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Adult Health
Final Exam
| Question | Answer |
|---|---|
| Primary Prevention | - Health promotion, risk asst and management, and disease prevention ex: exercise, nutrition, immunizations, wear seat belt |
| Secondary Prevention | -Behaviors that promote early detection of disease ex: mammogram, dental exam, physical, eye or ear exam |
| Tertiary Prevention | - Activities related to rehabilitation after disease is diagnosed ex: Breast reconstruction after mastectomy, rehab |
| Tumor | A mass or swelling |
| Neoplasm | Abnormal mass, no useful purpose |
| Benign neoplasm | -Harmless growth -no spreading -Can put pressure on surrounding organs |
| Malignant Neoplasm | -Harmful mass -Can spread to organs and adjacent tissue |
| Cancer | -Ability to proliferate cells is altered |
| Adenocarcinoma | -Glandular tissue -Ex: Breast, lung, thyroid, and pancreas |
| Carcinogens | -Tobacco,asbestos,coal tar,soot (lung) -Smoked,salty,pickled food (oral,stom) -Fumes,alcoholism(stom,colon) -Benzene,ethylene oxide (leukemia) -Prolonged UV rays (melanoma, basal cell) -Alcohol (liver) -Viruses(stom,bladder, liver,lymphoma) |
| 4 Causative Agents | -Radiation -Chemicals -Viruses (HPV, Hep B & C, H.Pylori) -Physical Agents |
| Cell Cycle Phases | -G0-At rest from cell division, longest phase -G1-RNA synthesis, variable phase,happens different amount of time in cells -S-DNA synthesis,High number = poor prognosis - G2-Prep for mitosis, make more RNA, short phase - M-cell division,mitosis |
| Malignant Cell Characteristics | -Loss of control of Mitosis -Decrease Specialization -Decrease cell boundary respect -Almost immortal -Irreversibility -Altered cell structure -Transplantability -Ability to create protective structures to support own survival |
| Neoplasm, Tissue of Origin | -Fibroma - benign fibrous tissue often in uterus, can grow to the size of a 9 mo pregnancy -Lipoma-benign fat tumors -Leiomyoma-benign tumor of smooth muscle -Sarcoma-malignant tumor of connective tissue,cartilage,bone |
| TNM staging of tumors | T-graded 0-4, primary tumor size N-graded 0-3, regional lymph nodes M-graded 0-3, metastasis -Angiogenesis - ability of tumor cells to secrete substance that stimulates blood vessel growth |
| Radiation Therapy | -60% of pts -Targets rapidly multiplying cells but kills other cells within it's path -Primary tx = cure -Adjuvant -Palliative -Goal - control tumor growth size |
| How Radiation Works | -Cell radiosensitivity -Damages DNA, cell can't reproduce -Damages all cells w/in field (normal cells can repair themselves) -Not dependent on cell cycle -O2 free radicals are formed -interact with surrounding tissue causing cell damage |
| Nursing Interventions:Radiation Therapy | -Keep skin dry -Use warm/cool water,mild soap only -Ink marks -Avoid powder,lotions,deodorant on radiated skin -Avoid clothing friction -Use electric razor only -Protect from sun exposure,and chlorinated pool -Control D if pelvic radiation |
| Side effects of Radiation | -Skin reaction - mild redness to 3rd degree skin reaction -Fatigue -Site specific:mucositis, xerostomia,esophagitis,dysphagia, alopecia,bone marrow suppression |
| Chemotherapy | -IV -Cure,control,or palliation -Use when: disease is widespread, not localized, risk of hidden disease is high, tumor can't be resected d/t location or size, tumor is resistant to radiation therapy -Adjuvant chemo |
| How Chemo Works | -Diff drugs target diff cell phases -Generally need more than one exposure to effect death of all cancer cells -Drugs used in comb0,or w/ radiation -Classification according to effect on cell cycle some are cell-cycle specific, some not |
| Nursing Care during Chemotherapy | -Alopecia -GI effects -Anorexia -Stomatitis -Pain -Mylelosupression -All effects are related to rapidly reproducing cell destruction |
| Pain | -From tumor pressure or V -From extravasation of chemo (apply ice immediately, stop IV fluid, leave needle in, aspirate any drug) -Antihistamine - antidote -Liberal analgesics - If the patient says they have pain, they have pain |
| Neutropenia | -Seen 7-14 days after chemo -Increased potential for infection -Protective isolation - limit visitors -Steroids used for tx add to infection potential - inhibit immune system |
| Nursing Interventions and Neutropenia | - Good hand washing -Frequent oral care -Don't share eating utensils -Fevers - treated as emergency -Avoid ppl w/ infections -Avoid animal feces -Avoid fresh flowers |
| Anemia | -Blood loss -Altered hemoglobin -Altered hematocrit -fatigue,dizziness,dyspnea, tachycardia -Blood transfusion, packed red cells |
| Thrombocytopenia Interventions | -Shave w/electric razor -Prevent dry cracked skin -Good oral care -Avoid C,enemas,rectal temps -Pressure on bleeding for 10 min -Avoid IM,SQ -Watch for tarry stools,blood in urine |
| Thrombocytopenia Interventions | -Watch for petechia -Watch for change in LOC,early sign of intracranial bleeding |
| Phases of Wound Healing | -Vascular Response (immediate) -Inflammation -Proliferation or Resolution -Maturation or Reconstruction |
| Vascular Response | -Immediate after an injury -Constriction - w/in seconds after you are injured,to control bleeding,reduce bacterial entry |
| Vascular Response:Clotting | -Platelets: stick together to control bleeding initially -Fibrin: cause clot to form |
| Vascular Response: Capillary Dilation | -15 minutes after injury -Allow plasma to flow into area and dilute any toxins that may be present |
| Inflammation Phase | -Begins the moment of the injury -May extend 4-6 days -Limits the effect of pathogens -Fibrinogen -WBCs (neutrophils begin phagocytosis, macrophages mature monocytes, eosinophils/basophils |
| Bacterial Infection | -Leukocytosis: > 10,000 -Neutrophils - 1st line of defense -Segs respond immediately -Bands also respond (major infection) -Total lymphocytes maybe normal range |
| Primary Intention | -Use of stitches or sutures to close -Little scarring -Low infection -Usually occurs through collagen synthesis |
| Secondary Intention | -Wound left open to heal -Longer (inflammation, proliferation,maturation) -Ex: Pressure Ulcer -May need skin or muscle flap |
| Tertiary Intention | -Infections -Wound left open -Ex: wound dehiscence (wound that has burst open) -Contaminated, high risk of infection -Promote healing from inside out -Wound vacs |
| Intrinsic Factors | -Infection:Prolong inflammation process -Foreign Body -Inadequate blood supply(CVD,less fibroblast,need good arterial flow for healing) -SMOKING-vasoconstriction, decrease 02,increase CO -Neuropathy-Can't feel area around injury, inadeaquate bf to are |
| Extrinsic Factors | -Malnutrition (protein, vit C, carbs) -Diabetes - suppress immune system and healing -Steroids - impair all phases of healing |
| Medical Management | -Control edema (Rest Ice Compression Elevation) -Reduce inflammation -Monitor systemic responses (temp-only give antipyretics for fevers over 101*, HR - increase, BP-increase, WBC-increase) |
| Incisions | -Assess ever 8h -Heal in 3-5 days -Asepsis -Don't clean unless ordered -Monitor for drainage -Don't apply pressure -Sutures/staples removed in 7d to 2wks -Glue -Drainage devices |
| Non-Opiod Analgesics | -Aspirin: not with viral infections at any age -Salicylate salts: fewer gastric side effects -Acetaminophen: action not known -NSAIDS: +bone pain |
| Opiod Analgesics | -Morphine -Codeine -Oxycodeine -Hydromorphone -Meperidine |
| Adverse effects of Opiods | -Respiratory Depression -C -N/V -Hypotension -Skin effects -Urinary retention |
| Fluid Compartments | -60% body weight composed of water in an adults - decreases with age -Two Compartments:Intracellular-66% Extracellular - 33% -Interstitial Fluid (b/w cells) -Vascular compartment (blood in veins and arteries and lymph in the lymphatic system) |
| What regulates fluid balance? | -Thirst Mechanism:Decrease w/age, regulated by menstrual cycle and aldosterone -Kidney:From adrenal glands, promotes Na retention, water goes to ECF -Aldosterone: causes more Na to be released |
| -Atrial natriuetic peptide/brain natriuetic peptide:from post pit., prevents diuresis&urination -ADH:Water Regulation-alcohol inhibits ADH secretion,so nephrons in kidneys to become less permeable to water=more water leaving body could be dehydration | |
| Hemodilution | -Hemodilution(Fluid overload) and dehydration affect hematocrit level in opposite directions -Critical Values: >55% dehydration < 35% fluid overload |
| Sodium | -Major component of ECF -Regulation:Intake (dietary, meds)/Output, Kidneys, Hormones (Directly - aldosterone, Indirectly - ADH,BNP) -Hyponatremia: <135 fluid overload -Hypernatremia:>145 dehydration |
| Blood Urea Nitrogen | -Measures end-product of protein metabolism -Regulated by: Kidneys and liver, diet-protein intake, hydration status, drugs -Blood level - increases with age -Elevates with dehydration and renal failure -Creatinine: Directly reflects kidney function |
| Dehydration | -Hypovolemic "dry" -Fluid loss (blood,sweat,urinate, vomit, D, wound drainage, nasal gastric tubes, burns) -Shift of fluid b/w compartments -ECF deficit for ICF deficit |
| Dehydration: Levels of Severity | -Mild: Loss of 1-2 L or 2% of body wt -Moderate: Loss of 3-5 L or 5% of body wt -Severe: Loss of 5-10 L or 8% body wt |
| Third Spacing | -Excess fluid in the body leaves the vascular space (blood vessels); occurs very frequently after surgery -Gets into the tissues -Causes swelling (edema): extremities, sacrum, peri-orbital areas - |
