea

Front 101

dm diet

Back 101

Nutrient Aim for
Carbohydrates 45% to 65% of daily calories
Protein 15% to 20% of daily calories
Fats 20% to 35% of daily calories

Front 102

metabolic syndrome

Back 102

* Abdominal obesity (excessive fat tissue in and around the abdomen)
* Atherogenic dyslipidemia (blood fat disorders — high triglycerides, low HDL cholesterol and high LDL cholesterol — that foster plaque buildups in artery walls)
* Elevated blood pressure
* Insulin resistance or glucose intolerance (the body can’t properly use insulin or blood sugar)
* Prothrombotic state (e.g., high fibrinogen or plasminogen activator inhibitor–1 in the blood)
* Proinflammatory state (e.g., elevated C-reactive protein in the blood)

Front 103

metabolic syndrome care

Back 103

# eight loss to achieve a desirable weight (BMI less than 25 kg/m2)
# Increased physical activity, with a goal of at least 30 minutes of moderate-intensity activity on most days of the week
# Healthy eating habits that include reduced intake of saturated fat, trans fat and cholesterol

Front 104

lispo aspart

Back 104

onset less then 15 min
peak 1-2 hrs
duration 3-4

Front 105

regular

Back 105

onset 0.5-1hr
peak2-3
duration 3-6

Front 106

nph

Back 106

onset 2-4
peak 4-10
duration 10-16

Front 107

gargline

Back 107

onset 2-4
peak peakless
duration 20-24

Front 108

dm sick days

Back 108

ype 2 diabetes. Check your blood sugar levels four times a day. If your blood sugar level is higher than 300 mg/dL, check your urine for ketones.

Front 109

dm sick call md if;

Back 109

iabetes complications can quickly become dangerous. Contact your doctor if:

* Your blood sugar level is higher than 300 mg/dL
* Your blood sugar level is higher than 240 mg/dL for more than 24 hours
* Your urine ketone level is moderate to high
* You feel sleepier than usual or can't think clearly
* You're unable to keep fluids down or vomit for more than six hours
* You have diarrhea for more than six hours
* You feel confused and can't think clearly
* Your lips and tongue appear dry and cracked

Think prevention

Front 110

dka tx

Back 110

Treatment Goals
• Immediate replacement of fluids to correct hypovolemia
• Administration of insulin
• Replacement of electrolytes to correct imbalances
Collaborative interventions
• Ensure airway
• Oxygen administration
• Establish IV access with large bore catheter
• Fluid resuscitation 1Liter per hour until UOP 60ml/hr and BP has stabilized
• Continuous IV insulin (0.1 U/kg/hr)
Ongoing monitoring
• VS, LOC, cardiac rhythm, oxygen saturation, UOP
• Breath sounds for overload
• Serum glucose and potassium
• pH and anticipate Na bicarb administration

Front 111

hnnk assessment

Back 111

Sweating, tremor
• Blurred vision, weakness, hunger
• Confusion, vertigo, behavior changes
• Parasthesias, anxiety, chilling, incoordination
• Slurred speech, palpitations, nausea, headache
• Stupor, seizures, coma

Front 112

hypoglycemia sx

Back 112

# nervousness,
# sweating,
# intense hunger,
# trembling,
# weakness,
# palpitations, and

Front 113

malnutrition

Back 113

Malnutrition is a general term for a medical condition caused by an improper or insufficient diet.

Front 114

marasmus

Back 114

The malnutrition associated with marasmus leads to extensive tissue and muscle wasting, as well as variable edema. Other common characteristics include dry skin, loose skin folds hanging over the glutei, axillae, etc. There is also drastic loss of adipose tissue from normal areas of fat deposits like buttocks and thighs. The afflicted are often fretful, irritable, and voraciously hungry

Front 115

tx

Back 115

It is essential to treat not only the symptoms but also the complications of the disorder, including infections, dehydration and circulation disorders, which are frequently lethal and lead to high mortality if ignored.

Ultimately, marasmus progresses to the point of no return when the body's machinery for protein synthesis, itself made of protein, has been degraded. At this point, attempts to correct the disorder by giving food or protein will fail to prevent death.

