Exam #4 Renal (Quiz #8) Urinary tract Infection (UTI) Infection of the bladder, kidney, urethra, or prostate Classified according to region and primary infection site Lower UTIs Urethritis (inflam of urethra) Prostatitis (inflam of prostate) Cystitis (inflam of bladder)-most common form of UTI; 2nd most common site in body for infection, 1st is resp tract Causes Bowel incontinence, procedures requiring instrumentation, sexual activity, urinary obstruction or calculi, and improper cleaning (esp. in kids) Pathogens enter urinary tract by 1 or 2 routes Ascending from mucous membranes of the perineal area to the lower UT (most common) E. coli is most common (90%) Most frequent in adult females (short straight urethra) From the blood-rare and usually associated with previous damage or scarring of the UT UTI categorized as Uncomplicated- isolated incidence of UTI Complicated: more than 2 UTIs in a year, related to functional, anatomic, metabolic, or neurological disorders, r/t antibiotic resistant pathogens Any UTI in a male is considered complicated (prostate enlargement, STD, or structural deformity of GU tract leading to urinary stasis) Urinalysis (UA)-shows presence of blood cells or bact-bact counts of 100-100000 are indicative of infection Manifestations Dysuria-painful or difficult urination Urinary frequency and urgency Nocturia-2+ awakenings at night top urinate Urine may be cloudy and foul smelling Voiding in small amts Pyuria-excess mucous and WBCs in urine Hematuria-blood in urine Malaise, chills, fever, N&V Low back and suprapubic pain Older pts may not have classic S&S but may present with nocturia, incontinence, confusion, behavior changes, lethargy, anorexia Tx Meds: Bactrim, Macrobid, Amoxil, Keflex, pyridium (UT analgesic-urine and semen turns orange) ( fluid intake (3L/day, 8-10 glasses/day) Cranberry juice-maintains acidic urine which inhibits bacterial growth Void every 2-4 hrs Cleanse perineal area front to back Urinary calculi (kidney stones) Defined as masses of crystals composed of minerals that are normally excreted in the urine Majority are calcium Stones may develop and cause obstruction at any point in the urinary system 3 factors present to form stones Saturated urine Urinary organic material (mucoproteins) Deficiency of substances that hinder stone formation (pyrophosphate and nephrocalcin) Causes Dehydration, immobility, excess dietary intake of Ca Manifestations Sudden, severe, intermittent pain of flank and upper outer ABD on affected side Vary with location and size Pain may radiate to suprapubic region N&V, pallor, cool and clammy skin Urgency and frequency (when lodged where ureter joins bladder Hematuria Fever and chills Most pass spontaneously (<6mm) Greatest dangers: obstruction and kidney infection-either could lead to loss of a kidney Tx Diagnostic tests: KUB x-ray, IVP (intravenous pyleography), ultrasound, CT scan Pain meds-narcotics and NSAIDs Antiemetics Antimicrobials ( fluid intake (3L/day) strain urine lithotripsy cystoscope (scope passed through urethra and bladder into the ureter to remove stone) surgical removal of stone urethral stent-placed for drainage of infected kidney Zyloprim med- ( risk of forming kidney stones in pts with high urinary calcium or uric acid levels Pyelonephritis Inflam disorder affecting the renal pelvis and the functional portion of the kidney tissue Acute and chronic Most common cause is E. coli (85%), but viruses or fungi can cause it Spread through blood or ascend through UT (most common) Inflam response in kidney, grossly edematous and localized abscesses may form, tissue damage occurs primarily of the tubules (altered reabsorption and secretion), scar tissue forms Onset is rapid with fever and chills, malaise, vomiting, flank pain, costovertebral tenderness, urinary frequency, and dysuria Older pts may present with behavior changes, confusion, incontinence, or general deterioration Chronic renal failure and end-stage renal failure may develop with chronic pyelonephritis; HTN may develop as renal tissue is destroyed-most common sign of chronic pyelonephritis Manifestations Frequency, dysuria, CVA tenderness, flank pain Frequently experiences sx of cystitis for several days Urine may be cloudy or bloody, foul smelling Fever, chills, malaise, acute distress Tx Analgesics for pain Meds: Bactrim, macrodantin, septra, cipro, pyridium ( fluid intake (3L/day) cranberry juice-acidic urine Void every 2-4 hrs Proper perineal hygiene Polycystic kidney dz Hereditary dz characterized by cyst formation and massive kidney enlargement 2 forms Autosomal dominant-adult Autosomal recessive-infantile Adult form is slow, progressive-accounts for 10% of pts with end-stage renal dz who require dialysis and or kidney transplant Also develop cysts elsewhere in body (spleen, liver, pancreas) 10% of affected pts develop subarachnoid brain hemorrhage from a congenital aneurysm cysts affect the nephron of the kidney, as cysts fill and enlarge, kidneys enlarge, renal blood vessels and nephrons become obstructed and tissue is destroyed manifestations HTN-due to activation of the renin-angiotensin system Lumbar pain-due to enlarged kidney Widening ABD girth due to enlarged kidney Swollen or tender ABD caused by the enlarging kidney mass Tx Antibiotics for infection Hydration to maintain fluid balance Surgical drainage of cystic abscess Dialysis or kidney transplant for progressive renal failure Nephrectomy no recommended-dz occurs bilaterally and the infection could occur in the remaining