| Fluid Volume Deficit: Subjective | -Complaints of Dizziness, feeling confused, weakness, constipation -Caused by low BP, not enough fluid, not enough O2 or changes in Na |
| Fluid Volume Deficit: Objective | -Weight Loss**(Most accurate mst of fluid balance=accuracy of weights,1kg of weight=1 L of fluid -Changes in vs -Dry mucous membranes -Changes in skin turgor -Flattened veins -Confusion -I-Na,osmolality,hematocrit,BUN -I-urine specific gravity |
| Fluid Intake | -Normal = 1500 - 2000 mL daily -800 mL from food |
| Complications of Fluid Volume Deficit | -Cardiac Output: alteration or decreased -Urinary Output: decreased -Impaired mucous membranes -Risk for injury -Cognitive impairment |
| Output | -Should be at least 30 mL of urine per hour -240 mL per 24h |
| Isotonic Solutions | -Normal saline (0.9%) or Lactated Rings -Amounts of electrolytes and water are close to plasma level -Caution: LR can alter acid-base balance, don't use in alkalotic state, don't use for liver failure -Considered volume expander |
| Hypotonic Solutions | -5% Dextrose in water (D5W, 45% normal saline -Used for flood losses sever intracellular dehydration -Pushes fluid back into cells -Fluid, no electrolytes (Dextrose is metabolized and water is left; electrolyte status can become diluted) |
| Hypertonic Solution | -D5 0.45 NACL, D5 0.22 NS, D5 0.9 NS -Adds both water and electrolytes -Extra solutes pull fluid from ICF back into ECF -Good for postoperative swelling -Food for pts with mild to moderate fluid overload |
| Hypervolemia | -Excess fluid volume -R/T to pts in ability to control: fluid volume shift to ECF or ICF either in the vascular space, b/w cells or in cells, increased intake, decreased output, and some diseases (CHF, kidney failure, pit disease) |
| Hypervolemia AEB | -Edema -Pulmonary congestion (hear crackles) -Changes in vs (BP increase) -Changes in neck veins (NVD) -Neurologic changes (confusion d/t brain swelling) -Decreased osmolality,hematocrit,NA and BUN |
| Hypervolemia: Diagnostic Findings | -Plasma: below 75 -Chest x ray -Sodium: < 135 -BUN: < 8 -Hematocrit: <45 |
| Cause of 3rd spacing | -Surgery -Heart Failure (ventricles aren't able to pump or push fluid into system and so it backs up into body/lungs) -Kidney failure - fluid can't get out |
| Hyponatremia | -Low sodium -Very common in elderly -Plasma volume <135 - Excessive Na loss through fluid losses such as GI losses, 3rd spacing, burns -Not enough aldosterone from adrenal glands (addison's) -Kidney disease |
| Hyponatremia: Assessment | -No symptoms if moderately low -N/V/D, cramping -Crackles (rales in lungs) -With critically low values cause lethargy,weakness, hallucinations, seizures, and coma possibly death, hypotension |
| Hypernatremia: Assessment | -Confusion -N/V -Restless, agitated -Seizures -Coma -Respiratory paralysis -death |
| Nursing Interventions: Hyponatremia | -Fluid Restriction <1500 per 24 h -High Na foods -IV (slow) replacement -Medication: inhibit ADH -Monitor Na levels -Treat N w/ anti-emetics |
| Hypernatremia | -Sodium retention or fluid losses will raise the serum sodium level (lots of urine output, D, burns) -Excessive aldosterone secretion |
| Nursing Interventions: Hypernatremia | -Fluid replacement (IV or oral) -Encourage fluids -Low Na foods -IV (slow) replacement: Hypotonic (D5W, 0.45 NS) -Meds: Diuretics |
| Potassium | -Major ICF -Maintains acid-base balance in the body -Very important in regulating membrane potentials in neuromuscular tissue and the heart |
| Hypokalemia | -Low dietary intake -GI losses, sweat -other electrolyte imbalances -Renal disease -Medications: Diuretics, steroids, insulin |
| Hypokalemia: Symptoms | -Fatigue, Decreased Reflexes, paresthesia, irritability to seizures an coma -Fibrillation, ECG changes, decrease musc contraction -Muscle weakness and cramps -Anorexia and N |
| Hypokalemia: Interventions | -Monitor Cardiac precautions -K+ supplements (take with food) -IV - 10-20 mEq in 50-100 ml fluid over 1h max rate, never push meds, must be diluted on IV pump device, not gravity |
| Hyperkalemia | -Greater concerns the higher it is -Associated with: renal failure, cellular injury, IV infusions -Cellular changes - Decrease cell excitability: neural, cardiac, muscle |
| Hyperkalemia: Assessment Findings | -Cardiac: HR faster,extra beats,tall peaked T wave, P wave almost nonexistent, QRS widened -Gastric: N/V,anorexia,D -Muscular irritability, twitching |
| Hyperkalemia: Interventions | -Dietary restriction -Increase urine output: Diuretics -Hydration -Meds |
| Hypocalcemia | -Reciprocal with Phosphorous -Associated with: Inadequate diet(Ca, Vit D), Decrease parathyroid hormone, pancreatitis,GI malabsorption, meds,cancer -Cellular changes: increased cell excitability (cardiac, muscle) |
| Hypocalcemia: Assessment | -Parathesis:numbess, tingling hands, feet, lips -Emotional lability -VS changes -Chvostek's sign (tap cheek of facial nerve, see twtiching) -Trousseau sign (use BP cuff and see hand, fingers twitching) -Low albumin levels |
| Hypocalcemia: Interventions | -Increase intake: Ca, Vit D -IV replacement: Ca chloride, Ca gluconate -Patient safety: fall risk, bleeding risk, cardiac arrhythmias |
| Hypercalcemia | -Associated with: Cancer with metastasis, hyperparathyroidism, thiazide diuretic therapy, excessive intake, prolonged immobilization, metabolic acidosis -Cellular changes: decrease cell excitability (cardiac, muscular); production of renal stones |
| Hypercalcemia: Assessment | -N/V -Anorexia -Lethargy -Muscle Weakness -Kidney stones or hx of kidney stones |
| Hypercalcemia: Interventions | -Identify pt at risk -Dietary restrictions foods high in Ca -Hydration with diuresis (IV normal saline with lasix) -Meds |
| Magnesium | -Major ICF cation -Most is in soft tissue,bone, muscle with only 1% in blood -Important for cardiac electrical function -Low Mg can contribute to low K+ and low Ca++ -Treat low Mg++ before treating K+ and Ca++ -Mg is used to treat toxemia in pregnan |
| Hypermagnesemia | -Most cases are caused by renal failure |
| Hypomagnesemia | -Associated w/ low K and low Ca -Inadequate food intake -IV nutrition/fluids -ETOH abuse -Malabsorption syndromes -Low Mg++=Trousseau and Chvostek signs -Low Mg + Low K Increases risk for cardiac electrical problems (ventricular arrhythmias) |
| Carbohydrates | -Mono,Di: milk,cane sugar,beet sugar,fruits -Polysaccharides:grains,legumes, root veggies -Are converted to glc, excess converted to glycogen or fat -Recommended daily intake = 125-175g, most should be complex carb (poly) like milk, whole grains |
| Protein:Complete | -Eggs, Milk Products, Meat -Meet body's AA needs for tissue growth -Building blocks of protein - AA -Recommended daily intake: 56g men, 45g women |
| Vitamin A | -Found in fish oil (Salmon,walleye) egg yolks,animal liver,fortified milk,margarine -Orange veg and fruits -Needed for vision, skin, repro, cell membrane structure -Deficit - night blindness -Excess - dry lips, bone pain, hair loss |
| Vitamin D | -Formed by action of sun on skin -Necessary for blood Ca stability, clotting, bone formation, neuromuscular function -Deficit - has to do with how much Ca gets used, joint pain -Excess - calcification of soft tissues |
| Vitamin E | -Veg oil,margarine,whole grains,dark green veg; additive product (oil, margarine) -Antioxidant - prevent oxidation of vit A&C necessary for cell membrane integrity -Deficit-lipid absorption problems -Excess - liver/kidney failure |
| Vitamin K | -Synthesized by coliform bacteria in large intestine -Green leafy veg,cabbage, cauliflower, pork -Essential for formation of clotting protein -Deficit - bruising -Excess - hemolytic anemia (cells lysed), jaundice in babies (CBD block) |
| Vitamin C | -Citrus fruit,potatoes,tomatoes,grn leafy veg -Help form connective tissue, conversion of cholesterol to bile salt -Antioxidant and vasoconstrictor (watch pts w/HTN) -Deficit-dry mouth,hair loss, itching -Excess-GI upset |
| Anuria | -Urine output <100 ml/24 |
| Oliguria | -< 30 - 50 ml per hour or 100-400 ml/24h |
| Polyuria | -Unusually large amounts of urine output |
| Frequency | -Voiding more often then every 2 hours |
| Urgency | -Strong sudden urge to void |
| Dysuria | - Burning on urination |
| Nocturia | -> need to urinate at night |
| Hesitancy | -Difficulty starting a stream of urine |
| Residual | -Urine left in the bladder after voiding |
| Retention | -The amount of urine left in the bladder |
| Cystitis | -UTI -Most common type -Prevalence 8x higher in women -Increases during hospitalization -Wipe from front to back -More common with increased sexual activity, poorly fitting diaphragms, tight clothing, wet bathing suites, indwelling catheters |
| UTI Causative Organisms | -E Coli (80%) -Klebsiella -Enterobacter and proteus -Chlamydia trachomatis -Trichomonas vaginalis -Neisseria gonorrhea |
| UTI signs and symptoms | -Burning -Frequency -Urgency -Cloudy urine -Inability to void -Malaise -Mental status changes - in elderly might be first sign |
| UTI Medical Management | -Inhibit bacterial growth (antibiotic) -Meds (can affect bc) -Diet Modification (avoid high caffeine, spicy foods) -Increase fluid intake (3-4L/d) -Prevent complications |
| Urosepsis | -Gram-Negative bacteremia originating in the gu tract -Can lead to septic shock and death without aggressive, immediate tx -Elderly,Indwelling cath,Untreated UTI -Ecoli most common cause -Chemo Observe for:I temp,change in mental status,Low bp |