Front 116

kwashiorkor

Back 116

Kwashiorkor is a type of malnutrition with controversial causes, but it is commonly believed to be caused by insufficient protein intake

Front 117

symptoms

Back 117

Symptoms of kwashiorkor include a swollen abdomen known as a pot belly, as well as alternating bands of pale and dark hair (flag sign) and weight loss. Common skin symptoms include dermatitis and depigmented skin.

The swollen abdomen is generally attributed to two causes: First, the appearance of ascites due to increased capillary permeability from the increased production of cysteinyl leukotrienes as a result of generalized intracellular deficiency of glutathione. It is also thought to be attributed to the effect of malnutrition on reducing plasma proteins, resulting in a reduced oncotic pressure and therefore increased osmotic flux through the capillary wall. A second cause may be due to a grossly enlarged liver due to fatty liver. This fatty change occurs because of the lack of apolipoproteins which transport lipids from the liver to tissues throughout the body.

Victims of kwashiorkor fail to produce antibodies following vaccination against diseases, including diphtheria and typhoid. Generally, the disease can be treated by adding food energy and protein to the diet; however, it can have a long-term impact on a child's physical and mental development, and in severe cases may lead to death.

Front 118

lab test for malnutrition

Back 118

# CBC (Complete Blood Count)
# CMP (Comprehensive Metabolic Panel)
# Albumin
# Total protein

# For nutritional status and deficiencies: Prealbumin (is decreased in malnutrition, rises and falls rapidly, and can be used to detect short-term response to treatment)
# Iron tests (such as Iron, TIBC, and Ferritin)
# Vitamin and minerals (such as B12 and Folate, Vitamin D, Vitamin K, Calcium, and Magnesium)

Front 119

cvad veins

Back 119

The main veins used for central venous access are:
n Internal and external jugular and subclavian veins
(all types of CVADs).
n Cephalic and basilic veins (for peripherally inserted
central catheters).
n Occasionally the femoral veins.

Front 120

skin tunneled cathathers

Back 120

broviac and hickman

Front 121

cvad insertion complications

Back 121

Hydrothorax
n Haemothorax
n Pneumothorax
n Cardiac arrhythmias
n Cardiac tamponade
n Thoracic duct trauma
n Brachial plexus injury
n Air embolism
n Catheter embolism
n Haemorrhage
n Misdirection or kinking

Front 122

cvad managment principles

Back 122

n Prevention of infection.
n Maintaining a closed IV system.
n Maintaining a patent device.
n Preventing damage to the device

Front 123

tpn assesment

Back 123

1. Assess temperature and I&O every shift.
2. Assess for signs/symptoms of catheter-related complications according to
Hospitals Central Venous Access Device procedures.

Front 124

tpn labs

Back 124

*3. Monitor:
●Na, K, Cl, HCO3, BUN, CR, Gluc, Mg, PO4, AST, ALT, alkaline phosphatase,
triglycerides.

Front 125

notify md

Back 125

4. Report to MD:
●nausea/vomiting
●blood glucose:
−adults: >180 mg/dl, <70 mg/dl
signs/symptoms of infection (systemic or at IV site)
−temperature:
adults: >38.5° C (oral)
−rigors/shaking chills
●sudden/unexpected cessation of TPN
●dislodgment of central venous access device

Front 126

tpn care

Back 126

Weigh patient every Monday/Wednesday/Friday or as ordered.
6. Prep all TPN connections with alcohol vigorously for seconds prior to entering.
NOTE: Line connections must be sterile.
7. Connect filter to the end of the TPN tubing, below the pump; change filter daily.
8. Change TPN tubing and needleless access cap every 24 hours for TPN with lipids and every 48 hours for TPN without lipids.
9. Infuse TPN via infusion pump.
*10. Stop adult TPN one day before surgery.

