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Adult Health 1
Exam 2
| Question | Answer |
|---|---|
| Mouth | -Lips and Cheeks -Hard and soft palate -Tongue -Saliva -Teeth |
| Pharynx | -Oropharynx -Laryngopharynx -Both are skeletal muscle lined with mucous membranes -Both produce mucous to help move food as it is swallowed |
| Esophagus | -10 in. muscular tube connecting mouth to stomach -Passed through the diaphragm (Hiatus Hernia) -Gastroesophageal sphincter keeps stomach contents from abcking up into the esophagus except in GERD |
| Stomach | -UL abdomen,10in long,can hold 4 L -Pyloric sphincter controls emptying into duodenum -Protein digestion begins; mechanical breakdown of food -Mucous and acids -Empty time is 4-6h,liquids faster |
| Small Intestine | -Pyloric sphincter(won't open until at right consistency) to ileocecal junction -Absorb nutrients -20ft long,1 in diameter: Duodenum(ducts from pancreas and liver, breakdown fat), jejunum, ileum -Food chemically digested and MOST food absorbed |
| Liver | -Largest gland in RUQ,4 lobes -Secretes bile -Store fat soluble vit -Store&release food into circ -Produce clotting factor -Produce fat from CHO&protein -Store&release glc -Kupffer cells remove debri from bld -Shouldn't be able to palpate liver |
| Gall Bladder | -Bile produced in liver but stored in gall bladder -Inferior to liver -Fatty food stimulate GB to secrete bile into cystic duct -Cystic duct joins hepatic duct to form common bile duct, opens into duodenum |
| Pancreas | -B/w stomach and SI -Secrete pancreatic juice through pancreatic duct-join the common bile duct -Juice is alkaline, balance PH -Break down all categories of food -Secreted insulin |
| 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 |
| Protein: Incomplete | -Legumes, nuts, grains, cereals, vegetables -Lack one or more AA needed by the body |
| Fats | -Saturated:milk,meat,plants; butter>than margarine -Unsaturated:seeds,nuts,veg.oils -Thicker=more saturated -30% or less of total cals -Digested in duodenum -Consumption of more than required by body results in storage as adipose tissue |
| Vitamins | -Facilitate the body's use of carbs, protein and fat -All must be ingested except D&K -Fat Soluble: ADEK - absorption inhibited by high fat intake, bind to ingested fat and are absorbed as fat is absorbed -Water soluble: B,C |
| 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 B | -B1-meat,liver,green leafy veg, whole grains(nerve function) -B2-liver,egg whites,milk,whole grain(breakdown) -B6-meat,poultry,fish,potatoe, spinach(form antibodies,HGB) -B12-liver,meat,poultry,fish,milk, eggs (helps use of folic acid, carbs) |
| 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 |
| Other Water Solubles | -Niacin-meat,poultry,fish,liver, peanuts,grn leafy veg;skin, nerves,GI -Biotin-liver,egg,nuts,legume; breakdown fa&carb -Pantothenic acid-meat,whlgrains, liver,legume;steroids&HGB -Folic Acid-liver,dark grn veg, beef,eggs,whl grain;rbc,g&d,NS) |
| Minerals | -Calcium,iron,phosphorus,zinc,iodine, fluoride,selenium,potassium -Best sources-veg,legumes, milk, meats -Work with other nutrients to maintain structure and function of the body |
| Based on 2000 Cal Diet | -Grains: At least 3oz -Veggie: 2.5 cups -Fruits: 2 cups -Milk: 3 cups -Meats/Beans: 5.5 oz |
| Therapeutic Diets: Liquid | -Clear liquid: most restrictive,tea, clear pop,popsicle,broth,sherbert -Full liquid: coffee,milk, cream of wheat, cream soups, pudding, ice cream (not oatmeal) |
| Therapeutic Diets | -Soft (teeth trouble,no teeth) requires little chewing,bake meats, breads, cooked veg, canned fruits -Mechanical Soft: (poor/no teeth) regular diet with ground meats -Regular diet -No added salt-no salt packet on tray |
| Anthropometric Assessment | -Objective ways to measure -Ideal body weight v. actual weight -Waist measurement -Triceps skinfold thickness -Midarm circumference |
| BMI | -Weight divided by height in inches, divided by height in inches, multiplied by 703 -Only measure with client standing |
| Waist Measurement | -Measure waist just above hip bones, while standing -Greater than 35 inches for women or greater than 40 inches for men, put you at increased risk for health problems, even if BMI is good |
