Final Exam Flashcards
manifestations of hypokalemia
weak irregular pulse, orthostatic hypotension, confusion, lethargy, coma, decreased motility (decreased bowels sounds), nausea, vomiting, skeletal muscle weakness, decreased deep tendon reflex, parasthesias, shallow resp., EKG changes
causes of hypokalemia
potassium loss (d/t meds, increased aldosterone, vomiting, diarrhea, NG tube prolonged suction, diaphoresis, impaired K reabsorption (kidney disease)), inadequate potassium intake, movement from ECF to ICF (alkalosis, hyperinsulinism), dilution of serum potassium (water intox., IVF with potassium deficient sol.)
EKG changes with hypokalemia
ST depressions, shallow flat or inverted T wave, prominent U wave
management of hypokalemia
monitor heart rhythms (cardiac monitor, focused cardiac assess.), assess resp., GI, and renal (urine output, BUN, creatinine), monitor electrolytes, hold potassium-wasting meds, replenish potassium (potassium rich food)
replenishing hypokalemia
levels 2.5-3.5 supplement orally, less than 2.5 supplement IV
causes of hyperkalemia
excess K intake (food, meds, or IV sol.), decreased K excretion (K sparing meds, NSAIDs, ACEI, renal disease, adrenal insufficiency), movement for ICF to EXC (tissue damage, acidosis, hyperuricemia, hypercatabolism)
manifestations of hyperkalemia
slow irregular pulse, dysrhythmias, hypotension, weakened skeletal muscles, increased motility, hyperactive B.S., diarrhea, muscle spasms, cramping, parasthesias, profound weakness and paralysis in extrem. at late and lethal levels
EKG changes of hyperkalemia
peaked T waves, flat P waves, widened QRS complex, Prolonged PR interval
management of hyperkalemia
limit/discontinue intake of K, increase excretion (potassium wasting diuretics, kayexalate for renal impairment, IV hypertonic glucose with insulin, IV calcium to prevent myocardial excitability, monitor K levels, assess cardiac function continuously
causes of hypocalcemia
inadequate oral intake (alcoholism), malabsorption (lactose intol., celiac disease/crohns disease, inadequate vit. D intake, ESRD), increased excretion (renal disease, diarrhea, wound drainage-especially GI), decreased ionized fraction of calcium (chelate or binding meds, acute pancreatitis, hypophosphatemia, removal/drainage of parathyroid glands)
manifestations of hypocalcemia
bradycardia, hypotension, diminished pulses, irritable skeletal muscles (twitching, cramp, tetany, seizure), decreased resp., paresthesias, hyperctive deep tendon reflex, anxiety, irritability, increased GI motility, hyperactive BS, cramping, diarrhea, positive trosseau’s and chvosteks
EKG changes with hypocalcemia
prolongs SR and QT
management of hypocalcemia
replenish Calcium (IV Slowly), increase vit. that increase absorption (vit D, aluminum hydroxide to reduce Phosph, have 10% cal. gluconate available for acute deficit), reduce environmental stim., seizure precautions, monitor EKG for changes (especially w/ IV calcium), educate calcium rich foods
trosseaus sign
carpal spasm induced by inflation of BP cuff
chvosteks sign
contraction of facial muscles in response to light tap over facial nerve in front of ear
isotonic dehydration
equal loss of water and electrolytes; decreased circulating blood causing inadequate tissue perfusion
hypertonic dehydration
water loss > electrolyte loss (causing hypernatremia); fluid moves from intracellular into plasma (cells shrink) d/t alterations in plasma electrolytes
hypotonic dehydration
electrolyte loss > water loss (causing hyponatremia); fluid moves from plasma and interstitial space into cells (cells swell) d/t fluid shifting between compartments and decreasing plasma volume
fluid volume deficit manifestations of lab findings
increased serum osmolarity, increased hematocrit, increased BUN, increased serum sodium, increases urine Specific gravity
fluid volume deficit management
