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44 Cards in this Set
- Front
- Back
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HIV
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• Retrovirus
• Selectively infects and destroys CD4 lymphocytes – Normal CD4 count is >500, CD4 % is 40% or > • CD8 count rises as the body tries to turn off the immune system – DIAGNOSTIC TESTING – Current tests rely on antibody formation which usually occurs in 6 weeks after exposure (90%, 99.7% by 3 months) – ELISA/ Western blot • Positive Elisa with negative or indeterminate WB should be repeated in 4 weeks • False positives most common in pregnancy and autoimmune diseases – “window” refers to the time between infection and antibody formation (now 3 months) – PCR (polymerase chain reaction) detects actual virus in the blood (positive about 2 weeks post exposure) – Oral test kit available (Orasure), some recommend confirmation with blood test – New rapid HIV test blood available, 20 minutes • Average time 10-11 years • CD4 count drops about 80/year, viral load climbs (CD4 < 500 risk of OI) • Classification and Staging System (p. 365) • NO SX SX, no C Sx AIDS ind • 1-CD4 >500 A1 B1 C1* • 2-CD4 200-499 A2 B2 C2* • 3-CD4 <200 A3* B3* C3* *By CDC def these patients have AIDS • CLINICAL MANIFESTATIONS of Immune System Decline • The following symptoms will put the client into a category B – Candidiasis – Cervical dysplasia – Herpes – ITP – Listeriosis – PID (pelvic inflammatory disease) – Peripheral neuropathy – CLINICAL MANIFESTATIONS AIDS : Category C – CD4 count 200 or less – PCP pneumonia – Kaposi’s sarcoma – lymphoma – MAC – TB – Cervical cancer |
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Transplants
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autografts-self
allografts-same species xenografts-different species Immunology and Transplantation T and B lymphocytes play a role in transplant rejection 2 major systems involved in an individual’s antigenic makeup HLA-human leukocyte antigens (100 antigens have been identified) ABO blood typing system Immunosupressive Therapy Azathiopurine (Imuran) metabolized in the liver, excreted by kidneys can cause pancreatitis, alopecia, hepatotoxic SE-bone marrow suppression Mycophenolate mofetil (CellCept) SE- N, V, diarrhea Antiemetics, antidiarrheal agents used monitor for leukopenia\infection Immunosupressive Therapy Cyclophosphamide (Cytoxan) Causes bone marrow suppression Force fluids, monitor for hematuria, skin changes, jaundice Many drug interactions Rapamune (Sirolimus) Can cause HTN, Cholesterol issues, Bone marrow supression Micophenolic acid (Myfortic) Teratogen, report any neuro type changes Immunosupressive Therapy Cyclosporine (Neoral, Sandimmune)* very common Also used for psoriasis, RA Nephrotoxic (monitor BUN and Creatnine), many drug interactions Can cause hypertension, hyperkalemia, hyperglycemia SE-gingival hyperplasia, photosensitivity, hirsutism Monitor for tremors, paresthesias Can cause seizures with high dose prednisone Avoid giving with grapefruit juice Immunosupressive Therapy Tacrolimus (Prograf) Monitor blood glucose, diabetes may develop Daily weights, I&O Monitor for GI side effects Monitor neurological status Monitor renal function Immunosupressive Therapy Monoclonal antibodies Given IV Not usually long term therapy Usually used to treat rejection and during the immediate perioperative period with kidney transplants Immunosupressive Therapy Corticosteroids (Prednisone, etc)* Topical, PO, IM, IV, NS, MDI Used for many disorders, many side effects Sodium retention- edema, BP, low Na diet, weigh periodically Hyperglycemia- blood sugars Hyperlipidemia- Diet GI bleeding- with meals, monitor GI symptoms, stool for blood Cataracts Immunosupressive Therapy Corticosteroids, continued Osteoporosis- exercise, calcium Growth delay in children Hypokalemia Masks signs of infection, delay wound healing Behavioral changes Vascular and skin fragility HPA axis suppression (2 weeks) medic alert bracelet, education regarding administration, what to do if can’t be taken Rejection Organ rejection Monitor for signs of organ malfunction Hyperacute within 48 hours of transplantation caused by antibodies-mediated response seen primarily with kidney transplants usually not reversible Rejection Organ rejection Acute 1 week to 3 months post transplant humoral and cellular immune system treated with steroids and monoclonal antibodies Chronic rejection after 3 months cellular and antibody mediated response major unresolved problem as it is less responsive to medications Major cause of death after the first year post transplant Rejection Organ rejection Graft Versus Host Disease seen in allogeneic bone marrow transplants donor’s cells recognize the recipient’s cells as foreign and attack them symptoms are seen in the liver, skin, and GI tract |
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Immunity
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CBC with differential
Neutrophils, called segs or granulocytes, mature WBC, 60-70% Bands increased with bacterial infection (1-5%), Left shift Monocytes, become marcophages in tissue Basophils, release substances that cause inflammation Eosinophils, increased with parasitic infection, people with allergies Lymphocytes increased with viral infection (38%),Right shift Hypersensitivity Reactions Type I- Immediate or Anaphylactic (IGE mediated), runs in families, fairly common, most common are to penicillin and bee stings. Mast cells go out systemically and cause an overreaction, productions vasodilatation, smooth muscle contractions, increased vascular permeability, increased mucous gland secretion, bronchial constriction Type II –Antibody mediated- Antigen-antibody reaction which destroys cells (cytotoxic) - blood transfusion reaction Type III -Antigen-antibody reaction which causes inflammation (immune complex) - autoimmune diseases Type IV- T lymphocytes destroy antigens - contact dermatitis, tissue transplant rejection Type V- Stimulatory, autoantibodies that mimic the hormone itself - Grave’s disease, hyperthyroidism |
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Sodium
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Normal sodium level-135-145 mEq/L
Controlled by: aldosterone osmolality renin mechanism Functions to: regulate the osmotic pressure control neuromuscular function via Na/K pump acid-base balance Hyponatremia A decrease in the amount of Na in relation to the amount of water. Causes: – Water intoxication – Dilutional hyponatremia (CHF and renal failure, caused by fluids expanding) – SIADH (syndrome of inappropriate anti diuretic hormone) – True hyponatremia – Starvation hyponatremia Signs and Symptoms of Hyponatremia-(CNS changes) Water retention causes brain cells to swell and dehydration causes brain cells to shink Change in CNS level-maybe be decreased (apathy/lassitude) or increased (irritability) N/D-abd.cramping Weight gain and edema Hypotension or hypertension Decreased skin turgor Treatment for Hyponatremia Depends on the cause -for increased water-restrict fluids -for Na loss-give sodium -for malnutrition-improve nutrition Nursing responsibilities for Hyponatremia Maintain accurate intake and output records Weight patient Obtain vital signs Regulate IV fluids Be alert to CNS changes Hypernatremia Condition that occurs when water losses exceed sodium losses or when water intake is inadequate Causes: -excessive water losses -increased sodium intake Signs and Symptoms of Hypernatremia-(CNS changes) -changes in CNS level-maybe incrased or decreased -dry sticky mucous membranes -flushed skin -oliguria -restlessness, confusion -edema (if hypervolemia is present) -muscle twitching to muscle weakness/decreased DTR Treatment of Hypernatremia Depends on the cause -for decreased water-give water -for increased sodium-give salt free solutions Nursing responsibilities for hypernatremia -maintain accurate intake and output records -be alert for CNS changes -administer fluids as ordered |
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Potassium
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Potassium
Normal values-3.5-5.5mEq/L Functions -controls intracellular osmotic pressure -regulates acid-base balance -maintains neuro/muscular function via the Na/K pump Regulated by: -kidneys -Aldosterone – causes sodium retention and potassium excretion -Na/K pump Hypokalemia Causes – Diuretic therapy-most common – Excessive use of digitalis/steroids – Gastric losses via wound drainage/NG suction – Vomiting/diarrhea – Infusions of K free IV fluids – Cushing syndrome (aldosterone problem) – Renal disease – Water intoxication – NPO status Signs and Symptoms of Hypokalemia Muscle weakness/decrease reflexes Abdominal distension, flatulence progressing to paralytic ileus Dysrhythmias-PVCs initially Ventricular fibrillation EKG changes-flat or inverted T wave, presence of a U wave, ST segment depression, peaked P wave (can also be caused by increase intracranial pressure) presence of a U wave indicates low potassium level and is the only time you will see it Treatment for Hypokalemia Oral K supplements Parental administration – Maximum amount-5-10 mEq/hr – May need cardiac monitoring – Can not be given SQ, IM or IVP – Should check renal function first Hyperkalemia Causes of increased K – Renal failure – Crushing injuries/burns – Excessive K in IVs/potassium containing foods – Addison’s disease (opposite of Cushing’s syndrome, retain NA and excrete K) – MI – Hemorrhage/shock – Blood transfusions(Whole blood/packed cells) – Uncontrolled diabetes Signs and Symtoms of Hyperkalemia Muscle spasticity progressing to flaccid paralysis Diarrhea/nausea Cardiac manifestations-most lethal bradycardia hypotenstion Ventricular fibrillation EKG changes-tall, tented T wave, wide QRS, prolonged PR interval, flat or absent P wave, ST segment depression Treatment of Hyperkalemia Kayexalate enema or po IV glucose and insulin – almost immediately drops K levels Limit po intake Dialysis Take K out of IV fluids Correction of acidosis CA salts (protection) Nursing responsibilities with Hyperkalemia Be alert to K values EKG changes Fresh blood transfusion |
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Magnesium
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Magnesium
