Pathophysiology Final-Exam-Concept-Review NR 283, Exams of Nursing

Download Pathophysiology Final-Exam-Concept-Review NR 283 and more Exams Nursing in PDF only on Docsity! lOMoARcPSD|28205643 Pathophysiology Final- Exam-Concept-Review NR 283 Chapter 17 Gastrointestinal Final Exam Concept Review Pathophysiology causes signs and symptoms Hiatal Hernia sliding or - shortening of the esophagus - weakness of the diaphragm muscles - heartburn/pyrosis (brief substernal burning sensation + sour taste) - frequent belching (gas) Complication: strangulation paraesophageal - ↑ abdominal pressure (from pregnancy) - ↑ discomfort when laying down, bending over, coughing part of stomach - trauma - dysphagia (esophagus inflammation/food mass compress protrudes  thoracic cavity esophagus) - persistent, mild, substernal chest pain radiate  shoulder/jaw - infection by many types of microorganisms (bacteria + viruses) - anorexia, nausea, vomiting  hematemesis: indicates ulceration + bleeding in stomach - epigastric pain/cramps/general discomfort - fever - headache - diarrhea (some w infections) Acute Gastritis - allergies to foods (shellfish or drugs) - radiation or chemotherapy gastric mucosa is - ingestion of corrosive or toxic substances - excessive EtOH intake inflamed - ASA/ulcerogenic drugs ingestion (esp. on empty stomach) (red + edematous) - ingestion of spicy/irritating foods (hot peppers, if unaccustomed to spicy diet) Chronic Gastritis - seen in individuals with:  abuse alcohol  chronic peptic ulcers - H. pylori, NSAIDs, alcohol, tobacco - autoimmune d/o: pernicious anemia - elderly - mild epigastric discomfort atrophy of stomach - anorexia mucosa w/ loss of - intolerance for certain foods (spicy or fatty foods) secretory glands Peptic Ulcer Disease (PUD) break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum - H. Pylori, NSAIDs, Zollinger Ellison Syndrome - duodenal: ↑ acid secretion more common - gastric: impaired mucosal defenses more common - person inflected w Helicobacter pylori may develop ulcers - damage to mucosal barrier predisposes development: inadequate blood supply (caused by vasoconstriction)  excessive glucocorticoid secretion or medication  ulcerogenic substances break down mucous layers (ASA, NSAIDs, EtOH)  atrophy of gastric mucosa (chronic gastritis) - epigastric burning or aching (2-3 hrs after meals + PM) - localized pain (usually following stomach emptying)  may be initiated by intake of spicy food @mealtime - heartburn, weight loss, N/V (after EtOH or irritating food)  some: weight gain b/c ↑ frequency of food intake relieves abd discomfort btwn meals - iron deficiency anemia - presence of occult blood in the stool (Dx indicator) duodenal ulcer – occurs in the proximal duodenum  painful when abd full gastric ulcer – found in the antrum of the stomach + painful when abd empty Cholelithiasis Gallstones formation (solid material -calculi- that forms in the bile) - idiopathic - - idiopathic, but risks: obesity, middle age, female, Native American ancestry, gallbladder or pancreatic disease - occurs twice as often in females - high cholesterol in the bile - high risk: obesity, high cholesterol intake, multiparity-several children, oral BCP or estrogen supplements - more common in PMHx of hemolytic anemia, alcoholic cirrhosis, biliary tract infections - frequently asymptomatic - larger gallstones may obstruct flow of bile in cystic/common bile duct  may need surgical intervention  severe pain waves (biliary colic) in RUQ/epi  back/shoulder R  N/V  pain continues: jaundice develops as bile backs up into liver & blood - pain ↑ for some time, then may ↓ if the stone moves on - obstruction persists: risk of a ruptured gallbladder Hepatitis inflammation of the liver Hepatitis A (HAV): transmitted by fecal-oral route in areas of inadequate sanitation or hygiene  contaminated water or shellfish or food  sexual transmission through anal intercourse - goes away; ø come back Hepatitis B (HBV): transmitted through infected blood; body secretions  body fluid (sexual contact)  tattoo  body piercing - last 6 months, then come back  cirrhosis Hepatitis C (HCV): transmitted by post-blood transfusion  IV drug use - 20% leave; 80% latent  chronic liver CA/cirrhosis Hepatic Encephalopathy -impaired cerebral fxn- - neurological syndrome caused by an accumulation of toxins in the blood steam d/t liver failure - altered LOC - confusion - memory loss - convulsions - asterixis: tremor of the hand - coma - jaundice: yellow