| IC Symptoms and Damage | -Bladder tenderness -Urinary urgency -Frequency (60+/day) -Nocturia -Dyspareunia - painful intercourse -Variable manifestations Damage: ulcerations and hemorrhages in bladder wall |
| Bladder Cancer | -Most frequent neoplasm of urinary tract -Strong correlation with smoking -Industrial exposure -Chronic cystitis -Pelvic Radiation |
| Bladder Cancer Manifestations | -Painless hematuria (85% of all cases) Typically first sign; Amt not significant to stage of disease -Initially intermittent bleeding -Obstruction |
| Urinary Calculi | -Commonly called stones -Causes: urinary stasis, supersaturation of urine |
| Types of stones | -Calcium - 90% (phosphate or oxidase) -Oxalate (soy bean based products) -Struvite (bacteria) -Uric acid (GOUT) -Cystine (autosomal recessive disorder) -Xanthaene (rare) |
| Urinary Calculi Symptoms and Dx | -Sharp sudden onset of pain -Infection -N/V -KUB -IVP -Cystoscopy |
| Urinary Retention | -Inability of bladder to empty: post void residual >100ml, detrusor failure in women, enlarged prostate in men -Manifestation of another pathologic condition -Causes: sensory input to/from bladder, muscle tension/anxiety, neurologic conditions |
| Urinary Incontinence | -4 Major types -Stress-force of exertion(laugh, preg,sneeze,radiation,overwt) -Detrusor over activity-urge incontinence (spontaneous bladder contract:parkinson,alzheimer,stroke) -Overflow-frequency,constant dribble,wk musc,block,tumor |
| -Functional:d/t physical, psychosocial of pharmacologic causes unrelated to urinary system (dementia,pharm,arthritis) | |
| Neurogenic Bladder | -Bladder dysfunctions caused by lesions of CNS/PNS -Uninhibited-constant urine flow -Sensory-bladder can't sense fullness -Motor-no contraction -Autonomous-can't start flow -Reflex-no sensation but bladder contracts |
| Hydronephrosis | -Distention of the renal pelvis caused by obstruction of normal urine flow -Tx:relieve obstruction&prevent infection |
| Nephrotic vs Nephritic | -Nephrotic: leaking protein, failure of glomerular basement wall -Nephritic: usually see hematuria or blood in urine |
| Acute Renal Failure | -Abrupt loss of Kidney function (days to weeks, can be life threatening) -GFR decrease, serum creatinine and BUN increase -Urine output Decrease |
| Non-oliguric | -Excrete as much as 2000 ml/24h with increase in GFR, BUN, and Creatinine |
| Classifications | -Pre-renal: decrease bf to kidney (cardiac issues) -Intra-renal: structures w/in kdineys-trauma, infection -Post-renal: obstruction in urinary tract-BPH, tumors |
| Nursing Asst:Pre-Renal | -Tachycardia -Hypotension -Dry mucous membranes -Flat neck veins -Coma |
| Nursing Asst:Intra-renal | -Hypovolemia -Vomiting -Diarrhea -Cool -Lethargy -Confusion |
| Chronic Kidney Disease | -Kidney damage for 3 months as defined by structural or functional abnormalities with or without decreased GFR or a GFR of 60ml/min/1.73m2 or less, with or without kidney damage |
| Cause of CKD | -Diabetes (40%) -HTN -Inflammation -Heredity -Chronic Infection -Obstruction -Accidents |
| Stage 1: CKD | -Normal or decreased GFR -Structural or functional abnormality of kidney markers of kidney disease -May have normal BP -No serum lab abnormalities -No symptoms Action:Dx,Tx,slow progression, tx comorbidities, CVD risk reduction |
| Stage 2: CKD | -GFR 60-89 -Generally asymptomatic -HTN usually develop -Lab abnormalities may or may not be present -Action: estimate progression |
| Stage 3: CKD | -GFR 30-59 -Lab abnormalities may be present indicating anemia, bone disease and disorder of Ca and Phosphorus -Usually asymptomatic -HTN usually present -Action: evaluate and treat complications |
| Stage 4: CKD | -GFR 15-29 -Symptoms: mild fatigue, anorexia, edema, impaired memory -HTN -Diabetes -Action: prepare for renal replacement therapy |
| Stage 5: CKD | -GFR <15 -Symptoms increase: malaise, wt loss/gain, trouble sleeping, anorexia,N/V, musc cramp, cognitive decline -Metallic taste from build up -Action: Renal replacement therapy |
| Diabetes | -Disorder of metabolism-the way our bodies use digested food for energy -Chronic,sytemic disease characterized by either a deficiency of insulin or decreased ability of the body to use insulin -Pancreas is responsible for insulin levels |
| Alpha Cells | -Produce glucagon -Stimulate breakdown of glycogen in liver (glycogenolysis) -Stimulated formation of carb in liver -Stimulate breakdown of lipids -Secretion is regulated by blood sugar -Secretion is regulated by blood sugar levels |
| Beta Cells | -Secrete insulin-helps glucose to move across the cell membrane, decrease blood glucose levels -Secretion is regulated by blood glucose level -Synthesize and secrete insulin |
| Delta Cells | -Produces somatostatin-inhibits the production of glucagon and insulin -Balances alpha and beta cell funtion -Acts as mediator |
| Classification of DM | -Type 1, Insulin dependent DM, juvenile onset -Type 2, Non insulin dependent DM, adult onset -Disease of pancreas or genetic disease -Gestational DM-during pregnancy |
| Type 1 | -Autoimmune disease -Often leads to absolute insulin dependency -Affects 10% of ppl with DM -Develops most often in children and young adults -Strongly inherited -Immune system fights beta cells |
| Type 2 | -Most common -usually diagnosed after 40 but seen in younger and younger ppl -Associated with older age, obesity,family Hx, previous gestational dm,physical inactivity, certain ethnic populations |
| Risk Factors Type 1 | -Genetic Predisposition -Exposure to environmental factors (viruses, smoked products, nitrates) -No known health promotion activity to prevent but regular exercise and balanced diet may limit the complications |
| Risk Factors Type 2 | -Hx of DM in parents of siblings -Obesity -Physical inactivity -HTN -Women with gestational diabetes hx -Race/ethnicity |
| Decreased Glucose Utilization | -Skeletal, cardiac, fat cells don't need insulin -Ingested glc can't be transported into cells, plasma level rise -Liver can't store glc as glycogen w/out adequate insulin -Blood glc level rise -Glc appears in urine -Dehydration appears-osmotic diu |
| Increased Fat Mobilization | -Muscle cry for glc so fat stores broken down -Ketones fomred as byproduct and produce hydrogen ions-measure in urine and smelled on breath -Lipid breakdown increase lipid level - lead to arteriosclerosis |
| Increased Protein Utilization | -AA converted to glc in liver, further elevate glc level -Insulin needed to build protein -Type 1 often appear emaciated d/t constant protein breakdown |
| Symptoms of DM | -Cardinal: POLYURIA,POLYDYPSIA, POLYPHAGIA -Weight loss (type 1) -Blurred vision -Pruitis,vaginitis -Weakness,fatigue,dizziness -Asymptomatic (type 2) -Slow healing wounds, dark patches |
| Diagnosis of DM | -Symptoms + postload glc > or = 200 -Fasting glc > or = 126 -2 hr post GTT > = 200 -Glycosylated Hemoglobin not used for dx -FBS 110-126 |
| Normal | -FBS: < 100 -Glucose Tolerance: < 140 |
| Hypoglycemia | -Etiology: insulin od, omitting meals, vomiting, over exercise without carbs, alcohol intake -Normal feedback loop is dirupted |
| Hypoglycemic symptoms | -Early signs (adrenergic: increaseing epinepherine, shaky, irritable, tachycardia, hunger, pale, paresthesias -Later signs (neuroglycopenic): lack of glc avail to brain, Ha, slurred speech, blurred vision, confusion, lethargy, coma, sz, death |
| Tx of Hypoglycemia | -Depends more on symptoms than blood glucose levels -Start with 10-15g of CHO (4oz OF, 6oz regular soda, 8oz 2% milk, 4tsp sugar) -20-30g of CHO (double above, glucagon, 1mg subq or IM) -50% dextrose IV (glucagon IM or IV) |
| Chronic Complications | -Eyes,heart,kidneys,brain, Macrovascular (larger vessels) -CAD,crebrovascular disease,HTN,peripheral vascular disease -Occur years before symptoms of DM even appear |
| Microvascular complications | -Retinopathy -Nephropathy -Damage to smaller blood vessels -No symptoms early -Late symptoms-swelling, proteinuria, renal failure -Checking urine protein is important |
| Neuropathic Complications | -Most common problem -Numbness,tingling,pain |
| Musculoskeletal System | -Movement/Positioning -Provides:support,protection, movable frame,storage for Ca and other ions (I movement of Ca stimulate osteoclasts to break down bone and release Ca 1)stimulate osteoclasts 2)reabsorb bone 3) new bone-osteoblasts -Bone marrow fx |
| Bone Marrow Function | -Osteoblasts - bone forming in bone matrix -Osteocytes - bone matrix, mature osteoblasts -Osteoclasts - remove old, damaged bones-growth and repair |
| Stages of Bone Healing | 1) Hematoma or inflammatory (1-3d) 2) Fibrocartilage formation (3d - 2wk) 3) Callus formation (2-6wk) 4) Ossification (3-24wk) 5)Consolidation and remodeling (6wk - 1y) |
| Osteoarthritis: Definition | -Painful, degenerative joint disease that often involves the hips, knees, neck, lower back or the small joints of the hands |
| Osteoarthritis | -Oldest and most common -Not just associated with aging -Cartilage deterioration, joint destruction -Chronic, incurable -Affects weight bearing joints -Obesity major risk factor |
| OA Assessment: Subjective | -Pain and stiffness that increases with activity and decreases with rest -Pain worse at the end of the day -Pain relieved by rest -Mild tenderness in joint areas -Joints lock give way when going down stairs -Symptoms:worsening pain,limit of movement |
| OA Assessment: Objective | -Crepitus/grating noise -Deficient ROM -Joint enlargement -Heberden's nodules DIP -Bouchard's nodules PIP |
