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

Download NR 283 Pathophysiology Final Exam Concept Review Latest and more Exams Nursing in PDF only on Docsity! 1 NR 283 Pathophysiology Final Exam Concept Review ***For all previous content covered on previous exams, please consult your previous concept review sheets. This is not an all-inclusive list for topics to be covered. Please be sure to consult your syllabus and learning plan. This is a comprehensive final. ***Be sure to cover pathophysiology, etiology, clinical manifestations, nursing considerations, diagnostic tests for the following topics: Endocrine SIADH • Is due to excess ADH, which causes retention of fluid • In some cases, the additional ADH is temporary, triggered by stress or may be secreted by an ectopic source • The signs are related to severe hyponatremia which causes metal confusion and irritability. Diuretics and sodium supplements are used to correct the problem DI Antidiuretic Hormone (Vasopressin) • Diabetes insipidus results form a deficit of ADH. This deficit may originate in the neuro. • In some cases, the condition is considered to be a nephrogenic, when the renal tubules do not respond to the hormone • S/S: polyuria with large volumes of diluted urine and thirst, eventually causing severe dehydration Hypo/hyperthyroidism Hypothyroidism Hyperthyroidism Serum levels of T3 and T4 Low High Metabolic Rate Low High Goiter Present with endemic goiter Present with Graves disease Skin Pale, cool, with edema Flushed and warm Temperature tolerance Cold intolerance Heat intolerance Eyes No changes Exophthalmos with Graves disease Cardiovascular Bradycardia, enlarged heart Tachycardia, increased blood pressure Nervous system Lethargic, slow intellectual functions Restless, nervous, tremors Body Weight Some weight increase with decreased appetite Thin, but increased appetite 2 Hypothyroidism: -Mild hypothyroidism is very common and easily treated by replacement doses of thyroid hormone. -Severe types: Hashimoto’s thyroiditis (destructive autoimmune disorder), Myxedema (severe in adults), Cretinism (untreated congenital hypothyroidism) -Diagnostic test: checks of blood levels, serum levels • Mild hypo is a very common and is easily treated by replaced doses of thyroid hormone • Several forms 1. Hasimoto- a destructive autoimmune disorder 2. Myxedema- severe hypo in adults, refers to nonpitting edema manifested as facial puffiness and thick tongue 3. Cretinism- untreated congenital hypo, may be related to iron deficiency during pregnancy or development defect Overweight, no appetite, thin hair, fatigue, constipation, thick, dry Diagnostic Test: Current test for thyroid disorder include check of blood levels of t4 and t3 as well as serum TSH levels and uptake of radioactive iodine Hyperthyroidism: -Increased T3 & T4, Graves disease is an example of hyperthyroidism. • These are varying forms of hyperthyroidism with increased t3 and t4 secretion • Graves diseases occurs more frequently in women over 30 years of age and is related to an autoimmune factor • It is manifested by the signs of hypermetabolic, toxic goiter, and exophthalmos (protruding eyes and decreased blink and eye movements) • It is also increased stimulation of the SNS • S/S: increased body temp, sweating, soft silky hair and skin, reduced BMI, insomnia, hyperactive, always skinny no matter how much they eat, go diarrhea all the time Hypo/Hyperparathyroidism: Hyporparathyroidism- -Causes: May be caused by a congenital lack of the four parathyroid glands, following surgery or radiation in the neck region, or as a result of an autoimmune disease -Hypoparathyroidism leads to hypocalcemia or low serum calcium levels -Hypocalcemia affects the nerve and muscle functions in different ways. Low serum calcium levels result in weak cardiac muscle contractions but also increase the excitability of nerves, leading to spontaneous contraction of skeletal muscle. This causes muscle twitching and spasms, commonly known as tetany, which is usually observed first in the face and hands. Hypocalcemia doesn’t weaken skeletal muscle contractions because sufficient calcium is stored in skeletal muscle cells. 5 -Type 1 diabetes is a major factor predisposing to strokes (cerebrovascular accident), heart attacks, myocardial infarction, peripheral vascular disease and amputation, kidney failure, and blindness. Type 2: Decrease effectiveness of insulin. May involve decreased pancreatic beta cell production of insulin, increased resistance by body cells to insulin, increased production of glucose by the liver, or a combination of these factors. This form of diabetes may be controlled by adjusting the need for insulin by: Regulating dietary intake, increase use of glucose, such as with exercise, reducing insulin resistance, stimulating the beta cells of the pancreas to produce more insulin. Type 2 is a milder form of diabetes, often develops gradually in older adults, more so those whom are over weight. There has been an increased incidence with adolescents and younger adults who are identified with metabolic syndrome, a complex of several pathophysiologic conditions marked by obesity, cardiovascular change, and significant insulin resistance due to increased adipose tissue. This form of diabetes increases with age approximately half the cases are found in persons older than 55. African