or green pigmentation of the skin 2 types: Obstructive & Hemolytic Hepatic Encephalopathy cause signs and symptoms - acute BL kidney dz (pyelonephritis; glomerulonephritis = ↓ GFR) - develops rapidly - itching, fatigue, confusion - uremia  malaise, fatigue, disorientation, drowsiness - severe and prolonged circulatory shock or - cardiovascular: hypertension, atherosclerosis, heart failure  tubule necrosis (ischemia) cardiomyopathy, edema, dysrhythmia Kidney Failure kidney fail to function both kidneys must be involved - nephrotoxins (drugs, chemicals, toxins)  tubule necrosis + obstruction of blood flow - mechanical obstruction (calculi, blood clots, tumors)  block urine flow  acute renal failure - pulmonary : pulmonary edema - circulatory: anemia - immune: ↑ risk of infection - GI: anorexia, N/V - integumentary: pruritus, dry skin, bruising, petechiae Treatment: - oliguria stage: dialysis nml body fluids+maintain homeostasis - ↑ UOP - drugs to stimulate ↑ erythropoiesis and ↓ phosphate lvls - uremic stage: organ transplant + dialysis Chapter 9 Musculoskeletal Sprains/Strains — RICE + immobilization often used to prevent tissue damage + promote healing  Sprain: a tear or injury in a ligament  Strain: a tear in a tendon – grade I, grade II, grade III  Avulsion: ligaments or tendons completely separated from bony attachments bone tore off, but still connected to tendon Dislocations —  Separation of two bones at a joint, with loss of contact between articulating surfaces  Usually accompanied by significant soft tissue damage to ligaments and tendons  Distortion of joint usually evident  May recur repeatedly, requiring surgery causative factors signs and symptoms complications Compartment Syndrome — edema within one area of compartment of the limb that is between layers of dense connective tissue (fascia) - tight cast - ischemia and infarction of tissue may occur because of compression of arterial blood supply - dead tissue may become  gangrenous, requiring amputation Osteoporosis — ↓ in bone mass + density; bone resorption rate exceeds bone formation = loss of compact bone - deficits of calcium, vitamin D, or protein - age 50+ years - ↓ mobility or sedentary lifestyle - lower BMI - hormonal factors  ↑ corticosteroids or parathyroid hormone (PTH)  ↓ estrogen or testosterone - asian or european ancestry - cigarette smoking - Cushing’s syndrome or medication - ↑ caffeine intake  compression fractures of vertebrae, wrist, hip, or femoral neck/femur  kyphosis and scoliosis Osteomalacia/Rickets — results from deficit of vitamin D + phosphates - intake of phenobarbital - dietary deficits - lack of sun exposure - malabsorption - children: weak bones + other skeletal deformities - adults: soft bones  compression fx Disuse Atrophy – immobilization, inactive muscle, and chronic illness (osteoporosis, fx)  loses strength, endurance, and mass quickly - muscle cell size is ↓ when the muscle is not used - may occur within a short period of time when a fractured limb is placed in a cast or the pain of arthritis limits movement - may be secondary to nerve injury  resultant flaccid paralysis - nutritional deficiencies: particularly protein, 2/2 anorexia or Crohn disease  atrophy - prolonged bed rest - atrophied muscle  weak and flaccid - weak skeletal muscle 2/2 degenerative △ involving accumulations of fatty or fibrous tissue - ↓ muscle mass with aging = ↓ # muscle cells and ↓ in size (diameter) of the fibers - diminished muscle strength which may vary with the individual’s degree of activity and general health status Fractures —  Complete: bone broken  separate pieces  Incomplete: bone only partially broken  Open (compound): skin broken  Closed: skin not broken  Simple: single break, maintaining alignment and position  Comminuted: multiple fractures and bone fragments  Compression: bone crushed or collapsed into small pieces  Impacted: one end forced into adjacent bone  Pathologic: results from weakness; occurs with little stress  Stress: fatigue fractures  Depressed: skull fractured & forced into brain causes signs and symptoms Osteoarthritis – degenerative joint disease; wear and tear joint disease - primary form : weight-bearing, obesity, aging - secondary form : post trauma or repetitive use - genetic factors thought to play a role - weight-bearing joints most frequently affected but finger joints also involved - aching pain w/ weight-bearing + movement - joint movement is limited - limited recreational + social activities