| Phamacotherapy for OA | -Acetaminophen:DRUG OF CHOICE -NSAID:Motrin -Capsacin cream -Steroid injections-cortisone, decrease pain,many SE -Hyaluronan injections-allows for smooth musc. movement: >synovial fluid production -COX-2 drugs:celebrex -Supplements |
| Osteoporosis | -Systemic skeletal disorder that compromises bone strength&I risk of bone fracture -2 components of bone strength: density and quality -Risk factors:women-small body,underwt,older,hx of OP) -Med Mngt: prevent loss of bone mass & bone resorption |
| Risk Factors: Major | -Hx of fractures as an adult -Hx of fragility or low trauma fractures 1st degree relative -Low body wt (<128) -Cigarette smoking** -Steroids use for > 3 months |
| Paget's Disease | -Tibia,lower spine,pelvis,head -Viral infection can begin process -Rare under 40 -Can be asymptomatic |
| Osteomalacia | -Inadequate vit D -Decalcification and softening bones, Asian and women more prone, vegan-similar to rickets in children -CM: fatigue, malaise,bone pain, muscle weakness -Daily vit d replacement, ensure adequate ca and phosphorus intake |
| Gout and Gouty Arthritis | -Uric acid lab levels -Metabolic acid of purine- mostly in big toe -Develop in stages -NSAIDS, allopurinal prevent flareups -Primary: inherited, more common in men -Secondary: acquired with renal disorders |
| Rhabdomylosis | -Can see as side effect from statins: rare occasion -Trauma – break down of muscle fibers, Electrical burns,Ischemic conditions,Prolonged immobilization -I creatine kinase (CK) – 5X normal value, Hyperkalemia ,HBG and myoglobin in urine |
| Fracture Classification | -Closed – deformity but no opening, skin in tact -Open: Grade I–wound w < 1 cm, minimal contamination - lacteration Grade II – greater than 1, moderate contamination Grade III – greater than 6-8 cm with extensive damage and high contamination |
| Closed Reduction | -Manual traction applied to move fx fragments&align bone -Should be performed as soon after injury as possible, wait until swelling goes down to fix it -Immobilization device must be applied right after Xray confirms bone alignment (i.e.cast) |
| Open Reduction and Internal Fixation | -Sx -Surgeon realigns fx -Tx of choice for compound fx’s -Femoral and joint fx’s are treated with ORIF -Maintains immobilization and prevents deformity -Screws, plates, pins, wires or nails are used to maintain the alignment |
| External Fixation | -Immobilization -Support -Maintain position -Common sites:face,jaw, extremities,pelvis,ribs,fingers and toes -Around the clock medication |
| Traction | -Use since prehistoric times!! -Application of a pulling force to an injured part or extremity while counteraction pulls in opposite direction hands (manual traction) -Weights (more common) -Not as prevalent today |
| Nursing Implications: Traction | -Never interrupt the wts of skeletal traction -Skin traction,remove wts only w intermittent skin traction -Dont wedge foot or place it flush with foot board of bed -Maintain line of pull/dont knot ropes -Wt should hang freely at all times |
| Synthetic/Fiberglass Cast | usually dries within 30 min Cooler and more lightweight Generates heat while drying Tell the patient he/she will feel heat under cast during this time OK to use a cool blow dryers |
| Plaster Cast | Plaster-may take 1-2 days to dry completely when dry the cast is odorless DO NOT cover with blanket or towel while drying! DO NOT use a blow dryer at this time! WHY? – can burn patient and can crack cast |
| Cast Application | Pad over bony prominences w/o wrinkles while cast wet support the cast with open,flat palm of hand at all times-avoid using fingertips avoid rapid cast drying wexcessive heat use pillows to elevate keep edges smooth turn q2h,Turn toward unaffected li |
| Cast Care | Provide/teach correct skin,cast care bathe only accessible skin apply lotion only to exposed skin, skin under cast use alcohol-will dry inspect for loose plaster avoid using powder in cast inspect padding Do not insert any foreign object under cast! |
| Delegation | LPNS can gather information, provide educational materials but not evaluate learning and perform most interventions. They do not plan care Nursing assistants CAN measure and gather data; they CANNOT assess, teach, evaluate or plan care. |
| Compartment Syndrome | -Asst,Prevention is the key -Monitor NV status of injured limb unrelieved,increase in pain in affected limb Pain w passive stretch of toes or fingers mottled skin excessive swelling poor cap refill paresthesia inability to move toes or fingers |
| Compartment Syndrome: Late Symptoms | pallor dim,absent pulses cold skin -Arterial occlusion from swelling of soft tissues 2nd to bone trauma Assess peripheral nerve function q1h for 1st 24 hours -poor venous return results in edema which impedes arterial flow and nerve impulse |
| Fat Embolism | Most often seen with femur fx Pathophysiology: fat globules enter the vascular space and become emboli eventually travel to the lung pulmonary embolus can cause death Fat embolisms usually occur 12-36 hrs. post injury |
| Classic Signs of Fat Embolism | tachypnea> 30/min sudden onset of chest pain or dyspnea restlessness, apprehension, anxiety confusion **impending doom elev temp >103 inc pulse rate >140 petechial skin rash of neck, conjunctiva, axilla, or chest |
| Hemorrhage/Hematoma Formation | Bleeding or Hemorrhage due to trauma monitor for s/s of shock/hemorrhage > pulse or < BP UO = <30cc/hr restless, agitated, change in mental status > RR < peripheral pulses cool, pale or cyanotic skin thirst |
| Lower GI problems: Inflammatory Disorders | -Can be in any portion of the bowel -Clostridium Dificile (large dose of antibiotics, on antibiotics >7d, contagious and pt in isolation, MUST wash hands) -Gastroenteritis-inflammation of stomach and small bowel-pain&D (can have N&V,fever,anorexia) |
| Appendicitis: Symptoms | -Appendix ruptures=no pain but peritonitis develop -DON'T do enema w/appendicitis= rupture -Acute ab pain,comes in waves -Feeling of pressure to pass gas -Pain starts in epigastrium, localizes to RLQ -Guarding of ab by drawing up legs -Tx=appendecto |
| Nursing Issues with Appendicitis | -Never give enema or laxative -Never apply ab heat -Assess for rebound tenderness= when push down=no pain, but when let go have pain -Assess for pain that abruptly changes and ab becomes rigid or board like-rupture - |
| Pathophys of Peritonitis | -Systemic effects -Inflammatory process shunts blood to site diverting it from other organs -Peristalsis stops, fluid&air in bowel I ab pressure -O2 needs are I by inflammation -Ventilation D d/t pain&ab pressure |
| Symptoms of Peritonitis | -Diffuse/localized pain -Rebound tenderness -Severe rigidity -Distention -Anorexia, N, V -D or absent bowel sounds -Fever -Can cause severe systemic problems |
| Clinical Manifestations of Crohn's and UC | -Ab pain -D,V -Fluid imbalances -Wt loss -Fever in acute phase-flare-up -Hemorrhoids-varicose veins of rectal area -Perianal abscess w/ crohn's |
| Ulcerative Colitis | -Predominant symptom-rectal bleeding -20 or more stools per day -Colicky pain in LLQ -Can have severe dehydration w/ D K -Symptoms worse with stress, poor diet, laxatives or antibiotics |
| Irritable Bowel Syndrome (IBS) | -Dysfunction in bowel motility:D alternate with C -Seen in middle age, very common -Risk factors:diet high in fat, gas producing food, lactose, carbonated bev, caffeine, alcohol, smokers, high stress |
| Pathophys of IBS | -Alternating D/C -Hypersensitivity of bowel wall to distension,alter peristalsis -Crampy pain in LQ -Hypersecretion of bowel mucous -Flatus,N,anorexia -Relief of pain w/defecation -Fiber,fruit,alcohol,caffeine,fatigue irritate sx -Connection to ser |
| Symptoms of Colon Cancer | -Rectal Bleeding** -Change in bowel habits, shape of stool -Ab pain -Wt loss -Anorexia -Anemia |
| Candidiasis-Moniliasis | -Thrush -Candida-albicans-yeast like fungus -Immunosupression,DM,ATB/Steroid Rx, tube feeding -Secondary inf -Pt on chemo |
| Nursing Care of oral Disorders | -Best to use warm saline -Avoid anything alcohol based (mouth wash) -Analgesia 30-45 min b/f meals -Small, frequent feedings |
| Esophageal Disorders: Dysphagia | -Difficulty swallowing -Clinical manifestation of an esophageal disorder -Obstructive cause:tumors, congenital defects,hiatal hernia -Motility Cause:DM,parkinson's, stroke |
| Symptoms of GERD | -Heartburn,dysphagia,salty secretions in mouth (water brash) -Pain described as burning that moves up and down -If severe,spasm may radiate to neck,back,jaw, an mimic a cardiac episode: treat w/nitro -Pain relieved by fluids or antacids |
| Medications for GERD | -Antacids: 1h ac or 2-3h pc, relief 10-30m,neutralize gastric acid,sooth mucosal lining -H2: 1h b/f or after antacids BID,taper to prn,inhibit histamine in parietal cells -PPI:tx failure,30ac daily,completely control acid secretion |
| -Antiemetic Cholinergic: increases LES pressure, increases gastric emptying, 30-60 ac | |
| Radiography | -Ab flat plate: simple xray (tumors,gas patterns,fluid collection) -Upper GI:barium swallow (stool white)(esophagus,stomach,duodenum,jejunum, NPO after midnight, scheduled AFTER other ab tests) -Lower GI:barium enema (sigmoid colon,rectum) |
| -CT scan:npo after bfast, masses, inflammation, abscesses | |
| Chronic Gastritis | -> 6mo -Type A (autoimmune):fundus of stomach,loss of parietal cells -Type B (most common):H pylori,peptic ulcer disease, gastric sx -Complications:blding,pernicious anemia, gastric cancer -PPI changed this, not so much bleeding |