Americans, Hispanic Americans, and native Americans are ones with the highest prevalence. Types of diabetes: • Prediabetes- an early manifestation of Type 2 diabetes • Latent autoimmune diabetes in adults-a slow onset of type 1 autoimmune dibetes • Maturity onset diabetes of the young- a rare form caused by a mutation in an autosomal dominant gene • Diabetes Insipidus- diabetes not related to blood sugar levels, but an insensitivity of the kidneys to ADH Pathophysiology: insulin deficit will lead to the following events: Initial stage: 1) Insulin deficit results in decreased transportation and use of glucose in many cells of the body. 2) Blood glucose levels rise-hyperglcemia 3) Excess glucose spills into the urine (glucosuria) as the level 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, resulting in large volume of urine to excreted (polyuria), with the loss of fluid and electrolytes from the body tissues 5) Fluid loss through the urine and high blood glucose levels draw water from the cells, resulting in dehydration 6) Dehydration causes thirst (polydipsia) 7) Lack of nutrients entering the cells stimulates appetite (polyphagia) Progressive effects: If the insulin deficit is severe or prolonged, the process continues to develop, resulting in additional consequences, ultimately, diabetic ketoacidosis. This occurs more frequently in persons with Type 1 diabetes. 8) Lack of glucose in cells results in catabolism of fats and proteins, leading to excessive amoints of fatty acids and their metabolites, known as ketones or ketoacids, in the blood. 9) Ketoacids are excreted in urine- ketonuria. Some diabetic patients test their urine for ketones 10) As dehydration develops the glomerular filtration rate in the kidney is decreased and excretion of acids becomes more limited, resulting in decompensated metabolic acidosis, which has life threatening potential. Signs & Symptoms: Type 2: weight gain or increased abdominal girth Type 1: weigh loss is common 6 Fluid loss is significant. Polyuria is indicated by urinary frequency, which is often noticed by the patient at night with the excretions of large volumes of urine. Thirst and dry mouth occur in response to fluid loss. Fatigue and lethargy develop. Weight loss may follow. Appetite is increased. Typically the three Ps, polyuria, polydipsia, and polyphagia- herald the onset of diabetes. Diagnostic test: Fasting blood glucose level, glucose tolerance test, and the glycosylated hemoglobin test are used to screen people with clinical and subclinical diabetes. Treatment: 1) Diet and exercise 2) Oral medication to increase insulin secretion or reduce insulin resistance 3) Insulin replacement Complications: can be acute or chronic Acute: -Hypoglycemia- insulin shock. Precipitated by an excess amount of insulin, which causes a deficit of glucose in the blood. It usually occurs in patients with type 1 diabetes, usually suddenly, following strenuous exercise, error in dosage, vomiting or skipping a meal after taking insulin. 1) excess insulin in blood 2) increased transport of glucose into cells 3) hypoglycemia decreased CNS function 4) stimulates SNS 5) increased gluconeogenesis 6) excess insulin transports glucose into cells 7) no glucose intake 8) blood glucose levels decrease further 9) neurons can’t function 10) coma and death -Diabetic Ketoacidosis: insufficient insulin, which leads to high blood glucose levels and mobilization of lipids. More common in Type 1. S/S: dehydration, metabolic acidosis, electrolyte imbalance -Hyperosmolar Hyperglycemic Nonketotic Coma: usually in type 2. Patient is usually older and has an infection or has overindulged in carbohydrates=hyperglycemia and dehydration develop. Chronic complications: usually when blood glucose is poorly controlled. The insulin deficit and glucose excess cause a number of alterations in metabolic pathways involving carbohydrates, lipids, and proteins. Vascular problems: Macroangiopathy Atherosclerosis in large arteries, related to hyperlipidemia, hypertension, and degenerative changes in the intimal layer of • Myocardial infarction (heart attack) • Cerebrovascular accident (stroke) • Peripheral vascular disease (ischemia, Clinical signs: • Weakness, confusion • Pallor • Diaphoresis • Tremors • Tachycardia 7 Thickening of the capillary basement membrane, leading to occlusion or rupture. Microaneurysms, neovascularization, and fibrosis Leads to blindness Note- in addition to ischemia, there is also a metabolic abnormality that causes degeneration of myelin and deficit of myo- inositol, essential in the conduction of nerve impulses. • Kidneys, diabetic nephropathy, chronic renal failure • Eyes, retinopathy • Nervous system, neuropathy in the central nervous system and peripheral nerves, decreased function of sensory, motor, and autonomic nervous system fibers Microangiopathy Neuropathy- leads to impaired sensations, numbness, tingling, weakness, and muscle wasting. Results from ischemia and altered metabolic processes. Degenerative changes occur in both unmyelinated and myelinated nerve fibers. The risks of tissue trauma and infection are greatly increased when vascular impairment and sensory impairment coexist. Autonomic nerve degeneration develops as well, leading to bladder incontinence, impotence, and diarrhea. May cause dizziness when a person stands. Infections: most common and tend to be more severe in