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NR 283 Final Exam Concept Review / NR283 Pathophysiology Final Exam Study Guide (Latest):, Exams of Public Health

NR 283 Final Exam Concept Review / NR283 Pathophysiology Final Exam Study Guide (Latest): Pathophysiology: Chamberlain NR 283 Pathophysiology Final Exam Concept Review Skull Fractures Increased Intracranial Pressure- The cranium is a closed box, whatever is in there (brain, blood, CSF), is all that it can hold. If you increase the amount of something in the skull, the volume of the other content has to decrease There are 4 stages of increased ICP that are seen: • Stage 1 o The blood vessels will compensate by constricting to decrease the volume in the brain o The ICP does not increase at this point and there are no manifestations • Stage 2 o Expansion of the contents in the cranium start to occur o This will cause the ICP to start to rise because there is no more extra room left in the brain o CM will be subtle and transient: changes in LOC: confusion or drowsiness • Stage 3 o The ICP is continuing to increase o Brain tissue will start to become hypoxic and the patient w

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NR 283 Final Exam Concept Review / NR283 Pathophysiology Final Exam Study Guide (Latest): Pathophysiology: Chamberlain

NR 283 Pathophysiology

Final Exam Concept Review

Skull Fractures

Increased Intracranial Pressure- The cranium is a closed box, whatever is in there (brain, blood, CSF), is all that it can hold. If you increase the amount of something in the skull, the volume of the other content has to decrease

There are 4 stages of increased ICP that are seen:

  • Stage 1

o The blood vessels will compensate by constricting to decrease the volume in the brain o The ICP does not increase at this point and there are no manifestations

  • Stage 2

o Expansion of the contents in the cranium start to occur

o This will cause the ICP to start to rise because there is no more extra room left in the brain

o CM will be subtle and transient: changes in LOC: confusion or drowsiness

  • Stage 3

o The ICP is continuing to increase

o Brain tissue will start to become hypoxic and the patient will start to deteriorate o CM: Decreased levels of arousal, bradycardia, pupil changes, hyperventilation

  • Stage 4

o Because of the high ICP, the brain tissue will start to shift or herniate to a compartment that has lower pressure

o The part of the brain that herniates impairs blood supply to that area and can cause areas of hemorrhage

o There are different types of herniation depending on where the brain tissue goes o Some places of herniation are not reversible

Parkinson’s Disease - is a common movement disorder

  • It typically begins after the age of 40
  • The cause is unknown, but it may be caused by a combination of genetics and environmental factors
  • The basal ganglia deteriorates and there is a loss of the neurons that produce dopamine
  • This results in a loss of dopamine which causes excessive excitatory activity which gets manifested as the CM of parkinsonism
  • Secondary parkinsonism o Presence of parkinsonism manifestations, but with a different cause

o Typically caused by head injuries, infection, toxins, and medications (most common) Classic CM of Parkinson:

o Resting tremors

Pill rolling tremor o Rigidity or muscle stiffness o Bradykinesia/Akinesia’s

Leading to gait and movement problems o Dysarthria

Impaired speech o Dysphagia

Impaired swallowing o Drooling

Depression is also a major CM

MS-( Multiple Sclerosis) 3 specific Neurological disorders

  • The first is Multiple Sclerosis, which is a common acquired autoimmune inflammatory disorder involving the destruction of axonal myelin in the brain and spinal cord

It is more common in females and the average age of onset is 20-

  • MS involves an autoimmune process that develops after an individual has had a viral infection that affected the nervous system
  • Because of the inflammatory process, the axons of the neurons get inflamed and demyelination of the axons occurs
  • Scar tissue is also formed over the damaged axon which will interfere with the conduction of nerve impulses
  • Neurons will eventual die and brain atrophy will occur
  • As more and more neurons are affected, the person will have to deal with a progressive interference with functions that are controlled by the nervous system, which can be just about anything depending on which part of the brain is affected
  • CM: May be unpredictable, transient, or last for hours to weeks o 2 initial symptoms:

Vision problems

Sensory impairm ent (paresthesia’s) o Other CM include: Dysphagia, muscle weakness, communication difficulty, fatigue, paralysis, incontinence, tremors, slurred speech. ALS- Amyotrophic lateral sclerosis