d/t pain - difficulty walking - predisposition to falls - in temporomandibular joint (TMJ): difficulty chewing and speaking - bony enlargement of distal interphalangeal joints Rheumatoid Arthritis – autoimmune disorder  chronic systemic inflammatory disease - exact cause not known - links to viral infections - genetic factor present - familial predisposition - ↑ incidence in women than in men - affects all age groups - affected joints are painful + stiffness - redness and swelling of joints - joint involvement includes small joints and is BL - joint movement impaired  fixed and deformed Gout – results from deposits of uric acid and crystals in the joint  inflammation - forms tophus: large hard nodule of urate crystals  occurs in feet and big toe - uric acid and crystals form d/t inadequate renal excretion, chemotherapy, metabolic abnormality, and/or genetic factors (40 y/o+ and males) - tophi  local inflammation and occur after the first attack of gout - inflammation  redness, swelling, pain Chapter 25 Immobility Contracture – fibrotic/scar tissue (of collagen fiber) is nonelastic  tends to shrink over time  may restrict the joint ROM  result in fixation and deformity of the joint Dermal Ulcers – sore that develops on the skin followed by destruction of the tissue surrounding it  complete skin lost Cardiovascular Effects from Pressure Ulcers :  Orthostatic Hypotension – prolonged immobility  drop in blood pressure occurring when a person changes position (rises from a supine to a standing position) o Short period of dizziness o Fainting o Pallor and sweating o Rapid pulse  Deep Vein Thrombosis – immobile  blood pooling– stasis  ↑ capillary pressure and edema  promotes thrombus formation (in veins)  DVT Respiratory Effects from Pressure Ulcers : ↑ mucous secretions in lungs  Pneumonia – frequently lead to infection; or caused by aspiration of food or water intake (occurs more easily when the patient is immobilized or in supine position)  Atelectasis -– obstruction of airway and collapse of the lungs; or caused by aspiration of food or water intake (occurs more easily when the patient is immobilized or in supine position) Gastrointestinal Effects from Pressure Ulcers :  Constipation – caused by muscle inactivity and body position; reduced food, fiber, fluid intake (#1 common) Urinary Effects from Pressure Ulcers : stasis of urine in bladder  Kidney Stones – more likely in people with hypercalcemia  Bladder Infection – common if catheters are used Paraplegia – paralysis of the lower body half (or upper body half) Quadriplegia – paralysis to all four limbs and trunk Hemiplegia – paralysis on one side of the body Diplegia – symmetrical Paralysis in any location of the body (BL) co ns id er ati on Chapter 16 Endocrine ***Be sure to cover pathophysiology, etiology, signs and symptoms, diagnostic tests for the following endocrine topics: Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) — excess of ADH - increased ↑ ADH = holds into more water (↓ UOP); edema  treatment: diuretics + sodium supplements = ↓ NA+ (stays with fluid; hyponatremia) = ↓ BP  may be temporary, triggered by stress; may be secreted by an ectopic source, such as a tumor Diabetes Insipidus (DI) — deficit of ADH - decreased ↓ ADH = holds onto less water (↑ UOP – poured urine, clear, no urea) = ↑ Na + (stays behind  secreted by ectopic source, an adenoma when fluid leaves; hypernatremia – dehydration, thirst) ↑BP  may originate in the neurohypophysis (posterior lobe of the hypophysis (pituitary gland)) o Head injury or surgery o Possible genetic problem o Replacement treatment required Diabetes Mellitus Type I insulin dependent autoimmune destruction of beta cells (insulin) in pancreas  glucose build up in blood  cells starve DM I & DMII both Diabetes Mellitus Type II non-insulin dependent; ↓ effectiveness of insulin/relative deficit of insulin pancreas works  makes insulin  receptor sites don’t work; does not respond to insulin pa th op hy sio lo gy Initial Stage 1. insulin deficit = ↓ transportation + use of glucose in many cells of the body 2. ↑ BGL hyperglycemia 3. excess glucose  urine (glucosuria) as the lvl of glucose in the filtrate exceeds the capacity of the renal tubular transport limits to reabsorb it 4. glucose in urine exerts osmotic pressure in the filtrate = polyuria w the loss of fluid + electrolytes (Na+ and K+) from the body tissues 5. fluid loss through the urine and ↑ BGL draw water from the cells  dehydration 6. dehydration  