Front 127

emergency tpn measures

Back 127

FOR SUDDEN/UNEXPECTED CESSATION OF CENTRAL TPN, infuse a
MEASURES: dextrose-containing solution at the same rate for at least 4-6 hours or until new
TPN is hung:
•adults: D5W
fluid concentration similar to TPN dextrose
concentration
•establish peripheral IV access as soon as possible to continue appropriate dextrose
infusion.
14. Notify MD for sudden/unexpected cessation

Front 128

nursing care of tube feedings

Back 128

check placement
check bowel sounds
use liquids rather pills
dilute viscus
elevate hob check risdula
asess for complicatiopns
check placement q 8 hrs
or every feeding
discard after 8 hrs
change tubing q 24 hrs

Front 129

200-499

Back 129

immune problems start to occur with hiv

Front 130

cbc lab values

Back 130

rBC's 3.5-5.5 million cells/mcL
Hemoglobin Male 14.0-18.0
Hemoglobin Female 12.0-16.0
Hematocrit Male 40-54%
Hematocrit Female 36-48%
Platlets 150,000-400,000/ cubic millimeters
Leukocytes 5,000-11,000 per cubic millimeter

Front 131

neutrophils

Back 131

increase with inflammation or bacteral infx

decrease w/ bone marrow or severe prolonged infx

Front 132

bands
immature neutrophils

Back 132

increase with serouis bacterial infx

Front 133

increase lymph

Back 133

viral infx

decrease with t and b cells w/ hiv or steriod use

Front 134

plasma cells produce ab.

t cytotoxic cells destroy pathogens.

nk cells in cell mediated immunity

Back 134

cytokins messangers

Front 135

igg

Back 135

placenta

Front 136

iga

Back 136

protects body surfaces

Front 137

igm

Back 137

immune responce

Front 138

ige

Back 138

allery

Front 139

humoral immunity

Back 139

plama cells produce ab igg

Front 140

b cells

Back 140

diff in to plama cells

Front 141

b lymp

Back 141

memory cells

Front 142

t cells

Back 142

cell mediated immunity
macrophages and natural killer cells

Front 143

eosenophils

Back 143

increase with parasite
decrease with steriods

Front 144

gastrostomy tube feeding

Back 144

Lesson 42. Gastrostomy Tube Feeding

1-42. GASTROSTOMY TUBE FEEDING

A gastrostomy tube feeding should be treated as a normal meal. The procedure must never be rushed, and the atmosphere should be pleasant and relaxing for the patient. The prescribed feeding may be a commercially prepared formula or a special preparation from the hospital food service. The procedure for administration of a gastrostomy tube feeding is as follows.

a. Review the patient's clinical record to verify physician's order for the amount and type of tube feeding.

b. Wash your hands.

c. Collect the necessary supplies and equipment.

(1) Feeding solution, as prescribed.
(2) Large bulb syringe or catheter tip 50cc syringes.
(3) Tap water.
(4) Graduated container for measuring.

d. Prepare the tube feeding, as ordered.

(1) For 1/4, 1/2, or 3/4 strength feeding, mix the solution with the appropriate amount of water to obtain the desired strength.
(2) Always check the label of a commercially prepared formula for expiration date.
(3) When mixing a feeding formula, label with date, time, and initials.
(4) Warm solution to room temperature to prevent cramps and gas formation.

e. Approach and identify the patient and explain procedure.

f. Provide for patient privacy.

g. Place patient in semi-fowler's position in bed to promote digestion.

h. Fold top linen down to expose gastrostomy tube and protect area with towel.

i. Attach the syringe to the clamped gastrostomy tube.

(1) Remove plunger if using a 50cc catheter tip syringe.
(2) Remove bulb from bulb syringe.

j. Check patency of the tube by pouring a small amount of water from the graduated container into the syringe.

(1) Remove clamp.
(2) If water flows freely, the tube is patent.
(3) If water does not flow its not.

k. Pour feeding solution into the syringe.

(1) As solution flows into the stomach, tilt the syringe to allow air bubbles to escape.
(2) Add more solution to the syringe when about one quarter of it remains.
(3) Increase or decrease the flow rate by raising or lowering the syringe.
(4) Depending upon the solution's consistency, and the amount, feeding may take 10 to 20 minutes.

l. After administering the ordered amount of feeding solution, flush the tube with 30 ml of water to clear the feeding solution residue.

m. Clamp or plug the tube to prevent leakage.

n. Instruct patient to remain in a sitting position for 30 minutes to enhance normal digestive process.

o. Record feeding on intake and output record. Record procedure and the patient's tolerance in the nursing notes.

p. Check back with the patient. He should not feel overly full or nauseated. . Gastric distress may require adjustment of feeding schedule.