| Triceps Skinfold Thickness | -Midpoint b/w olecranon and acromion process -Grasp skin and fat and pull it away from the muscle -Apply caliper for 3 seconds -Repeat 3x and average the readings -Standard male: 12.5 -Female: 16.5 |
| Midarm Circumference | -Midpoint between olecranon and acromion process -Standard - 29.3 -Female - 28.5 |
| Other Assessments | -Lab tests-urine protein,total protein, blood test (serum protein) -Oral Asst. - lesions on lips, tongue, mucous membranes -Abdominal Asst. - inspect, auscultate, percuss, palpate; attention to liver |
| Obesity | -Central (upper body) v. Peripheral (lower body, more difficult) -An excess of adipose tissue -Not defined as behavior -Not defined as overeating -It is a DISEASE |
| Disease of Obesity | -Recognizable etiologic agents (sedentary lifestyle,eating portions) -Identifiable signs&symptoms: excess adipose tissue,increase size of fat cells,insulin resistance,increase glucose, increase cholesterol&triglyceride -Consistent anatomical alterations |
| Treatment Options: Obesity | -Weight loss programs -Healthy eating habits-low cal -Change in attitude about control of weight -Behavior modification CRITICAL -Meds: Amphetamines and other app. suppressors -Surgery: gastroplasty, vertical banding, gastric bypass |
| Treatments: Medications | -Meridia acts on CNS to trick brain into feeling full -Xenixcal inhibits lipases needed to breakdown fat-so not absorbed |
| Malnutrition | -When nrnt availability is consistently inadequate or excessive -Primary-nutrients not delivered to upper GI (famine,anorexia,diet) -Secondary-Upper GI fails to absorb metabolize or use nutrients (crohn's) -More than 1/2 of all hosp pts are malnourishe |
| Risk factors for Malnutrition | -Age (infants,elders) -Poverty,homelessness -Functional health problems-mobility -Oral or GI disease -Chronic pain or chronic disease -Med that affect appetite |
| Consequences of Malnutrition | -Cardiac: D cardiac mass,postural hypotension -Pul:D diaphragm & resp strength, D exercise tolerance, inability to clear secretions -Immune:I incidence&severity of inf -Wound healing delayed,skin dry,nails brittle,periodontal disease,wt loss |
| Consequences of Malnutrition | -Skeletal/Musc strength: fatigue, risk of falling -GI Function: Impaired lipid absorption - Diarrhea |
| Tx of Malnutrition | -Define nutrients required:Hx, observation,labs -Determine route of feeding: oral including supplements, parenteral (IV, tube feeding) |
| Oral Supplements | -Milk-based: ensure, fortisip, jevity -Lactose-free: boost, probalance -Disease specific: nephro, respicare -Nutrition bar: protein bar, power bar, boost bar |
| Nursing Issues: Nutrition | -Feeding self care deficit: appearance of food, social interaction, minimize fatigue, decrease stimulation -Impaired swallowing: assess swallowing, speech therapy, food to unaffected side of mouth, watch consistency of food, sitting in chair |
| Urinary Assessment:Health History | -Urgency -Frequency -Dysuria -Nocturia -Urine description -Pain -Exposures -Meds -Surgeries |
| Urinary Assessment:Family History | -Urine dysfunction -Cancer -Frequent UTI's |
| Urinary Assessment: Current Health | -Back pain -Flank pain |
| 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 Dx Testing | -Urine Culture: clean catch, straight cath, indwelling cath, urine culture and sensitivity -Wash hands,separate labia, void and start stream and catch urine after starting stream; men avoid catching very end of stream |
| 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 |
| Urethritis | -Inflammation of the urethra -STDs, lubricants, sprays (irritants) |
| Ureteritis | -Inflammation of the ureter -Pylonephritis |
| 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 |
| Interstitial Cystitis (IC) | -Painful bladder disease -Non-infectious/abacterial -Patho is poorly understood - possibly autoimmune? -Occurs mostly in women |
| IC Symptoms and Damage | -Bladder tenderness -Urinary urgency -Frequency (60+/day) -Nocturia -Dyspareunia - painful intercourse -Variable manifestations Damage: ulcerations and hemorrhages in bladder wall |
| IC Medical and Nursing Management | -Meds: antihistamines, musc. relaxants, elmeron, analgesic, anti-inflammatory -Surgery rarely used -Avoid alcohol, spicy, citrus foods |