kidney Acute Renal Failure (ARF) Rapid breakdown of kidney function that occurs when high levels of uremic toxins (waste products of the body?s metabolism) accumulate in the blood ARF occurs when the kidneys are unable to excrete the daily load of toxins in urine Based on amt of urine that is excreted over a 24 hr period-pts with ARF are separated into 2 groups Oliguric: pts who excrete <500mL/day Nonoliguric: pts who excrete >500mL/day Urine is of poor quality (contains little waste) because blood is not well filtered, despite the fact that an adequate volume of urine is excreted Both kidneys are failing when ARF occurs 3 types (named for location within renal system) Prerenal ARF Characterized by inadequate blood perfusion to kidneys, which leaves them unable to clean blood properly Many pts with prerenal ARF are critically ill and experience shock-very ( BP There is often poor perfusion within many organs, which may lead to multiple organ failure Hypovolemic and cardiovascular failure Postrenal ARF Caused by an acute obstruction that affects the normal flow of urine out of both kidneys The blockage causes pressure to build in all of the renal nephrons Excessive fluid pressure ultimately causes the nephrons to shut down The degree of renal failure corresponds directly with the degree of obstruction Intrarenal ARF- ischemia, toxins Manifestations The most common sx is ( UO (oliguria) which occurs in 70% of pts Kidney can?t eliminate waste products leading to azotemia (( blood levels of urea, creatinine, and uric acid), fluid retention, electrolyte imbalance and metabolic acidosis Na and water retention leads to edema and ( risk for CHF and pulm edema Impaired renal elimination leads to hyperkalemia, hyperphosphatemia, hypocalcemia Edema, anemia, hypotension due to hypovolemia, proteinuria, tachy, lethargy, cool, clammy skin, crackles Dx Hyperkalemia, Hyponatremia, hyperphosphatemia, metabolic acidosis ( BUN and Cr blood level of Cr typically ( by 0.5 mg/dL every day Cr is more accurate than BUN because it is not affected by proteins in the diet or fluid status BUN:Cr should be 10:1 Cr doesn?t ( unless ¼ of nephrons aren?t functioning Tx Blood volume expanders Diuretics ( CHO diet that is ( in pro, Na, and K fluid restriction dialysis Chronic Renal Failure (CRF) Gradual loss of entire nephron units (over mos to yrs) leading to an inability of kidneys to produce sufficient urine GFR (glomerular filtration rate) is <20% of norm Cr >5 mg/dL Functional capacity of entire nephron is lost and renal mass is ( leading to progressive deterioration of glomerular filtration, tubular secretion and reabsorption Eventually the kidneys are unable to excrete metabolic waste and regulate fluid electrolyte balance 3 stages of renal failure early stage (renal impairment); unaffected nephrons compensate for lost nephrons compensate for lost nephrons (BUN 20-50 mg/dL) 2nd stage (renal insufficiency); more than 75% of functional renal tissue is destroyed (BUN>100 mg/dL; Cr >5 mg/dL) 3rd stage (end stage renal dz-ESRD); GFR is <20% (BUN> 200 mg/dL; Cr >5 mg/dL) most common causes of CRF: diabetic nephropathy, HTN, Glomerulonephritis, cystic kidney dz Manifestations Early stage: free of sx, BUN, and Cr are normal 2nd stage; rise in BUN and Cr; oliguria 3rd stage: sharp ( in BUN and Cr; oliguria and uremia hypervolemia, hypocalcemia, hyperkalemia, azotemia, metabolic acidosis, anemia, peripheral neuropathy (due to accumulation of toxins) Dx ( BUN and Cr, electrolytes (Hyponatremia, hypocalcemia), CBC (severe anemia and thrombocytopenia), ABGs (metabolic acidosis) Tx Diuretics, digitalis, anti HTN, Na HCO3, Ca supplements, Vit D, Iron and folic acid ( CHO, ( Na, K, and pro diet transfusions Dialysis Renal transplant Glomerulonephritis Bilateral inflam of cap loops of glomeruli (often following a strep infection) Acute and chronic Acute post streptococcal Glomerulonephritis is most common Acute Circulating antigen-antibody immune complexes are formed and trapped in glomerular membrane, causes inflam and edema; causes glomerular caps to allow plasma proteins and blood cells to escape into urine Sx usually subside in 10-14 days and 60% recover completely Other 40% may have impaired renal function leading to renal failure Chronic Slow progressive destruction of glomeruli with impaired renal function; kidneys ( in size symmetrically and become granular; eventually all nephrons are destroyed (causes: Lupus, DM, unknown) Manifestations Acute: Hematuria, proteinuria, Na and water retention, HTN, azotemia, fatigue, anorexia, N&V, oliguria, SOB Chronic: develop insidiously, often unrecognized until renal failure is evident Dx Throat cultures, Sed rate, BUN and Cr, electrolytes, kidney scan, biopsy Tx Immunosuppressive meds (to ( risk of ESRD) NSAIDs Antibiotics Anti HTN Fluid restrictions Diuretics Correct electrolyte imbalances Dialysis or kidney transplant for chronic Glomerulonephritis Musculoskeletal Fractures (fx) Break in continuity of a bone Causes Trauma (kids and young adults), Falls, Sports injury, child abuse (previous hx of fx) Pathological fx (elderly)- osteoporosis, infection, tumor, long term use of steroids Stress fx Rapid ( in training level of athlete Young athletes-perform at early ages Beginning of new physical activity Common in endurance sports-running Classification Open-break in skin-compound-subject to infection, osteomyelitis, and delayed healing Closed-no break in skin-healing chances are better Direction of fx line Transverse-straight