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Pathology Exam 4
Endocrine:
Diabetes Mellitus:
This is defined as a lack of or inadequate secretions of insulin, or insulin resistance resulting in hyperglycemia. It is the most common chronic disorder of the endocrine system Pancreas (beta cells of inlets of Langerhans) fails to secrete an adequate amount of insulin (hormone responsible for glucose metabolism) Lack of adequate insulin secretion results in inappropriate hyperglycemia Obesity, especially when centralized in abdomen, may lead to insulin resistance The two types are:
Diabetes type I:
Insulin dependent due to destruction of the pancreatic cells. This means that no insulin is produced from beta cells of pancreas and that insulin MUST be received exogenous. Cause: Occurs as a result of genetic, environmental, or immunological factors that damage the pancreatic beta cells. Pathophysiology: Damage to the beta cells leads to uncontrolled production of glucose by the liver which results in hyperglycemia. Elevated glucose serum Renal threshold is 180-200 anything after that gets spilled into the urine. Since glucose is highly osmotic fluids follow it and get out of the body in large amounts of urine; the excessive amount of urine is known as POLYURIA Since there is an excessive loss of fluids this leads to POLYDIPSIA which is extremely thirsty. Since there is a lack of insulin the body is not allowed to use carbs as the source of energy but instead it uses proteins and fats for energy which this leads to a weight loss. The use of fat leads to ketones production which causes acidosis in the body. Failure to receive insulin leads to the continue of fat metabolism which produces ketones body that lead to acidosis.
The breakdown of nutritional stores leads to excessive hunger known as POLYPHAGIA DKA: Diabetic Ketoacidosis: ( Caused by lack of insulin & ketosis) Type 1 diabetes glucose 300- Results in severe metabolic, fluid and electrolyte disturbances and it is a life threatening condition of hyperglycemia and metabolic acidosis requiring immediate action. The cause of acidosis in diabetes type I is that you use fat metabolism which leads to the buildup of ketones and that leads to acidosis!! Symptoms of DKA: is the fruity breath odor Hyperglycemic-hyperosmolar state (HHS) – hyperglycemia – primarily type 2 but can be both (glucose is usually much higher 1000- Hypoglycemia – neuro problems, need sugar Metabolic Syndrome – combo of Co-morbidities: elevated triglycerides, elevated glucose, high BMI, High LDL – “ticking time bombs” can have sudden death
THE CLASSIC SIGNS FOR
DIABETES TYPE 1: ARE
POLYURIA,
POLYDIPSIA AND
POLYPHAGIA.
Signs and Symptoms:
Polyuria Polydipsia Polyphagia Glucosuria Fatigue Weight loss Nausea/ vomiting/ abdominal pain.
Lab values: Fasting normal blood glucose levels are 80- Below 80 is hypoglycemia 100-125 : prediabetic 126 and above: hyperglycemia HbA1C: glycosylated hemoglobin A1C to test for it. Normal: 3.9 – 6.9% Poor level: increased above 6-8% Serum glycosylated hemoglobin levels: increased (greater than 7%) Urine for glucose and ketones: positive Urine for protein: positive Serum K: decreased (hypokalemia) Education to client: Signs and symptoms of hypo(irritability, fatigue, weakness, tremors, headache, possible coma) and hyperglycemia Self-injection of insulin or oral hypoglycemic agent Self-monitoring of glucose Proper dietary management Teach proper diabetic wound care Teach sick day rules: Increase or maintain insulin Monitor glucose more often Q2-4H Maintain fluid intake Proper exercise Chronic complications: Nephropathy: This is the leading cause of chronic kidney disease; it is associated with the increased work demand and micro albuminuria imposed by poorly controlled blood glucose.
Retinopathy: Leading cause of blindness; closely linked to elevations in blood glucose and hyperlipidemia; seen in persons with uncontrolled diabetes. Neuropathies: Affects somatic and autonomic nervous system. Results from the demyelinating effect of long term uncontrolled diabetes. What causes a diabetic patient to develop ulcers in the extremities? Due to neuropathy they have decreased in peripheral sensation, that patient aren’t able to detect early warning signs for disease process.
1. Diff between type 1 & 2: Type 1: chronic autoimmune; lack of insulin prod. Genetic predisposition or environmental triggering event. Usually children and young adults Type 2: insulin resistance. Mostly people older and overweight.