| 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 |
| Bladder Cancer Diagnostic Tests | -Cytoscopy -Biopsy -IVP (Intravenous pylogram) -MRI -CEA (Carcinogenic embryonic antigen) |
| Bladder Cancer Medical Management | -Chemo -Radiation -Surgical: Transurethral resection of Bladder, Partial cystectomy, Radial cystectomy (all bladder removed and stoma put in) |
| Bladder Cancer Palliative Care | -Nephrostomy Tube: obstruction and urine can't drain past tumor - goes into renal pelvis and urine empties out into bag -Ureterostomy: Tumors in ureter - remove from bladder and pouch them to outside |
| Urinary Calculi | -Commonly called stones -Causes: urinary stasis, supersaturation of urine |
| Predisposition of Stone Formation | -Immobility -Dehydration -Metabolic disturbances -History of stones -High mineral content in water -UTI's |
| 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 Calculi Medical management | -Increase fluid to 3-4L a day -Reduce pain -Prevent calculi formation -Dietary changes |
| Urinary Calculi Surgical Management | -Cysto -Lithotripsy: Laser, Extracorporeal shock wave (pt lays in water and shoots pulse waves - crush stones) -Open surgical procedure (percutaneous, go through back or larger procedure and go through side; invasive and has long recovery period) |
| 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 |
| Benign Prostatic Hypertrophy | -Blocks urethral outflow -Age, diabetes, cvd -Enlarge prostate -Risk factors: bph, prostate cancer -PSA (prostate specific antigen) |
| BPH: Clinical Manifestations | -Slow Develop:prostatic hyperplasia,prostratic hypertrophy smooth musc,I musc tone@bladder neck&prox urethra,constrict urethral lumen -Incomplete empty of bladder -Urine stasis,UTIs,pylonephritis -Hydroureter,Hydronephrosis -UTIs lead to pyelonephrit |
| BPH Nursing Management | -Encourage fluids -Concentrated urine is an irritant -Reduce caffeine and alcohol -Avoid alpha-adrenergic agonists -Diphenhydramine -Care with antidepressants, antiphycholics, CCB |
| Surgical Management of BPH | -Transurethral resection of prostate -Prostatectomy -Post-Op complications: bleeding, infection, incontinence, erectile dysfunction |
| Post-Op Nursing Care | -Manage continuous bladder irrigation -Document urine color (clear to pink) |
| Continuous Bladder Irrigation | -Insertion of 3 way cath -Continuous infusion of 0.9% solution -Presence of clots: increase irrigation rate -Total output minus the amount of irrigation rate = urine output -Cath patency is critical |
| 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 |
| Urinary Incontinence | -Functional:d/t physical, psychosocial of pharmacologic causes unrelated to urinary system (dementia,pharm,arthritis) |
| Urinary Incontinence: Medical and Nursing Management | -Kegal exercises -Bladder training -Monitor fluid intake (at least 0.5oz of fluid for every pound of body wt) -Use of incontinence products -Coping-self esteem issues,hygiene,skin integrity |
| 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 |
| Diabetes Mellitis | -HTN -Hypotension-doesn't deliver enough blood -Rhabdomylosis-traumatic injury to musc,release particles clog kidneys -CVD-CO and circulating blood vol -Peripheral Vascular Disease-Thromboembolic disease |
| Nephrotoxins | -Anitbiotics - decrease amount -Heavy metals -Poisons -Analgesics -Contrast dyes |
| Hydronephrosis | -Distention of the renal pelvis caused by obstruction of normal urine flow -Tx:relieve obstruction&prevent infection |
| Glomerulonephritis | -Caused by immunologic reaction that produces proliferation and inflammation in glomerular structure -Acute (fluid retention,edema) or chronic -Manifested by nephrotic syndrome, nephritic syndrome |
| Nephrotic Syndrome | -Protein wasting-urine foamy, 2ndary to diffuse glomerular damage -Cause:glomerulonephritis,systemic disorders,allergic reactions -Complications:ECF accum,renal failure |
| Nephrotic Syndrome Tx | -Heal leaking glomerular basement membrane and stop the protein from leaking into the urine -Maintain fluid and electrolytes -Reduce inflammation -Prevent thrombosis -Minimize protein loss -Emotional support |