  • Also known as Lou Gehrig’s Disease

It diffusely affects the upper and lower motor neurons of the brain and spinal cord

  • The exact cause is unknown
  • Thoughts are that it may be due to:

o Genetics o A virus

o Deficiency of nutrients supplied to the neurons o An autoimmune disorder

The pathological feature of ALS is that the motor neurons in the body get destroyed, and the other non-motor neurons start to degenerate as well

  • As the neurons die, the muscle fibers that they supply become atrophied
  • This will lead to progressive muscle weakness, eventually causing respiratory failure because of the weakness of respiratory muscle, and eventual death
  • The initial symptoms are related to which motor neurons are affected

CM:

o The hallmark sign of ALS is muscle weakness

o The muscles may develop twitching or spasms as well and eventual atrophy o Difficulty speaking and swallowing. Depression is huge

MG- (Myasthenia Gravis) The last disease is Myasthenia Gravis which is an acquired autoimmune disease that affects the transmission of nerve impulses between the motor neuron and its innervated muscle cells

  • The cause is unknown
  • But it is commonly associated with other autoimmune disorders or problems with the thymus gland ( a gland located near the sternum that plays a big role in the immune response)
  • What happens is that acetylcholine receptors are no longer recognized as “self” (hence the autoimmune problem) and autoantibodies are produced against these receptors
  • The autoantibodies bind to the receptor and block the binding of acetylcholine
  • Eventually the receptor sites are destroyed
  • This will lead to a decrease in the transmission of nerve impulses and a lack of muscle depolarization
  • CM: muscle fatigue and weakness that is progressive o Difficulty speaking, chewing, and swallowing
  • In myasthenia gravis, there are 2 crisis states that can occur. We are only going to focus on one:

Myasthenic crisis:

o Occurs when severe muscle weakness causes extreme paresis/paralysis, respiratory insufficiency and difficulty swallowing

o This patient is in danger of going into respiratory distress

Huntington’s Disease - is a rare hereditary autosomal disorder of the basal ganglia (which controls our movement along with the frontal lobe)

It is also known as chorea which is the main CM seen with Huntington

There is severe degeneration of the basal ganglia and development of protein tangles that contribute to the loss of neurons

This leads to alterations of motor and mental functioning

CM:

o Progress slowly o Chorea

Irregular, uncontrolled excessive movements

Begins in arms and face o Athetosis

Writhing movements o Ballism

Flinging movements

Review A&P of the brain and cranial nerves

Spinal Cord Injury- Spinal cord trauma most commonly occurs due to injuries that result from:

o Acceleration, deceleration, or deformation forces that are applied to the spinal cord

  • These forces compress the tissues, pull on the tissues, or shear tissues so that they slide against one another
  • Damage may be to not only the spinal cord, but to the bones, the ligaments, and the joints as well
  • The leading cause of spinal cord trauma is due to motor vehicle accidents, but they can also be caused by falls, sports, and violence
  • The most common place on the cord for injuries to occur is:

o C 1, 2, 4-7 o T1-L

o Because these are the most movable parts of the vertebra

  • When the injury occurs, hemorrhage and swelling will occur at the site
  • Cord swelling increases the degree of dysfunction o This is especially life-threatening in the cervical region because it may affect the working of the diaphragm and the brain stem
  • Within 24-48 hours after the injury, the hemorrhage will start to become reabsorbed

Any axons that were damaged in the area will be removed

Within 3-4 weeks of the injury, the part of the cord that was injured will be replaced with fibrous tissue and the meninges may thicken as well

Spinal shock is the loss of normal body activity below the level of the spinal cord injury This involves a complete loss of all normal reflex functions, such as:

o Skeletal muscle function o Bladder and bowel function o Sexual function o Temperature control

  • Spinal shock typically lasts 7-20 days, but can last up to 3 months
  • It stops when reflex activity has reappeared
  • The specific CM of spinal cord injury really depend on what level the injury is at One complication of spinal cord injury is something called autonomic dysreflexia
  • This is a massive cardiovascular response to stimulation of the SNS
  • It involves sensory stimulation of the body, below the level of spinal cord injury o Most commonly seen with bladder or bowel distension
  • Some type of sensory stimulation occurs below the level of injury
  • The stimulus travels up the cord until it reaches the area of injury and it gets blocked
  • Because the impulse cannot reach the brain, the SNS is activated causing constriction of the blood vessels and HTN
  • The brain will sense the HTN, and will attempt to send messages via motor neurons to the heart and the vessels to dilate to decrease the BP
  • Unfortunately because the motor neuron impulse cannot pass the area of injury of the spinal cord, HTN remains and leads to problems with regulation of BP