Thyroid stimulating hormone: decreased Serum thyroxin: decreased Serum triiodothyronine: increased T3 uptake test: increased T3 and t4 elevated
Addison’s disease: (Adrenal insufficiency)
Chronic adrenocortical insufficiency as a result of destruction of the adrenal glands Autoimmune Destruction: o Disorder in which all the layers of adrenal cortex are destroyed. Results in a decreased production of cortisone and aldosterone (HYPOFUNCTION) Adrenal cortex hypofunction results in decreased production of cortisone and aldosterone Causes include destruction of adrenal gland because of trauma, infection, hemorrahage into gland, or sudden stress Causes include: pathophysiology Destruction of the adrenal gland because of trauma, an infection, hemorrhage into gland or sudden stress. This disease is aka Gradual destruction of adrenal cortical tissue leads to hypo function of adrenal glands Insufficient hormonal secretion of mineralocorticoids and glucocorticoids results in deficient aldosterone, cortisol, and androgens Insufficient levels of aldosterone lead to decreased NA+ absorption and increased NA+ excretion Hypotension occurs as a result of hypovolemia Hyperkalemia because K+ is retained Addisonian crisis can occur which is an acute insufficiency of adrenocortical hormone from a lack of cortisol during stress, such as surgery or pregnancy or when exogenous corticosteroid therapy is abruptly discontinued. Requires lifelong therapy of hormone replacement.
Adrenal hormones decrease and ATCH levels increase cause of lack of feedback inhibition Autoimmune destruction is the most common cause Glucogenesis in liver decreases resulting in hypoglycemia GFR decreases causing improper filtration and accumulation of toxins; kidneys can still produce urine, although they aren’t filtering it Decreased gastric acid secretion Decreased urea excretion & anorexia/wt loss HYPERKALEMIA, HYPONATREMIA (cause of decreased aldosterone), HYPOVOLEMIA K retention (more K+ in plasma) resulting in acidosis Signs and symptoms: Neurosis and depression Hypotension Muscle weakness Fatigue Skin hyperpigmentation Diarrhea Nausea Vomiting Weight loss. Hyperkalemia, hyponatremia, hypoglycemia, weight loss Diagnostic tests: Serum sodium: low (hyponatremia) Serum potassium: high (hyperkalemia) Serum cortisol: low Serum ACTH: high Serum aldosterone levels: decreased ABG: metabolic acidosis (decreased HCO3) MONITOR THE PATIENT FOR POTASSIUM AND HYPERKALEMIA!!!!
Cushings Disease :
Excess corticosteroids (hypercortisolism) Hypercholesterolism & hyperaldosteronism
Somatostatin analog to suppress ACTH Priority nursing diagnoses: excess fluid volume, risk for infection, risk for injury, activity intolerance, anxiety, deficient knowledge, risk for impaired skin integrity
MUSCULOSKELETAL
Osteoporosis : related to aging and decreased estrogen levels, an imbalance between bone reabsorption and
bone formation, bones are becoming brittle; bone is being broken down (reabsorption) Defined as a musculoskeletal disorder characterized by loss of bone mass Disease process predisposes clients to fractures Classifications: type 1: associated with early postmenopausal estrogen deficiency Type 2: senile osteoporosis associated with calcium deficiency Pathophysiology: An increase in osteoclast activity and a decrease in osteoblast activity lead to rate if bone resorption that exceeds rate of bone formation Outer cortex (outer surface of bone composed of hard, cortical bone) of diaphysis and metaphysic become thinner secondary to enlargement of bone Advanced disease process leads to loss of trabeculae (spongy bone containing red bone marrow located in metaphysic of long bones) from cancellous bone (spongy bone located towards interior of bone containing red or yellow bone marrow) and thinning of cortex; these changes increase risk for bone fracture. Signs and symptoms: Loss of height, kyphosis, low back pain, fractures of forearm, spine, and hip Calcium loss Risk for fractures For early prevention @ young age take calcium and any preventative measures such as: exercising
Rheumatoid Arthritis:
Chronic autoimmune systemic disease ; inflammatory process that affects connective tissue Characterized by chronic inflammation of bilateral joints and surrounding structures; multiple joints are usually involved. Unknown etiology but seems to be related to autoimmune processes in middle age Systemic complications: vasculitis, anemia, and extrasynovial rheumatoid nodules on heart, lungs, eyes, or spleen. Pathophysiology Exposure to a virus may initiate inflammatory response; immunoglobulin G is formed in response to antigen, but for an unknown reason, body produces autoantibodies against IgG Rheumatoid factors combine with IgG to form immune complexes Synovial membrane (located within joint capsule and responsible for producing synovial fluid to lubricate joint structures) hypertrophies and thicken secondary to chronic inflammation Signs and symptoms Initially may present with vague systemic symptoms such as anorexia, weight loss, fever, and loss of energy Inflammation Swelling Decreased movement of joints in hand, feet, wrists, and elbows As RA progresses joints of knees, hips, and cervical spine may be involved.