| Nephritic Syndrome | -Clinical manifestation: hematuria -and at least one of the following: oliguria U0<400ml in 24h -HTN -Elevated BUN -Decreased GFR |
| Nephrotic vs Nephritic | -Nephrotic: leaking protein, failure of glomerular basement wall -Nephritic: usually see hematuria or blood in urine |
| Kidney Function | -Clean blood&remove waste -Filter waste -Maintain body chemical balance -Control BP -Help make RBC |
| Glomerular Filtration Rate | -Best measure of kidney function -Normal aging can decrease number -To identify stage of CKD need: serum creatinine level, age, race and gender |
| 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 |
| Chronic Renal Failure | -Aka end stage renal disease -Progressive and irreversible -Could be from ARF that has now turned chronic |
| CRF Treatment Options | -Hemodialysis -Peritoneal Dialysis -Transplant -No treatment |
| Protect Kidney Function | -Keep BP under control -Reduce proteinuria -Hemoglobin HgA1C < 7 -Medication adjustments for GFR < 50 -Avoid nephrotoxic drugs -Education -Early referral to nephrologist |
| 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 |
| When blood glucose drops... | -Low blood glucose causes alpha cells to release glucagon which travels to liver, glycogen is broken down in the liver and released into the blood stream, and blood sugar rises -Normal compensatory Mechanism |
| 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 |
| When Blood Glucose rises... | -High blood glucose causes beta cells to secrete insulin, which encourages the cells to take up more glucose, liver produces glycogen from excess glucose and blood glucose goe sdown -Normal compensatory Mechanism |
| 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 |
| Gestational DM | -Glucose intolerance first diagnosed during pregnancy -Affects about 5% -Symptoms generally disappear after termination of pregnancy |
| Pathophysiology of DM | -Insulin is needed in a prescribed amt for glucose to get into cells - unlocks door (Nerve,intestine, kidney don't need insulin to use glc) -Low glc levels stimulate release of stored glc -High glc levels stimulate pancreas to release more insulin |
| Etiology of Type 1 DM | -Hereditary traits -Environmental factors trigger-chemical toxin in smoked meat -Viruses trigger autoimmune response (Islet antibodies, presence dx preclinical dm) -Obesity is factor but less than type 2 -Symptoms appear after 80% of beta cells destro |
| Etiology of Type 2 DM | -Hereditary traits - mostly with identical twins -Obesity if major factor -Impaired liver/Muscle tissue sensitivity to insulin -Impaired insulin secretion |
| Stages of Development, Type 1 | 1)Genetic Predisposition 2)Environmental trigger (strong in spring,fall) 3)Active autoimmune response (ICA accumulate) 4)Progressive beta cell destruction (increase in ICA) 5)Overt symptoms develop (honeymoon period,3-12 mo pancreas produce insulin) |
| Stages of Development, Type 2 | 1)Specific cause unknown,strong genetic 2)No beta cell destruction (chronic I BGL,beta cell insufficient) 3)Desensitization (body used to high glc) 4)Insulin resistance 5)Muscle/fat tissue unable to move glc into cells w/out insulin |
| Development of Genetic Forms | -Genetic in beta cells -Genetic defect in insulin action, associated with growth syndrome abnormalities -Pancreatic disease-pancreatitis, cancer,trauma,inf -Drug/chemical induced:rat poison, glucocorticoids, nicotinic acid |
| 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 |
| Major Metabolic Issues in DM | -Decreased glucose utilization -Increased fat mobilization -Increased protein utilization |
| 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 |
| Prediabetes | -IGF impaired glucose 100-125 -IGT impaired glucose tolerance 140-199 -After 2 h of eating a meal blood glucose should return to normal |
| Treatment Options | -No cure, but tx is available -Proper nutrition -Regular physical exercise -Meds: Oral, Insulin, Aspirin (prevent clots and cvd) |
| Sulfonylureas | -Used since 1950s -Diabeta,Glucotro,Amaryl,Micronase -Stimulate beta cells to secrete insulin -Mild diuretic -Take 1-2 times per day b/f meals -Used for type 2 |
| Biguanides | -Metformin (glucophage) -Makes muscle cells more sensitive to insulin -Decrease glc produced by liver -Decrease LDLs and triglycerides -Decrease amount of insulin needed in type 2 -Take 1-3 times per day with meal |