diabetics, probably because of the vascular impairment, which decreases tissue resistance, the delay in healing because of insulin deficit, and the increased glucose levels in body fluids that support infection. Cataracts: clouding of the lens of the eye Pregnancy: both mother and fetus, maternal diabetes may become more severe, control is more difficult with the continual hormonal and metabolic changes, and there is an increased incidence of spontaneous abortions and abnormalities in infants born to diabetic mothers. Newborn infant is typically larger than average and is predisposing to complications. Musculoskeletal Sprains/Strains A tear in a ligament is called a sprain A tear in a tendon is called a strain Ligaments and tendons support the bones in a joint and can easily be torn when excessive force is exerted on a joint. In some cases, the ligaments or tendons can be completely separated from their bony attachments, a problem known as avulsion. Sprains and strains are quite painful and are accompanied by tenderness, marked swelling, and often discoloration due to the hematoma formation. Bleeding into the joint capsule delays healing. Strength and range of movement in the joint are limited. Diagnosis requires x-rays and other tests to rule out the presence of a fracture and determine the extent of damage. After a tear occurs, inflammation and then granulation tissue develops at the site. Collagen fibers are formed that create links with the remaining tendon or ligament, and eventually the healing mass is bound together with fibrous tissue. A tendon or ligament requires approximetly 6 weeks before it’s strong again. Stress on a tendon in the early stage will reopen the tear and lead to the development of excessive fibrous tissue in the tendon and the arterial wall. gangrene, and amputation affecting legs) 10 - Dead tissue may become gangrenous, requiring amputation - A TIGHT CAST CAN CAUSE COMPARTMENT SYDROME!!! Arthritis-Gout, RA, Osteoarthritis • Rheumatoid Arthritis (RA) - Is considered an autoimmune disorder causing chromic systemic inflammatory disease - Higher in women and men and increase in older individuals Patho: - The disease often commences rather insidiously with symmetric involvement of the small joints such as fingers, followed by inflammation and destruction of additional joints - The first step for developing is having an abnormal immune response causing inflammation of the synovial membrane with vasodilation, increased permeability and formation of exudate, causing the typical red, swollen, and painful joints synovitis appear to result from the immune abnormality - 1. Synovitis- inflammation recurs, synovial cells proliferate 2. Pannus formation- granulation tissue from the synovium spreads over the articular cartilage. This is called granulation tissue pannus, release enzymes and inflammatory mediators, destroying the cartilage 3. Cartilage erosion- cartilage is eroded by the enzymes from the pannus and in addition, nutrients that are normally supplied by the synovial fluid to the cartilage are cut off. 4. Fibrosis- pannus between the bone ends becalm fibrotic limiting movement 5. Ankylosis- joint fixation and deformity develop Signs and Symptoms: - Affected joints are extremely painful - Stiffness in joints - Redness and swelling in joints - Eventually the joint becomes fixed and deformed • Gout (Gouty Arthritis) - This form of joint disease is common in men older then 40 years - Results from deposits of uric acid and urate crystals in the joint that then cause an acute inflammatory response, uric acid is a waste product, normally excreted through the kidneys - Hyperuricemia- may develop if renal excretion is not adequate or a metabolic abnormality, often a genetic factor such as a deficit of the enzyme uricase, leading to elevated levels of uric avid - A sudden increase in serum uric levels usually precipitate an attack of gout - Gout often affects a single joint, usually in BIG TOE - Causes inflammation which then leads to redness and swelling of the joint and severe pain - Diagnose is confirmed by examination of synovial fluid and blood test - Tophus – is a large hard nodule, consisting of urate crystals that have been precipitated in soft tissue or bone causing a local inflammatory reaction - USUALLY IN MEN EATING REDMEAT AND ALCOHOL • Osteoarthritis - May be called a degenerative or wear the tear joint disease - Men are affected more than women - It is a major cause of disability and absence from the workplace 11 Patho: Is a condition 1. The articular cartilage of weight bearing joints in particular (hips and knees) is damaged and lost through structural fissures and erosion resulting from excessive mechanicals stress 2. The surface of the cartilage becomes rough and worn, interfering with easy joint movement 3. Tissue damage appear to cause release of enzymes from the cells, which accelerates the disintegrating of the cartilage 4. Eventually the subchondral bone may be exposed and damaged, and cysts and osteophytes or new bone spurs develop around the margins of the bone 5. Pieces of the osteophytes and cartilage break off into the synovial cavity, causing further irritation 6. The joint space becomes narrower (easily seen on x-rays) 7. There may be secondary inflammation of the surrounding tissue in response to altered movement and stress on the joint Etiology: - Primary