| Peptic Ulcer Disease | -Seen in all parts of upper GI -90% b/c of H pylori -Helivax vaccine -Aspirin,NSAIDS breakdown gastric lining allow acids to damage mucosa -Stress stimulates vagus nerve, I acid production, I gastric motility -Stress ulcers occurs in critically ill |
| Aggressive v Defensive Factors | Aggressive (acid) -stomach acid -H pylori - if hubby has it, wife prob does too -smoking -alcohol Defensive -mucous -adequate bf to stomach lining -balanced diet |
| Symptoms of GI ulcer | -Acute pain-burning,gnawing,cramping -Gastric: food causes pain,V relieves pain -Duodenal ulcer:pain on empty stomach, food eases pain -N,V most freq in gastric -Blding if ulcer erodes thru bld vessel |
| How to check for Tactile fremitus | -Place hands on chest while patient says 99 -Increased vibrations=fluid in lungs -Decreased vibrations=air in lungs, obstruction (pneumothorax), emphysema |
| Resonance | -Hyper resonance- normal only in chronic obstructive disease, children, and very thin pts -Dull-abnormal,mass/tumor,pneumonia -Flat-over bony prominence -Tympanic-air in peripheral space (pneumothorax) |
| Auscultation | -Vesicular-peripheral -Bronchial-meniculum -BV-1st,2nd ic space b/w scapula and where trachea divides |
| Adventitious breath sounds | -Crackles/Rales:popping,sudden opening sounds when alveoli are fluid filled, doesn't clear with cough, inspiration/expiration, can come and go -Rhonchi:air pass through airway narrowed w/fluid, snoring,clears w/cough,expiration ex:bad cold |
| -Wheezes:high pitched musical sounds caused by bronchoconstriction, can be heard w/out stethoscope, foreign bodies, fluid can cause -Pleural Friction Rubs: grating sound, pleuritis, inflammation of pleura | |
| Definitions | -Eupnea-breathing is normal -Tachypnea-breathing is fast -Dyspnea-trouble breathing -Exertional dyspnea-when i lift things, lose my breath -Orthopnea-can't breathe lying flat -Parozysmal nocturnal dyspnea-sat up in bed and couldn't catch breath |
| -Hypoxia-low oxygen -Hypoxemia-low oxygen in blood -Anoxia-no oxygen in bld or tissues -Hemoptysis-coughing up blood -Atelectasis-collapse of alveoli in lower lobes | |
| Normal drive to breathe | -Brain gets the signal that there is a high CO2 level -Arterial blood levels |
| pH | -Normal serum pH = 7.35 - 7.45 - < 7.35 = acidosis - > 7.45 = alkalosis |
| Obtaining Arterial Blood Gases | -Draw bld from artery to measure O2, CO2,pH, bicarb, base excess -Also measure electrolytes -Usually draw from radial artery -Done by MD,PA,NP,RT,RN |
| -Sample must be collected in a syringe with agent to prevent O2 metabolism which would falsely lower the reading&placed on ice in a syringe -Allen test (pg 180) -ABG test = painful -Hold pressure at site for 5 min after drawing blood | |
| ABGs: Normal Levels | -PaO2 (80-100mmHg) -PaCO2 (35-45 mmHg) reflects acid base balance -pH (7.35 - 7.45) -Bicarbonate (22-26 meq/L) represents acid-base balance -Base Excess - -1 to +1 |
| Important Concepts: ABGs | -If blood pH < 7.35 = acidotic or has acidosis -If blood pH > 7.45 = alkalotic or has alkalosis -If CO2 > 45 = hypercarbic AND acidotic -If CO2 < 35 = hypocarbic AND alkalotic |
| -O2=91,CO2=50,pH=7.33,HCO3=24 -O2=87,CO2=33,pH=7.48,HCO3=22 | -Respiratory Acidosis -Respiratory Alkalosis |
| CT | -More sophisticated multidimensional images than xray -Radioactive dye is given -Assess for iodine allergies -NEED TO KNOW CREATININE IF DYE IS GIVEN -Can use CT scan for interventions like biopsies |
| Bronchoscopy | -Scope inserted into airway for:examination,tissue specimen,removal of foreign bodies,suctioning of thick secretions,remove lesions -Pre:NPO 6h,sedation,sore throat-numbed and affects swallowing -Post:monitor vs,suction,assess swallowing-check gag refle |
| Thoracentesis | -MD insert cath into lung,drain fluid/air,fluid can be checked for inf,cancer cells,insert med -Pre:painful,sit up and lean over table,topical anesthetic,10-15min -Post:xray-check for pneumothorax,turn to unaffected side,monitor vs&subq crepitus |
| Pulse Oximetry | -SaO2 -Non-invasive and continuous -Measure amt of hemoglobin saturated w/oxygen through fractionated light -Normal = 92-100 -Problems: affected by motion, poor circ, cold |
| Asthma Asst | -Dyspnea,chest pain, feel anixous, can't stop coughing -Objective: nasal flaring,cyanosis,use of acc musc,wheeze, tachypnea/cardia, pursed lip breathing,cough-night time |
| Classification of Asthma Severity | 1)Mild intermittent:sx<2xwk,brief exacerbations;no prob w/lung fx 2)Mild Persistent:sx>2xwk but < 1time/d;exacerbation may affect activity 3)Moderate Persistent:daily sx w/daily use of inhaler;exacerbation affect activity |
| 4)Severe Persistent:continual sx;limited physical activity, freq exacerbations | |
| Medications for Asthma | -Beta2:Bronchiolators,oral -Short,long acting -SE:tremor,nervousness, HTN,tachycardia,oral candidiasis (rinse mouth) -Albuterol,Proventil,Theophylline -Most pts start out on short-acting and progress to long-acting or oral as disease progresses |
| -Inhales Steroids (corticosteroids) -Inhaled, oral (sicker pt) -Reduced inflamm -D mucous production -Make receptors more receptive to beta agonists -SE:thrush,dysphonia -rinse mouth -Use spacer to reduce SE -Beta2 combined with steroid | |
| -Oral Steroids -More prone to inf d/t immuno-suppression -Bone loss d/t dimineralization -I BS b/c cortisol -Fluid retention d/t aldosterone -Stomach ulcers d/t affects protective layer of stom -Suppression of growth in kids | |
| Oral Steroids -Give smallest dose in am b/c of hormone levels -Used as disease progresses or if there are exacerbations -Tapered slowly so that inherent adrenal function returns | |
| -Leukitriene Modifiers -Tremendous benefit (good drug,less SE) -Reduce bronchoconstriction, inflamm, mucous production -Singulair | |
| Medication Management for Long term Control | 1)Mild Intermittent:short act bronchodilator prn 2)Mild Persistent:low dose inhaled steroids daily 3)Moderate Persistent: low-med dose inhaled steroids daily, long acting beta 2 daily 4)High dose inhaled steroids daily,long acting beta2 daily |
| COPD | -Emphysema,Chronic Bronchitis -Chronic airflow limitation* -Can include bronchial edema, decreased elastic recoil -Risk factors: smoking,chronic resp inf, environment |
| Chronic Bronchitis | -I mucous produc(I goblet cells, I mucous glands) -Impaired cililary func -Thick mucous cause air trap/alveolar collapse -I risk inf -Retain CO2 -Hypoxemic -Polycythemic:high rbc,hgb b/c pt have chronic low O2,body thinks need more,make more rbc |
| Chronic Bronchitis: Signs and Symptoms | -Productive cough -Decreased exercise tolerance -Wheezing -SOB -Copious sputum -Freq pul inf -Chronic hypoxemia -Chronic I Co2 -High hgb -Finger nail clubbing |
| Emphysema | -Aleolar wall destroyed d/t conn tissue destruction -Deficiency in alpha1 antitrypsin -I dead space in lungs-non functioning lung tissue -I work of breathing -Co2 retention is less of problem |
| Emphysema: Signs and Symptoms | -Progressive dyspnea on exertion, progress to dyspnea @rest -Barrel chest -Hyperresonance -Clubbing of fingers -Wt loss -High Co2 -High hgb -Rt heart failure -Hypoxemia |
| Complications of COPD | -Inf -Collapsed lung -Worsens @night -More likely to go into resp failure and need ventilator after acute illness -May need home O2 |
| Medications for COPD | -Bronchodilators -Steroids, oral and inhaled -OXYGEN IN LOW DOSES: Low flow (1-3L/min); Low flow venturi mask; Nasal cannula (1-3L) |
| Pulmonary Emboli | -Occlusion of portion of blood vessel in pul vascular system -Can be lethal depending on size -Mortality rate,50,000 unchanged in over 20y -Silent Pulmonary emboli -High risk:major surgeries,long plane rides, sit for a long time, vascular disorders |
| Pulmonary Emboli: Causes | -Thrombosis related (80%) -Prolonged bed rest -Obesity -Long operations -Long plane flights -Afib -Rt side hrt failure -CHF -Pelvix fx or large bone |
| Virchow's Triad: What you need to create an emboli | -Blood stasis: pooling -Blood coagulation alterations: coagulation disorders -Vessel wall abnormalities: atherosclerosis, DM |
| Diagnostic findings of Pulmonary Emboli | -Some have no symptoms -Dyspnea (81%) -Sudden pleuritic pain -Tachycardia,tachypnea -ECG changes |
| Asst Findings Pulmonary Emboli | -Dyspnea -Apprehension -Diaphoresis -Syncope -Chest pain -Rales -Fixed splitting of S2 -Murmur -Cyanosis -Fever -Shock -Cough, hemopysis |
| **Serum lab tests that represent clotting** | -PT (prothrombin time), extrinsic pathway: normal = 11-13sec -INR (international radio), extrinsic pathway: normal: 0.8-1.2 (used more often than PT) -PTT (partial thromboplastin time),intrinsic pathway: normal=21-35 sec |
| Anticoagulation Therapy for PE | -Heparin Drip (blocks promthrobin-thrombin) -I PTT to 2-2.5 times normal (>70) -WON'T dissolve clot, prevent others from devloping -Bld draws q4h until established level -Only give IV, coumadin for home |
| Anticoagulation Therapy for PE | -Coumadin -Oral, depresses clotting factors -Begin 3-5 days before d/c heparin -PT 2x normal (>26 sec) -Most often we follow INR and keep it in 2-3 -Continue therapy for approx 6 months |
| Arteries | -3 Layers: Intima (single layer of endothelial cells,elastic membrane); Media (near vessel lumen receive O2/nutrients by direct diffusion in small arteries;vasa vasorum in larger arteries); Adventia (conn tissue,nerve fibers,vasa vasorum) |
| Three types of Arteries | -Large Elastic -Medium Muscular (HTN) -Small (within tissues and organs) |