polydipsia 7. lack of nutrients entering the cells stimulates appetite (polyphagia). ca us es - autoimmune - (weak) genetic link - acute onset in children and adolescents - slow and insidious onset (usually 50 years+) - (strong) genetic link - black - lifestyle choices - hispanic - obesity - native American sig ns a nd sy m pt om s - weight loss - ↓ insulin = ↓ transport and use of glucose in many cells  polyphagia and fatigue - excessive glucose in urine (dehydration, polyuria, polydipsia) - nocturia w the excretion of large volumes of urine - BGL rise (hyperglycemia) - dry mouth - itchy skin - blurred vision 3 P’s: polyuria, polydipsia, polyphagia - weight gain - ↑ abdominal girth co m pl ic ati on s ACUTE - diabetic ketoacidosis (DKA)  occurs in insulin- dependent clients = insufficient insulin in blood  high BGL > 450  s/s: dehydration, rapid and deep respiration, metabolic acidosis, electrolyte imbalances (abd cramp, N/V), ketone urine, acetone breath (musty/fruity) - hypoglycemia (insulin shock) ACUTE  common with insulin replacement treatment; can occur because of excess oral hypoglycemic drugs  low BGL; excess insulin in body  s/s: diaphoresis, tremors, confusion, staggering, hungry, pale, sz, coma, death  immediate admin of glucose is req to prevent brain damage - vascular problems: ↑ atherosclerosis CHRONIC - microangiopathy: obstruction or rupture of small capillaries + arteries  neuropathy, retinopathy (cataract; glaucoma); chronic renal failure - macroangiopathy: affects large arteries  = abnml lipid levels  MI, CVA, PVD  peripheral neuropathic diabetic foot ulcer - neuropathy: ischemia in microcirculation to peripheral nerve  paresthesia, numbness, tingling, impaired sensation, muscle wasting - infections: fungal, gingivitis, periodontitis, dental caries, UTI - pregnancy: gestational diabetes  insulin only  stillbirth, v. ill baby, ↑ size + weight of infants; hypoglycemia in 1st hrs postnatally  does go away when baby is born ACUTE - HHNK syndrome (hyperglycemic hyperosmolar nonketotic diabetic coma)  insidious onset, occurs in older clients  s/s: hyperglycemia (BGL > 1000), severe dehydration, electrolyte imbalances, nerve pain, fatigue di ag no sti c te st s - glycosylated hemoglobin (HbA1c) - fasting blood glucose level - glucose tolerance test  clinical and subclinical diabetes  monitors long-term control every 3 months  RBCs lives for 120 days nu rs in g s & pa tie nt ed uc ati on - diet △ - regular exercise to ↓ BGLs  ↑ fiber; ↓ lipids; ↓ simple carbs - reduce insulin resistance by ↓ BMI to nml range - monitor BGL - medication to stimulate beta cells of the pancreas  produce more insulin - routine f/u + blood testing - insulin dependent: proper administration of insulin to maintain BGL in nml range CVA Types Definition of Deficits Signs and Symptoms Prognosis Tr an sie nt Isc he m ic A tt ac ks - temporary reduction of blood flow to the brain: recovery within 24 hrs - may occur singly or in a series - from temporary localized ↓ blood flow in brain  partial occlusion of artery ▪ vascular spasm  atherosclerosis ▪ small embolus  local loss of autoregulation - patient remains conscious - intermittent short episodes of impaired function  muscle weakness in arm/leg - visual disturbances - numbness and paresthesia in face - transient aphasia or confusion may develop - attack may last a few minutes or longer, but rare is > than 1-2 hrs - repeated attacks = warning sign for obstruction related to atherosclerosis Ce re br ov as cu la r Ac ci de nt s - lack of blood  an infarction of brain tissue  total occlusion of a cerebral blood vessel o  ischemia  rupture of cerebral vessel o  hemorrhage + ↑ ICH - 5 min of ischemia  irreversible nerve cell damage - depends on location of obstruction, size of artery & fxnal area involved - lack of voluntary movement or sensation on opposite side of body - initially flaccid paralysis; spastic paralysis develops weeks later - ↑ functional deficits - coma, LOC, death - 5 minutes of ischemia causes irreversible nerve cell damage  central area of necrosis develops ▪ all function lost  surrounded by area of inflammation; zone will regain fxn s/p healing He m or rh ag e St ro ke - intracerebral hemorrhage - caused by occlusion of large arteries (internal carotid artery or the middle cerebral artery) or a hemorrhage  mass of blood compresses and displaces tissue - complicated by secondary effects of bleeding - usually begin suddenly with a blinding headache and increasingly