form of it is associated with obesity and ageing - Secondary form- follows trauma or repetitive use - Genetic factors play a role - Weight bearing joints are frequently effected Signs and Symptoms: - Arching pain with weight bearing and movement - Joint movement limited - Recreational and social activates become limited because of pain - Walking is difficult - Predisposition to falls - TML syndrome and speaking is difficult - Bony enlargement of distal interphalangeal joints Treatment: - Any stress on the joint should be minimized and rested - Canes or walkers should be used - Shoe inserts - Mild exertion Ankylosing Spondylitis - Is a chromic progressive inflammatory condition that affects the sacroiliac joints, intervertebral spaces, and costovertebral joints of the axial skeleton - The disorder is more common in men - The cause is not fully determined, but it is deemed an AUTOIMMUNE DISORDER WITH A GENETIC BASIS Patho: 1. The vertebra joints first become inflamed 2. Fibrosis and calcification or fusion of the joints follows 3. Inflammation begins in the lower back at the sacroiliac joints and progresses up the spine, eventually causing a typical “poker back” 12 4. Kyphosis develop as a result of postural changes necessitated by the rigidity and loss of normal spinal curvature 5. Osteoporosis is common and may contribute to kyphosis because of pathologic compression fracture of the vertebrae 6. Lung expansion may be limited at this stage Signs and Symptoms: - Lower back pain, morning stiffness, pain when lying down, spine becomes rigid - Systemic signs fatigue, fever, weight loss Osteomalcia/Rickets • Rickets (kids)/Osteomalcia(adults) - Result from a deficit of vitamin D and phosphates required for bone mineralization - They occur with a dietary deficit, malabsorption, prolonged intake of phenobarbital, or lack of sun exposer - Vitamin D is required for the absorption of calcium and the lack of it results in cartilage forming at the epiphyseal plate leads to weak bones - In children, leads to weak bone and other skeletal deformities, there height is usually below normal - In adults, may lead to soft bones, resulting in compression fractures • Paget’s Disease - Usually doesn’t show until they are 40 - BIG JAW • Osteomyelitis - Bone infection usually caused by bacteria and sometimes fungi Osteoporosis Common metabolic bone disorder characterized by a decrease in bone mass and density, combined with loss of bone matrix and mineralization. Estimated for prevalence run as high as 10 million in the United States, with many more having low bone mass, and therefore increased risk. Although women have a higher risk of osteoporosis, a significant number of men also have been diagnosed. Osteoporosis occurs in two forms: primary, including postmenopausal, senile, or idiopathic osteoporosis, and secondary, affecting men and women, following a specific primary disorder such as Cushing’s syndrome. - Is a common metabolic bone disorder characterized by a decrease in bone mass and density, combined with loss of bone matric and mineralization - USUALLY involved the hip - Regular bone mass density test is recommended in 50 year or older - Two forms 1. Primary- postmenopausal, senile, or idiopathic osteoporosis 2. Secondary- affecting men and women, following a specific primary disorder such as Cushing syndrome Patho: - During the continuous bone remodeling process, bone reabsorption exceeds done formation, leading to thin fragile bones that are subject to spontaneous fractures 15 ischemia causes irreversible nerve cell damage. A central area of necrosis develops, surrounded by an area of inflammation and function in this area is lost immediately. The tissue liquefies leaving a cavity in the brain. - The development and effects of a stroke vary with the cause. There are three common categories: Thrombus, Embolus, Hemorrhage Thrombus Embolus Hemorrhage Predisposing condition Atherosclerosis in cerebral artery Artherosclerosis or systemic source Hypertension- arteriosclerosis Onset Gradual- may be preceded by transient ischemic attacks Often occurs often at rest Sudden Sudden often occurs with activity Increased ICP Minimal Minimal Present; often high Effects Localized- may be less permanent damage if collateral circulation has been established Localized unless multiple emboli are present Widespread and severe- often fatal Etiology: Include diabetes, hypertension, systemic lupus erythematosus, elevated cholesterol levels, hyperlipdidemia, artherosclerosis, a history of TIA’s, increasing age, obstructive sleep apnea, and heart disease. The combination of oral contraceptives and cigirrate smoking has been well documented as a causative factor. Signs & Symptoms: FAST.. Face, arm, speech, time Patho: - A stoke is an infarction of brain tissue that results from lack of blood - Tissue necrosis may be an outcome - A central area of necrosis develops, surrounded by an area of inflammation, and function in this area is lost immediately - Caused by HTN, aneurysms, tumors, trauma - Mass of blood compresses and displaces tissue - Edema, Ischemia - Blood eventually will be reabsorbed Risk factors for stroke: 1. Diabetes 2. Hypertension 3. Systemic Lupus E. 4. Elevated cholesterol 5. Hyperlipidemia 6. Atherosclerosis 7. Smoking Signs and Symptoms F - FACE A- ARM S- SPEECH 16 T- Time to call 911 Traumatic Brain Injury Brain injures