Joint deformities Swan neck deformity: hyperextension of PIP joints with flexion of DIP joints Ulnar drift: joint deformity characteristics of RA; characterized by displacement of fingers laterally toward little finger of same hand Boutonniere deformity: flexion of PIP joint and hyperextension of DIP joint Osteoarthritis : “wear and tear” arthritis, overuse of joints Defined as a form of arthritis with progressive destruction of cartilage in both synovial joints and vertebrae Most common form of arthritis, also referred to as degenerative arthritis; is a chronic, progressive, nonsystemic disease Primary idiopathic: unknown etiology but risk factors usually present Secondary disorder: results from conditions that predispose to degenerative changes in joints, such as RA, DM, congenital deformities, joint trauma, or repetitive joint movement during sports or work activities Pathophysiology Primary idiopathic OA: articular cartilage decreases friction during joint movement and displaces force of workload onto subchondral bone, thereby decreasing stress within joint itself. o Type II collagen (normally present in healthy articular cartilage) contains proteoglycans (macromolecules that provide elasticity and stiffness to articular cartilage, allowing it to resist compression) o Clients in primary idiopathic OA may have some type of malfunction in production of proteoglycans and collagen; however, these substances are destroyed faster than they can be synthesized. o Type II collagen is eventually replaced with type I collagen (normally present in skin and tendons); with disease progression, composition of articular cartilage is altered and unable to perform its original function o In response to changes in articular cartilage, synovitis (inflammation of a synovial joint) often occurs within joint; subchondral bone responds to cartilage damage by producing osteophytes (outgrowths of bony tissue often referred to as spurs) Secondary OA o Repetitive movements that apply excessive workload to joints results in breakdown of cartilage and changes in subchondral bone o Ability of cartilage to lubricate joint becomes depleted and friction increases between joint surfaces during joint motion o Joint narrowing occurs with cartilage breakdown,and synovitis and formation of osteophytes occurs with disease progression Signs and symptoms o Dull, aching pain in affected joint with movement and weight bearing and relieved with rest o Numbness or tingling at night, associated with disease progression secondary to nerve damage o Crepitus with joint movement o Edema and stiffness in affected joint o Decreased ROM and ability to participate in activities of daily living o Symptoms vary in severity and may range from mild intermittent discomfort t complete disability o Morning stiffness o Inflammation Similar to RA but not as severe Common in athletes, but is one of the 10 most disabling conditions in developing countries UNILATERAL more localized (pitcher’s shoulders, dancers ankles, basketball player’s knee)
o Neuronal injury o Ischemia o Increased vascular permeability o Compromised blood flow o Hypoxemia, hypotension Vertebral Injuries: Subluxations Fractures Dislocations Compressions Damage to ligament or vertebrae: burst, shatter Flexion/bending movements, compression Spinal Cord Injuries: Direct damage – directly to cord Ischemia – directly to cord Indirect damage – vertebral fractures that effect the spinal cord Spinal Cord Shock: Immediate response to SCI – will see the following: Flaccid paralysis Loss of tendon reflexes BELOW level of injury Lack of somatic/visceral sensations BELOW level of injury Loss of bladder/bowel function Vasodilation, hypotension, increase venous capacity Level of damage determines what parts of the body will be affected – see chart below Central Cord Syndrome Injury is predominantly in the central gray or white matter of the cord (most common incomplete injury): motor loss to upper extremities greater than lower extremities, variable amount of sensory loss and bladder dysfunction. Anterior Cord Syndrome Damage from infarction of the anterior spinal artery; results in damage to the anterior two thirds of the cord (associated with flexion injuries of cervical spine): Complete paralysis, hyperesthesia, and hypalgesia below level of injury. Touch, position, pressure, and vibration is preserved. Brown-Sequard Syndrome Damage to the hemi-section of the anterior and posterior cord (associated with penetrating wounds): Ipsilateral loss of motor, position, and vibration below level of injury. Autonomic Dysreflexia Common with thoracic & lumbar injury Exaggerated SNS response Extreme HTN, RR, HR, Pallor, goosebumps Baroreceptor reflex