| Alpha-Glucosidase Inhibitor | -Acarbose (precose), glycet -Delays digestion of complex carb, so glucose levels peak later after meals -Take with every meal -Used in type 2 DM |
| Meglitinides | -Prandin,Starlix -Stimulated beta cells to secrete insulin -Take 30 min before each meal -Used in type 2 DM |
| Thiazolidinediones | -Avandia,Actose,Resulin -Increase insulin action at receptors in liver and peripheral tissue -Decrease triglycerides -Take once daily before breakfast -Used in type 2 DM |
| Humalog Insulin Lispro | -Clear -Onset-5-10 minutes -Peak-30-90 minutes -Duration-3-5h |
| Novolog | -Clear -Onset-5-10m -Peak-40-50m -Duration-3-5h |
| Regular | -Clear -Onset-30m -Peak-1-2h -Duration-4-6h |
| NPH | -Cloudy -Onset-1-2h -Peak-4-6h -Duration-8-24h |
| Lente | -Cloudy -Onset-1-2h -Peak-6-15h -Duration-10-24h |
| Ultra lente | -Cloudy -Onset-4-6h -Peak-8-30h -Duration-24-36h |
| Insuline glargine (Lantus) | -Clear -Onset-w/in few minutes -Peak-Absorbed into blood slowly so there is not time of greatest effect -Duration-24h |
| Insulin Pump | -CSII-Continuous Subcutaneous Insulin Infusion -Catheter and needle replaced q 2-3 days -Improved HbA1c reduced risk of hypoglycemia -Uses fast acting insulin so less variability of glc levels -Helps controls glucose spikes after meals/snacks |
| Effects of Insulin Pump | -Improved retinopathy -Required edu abt pump has empowered pts to take control -sooner=better -Early CSII use - longer honeymoon period, and preserved beta cell function -Requires indiv. dosing algorithims -Still require very frqt glc testing |
| Pulmonary Insulin Delivery | -Studies being done -Human trials underway -Dosing difficulty -Lung fnc,allergies = issue -Increase antigen production |
| Other Tx options | -Pancreatic Islet Transplantation (type 1) -Acupuncture (pain from neuropathy) -Biofeedback (learn to recognize clues) -Chromium,Magnesium,Vanadium -Cinnamon, high intake of coffee |
| Tx with Diet | -Goals (esp type 1) -Eat bfast w/in 1h of insulin dose -Eat carb 3h later -Eat lunch 4-5h after am insulin -Eat supper at regular times -Eat bedtime snack consistently -Dietician should provide initial intructions |
| Serving Method | -Grains/Starches: 6-11 servings -Veg: 3-5 servings -Fruit: 2-4 servings -Milk: 2-3 servings -Meat and Substitutes: 4-6 servings -Fats,sweets,alcohol: special treats only |
| Grains | -1 slice of bread -1/4 of bagel -1/2 english muffin -1 6in tortilla -1/2 cup cooked cereal -1/3 cup cooked pasta/rice |
| Vegetable | -1 cup raw -1/2 cup cooked -3/4 veg juice -Starchy vegetables like potatoes, corn peas and lima beans are counted as starch/grain |
| Fruit | -1/2 cup canned fruit -1 small fresh fruit -2 TBS dried fruit -1 cup melon or raspberries -1 1/4 cup whole strawberries |
| Milk | -1 cup non fat, low fat milk -1 cup yogurt |
| Meat | -1 oz meat -1/4 cup cottage cheese -1 egg -1 TBS peanut butter -1/2 cup tofu |
| Fats, Sweets | -1/2 cup ice cream -1 small cupcake/muffin -2 small cookies -Not as nutritious as meats and vegetables and should be limited |
| Glycemia Index | -Measures how fast a food is likely to raise your blood sugar -Glucose is given 100GL, and other foods are identified in relation to glucose -Higher numbers mean quicker rise in blood sugar |
| Acute Complications | -Diabetic Ketoacidosis -Hyperglycemic, Hyperosmolar, Nonketotic Syndrome (HHNS) -Hypoglycemia |
| 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) |
| Hypoglycemic Unawareness | -Person is unaware that they are hypoglycemic and don't initiate treatment -Repeated episodes of hypoglycemia seem to epinephrine response so the physiologic symptoms are less apparent -Usually have higher target blood glucose especially at night |
| Somojyi Effect | -Rebound high blood glucose -After episodes of untreated nighttime hypoglycemia -Caused by secretion of counter regulatory hormones: glucagon, epinephrine |
| Sick Day Management of DM | -Check bs every 4h -take regular med (oral and insulin) -Call MD if: vomiting or diarrhea for more than 8h, bs above 300 for 8h, bs below 70 for 8h, having trouble concentrating, thinking clearly |