Front 145

blood transusion components

Back 145

Component Description Indication for use
Red cell concentrate in Made following the removal Used to increase tissue oxygenation
additive solution of virtually all the plasma when this is critically reduced by
(generally 250-300ml) and the anaemia or hemorrhage
addition of 100ml of nutrient
solution
Platelets Platelet concentration in Used where deficiency (a platelet
plasma with red cell removed count below 50-100 x 109/l) or
functional abnormality is causing, or
may cause severe microvascular
bleeding, or if disseminated
intravascular coagulation (DIC) is
confirmed by laboratory results
Fresh frozen plasma (FFP) Made from plasma which is FFP is used for single coagulation
frozen within eight hours factor deficiency (if no concentrate
of donation is available) and for multiple factor
deficiencies if abnormal bleeding is
occurring or is likely to occur. FFP is
rarely indicated to immediately
reverse the effects of warfarin
Albumin 4.5 per cent albumin is an Contributes to the maintenance of
isotonic protein solution. blood viscosity, osmotic pressure
20 per cent albumin is a and blood volume
hyperoncotic agent
Cryoprecipitate Prepared from plasma and Given for bleeding and prior to
contains fibrinogen and surgery in patients with
clotting factors hypofibrinogenaemia

Front 146

blood compatiblites

Back 146

o compat with o
a compat w/a and o
b compat w/ b and o
ab compat w/ a/b/ab/o

Front 147

transfusion observations

Back 147

Blood transfusion
identify any pre-medication.
n That any special blood requirements, such as
gamma irradiation, are catered for in the unit.
Under no circumstances should one nurse, midwife
or doctor check a unit of blood for another member
of staff to connect. The compatibility report and the
prescription chart should be signed at the time that
it is checked at the bedside and both should remain
available near the patient during the transfusion.
Patient observation Ensure that the patient is
in a location that enables him or her to be conveniently
observed. Give the patient a means of
calling attention and ensure that he or she knows
how to use it. Alert the patient to report any of
the following symptoms immediately:
n Chest pain.
n Flushing.
n Shivering.
n Abdominal discomfort.
n Rashes.
n Shortness of breath.
n Pain in the loins or extremities.
n Blood in urine.
n A feeling of restlessness or anxiety.
n Feeling generally unwell.

Front 148

blood set up

Back 148

n Close the clamp on the giving set.
n Pull the tabs to expose the outlet port and
insert the spike into the blood component pack
outlet.
n Invert the bag and the giving set so that the
giving set is pointing upwards.
n Open the clamp and squeeze the blood up
through the first chamber and a third of the
way into the second chamber.
n Re-invert the bag, hang it up and run through
as normal so that the blood continues to the
end of the line.
Note that it is not necessary to prime a blood giving
set with saline as this prevents correct priming of
the line with blood.
Warming is not normally necessary and blood
components should never be put in a bowl of warm
water, on a radiator or in a microwave oven: this is
dangerous, as it will damage the cells. The use of
specialist blood warming devices is not normally necessary
and if one is to be used, it must be checked
regularly and calibrated by a qualified technician.
Only electronic or mechanical infusion pumps specifically
designed for the purpose of transfusion should
be used, as other pumps will damage cells

Front 149

hemolytic rxn

Back 149

haemolytic reaction is
caused by destruction of the donor red blood cells
by antibodies in the recipient’s plasma. It can occur
after only a few millilitres of blood are transfused,
although a delayed reaction can occur up to two
hours later. Haemolytic reactions can be fatal and
as such, a suspected haemolytic reaction must
always be responded to as a medical emergency. A
haemolytic reaction is indicated by:
n Breathlessness.
n Collapse.
n Tachycardia.
n Hypertension followed by hypotension