| Arterioles | -Principle point of resistance to blood flow -Sharp decrease in pressure and velocity -Changes from pulsatile to stead flow |
| Veins | -Larger diameters -Larger lumina -Thinner less organized walls -High volume,low pressure (go back to heart) -Reverse flow is prevented by venous valves in the extremities -Valve damage = varicose veins |
| Blood Flow | -Flow = pressure gradient/resistance -Pressure = arterial pressure -Flow = CO -Resistance = total peripheral resistance (depends on: size of vessel,fluid viscosity, length of vessel) |
| Regulation of Body Fluid Volume | -When sodium and water levels increase the total blood volume is increased -Disease that change kidney function alter BP:vasoconstriction= high peripheral vasc resistance; systolic = < 70, kidneys not getting O2 |
| Renin-Angiotensin-Aldosterone | -ADH now released d/t increased osmolaritiy, begins to reabsorb water to try to decrease serum omolarity -Increased reabsorption of water increases blood volume, increase venous return, which can increase stroke volume, thus increasing CO and bp |
| Blood Pressure | -Reflects left ventricular function -Systolic reading represents force of ventricular contraction -Diastolic reading indicates vascular resistance (afterload) -Pulse pressure-difference b/w systolic and diastolic, normal = 40 mmhg |
| Stages of Hypertension | -Normal 120/80 -Pre:120-139/80-89, No meds,need lifestyle mod -Stage 1:>140-159/90-99,Thiazides,consider ACEI,ARB,BB,CCB;<130/80 pts w/DM or CKD -Stage 2:>160/>100, two drug combo, thiazide +ACEI,ARB,BB,CCB |
| Preload | -Blood coming back to heart -Venous return that builds during diastole -Ventricles stretch just before contraction -Hypovolemia = increased preload |
| Afterload | -Increase in high bp, vasoconstriction -Resistance that the heart must overcome to achieve ejection -HTN- increase the word load of the heart |
| Types of HTN | -Primary (essential): no renal disease or tumor, just have HTN -Secondary: b/c of something else -Isolated systolic: get horrible news, nervous -Resistant (malignant): can be lethal, cardiac or brain insult |
| Smoking | -Smoking affects blood vessels in 2 ways -Endothelial damage (carbon and tar): fat,cholesterol,lipids can sneak into inner layer and build up plaque -Vasoconstriction (nicotine) |
| Pharmacotherapy: Diuretics | -Thiazide:first line -Loop diuretics (K+ wasting) Lasix -Potassium sparing: (>K+) aldactone,midamor |
| Pharmacotherapy: Beta-Blockers | -D HR,contractility,afterload,CO,renin secretion -<effectiveness in AA,elderly -Contraindicated in asthma -ED in men -Caution in DM -Reduce O2 (know hr,bp before admin) -olols |
| Pharmacotherapy: Calcium Channel Blockers | -Cause smooth musc relax,vasodilation block calcium to influx musc ->effect in AA when w/thiazide -D L ventricular wall stress by D afterload -Diltiazem,il,pine |
| Pharmacotherapy: ACE inhibitors | -Inhibits ACE so block PRODUCTION of angiotensin II -More effective in caucasian than aa -Better for diabetes, slow progression of nephropathy -Useful for asthmatics,hf,pvd -Can cause dry cough,1st dose htn,hyperkalemia,renal failure,angioedema -pril |
| Pharmacotherapy: Angiotensin II receptor blockers (ARB) "sartans" | -Block the ACTION of angiotensin II by blocking receptors -DON'T cause hyperkalemia,cough or angioedema -SE: low incidence of dizziness |
| What symptoms would your patient complain of if they had reduced/blocked arterial flow? | -Angina -SOB -Fatigue -Heart burn -Tightness -Tingling -Numbness -In the leg: poor pulse, cold |
| Arterial Assessment | -Weak/Absent pulses -Dependent rubor -Pallor with elevation -Hypertrophied toenails -Tissue atrophy -Ulcers -Gangrene -Absence of hair -Parasthesia -Tingling -Numbness |
| Intermittent Claudication | -Most important manifestation of chronic arterial occlusive disease -Pain that occurs when a muscle is forced to contract w/out adequate bld supply -Any musc claudicate,but is more common in lower -Reproducible pain |
| -Aortic-iliac disorders:pain in thighs,buttocks,hips -Femoral-popliteal:calf -Popliteal-tibial:leg and food | |
| Arterial Ulcers | -Arterial occlusion -Intermittent claudication with > pain at rest -Decreased/absent pulse -Pale color -Cool temp -Skin:thin,shiny,hair loss -Ulcers on feet,toes,heels -Gangrene may develop |
| Amputation: Post op | -Elevate stump to reduce edema -Wrap stump to reduce edema -Immobilize knee in BKA -Trapeze to assist in moving, developing upper body strength -Phantom Limb sensation:normal for up to 2 years after surgery |
| Abdominal Aortic Aneurysm (AAA) | -Most common in men 40-70 -Large diameter and stress on area>susceptibility to rupture -Most are asymptomatic -Pt may c/o pulsating mass,back or groin pain -Mottling of extrem -Often,incidental finding on x-ray,ct,ultrasound -Operable if >/5cm |
| AAA surgical repair | -Major surgery -Recommended for >6cm or 4-6cm good surgical risk -Incision for xiphoid process to symphysis pubis |
| AAA: Post op | -Risk for hemorrhage/fluid vol deficit -Monitor vs -Monitor UO (30-50ml/hr) -Monitor abdominal girth -Maintain Hgb > 8 -Monitor for hypovolemia |
| Hemostasis and Clot Formation | -Damaged blood vessels have several events that occur to prevent excessive blood loss -3 stages: Vascular Spasm (vessel clamps down) Platelet plug formation (1st to site-make sticky plug) Coagulation |
| Parenteral Anticoagulants (SC/IV) | -Heparin sodium:wt based,can be reversed by protamine (1mg protamine per 100 units hep), monitor PTT,platelet,hematocrit -Low molecular wt SC heparin:longer half life,need less lab monitor,lovenox, fragmin, therapeutic w/in 30min |
| Lovenox (enoxaparin sodium) | -Current recommended dosage is 1mg/kg SC every 12h -New tx protocols: 1.5mg/kg qd for acute DVT w/concurrent warfarin sodium therapy; w/average LOS of 1.1d; continue at outpatient |
| Oral: Coumadin | -Reversible w/Vit K (not immediate) -Dosage based on INR: should be in 2-3 range, 2.5-3.5 for prosthetic mechanical heart valve -Don't use PT to determine dosage -Affect extrinsic clotting -Monitor PT/INR -Has a half life of 0.5-3d |
| -Watch for bleeding: Overt (frank-nose bleed) Covert (tarry stools,blood in urine, NG drainage) -Inform medical specialists if an invasive test is planned -Green leafy veg can counteract effect -Caffeine counteracts effect -Many drug and herb reaction | |
| Antiplatelet Agents | -Inhibit platelet aggregation, usually by inhibiting synthesis of thromboxane A2 -Arterial thrombi: primarily platelet aggregates, antiplatelet agent used -Venous thrombi: primarily fibrin and RBC, so anticoagulant drug used |
| Deep Vein Thrombosis | -Age>40 -Sx>30 min -Venous stasis -Heart attack/disease -Pregnancy -Trauma -ERT/Oral contraceptives -Malignancy -Obesity -Family hx -Dehydration -Long plane flights |
| DVT: Clinical Manifestations | -50% are asymptomatic -Unilateral swelling distal to site -Pain -Redness,warmth of leg -Low grade fever -First sign may be PE -Homan's sign:doesn't always mean DVT |
| Nursing Management DVT | -Elevate legs -Compression stocks -DON'T MASSAGE LEGS -DON'T USE EPC IN AFFECTED LEG -Monitor anticoagulation: bleeding,bruising,flank pain -Monitor for PE: acute/lethal complication of DVT,SOB,maintain airway,chest pain,hemoptysis |
| Varicose Veins | -Permanently distended veins from loss of valve competence:congenital, trauma/obstruction to valves -Not necessarily from prolonged standing -C/O aching,heaviness,itching, swelling -Early Rx:compression hose |
| Venous Ulcers | -Venous Occlusion -Pain is aching -Normal pulses -Brown pigmentation over time -Normal temp -Marked edema -Ulcers medial side of legs -NO gangrene |
| Lymphadema | -Accumulation of lymphatic fluid in interstitial spaces:cause: swelling, usually arms&legs; surgical removal of lymph nodes or damage -Can be bilateral,unilateral -C/O of dullness or heaviness in limb, not necessarily pain |
| What if the pump (heart) is Ineffective? | -Decreased bf to organs and tissues -Decreased O2 delivery -Impaired waste removal -Kidney function impaired 1st b/c require high bf -All organs will fail eventually |
| Functional Diseases | -Corornary Artery Disease: impaired bf to pump b/c arteries that supply myocardium are partially occluded d/t atherosclerosis -Heart Failure: pump is damaged so CO of blood is decreased |
| Heart Failure | -RHF is caused by LHF usually -Pump failure could be a result of CAD because fluid backs up into lungs -COPD can cause RHF as well |
| Electrophysiology Problems | -CAD: circ to myocardium and electrical system is impaired; impedes musc function and creates alterations in rhytm (v fib) -HF: ineffective pump and altered anatomy can cause changes |
| Terms | -Contractility: pump part of the heart -Conduction: electrical system in heart -Cannot have one part function without the other |
| Cardiac Output | -Amount of bld ejected by the L ventricle in 1 min -HR x SV -Normal=4-8 L/min -Measurement: swan-ganz cath in hosp or during cardiac procedures |
| Cardiac Index | -CO x body surface area -2.5 - 4L/min -Individualized measurement -Watch in people who have had heart surgery |
| Preload | -Forced used to stretch cardiac musc ->EDV causes>preload > venous return -Affected by: fiber length,stretch,vol, wall stress -Frank-Starling law:> stretch = > force of contraction |
| Measuring preload | -BP -Hydration status -Cap refil -JVD -Lung sounds -Weight |