oral rehydration/ IV: isotonic dehydration rehydrate with isotonic fluids, hypertonic dehydration with hypotonic, hypotonic dehydration with hypertonic
fluid volume deficit manifestations of assessment
weak/thready/diminished pulse, decreased BP/ortho., flat neck veins, decreased RR/dyspnea, lethargy/coma, muscle weakness, fever, decreased urine output, decreased skin turgor, dry mouth, diminished bowel sounds, constipation, thirst
process of stroke
cerebral anoxia- lack of O2 to the brain which can cause cell damage, cerebral infarction- death of brain tissue from lack of O2/blood supply, cerebral edema- brain swelling (compensatory mechanism that can damage the brain further due to increased ICP), cerebral dysfunction- portion of brain that lost function d/t death
2 types of stroke
hemorrhagic or ischemic
2 types of ischemic strokes
thrombotic or embolic
manifestations of ischemic stroke
sudden severe headache; weakness/numbness; difficulty speaking/understanding speech; loss of balance/difficulty walking/dizziness; confusion/altered LOC; dysphagia; facial droop to one side
manifestations of hemorrhagic stroke
sudden severe headache (worst headache of pt life); weakness/numbness; N/V; difficulty speaking/understanding speech; vision problems; loss of balance/difficulty walking/dizziness; confusion/altered LOC; seizures
nursing intervention of acute phase of stroke
maintain airway, supplemental O2, neuro exam- monitor ICP within first 72 hours, elevate HOB and place pt on side to prevent aspiration, foley catheter, fluid and electrolyte admin., medication admin., quiet environment, seizure precautions
nursing interventions of post acute phase of stroke
position 2 hours on unaffected side and 20 minutes on affected side, antiembolism stockings, ROM exercises, eval. gag reflex and ability to swallow, NPO to begin and advance as tolerated
what is a seizure
abnormal, sudden, excessive discharge of electrical activity in the brain
3 main types of seizures
focal onset- localized to one area of brain, generalized onset- more wide spread brain activity, unknown onset
6 types of seizures
tonic-clonic (gen), absence (gen.), myoclonic, atonic/akinetic, simple partial (focal), complex partial (focal)
general stroke symptoms
sudden weakness, numbness, difficulty speaking, loss of coordination
non-modifiable risk factors for stroke
age, gender (males higher risk), ethnicity (african americans higher risk), genetics
modifiable risk factors for stroke
HTN, atherosclerosis, Afib, anticoag therapy, stress, obesity, oral contraceptives, DM
primary cause of stroke
HTN
embolic ischemic stroke
clot/debris that travels to brain; sudden severe symptoms; less common warning signs; pt remains conscious but complains of headache
thrombotic ischemic stroke
build up of plaque in artery in brain; gradual onset compared to other strokes; no decrease in LOC in first 24 hours; s/s progressively worsen as infarction and edema occurs
common stroke assessment findings
agnosia, apraxia/dyspraxia, hemianopsia, neglect syndrome, proprioception alterations, aphasia
agnosia
inability to recognise familiar objects/people
apraxia/dyspraxia
loss of ability to carry out skilled movements or gestures
meds used to prevent strokes
anticoag therapy, antiplatelet, antihypertensive, dyslipidemia
acute stroke management
CT without contrast to identify if hemorrhagic or ischemic; if ischemic then use thrombolytic therapy
window for administering thrombolytic therapy
3.5-4 hours after onset of altered status
epilepsy
disorder characterized by chronic seizure activity; indicates CNS or brain irritation
causes of seizures
genetics, tumors, trauma, circulatory or metabolic disorders, toxicity, infection
status epilecticus
rapid succession of epilectic spasms without intervals of consciousness; can occur with any type of seizure
what is the danger of seizures?