across bone-break is clean, also called a simple fx Oblique-less than right angle Spiral-circles throughout bone-due to twisting force, seen in sport injuries Type of fx Comminuted- bone fragments into many pieces-common in elderly with more brittle bone Compression-bone is crushed, common in pts with osteoporosis ex: vertebrae squeezed or crushed together Impacted- broken bones are forced into each other, wedged together-common in falls, esp. hip fx Segmental-clean break at one end; other end is in contact with the original bone-sports injury, falls Greenstick-bone breaks incompletely-as a green twig breaks- common in children, bones more flexible Depressed-bone is pressed inward-common in skull fx S&S Deformity-( or ( of limb length, bulging at fx site Pain-point of tenderness, ( with movement, muscle spasm due to shortening of bone length-rate 1-10 Paresthesias-numbness, tingling-swelling around nerve or damage to nerve, paralysis-rate-feeling to touch, pain, or lack of feeling Crepitus-grinding noise or feeling when bone edges rub together Edema/extravasation-leakage of blood and serous fluid into fx area=ecchymosis, swelling ( Perfusion-lack of pulses, pallor, mottling, cyanosis, coolness-check pulses-bounding/thready, intensity +1/thr +4, temp, cap refill >3secs Dx X-ray to reveal fx line and taken over time to gauge healing Bone scans Tx Casts-fx is first reduced-bones placed in correct alignment Used with simple fx Purpose to immobilize joint above and below fx so area can heal Straight traction- skin traction Noninvasive wraps around limb are applied and weights and pulleys are used to keep limb in alignment are overhead ? bed frames used Skeletal traction Pins are inserted into bone and weights and pulleys are applied, or an external fixation device can be used AKA: ORIF-open reduction and internal fixation ORIF Normal healing time Children 4-6 wks Adolescents 6-8 wks Adults 10-18 wks Complications Impaired healing Malnutrition, delayed union or nonunion Results from misalignment, mobility of fx site Fracture blisters Fluid collects between epidermis and dermis, occur in severe twisting injuries esp.: car accidents and falls Likely at ankle, elbow, foot Tx with early surgical intervention to reduce fx ( risk for infection Compartment syndrome Edema or bleeding accumulates between muscle and fascia Leads to constriction, lack of O2, cellular acidosis, anaerobic metabolism, tissue death and destruction Occurs in crush injuries, fx with burns, or a cast that is too tight S&S ( pain, swelling, pallor, weakness, ( sensation to touch, pulses and cap refill Tx Cutting cast to allow for expansion Fasciotomy-cutting fascia to relieve pressure Fat embolism syndrome Occurs when Fat globules leave bone marrow and enter the blood stream And/or release of catecholamines in response to injury (causes rapid mobilization of fatty acids) Results in fat embolus-travels to Lung-PE; extreme dyspnea, chest pain, ( O2 sat, tachy Brain-CVA; alteration in LOC, changes in sensation and perception levels DVT 3 factors leading to DVT venous stasis-pt immobilized-( of blood blow by 50% Injury to blood vessel wall-occurs from injury or surgery Altered blood coagulation-occurs from blood loss and body?s attempt t ( production of platelets and clotting factors S&S Swelling, leg pain, cramping, impaired orientation, ( ability to think Tx Thrombolytic agents to dissolve clots Heparin IV-prevents more clots from forming Vena cava filter-prevent clots from entering pulm system Reflex sympathetic dystrophy Cause is unknown-musculoskeletal trauma Refers to group of poorly understood post-traumatic conditions Persistent pain, hyperesthesia, swelling, changes in skin color, temp Tx: sympathetic nervous system blocking agents Shock Results from blood loss of from sepsis Blood loss from Pelvic fx=4.5 L Femur fx=2 L Elbow=1.5 L Results in hypovolemia-loss of blood and fluid volume S&S-hypotension, tachy, cardiac collapse Tx: blood replacement, IV fluids Infection Open fx is more likely to develop infection Any complication that ( blood supply ex: compartment syndrome can cause infection Pseudomonas, staphylococcus, clostridium are common Infection delays healing resulting in osteomyelitis Bone healing 1st stage-hematoma Starts immediately after injury Lasts approx 1 day Bleeding into site of fx and surrounding tissue Hematoma is formed around injury site Inflam response-vasodilation and edema 2nd stage-proliferation Starts 2nd day Lasts 6 days Fibroblasts enter and add a fibrin mesh to protect injured bone WBCs migrate to area to contain inflam-phagocytosis; removal of debris 3rd stage- callus formation Starts day 6 Lasts 10 days Osteoblasts invade clot to form a soft tissue around injured site Tissue changes into newly formed cartilage called callus Callus is sufficient to hold bones together but not for wt bearing 4th stage- ossification Starts 14th day Lasts 2-10 wks Ca and cartilage are deposited Leads to rigid calcification and permanent callus formation 5th stage-consolidation and remodeling Starts 10 wks after injury Lasts 2 mos-1 yr Osteoclasts are active=reabsorption of bone Bony overgrowth and excessive Ca are remolded into normal bone contour Osteoarthritis (OA)-degenerative joint dz (DJD) Demographics Most common form of arthritis Occurs equally between sexes At risk person >65 yo Patho-idiopathic (cause unknown) Loss of cartilage at ends of long bones, esp. knees, ankles, toes, fingers, hip ( formation of new cartilage-malfunction in production of