may involve skull fractures, hemorrhage and edema, or direct injury to brain tissue. An injury could be mild, causing only bruising of the tissue or it can be severe-life threatening, causing a destruction of brain tissue and massive swelling of the brain. The skull protects the brain but can also destroy it by means of bone fragments that penetrate or compress the brain tissue and by its inability to expand to relieve pressure. Types: -Various terms are used to classify and describe brain trauma, in some cases overlap as follows: • Concussion, mild traumatic brain injury- a reversible interference with brain function usually resulting from a mild blow to the head, which causes sudden excessive movement of the brain, disrupting neuroogic function and leading to loss of conciousness. Amnesia (memory loss) and headaches may follow a concussion but recovery with no permanent damage usually occurs within 24 hours. If concussions are recurrent it could lead to potential and progressive permanent brain damage • Contusion: bruising of brain tissue with rupture of small blood vessels and edema that usually results from a blunt blow to the head. The possibility of residual damage depends on the force of the blow and the degree of tissue injury. • Closed: head injury occurs when the skull isn’t fractured in the injury, but the brain tissue is injured and blood vessels may be ruptured by the force exerted against the skull. Extensive damage may occur when the head is rotated with considerable force. • Open: head injuries are those involving fractures or penetration of the brain by missiles or sharp objects. Signs and symptoms of head injuries: 1) Seizures 2) Cranial nerve impairment 3) Otorrhea or rhinorrhea 4) Otorrhagia- blood leaking from ear 5) Fever 6) Stress ulcers Hematomas-epidural/subdural/subarachnoid Second brain damage is caused by the development of additional injurious factors. A hematoma is a collection of blood in the tissue that develops from ruptured blood vessels, either immediately after the injury or after some delay. Hematoma can develop after surgery, they are classified by their location in relation to the meninges as follows: • Epidural hematoma: results from bleeding between the dura and the skull, usually caused by tearing of the middle meningeal artery in the temporal region. Signs of trouble usually arise within a few hours of injury, when the person loses consciousness after a brief period of responsiveness. • Subdural hematoma: develops between the dura and the arachnoid. Frequently there is a small tear in a vein, which causes blood to accumulate slowly. A hematoma may be acute or subacute. A chronic subdural hematoma may occur in elderly person, in whom brain atrophy allows more space for a hematoma to develop. Also, a tear in the arachnoid can allow CSF to leak into the subdural space, creating additional pressure. 17 • Subarachnoid hemorrhage occurs in the space between the arachnoid and pia is associated with traumatic bleeding from the blood vessels at the base of the brain. Because blood mixes with circulating CSF, a localized hematoma cannot form. • Intracerebral hematoma: results from contusions or shearing injuries and may develop several days after injury. Concussion Injuries are caused by: o Shaking (shaken baby syndrome) o Rotational and twisting motions o Acceleration and deceleration (whiplash) manifestations of each category have varying degrees of neurological dysfunction, such as loss of consciousness, headache, amnesia, mood changes, and sometimes permanent disabilities seen with the more severe injuries Skull Fractures • Compound fractures involve trauma in which the brain tissue is exposed to the environment and is likely to be severely damaged because bone fragments may penetrate the tissue the risk of infection is high • Depressed skull fractures involve displacement of piece of bone below the level of skull, thereby compressing the brain tissue • Linear fractures: are simple cracks in the bone • Comminuted: fractures consist of several fracture lines but may not be complicated • Compound fractures involve trauma in which the brain tissue is exposed to the environment and is likely to be severely damaged because bone fragments may penetrate the tissue and risk of infection is high. • Depressed skull fractures involve displacement of a piece of bone below the level of the skull, therby compressing the brain tissue. With this type of fracture, the blood supply to the area is often impaired, and considerable pressure is exerted on the brain. • Basilar fractures occur at the base of the skull and are often accompanied by leaking of the CSF through the ears or nose. These fractures may occue when the forehead hits a car windshield with considerable force. Cranial nerve damage and dark discoloration around the eyes are common • Contrecoup injury occurs when an area of the brain contralateral to the site of direct damage is injured as the brain bounces off the skull. This injury may be secondary to acceleration or deceleration injuries, in which the skull and brain hit a solid object, which causes the brain to rebound against the opposite side of the skull. Increased Intracranial Pressure • When the skull contains brain tissue, blood, and CSF, Q When ICP increases, the body initially attempts to compensate by shifting more CSF to the spinal cavity Q FIRST