Normal value-1.5-2.5 mEq/L Problems with magnesium usually seen with potassium and calcium imbalances Functions – Activates many enzyme systems – Has sedative effect on the CNS – Facilitates transport of Na and K across the cell membrane Hypomagnesium Causes – Impaired absorption (malnutrition/starvation) – Too rapid excretion thru the kidneys – Inadequate intake – Citrate (blood products) – Diuretic therapy – Renal failure Signs and symptoms of hypomagnesium Neuromuscular irritability-tingling, twitching, tetany Hallucination/agitation/personality changes Hypertension Positive chvostek’s sign/Trousseau’s sign Ventricular irritability-PVCs, VT, VF Treatment for Hypomagnesium IM or IV magnesium sulfate – Watch for symptoms of hypermagnesium – IV rate not to exceed 150 mg/min – Do not give in renal insufficiency – Watch for resp. depression or heart block – Check deep tendon reflexes and RR – Calcium gluconate is antagonist Hypermagnesium Causes – Renal failure – Excessive use of magnesium containing antacids – Ingestion of cathartics (Epsom’ salts, MOM) – Hyperalimentation Signs and symptoms of Hypermagnesium Diminished reflexes Resp depression Hypotension Flush, feeling of warmth, sweating Bradycardia Drowsiness Treatment for Hypermagnesium Calcium gluconate Stop administering any magnesium Hydration dialysis |
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Calcium
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Calcium
Normal level- – 4.5-5.8 mEq/l – 8.5-10.5 mg/100cc – Majority of calcium is found in the bones – Only small percent found in the serum The Calcium Train and its mystery passenger If you know the signs of hypocalcemia, hypercalcemia is the opposite Ca and Mg go together (the mystery passenger) Ca and Phosphorus go in opposite directions Hypocalcemia Causes – Hypoparathyroidism especially after thyroid or parathyroid surgery/thyroid radiation – Decreased absorption from the intestines – Low Levels of vitamins D – Inadequate calcium intake – Renal disease – Diarrhea/draining wounds Signs of Symptoms of Hypocalcemia Parathesias of nose, ears, fingertips, toes, tingling, twitching Tetany/seizures Cardiac irregularities-prolonged QT interval Trousseau’s sign (thumb adduct and wrist will flex with blood pressure cuff on inflated to 20mm Hg) Chvostek’s sign (tap patients facial nerves and contraction will occur) Painful muscle spasms (Charley horse) seen early Treatment of Hypocalcemia IV calcium Po calcium Vitamin D supplements Nursing Responsibilities for Hypocalcemia Observe for changes in neuromuscular irritability Seizure precautions Decrease stimulation Administer digitalis preps with caution Have trach tray ready (after thyroid surgery) Prevention of injuries (esp to bones) Hypercalcemia Cause – Primary hyperparathyroidism – Multiple myeloma/metastatic cancer – Vitamin D overdose – Over use of aluminum hydroxide gel (calcium containing antacid) – Paget’s disease – Renal failure – Prolonged bedrest/immobility Signs and symptoms of hypercalcemia Lethargy leading to coma Anorexia/N and V/dehydration Constipation Decreased QT intervals on EKG Renal stones Pathological bone fractures Severe muscle weakness/decreased DTRs Treatment of Hypercalcemia Definitive treatment-remove the cause Hydrate with NS Oral phosphate Mithracin Nursing responsibilities for Hypercalcemia Encourage mobility when possible Strain urine if kidney stones suspected Observe for CNS and musculoskeletal changes |
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Radiation Therapy
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Definition-the movement of energy through a space or medium. Therapy is based on the concept that rapidly reproducing malignant cells are more sensitive to radiation than normal cells
Protection of Health Care Workers Time-limit the amount of time in close proximity to the patient (30min/8hrs) Distance-increase the distance from the radiation source (6 ft) Shield-use lead barriers Factors that influence side effects Body site irradiated Dose of radiation given Extent of body treated Method of radiation Skin Care First degree reaction-destroys hair roots Second degree reaction-sweat glands are destroyed. Hair loss may be permanent. Skin is bright red erythema Third degree reaction-skin has dark purple areas, may have blisters and scabs. Hair loss and sweat gland damage is permanent. May need to stop treatment for healing Fourth degree reaction-rare Ways to minimize skin damage (pg 420) Avoid sun exposure, trauma to the skin, adhesive tape Use caution with soaps No bath salts, perfumes, ointments or lotions No heat lamps, heating pads, ice packs Wear soft, cotton lightweight clothing May have medicated ointment prescribed Other Side Effects-usually from dead cancer cells entering bloodstream Scalp with hair loss Head and Neck Chest and lungs Abdomen Pelvis Bone marrow Internal Radiation Definition-the use of high energy radioactive sources placed into or directly on the body to treat a disease. General Precautions to Internal Radiation Private room Radioactive sign on the door Wear film badge Encourage self care Rotate care givers Limit visitors Precautions if implant is dislodged |
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Chemotherapy
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Side Effects of Chemo (most problematic) pg 423
Bone marrow depression-a decrease in the number of circulating blood cells (both RBC and WBC and platelets) Neutropenia-decrease in number of WBC. Patient will need neutropenic precautions (reverse isolation) Anemia-decrease in number of RBCs Thrombocytopenia-decrease in number of platelets Nadir effect Because cells have different life spans lab values will reach their lowest point at different times. WBC will be lowest 7-10 days after treatment RBC will be lowest 7-10 days after treatment Platelets will be lowest 10 days after treatment Nursing care of the immunosuppressed patient (low WBC) pg 426-427 Good handwashing Prevent exposure to people with known infections Meticulous aseptic technique Adverse effects of Chemo-stomatitis (mucositis) Frequent assessments of the oral cavity Treatment – Mouth care with mild baking soda, Magic mouthwash (Avoid commercial mouthwash) – Nystatin swish and swallow – Viscous lidocaine (numbing solution) – Soft toothbrush, no floss – Lubricant to the lips – Avoid hot spicy food unless patient requests it and it causes no problems – Good fluid intake Adverse effects of chemo-pharyngitis Same as for stomatitis Adverse Effects of Chemo-Anorexia (pg 427) Anorexia may be due to: – Effect of chemo on hunger center in the thalmus – Nausea and vomiting – Stomatitis Patient may need enteral feedings or TPN Adverse effects of Chemo-nausea and vomiting CIN-Chemotherapy induced Nausea Occurs due to the effect of the chemo on the emesis center in the thalamus. The drugs are emetogenic (vomiting inducing) Offer small, frequent feedings Dietary counseling Cold bland foods Antiemetic meds-give liberally. Work best when given 30-60 minutes before eating Peripheral Neuropathy (PN) pg 430-431 Loss of sensory or motor function of peripheral nerves (permanent) Seen with nerve damaging chemo agents (antimitotics and platinum drugs) May have rapid onset/may be severe Seen long term/may be permanent Prevention of injury most important Chemo Brain Unsure why this happens Listen to the patient/Be supportive Know that this is real for the patient Renal Toxicity Some agents are nephrotoxic-examples-Cytoxan or methrotrexate Monitor BUN and creatinine Encourage increased oral intake-maintains hydration Observe for signs of hemorrhagic cystitis-dysuria, hematuria Pulmonary Toxicity (cumulative effect, once max is reached the drug can never be taken again) These agents have a cumulative effect on the pulmonary system. Example-Bleomycin Observe for pneumonia, CHF, SOB, coughing Cardiovascular Toxicity These agents have a cumulative effect on the cardiovascular system. Example-Adriamycin (solution is red) Observe for signs of CHF Obtain a baseline EKG Reproductive Toxicity Some agents are teratogenic. Example-methotrexate Sperm banking Birth control Toxicity for the Hepatic System Problem with chemo agents that are metabolized by the liver Monitor liver function test |
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Cancer
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Oncological Emergencies pg 434
Superior Vena Cava Syndrome (SVCS) – A disorder of venous congestion caused by obstruction of venous drainage in the upper thorax either by a primary tumor or a secondary tumor Signs and Symptoms-slow and progressive -SOB, headache, visual disturbances,facial edema Spinal Cord compression – A disorder caused by direct pressure on the spinal cord with compromised vascular supply to the area leading to spinal cord infarct or veretebral collapse. Signs and Symptoms-depend on the site of compression Early will be localized back pain and weakness in lower ext. Pericardial effusion/cardiac tamponade – An increased accumulation of fluid in the cardiac sac due to the tumor invasion or pericardial thickening after radiation Hypercalcemia-the most common oncological emergency Occurs in 10-20% of all cancer patients Signs and symptoms-may manifest as pathological fracture Tumor Lysis Syndrome The destruction of large numbers of tumor cells is happening quicker than the elimination of them. This results in electrolyte imbalances Can be prevented by good hydration Treat-the electrolyte imbalance A sign that the chemo is working SIADH – syndrome of inappropriate anti diuretic hormone DIC- Disseminated intravascular coagulation Septic Shock |
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Diabetes
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TYPE 2 DIABETES