severe neurologic deficits  effects are evident in both hemispheres  edema, ischemia and IICP can occur - cause severe, widespread effects coma, LOC, or death, almost immediately - in patient w/ severe HTN, arteriosclerosis, aneurysm, tumors, trauma Often High ↑ICP present Less successful outcome Is ch em ic St ro ke Th ro m bo tic St ro ke - blood clot forms occlusion of an artery by an atheroma - often develop in large arteries - predisposing condition: atherosclerosis in cerebral artery - gradual onset – maybe preceded by TIAs - occurs at rest - localized effects – may be less permanent damage if collateral circulation est. Minimal ↑ ICP - severe headache w/o known cause - numbness/weakness of the face, arm, leg  especially on one side of the body - trouble seeing in one or both eyes - confusion trouble walking, dizziness - loss of balance or coordination Em bo lu s - sudden obstruction caused by an embolus - lodging in a cerebral artery - predisposing condition - atherosclerosis (carotid artery) or systemic source (heart) - localized effects – unless multiple emboli are present Minimal ↑ ICP M id dl e Ce re br a l A rt er y (M CA ) - lack of blood supply to the middle cerebral artery supplies a large portion of the cerebral hemisphere - contralateral paralysis and sensory loss (primarily of upper body + arm) - aphasia occurs when the dominant hemisphere of the brain is affected - spatial relationships maybe more severely impaired if right side damaged - posterior cerebral artery supplies occipital lobe (if occluded)  visual loss An te rio r Ce re br a l A rt er y (A CA ) - occlusion of an anterior cerebral artery affects the frontal lobe - contralateral muscle weakness or paralysis - sensory loss in the leg - confusion - loss of problem-solving skills - personality changes Meningitis: infection + inflammation, usually of bacterial origin, in the meninges of the CNS, CFS, and ventricles  microorganisms reach the brain via blood, by extension from nearby tissue, or direct access through wounds  causative organisms : Neisseria meningitidis (meningococcus); Escherichia coli; Haemophilus influenzae; Streptococcus pneumoniae (pneumococcus)  s/s : sudden onset of severe headache, back pain, photophobia, nuchal rigidity (hyperextended, stiff neck) = meningeal irritation o vomiting, irritability, lethargy  to stupor (near unconsciousness) or seizures are common early indicators of ↑ ICP o F/C with leukocytosis = infection o rosecolored petechial rash/ecchymoses over body o different signs: feeding problems, irritability, lethargy, a typical high-pitched cry, and bulging fontanelles in the newborn.  Kernig sign - resistance to leg extension when lying with the hip flexed  Brudzinski sign - neck flexion causes flexion of hip and knee  potential complications: hydrocephalus, damage to the cerebral cortex may occur = mental retardation, seizures, or motor impairment  fulminant (rapidly progressive, severe) cases caused by highly virulent organisms: o frequently meningococcal, disseminated intravascular coagulation develops, with associated hemorrhage of the adrenal glands, or meningococcal septicemia may directly cause adrenal hemorrhage (Waterhouse-Friderichsen syndrome)  result in vascular collapse or shock and death  precaution : vaccine as a preventive measure for some types of meningococcal, S. pneumoniae, and H. influenzae meningitis Encephalitis: infection of the parenchymal or connective tissue in the brain and spinal cord  usually of viral origin, but maybe caused by other organisms ▪ infection may include meninges  necrosis and inflammation develop in brain tissue  some permanent damage  early s/s: severe headache, stiff neck, lethargy, vomiting, seizures, fever o Western equine encephalitis - arboviral infection spread by mosquitoes  more frequent in summer months  common in young children o St. Louis encephalitis affects older persons more seriously than younger individuals o West Nile fever caused by a flavivirus + spread by mosquitoes o Neuroborreliosis (Lyme disease) caused by Borrelia burgdorferi  transmitted by ticks  antimicrobial therapy  typical bull’s-eye lesion—sore throat, dry cough, fever, headache, cardiac arrhythmias, neurological abnormalities o Herpes simplex encephalitis spread from herpes simplex I  occurs occasionally  extensive necrosis + brain hemorrhage  precaution: avoid exposure to viruses that can cause the disease o practice good hygiene - wash hands frequently and thoroughly with soap