can cause brain damage
tonic/clonic seizures
may begin with aura; tonic phase consist of stiffening/rigidity of muscles in arms or legs for 10-20 sec followed by LOC; clonic phase consist of hyperventilation and rapid jerking of extrem. lasting 30 seconds; may lose control of bladder during clonic phase; postictal phase may take hours to recover
when to seek medical treatment for seizures
if seizure lasts longer than 5 min
myoclonic seizure
minor/brief generalized jerking or stiffening of extremities; can cause pt to fall to ground; pt is aware of the event
atonic seizures
sudden loss of muscle tone causing person to drop/fall to ground; both sides of brain usually affected; can happen to part or entire body; lasts less than 15 sec; pt not completely aware of event
simple seizure
occurs in one area of brain on one side; motor and sensory symptoms localized to specific area; pt remains conscious; rarely lasts longer than 1 hour; may experience aura
complex seizure
most common seizure in adults; consist of blank stare (usually involves temporal lobe); periods of altered behavior that pt is unaware of; lasts longer than 1 minute; pt loses consciousness for a second
nursing assessment of seizure
seizure HX, type of seizure, what happened before/during/after; were there prodromal signs/aura; loss of bladder? LOC?; details of postictal state
phases of seizure
prodromal phase, aura phase, ictal phase, postictal phase
nursing interventions for seizure
note time/duration; assess behavior at beginning/middle/end; lower pt to ground; support ABCs; remain with pt but do not restrain; remove tight clothing; note type of seizure; monitor incontinence; admin IV meds; monitor vitals; reorient pt
myasthenia gravis
chronic progressive neuromuscular disease characterized by severe weakness and abnormal fatigue of voluntary muscles; interruption of transmission of nerve impulses at myoneural junction
causes of myasthenia gravis
insufficient secretion of acetylcholine; excessive secretion of cholinesterase; unresponsiveness of muscle fibers to acetylcholine
what is the role of acetylcholine neurotransmitter
muscle contraction and movement
what is the role of cholinesterase
destruction of acetylcholine
assessment of myasthenia gravis
weakness, fatigue, difficulty with chewing and swallowing, dysphagia, diplopia, weak/hoarse voice, difficulty breathing, ptosis
nursing interventions for myasthenia gravis
monitoring of respiratory, swallowing, cough reflex, speech, muscle strength, myasthenic or cholinergic crisis; educate pt to wear medic alert, sit up when eating, conservation of muscle strength
treatment of myasthenia gravis
admin anticholinesterase meds which relieve muscle weakness by blocking acetylcholine breakdown at neuromuscular junction
myasthenic crisis
acute exacerbation of disease that is caused by rapid progression of disease, infection, too little meds, fatigue, or stress
manifestations of myasthenic crisis
tachycardia, tachypnea, HTN, dyspnea, cyanosis, incontinence, absent cough/swallow reflex
nursing interventions for myasthenic crisis
assess for symptoms, increase anticholinesterase meds as prescribed
osteoarthritis
breakdown of articular cartilage leading to damage of bone; osteophytes form in joint space that cause narrowing and decreased movement in joints; causes progressive degeneration
risk factors for developing osteoarthritis
old age, female, obesity, labor intensive occupations, sports
manifestations of osteoarthritis
pain when moving under stress that is relieved by stress; hard and bony stiff joints; morning stiffness for about 30 minutes; often impacts weight bearing joints like hips knees c-spine and l-spine
2 types of bony growths in osteoarthritis
heberden- distal; bouchard-proximal
assessment of osteoarthritis
joint crepitus; effusion d/t inflammation; non-systemic; x-ray + for decreased joint space and osteophyte formation; subchondral bones may appear thick
does osteoarthritis appear bilaterally?