CM:

o Extremely high BP o Pounding headache o Blurred vision o Sweating o Skin flushing

Seizures- A seizure is a syndrome that results from a sudden, explosive discharge of neurons

And is characterized by a sudden, transient alteration in brain function

A convulsion is a term that is sometimes applied to seizures o it usually refers to the tonic-clonic movements that are seen with some seizures Seizures can be caused by a number of things:

o Brain lesions or trauma o Biochemical disorders

o Sometimes seizures can be caused by stress, fatigue, stress, drugs, loud noises, or flashing lights

  • Epilepsy is a condition in which there is continuous seizure activity without a known cause

(everything has been ruled out but they are still having seizures)

  • Research has indicated that epilepsy may be due to an interaction between genetics and environmental factors
  • A specific group of neurons called epileptic neurons are responsible for the epileptic activity o They are hypersensitive and fire more frequently than normal

Seizures are classified in many ways: partial, complex, generalized, etc

Different phases of seizures- specifically those seen in the grand mal or tonic clonic seizures

  • Starting with the tonic phase of a seizure which is a state of continued muscle contraction due to the excessive excitation of the brain muscle
  • The clonic phase of a seizure is characterized by alternating muscle contraction and relaxation o This occurs when the neurons that inhibit activity start to work to stop the excess excitability to stop the seizure

o This will produce intermittent contractions or seizures that gradually decrease until it stops

o The post-ictal phase is the period of time immediately following the seizure

  • The specific CM of seizures will depend on the specific type
  • 2 common manifestations associated with the tonic clonic seizures:

o An Aura: a partial seizure that people will describe as a peculiar sensation or dizziness or numbness that occurs right before the seizure occurs

o A Prodroma: an early CM, such as malaise or a H/A, that occurs hours to days before the seizure

  • The most important manifestation associated with seizures is the increase in oxygen consumption o During a seizure your body is constantly contracting, so oxygen is quickly used and depleted

o Once oxygen has been depleted, your body will use glucose for energy which will cause your lactic acid levels to build-up

Finally, a continued seizure activity can cause brain injury and eventual irreversible damage if it does not stop

Meningitis- which is infection and inflammation of the meninges, CSF, and ventricles There are 3 types:

  • Bacterial o It is primarily caused by meningococcus or pneumococcus o The infection enters the CNS causing the inflammatory response

o In some cases the CSF will thicken leading to hydrocephalus and cerebral edema can occur leading to an increase in ICP o CM:

S/S of systemic infection: fever, tachycardia, and chills

S/S of Meningeal irritation: throbbing headache, photophobia, positive Kernig sign (when knee is bent, pain in head when leg is straightened), positive Brudzinski sign (involuntary lifting of legs when lifting up head)

Neurological signs: decreased LOC, hemiparesis, seizures

Aseptic meningitis or viral meningitis o Primarily caused by a virus

o CM are similar to bacterial but they are less severe o This form is self-limiting

  • Fungal meningitis o Chronic and less common form of meningitis o It will progress slowly o CM will mimic other neurological syndromes such as hydrocephalus or dementia

Encephalitis- Encephalitis is an acute, febrile illness that affects the nervous system leading to brain inflammation

It is most commonly caused by an arthropod or mosquito borne virus (like West Nile) and HSV

  • But it can also result from a complication of other viral disease
  • It involves all of the meninges of the brain and spinal cord
  • It can result in neuron damage, edema, hemorrhage, increased ICP, or necrosis

CM:

o Range from mild to life threatening

o The most dramatic ones are:

Fever

Delirium

Confusion progressing to unconsciousness

Seizures

Paralysis

***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- Syndrome of Inappropriate Diuretic Hormone antidiuretic hormone ) secretion leads to water intoxication and hyponatremia

Causes include trauma, stroke, malignancies (often in the lungs or pancreas), medications, and stress