and water after using the toilet and before + after meals TBI  producing physical, intellectual, emotional, social, and vocational changes Closed head injury : skull is not fracture, but brain tissue is injured  blood vessels may be ruptured by the force exerted against skull  extensive damage may occur when the head is rotated with considerable force - hematoma: classified by location in relation to the meninges - brain tissue trauma  loss of function in body part controlled by area of the brain o cell damage and bleeding  inflammation and vasospasm around injury site  ↑ ICP, general ischemia, dysfunction  some recovery may occur—scar tissue formation Open head injuries : involving fractures or penetration of the brain by missiles or sharp objects Contrecoup injury : area of the brain contralateral to the site of direct damage is injured  2/2 acceleration or deceleration injuries  skull + brain hit solid object o  brain bounces off the skull against the opposite side of skull = minor damage  concern with child  bc of shaking baby syndrome; damage to front and back of skull Extradural (epidural) hemorrhage or hematoma : between dura + skull, arterial; signs arise within few hours of injury  result from arterial bleed as bleeding grows  CM gets worse o brief period of responsiveness  LOC for a period of time o medical emergency Subdural hematomas : between dura and arachnoid, venous  hematoma maybe acute or subacute  tear in arachnoid  CSF to leak into subdural space; creates additional pressure o hematoma disintegrates about 7 days postinjury o hemolysis increases osmotic pressure → ICP Subarachnoid hemorrhage : arachnoid and pia (blood) mixes with CSF = no localized hematoma formation  assoc with traumatic bleeding from the blood vessels at the base of the brain Intracerebral hematomas: bleeding within the brain from contusions or shearing forces  may develop several days after injury  LOC, pupillary changes, respiratory changes Linear fractures: simple cracks in the bone Comminuted fractures: several fracture lines but may not be complicated Compound fractures: brain tissue is exposed to environment and is likely to be severely damaged because bone fragments may penetrate the tissue  risk of infection is high Depressed skull fractures: displacement of a piece of bone below the level of the skull  compressing the brain tissue  blood supply to the area is often impaired  considerable pressure is exerted on the brain Basilar fractures: occur at the base of the skull and are often accompanied by leaking of CSF through the ears or nose  may occur when forehead hits a car windshield w considerable force  CN damage and dark discoloration around the eyes are common Spinal Cord Injury: most commonly occurs d/t vertebral injury from hyperextension, dislocating vertebrae, compression (diving), penetrating injuries  Most injuries: in areas of the spine that provide more mobility but less support (ie, C1 to C7 and T12 to L2) lumbar vertebrae  Cervical spine injuries : may result from hyperextension or hyperflexion of neck with possible fracture  Dislocation of vertebra : may crush or compress spinal cord  Compression : causes injury to spinal cord when great force is applied to top of the skull or to the feet  Spinal cord damage : result directly from penetration injuries, such as stab or bullet wounds  Autonomic hyperreflexia (dysreflexia) o Massive, uncompensated cardiovascular response to SNS stimulation o Life threateninig o Caused by any type of sensory stimulation below the level of injury  Distended bladder or rectum are most common (bladder is full or fecal material in the rectal valve) o CM:  HTN  HA  Blurred vision  Face/skin flushed  bradycardia  Spinal shock: nml activity of the spinal cord ceases at + below the level of injury; sites lack continuous nervous discharges from the brain o Complete loss of reflex function o Condition may persist for days or weeks  Flaccid paralysis  Sensory loss at and below injured area  Absence of all reflexes  Loss of central control of autonomic function o Resolves with reappearance of reflex activity.  Tetraplegia (quadriplegia) - paralysis of all four extremities  Paraplegia - paralysis of the lower part of the trunk and legs  Ipsilateral paralysis and contralateral loss of pain and temperature sensation - depends on the point of decussation and location  Complications of Spinal Cord Injury o Urinary tract infections o Pneumonia o Skin breakdown o Spasm and pain o Depression