no but it can
management of osteoarthritis
decrease pain and stiffness, maintain/improve mobility, exercise to preserve joint, weight loss, OT/PT, orthotics and walking devices, NSAIDs/steroids, arthroplasty in severe cases
osteoporosis
bone resorption (osteoclast) > bone formation (osteoblast); causing thinning of bone
osteoporosis can lead to…
compression FX of T and L spine, FX of hips, FX of wrists; increased FX risk
risk factors for developing osteoporosis
small frame, female, ethnicity, aromatase inhibitor use, nutritional factors, autoimmune diseases, steroid use, immobility, diabetes
typical age range for onset of osteoporosis
men- 60 to 70
women- 50 to 60
manifestations of osteoporosis
low bone mineral density on DEXA scan, rounding of upper back (aka dowager humps), osteoporotic FX; otherwise can be asymptomatic
assessment of osteoporosis
X-ray + for radiolucency if significant demineralization (dark area indicative of low density); dual energy xray (DEXA) provides bone mineral density
prevention of osteoporosis
balanced diet rich in calcium and vitamin D, regular weight bearing exercises (20-30 per day)
why weight training for osteoporosis prevention
stimulates bone mineral density
management of osteoporosis
pharmacological therapy to improve bone density via bisphosphenates or alendronate; hip FX managed with replacement; compression FX managed conservatively
osteoporosis nursing interventions
educate pt on how to prevent worsening, pain management, improve bowel elimination to avoid FX, injury prevention
osteomalacia
inadequate mineralization of bone caused by Vitamin D deficiency; leads to soft and weakened bones
causes of osteomalacia
failure to absorb calcium; excessive calcium loss; GI disorders; liver disease; kidney disease; renal insufficiency; hyperparathyroidism; malnutrition
assessment of osteomalacia
X-ray + for general demineralization; X-ray can show compression FX; labs show low Ca, low Phosp, elevated alkaline phosphatase; bone biopsy shows increased osteoid
what is osteoid
demineralized cartilaginous bone matrix; aka pre-bone
management of osteomalacia
treat underlying cause f possible; Vitamin D, calcium supplements, sun exposure; if kidney disease is issue then admin of activated Vitamin D med; if dietary is cause then recommend change; severe deformities may warrant braces
why low calcium and low phosphorus in osteomalacia
bone is unable to mineralize
why elevated phosphatase in osteomalacia
increased bone turnover
septic arthritis
infection of joint; mortality for ingle infected joint is 11%
risk factors for developing septic arthritis
older age, diabetes, rheumatoid arthritis, skin infection, alcoholism, HX of joint surgery, IV drug use
manifestations of septic arthritis
warm, painful, swollen joint; decreased ROM; chills, fever, leukocytosis; half of all cases localized to knee
assessment of septic arthritis
infectious workup; aspirations, examination, and culture of synovial fluid (will be purulent pus); CT/MRI and bone scan
septic arthritis management
primary broad spectrum antibiotic, aspirate synovial fluid periodically (therapeutic aspiration), splinting, pain relief, progressive ROM, potential for joint fibrosis, monitor for reoccurrence
nursing interventions for septic arthritis
pain relief; improve physical mobility; control infection promote home, community, transitional care
3 types of fractures
closes or simple, open or compound/complex, intra-articular
avulsion FX
fx where fragment of one has been pulled away by tendon and its attachment
comminuted FX
fx where bone has splintered into severe fragments
compression FX
fx where bone has become compressed (common or vertebrae)
depressed FX
fx where fragments are driven inward (commonly seen in skull)
epiphyseal FX
fx through epiphysis
greenstick FX
fx where one side is broken and other is bent (common in children)
impacted FX
fx where bone fragment is driven into another bone fragment
oblique FX
fx occurring at angle across bone; ess stable than transverse FX
open FX/ compound FX
fx where bone is protruding through skin or mucous membrane; damage to skin or mucous membrane; increased risk for infection
pathologic FX
fx that occurs through area of diseased bone; can occur with or without trauma; ex. osteoporosis or bone cyst
simple FX
fx that remains contained in skin; no disruption of skin integrity
spiral FX
fx that twists around the bone shaft