proteoglycans Destruction of proteoglycans is > synthesis Type II collagen (normal) is replaced with Type I (abnormal) Results in Synovitis-inflam of joint Spurs-osteophytes-outgrowth of bony tissue at joint Secondary OA Causes Repetitive movements applies excessive workload to joints ( lubrication to joints ? aging Patho Same sequence as ( S&S-both forms Dull aching pain relieved with rest Numbness, tingling due to nerve damage Edema/stiffness ( ROM and ADLs Joint deformities Heberden?s-distal joint Bouchard?s-proximal joint Dx X-rays- narrowing of joints, spurs, deformity, fusion of joins Tx Drug tx-ASA, ibuprofen, indomethacin Injection of corticosteroids into joint-4-6 mos to ( mode formation Exercises to strengthen muscles esp. around knees, hips Canes, walkers Arthroplasty-replacement of all or part of joint with prosthesis Arthrodesis-surgical fusion of bones, esp. spine Osteoplasty-scraping and lavage (washing) of deteriorated bone from joint Osteotomy-cutting of bone-wedge to improve alignment Rheumatoid Arthritis (RA) Systemic inflam joint disorder Affects women more than men Occurs ages 30-50 Cause is unknown-thought to be genetic or viral Patho Exposure to virus-initiates antigen/antibody response IgG released and autoantibodies form-called rheumatoid factors-deposited in joints Chronic inflam and destruction of joint occurs Vascular granulation tissue-pannus-invades cartilage, bone, and surrounding tissue S&S Low grade fever Joint of hand, wrists, elbows, feet involved, move to knees, hips, cervical spine Swelling, tenderness Bilateral involvement Morning stiffness > 1hr Joint deformities Dx X ray Rheumatoid factor (+)- autoantibodies of IgG Aspiration of synovial fluid-ABC, cloudy Tx NSAIDs Corticosteroids DMARDs-Dz modifying drugs Gold salts Antimalarial rx Cytotoxic rx- methotrexate Immunosuppressive rx-cyclosporine Osteoporosis Patho Metabolic bone disorder Rate of bone reabsorption > bone production ( bone mass Loss of Ca and P Bones become porous, brittle, and prone to fix Primary osteoporosis Contributing factors Sedentary lifestyle Lack of Ca intake, poor diet intake Hormonal imbalance-endocrine-hypoparathyroidism Inadequate pro intake Classification Type I-postmenopausal, 51-75 yo-due to estrogen loss Type II-senile-70-85 yo- ( osteoblast and osteoclast Secondary osteoporosis Alcoholism Liver dz Immobility-paralysis Prolonged steroid and heparin tx S&S Fix of radius, vertebrae, femur Redness, warmth at joints Limited ROM Pain Loss of ht Muscle spasms Dowager?s hump with protruding ABD Dx X rays, CAT scans, bone scans-show density and/or degenerated sites Bone biopsy-honey comb look Ca and P levels usually normal Tx Biphosphonates- Fosamax, binds to Ca and P to inhibit osteoclastic activity Calcitonin-inhibits bone breakdown NaF- stimulate bone formation Gout Patho Collection of uric acid crystals in joints esp. feet, great toe, mid foot, ankle Results from ( urate production and/or ( excretion of uric acid Hallmark sign-hyperuricemia >7mg/dL Primary gout Occurs in men over 30 and postmenopausal women Pt tx with diuretics Genetic link Secondary gout DM HTN Obesity Leukemia Kidney dz Stages 1-asymptomatic hyperuricemia 2- acute gouty arthritis-painful swelling, tenderness-pt seeks help 3-characterized by exacerbations and remissions 4-chronic-without tx, tophi form (bumps filled with urate crystals-pinna of ear, feet, hands, outer sides of forearm, in cartilage, tendons) provoking factors that can cause an attack Stress Trauma Infection Hospitalization Wt reduction Excessive food intake Use of alcohol S&S Swollen joint Very red to purple Late S&S Tophi-hard yellow to white nodules-can ulcerate During an attack, intense pain-can?t stand covers on foot, can?t stand vibration of someone else walking on floor Initial acute attack-2nd attack-6 mos-2yrs or 5-10 yrs- then goes into chronic phase if it hasn?t been tx Tx-acute attacks Colchine-has anti-inflam effects NSAIDs-anti-inflam Corticosteroid injected into joint Tx-long term tx Allopurinol-inhibit formation of uric acid Probenecid, sulfinpyrazone- ( renal secretion of uric acid Adjunctive therapy Avoid alcohol- esp. beer and wine Avoid purine rich foods ((urate levels) ex: sweetbreads, lentils, anchovies, liver, sardines, kidneys For obese-wt reduction ( stress levels- talk with pt Neuro (Quiz #9) CVA (cerebrovascular accident) Sudden reduction in cerebral blood flow Abrupt loss of consciousness Can be preceded by a TIA (transient ischemic attack) Results in paralysis, temporary or permanent Caused by Thrombus- atherosclerosis of intracranial vessels, plaque causes blockage of blood flow-assoc with HTN, smoking, DM Embolism- a thrombus which originates outside of brain and flows to brain-oral contraceptives, embolus after surgery, endocarditis Hemorrhage- rupture of cerebral vessel due to HTN, aneurysm, trauma Patho Cell changes begin 4-5 min after ?blood flow and ?O2- O2 deprivation, permanent damage within 10 min Na pump fails-Na draws water into brain tissue=edema Blood vessels swell, circulation is ?, vasospasm results in infarction-tissue injury is trigger for this Inflam response-leads to more edema and cell death from pressure of edema S&S Vary according to artery affected CVA in one hemisphere causes S&S on opposite side of body CVA that damages cranial nerves affects the same side of body which the infarction occurs TIAs- last from seconds to hours but clear within 24 hrs Considered as a warning sign for CVA-TIAs reported in ½ of pts who then develop CVA