S/S include signs of fluid volume overload, changes in level of consciousness and mental status changes, weight gain, hypertension, tachycardia, anorexia, nausea, vomiting, hyponatremia, concentrated urine, decreased urine output, serum osmolality decreased

Nursing considerations include monitoring vital signs and cardiac and neurological status, providing a safe environment, particularly for the patient with changes in level of consciousness or mental status, monitoring intake and output and weight daily; monitoring fluid and electrolyte balance, monitoring serum and urine osmolality; restriction of fluids

DI (Diabetes Insipidus)- Kidney tubules fail to reabsorb water

Etiology includes stroke or trauma or may be idiopathic

S/S include excretion of large amounts of dilute urine, polydipsia, dehydration (decreased skin turgor and dry mucous membranes), inability to concentrate urine, increased urine output, urine very dilute, Low urinary specific gravity, fatigue, muscle pain and weakness, headache, postural hypotension that may progress to vascular collapse without rehydration, tachycardia, hypernatremia

Nursing Considerations: monitor vital signs and neurological and cardiovascular status, provide a safe environment, particularly for the patient with postural hypotension; monitor electrolyte levels and for signs of dehydration; maintain patient intake of adequate fluids; monitor intake and ouput, weight, serum osmolality and specific gravity of urine; instruct the patient to avoid foods and/or liquids that produce diuresis

Hyperthyroidism- Too much thyroid hormone (T3 and T4) Characterized by an increased rate of body metabolism

Common cause is Graves’ disease, also known as toxic diffuse goiter

S/S include: personality changes such as irritability, agitation and mood swings, nervousness and fine tremors of the hands, heat intolerance, weight loss, smooth, soft skin and hair, palpitations, cardiac dysrhythmias such as tachycardia or atrial fibrillation, diarrhea, protruding eyeballs (exophthalmos) may be present, diaphoresis (sweating), hypertension, enlarged thyroid gland (goiter)

Too much ADH (

Nursing Considerations: Provide adequate rest, provide a cool and quiet environment, provide a highcalorie diet, obtain daily weight, avoid administration of stimulants, administer sedatives as prescribed, administer antithyroid medications, administer blood pressure medication for tachycardia, prepare for thyroidectomy if prescribed

Hypothyroidism- Hyposecretion of thyroid hormones (T3 and T4) Characterized by a decreased rate of body metabolism

Causes: autoimmune disease, treatment for hyperthyroidism, radiation therapy, thyroid surgery, certain medications

S/S: lethargy, fatigue, weakness, muscle aches, paresthesias, intolerance to cold, weight gain, dry skin and hair and loss of body hair, bradycardia, constipation, generalized puffiness and edema around the eyes and face (myxedema), forgetfulness and loss of memory, menstrual disturbances, cardiac enlargement, tendency to develop heart failure, goiter may or may not be present

Hyperparathyroidism- Hypersecretion of parathyroid hormone (PTH)

Causes: Tumor, Hyperplasia, Genetics; secondary causes-severe calcium or vitamin D deficiency, chronic kidney failure

S/S: Hypercalcemia and hypophosphatemia, fatigue and muscle weakness, skeletal pain and tenderness, bone deformities that result in pathological fractures, anorexia, nausea, vomiting, epigastric pain, weight loss, constipation, hypertension, cardiac dysrhythmias, renal stones

Nursing Considerations: Monitor vital signs, particularly blood pressure; monitor for cardiac dysrhythmias, monitor for intake and output and for signs of renal stones, monitor skeletal pain, move the patient slowly and carefully; encourage fluid intake, administer furosemide (Lasix) as prescribed to lower calcium levels, administer phosphates, which interfere with calcium reabsorption as prescribed, administer calcitonin as prescribed to decrease the skeletal calcium release and increase renal excretion of calcium, monitor calcium and phosphorus levels, prepare the patient for parathyroidectomy as prescribed

Hypoparathyroidism-Hyposecretion of parathyroid hormone (PTH)

Can occur following a thyroidectomy because of removal of parathyroid tissue

S/S: Hypocalcemia and hyperphosphatemia, numbness and tingling in the face, muscle cramps and cramps in the abdomen or extremities, positive Trousseau’s and Chvostek’s sign, signs of overt tetany such as bronchospasm, laryngospasm, carpopedal spasm, dysphagia, photophobia, cardiac dysrhythmias, seizures; hypotension, anxiety, irritability, depression