| 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 |
| Cycle of foot wound | -Neuropathy -Minor trauma -Ulceration -Poor healing -Gangrene |
| 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) |
| Observation | -Gait -Body mobility -Posture -General joint motion -Balance -Note discomfort |
| Inspection | -Joint alignment, condition, ROM -Extremity symmetry and length -Muscle group symmetry, strength, presence of atrophy fasciculation -Bone deformities -Always compare one side to the other |
| Palpation | -Muscle groups: firm, symmetrical, nontender, masses, spasms -Joints: stable nontender, without heat or crepitus, bogginess, nodules -Muscle Strength: rate 5/5 |
| Related Systems | -Peripheral Nerve: sensation, cap refill, pulses, color, skin temp -Neurovascular: pain, pallor, temp, pulses, cap refill, mobility of affected joint, paresthesia |
| Musculoskeletal Diagnostic Tests | -X ray -CT -MRI -Bone scans |
| X-Ray | -Radiography -Always check for pregnancy when appropriate -Bone abnormalities -NOT soft tissue, tendon or ligament abnormalities |
| CT Scan | -2-3d x-ray pictures for organ, bones -Check kidney fx,contrast dye,can do without dye -Iodine allergies (shellfish) -Diabetics no glucophage -N,salty taste -Plenty of fluids after -Maybe NPO for GI issues -Lasts <30m -Invasive -Determine small f |
| MRI | -2-3d pic use powerful magnets&radio frequency waves -NO METAL (vascular stents, pacemakers,cochlear implants,jt implants,screws,staples) no angioplasty -Cover tattoos, permanent makeup -Assess claustrophobia -Very Noisy |
| 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 |
| Idiopathic OA | -Happens and we don't know why -65+y -F>M -Large weight bearing,joints,spine -Strong familial disposition -Autosomal recessive with genetic defects that destroy cartilage -Hormonal influence |
| Secondary OA | -M>F -Causes: trauma, inflammation joint disease (repetitive injury, wear and tear) |
| 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 |
| Medical Management | -Alternate exercise and rest -Tai Chi-increase fitness and flexibility -Assistance devices -Application of heat/cold -Joint protection and energy conservation -Medication for pain or inflammation: Can't effectively treat with just meds |
| 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 |
| Etiology and Risk Factors | -Peak bone mass attained by 20, consolidation cont. til 30 -I peak may be effective til 30 -Menopause:bone loss I, up15% loss of bone during premeno,also true if ovaries stop working -Men loss of bone assc w/d testosterone -60-80 is inherited |
| 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 |
| Risk Factors: Other | -Impaired vision -Estrogen deficiency -Low intake -Dementia -Poor Health -Falls -Sub optimal vit d level -Alcohol use > 2/d |
| Pathophysiology | -Bone undergoes continuous remodeling -Peak bone mass + Rate and duration of bone loss = skeletal integrity -Poor skeletal integrity = > fracture potential -Bone tissue lost,become brittle and no support |
| Effective Osteoporosis Tx | -Adequate Ca/Vit D intake -Hormone replacement -Weight bearing exercise -Avoid tobacco use and alcohol use -Med for severe osteoporosis |
| Meds for Osteoporosis | -Actonel, Fosamax-inhibit bone resorption -Evista-SERM (<breast cancer risk > DVT risk) -Miacalcin-slows bone resorption -Parathyroid hormone - bone building |
| 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 |
| Spinal Column Deformities | -Scoliosis-curvature of spine -Kyphosis-humpback -Lordosis-excessive inward curvature of lumbar spine |
| Scoliosis | -Congential or neuromuscular -Abnormal spine curvature -Braces,exercise -Spinal fusion-only in severe cases -Nonstructural if easily corrected with force bending |
| Kyphosis | -Posterior rounding of thoracic spine -Caused by osteomalacia -Osteoporosis and muscular dystrophy |
| Lordosis | -Inward curvature -Women who are pregnant obesity -Usually it is self correcting |
| Osteomyelitis | -Infection of bone and surrounding tissue; usually bacterial but can be viral or fungal; more in men; very difficult to treat; femur, tibia, sacrum and heel – most common -Pain, fever, malaise, redness, drainage -History recent trauma; new prosthesis |