SYMPTOM- Decreased level of consciousness. % General symptoms: Q - Severe headache occurs from stretching of the dura and blood vessels Q - Vomiting often projectile vomiting that is not associated with food intake, is the result of pressure 20 Signs and Symptoms: Muscle weakness, fatigue develops quick, diplopia and ptosis impair vision, speech becomes nasal monotone. Face appears droopy, chewing and swallowing difficult. The head droops, arms become weaker, muscle fatigue, upper respiratory functions are more frequent. Treatment: anticholinesterase agents Huntington’s Disease - Is an inherited disorder that does not manifest until midlife Patho: - Progressive atrophy of the brain occurs, with degeneration of neurons, particularly in the basal ganglia and the frontal cortex - The ventricles are dilated - There is a depletion of gamma- aminobutyric acid an inhibit neurotransmitter in the basal nuclei - Levels ACH in the brain also appear to be reduced Etiology: - Condition is inherited as an autosomal dominant trait and is carried on chromosome 4 - No diagnostic test available to identify affected individual before the onset of symptoms Signs and Symptoms: - At the onset mood swings, and personality changes develop as well as restlessness - May also be early indication of intellectual impairment, such as difficulty learning intellectual impairments such as difficultly learning new information - Loss of problem solving skills - Poor judgment - Personality changes Spinal Cord Injury Most commonly occurs due to vertebral injuries, resulting from: • Hyperextension: neck, with possible fracture. Usually damage to the disc and ligaments occurs, leading to disclocation, loss of alignment of the vertebrae, and compression or stretching of the spinal cord. • Dislocated vertebrae: may crush or compress the spinal cord and compromise the blood supply • Compression: cause injury to the spinal cord when great force is applied to the top of the skull or to the feet and is transmitted up or down on the spine. Diving into an empty pool, jumping from a height and landing on feet, or an object falling on standing persons head are examples of how this can happen. The shattered bone is compressed and protrudes, exerting pressure horizontally against the cord. The sharp edges of bone fragments may lacerate or tear nerve fibers and blood vessels. • Penetrating injuries: ex. Stab or bullet injuries -Because spinal cord injuries are often unstable, immediate appropriate immobilization is essential to prevent secondary damage. -Most common locations: cervical (1,2, 4-7) and T1-L2 lumbar vertebrae -Hemorrhage and edema form -Injured axons are removed 21 -Within 3-4 weeks, the injured area will be replaced by fibrous tissue -Spinal Shock • Normal activity of the spinal cord ceases at and below the level of injury; sites lack continuous nervous discharges from the brain • Complete loss of reflex function • Resolves with the reappearance of reflex activity Treatment: • A=complete: no motor or sensory function is preserved in the sacral segments S4-S5. • B=incomplete: sensory but not motor function is preserved below the neurologic level and includes sacral segments S4-S5. • C=incomplete: motor function is preserved below the neurologic level, and more than half of key muscles below the neurologic level have a muscle grade less than 3. • D=Incomplete: motor function is preserved below the neurologic level and at least half of key muscles below the neurologic level have a muscle grade of 3 or more. • E= Normal: Motor and sensory function are normal. Treatment and rehabilitation begin at the time of the injury. Care must be taken to immobilize the spine, maintain breathing, and prevent sock. Surgery may be required and ongoing care is needed. Seizures Uncontrolled, excessive discharge of neurons in the brain. The activity may be localized or generalized. There are many possible causes. The disorders are characterized by recurrent seizures, also called convulsions. -Epilepsy is the old term for recurrent seizures. - Seizure disorders are classified by their location in the brain and their clinical features, including characteristic EEG patterns during and between seizures. Classification of seizures: I. Partial seizures (focal) a. Simple 1. Motor 2. Sensory 3. Autonomic 4. Psychic b. Complex (impaired consciousness) 1. Temporal lobe or psychomotor c. Partial leading to generalized seizures II. Generalized (both hemispheres affected with loss of conciousness) a. Tonic-clonic b. Absence c. Myoclonic d. Infantile Spasms e. Atonic f. Lennox-Gastaut syndrome III. Unclassified 22 Seizures may be primary (idiopathic) or secondary (acquired) with an identified cause, such as post traumatic syndrome. Pathopysiology: results from sudden, spontaneous, uncontrolled depolarization of neurons, which cause abnormal motor or sensory activity and possibly loss of conciousness. Any physiologic change can trigger a seizure ex. Flashing lights. Seizures can last for minutes or seconds. Etiology: Many seizure disorder are idiopathic. Children with congenital disorders, such as cerebral palsy, may have seizures resulting from the brain damage. A seizure can be initiated by a tumor, hemmrhoge, high fever in an infant or young child (febrile seizure). Some systemic disorders such as renal failure, or hypoglycemia, may precipitate a seizure in an individual