Nursing Considerations: Monitor vital signs, monitor for signs of hypocalcemia and tetany, initiate seizure precautions, place a tracheostomy set, oxygen and suctioning equipment at bedside, prepare to administer calcium gluconate intravenously for hypocalcemia, provide a high-calcium, low- phosphorus diet, instruct the patient on administration of calcium supplements as prescribed, instruct the patient on administration of vitamin D supplements as prescribed, vitamin D enhances the absorption of calcium from the GI tract, instruct the patient on administration of phosphate binders as

prescribed to promote the excretion of phosphate through the gastrointestinal tract, instruct to wear a Medic-Alert bracelet

Cushing’s Syndrome/Disease - is a metabolic disorder characterized by abnormally increased secretion

(endogenous) of cortisol, caused by increased amounts of ACTH secreted by the pituitary gland

Cushing’s syndrome is a metabolic disorder resulting from the chronic and excessive production of cortisol by the adrenal cortex or by the administration of glucocoritcoids in large doses for several weeks or longer (exogenous or iatrogenic)

S/S: generalized muscle wasting and weakness, moon face, buffalo hump, truncal obesity with thin extremities, supraclavicular fat pads, weight gain, hirsutism (masculine characteristics in females), hyperglycemia, hypernatremia, hypokalemia, hypocalcemia, hypertension, fragile skin that bruises easily, reddish-purple striae on the abdomen and upper thighs

Nursing Considerations: Monitor vital signs, particularly blood pressure, monitor intake and output and weight, monitor laboratory values, particularly the white blood cell count, and serum glucose, sodium, potassium, and calcium levels; provide meticulous skin care, allow the patient to discuss feelings related to body appearance, administer chemotherapeutic agents as prescribed for inoperable adrenal tumors; prepare the patient for radiation as prescribed if the condition results from a pituitary adenoma; prepare the patient for removal of pituitary tumor (hypophysectomy, transsphenoidal adrenectomy) if the condition results from increased pituitary secretion of ACTH, prepare the patient for adrenalectomy if the condition results from an adrenal adenoma; glucocorticoid replacement may be required following adrenalectomy

Addison’s Disease-Hyposecretion of adrenal cortex hormones (glucocorticoids and mineralcorticoids)

  • Can be primary or secondary
  • The condition is fatal if left untreated

S/S: Lethargy, fatigue and muscle weakness, gastrointestinal disturbances, weight loss, menstrual changes in women, impotence in men, hypoglycemia, hyponatremia, hyperkalemia, hypercalcemia, hypotension, hyperpigmentation of the skin (bronzed) with primary disease

Nursing Considerations: Monitor vital signs, particularly blood pressure, weight, and intake and output, monitor white blood cell (WBC) count; blood glucose, potassium, sodium, and calcium levels; administer glucocorticoid or mineralcorticoid medications as prescribed; observe for addisonian crisis caused by stress, infection, trauma, or surgery

Patient education: avoid individuals with an infection, diet: high protein and high carbohydrate, normal sodium intake, avoid strenuous exercise and stressful situations; need for lifelong glucocorticoid therapy; avoid over-the-counter medications, wear a medic-alert bracelet, signs and symptoms of complications such as underreplacement and overreplacement of hormones

Hyperaldosteronism- Hypersecretion of mineralcorticoids (aldosterone) from the adrenal cortex of the adrenal gland

Most commonly caused by an adenoma

S/S: Symptoms related to hypokalemia, hypernatremia, and hypertension; headache, fatigue, muscle weakness, nocturia, polydipsia, polyuria, paresthesias; visual changes; low urine specific gravity and increased urinary aldosterone level; elevated serum aldosterone levels

Nursing Considerations: Monitor vital signs, particulary blood pressure; monitor for signs of

hypokalemia and hypernatremia; monitor intake and output and urine for specific gravity; Spironolactone (Aldactone) may be prescribed to promote fluid balance and control hypertension; this is a potassiumsparing diuretic and aldosterone antagonist, and patients need to be monitored for hyperkalemia, particularly those with impaired renal function or excessive potassium intake; administer potassium supplements as prescribed; prepare the patient for adrenalectomy; maintain sodium restriction, as prescribed, preoperatively; administer glucocorticoids preoperatively, as prescribed, to prevent adrenal hypofunction; monitor the patient for adrenal insufficiency postoperatively; instruct the patient regarding the need for glucocorticoid therapy following adrenalectomy; instruct the patient about the need to wear a Medic-Alert bracelet