within 2-5 yrs Weakness in lower face, arms, hands, fingers, legs, numbness, tingling of face, double vision, slurred speech Anterior Cerebral Artery Confusion, weakness, numbness on affected side (esp arm), paralysis of opposite side, incontinence, personality changes (flat affect, distractibility) Middle Cerebral Artery (mainly affects speech) Aphasia (can?t speak), dysphagia (trouble speaking and swallowing), dyslexia, dysgraphia (can?t write), hemiparesis on affected side Posterior Cerebral Artery Visual field cuts, sensory impairment, Dyslexia, coma, blindness Basilar Artery Dizziness, weakness on affected side, visual deficits, poor coordination, dysphagia, amnesia, ataxia (unsteady gait) Internal Carotid Artery HA, weakness, paralysis, numbness, altered visual disturbances-blurring affected side, altered LOC, bruits over carotid artery, aphasia, dysphagia, ptosis Can clear out with surgery Dx Cerebral angiography-details disruption of circulation-best test for examining the entire cerebral artery MRI-identifies areas of ischemia or infarction PET-positron emission tomography-identifies areas of altered metabolism surrounding lesions not detected by other tests Lumbar puncture-reveals changes in CSF-blood, WBCs Tx Thrombolytic therapy-plasminogen activator given within 1st 3 hrs of stroke to restore circulation to affected brain tissue and limit brain injury Anticonvulsants- to tx or prevent seizures, phenobarbital, Dilantin Corticosteroids-dexamethasone to ? cerebral edema Anticoagulants-heparin to ? risk of further stroke Analgesics- to relieve HA Seizure disorder- Epilepsy Patho Brain neurons depolarize easily-hyperexcitable Resting membrane potential is less or can be a lack of inhibitory substance On stimulation-electrical current spreads from cell to cell Brain?s demand for O2 increases Hypoxia ensues-brain damage Inhibitory substances cause seizure to stop If no inhibitory substances-status epilepticus-life threatening Primary seizure disorder-cause unknown Secondary seizure disorder-structural changes or metabolic alterations Causes: birth trauma (anoxia), infectious dz (meningitis, encephalitis), ingestion of toxins (mercury, lead), brain tumors, head injury, metabolic disorders (hypo/hyper glycemia), CVA Types of seizures Partial-involves part of the brain Localized areas of brain are affected Simple partial seizures S&S-presents with flashing lights, smells, hearing hallucinations Autonomic sx-sweating, flushing, pupil dilation No alteration in consciousness Lasts a few seconds Jacksonian March- motor involvement-involves one part of body Complex partial seizure Amnesia occurs during and after During seizure pt can follow simple commands Lasts for 1-3 min Generalized seizures Can be convulsive or nonconvulsive Involves generalized area of brain Types Absence seizures Often seen in children Begin with brief changes in LOC Blinking, rolling of eyes, blank stare Pt maintains posture Continues preseizure activities Lasts 1-10 secs Can occur up to 100x/day Myoclonic seizures Single jerk of one or more muscle groups Involuntary jerks-lasts few secs Consciousness is not lost Generalized tonic-clonic seizures Loud cry-air rushes from lungs over vocal cords Falls to ground Body stiffens-tonic phase Then body relaxes- clonic phase Tongue biting Incontinence Labored breathing Apnea Cyanosis Lasts 2-5 mins After-confused, difficulty talking, fatigue, HA, muscle soreness, may fall into deep sleep Atonic seizure Loss of postural tone Loss of consciousness Young children Called ?drop attack? Status epilepticus Most life threatening Continuous tonic-clonic seizure Resp distress with hypoxia-trigger and result Results from acute withdrawal of anti-convulsant meds, head trauma, metabolic disorders (acidosis), septicemia, encephalitis Dx MRI Electroencephalogram (EEG) Skull x rays-fractures Chemistry-hypoglycemia, electrolyte imbalances Tx Drug therapy-Dilantin (phenytoin), phenobarbital, gabapentin (Neurontin) Status epilepticus- IV diazepam (Valium), Dilantin, phenobarbital Dextrose for hypo glycemia Surgery to remove underlying cause ex: tumor, vascular problem (aneurysm), focal surgery Spinal cord injury Results from forces applied to head or spinal column Forces Hyperflexion-forward movement of head Hyperextension-backward movement of head Compression-force from top of head through spinal column Patho Hemorrhage into spinal cord Impedes with circulation Edema-? blood supply Cord becomes ischemic Inflam rxn Phagocytes and macrophages come within 48 hrs of injury Collagen replaces normal tissue-scarring Loss of function according to level of injury C1-C3; no control of head, neck, diaphragm, dependent care, respirator, no bladder or bowel control, wheelchair C4; sensation in head, neck, and some control of head and nick, diaphragm movement, dependent care C6; use of shoulder, extension of wrists, dependent care-can transfer selves to wheelchair C7-C8; extends elbows, flexes wrists, use of some fingers, dependent care, manual wheelchair T1-T5; paraplegia with use of diaphragm, arm function, bladder and bowel T6-T12; paraplegia-no ABD reflexes present, no bladder or bowel control, sensation to groin L1-L5; bowel and bladder dysfunction, lower leg weakness, hip and knee movement S1-S5; loss of bladder, bowel, sex function, no paralysis of legs, loss of sensation to scrotum, perineum, anus, anal area, and upper inner aspect of thigh S&S Resp ? cough reflex Limited chest expansion ? vital capacity Cardiovascular Orthostatic hypotension ? venous return Paroxysmal HTN Hypercalcemia GU Urinary retention or incontinence Neurogenic bladder Impotence ? vaginal lubrication Musculoskeletal Contractures Bone demineralization Muscle spasms Pathological fx Integument Decub ulcers Psychosocial Loss of body functions Change in self-image Dependent role Financial debt Thoughts of suicide Complications Spinal shock Immediate response to spinal cord injury Complete or partial transection of cord Begins within 1 hr of injury and can last for 6 wks Parasympathetic dominates Hypotension < 100mm/Hg Bradycardia <60 bpm Flaccid muscles Loss of sensation, pain, touch, temp Loss of ability to perspire Autonomic dysreflexia Exaggerated sympathetic response in pts with a T6 injury or above Abnormal triggers such as a full bladder or bowel causes following: Bradycardia HTN Severe HA Goose flesh skin below injury Remove stimuli-ex: full bladder, bowel-avoid bradycardia, HTN, need for pain meds Neurogenic shock Most frequent in cervical injury Results form loss of autonomic function and results in following changes Orthostatic hypotension Bradycardia Hypothermia Can?t sweat below level of injury Dx Spinal x rays to detect fx MRI- reveals spinal edema and compression Lumbar puncture- increase in pressure from edema Tx Cervical collar, skeletal traction, halo devices High dose of dexamethasone (prednisone) to ? inflam of spinal cord Vasopressors to tx hypotension and bradycardia Team approach to help with disabilities Movement Problems Parkinson?s Disease Patho ? dopamine production Dopamine is responsible for control of movement Cause unknown S & S ? in speed of movement to carry out tasks Masked face and monotonous tone Tremors especially at rest (?pill rolling?) Legs suffling gait Brdaykinesia ? slowing of voluntary movement Dx No tests to mark Parkinson?s Tx Levodopa ? restores dopamine levels Myathenia Gravis Patho Destruction of acetylcholine receptor sites in the muscle ? likely from autoimmune disease Lack of receptor sites for acetylcholine Results in muscle?s inability to contract S & S First seen in muscles of eye Ptosis Diplopia Incomplete closure of eyelid Reduced facial expression Difficulty chewing and swallowing Respiratory failure Dx Tensil test ? stimulate muscle receptor sites temporarily so muscles contract Tx Anticholinesterase (neostigmine) ? restores muscle function Corticosteroids ? relieves symptoms Multiple Sclerosis Patho Myelin sheath of the brain and spinal column are destroyed Destruction of sheath causes an interruption of nerve conduction Plaque formation occurs in white matter of brain and spinal column Inflammation occurs around the plaque and normal tissue Astrocytes appear and form scar tissue replacing the nerve axons with scar tissue Leads to permanent disability Cause unknown ? associated with: Genetics Autoimmune Childhood viral infections ? slow acting viral infections could alter immune response Risk factors Family Hx 20-40 years old Cool and cold environments Recent viral infection S & S Patter = exacerbations and remissions Motor Fatigue Tremor Ataxia Eyes Diplopia Blurred vision nystagmus Head Slurred speech Dysphagia Sensory ? response to Phys. Ex To touch, vibration, pain, temperature Numbness, tingling (?pins and needles) sensation hyperesthesia Emotional Irritability/ hyperexcitability Apathy/depression Can change rapidly Cognitive Memory loss Poor judgment Inappropriate responses Dx Cerebrospinal fluid ( mononuclear cells and IgG Positive myelin basic protein (MBP) MRI Tx Immunosuppressant therapy Antiviral drugs Corticosteroids Interferon-alpha Antibiotics Antispasmodics Dementia Alzheimer?s Disease Patho Loss of blood perfusion to the brain (lobes, frontal, temporal, cerebral cortex) Amyloid ? starch like protein accumulates in brain tissue Loss of nerve cells Brain atrophies Progresses to all areas of the brain Deficit in neurotransmitter ? acetylcholine End result = memory impairment and deterioration of intellect Causes Genetic ? demonstrates a familial tendency of early AD Deficiency of neurotransmitters are documented Acetylcholine, NE, Serotonin Environmental ? infection with slow growing virus Autoimmune response S & S First Stage (2-4 years) Forgetfulness Recent memory loss ? ability to concentrate Lack of spontaneity, social withdrawal Second Stage (may last several years) Progressive forgetfulness, memory loss Language disturbances = poor choice of words, echolalia Motor ? ability for direct function Shaking uncontrollably Mental Deterioration = delusions, hallucinations, wandering syndrome (sundown syndrome) Terminal Stage (1-2 years) Inability to recognize family/friends Incontinence Inability to eat Dx EEG ? electroencephalogram = measures brain waves (? with AD) CT Scan ? shows brain atrophy MRI ? shows brain atrophy PET Scan ? shows ? metabolic activity of brain, can be used to Dx early disease Tx No cure Requires extensive family support Reverse acetylcholine destruction with meds Cognex, Aricept, Exelion (improve memory) Tranquilizers to treat agitation Skin (Quiz #10) Candidiasis Yeast like fungus found in vagina, GI tract, skin, and mucous membranes Favorable growth factors: warm, moist environment, change in pH, ? blood glucose, or change in immune system Can also be a result from antibiotic therapy (suppresses protective flora) At risk: DM, Cushing?s dz, poor nutrition, debilitation (? resistance to infection), immunocompromised pts, pts receiving antineoplastic therapy Can reside on skin folds of ABD, inguinal