• Diagnosis • FBS >125 (recommended test) • RBS 200 or > with symptoms • OGTT 75 gm CHO • FPG >125 or 2 hr > 200 TYPE 2 DIABETES • Prevention/early diagnosis • Weight control • Avoid foods with a high glycemic index • Regular exercise (150 minutes/week) • High fiber diet • FPG (fasting plasma glucose) every 3 yrs starting at age 45 • Age 30 for high risk groups esp AA and Hispanic • Age 30 with risk factors • Intervention with impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) Now called pre-diabetes. • Macrovascular disease actually starts during this period of time TYPE 2 DIABETES • Goals of therapy • Pre-prandial blood glucose 90-130 • nl<100 • Post-prandial (2 hr) blood sugar <180 (nl <140) • Hemoglobin A1C <7% • nl 4-6 TYPE 2 DIABETES • Treatment • Sulfonylureas- glipizide (Glucotrol and XL), glyburide (Diabeta, Micronase), micronized glyburide (Glynase Pres Tab), glimepiride (Amaryl) • increase insulin secretion from pancreas • will cause weight gain • can cause hypoglycemia, cannot skip meals • avoid ETOH (alcohol), decreases metabolism of drug • sulfa allergy may preclude use TYPE 2 DIABETES • Treatment • Meglitinide (Prandin), nateglinide (Starlix) • Increases insulin production by the pancreas • Take before each meal • Good for persons with erratic eating habits • Elderly TYPE 2 DIABETES • Treatment • Acarbose (Precose), Miglitol (Glyset) • Interferes with absorption of CHO from duodenum, digested later in colon • SE is GI problems (flatus) • SE decrease over time • Not systemically absorbed • Taken with first bite of each meal • Cannot treat hypoglycemia with regular sugar • Use laxatives TYPE 2 DIABETES • Treatment • Rosiglitazone (Avandia), pioglitazone(Actos) • Increases insulin sensitivity at cell level by changing the cell membrane structure to increase insulin receptors • Takes 2-4 weeks to see full effect • Can be hepatotoxic • monitor for S&S, LFT monitored frequently • Patient may gain weight • Some patients experience significant edema • Can precipitate or worsen heart failure due to fluid retention • Recent concern of association with increased risk of MI (Avandia) • rosiglitazone and glimepiride (Avandaryl) TYPE 2 DIABETES • Treatment • Metformin (Glucophage, Glucophage XR, Riomet, Fortamet, Glumetza) • Decreases glucose absorption by the gut • Good for overweight, tend to loose weight • Favorable effect on lipid profile, no hypoglycemia • Side effects- flatus, diarrhea, decreases with time • Contraindicated with renal impairment • Stop 48 hrs before any studies using dye, wait 48 to restart • Contraindicated in liver disease, alcohol abuse • New formulations called • Glyburide and glucophage (Glucovance) • Rosiglitazone and metformin (Avandamet) • Glipizide and metformin (Metaglip) • Pioglitazone and metformin (Actoplus met) TYPE 2 DIABETES • Treatment • Exenatide (Byetta) (approved June 1, 2005) • New class of drugs, incretin mimetics • Can be used as monotherapy or with other oral agents • SC injection BID up to 60 minutes before the breakfast and evening meal • Comes in a pen, 5mcg or 10mcg per dose • New warning about pancreatitis • Action • Lowers postmeal and fasting glucose levels • Stimulates the pancreas to produce insulin • Slows food absorption • May cause weight loss • Can cause hypoglycemia TYPE 2 DIABETES • Treatment • Sitagliptin (Januvia) • Inhibits the activity of enzymes that break down incretins which play a role in insulin synthesis and release from the pancreas • Adjunct to diet and exercise in type 2 diabetes • Can be monotherapy or with other oral agents • Given orally once daily TYPE 2 DIABETES • Treatment • Insulin • Indicated when BS cannot be controlled with oral agents (can combine oral agents) or during periods of stress such as infection • if an acute event may add SS only using short acting insulin • Combination of evening intermediate or long acting with daytime oral agent often used first • Split mix used commonly 70/30, 75/25, 50/50 TYPE 2 DIABETES • Treatment • Pramlintide (Symlin) • Injectible, SQ, before meals into abdomen or leg, rotate sites • Used with insulin or oral agents • Lowers blood sugar during the 3 hours after a meal • Slows absorption, decreases liver glucose, increases satiety • Risk is hypoglycemia • CANNOT be mixed with insulin • Stored like insulin (up to 30 days at room temperature) • Vials 0.6mg/ml solution, given in micrograms • Also used for type 1 diabetics TYPE 2 DIABETES • Treatment- hypertension • Goal is BP <130/80 to preserve renal function • <125/75 if sign proteinuria already present • Control of BP more important than control of BS in preventing renal deterioration • ACE inhibitors or angiotensin receptor blockers are the drugs of choice to preserve renal function • High glucose load stresses the kidneys • ACE inhibitors and ARB’s lower the GFR and normalize pressure within the nephrons • Renal function, K must be monitored • SE is cough, edema TYPE 2 DIABETES • Treatment-hyperlipidemia • Goal is LDL <100, <70 with CAD • HDL >40(men),>50(women) • TG <150 • Lifestyle changes • increase exercise • low fat diet • no smoking TYPE 2 DIABETES • Treatment-hyperlipidemia • Medications • *HMG Co A reductase inhibitors (statins) • monitor for liver toxicity • myositis (generalized muscle weakening) • Bile acid binding resins • Gemfibrizil (TG) • Niacin (may raise BS levels) • ASA (aspirin) daily if > 40 years of age or with risk factors TYPE 2 DIABETES • Complications -hypoglycemia • <70 with or without symptoms, <80 with symptoms, <90 at bedtime or overnight • Too much insulin or not enough food • S&S • increased sympathetic activity (cold, sweating, irritable, headache) • decreased CNS glucose • pallor, diaphoresis, nervous, irritable, H/A, weak, shaky, diaphoresis, decreased LOC • Treatment • Check BS if in doubt treat for hypogycemia • Check BS in 15 min, >80, snack if next meal >60 minutes • Give 15-20gms CHO • Glucagon (SC/IM, 1mg), IV D50 if severe • Cold and clammy need some candy, hot and dry is sugar high • be aware that client may be taking drugs that may blunt the symptoms of hypoglycemia such as beta blockers (diabetics taking beta blockers is contraindicated) TYPE 2 DIABETES • Complications –HHS (HHNC*) type 2 • Hyperglycemic-hyperosmolar state (HHS) • Mortality 70% because it develops slowly and is diagnosed late • Pathophysiology • caused by deficiency of insulin but enough to prevent ketosis • persistent hyperglycemia causes osmotic diuresis with loss of water and electrolytes (Na and K) • severe dehydration results • develops slowly and diagnosed late (elderly) • Etiology • acute illness such as infection • meds (diuretics, corticosteroids) TYPE 2 DIABETES • Complications -HHS • Signs and symptoms • polyuria, polydipsia • hypotension, tachycardia • profound dehydration • neurological changes TYPE 2 DIABETES • Complications -HHS • Treatment • Treat underlying cause • Fluids (NS or .45% NS) to re-hydrate • Elderly must re-hydrate carefully • Electrolytes, K may be WNL and then drop when pt is treated as K moves back into the cells • Insulin IV TYPE 1 DIABETES • Treatment (Insulin, continued) • Formulations • Insulin lispro (Humalog), insulin aspart (Novolog), insulin glulisine (Apidra) • onset <15 min, peaks 1 hr, lasts 3-4 hrs • take when you sit down to eat (0-15 minutes before eating) • Insulin glargine (Lantus), insulin detemir (Levemir) • No peak, lasts 24 hours • Clear • Do not mix with any other insulin • Usually given at bedtime • Humulin R U500- clear, for >200u/d, only SQ, lasts 24 hours • Humalog mix 75/25, 50/50 • Insulin lispro protamine and insulin lispro Complications • DKA (mortality about 10%) • Etiology • Infection*, stress, too much food, not enough insulin, meds • Signs and symptoms • dry, flushed skin, fruity breath odor, Kussmaul respirations (deep and rapid, exhaling CO2 to try to get rid of acids), change in LOC, nausea, vomiting • Treatment (much like HHS plus treating acidosis) • fluids, insulin, electrolytes, treat underlying cause • education TYPE 1 DIABETES Complications • Somogyi effect • gluconeogenesis and glycogenolysis occurs during sleep due to hypoglycemia • am BS high • need to check BS at 2-3 am to identify • treated by moving supper NPH to bedtime or give HS snack |
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Respiratory - General
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– crackles – fluid, typically cardiac
– rhonchi, typically congestion of the bronchi – wheezing, narrowing of the airway Chest contusion • Hemorrhage in and around the alveoli • Hypoxemia occurs o Develops over time, bloody sputum, crackles, decreased breath sounds o Rx oxygenation/ventilation, ARDS may develop |
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TB
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Laboratory Assessment
• QuantiFERON-TB Gold (QFT-G) o Results in < 24 hours, acute care setting • + tuberculin skin testing (Mantoux) o 10mm induration (48-72 hours) o Indicates exposure or dormant disease o 5mm induration for immunocompromised patients o Anergy –failure to respond due to ↓ immune function o Once positive no further skin tests should be done • chest x-ray • sputum culture confirms the diagnosis o takes 1-4 weeks for results o Used to determine treatment effectiveness Treatment • isolation until symptoms subside, 3 negative smears not infectious • initial regimen is with 4 drugs (6 months of treatment) • number can be altered when susceptibility testing is completed • DOT (directly observed therapy) has increased success of treatment • Combined drugs in a single tablet improves compliance • patients can be held against their will for treatment if they do not comply • lifestyle changes to improve health Isoniazid (INH) • Dosing 200-300 mg daily or 600-900 mg 2X/week • used for treating positive skin tests and active disease • SE: peripheral neuritis (tingling, numbness – can be prevented by taking vitamin B-6), rash, fever, hepatitis, anemia , • Prone to PN-take daily dose of 6-50mg • Liver function tests may be checked monthly during therapy • ETOH (alcohol) increases risk of hepatitis and interferes with drug metabolism • aluminum containing antacids decrease absorption • Take on an empty stomach Rifampin • Dosing- 500-600 mg daily or 2x/week one disease is under control • SE: hepatotoxicity, GI disturbance, flu-like symptoms, thrombocytopenia, can alter color of urine, can cause issues with contact lenses, interferes with birth control pills and blood thinners, decreases affects of HIV medication • LFT’s and/or platelets may be monitored • Body fluids turn orange • Decreased effectiveness of BCP, anticoagulants, NNRTIs • Rifamate is INH and rifampin in 1 tablet Ethambutol • Dosing 750-1500 mg daily or 2500-5000mg 2X/week • SE-optic neuritis (can lead to blindness, only reversible if caught early), asymptomatic hyperuricema • Report any visual changes immediately • Ask about history of gout-drug inhibits excretions of uric acid • Avoid alcohol –hepatotoxic, can also cause severe N/V if taken with alcohol • Drink 8 0z of water with dose, ↑ fluid intake • May be taken with food for GI upset Pyrazinamide (PZA) • SE: ↑ uric acid, hepatitis, arthralgia, GI upset, photosensitivity • uric acid, LFT may be checked • give with food • drink 2 liters of fluid daily • Rifater is INH, rifampin, pyrazinamide in a single tablet |