Pheochromocytoma-Catecholamine-producing tumor usually found in the adrenal medulla, but extra adrenal locations include the chest, bladder, abdomen, and brain; typically is benign tumor but can be malignant

Excessive epinephrine and norepinephrine secreted

S/S: paroxysmal or sustained hypertension, severe headaches, palpitations, flushing and profuse diaphoresis, pain in the chest or abdomen with nausea and vomiting, heat intolerance, weight loss, tremors

Complications: hypertensive crisis, hypertensive retinopathy and nephropathy, cardiac enlargement, dysrhythmias, heart failure, myocardial infarction, increased platelet aggregation, and stroke; death can occur from shock, stroke, renal failure, dysrhythmias, or dissecting aortic aneurysm

Nursing Considerations: Monitor vital signs particularly blood pressure and heart rate; monitor for hypertensive crisis; monitor for complications that can occur with hypertensive crisis, such as stroke, cardiac dysrhythmias, myocardial infarction; prepare to administer antihypertensive agents to control hypertension; monitor serum glucose level; promote rest and a nonstressful environment; provide diet high in calories, vitamins, and minerals; prepare for an adrenalectomy

It is important to avoid stimuli that can precipitate a hypertensive crisis, such as increased abdominal pressure and vigorous abdominal palpation

Diabetes Mellitus (DM)- A group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both

Normally, a certain amount of glucose circulates in the blood.

Major sources of glucose are absorption of ingested food in the GI tract and formation of glucose by the liver from food substances

Diabetes is especially prevalent in the elderly; as many as 50% of people older than 65 years of age has some degree of glucose intolerance. People 65 years and older account for almost 40% of people with diabetes.

Risk Factors

Family history

Obesity

Race/ethnicity- (African Americans, Hispanics, Native Americans, Asian Americans, Pacific Islanders)

Age- greater than or equal to 45 years old

Impaired fasting glucose or impaired glucose tolerance

Hypertension

HDL/Triglyceride level- HDL less than or equal to 35 and or triglyceride level greater than or equal to 250

History of gestational diabetes or delivery of babies over 9 lbs 7 tips for managing diabetes

Healthy eating

Being active

Monitoring

Taking medication

Problem solving

Healthy coping

Reducing risks Patho-

Insulin secreted by beta cells

Insulin levels increase after meals consumed

During fasting periods insulin and glucagon is released Liver produces glucose through

Glycogenolysis – the breakdown of glycogen to glucose which occurs in the liver & muscles

Glyconeogenesis- the making of glucagon

Prediabetes is classified as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) and refers to a condition in which blood glucose concentrations fall between normal levels and those considered diagnostic for diabetes

Type I Diabetes-(genetics/juvenile) Insulin producing beta cells in the pancreas are destroyed by an autoimmune process, genetic susceptibility, or environmental factors

Requires insulin, as little or no insulin is produced

Onset is acute and usually before 30 years of age

5 – 10% of persons with diabetes

People do not inherit type 1 diabetes itself but rather a genetic predisposition toward development of type 1 diabetes.

Autoimmune: abnormal response in which antibodies are directed against normal tissues of the body, responding to these tissues as if they are foreign

Environmental factors such as viruses and toxins that may initiate destruction of beta cells are being investigated

Destruction of beta cells results in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but instead remains in the bloodstream and contributes to postprandial (after meals) hyperglycemia.

Because insulin normally inhibits glycogenolysis and gluconeogenesis, these processes occur in an unrestrained fashion in people with insulin deficiency and contribute further to hyperglycemia. In addition, fat breakdown occurs, resulting in an increased production of ketone bodies, which are the by products of fat breakdown.

S/S- polyuria(increased urine), Polydipsia(increased thirst), polyphagia(increased hunger), weigth loss, fatigue, frequency of infections, rapid onset, insulin dependent, familial tendency, peak incidence from 10 to 15 yrs, glycosuria.