stress FX
fx resulting from repeated loading of bone and muscle
transverse FX
fx that is straight across bone shaft
manifestations of bone FX
loss of function, shortening, crepitus, edema, deformity, ecchymosis
assessment of FX
health HX, comorbidities, vital signs, respiratory status, LOC, s/s of shock, neurovascular assessment of extremity, bowel/bladder elimination, bowel sounds, I/Os if hip FX, skin condition, anxiety and coping
management of FX
immediate immobilization, cover open wounds, FX reduction and then immobilize if needed
3 types of FX reduction
closed reduction- manual traction; open reduction- surgical intervention; delayed reduction- waiting for pt to stabilize prior to intervention
2 types of immobilizations
external fixation- casts and bandages; internal fixation- plates and screws
nursing interventions of FX
elevate, monitor for neurovascular compromise (5 Ps), monitoring for normal elimination, isometric muscle exercises, encourage ADLs and independence, pain management, pt education, wound care
risk factors for FX healing
over 40 years of age, corticosteroid use, NSAID use, avascular necrosis, bone loss, tobacco use, comorbidities, local trauma, inadequate immobilization, malalignment, premature weight bearing, infection, local malignancy
acute FX complications
shock, fat embolism, compartment syndrome, DVT, PE, DIC, infection loss of bladder control in hip FX, hemorrhage
chronic FX complications
delayed union of bone, malunion of bone, AVN of bone, complex regional pain syndrome (CRPS), heterotrophic ossification (benign bone growth in atypical location)
5 Ps of neurovascular assessment
pain, pulse, pallor, parasthesia, paralysis
assessment of casts, splints, braces
assess injury, treat lacerations and wounds, assess neurovascular status (5 Ps)
complications associated with casts, splints, braces
pressure injuries, disuse syndrome (muscle weakness/wasting and joint stiffness), acute compartment syndrome
compartment syndrome
increased pressure within compartment that impairs blood flow and compromised tissue viability
management of compartment syndrome
fasciotomy
hypertension classifications
primary- unknown cause; secondary- caused by another factor and need to target underlying cause; malignant- HTN crisis
interventions for HTN prior to medications
lifestyle modification for 1-3 months such as reducing alcohol, sugar, sodium, fat, stress, and increasing exercise
causes of primary HTN
aging, family HX, African American race, sedentary lifestyle, smoking, alcohol, HLD
causes of secondary HTN
results from other conditions like CV disorders, renal disease, endocrine diseases, pregnancy, meds, sleep apnea
assessment for HTN
History: family HX, current meds, perception of diseases; Signs and symptoms: dietary pattern, headache, visual changes, neurological assessment, lab tests; Physical exam: obtain 2 BP on both arms when supine and then standing, compare to prior, assess weight, assess for JVD, HR, dysrhythmias, S3, enlarged heart on Xray
common end organ damage from HTN
cerebrovascular damage, vasculopathy, heart disease, nephropathy
cerebrovascular damage resulting from HTN
acute HTN encephalopathy (confusion), stroke, vascular dementia, retinopathy
vasculopathy from HTN
atherosclerosis, aortic aneurysm
heart disease from HTN
left ventricular hypertrophy, coronary artery disease, MI, HF, atrial fibrillation
nephropathy from HTN
proteinuria, renal failure
non-pharmacological interventions for HTN
weight reduction, sodium reduction (less than 2g/day), reduce alcohol and caffeine, exercise, smoking cessation, stress reduction, monitor BP
older adult considerations HTN
isolated systolic HTN d/t age related loss of elasticity of carotid and aorta; hard to treat due to low DBP; medication issues because of failure to remember, polypharm, expensive, orthostatic hypotension
HTN urgency
BP > 180/120 with no evidence of end-organ damage; pharmacological interventions used to normalize BP within 24-48 hours
coronary artery disease
narrowing or obstruction of 1 or more coronary arteries due to atherosclerosis; leads to inadequate perfusion and oxygenation of myocardial tissue
effects of coronary artery disease can lead to
HTN, angina, dysrhythmias, MI, heart failure, death
collateral circulation
vascular system is generated around the obstruction to bypass and perfuse; takes ~ 10 years to form
modifiable ris factors for CAD