area, or under breasts of those who are obese Uncircumcised males Manifestations: Candida releases toxins that irritate the skin Red, edematous area with well defined borders As progresses, may have white patchy areas with scaling Severe=pustules Itching and burning accompany rash Prevalent sites=skin folds, under breasts, axillae, groin, perineal area, scrotum Oral candidiasis 9thrush)=formation of creamy white coating, white plaques or flaking on red inflamed tongue or mucous membrane Lesions may develop into shallow ulcers Papillae on tongue may appear large Plaque can be removed, but=bleeding Slight fever or GI irritation may accompany thrush With tx, infection is generally cleared in 3-7 days Tx Topical, antifungal drugs Oral candidiasis treated with oral suspensions of nystatin (swish and swallow) Severe cases tx with antifungal and topical steroids or PO Cellulitis Bacterial infection of dermis and subcutaneous tissue Caused primarily by GAS or S. aureus At risk DM, HIV, CA, neoplasms, pts on antineoplastic therapy, pts with poor circulation, pts with previous trauma to skin or existing skin ulcers Manifestations Usually found on lower legs, ears, and face appearing a few days after infectious organism invades skin Local swelling, tenderness, warmth, and pain Bright red patches or plaques with indefinite borders Edema at site Skin tender and warm In later stages, pustules, abscesses, and necrosis may develop Secondary infections of site can occur Tx Systemic antibiotics Resistant strains tx with vancomycin Lower extremities elevated to ? swelling Herpes Zoster Caused by varicella zoster (same virus as chicken pox) Acute inflammation along a dermatome of the skin Decline in immunity, stress, or aging may cause a reactivation of latent varicella zoster virus Initial exposure to chicken pox, the virus travels down to nerve fibers to dorsal ganglion cells where it resides in a dormant state After it is reactivated, it replicates in affected sensory ganglion The virus moves through the sensory nerve pathways to skin where it creates pain, vesicles, and crusting Inflam response along nerve pathways and neuronal necrosis causes the intense pain Manifestations Before eruption of lesions-itching, pain, tenderness at site Lesions appear bubbly, underlying skin is red and swollen Vesicles usually develop in the posterior surface of the body and move peripherally along unilateral dermatomes to anterior body surface 1-2 weeks- crusts fall off Primary sites are facial, thoracic, or cervical nerve roots Pain is intense Permanent blindness can result when the virus develops in ophthalmic division of trigeminal nerve Tx Antiviral rx (Zovirax) Antibacterial cream to prevent secondary infections Topical anesthetic agents to ? pain Narcotics for severe pain Amitriptyline (antidepressant) for sedative effect Eczema (dermatitis) Inflam skin response to any injury is agent Clothing, cosmetics, cleaning products, occupational exposure, plants metal alloys (jewelry), additives, dyes, soap, latex products Life long problem with periods of exacerbation and remission Manifestations Vesicle formation, oozing, crusting, itching, erythema, scaling Can range from mild (itchy, hot, dry skin) to severe forms with raw, bleeding and broken skin Tx Removing source or irritant or allergen Antipruritic creams (anti-itch) Topical steroids Washing affected areas to remove further contamination by irritant or allergen Severe cases=oral antihistamines, systemic corticosteroids, wet dressings Psoriasis Common, chronic inflam skin dz Cause uncertain, but thought to be T-cell immune response to??? Skin trauma is a common precipitating factor in individuals predisposed to the disorder Manifestations Areas affected: scalp, hairline, elbows, knees, and sites of trauma Circular, patchy appearance of all sizes covered with heavy, dry, silvery scales Erythema Extent of inflammation determines the size and distribution of the lesions Tx Goal: suppress clinical manifestations Corticosteroids and emollients used in mild cases Systemic corticosteroids, antimetabolites, topical agents, and hospitalization in severe cases Basal cell carcinoma Malignant lesion arising from epithelial cells Most common sites are areas of skin exposed to sun (face and neck) Sun exposure and age are most common risk factors UV light exposure creates DNA mutations in p53 gene which allows CA cells to grow and become more aggressive At risk Older adults and light skinned individuals Manifestations Begins with slightly elevated pearl colored nodule Growth rate is slow As lesion grows, it frequently ulcerates Usually center of lesion is depressed Prognosis Good with early dx and tx; metastatic spread is rare Tx Surgery, radiation therapy Squamous cell carcinoma Malignant of epidermis Grows more rapidly than basal cell tumors Can metastasize Tumors can be localized or invasive and spread through the lymph Tumors are firm Surface is elevated with granular quality that bleeds easily Most arise from skin lesions (sun damaged skin, warts, calluses, scars, ulcerated skin) Cause unknown, but sun exposure and aging are most common risk factors Mutation is p53 gene is part of mechanism Manifestations Face and neck most common areas Lesions are scaly, slightly elevated with irregular border, and usually have shallow chronic ulcer Later lesions grow outward, show large ulcerations and have persistent crusts with raised, erythematous borders Prognosis Remains confined at epidermis for a long time-but at some unpredictable time, the lesion penetrates dermis and metastasizes to regional lymph nodes Invasive squamous cell carcinoma can be slow or fast growing with metastasis Prognosis good Cure with early dx and tx Tx Surgery, radiation Reconstructive surgery-extensive tumors With metastasis, combination of radiation and antineoplastic therapy Malignant melanoma CA lesion arising from epidermal melanocyte cells Most commonly arise from existing mole (nevus) Nevus is benign aggregation of melanocytes Nevus with diameter ? 