| Afterload | -SV is inversely related -Initial resistance that must be overcome by the ventricles to develop force and contract to open semilunar valves, push bld -Resistance: L=systemic vasc R=pulmonary vascular |
| Swan Ganz Catheter | -Special IV that goes into heart and measures: central venous pressure, pulmonary artery pressure, cardiac output |
| Measuring Afterload | -Blood pressure -As blood pressure goes up, resistance goes up -As resistance increases, so does the workload on the heart |
| Cardiac Symptoms | -Chest pain (angina) -Palpitations (heart pounding, sob, ventricular arrhythmias) -Tachcardia |
| Respiratory Symptoms | -Cyanosis -Dyspnea |
| Related Symptoms | -Fatigue -Syncope -Weight gain -Irritability |
| Heart Sounds | -S1 closure of mitral and tricupid, happens with onset of systole -S2-closure of pulmonary and aortic, end of systole -S3-normal in children -S4-Atrial kick, HF,ventricles stiff -Pericardial friction rub-fluid -Murmurs-blowing sounds |
| Exercise Stress Tests | -Treadmill-with or without dye, non invasive -Women can pass but have disease -Balanced ischedmia in heart will show normal -Dipyridamole Thallium-hold caffeine 24h, NPO, hold theophylline,aminophylline |
| Cardiac Cath | -Invasive -Pre: NPO, iodine allergy, bleeding time, kidney function -Post: bedrest for femoral for 6h, asses insertion site and check pulses distal q1hx6h, force fluids |
| Cardiac Enzymes | -Triponin I- only there is there is heart damage done |
| Cholesterol Levels | -HDL (healthy): >40, >60 ppl with CHD -LDL (lousy): <160 w/0-1rf, <130 w/2+rf, <100 w/ CHD -Triglycerides: <150 |
| Cholesterol Management | -Overall goal = maintain total cholesterol <200 -LDL contributes the most in development of CAD -Statin Drugs: Lipitor and Crestor (reduce LDL,triglyceride, Increase HDL); Adverse effects: musc weakness, liver toxicity |
| Obesity and Diabetes | -BMI: normal = 19-25, BMI = 25-30 (overweight), BMI = 30 (obesity) -Diabetics: Keep fasting blood sugar <112 -HbA1c: <7% |
| Contributing Risk Factors | -Stress -Homocysteine levels -Elevated C-reactive protein -Menopause -Bacterial contamination |
| Pathophys of CAD: Atherogenesis | -Phase 1: <30y, clinically silent Type I,II,III lesions -Phase 2:may be clinically silent, STABLE ANGINA, vulnerable plaque; Type IV, Va lesions -Phase 3:Disruption of lesion w/thrombus,ACS,TypeVI lesion |
| -Phase 4:>degree of occulsion, ACS -Phase 5:thrombus over disrupted lesion calcifies, crhonic angina and sometiem collateral circ, Type Vb-c | |
| Coronary Arteries:Left | -Divides into: left anterior descending which supplies anterior myocardium -Circumflex-supples post wall, bld to av (10%) node and SA (45% of pop) node |
| Coronary Arteries: Right | -Supplies: blood to inferior and right side of heart -blood to AV node (90%) and blood to SA node (55%) |
| Angina Pectoris | -clinical syndrome characterized by discomfort in chest,jaw,shoulder,back or arm -transient -d/t lack of o2 to cardiac cells -caused by atherosclerosis -doesn't mean you're having heart attack -bld supply<bld demand |
| Stable Angina | -Pain/discomfort triggered by predictable degree of exertion/emotion -stable pattern of symptom -Pain/discomfort relieved by: nitroglycerin or rest |
| Unstable Angina | -Triggered by unpredictable exertion or emotion -May occur at night -I in freq,quality,severity, duration -Medical Emergency:call 911 -Nitro may not relieve pain, nor rest -Has progressed and could mean pt is having MI |
| Variant Angina | -Prinzmetal's -Similar to classic angina; last longer -Caused by arterial spasm,not blockage -Usually occurs b/w midnight and 8am -Occurs at rest w/out precipitating factor |
| Other Angina | -Nocturnal-occurs during REM -Intractable-nothing you do makes it go away -Postinfarction-after a heart attack still having ischemia |
| Assessment of Angina | -Characteristics:dyspnea,pallor,sweating, faintness,palpitations,dizziness,GI -Aggravation: activity -Relieving factors: nitro, rest, time |
| Diagnostic Tests for Angina | -EKG -Stress test -Cardiac Cath -Echocardiogram |
| Treatment of Angina | -Relieve discomfort (MONA) -Restore bf -Prevent further attacks -Pharmacotherapy:Nitro most common; beta blockers (reduce O2 demand), Aspirin (prevent platelet aggregation) |
| Nitro | -Anticipate side effects: headaches,orthostatic hypotension -Monitor BP -Remove transdermal patches at night -Rotate sites |
| Other meds for Angina | -Morphine Sulfate: 2-6mg IV until pain relieved, decrease pain and workload on heart -CCB: vasodilator, open coronary arteries -Antiplatelet meds: aspirin,plavix, decrease stickiness of platelets -Lipid-lowering agents |
| Emergency Treatment for AMI | -First 24h greatest risk for sudden death -ER-door to needle time (thrombolytic therapy w/in 30min or angioplasty w/in 1h) -4 Ds: door, data, decision, drug |
| AMI Pathophys | -3 zones of infarction: Infarct and necrosis; pneumbra (hypoxic); ischemia (reversible) -Most common sites: Anterior (LAD), Posterior (RCA, L circ), Inferior (RCA) |
| All Suspected patients get MONA | -Morphine -O2 -Nitro -Aspirin |
| Myocardial Infarction | -Lack of O2 to cardiac cells beyond the occlusion in a coronary artery d/t blockage or spasm in artery -Causes cell death -Cell death = tissue death -Tissue death = organ death -Main cause of death=arrhythmias -Longer the ischemia=greater cell dea |
| When do coronary arteries receive blood? Most common site for AMI? Time of day are AMIs most likely to occur? | -Diastole -Anterior Wall -In the morning |
| Medical Treatment for MI | -Diagnose type of MI -Reduce pain -Monitor cardiac rhythm -Improve perfusion -Primary angioplasty -Stenting -CABG |
| Thrombolytic Agents | -Dissolve the clot (urokinase,streptokinase) -ABSOLUTELY contraindicated for hemorrhagic stroke, intracranial tumors, active internal bleeding -RELATIVELY contraindicated with recent trauma, current use of anticoagulants,recent surgery, pregnancy |
| Complications Post MI | -Arrhythmias -Cardiogenic Shock (fluid overload) -CHF -Pulmonary edema -Pulmonary embolism -Recurrent MI -Pericarditis -Renal failure -Anxiety and Fear |
| Alteration in Comfort | -Pain means myocardial tissue death, PRIORITY! -Limit visitors unless patient requests -Calm environment -Administer morphine -Verbalize relief of pain w/in 15-20 mins |
| Normal Wave Form | -Depolarization= contract -Repolarization = relax |
| Dysrhythmias vs Arrhythmias | -Most like to cause death in 1st 24h -Continuous ECG monitoring -Heart tones -Monitor for ECG changes -Give anti-dysrhythmics -Monitor K+ |
| Blood Brain Barrier | -Essential barrier to provide the best environment for the neurons (keeps parasites, bacteria out) -Certain substances can not enter, or enter very slowly – many medications are not able to pass this barrier -Water, glucose, oxygen go through quickly |
| Level of Consciousness | -Glasgow Coma Scale 1-15 (used for unconscious states) – below 9 is some level of coma: Best Eye Opening, Best Motor Response, Best Verbal Response |
| Neuro Checks | -Will depend on level of injury -LOC (orientation X4) The most important indicator of neurologic function** |
| Cranial Nerves Testing | I-Olfactory–smell II-Optic–visual acuity, periph vision,eye position III-Occulomotor,IV-trochlear,VI-abducens – shape,size of pupils,nystagmus(lateral shaking of pupil),reaction to light & accommodation V-Trigeminal-face sensation,chewing,jaw musc |
| VII-Facial–taste,expression,corneal reflex VIII-Acoustic – whisper test, watch tick IX-Glossopharyngeal – gag, say ah X-Vagus – check voice for hoarseness, swallow reflex | |
| XI-Spinal accessory – shrug shoulders, turn head, move head against resistance XII-Hypoglossal – deviation of tongue, asymmetry | |
| Motor Assessment | Muscle strength 5 point scale 0/5= contraction, movement absent 1/5= trace of contraction 2/5= movement with gravity only 3/5= movement against gravity 4/5= full ROM but with some weakness 5/5= Full ROM, normal strength |
| Gait Disturbances | Ataxic – staggering (drunk) Dystonic – irregular, poor direction, like ataxic but weirder Dystrophic – broad based – waddling Equine – high steps (like a show horse) – help maintain balance Festinating – on toes fast pace |
| Hemiplegic – one arm and leg swing wide with each step Parkinsonian, short shuffling, leaning forward, dangerous gait, look at the floor, feet close together | |
| Scissor steps- slow, short steps, with legs crossing Steppage – foot and toes high, foot slaps down (similar to equine) | |
| Sensory Assessment Terms | -Stereognosis-ability to feelfamiliar object wout looking -Absence=astereognosis -Graphesthesia-ability to recognize a written symbol -Extinction-simultaneous stimulation 2-point stimulation- ability to differentiate 2 pin pricks from 1 |
| Abnormal Sensations | Paresthesia- distorted sensation Light touch feels like burning pain Dysesthesia – localized, irritating sensation Prickly, crawling Hypoesthesia- reduced sensation Hyperesthesia- abnormal excessive sensation |
| Response to Painful Stimulation | Localization- push away source of pain Flexion withdrawal- move purpose Decorticate Flex withdrawal-moves wout purpose, grimacing Abn Flex-adduct,internally rotate wrists,arms,extend legs Abn Extend- extend,pronate,extend legs,arch back |
| Superficial Reflexes | Corneal- touch cornea Pharyngeal- touch posterior pharynx with cotton tip applicator Abdominal- stroke skin at umbilicus Anal- stroke perianal region Plantar- stroke sole of foot |
| Deep Tendon Reflex | Causes the muscle to stretch Bicep jerk Tricep jerk Brachioradial jerk Knee jerk Ankle jerk |