BMI>30, DM, HTN, alcohol use, high LDL and low HDL, tobacco use
non-modifiable risk factors for CAD
65 years and older, family HX, genetic predisposition
manifestations of CAD
early on is asymptomatic, chest pain, dyspnea, syncope, cough/hemoptysis, palpitations, excessive fatigue
diagnosing CAD
EKG: ischemia = depression and infarction = elevation; Lipids: elevated cholesterol, stress tests, cardiac cath
cardiac cathertirzation
angiogram used to diagnose CAD; injected dye into arteries to identify atherosclerotic plaques blocking off blood flow (plaques do not illuminate)
treatment for CAD
tobacco cessation, manage HTN, low cal, low sodium, low fat, low cholesterol, increased dietary fiber, control Dm, reduce stress, reduce alcohol, pharmacological management
lymphedema
increase in lymph due to obstruction of a vessel; can be primary or secondary (d/t other condition)
treatment of lymphedema
ambulatory compression stockings, manual drainage, physiotherapy, skin care
TIA or transient ischemic attack
temporary neurologic deficit resulting from temporary blood flow impairment; seen as a warning sign for potential impending stroke; requires medical attention to rule out infarction
manifestations of TIA
transient/short-lived symptoms; same as ischemic stroke: weakness/numbness; difficulty speaking/understanding speech; vision problems; difficulty walking/loss of balance/dizziness; facial droop to one side
tuberculosis
highly contagious communicable disease caused by M. tuberculosis; airborne; exudative response causes nonspecific pneumonitis and granulomas in lung tissue; onset is insidious and pt are unaware until disease is advanced
risk factors for developing tuberculosis
elderly, <5 years of age, unpasteurized milk if cow is infected, homeless, low socioeconomic group, minorities, refugees, frequent contact with untreated/undiagnosed individual, crowded living areas, malnutrition, immune dysfunction, alcohol abuse/IV drug use
causes of tuberculosis
bacteria forms tubercle lesion and immune system encapsulates tubercle leaving scar; if no encapsulation then bacteria can enter lymph and cause inflammatory response called granulomatous inflammation leading to primary lesions forming
active phase of tuberculosis
infection causes necrosis and cavitation in lesions that can rupture and spread necrotic tissue damaging various parts of the body; need xray to confirm because a recent BCG vaccine can cause positive PPD/mantioux test
manifestations of tuberculosis
may be asymptomatic in primary phase, fatigue, lethargy, anorexia, weight loss, low grade fever, chills, night sweats, persistent cough (can be blood streaked but usually dry), chest tightness, dull aching chest pain with cough
testing for tuberculosis
chest xray may show cessation and inflammation, advanced may show partial obstruction of bronchus from endobronchial disease (wheezing and dyspnea present), TB skin test (positive result does not mean active), quantiferon TB gold test (sensitive and rapid blood test), sputum culture for confirmation
managing tuberculosis
goal is to prevent transmission, reduce symptoms, prevent progression; risk of transmission decreases after 2-3 weeks of treatment; treatment for up to 12 months; educate importance on medication compliance; well balanced diet; sputum culture every 2-3 weeks until 3 negative tests consecutively
emphysema
air sacs enlarged and damaged causing hyperinflation and breathlessness; pink puffer; barrel chest
atelectasis
collapse of alveoli; can be acute or chronic; occurs as result of ventilation; can be caused by reduced ventilation or obstruction; at high risk for developing when post op
clinical manifestations of COPD
cough, exertional dyspnea, wheezing/crackles, sputum production, weight loss, barrel chest, accessory muscle use, prolonged expiration, orthopnea, cardiac dysrhythmias, congestion/hyperinflation of chest xray, ABG show acidosis and hypoxemia, decreased capacity of pulmonary function test
management of COPD
monitor vital signs, admin O2, fowlers position and leaning forward, respiratory treatments chest physiotherapy, educate on tripod breathing and pursed lip, bronchodilators, corticosteroids, mucolytics, antibiotics, high calcium and high protein diet, 2-3L fluid, suction as needed
causes of atelectasis
foreign body, tumor/growth, altered breathing patterns, retained secretions, pain, prolonged supine position, increased abdominal pressure, reduced lung volumes from muscular/neurological disorders, surgery