6mm is considered highly suggestive for developing malignant melanoma Most common are superficial spreading; pattern of tumor growth is horizontally along skin surface Nodular melanoma has ? potential of becoming metastatic because it grows vertically into deeper tissue Cause unknown, but sun exposure=risk Prognosis Depends on extent of metastasis, initial lesion site and depth, lesion thickness, stage of dz process Initial lesions on extremities have most favorable prognosis Lesions on trunk, head, neck=poorest prognosis Lesions > 4mm thick=poorest prognosis 10 yr survival rates have ?, but mortality rate continues to ? 5 yr survival rates best for nonmetastatic lesions that are dx and tx early Manifestations Most lesions are slightly raised, black or brown Irregular borders and surfaces uneven May ulcerate and bleed Surrounding erythema, inflammation, and tenderness Dark melanomas are frequently mottles with red, blue, and white shades Diff colors represent diff concurrent processes: melanoma growth (blue), inflammation (red), and scar tissue (white) Tx For premalignant melanoma lesions Suspicious pigmented nevi should be removed Indications for biopsy and removal include Changes in size or color of mole Irregular notched margins Nodularity Ulceration Scab formation Itching, oozing, bleeding For malignant melanoma lesions Surgical excision Dissection of regional lymph nodes Antineoplastic therapy for metastatic dz Prostate Benign prostatic hyperplasia Enlargement of the prostate gland Prostate enlarges as nodules form and grow and glandular cells enlarge Resulting hyperplasia leads to hypertrophy of gland Hyperplasia, not hypertrophy, causes the major prostatic changes During early stages, detrusor muscle hypertrophies to help bladder force urine out against ? resistance As obstruction progresses, the detrusor muscle decompensates and the bladder is unable to empty all of the urine ? volumes of urine are retained until urinary retention becomes a chronic problem Amt of urine retained can be large-producing uncontrollable over flow incontinence with any ? in ABD pressure Progressive bladder distention causes outpouchings in the bladder wall and some neural degeneration of smooth muscle cells occur Ureters may become obstructed-calculi, bladder and kidney infections Etiologic factors are uncertain, but several agents appear to play a role in BPH ? testosterone, ? estrogen, stimulation of alpha adrenergic nerve endings that interfere with opening of bladder sphincter, and smoking BPH is most common benign tumor in men Sx of BPH usually begin after age 55 with approximately 25% of men reporting obstructive voiding At 75 yrs, 50% report a ? in the force of urinary stream Manifestations ? or interrupted urinary flow Difficulty starting micturition Inability to empty the bladder ? frequency of urination Gradual worsening of obstructive sx Weak urinary stream ABD straining to void Hesitancy Intermittency Incomplete bladder emptying Dribbling Frequency Nocturia Urgency Incontinence Possible hematuria Renal insufficiency and if un tx, renal failure Prognosis Development of BPH occurs over a prolonged period Changes within the urinary tract are slow Reversing progressive BPH is impossible Dx Enlarged prostate with rectal palpation ? BUN and Cr (renal dysfunction) UA showing hematuria and WBCs more than 100,000-UTI ? PSA (prostate specific antigen)-prostate carcinoma must be ruled out Tx Alpha adrenergic blocking drugs to relax the smooth muscle of bladder and prostate Antiandrogen drugs-cause the prostate gland to shrink TURP-transurethral resection of prostate Indwelling catheters-difficult with BPH pts Suprapubic catheters Prostatic carcinoma Majority are adenocarcinomas Begins in the periphery of the posterior lobe Normally grows slowly Sometimes grows rapidly with metastasis to bladder (direct extension); also through lymph and circulation At risk Most common male cancer and 3rd leading cause of death among men in US Manifestations Unless BPH is present, manifestations are absent at the time of digital examination Dysuria-difficulty urinating Excessive urinary frequency Slow, small urinary stream Inability to empty bladder Nocturia Urinary obstruction is rare unless BPH is present Rectal pressure from tumor causes changes in stool and painful BM Painful ejaculation Late stages=hip or back pain and sensory or motor changes from spinal cord pressure Late in dz-thrombophlebitis, and lower extremity lymphedema Dx PSA-prostatic specific antigen-specific for prostate CA Useful in detecting and staging; monitoring response to tx and detecting recurrence before it becomes clinically evident 24% of men with moderate elevations of PSA are found to have prostate CA ? BUN and Cr-advanced CA with urinary retention or urethral obstruction Tx Controversial-if prostate removed-can?t get an erection Based on staging and grading of tumor, pts age Radiation therapy Prostatectomy Antineoplastic therapy
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