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Lung Cancer
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Signs and symptoms – table 32-5 in book
• persistent cough unresponsive to treatment * • hemoptysis * • dyspnea * • wheezing * • pain • fatigue • weight loss Diagnostics • chest x-ray • sputum cytology • bronchoscopy and biopsy • CT and MRI used for diagnosis and staging Nonsurgical Management • Chemotherapy- small cell lung cancer (SCLC) o Alone or adjuvant with surgery o Platinum-based agents • Targeted therapy • Radiation o In combination with surgery or chemo • Photodynamic (PDT) o Small bronchial tumors o RF bronchial hemorrhage, fistula formation, hemoptysis o Photosensitivity up 3 months after treatment Thoracic surgery • Pneumonectomy (removal of entire lung)- no chest tube post-op • lobectomy/segmental resection, wedge resection • chest tube post-op • Open thoracotomy or thoroscopy with MIS Postoperative Care • ventilation, lung re-expansion, oxygenation • chest tubes, TCDB, spirometer, resp tx • Pain management necessary so patient will cough • nutrition • positioning, semi-fowlers • ambulation, pleurovac below chest level • arm exercises, passive to active • Other meds- Bronchodilators, antibiotics, corticosteroids Nursing Concerns Incision • be sure tubes are patent and not kinked o blood on the dressing is unusual due to chest tube, should be reported o subcutaneous emphysema- caused by air leaks from the pleural space into SQ tissues not abnormal, monitor, report if worsening o may need a larger chest tube or more suction • patients with a pneumonectomy should not have SQ emphysema- report, air leaking from bronchial stump Chest tube • used for 48-72 hours (report > 100mL/hr output) • Dressing chg every 8 hrs after first 24 hours • Lack of tidaling may indicate obstruction • X-ray used to confirm re-expansion • do not clamp→ tension pneumothorax o Resp distress, tracheal deviation Pneumonectomy • Surgeon will order positioning, most on operative side • monitor trachea deviation caused by mediastinal shift if air leak occurs |
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Respiratory Diagnostic Tests
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ABG’s for oxygen and CO2 levels
CBC, COPD will typically produce more RBC’s to carry oxygen, WBC’s for infection, Sputum analysis X-ray, CT, MRI PFT (Pulmonary function test) Peak flow meters Skin testing for TB Bronchoscopy Concern is loss of gag and swallow reflex Monitor breath sounds |
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Angina
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Beta Blockers end in “olol”
Examples-Inderal, lopressor, Tenormin Decrease the patient’s heart rate and therefore decrease oxygen demands Calcium Channel blockers “CA” Examples-Calan, Verapamil, Procardia, Cardizem Work by preventing the flow of calcium into the cells resulting in relaxation of the smooth muscles of the myocardium (desired effect) and a reduction in myocardial contractility (a undesired effect). The desired effect outweights the undesired effect |
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CAD/MI
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Left coronary artery - “Widow Maker”
Left Anterior Descending artery (LAD)-supplies blood to the anterior 2/3 of the septum, the anterior and apical portion of the left ventricle and a portion of the right ventricle, blood pressure is a good indicator of function, low blood pressure could indicate a blockage Left circumflex artery-supplies blood to the left atrium, lateral wall of the left ventricle and a portion of the posterior wall of the left ventricle, blood supply for the SA node in most people, those with blockages need to be monitored for electrical disturbances Right Coronary Artery-supplies blood to the right atrium, the right ventricle, posterior third of the septum and the inferior and posterior left ventricle Pre-load - Increased preload indicates cardiac failure/hypervolemia Decreased preload indicates hypovolemia Afterload-the tension and stress that develops in the walls of the ventricle during systole (resistance that the ventricle must pump against) Increased with hypertension/vasconstriction Decreased in vasodilation Inotropic-increases the force of myocardial contractions Chronotropic-increases the rate of myocardial contractions TEE-Transesophageal Echocardiography Allows ultrasonic imaging of the cardiac structures and the great vessels via the esophagus Contraindicated in esophageal surgery, dysfunction or malignancy Should be NPO 4-6 hours prior to test and until the gag reflex returns Check allergies/check consent Acute Coronary Syndrome A syndrome seen in patients with coronary atherosclerosis in which there are varying degrees of coronary artery occlusion (rupture) which may end on myocardial infarction or sudden cardiac death. Includes unstable angina and MI Diagnostic Studies for MI-Non specific CBC-Usually shows up in a few hours after pain begins and lasts up to 3-7 days. Gives baseline Electrolytes-assess for imbalances/gives baseline ESR-erythrocyte sedimentation rate-increased due to inflammation. Rises during the first week after an MI and remains elevated for several weeks – indicates inflammation Blood coagulation studies-used to monitor coagulation therapy (Heparin, TPA) BUN and creatinine-indicator of renal function Myoglobin-a very early marker for MI. Becomes elevated 2 hours after pain, declines in 7 hours. Is not cardiac specific Serum Lipids-used more as a risk for CAD C-Reactive Protein-tells us about inflammation. If elevated may need to change life style or may need to be on a cholesterol lowering agent Diagnostic studies for MI-specific Troponin level-indicator of myocardial damage. Become elevated within 3 hours after onset of pain and returns to normal in 14 days Normal value-negative CK (creatine kinase) and CK isoenzymes-useful indicator of myocardial muscle damage CK-MB-specific for myocardial damage Normal values-less than 99U/L in males less than 57 U/L in females Becomes elevated in 3-6 hours after a MI, peaks in 12-18 hours and returns to normal in 3-4 days EKG changes Pronounced Q wave ST segment increases (STEMI) T wave inversions Antiplatelet agents- Aspirin- primary antiplatelet agent used in pre-hospital care/emergency room for suspected MI May be taken as a preventive therapy Other antiplatelet agents-Plavix and Ticlid Fibrinolytics Need to be given within 6 hours after onset of MI Work by lysising the clot that is obstructing the the coronary artery May cause reperfusion heart dysrhythmias Patient must be monitored for bleeding tPA, reteplase, streptokinase-examples Glycoprotein Iib/IIIA receptor inhibitors- Prevent platelet aggregation and clot formation Used for ACS (unstable angina and non Q wave MI Monitor for bleeding Aggrastat, Integrelin, ReoPro-examples Core Measures for MI (assuming there is no contraindications) Aspirin on arrival to ED and at discharge ACE inhibitor/angiotensin receptor blocker at discharge Smoking cessation class BETA blocker at discharge Thrombolytic therapy within 30 minutes of ED PCI (percutaneous coronary intervention) within 90 minutes of ED |
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CHF
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Left Sided Heart Failure
Left ventricular CO is less than the volume of blood received from the pulmonary circulation Can be systolic or diastolic heart failure Right Sided Heart Failure Right ventricular CO is less than volume received from the peripheral circulation Can be due to left sided HF, or some problem with pulmonary constriction S/S of Left heart failure (pulmonary in nature) Dyspnea Dyspnea on exertion Orthopnea Paroxysmal noctural dyspnea Fatigue Pain Anxiety Edema Rales and rhonchi S/S of Right heart failure (systemic in nature) Peripheral edema Ascites Distended neck veins Diuresis at rest May also include S/S of left heart failure Diagnosis of Heart Failure Clinical symptoms Chest Xray BNP level (brain natriuretic peptide) tells that fibers in the right atrium are being stretched and that there’s too much fluid in that chamber of the heart, can get up as high as six thousand but could be zero in a person without heart failure, if there’s anything about zero it indicates heart failure Microalbuminuria-early warning indicator |
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Pulmonary Edema
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Definition-medical emergency resulting from heart failure, patients are basically drowning in their own secretions
Pathophysiology-Fluid is forced into the alveoli due to increased pulmonary capillary pressure due to a decrease in CO S/S of Pulmonary Edema Restlessness/uneasiness Profound dyspnea Pallor Blood tinged secretions Wheezing Cyanosis tachycardia Interventions Place in High Fowler’s position Oxygenate-may need intubation Morphine – vasodilator, decreases preload so fluid goes to the periphery, decreases anxiety and decreases respiratory rate Diuretics Inotropic agents-improve cardiac output Vasodilators-decrease afterload |
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Pulmonary Embolism
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Risk factors for PE
Any condition that causes – Venous statsis – Hypercoagulability, dehydration – Vascular wall damage S/S of PE Depends on the size or number of PE May be asymptomatic Dyspnea Tachypnea Tachycardia Pleuritic CP (chest pain) Hemoptysis Distended neck veins Syncope Hypotension Low grade fever petechiae Diagnostic tests for PE Patient history ABGs, EKG and Chest X-ray V/Q perfusion scan (ventilation/perfusion scan)-will show high probability (p. 566 in Iggy) Pulmonary angiography-most definitive D-dimer Medications for PE Anticoagulants- – Heparin Drug of choice Inhibits coagulation/does not dissolve clots IV bolus given followed by a continuous infusion Monitor PTT Protamine sulfate-antagonist Coumadin Given po/IM Started while patient is on Heparin Monitor PT/INR Vitamin K-antagonist Thrombolytic agents Works to dissolve a clot Not usually used for routine PE because it does not seem to change the outcome May not be used on post operative patients due to potential for bleeding Examples, streptokinase, tPA |
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Aneurysm
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Causes of aneurysms