manifestations of atelectasis
dyspnea, cough, sputum production, hypoxemia, decreased breath sounds, crackles, respiratory distress, tachycardia, tachypnea, pleural pain, central cyanosis
prevention of atelectasis
frequent turning, early ambulation, lung volume expansion maneuvers like deep breathing and coughing and incentive spirometers, positive end respiratory pressure (PEEP), CPAP
diabetes mellitus
chronic disorder of impaired carbohydrate, protein, and lipid metabolism; primarily carbohydrate; deficiency of insulin results in hyperglycemia
sub categories of DM
Type 1, Type 2, and metabolic syndrome (pre-diabetes)
complications of DM
microvascular complications, macrovascular complications, reduced healing causing increased risk of infection
type I DM
nearly absolute deficiency of insulin due to autoimmune primary beta cell destruction (negligible insulin); if insulin is not given then fat is metabolized for energy causing DKA; genetic
type II DM
relative lack of insulin or resistance t the action of insulin; insulin is sufficient to stabilize fat and protein metabolism but not carbohydrate; develops over time
metabolic syndrome
coexisting risk factors for developing type II diabetes; risk factors include abdominal obesity, hyperglycemia, HTN, high triglyceride levels, low HDL
assessment of DM
polyuria, polydipsia, polyphagia, hyperglycemia, weight loss, blurred vision, slow wound healing, vaginal infections, weakness/parasthesias, signs of inadequate circulation of feet, signs of accelerated atherosclerosis
A1C diagnostic for diabetes
> 6.5
primary intervention for type II DM
exercise, diet, and lifestyle; if not working after 6 months than oral hypoglycemics and maybe insulin prescribed
only oral hypoglycemic not contraindicated in
SGLT-2 inhibitors
dawn phenomenon
hyperglycemia on morning awakening resulting from excessive release of GH and cortisol early in morning; treatment is increase in insulin dose or change in administration timing
somogyi effect
normal/elevated glucose at bedtime, hypoglycemia around 2am causing increase in production of counterregulatory hormones; blood glucose rebounds by 7am in response to counterregulatory hormones and pt is hyperglycemic; treat with decreased insulin and or having large bedtime snack
hypoglycemia
<70 mg/dL or rapid drop from elevated level; caused by too much insulin, too much oral hypoglycemic, too little food, or too much exercise
signs and symptoms of hypoglycemia
cold, clammy, headache, lethargy, AMS, hungry, tachycardia, jittery, angry
assessment of hypoglycemia
mild is 40-70: fully awake with neurogenic symptoms like tremors, palpitations, sweating, hunger; moderate is 20-39: s/s of worsening hypoglycemia like dizziness, drowsiness, and weakness; severe is <20: severe neuroglycopenic symptoms like delirium, seizure, coma, and death
hypoglycemia interventions
check BGL, 15/15 rule- if symptomatic or below 70mg/dL give 15 gram of simple carbs (4oz juice), recheck BGL in 15 min and administer another 15g, if still below 70 after 45 g sugar admin 15-50 ml of 50% dextrose or 1mg glucagon; pt should then eat snack
DKA
life threatening complication of type I that can occur with severe insulin deficiency; too much breaking down of fats producing ketones which are acidic; hyperkalemia can be seen (H into cell and K out into blood stream)
assessment of DKA
precipitated by infection, stress, inadequate insulin, or can be sudden; glucose >300 Cr > 1.5, urine has ketones, K elevated with acidosis, ABG show acidotic, dehydrated, polydipsia, polyuria, weight loss, dry skin, sunken eyes, lethargy, coma
Interventions for DKA
restore blood volume, IV insulin with infusion of NS or 1/2 NS with dextrose added; monitor K and correct imbalances in electrolyte; cardiac monitoring if needed
HHS- hyperosmolar hyperglycemic syndrome
extreme hyperglycemia without ketosis/acidosis; more often inn Type II diabetes; enough insulin is present to prevent breakdown of fts for energy (no ketosis); need to have neurological side effects present
assessment of HHS
gradual onset precipitated by infection, stressors, poor fluid intake; neurological symptoms from altered CNS function; dehydration and electrolyte imbalance from high glucose displacing electrolytes; polyuria, polydipsia, weight loss, sunken eyes, dry skin, lethargy, coma; glucose >800, hypokalemia, hyponatremia, elevated creatinine, negative urine ketones; ABD does not show acidosis