| Abnormal Reflexes | Babinski Snout- tap around mouth, pursing Rooting- stroke side of face, mouth opens & head turns toward stim. Sucking- touch lips, lips tongue and jaw move forward |
| Coma | Sustained unconsciousness No response to verbal stimuli Varying response to painful stimuli No voluntary movement Often altered respirations Often altered pupil response No blinking **Consciousness = wakefullness, aware of self/surounding |
| Causes of Coma | -Lesion putpressure on brain stem,esp RAS Gunshot,Auto accident,blding in head,tumor Sx generally unilateral -Metabolic disorders affect brain supply of glc or O2 Hypoxia,blood loss,ischemia from cardiac condition,DM Sx usually bilateral |
| CVA | Neurovascular deficit resulting in decreased blood flow to brain Ischemic Thrombus Embolus Hemorrhagic Neurologic deficit Determined by area or brain injured |
| Risk Factors for CVA | Hypertension DM Sickle Cell Anemia ï‚‚ Substance Abuse Atherosclerosis Obesity Oral contraceptives Anything that can change the lumen of a blood vessel |
| Thrombic CVA | Thrombus forms at bifurcation Carotid, vertebral, basilar arteries Cause is atherosclerosis- platelets get stuck in small lumen Occur rapidly and progress slowly Swelling in brain Often occur during sleep Lacunar CVA with DM Collateral circulation |
| Embolic CVA | Thrombus mobilizes and occludes flow Usually in middle cerebral artery or carotids Generally more deficits – no time for collateral circulation to form Source of clot Carotids- plaque Left ventricle – artial fibrillation |
| Hemorrhagic CVA | Aneurysm Trauma- head injury Hypertension Rapid onset, rapid progression Most fatal prognosis Often see seizures – blood irritation Avoid increasing bleeding |
| Transient Ischemic Attack | Temporary neurologic symptoms caused by short term hypoxia Autoregulation fails Return to full function possible Serves as warning of possible CVA |
| Deficits of CVA | Hemiparesis, contralateral- weakness Hemiplegia, contralateral- paralysis Aphasia Receptive Expressive Global Dysarthria- often called dysphasia Dysphagia- not dysphasia |
| Apraxia- can’t make purposeful movements Vision changes Homonymous Hemianopsia Visual loss in same half of each visual field Horner’s Syndrome Eye paralysis, ptosis, constricted pupil, no tearing | |
| Agnosia- can’t recognize familiar objects through senses Unilateral neglect Behavior changes Incontinence | |
| Right CVA | Confusion, usually pleasant Impulsive Poor judgment Distracted Left sided paresis or paralysis |
| Left CVA | Usually alert Aphasia, more severe mobility issues Easily frustrated Emotional, crying Right sided paresis or paralysis |
| Epilepsy | Recurrent episodes of one or more: Loss of consciousness Convulsive movements Sensory phenomena Behavior abnormalities Caused by any process that disrupts the nerve cell membrane causing hyperexcitability Drugs, head injury, tumors |
| Focal (Partial, Simple) Seizures | Most common Abnormal discharge from 1 specific part of brain Often begin in upper extremity&moves to entire side of body–Jacksonian march Somatosensory affects certain sense Tingling, seeing flashing lights, strange taste, strange smell, slurred speec |
| Complex Partial Seizure | Often called temporal lobe seizure Automatisms- purposeless, repetitive activities while in a dream-like state Often seen as psychotic behavior Last 2-3 minutes, some up to 15 Patient is unaware of activity during seizure and is drowsy postictal |
| Generalized Seizures | What distinguishes generalized seizures from partial seizures is that there is always a loss of consciousness in generalized seizures Tonic-clonic or absence Various manifestations exist, but both hemispheres are generally involved |
| Absence Seizures | Usually in children age 4-puberty Vacant stare, unaware of environment, unresponsive, rarely fall (not in a conscious state) Lasts 5-30 seconds, 100 X per day Interferes with learning, postictal confusion Trigger, ↓ blood sugar, photic stimulation |
| Myoclonic Seizure (generalized) | Involves sudden uncontrollable jerking movements of a single muscle group or near muscle groups Loss of consciousness and confusion postictally |
| Tonic-Clonic Seizures | Sudden loc Tonic-body stiff,fall,cry,eyes open,pupils fixed,apnea (15-60 sec) Clonic-rhythmic jerk,incontinent,bit tongue/lip,excess saliva,hyperventilation (2-5 min) Post ictal-stupor/coma up to 1h quiet breathing,confusion,tired,deep sleep. |
| Trigger for Seizures | Hunger(↓ BS) Fatigue, lack of sleep- cell excitability Hyperventilation-  CO2 Sensory stimuli – strobe light, loud sounds, certain music Certain odors Emotional stress Fever, ETOH, injury, menstruation Will be different for each patient |
| Nursing Interventions | Protection- padded rails, bed in low position at all times Airway maintenance- tongue blades not used unless inserted before the tonic clonic phase Roll on side if possible, loosen clothing around neck Do not restrain Reorient after seizure |
| Anti-seizure meds | Phenobarbital (10-25 day onset) Therapeutic blood level 10-40 PO, IV |
| Dilantin (5-10 day onset) Therapeutic blood level 10-20 PO, IV, (IM causes tissue breakdown) Precipitates in dextrose solutions Gingival hyperplasia, rash, blood dyscrasias, slurred speech, ataxiaMuscle pain, fever, rash | |
| Status Epilepticus | Medical Emergency! Seizures in succession or continuous seizures for 30 minutes or longer Caused by sudden withdrawal of meds Glucose and oxygen to brain becomes inadequate- permanent brain injury Treat with IV anti seizure meds or Valium |
| Trigeminal Neuralgia | Intermittent episodes of intense pain in face Entrapped trigeminal nerve, compression, tumor Triggered by touch, cold, talking, chewing, brushing teeth No diagnostic test |
| Treatment of Trigeminal Neuralgia | -Tegretal -to decrease the irritability of the nerve cells (neurons) Anti spasmotics- Baclofen- to ↓ muscle spasms in face Nerve blocks and peripheral neurectomy help to alter the perception of the pain- can affect facial movement |
| Bell's Palsy | Affects motor portion of the facial nerve (5th cranial nerve) Unilateral paralysis of the muscles of expression – can’t show teeth, smile, raise eyebrows Symptoms generally improve in a few weeks |
| Carpal Tunnel Syndrome | Entrapment of medial nerve Sensory/motor changes in thumb, index, middle finger, & radial aspect of ring finger Associated with gout, pregnancy, hypothyroidism, and repetitive use of hands and wrists |
| Testing | Tinel’s sign- tingling in hands,fingers when wrist tapped Phalen’s test- numbness,tingling when wrist forcefully flexed for 20-30 sec Wrist compression test-30 sec of pressure over the flexor retinaculum EMG can also be done to definitively diagnose |
| Parkinson's Disease | Chronic, progressive Caused by loss of dopamine Cardinal symptoms Resting tremors (pill-rolling) Rigidity Bradykinesia- slow, shuffling gait Flexed posture – trunk, neck, limbs Freezing movements (akinesia) |
| Nursing Assessment | Stooped posture,loss of balance, little facial expression,Shuffling,propulsive gait, leaning forward Speech Monotone,drooling,aphasia Eating- dysphagia Handwriting Progressive micrographia Hand tremors- pill-rolling (resting) Restlessness- pacing |
| Huntington's Disease | Degenerative, genetically transmitted Abnormal movement- chorea Begin subtly and become dramatic Intellectual decline Emotional disturbances Progressive, fatal from respiratory complications No known treatment |
| Multiple Sclerosis | Chronic, progressive, demyelinating Onset age 20-40, in cold climates Immune disorder? As myelin degenerates, plaque forms causing inflammation, edema, scarring Nerve impulse does not conduct appropriately Exacerbations & remissions are classic |
| Symptoms of MS | Vary widely Weakness/paresthesia in 1 extremity Vision changes/loss Incoordination cerebellar involvement Bowel/bladder dysfunction spinal cord involvement (constipation) Fatigue Memory loss, confusion Characterized by relapsing-remitting |
| Guillain-Barré Syndrome (GBS) | Inflammatory, unknown cause Degeneration of myelin on peripheral nerves Often preceded by URI, or GI infection Cytomegalovirus, Epstein-Barr, Campylobacter jejuni are thought to be causes Associated with HIV |
| Symptoms of GBS | Initial phase Ascending weakness,evolve over h/d Plateau phase-no progression of sx Loss of deep tendon reflexes Paresthesia Resp musc weakness Recovery phase-6 mo.-2y Remyelination in descending pattern Not always complete recovery of motor/senso |
| Myasthenia Gravis | Autoimmune disease Loss of acetylcholine receptors in postsynaptic neurons of neuromuscular junction Cause unknown Young women > men Older men > women |
| Symptoms of MG | Increasing weakness with muscle use Ptosis, diplopia most common Dysphagia, nasal speech Weak peripheral muscles Respiratory depression Tensilon test- definitive diagnosis Atropine as antidote |
| Pathophys of MG | ACH- neurotransmitter needed for proper muscle function Antibodies occupy the ach receptor sites Cholinesterase (acetylcholinesterase) stops the action of ach. Cholinesterase inhibitors are drugs that prevent the breakdown of ach. -No cure |
| Complications of MG | Myesthenic Crisis Insufficient med (sudden stop) Treat w/cholinesterase inhibitor Possible mechanical ventilation Extreme musc weakness |
| Cholinergic Crisis Over med Abd cramping,excessive lung secretions, severe musc weakness Possible mechanical ventilation Treat w/Atropine |
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