Type II diabetes- Insulin resistance refers to decreased tissue sensitivity to insulin. Normally insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism. In type 2 diabetes, these intracellular reactions are diminished making insulin less effective at stimulating glucose uptake by the tissues and at regulating glucose release by the liver

Despite the impaired insulin secretion, there is enough insulin present to prevent the breakdown of fat and the accompanying production of ketone bodies, therefore DKA(diabetic ketoacidosis) does not typically occur in type 2 diabetes, however uncontrolled type 2 diabetes may lead to hyperglycemic hyperosmolar nonketotic syndrome

Because type 2 diabetes is associated with a slow, progressive glucose intolerance, its onset may go undetected for many years.

More common in persons over age 30 and in the obese

Slow, progressive glucose intolerance

Treated initially with diet and exercise

Oral hypoglycemic agents and insulin may be used

CM- Polyuria, polydipsia, recurrent infections, visual changes, fatigue, low energy, skin infections, vaginal discomfort, HbAc high 6.5%, FBS high 126mg/dL, prediabetes FBS 100-125mg/dL, Metabolic Syndrome.

Endocrine Control for DM-

  • Insulin: lowers blood glucose by facilitating glucose transport across cell membranes of muscle, liver, and adipose tissue
  • Glucagon: Increases blood glucose concentration by stimulation of glycogenolysis and glyconeogenesis
  • Somatostatin: delays intestinal absorption of glucose
  • Glucocorticoids (mainly cortisol): affects metabolism of all nutrients, regulates blood glucose levels, affects growth, has anti-inflammatory action, and decreases effects of stress

Musculoskeletal

Sprains/Strains- A sprain is a tear or injury to a ligament

  • A strain is a tear or injury to a tendon
  • An avulsion is a complete separation of a tendon or ligament from its bony attachment site
  • Dislocation is the complete loss of contact between 2 bones in a joint
  • Subluxation is a partial loss of contact
  • They are typically associated with bone fractures, most commonly the fingers and shoulder
  • However they can also be associated with other musculoskeletal disorders that affect the stability of muscles, bones, or joints.

Fractures-A fracture is a break in the continuity of bone Fractures are classified in many ways:

  • A complete fracture is when the bone is broken entirely:

o Open – when the skin is broken and the bone pushes through

o Closed – when the bone does not push through the skin, the skin remains intact o Comminuted – the bone has been broken into 2 or more fragments o Linear – the bone has been broken at a parallel to the long axis of the bone o Oblique – the bone has been fractured at an angle to the long axis o Spiral – the bone has a fracture that encircles the entire bone o Transverse – the bone has a fracture perpendicular to the long axis o Impacted – the bone has been fractured and the 2 parts get pushed together o Pathologic – the bone has fractured at a part of bone that has been weakened by an

Neurological

Levels of consciousness/arousal- Full consciousness is a state of awareness of yourself and the environment and the responses to that environment

  • Consciousness involves both arousal and awareness:

o Arousal is a state of being awake and being able to respond to stimuli o Awareness is a state of being aware

  • Both are mediated by the reticular activating system in the brain stem, where all our vital reflexes are controlled.
  • When brain function from the cerebrum is lost, your RAS can maintain someone in a vegetative state

Alterations in arousal can be classified in 3 ways:

Structural causes:

o Include infection, brain tumors, trauma Metabolic causes:

o Hypoxia, electrolyte changes, hypoglycemia, medications or toxins Psychogenic causes: o Uncommon

o Sign of a psychiatric disorder

Locked-In syndrome- Cerebral death occurs when permanent brain damage has occurred and the person is unable to respond to any stimuli, BUT the brain stem is still functioning and is able to maintain internal homeostasis and keep the body functioning

People who have experienced cerebral death can have 1 of 4 final outcomes:

o They may remain in the coma for life o They may emerge into a persistent vegetative state:

The person is unaware, does not speak or follow commands But they may open their eyes and have a normal sleep cycle

If the person remains in a vegetative state for greater than 12 months, it is considered a permanent state

o They may progress into a minimal conscious state

They may be able to follow simple commands

Have simple speech, such as speaking yes and no

Have some spontaneous movements such as smiling o Or they may be in what’s called a locked-in syndrome

The body is fully conscious, but there is complete paralysis of the muscles

The only thing they are capable of is eye movement

Cerebral vascular accident-They are the leading cause of disability and the third leading cause of death in the US