| Septic Arthritis | -Pathogens – invade synovial membrane -Joint pain, swelling, tenderness, warmth in single joint -Plus acute systemic reaction – become septic |
| Bone Tumors: Malignant | Causes:Unknown: past trauma?, exposure to abestos, radium, dioxin; 5% have association with heredity Nighttime bone pain – can be missed because children complain of this when having growth spurts; recent fractures, fever, chills, pulmonary problems |
| Disorders of the Foot | -Hallux valgus (bunion) – 1st metatarsal,common women b/c of shoes can also be congentital -Morton’s neuroma- seen in athletes,excessive pressure in medial plantar nerve;sx mostly w anti inflam -Hammer toe – family hxtreat w special shoes,pads/sx |
| Muscular Dystrophy | -Genetic, effects males almost exclusively -Progressive weakness,Skeletal muscle wasting,Disability and deformity -Diagnosis – most common is duchene’s MD -Treatment Symptomatic and supportive;I CK lab /musc biopsy;pt usually die from cardiac failure |
| 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 |
| Neurovascular Assessment:MS | -High risk for ischemia -Deformity -Loss of function in affected limb |
| Bone Healing | -Inflammatory(vascular compromise can delay healing)Hematoma: 1-3 d -Fibrocartilage formation (osteoblast form fibrocartilage, stabilize fx):3d–2wk -Callus formation (most important stage,if don’t have this then 4 and 5 don’t occur):2–6wks |
| Bone Healing contd | -Ossification:3wk-6 mo -Consolidation/remodeling (excess callus removed,time period effected by musc,wt bearing&age:6wk–1y |
| Influences on Bone Healing: Positive | -Location -Minimal damage to soft tissue -Anatomic reduction -Effective immobilization -Weight-bearing on long bones |
| Influences on Bone Healing: Negative | -Wide separation of bone fragments or distracted by traction -Severe commuted fx or damage to -soft tissue -Bone loss -Inadequate fixation -Infection -Impaired circulation -Location -Tobacco/ETOH use |
| Fractures | -A fracture is any disruption in the normal continuity of a bone -Results from:Mechanical overload of the bone,Stress on the bone,Amt of force applied tobone (Direct-object hits bone,Indirect-powerful musc contraction) -Trauma leading cause of most fx |
| Risk Factors for Fractures | -Osteopenia (steroid use) – pre-osteoporosis -Osteoporosis (demineralization) -Neoplasm -Postmenopausal estrogen loss -Protein malnutrition -High risk activity (recreation or employment) -Domestic violence -Malignancy |
| 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 |
| Asst. of Fracture | -Assessment:Observation,Inspection, Palpation -Questions Do you have pain? describe and rate Do you feel as if the area is swollen? Can you move this area? Cause of fx? |
| Clinical Manifestations: Fracture | -Depend on cause,classification, type&site of fx -pain w or w/o movement or wt bearing -swelling -inability to move or loss of function -discoloration/ecchymoses -crepitus -deformity -neurovascular changes -Hypovolemic shock (fluid volume deficit) |
| Fracture Findings: Deformity | -swelling may be due to local hemorrhage -muscle spasms can cause limb shortening -rotational deformity or angulation |
| Fracture Findings: Swelling | -edema may appear quickly -localization of serous fluid at the fx site and / or -pooling of blood into surrounding tissues |
| Fracture Findings: Bruising and Musc Spasm | -Bruising (ecchymosis) subcutaneous bleeding at the fx site -Muscle spasm frequently accompanies fxs involuntary muscle spasm acts as a splint to decrease further movement of fx fragments |
| Fracture Findings:Pain, Tenderness, Loss of function | -Pain:If pt is neurologically intact pain accompanies a fx,the intensity and severity may vary -Tenderness:caused by underlying injuries -Loss of function:either from pain or loss of lever-arm function in the affected ext. Paralysis-nerve damage |
| Fracture Findings:Crepitus, NV changes, Shock | -Crepitus caused by bone fragments rubbing together to create grating -NV changes damage to peripheral nerves or to those vasculature structures Numbness, tingling -Shock-blood loss or other injuries may need tx for hypovolemic shock |
| Treating Fractures | -Elevate -ICE -Opioids, maybe even a PCA pump initially and administer routinely -Move slowly -Collaborate with MD to promote adequate pain relief |