who has no previous history of seizures. Sudden withdrawal from sedatives or alcohol can preicipate seizures as well as cocaine. Precipitating factors, or triggers can include, physical stimuli, such as loud noises or bright lights, or biochemical stimuli, such as stress, excessive premenstrual fluid retention, hypoglycemia, change in medication, or hyperventilation. Awareness and avoidance of the potential precipitating factors in an individual can reduce the frequency of seizures. Signs and symptoms: Generalized seizures: Absence seizure- more common in children, last for about 5-10 seconds and can occur many times during the day. There is a brief loss of awareness, usually child stares into space and then resumes activity. No memory of episode is retained. Tonic-clonic seizures are a type of generalized seizure that may occur spontaneously or after simple seizures. There is a pattern for this type which usually ends spontaneously. • Prodromal signs occur- nausea, irritability, depression, muscle twitching some hours before seizure • Aura- peculiar visual or auditory sensation, immediately precedes loss of conciousness. • Person falls to floor, loss of conscious • Strong tonic muscle contraction, resulting briefly in flexion is followed by extension of the limbs and rigidity in the trunk. • Air is forced out of lungs, jaw is clenched tight and respirations cease. • Clonic stage follows, in which muscles alternately contract and relax, resulting in series of forcefully jerky movements that involve the entire body. Increased saliva (foaming at mouth), bowl and bladder incontinence can occur. • Contractions subside, body is limp, conciousness slowly returns • Person is confused and fatigue with aching muscles, usually falls into a deep sleep=postictal period. Hypoxia can be current at the wake up stage of seizure. Partial seizure: manifested by repeated motor activity such as, jerking or turning the head or eye aside, jerky movements of lef, or by a ssensation such as tingling that begins in one area and may spread. Auditory or visual experiences may occur. Memory and conciousness remain, although awareness is reduced. A jacksonian seizure is a focal motor seizure in which the clonic contractions begin in a specific area and spread progressively. Diagnostic test: medical history, description of seizure, EEG will determine the type and location of seizure, an MRI can detect any structural abnormality in brain. . Treatment: Anticonvulsant drugs Meningitis/Encephalitis • Meningitis 25 • Virchow-s triad 1. Venous Stasis 2. Hypercoagulability 3. Blood vessel damage they are increase chances of a deep vein thrombosis Where do DVT originate?? Femoral Veins or legs Pneumonia • Initially when a person is immobilized, there is less demand for oxygen because of metabolism is decreased, could be an infection that is increasing the resting rate of metabolism • A patient is supine in bed, deep breathing and coughing become more difficult because chest expansion is restricted by the body weight and the upward pressure of the abdominal contents • When a person is immobilized, secretions build up in the airway and are difficult to remove because the cough mechanism is less effective • Hypostatic pneumonia- the obstruction of the airway and collapse of the lung (atelectasis) • Pneumonia and atelectasis may result from aspiration of food or water intake, which occurs more easily when the patient is immobilized or in a supine position • Respiratory therapy includes breathing exercise may be helpful Atelectasis • Pneumonia and atelectasis may result from aspiration of food or water intake, which occurs more easily when the patient is immobilized or in a supine position Constipation Digestive System Effects: • Major problems associated with immobility and the gastro tract is constipation!! • Elimination if affected by the slower passage of feces through the intestine due to muscle inactivity and body position which results in harder stool ] • Patients who are ill, have reduced food, fiber and fluid intake in their body • When a person is inactive appetite is often reduced leading to decreased dietary intake which results in negative nitrogen balance (protein deficit) • The lack of protein imbalances contributes to a low hemoglobin level and delays in healing!! • In some cases, immobility can lead to obesity Kidney Stones Caused by immobility Bladder Infection Caused by immobility Nerve Damage • Continuous pressure on skin and underlying tissue will stimulate receptors • Spasms may occur because of nerve damage, muscle innervation may have issues 26 • Effects of pain may lack of control over the environment Delayed Growth in Children • Normal growth often delayed • Contractures and loss of muscle may tone away and affect: hip, spine, hands and feet, • Mobility does return! Catch up on growth! • Depending on the underlying condition, deformities may develop in the hips, spine, hands, and feet • Other development delays are common when sensory and experimental stimulations are decreased Environmental Factors Results of Heavy Metal Damage- Lead and mercury are examples of heavy metals -Hemolytic anemia, inflammation and/or ulceration of digestive treact, inflammation of the kidney tubules, damage to the nervous system Acid/Base Injury Acid and bases can cause corrosive damage to living tissue which is classified as a chemical