Pathophysiology:
- Influencing Factors o Spinal cord is located in relatively small space o Peculiarities of spine: canal space varies - Wider in children o Wide canal allows cords more space to move without compression - Narrower o Congenital abnormalities, cervical spondylitis, age, osteoarthritic changes o Variability of vascular supply o Presence of Osteophytes - Also called “bone spurs” - Boney growth that indicated degeneration of the spine - Occurs with aging and is not painful
- Mechanisms o Concussion o Compression o Contusion o Hematomyelia: hemorrhage within cord - Usually caused by trauma - Hematomyelia and edema can transfer above the injuryà leads to syringomyelia or chronic spinal cord disease o Transection: actual (rare) or functional o Overstretching o Edema o Ischemia
- Vascular Pathology o Injury increases permeability of blood vesselsà Edemaà decrease in blood flow
Failure of compensatory mechanism causes ischemia, hypoxia, herniation, and brain death Brainstem reflects final effort to maintain cerebral perfusion (cushing triad or response) Decorticate: flexor posturing indicating corticospinal tract lesions Decerebrate: extensor posturing indication brainstem injury TRAUMATIC BRAIN INJURY – TBI Head injury describes all structural damage to the head CAUSES MVC Pedestrian impacts Falls Assaults Types of injuries TYPES OF INJURY Skull fractures Brain injury Vascular damage Primary vs. Secondary Injury Classifications Mild, Moderate, Severe Mild head injury Microscopic changes in neurons and neuroglia Ex. Concussion Moderate head injury Small hemorrhages and swelling of brain tissue occurs Contusions are visualized on CT Brain Severe head injury Extensive mechanical and secondary damage to brain structure Contusions, intra-cerebral, subdural, subarachnoid and epidural hemorrhages evident on CT scan Secondary Injury Ischemia: Results from hypotension, hypoxia (most common cause of secondary brain injury) Hypotensive – they get lethargic/weak – due to decreased oxygen and glucose to the brain Impaired regulatory mechanisms o Unable to maintain adequate blood flow o Unable to maintain adequate oxygen supply Cerebral edema – increase fluid causes increase pressure Increased ICP: (Monroe Kelly hypothesis – if the volume of one sub increases in the brain, the volume of the others decreases) ex. Increase CSF, blood flow will decrease to maintain pressure, too much tissue
edema, the body will slow down on influx of blood and CSF – self preservation but it doesn’t really work – it actually is more damaging Brain herniation: increase in intracranial pressure – the brain will suffer, it will try to find a way to find a way out – the foramen magnum the hole were the brain stem, nerves, vessel go into the brain – the swelling will cause brain matter to push down into the foramen and starts to effect the brain stem (basically supports life) The brain stem begins to get compressed by the brain tissue being pushed into the foramen – usually patients don’t survive that – called brain death. Vitals will have severe fluctuations. Patient’s spine and neck need to be aligned so as to not cause additional intracranial pressure. Anything that causes an increase in intra-thoracic pressure will also raise the intracranial pressure. (Coughing or nose blowing) Epidural Hematoma Develops between the inner bones of the skull and the dura Tear in middle meningeal artery Arterial in origin Subdural Hematoma Develops in the area between the dura and the arachnoid (subdural) space Venous bleed Traumatic Intracerebral Hematoma Single or multiple Occur in any lobe of the brain (> frontal/temporal due to falls Coup-contracoup : hit head in front and then back (usually seen in mva) Racoon eyes: blood that drains in to the orbital sockets from an intracrainal bleed that accumulates in that space Clinical Manifestations Alterations in sensory, motor and cognitive function Changes in level of consciousness Brain death if severe Pupillary changes Hemodynamic and respiratory instability Diagnosis: CT Brain Management Cranial surgery: remove hematoma Measure to decrease ICP Support ABC’s Health Promotion Educate on safe behaviors Nursing Interventions Positioning NPO Supportive measures to decrease ICP Medication administration Normal Cranial Cavity Blood: 10% Brain tissue: 80% CSF: 10% Normal ICP: 0-15 mm Hg Monro-Kellie Hypothesis Reciprocal compensation occurs within 3 compartments