| Reducing Fractures | -1st step reduction or bone setting -Reduction:alleviates compression or stretching of nerves&bld vessels. -Very painful&requires sedation, local/general anesthesia -Not all require reduction may splint or cast |
| 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 |
| Nursing Implications: Internal Fixation | Assess -Wound&device drainage -Lung sounds -Bowel sounds -Admin meds (analgesics &antibiotics,stool softeners) -Assure proper alignment -PT, OT -Encourage early mobilization, coughing and deep breathing – prevent pneumonia |
| External Fixation | -Immobilization -Support -Maintain position -Common sites:face,jaw, extremities,pelvis,ribs,fingers and toes -Around the clock medication |
| Halo Brace/External Fixator | -Used to stabilize cervical fractures -Incomplete cervical fractures -A complete fracture would cause permanent changes depending on the level of injury (C1-C7 |
| 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 |
| Purpose of Traction | -Reduce,realign,,promote healing -< musc spasms,surgical reduction, low back pain,whiplash,sometimes do w pts who can’t do surgery -Immobilization to prevent tissue damage -Prevent/treat deformities -Rest -reduce and treat dislocations |
| Purpose of Traction | -prevent contractures -expand a joint space -arthroscopy -prior to major joint surgery |
| Skin Traction | Skin -force directly applied to skin -Skin strips, boots, foam splints Buck’s traction -low weights used (5-7#) -High risk for skin breakdown |
| Skeletal Traction | -Uses pins to apply force to the bone i.e. distal femur, proximal tibia, and proximal ulna -Tolerated for long periods -Weights >10 # -Disadvantages:prolonged bedrest and immobility |
| Traction Types | -Cervical chin, skeletal, i.e. Crutchfield tongs, halo -Upper Extremity side arm overhead 90/90 -Lower Extremity Buck Balanced suspension |
| 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 |
| Complications of immobility | formation of pressure ulcers formation of renal calculi deep vein thrombosis pneumonia paralytic ileus loss of appetite |
| 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! |
| Clinical Manifestation: Hip Fracture | shortened abducted externally rotated absent or weak pulses discoloration cool to touch inability to move affected leg or foot Inability to bear weight |
| 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. |
| Complications of Fractures | Neurovascular compromise Compartment syndrome Fat embolism syndrome Thromboembolism Infection Osteomyelitis Hemorrhage/hematoma Avascular necrosis |
| Neurovascular Complications | compare affected limb to other limb dim or absent pulses numbness or tingling cap refill exceeding 3 sec pallor, blanching, cyanosis, coolness inability to flex or extend ext. |
| 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 |
| Thromboembolism: DVT and PE | DVT results from formation of a clot in a deep vein in the lower extremities caused by venous pooling If the clot travels into the pulmonary circuit, then we call it a pulmonary embolus (PE) |
| Clinical Manifestations of DVT | Positive Homan’s sign (dorsiflexion of the affected foot) causes pain in the gastrocnemius CONTROVERSIAL Calf tenderness, warmth, redness, swelling low grade fever edema Diagnosis - venous ultrasonography |
| High Risk | > 40 years obese patients with multiple trauma or hx of circulation deficits and patients on estrogen therapy (birth control, hormone therapy) Patients with systemic infection Tobacco users Pts w malignancy (cancer dt I platelets) |
| Osteomyelitis | Infection of bone after a break or bedsores,sometimes w resistant bacteria Hard to cure IV antibiotics 4-8 wk Usually need surgical debridement as well(clean out the infection) Can become chronic Fever, pain, malaise are common subjective symptoms |
| 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 |
| Avascular Necrosis | Loss of blood supply to bone-death of bone primarily in fx proximal to the femoral neck Result of local circ compromise Xray shows collapse of femoral head Pain occurs mo to y after fx repair Replace w prosthesis is required prompt sx repair after |
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