Atherosclerosis Congential birth defects Trauma Infections Connective tissue disorders Risk factors for Aneurysms Smoking Hypertension Genetic predisposition Types of aneurysms Fusiform-uniform dilation all around the aorta Saccular-saclike-narrow neck, balloon shape Dissecting-involves a separation or tear in between the layers of the blood vessel which can extend so that there is an accumulation of blood in this new cavity Ruptured-break in the blood vessel S/S of aneurysms Asymptomatic Leaking or ruptured-may c/o severe pain, signs of shock, decreased RBC, increased WBC Abdominal-palpable mass, systolic bruit, c/o abdominal pain or back pain Thoracic-chest wall pain, back, flank, abdominal pain, dyspnea, cough, wheezing Surgery Usually only done if greater than 6 cm Major surgical procedure Diseased area is replaced with a graft or stents |
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EKG
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EKG complexes
P wave represents depolarization of the atria P-R interval-represents the conduction time between the SA node thru the AV node The PR interval should be between 0.12-0.20 seconds A longer PR interval represents a delay through the AV node (and is one of the ways that heart blocks are determined) QRS complex – Represents ventricular depolarization – The first downward deflection is called a Q wave – The first upward deflection is called a R wave – The first downward defection following an upward deflection is called a S wave QRS interval – Represents the time involved in ventricular depolarization – Normal QRS interval should be no greater than 0.12 seconds |
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Endocarditis
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Infective Endocarditis (endocardium is inside, lines the valves) pg 783
Definition-infection of the endocardium in which the valves of the heart are most often affected but may involve any area of the endocardium Can be acute or chronic Acute Endocarditis is most often caused by a staph infection and may cause rapid destruction of the tissue resulting in death in days to weeks if left untreated, anyone with valve problems is at risk Persons at risk for endocarditis Patients with rheumatic valvular disease, congential heart disease or degenerative heart disease Patients who have had a valve replacement Immunosuppressed patients IV drug abusers and body piercings Infectious Endocarditis May be preceded by dental procedures, minor surgery, open heart surgery, invasive procedures IV drug users. Occurs when bacteria in the blood becomes lodged on the valve resulting in infectious growth or “vegetation”. Vegetation can break off and form an emboli. Most commonly develops on left side of the heart because left side has more pressure. S/S of endocarditis Fever/chills Fatigue Anemia Anorexia Weight loss Murmur Heart failure Petechiae Janeway lesions-nontender, macule on palms of hands and soles of feet Osler’s nodes-small, raised, tender, bluish areas on the fingers and toes Diagnostic tests for Endocarditis Blood cultures CXR ECHO (TEE – echocardiogram through the esophagus) Cardiac cath Treatment for Endocarditis ID the infecting organism Antibiotic therapy (usually IV antibiotics, requires prolonged hospitalization) Surgical valve replacement Nursing Care for Endocarditis ID patients at risk Notify all MDs, including dentists Good oral hygiene Assess for S/S of endocarditis |
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Valvular Heart Disease
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A and P of Valves
Tricuspid valve-separates the right atrium from the right ventricle Mitral valve-separates the left atrium from the left ventricle Pulmonic valve-separates the right ventricle from the pulmonary circulation Aortic valve-separates the left ventricle from the aorta Stenosis-the orifice is restricted and forward blood flow is restricted. An increased pressure is needed to push the blood through the valve. Regurgitation (insufficiency)-the valves fail to close properly and the blood is allowed to flow backwards Mitral Stenosis Most often occurs due to Rheumatic Fever Because of the stenotic valve the pressure in the LA increases which causes the LA to dilate. This causes fixed left sided cardiac output which causes an increase in pressure in the pulmonary vascular bed which causes pulmonary congestion which causes right heart failure Patients with mitral stenosis are at risk for the development of atrial fibrillation due to the dilate LA. S/S of Mitral Stenosis CXR-will show enlarged LA Symptoms of right sided (the body – edema, ascites, jugular vein distention, etc.) and left sided heart failure (pulmonary in nature) Heart sound changes-opening snap with diastolic murmur Diagnostic tests for Mitral Stenosis Clinical symptoms (left and right sided heart failure) EKG CXR ECHO (definitive diagnosis) Cardiac cath Once the patient becomes symptomatic they have a life expectancy of 5-10 years unless they have a valve replacement Interventions for Mitral Stenosis Digixon Diuretics Beta Blockers Calcium Channel Blockers Low sodium diet Try to convert atrial fibrillation. If a. fib continues will need anticoagulation therapy. Also if ventricular rate is fast may need Amiodorane or a beta blocker to slow down rate All patients with valve disease should be on prophylactic antibiotics prior to any invasive procedure Surgical interventions for Mitral Stenosis Mitral commissurotomy-splitting of the fused mitral valve leaflets Mitral valve replacement-replacement of the valve with either an artificial or bioprosthetic valve Balloon Valvuloplasty-catheter with a balloon is threaded into the valve and the balloon is inflated opening up the valve. Mitral Regurgitation The insufficient mitral valve allows blood from the LV to re-enter the LA during systole which causes the LA to dilate. The LV has to hypertrophy to maintain the cardiac output and eventually heart failure occurs Causes of Mitral Regurgitation Rheumatic heart disease Ruptured papillary muscle S/S of Mitral Regurgitation Signs and symptoms of right and left sided heart failure Diagnostic tests for mitral regurgitation Clinical symptoms Blowing, high pitched systolic murmur S3 CXR EKG ECHO Cardiac cath Treatment for mitral regurgitation Supportive Low sodium diet Diuretics Digixon Beta Blockers May need surgical replacement or repair to own valve (mitral valve annuloplasty Mitral Valve Prolapse – mostly seen in women One or both of the leaflets may be floppy and “prolapse” back into the atria during systole. May also have mitral regurgitation S/S of mitral valve prolapsed (rule out MI first) Asymptomatic Atypical chest pain Palpitations Fatigue Dizziness Dyspnea Anxiety Aortic Stenosis – mostly seen in men (approximately 80%) As the left ventricle tries to push blood through the stenotic aortic valve there is an increase in LV systolic pressure which eventually leads to LV failure. Eventually the patient will develop heart failure as the LV can not push blood forward. S/S of aortic stenosis Angina-due to the fact that the oxygen demands of the myocardium are not being met, first classic symptom Syncope-due to the fact that the brain is not getting the blood supply that it needs Dyspnea-due to the development of pulmonary congestion because the LA can not completely empty. Later S/S of Aortic Stenosis Fatigue Weakness Orthopnea PND Peripheral edema JVD ascites Classic S/S of Aortic Stenosis Angina, Syncope, Dyspnea Diagnostic Tests for Aortic Stenosis Harsh, rough, mid-systolic murmur Cardiac cath CXR ECHO EKG Interventions for Aortic Stenosis Digixon Beta Blockers Low sodium diet Diuretics Nitro for angina Balloon valvuloplasty May need valve replacement Aortic Regurgitation Because the aortic valve does not close completely there is a backflow of blood from the aorta to the LV during diastole. This causes the LV to dilate and then hypertrophy develops as the heart tries to compensate with a more forceful and rapid ejection of blood S/S of Aortic Regurgitation May take many years to develop Widened pulse pressure Other symptoms similar to other valve problems Diagnostic tests for Aortic Regurgitation Soft, blowing, aortic diastolic murmur EKG Cardiac cath ECHO Angiography CXR |
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Anemia
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Anemias
• Nutritional -Iron Deficiency -Vitamin B12 Deficiency -Folic Acid Deficiency • Hemolytic -G6PD -Immunohemolytic • Aplastic Iron Deficiency Causes Inadequate supply of iron (2/3 stored in HG, rest stored in liver, bone marrow, spleen, muscles) Body cannot synthesize hemoglobin Fewer number of RBCs, smaller and pale in color Chronic Bleeding Menstrual bleeding GI Inadequate intake or malabsorption (not enough leafy vegetables, meat, dairy products) Additional manifestations ● Brittle nails ● Smooth sore tongue ● Cheilosis (cracks in the corners of their mouths) ● Pica (eating things like dirt, clay) Vitamin B12 Deficiency RBC Macrocytic – large but mis-shapen in the membranes Fragile, short life span Do not carry O2 Pernicious anemia Failure to absorb B12 Strict vegetarians (no dairy) Gastric or ileal resections • Manifestations – can all be reversed with treatment Pallor, slight jaundice Sore beefy red tongue Diarrhea Paresthesia Proprioception – lack of sense of space Balance difficulty due to spinal chord involvement • Treatment ↑ intake of meats, dairy Parenteral Vit B12 replacement forever (Z-track, very irritating to the skin) weekly at first them monthly once normalized Shillings test – if it shows up in the urine after the shot they are absorbing B12 Folic Acid Deficiency (required for DNA synthesis and RBC production) • Causes Chronic malnourished Elderly Alcoholics (alcohol suppresses the metabolism of folic acid) Increased need Pregnancy Rapid growth Malabsorption Crohn’s disease Chronic alcoholism Medications Celiac’s disease Certain drugs (methatrexate), oral contractions and anticonvulsants • Manifestations Pallor, SOB, fatigue Glottis, cheilosis Diarrhea No neuro symptoms • Treatment Folic acid supplement ↑ intake of green leafy vegetables, fruits, meats, cereals Hemolytic Anemia • Premature lysis of RBCs • ↑ bone marrow production with ↑ reticulocytes • Normocytic & normochromic RBCs • Intrinsic (within RBC) • Extrinsic (outside RBC) Drugs, bacterial infection & toxins, trauma (sulfa drugs, aspirin, high doses of vitamin C, thiazaide diuretics, etc) • RF acute renal failure |
