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Adult Health

Final Exam

QuestionAnswer
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  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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