Three commonly seen risk factors for a CVA include: HTN, DM, and smoking CVA’s can be classified in different ways:

Hemorrhagic Stroke:

  • It is typically caused by chronic HTN problems, but can also be caused by ruptured aneurysms, bleeding tumors, or bleeding from a head trauma
  • The hemorrhage can be tiny or massive
  • As bleeding continues into the brain tissue, a mass of blood is formed
  • Brain tissue that is next to the bleeding area can become deformed, compressed, or displaced
  • This will produce edema, increased ICP, and ischemia of brain tissue
  • The hemorrhage will eventually resolve through reabsorption, and will leave a cavity in the brain where it was
  • CM: vary depending on what part of the brain is affected A thrombotic CVA:
  • An occlusion of one of the arteries of the brain
  • Most commonly this is caused by atherosclerosis
  • The CVA occurs when parts of the clot detach, travel upstream, and obstruct blood flow causing ischemia

An embolic CVA:

  • This is caused by a piece of plaque that has broken off of a clot that is elsewhere in the body, beyond the brain
  • People who have embolic CVA’s are at a higher risk for developing more because the cause is still there (such as atherosclerosis of the heart)

A TIA

  • Is a brief episode of neurologic dysfunction due to platelet clumps or a partial obstruction
  • People who have TIA’s are at a higher risk for developing a CVA

Traumatic Brain Injury-A major head trauma is a traumatic insult to the brain that is capable of producing many changes to an individual, including physical, emotional, social, and intellectual Major head traumas can be caused by car accidents, falls, sports injuries, or violence There are 2 main types of head trauma’s:

o Closed

When the head strikes a hard surface (wall) or an object hits the head (baseball), and the skull and meninges remain intact

These are the most common

o Open

Commonly caused by severe accidents or bullets

The skull is broken and the brain gets exposed to the environment Brain damage from trauma can be categorized as:

o Focal: affecting one area of the brain o Diffuse: affecting more than one area of the brain

Hematomas-epidural/subdural/subarachnoid

Extradural/Epidural hematoma/hemorrhage

o Usually the result of a skull fracture that has tore an artery!!!! (Arterial bleed!, not venous)

o Because arteries have a higher amount of pressure than veins do, the blood will accumulate quickly in the epidural space

o The individual will lose consciousness at the time of the injury, but regain it for a period of time

o This type of hematoma can be very deceiving, because the patient will feel okay, but the bleed is still occurring and is starting to accumulate

o Eventually when the bleed grows big enough, the person will develop a worsening headache, vomiting, confusion, and seizures

o Soon the brain will herniate, LOC will be lost, and the person may die o Epidural hematomas are considered medical emergencies

Intracerebral hematomas Bleeding in the brain

o Common in the frontal and temporal lobe

o It can cause increased ICP, Decreased LOC, pupil and respiratory changes

The third type of bleed caused by a focal injury is a subdural hematoma

It is bleeding between the dura and the brain, usually associated with a torn vein Subdural’s can be classified as:

Acute:

o Develop rapidly with CM of headache, and some type of neurological change

o CM will worsen over time and quickly progress to loss of consciousness, respiratory changes, and pupillary changes and brain herniation

Chronic

o Develop over weeks to months

o Typically seen in the elderly because their brain has atrophied, leaving more room for the bleeding

o Can be caused by what is considered a very insignificant head trauma o CM: Chronic headaches

Vague symptoms – patient can have symptoms that are sometimes mistaken for dementia

Based on the degree of the bleed, increased ICP and eventual herniation can occur

Subarachnoid hemorrhage (SAH) is the escape of blood from a defective or injured vessel into the subarachnoid space. Individuals at risk for a subarachnoid hemorrhage are those with intracranial aneurysm, intracranial arteriovenous malformation, hypertension, or a family history of SAH, and those who have sustained head injuries. Subarachnoid hemorrhages often recur, especially from a ruptured intracranial aneurysm.

CM- Early manifestations associated with leaking vessels are episodic and include headache, changes in mental status or level of consciousness, nausea or vomiting, and focal neurologic defects. A ruptured vessel causes a sudden, throbbing, “explosive” headache, accompanied by nausea and vomiting, visual disturbances, motor deficits, and loss of consciousness related to a dramatic rise in intracranial pressure. Concussion