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Thrombocytopenia
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Autoimmune Thrombocytopenia (ATP)
Thrombotic Thrombocytopenic Purpura (TTP) Heparin Induced Thrombocytopenia (HIT) Autoimmune Thrombocyctopenic Purpura (Also called ATP or ITP) – without clotting Antibody directed toward the person’s platelets, production of platelets is normal Symptoms Ecchymoses, petechiae, bleeding, anemia IC bleed can cause neuro symptoms Labs (low platelet count and HNH) normal platelet is 150,000 to 400,00- but treatment normally doesn’t start until below 50,000 Treatment is immunosuppressive drugs (steroids but increases risk for infection) Corticosteroids or azathioprine (Imuran) Platelet transfusions – if below 20,000 but spleen will still keep destroying platelets Splenectomy – platelets are destroyed by the spleen No contact sports due to risk for bleeding Most common in women ages 20-40 people with other autoimmune disorders Assess for CNS changes associated with brain bleeds Thrombotic Thrombocytopenic Purpura (TTP) – with clotting Disorder of platelet aggregation leading to a low platelet count Platelets clump in small vessels so they can’t be used to clot elsewhere Autoimmune Manifestations are renal failure, MI, stroke because that’s where clumping can occur Fatal in 3 months if not treated Treatment Prevent clumping/stop underlying autoimmune process Plasma pheresis – take out plasma and replace with fresh frozen plasma from donor FFP infusions Platelet aggregation inhibitors ASA, alprostadil (Prostin), Plavix Immunosuppressents to slow down/stop the disorders |
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Blood disorders diagnostic testing
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Leukemia - Lab assessment
Decreased H&H Decreased platelets Altered WBC (low, normal, elevated: usually 20,000 to 100,000) not an increase in the amount necessarily but in the type Clotting times/factors increased Bone marrow aspiration/biopsy identifies types Diagnostics Medical History Physical exam CBC, electrolyte, ESR, renal/LFT Bone marrow biopsy Positron Emission Tomography (PET) CAT scan Lymph node biopsy Ann Arbor Staging Criteria Non-Hodgkin’s |
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Skin
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Skin Cancer
Normal age related changes seborrheic keratosis, rarely develop into malignancy actinic keratosis, have malignancy potential – 25% become squamous cell carcinoma Squamous cell carcinoma on sun exposed or chronically irritated areas irregular, soft, red, ulcerative can metastasize Basal cell carcinoma sun exposed areas of older, fair individuals pearly raised lesion with depressed center rarely metastasizes Seborrheic Keratosis Actinic Keratosis Squamous Cell Carcinoma Basal Cell Carcinoma Basal Cell Carcinoma Skin Cancer Melanoma on the increase due to sun exposure, thinning ozone layer ABCD (asymmetry, borders, color, diameter) high rate of metastasis always excised Skin Cancer Melanoma Treatment (all skin cancers) excision freezing topical agents (chemo) systemic chemo for melanoma Biotherapy using interferon for melanoma Skin Cancer Family / patient teaching avoid causative agents direct sunlight, tanning booths sunscreen when in sun, reapply q 2 hr nutrition balanced diet important in maintaining intact, healthy skin monthly skin checks using mirror pigmented areas, moles, newly acquired skin growths, changes in lesions, itching , pain Periodic skin exams by dermatologists UVA penetrates epidermis, UVB penetrates to the dermis |
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Stomach Cancer
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Second leading cause of cancer death in world
5 year survival rate is low Cancer is usually advanced by the time of detection Pathophysiology Most gastric cancers are adenocarcinoma and will be either intestinal (contained) or diffuse (scattered). Gastric cancers usually spread through the wall of the stomach into the lymphatic system Causes Presence of H. Pylori bacteria due to chronic inflammation Increased risk with pernicous anemia, gastric polyps, chronic gastritis, achlorhydria (no hydrochloric acid) Increased risk with ingestion of certain foods (salt, nitrates) Smoking and increased alcohol use (controversial) Family history Previous gastric surgery (increased risk of developing gastritis) Prevention Get rid of H. pylori bacteria Make sure gastritis heals No smoking Limit alcohol Consume well balanced diet Genetic counseling with family history Diagnosis History H. pylori Food intake Family history Smoking/alcohol use Diagnostic Tests Low hemoglobin and hematocrit Stool positive for occult blood Elevated CEA, usually only seen in infants, in adults may indicate cancer Double contrast upper GI series-done first CT scan to stage the disease and see extent of spreading EGD (esophagogastroduodenoscopy)-definitive Clinical Manifestations Asymptomatic-early Indigestion/abdominal discomfort-common Epigastric/back pain-common and early Weight loss Nausea and vomiting Weakness, fatigue, anemia Metastasis may show up as hepatomegaly (enlarged liver) or enlarged lymph nodes Treatment Depends on the stage of the disease Non Surgical Management May or may not get chemo alone or with other therapy Chemo agent more effective if given in combination of two chemo agents Radiation: limited Surgical Intervention Treatment of choice Usually have total or subtotal gastrectomy with Billroth I (duodenum attached to stomach) or II (jejunum attached to stomach) Preoperative care-same as for any patient having abdominal surgery Post operative care Same as for other abdominal surgery T, C, DB-assess breath sounds Observe for bleeding/infection Nutritional support-feeding tube, TPN, dumping syndrome (small meals, don’t drink while eating, low to moderate carb diet, high protein diet) Emotional support Practice Question: Which statement about general principles of diet therapy for patients with dumping syndrome is true? A. Patients with dumping syndrome should have liquids between meals only. B. Patients with dumping syndrome should be encouraged to eat diet high in roughage C. Patients with dumping syndrome should eat a high carb diet. D. The diet for a patient with dumping syndrome must be low in fat and protein. |
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Colon Cancer
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Colorectal Cancer
Colon and rectal cancer-very common Often metastasis to liver Can be screened for Pathophysiology Adenocarcinomas are the most common (tumors that develop from the glandular epithelial tissue of the colon) They usually develop slowly over many years Initially start in the mucosa and takes a long time to spread through the layers of the stomach to get into the lymphatic system Risk Factors Occurs more commonly in families Age-most occur after 50 years of age Presence of adenomatous polyps Consumption of foods that decrease bowel transit time Co-morbity of inflammatory bowel disease Prevention Balance diet NSAIDs (aspirin)-decreases risk of colon cancer Exercise MVI (multi vitamins) Female Hormone Therapy-Oral contraceptives Regular screening-very important-to include FOBT (fecal occult blood testing) Diagnosis Ask routine history questions plus: Change in bowel habits-very common Blood in stool Feeling of fatigue Recent weight loss Complaints of abdominal fullness and pain Clinical manifestations Change in bowel habits/stool-common Anemia - common Rectal bleeding-hematochezia - common c/o gas pains, cramping Constipation/straining to have BM Narrowing of the stool May see abdominal mass Hypoactive or absent bowel sounds Steatorrhea – fat in the stool Diagnosis FOBT (fecal occult blood test) Decreased hemoglobin and hematocrit Elevated CEA Barium enema CT scan/liver scan Colonoscopy-definitive method Treatment Depends on how advanced the disease is Non Surgical management Radiation May be done pre op or post op May be done for palliative therapy Rectal cancer almost always includes radiation therapy Chemotherapy Drug of choice is 5FU with or without leucovorin New drug-oxaliplatin (Eloxatin) may be added Bevacizumab (Avastin)-new antiangiogensis med which decreases blood supply to tumor Cetuximab (Erbitux)-slows cell growth Surgical Intervention Depends on location of tumor and extent of disease Colon resection Colectomy Colostomy Abdominal perineal resection – removal of sigmoid colon, rectum and anus Preoperative care Same as for all abdominal surgeries May consult ET nurse (ostomy nurse) Bowel prep Educate patient about what to expect postop Postoperative care NG tube care Ostomy/wound management Routine care for abdominal surgery Practice question: Colonoscopy with biopsy is the definitive test for the diagnosis of CRC? TRUE FALSE Malabsorption Syndrome Inability of the gut to absorb nutrients due to problems with the intestinal mucosa Depending on where in the intestines the problem occurs will depend on which nutrients are not being absorbed Occurs commonly after gastric surgery Clinical manifestations Diarrhea-common Steatorrhea-common Weight loss Bloating/excessive gas Decreased libido Easily bruised Anemia Bone pain edema Diagnosis Lab values depends on the nutrient being lost Intervention Supplements for the lost nutrients Avoid things that cause malabsportion to get worse Practice questions: Constipation is a classic symptom of malabsorption TRUE FALSE The Schilling test measures urinary excretion of vitamin B12 for dxg of pernicious anemia and a variety of other malabsorption syndromes. TRUE FALSE |
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Oral Cancer
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Premalignant