burn. The classification of the type of chemical burn follows the same standard system as thermal burns. Acids and bases can be found in numerous household products as well as in labs and manufacturing facilities. In addition to acids and bases, strong oxidizers, reducing agents and solvents can also cause chemical burns. Treatment will depend on the specific chemical causing the burn. In general, first aid involves rinsing off the chemical with water or a neutralizing solution. In some cases, involving lipophilic chemicals such as hydrofluoric acid, the burn symptoms may not be immediately obvious but may appear hours later. Inhalants - Inhalants can be classified as particular (such as asbestos and silica, or gaseous, such as sulfur dioxide and ozone; or they may arise from solvents, such as carbon tetrachloride - Sources of toxic inhalants include factories, laboratories, mines, spectacles, and aerosols, paints, glues, act - Cigarette smoking predisposes the smoker to lung disease, including emphysema, bronchitis, and lung cancer, and also to bladder cancer, peptic ulcer, and cardiovascular disease Chemical Types and damage Damaging the cell membrane eventually causing cell lysis, alteration, or interference in cellular metabolic pathways, causing cellular mutation that could lead to cancer. Abestos Still found in older building, where it was used for insulation. Exposure of the lungs to asbestos can cause a severe acute inflammation and subsequent scarring, which could lead to chronic problems such as mesothelioma, Malignant mesothelioma is a rare form of lung cancer that develops in the mesothelium and is often caused by exposure to asbestos. Other asbestos related diseases include asbestosis, pleural plaques, and pleural thickening. Chronic asbestos related diseases often take a long time to manifest which leads to delated diagnosis and poor prognosis for recovery. 27 Pesticides A grouping of diseases and complications that can be caused by some type of exposure to pesticides. Depending upon the type of pesticide and amount of exposure these chemicals can cause a variety of both acute and chronic adverse health effects. Because their organs and body systems are still in process of developing infants and small children are especially sensitive to health risks that can arise due to exposure. Signs of acute exposure problems include diarrhea, nausea, vomiting, pinpoint pupils, rashes, headaches, irritation of the eyes, skin or throat. Chronic exposure can, with some chemicals, lead to aggravation of asthma problems, cause damage to the immune system, as well as increase the risk of certain cancers and birth defects. Treatment for a pesticide illness will usually depend on the specific chemicals involved. Hyperthermia An excessive elevation of body temperature. Syndromes associated with it are heat cramps, heat exhaustion, and heat stroke Hypothermia Usually involves fingers, toes, ears, or exposed parts of the face and can result in necrosis/gangrene. Systemic hypothermia usually involves many body tissues over a wide area and can result in tissue necrosis as well as hypovolemic shock Radiation -Body cells that are primarily affect: cells undergoing rapid mitosis such as epithelial tissue, bone marrow, and gonads Ionizing Radiation: arises from natural sources such as the sun and radioactive minerals in the soil, is an ongoing hazard. It includes x-rays and gamma rays as well as particles such as protons and neutrons. These rays and particles differ both in energy levels and their ability to penetrate body tissue, clothing, or lead. Light Energy Exposure to both visible light and UV rays can cause damage to skin and eyes. Cumulative damage is manifested by the development of skin cancers resulting from UV rays related to skin exposure , as seen frequently in older individuals. The UV damages the nucleotides in the cell’s DNA. Reducing exposure and routine use of skin lotions that block damaging ultraviolet rays, both UVA & UVB, is recommended to reduce the risk of skin cancer. Exposure of the eyes to strong UV radiation can also cause permanent damage depending on specific wavelength involved. The shorter wavelengths can cause corneal cell damage, UVA and B can cause lens damage, and the longer wave lengths have been implicated in muscular degeneration and reinal tissue damage. Visible laser light can also cause severe damage to the eyes. Two types of eye damage that can be caused by a laser beam are tissue thermal burns, affecting structures such as the cornea, and photochemical damage to the retina. Powerful lasers can also cause thermal damage. Noise Hazards Hearing impairment may result from excessive noise, for example, a single loud noise such as gunshot or a variety noise intensities can cause cumulative damage. A sudden, extremely loud noise may rupture the tympanic membranes or damage the nerve cells in the inner ear. Inner ear damage involving the nerves is usually irreversible. Cumulative damage caused by noise may result directly from noise in the workplace but is often associated with higher noise levels in urban areas and recreational sources such as rock music. Ear protection is now required in most noisy work environments. Because only soft or high-pitched sounds are lost initially, the effects of such trauma are often gradual and go unnoticed until they are well advanced. In some