Leukoplakia – most common in adults, most often see in men Slow developing changes in the oral mucousa Thick, white, firmly attached, slightly raised and sharply circumscribed patches (can not be removed by scraping) Small percentage become malignant after about 8 years Lesions on lips and tongue most likely to become malignant Causes Long term irritation to the oral membranes Poorly fitting dentures Chronic cheek chewing Broken teeth HIV infection Tobacco use Erythroplakia Red, velvety mucosal lesion on oral mucosa More likely to become malignant Usually seen on the floor of the mouth, tongue, palate and mandibular mucosa Malignant Tumors Types Squamous cell carcinoma Basal cell carcinoma Kaposi’s Sarcoma (discussed with HIV) Squamous Cell Carcinoma Most common of the oral cancers Usually found on lips, tongue, buccal mucosa, oropharynx Occurs because over many years cell changes take place in the oral cavity Early symptom is mucosal erythroplasia (lesions that are red, raised, and eroded) Risk factors Increasing age Tobacco Alcohol ingestion (combination with tobacco increases risk) Textile workers, plumbers, coal and metal workers Sun exposure Poor oral hygiene Poor dietary habits Human papillomavirus (HPV16) Basal Cell Carcinoma Usually occurs on the lips Asymptomatic, doesn’t usually spread Starts with a small scabbed area that does not heal and advances to an ulcerated area with a pearly border High risk factor is sun exposure Prevention Important Screening by dentist yearly Decrease sun exposure/wear SPF Stop tobacco use Decrease alcohol consumption Clinical manifestation Unusual lumps or thickened areas Red or white patches Sore that does not heal Soreness, pain, burning sensation Trouble swallowing or chewing Pain may radiate to ear Enlarged lymph nodes Diagnosis History/Physical exam CT scan/MRI Biopsy-definitive Toluidine blue solution for high risk persons-may have false positive (if solution turns blue it indicates cancer) results with inflammation Interventions Airway is the priority Assess breath sounds, oxygen saturation levels, respiratory rate Clear secretions-cough, suction Semi-fowler’s/high fowler’s position Prevent aspiration May need a trach Non Surgical Treatment Good oral care Q 2 hours No commercial or harsh mouthwash (use warm saline or baking soda) Soft bristle toothbrush Lubricant to lips Soft, bland, non-acidic foods Radiation Goal-get rid of the tumor while preserving function and appearance May be given alone or with chemo or surgery Can be given externally or internally Chemotherapy May be given alone or with radiation or surgery May receive more than one chemo agent Surgical treatments Type of surgery depends on the size, location of lesion, spread into the bone and lymph nodes If small enough can be removed under a local anesthesia More extensive lesions may require a partial or total glossectomy (tongue removal) and partial mandibulectomy with radical neck dissection Preoperative care Make sure patient understands what procedure is planned Possibility of trach, drains, IVs, ICU placement Changes with speech NPO Routine post op care-T, C, DB, out of bed Post operative care Airway, airway, airway Prevention of infection-good oral care, antibiotics, assessment Elevate HOB at least 30 degrees-prevents edema, prevents aspiration Pain control Nutrition-NPO with TPN/tube feedings, assess for trouble swallowing |
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Strokes
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Medical Emergency
Must make a diagnosis quickly to preserve brain tissue, medication must be administered within 3 hours of symptoms History- last time normal is very important When did it happen? – Ischemic-sleep – Hemorrhagic-activity Severity of symptoms – Hemorrhagic-gets worse – Embolic-gets better Glascow Coma Scale (GCS) Allows for a rapid neurological assessment Standardized assessment Scored on three areas-eye opening, motor response, and verbal response. The higher the score the better (15 is the best, 3 is the worst) Posturing Late sign of neurological deterioration Notify the physician immediately Decorticate position-arms, wrists, and fingers flex with internal rotation. Feet flex in Decerebrate position-rigid extension of arms and legs, pronation of the arms and plantar flexion of the feet. Dysfunction of the brainstem Aphasia-inability to use or comprehend language Alexia-reading problems Agraphia-difficulty with writing hemiplegia-paralysis on one side of the body Hemiparesis-weakness on one side of the body Remember that motor nerve fibers cross the midline before going to the spinal cord. Right hemisphere problems mean left sided paralysis Flaccid paralysis-extremities just all to the side-patient does not have the ability to hold them up Spastic paralysis-contractures (lack of movement) in a joint Agnosia-inability to use an object correctly Apraxia-inability to carry out purposeful motor activity Neglect Syndrome-unaware of one side of the body Ptosis-drooping eyelid Anaurosis fugaz-brief period of blindness in one eye Hemianopsia-blindness in half the visual field CT scan is most important Goal is to have the CT scan done and read within 45 minutes, can tell if it’s a hemorrhagic or ischemic stroke, don’t treat a hemorrhagic stroke because medication would make it worse and cause more bleeding Interventions Depends on the type of stroke (3 hour window for thrombolytics) ABCs-priority Monitor for signs of IICP (increased intracranial pressure) such as change in LOC, changes in behavior, changes in vital signs Dysarthia-slurred speech due to decreased muscle control of tongue-may also have swallowing problems Expressive aphasia-understands speech but can not answer Receptive aphasia-can talk but words don’t’ make sense. No understanding of spoken or written word Get speech therapy involved Look for other ways to communicate |
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Testicular Cancer
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– Testicular Cancer
– Leading cause of cancer deaths age 15-35 and on the increase – Etiology – trauma, orchitis (inflammation of the testes), family history, cryptochidism (non-distended testes at birth) DES exposure (pill used to fight morning sickness), exposure to carcinogens – Symptoms – often subtle – mass or swelling – heavy or dragging sensation – Testicular Cancer – Diagnosis – Workup done for mets – Biopsy will not be done because they don’t want it to spread – AFP, HCG can be produced by the tumor – Any testicular mass should be investigated further – Testicular Cancer – Treatment – orchiectomy (removal of testicle) – radiation/chemotherapy determined by cell type – Nursing considerations – body image/ effect on reproduction – sperm banking may be done – radical node dissection – high risk for bleeding, DVT – may have ejaculatory dysfunction – education regarding follow up – Prevention » TSE (after showering) |
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Breast Cancer
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– Breast cancer screening
– BSE and yearly physical – mammogram yearly starting at age 40 – if first degree relative has premenopausal breast cancer start 10 years before their cancer – normal findings on BSE • one breast larger than the other • bilateral nipple retraction • *bilateral milky discharge • fibrocystic changes – Risk factors – Age (usually peaks in the 60’s) – previous breast cancer – family history – nulliparity (no children after age 30) – early menarche, late menopause – ETOH – obesity – exogenous hormones – atypical hyperplasia – lactation decreases risk – Tamoxifen – anti-estrogen – causes menopausal symptoms – monitor for DVT, abnormal vaginal bleeding – Herceptin – Originally used only for women with recurrences after treatment – New studies show improved outcomes when used during the original treatment plan – Only used in women with HER2-positive breast cancer (tend to be the more aggressive types) » These cancers make too much of the HER2protein » Herceptin blocks the HER2 protein in cancer cells |
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Addison's disease
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Pathophysiology Inadequate secretion of ACTH by hypothalamus & pituitary
Causes Primary-Autoimmune disease, TB, metastatic cancer, AIDs, hemorrhage, Gr- sepsis, adrenalectomy, abdominal radiation, fungal lesions, drugs (mitotane) & toxins Secondary- pituitary tumors, hypophysectomy, high doses of radiation Clinical Manifestations Muscle weakness, fatigue, joint/muscle pain, anorexia, N/V, constipation/diarrhea, wt loss, salt craving, vitiligo – white patches where they lose pigmentation on skin, ↑ skin pigmentation, anemia, ↓BP, ↓Na, ↑K+, ↑Ca++ Laboratory & Diagnostic ↓ cortisol, ↓fasting BG, ↓Na , ↑K+, ↑Ca++, ↑BUN, Primary- ↑ACTH, ↑ESR CT, MRI,skull X-ray if problem is pituitary Interventions Goal- fluid balance, prevent hypoglycemia Cortisone replacement (give 2/3 dose in AM, 1/3 dose PM) Hydrocortisone or prednisone Fludrocortisones (Florinef)-causes Na reabsorption & K+ excretion ↑Na+ intake Emergency Mgmt- rapid infusion NS or D5NS, 100-300 mg Solucortef, hydrocortisone drip over 8 hrs, hydrocortisone 50 mg IM, histamine blocker IV, ↑K+ give insulin +D50W (shifts K+ into cells), Lasix, hypoglycemia give d50W & monitor BG hourly. Nursing Intervention Daily weight, accurate I&O, monitor for dysrhythmias, orthostatic hypotension |
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Cushing's Disease
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Cushing’s Disease (Hypercortisolism)
Excessive secretion of cortisol with affects metabolism, ↑ body fat, kills lymphocytes & shrinks organs containing lymphocytes (spleen, liver, lymph nodes) Endogenous secretion- bilateral adrenal hyperplasia, pituitary adenoma, malignant CA of lungs, GI tract, pancreas, Adrenal cancer Exogenous-use of mineral corticoids for disease (asthma, autoimmune disorders, organ transplant, cancer chemo, allergic reaction, chronic fibrosis) Moon face, buffalo hump, truncal obesity, HTN, dependent edema, ↑RF bleeding, muscle atrophy, osteoporosis, thin skin, striae, ↑ skin pigmentation, ↑RF infection, ↓ immune function & inflammatory response ↑ cortisol, ↑BG, ↑Na, ↓lymphocytes, ↓Ca+, ↓K+ Dexamethasone suppression testing Goal- ↓cortisol level, removal of tumor, restore body appearance to normal or acceptable. Aminoglutethimide (Elipten, Cytadren) and metyrapone (Metopirone) use different pathways to decrease cortisol production. For increased ACTH production, cyproheptadine (Periactin) may be used because it interferes with ACTH production. Mitotane (Lysodren) is an adrenal cytotoxic agent used for inoperable adrenal tumors causing hypercortisolism. Monitor for ↓ weight and ↑U/O, monitor electrolyte balance |
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Problems of the Thyroid
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Thyroid Gland- control metabolism. Calcitonin (secreted by thyroid) lowers serum calcium & phosphorous levels by reducing bone reabsorption.
Hyperthyroidism Pathophysiology ↑ secretion of thyroid hormone called thyrotoxicosis Causes Graves’ disease (autoimmune disorder), toxic multinodular goiter, excessive thyroid replacement Clinical Manifestations ↑ metabolism- diaphoresis, thin hair, smooth warm skin, SOB with exertion, ↑resp rate, palpitations, CP, ↑sys BP, ↑HR, dysrhythmias, wt. loss, ↑appetite, ↑BM, hypoproteinemia, muscle weakness & wasting, blurred vision, ↑tears, photophobia, ↑DTRs, insomnia, heat intolerance, low-grade fever, fatigue, restless, irritable, emotional liability, manic behavior, amenorrhea, ↑libido, goiter, exophtalmos, enlarged spleen Laboratory & Diagnostic ↑ T3, ↑T4, ↓TSH (graves disease), ↑TSH (secondary hyperthyroidism ↓WBC, Thyroid scan evaluates the position, size, and functioning of the thyroid gland, Ultrasonography can determine its size and the general composition of any masses or nodules. Interventions Drug therapy-propylthiouracil (PTU) [preferred drug] and methimazole (Tapazole)-block thyroid hormone production by preventing iodide binding in the thyroid gland. Iodine preps may be used prior to surgery to ↓ bld flow to thyroid→↓hormone release. Lithium – inhibit hormone release. Beta-blocker to ↓HR, palpitations, anxiety & diaphoresis Radioactive iodine (RAI) therapy –given in oral form, The thyroid gland picks up the RAI, and some of the cells that produce thyroid hormone are destroyed by the local radiation. Contraindicated with pregnancy- damage fetal thyroid gland. Because the thyroid gland stores thyroid hormones to some degree, the patient may not have complete symptom relief until 6 to 8 weeks after RAI therapy. Additional drug therapy for hyperthyroidism is still needed during the first few weeks after RAI treatment. No radiation precautions needed. Surgical Intervention Total or subtotal thyroidectomy-drug therapy 1st to have euthyroid function prior to surgery. HTN, dysrhythmias, ↑HR must be controlled during surgery Nursing Interventions Postop Mgmnt-VS q 15-30 min, maintain semi fowlers position, maintain head & neck alignment, humidified air, monitor for signs of ↓Ca++ (parathyroid injury)- tetany around mouth. Monitor for hemorrhage-inspect behind neck. Monitor respiratory status-stridor indicates laryngeal swelling, O2. Keep trach tray at bedside. Thyroid Storm-life threatening event occurs with Graves’ disease. Patient has sudden ↑ in metabolic rate → fever, tachycardia & HTN. Hypothyroidism Pathophysiology Under secretion of thyroid hormone Causes Hypothalamus & pituitary don’t secrete TSH, overtreatment of hyperthyroidism, Autoimmune thyroid destruction, thyroid cancer, Drugs-Lithium Clinical Manifestations ↓ metabolism- cool, dry, scaly skin, brittle nails & hair, poor wound healing, dyspnea, poor ventilation, ↓HR, ↓BP, dysrhythmias, enlarged heart, ↓activity tolerance, ↓temp, cold intolerance, slow intellectual functioning, lethargy, ↓DTRs, apathy, depression, anorexia, wt. gain, constipation, amenorrhea, ↓libido, impotence, fluid retention & edema, goiter, nutritional anemias, ↓U/O, thick tongue, hoarseness Provide safe environment with cognitive disturbance. Monitor for manifestations of ↓ cardiac output Laboratory & Diagnostic ↑TSH, ↓T3,↓T4, Interventions levothyroxine sodium (Synthroid, T4, Eltroxin- started with low doses and gradually increased over a period of weeks. Lifelong treatment Myxedema coma Brought on by acute illness, surgery, chemotherapy, sudden d/c of hormone therapy, sedatives & opioid use Lead to coma, resp failure, ↓BP, ↓Na+, ↓BG, hypothermia. If left untreated lead to death Nursing Interventions Assess for chest pain & dyspnea during initial treatment. Wear medic alert bracelet. Teach S&S of hypo & hyperthyroidism, adequate diet to prevent constipation-fiber supplements can interfere with absorption of thyroid hormone. Take drug on empty stomach. May need to ↑ dose if patient has insomnia or constipation. |
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SIADH
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SIADH (Syndrome of inappropriate antidiuretic hormone)
vasopressin (antidiuretic hormone [ADH]) is secreted even when plasma osmolarity is low or normal. A decrease in plasma osmolarity normally inhibits ADH production and secretion. Cancer and cancer treatment, recent head trauma, stroke, TB, pneumonia, lung abscess, chronic lung disease, pneumothorax, SLE Drugs- chemotherapeutic agents, general anesthesia, tricyclic antidepressants, opioids Water is retained, → dilutional hyponatremia. Anorexia, N/V, weight gain, lethargy, headaches, hostility, disorientation, and a change in level of consciousness, ↓ deep tendon reflexes, ↑HR, hypothermia Serum Na < 115 mEq/L. dilutional ↓H&H Fluid restriction - as low as 500 to 600 mL/24 hr. Dilute tube feedings with saline rather than plain water, and use saline to irrigate GI tubes. Mix drugs to be given by GI tube with saline. Diuretics Hypertonic saline (3% NaCl)- given slowly, monitor for worsening fluid overload Demeclocycline (Declomycin)-monitor for Candida. Monitor the patient's response to therapy to prevent the fluid overload from SIADH from becoming worse, leading to pulmonary edema and heart failure. Monitor for seizures, confusion. Safety with hyponatremia Oral care for thrush-, eat yogurt, daily weight |
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DI
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Diabetes Insipidus
ADH deficiency results in the excretion of large volumes of dilute urine (4-30 liters/day). Causes Neprogenic- inherited-renal tubules don’t respond Primary- defect in the hypothalamus or pituitary gland resulting in a lack of ADH production or release Drug induced- Lithium carbonate, demeclocycline (interfere with kidney’s response to ADH Clinical Manifestations Increase in the frequency of urination and excessive thirst. Signs of dehydration. U/O 4 liters > intake. Laboratory & Diagnostic ↓ urine specific gravity <1.005, ↑ H&H, ↑BUN Interventions chlorpropamide (Diabinese)-↑action of existing & stimulates production of ADH in hypothalamus, SE hypoglycemia Desmopressin acetate (DDAVP) is a synthetic form of vasopressin given orally or intranasally in a metered spray- mild 1-2 doses/24, severe 2-3 doses/24 hr. Nursing Intervention Monitor I/O, daily weights, monitor for dehydration, push PO fluids Home Care Patient teaching Permanent DI requires lifelong desmopressin or vasopressin therapy. Teach that polyuria and polydipsia are signals for the need for another dose. |
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Hip Replacement
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Preoperative care – usually only one hip replaced at a time
Post operative care – Positioning-flexion limited, no adduction, never let them cross their hip across the midline! Put adduction pillows between the knees – Wound care-drains – Activity-no severe flexion with elevated HOB, ROM, turn with abduction pillow, partial weight bearing with walkers and crutches, elevated chair/toilet seat – Medication-anticoagulant therapy, pain control Discharge-use of ambulatory devices, limited flexion and adduction, raise toilet seat, prophylaxis antibiotics Complications-dislocation (more common than in knee replacements, pain, difference in leg length, deviation, popping sound or patient feels popping), DVT, fat embolism Minimal invasive surgery New procedure that requires less hospital/recover time Joint is accessed by separating muscles instead of cutting them Smaller incisions Potential candidates-good health, not obese, motivated to participate in rehab, no prior joint injury Post op care the same |
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Knee Replacement
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Total Knee Replacement – not usually done until they can’t complete their ADL’s, usually don’t do both knees at the same time
Preoperative care Post operative care – Positioning-elevate leg on pillows for 48 hours, turn – Wound care-drains, watch for bleeding, bulky dressing at first – Activity-CPM, ROM exercises on extremities that were not operated on, light weight bearing in 1st post op day, sit in chair with legs elevated, knee brace – Pain control-PCA, epidural, ice Importance of CPM – continuous passive motion machine (page 328) Decreases post operative swelling Prevents adhesions Decreases pain Helps with early ambulation Prevents contractures Helps with healing Discharge-partial weight bearing and assistive devices, exercise, prophylaxis, antibiotics Complications-infection, DVT, fat embolism Fat Embolism-What do you remember? Occur 1-7 days after injury, clinical manifestations are hypoxemia, tachypnea, tachycardia, petechiae, fever, lipuria, chest pain, change in LOC, Notify MD, treat with oxygen, PEEP fluids (positive and expiratory pressure), steroids Total hip replacement – page 328 Preoperative care – usually only one hip replaced at a time |
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Lupus
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Systemic Lupus Erythematosus
chronic, progressive, inflammatory disorder that causes organ failure Characterized by remissions and exacerbations Survival rate better today, early diagnosis helps, better treatments available An autoimmune disorder which causes inflammation and damage to body organs Kidneys most commonly involved and the major cause of death Clinical manifestations “Wolf” Very individualized Butterfly rash-dry, scaly, raised rash on the face (distinguishing characteristic) Polyarthritis-joint changes similar to RA Osteonecrosis-due to steroid therapy which causes lack of blood supply to bone and necrosis Muscle atrophy/myalgia Fever/fatigue Renal symptoms-decreased UO, increased BUN/creatinine, protein and blood in urine Pulmonary-pleural effusions, pneumonia Cardiac-pericarditis, tachycardia, chest pain, myocardial ischemia Raynaud’s phenomenon Neurological manifestations Abdominal pain Hydroxychloroquine (Plaquenil)-same as RA (takes a long time to work, vision must be monitored) Patient education Skin protection Monitor for temperature-sign of exacerbation Psychological support during exacerbations Counseling regarding pregnancy |
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Rheumatoid Arthritis
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Clinical manifestations of RA
Early – Fever due to the inflammatory process – Weight loss (usually only a few pounds) – Fatigue – Generalized aching – Early morning stiffness lasting a few minutes to an hour or more-diagnostic if stiffness is of at least 6 months duration – very good indicator for diagnosis, usually don’t want to move in the morning but they should be encouraged to be mobile to preserve mobility, advise to take a hot shower in the morning Later – Frank articular inflammation – Joint swelling-diagnostic if 3 or more joints are involved for at least 6 months, joint swelling should be symmetrical – Pain – Tenderness – Warmth – Redness – Rheumatoid nodules-diagnostic, found in about 90% of people who have the disease, little bumps (eraser size) found underneath the joint that is a collection of debris Diagnostic test for RA History Physical exam Labs – no specific lab for diagnosis – Increased ESR – Mild leukocytosis – Anemia – Positive rheumatoid factor – not definitive X-rays show narrowing of joint spaces due to necrosis Biopsy Aspiration – thick fluid, not clean Medications for RA (page 341-342 chart) Salicylates – used to be first drug of choice but not anymore due to GI problems and toxicity (tinnitus), not usually tolerated very well Nonsteroidal anti-inflammatory drugs – first line, also cause GI upset, encourage to take with food Potent anti-inflammatory drugs (steroids) What do you already know about steroids? Watch out for systemic affects such as hyperglycemia, poor wound healing, risk for infection, risk of osteoporosis, fluid retention, Na retention. Usually used during acute exacerbations. Slow acting anti-inflammatory drugs-also called DMARDs (disease modifying antirheumatic drugs) – Antimalarials-plaquenil • Takes between 6-12 months to work • Side effects are GI upset and retinal edema (baseline eye exam and need eye exams Q 6 months) Immunosuppressive therapy-methotrexate (Rheumatrex), azathoprine (Imuran), cyclophosphamide (cytoxan) these are chemotherapy agents, can cause low WBC, low RBC, and low platelet count Biological Response Modifiers-patients with TB should not take because it can be reactivated, not usually given on a daily basis – Etanercept (Enbrel) – Infliximab (Remicade) – Adalimumab (Humira) – Anakinra (Kineret) |
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End of Life
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Signs and Symptoms of Approaching Death (Chart 9-1)
Coolness of extremities Increased sleeping Fluid and food decrease Incontinence Congestion and gurgling Slowed breathing and change in pattern Disorientation Restlessness Emotional Signs of Approaching Death Withdrawal Vision-like experiences Letting go Saying goodbye Patients at Risk for Poor Pain Control Elderly/children Cognitively impaired Unconscious patients Patients who deny pain Non English speaking patients Patients with history of substance abuse Pronouncement of death Absence of heart beat, respirations for one full minute General appearance of the body Lack of reaction to any stimuli Lack of pupil reflexes (fixed and dilated) Time of pronouncement Who pronounced the patient Who was present at the time of death Who was notified of the death (family, Translife,) Disposition of the body(if there’s to be an autopsy, touch nothing), remove tubes, put dentures in, close eyes, when patient is put in troud make sure zipper ends at feet Autopsy and organ donation consents Nursing Care at the Time of Death Inform family openly and honestly that the patient has died May need to repeat the information Post mortem care (Chart 9-6) Necessary paperwork Funeral home Trans Life |