diabetes insipidus
hyposecretion of ADH by posterior pituitary (too little ADH is reabsorbed); kidney fails to reabsorb water; Central DI is decreased ADH production; Nephrogenic DI is adequate ADH production but kidneys do not respond appropriately (very rare)
assessment of diabetes insipidus
large amount of dilute urine; polydipsia, dehydration, inability to concentrate urine, low urine specific gravity; fatigue and muscle weakness; headache; postural hypotension that may cause vascular collapse; tachycardia
intervention for DI
monitor VS, neuro status, cardio status, fluids, electrolytes, IOs, weight; maintain adequate fluid intake with IV hypotonic saline to replace urinary loss; avoid diuresing foods and liquids; vasopressin if indicated; ensure safe environment; pt education on prescribed meds
addisons disease
aka primary adrenal insufficiency; causes hyposecretion of adrenal cortex hormones like glucocorticoids(cortisol), mineralocorticoids (aldosterone), and androgens; commonly caused by autoimmune destruction; requires lifelong replacement of glucocorticoids; fatal if left untreated
addisons disease loss of glucocorticoids
leads to decreased vascular tone, decreased vascular response to catecholamines, decreased gluconeogenesis
addisons disease loss of mineralocorticoids
leads to dehydration, hypotension, hyponatremia, hyperkalemia
adrenal insufficiency assessment
lethargy, fatigue, muscle weakness, GI disturbances, weight loss, menstrual changes, impotence in men, electrolyte imbalance (hyponatremia, hyperkalemia, hypocalcemia), hypoglycemia, hypotension, hyperpigmentation of skin
interventions for adrenal insufficiency
monitor VS, weights, IOs; labs- WBCs, glucose, potassium, sodium, calcium; admin prescribed glucocorticoids and/or mineralocorticoids, monitor for s/s of addisonian crisis
addisonian crisis
medical emergency caused by acute adrenal insufficiency; caused by stress, infection trauma, surgery, or abrupt withdrawal of supplemental corticosteroids
assessment of addisonian crisis
can result in hyponatremia, hyperkalemia, hypoglycemia, severe headache, abdominal pain, weakness, irritability, confusion, severe hypotension, evidence of shock
interventions for addisonian crisis
admin of IV glucocorticoids, fluids, and electrolytes; monitor VS, neuro status, IOs, labs; oral glucocorticoids and mineralocorticoids following resolution
cushings syndrome
metabolic disorder causing chronic excessive production of cortisol d/t increased ACTH from pituitary; iatrogenic- cortisol coming from adrenal cortex resulting from prolonged admin of high dose glucocorticoids; can be caused by ACTH secreting tumors
cushings syndrome assessment
generalized muscle weakness and wasting, moon face, buffalo hump, truncal obesity with thin extrem., weight gain, hirsutism (masculinity in women), electrolyte imbalance (hypernatremia, hypokalemia, hypocalcemia), hyperglycemia, HTN, fragile skin, easy bruising, red/purple striation on abdomen and thighs
cushings syndrome interventions
monitor VS, weight, IOs; monitor labs- WBC, glucose, sodium, potassium; chemotherapeutic agents for inoperable adrenal tumors, removal of pituitary, adrenalectomy d/t adrenal adenoma; increased glucocorticoid during stress for those with lifelong therapy; assess for post op thrombus formation, medic alert bracelet
hypothyroidism
hyposecretion of thyroid hormones; decreased rate of body metabolism; T4 is ow and TSH is high
primary hypothyroidism
source of dysfunction is the thyroid gland that cannot produce necessary amount of hormones
secondary hypothyroidism
thyroid is not being stimulated by pituitary gland to produce hormones; anterior pituitary not releasing TSH
assessment of hypothyroidism
lethargy, fatigue, weakness, muscle aches, parasthesias, cold intolerance, weight gain, dry skin/hair, hair loss, bradycardia, constipation, myxedema (edema around eyes and face), forgetfulness, menstrual disturbances, goiter, cardiac enlargement
hypothyroidism interventions
monitor VS, admin thyroid replacement as prescribed, assess for constipation, educate pt on therapy compliance, monitor for signs of hypo/hyperthyroidism, encourage low cal low cholesterol low sat fat die, include fiber, plenty of fluids for constipation, provide warm environment, avoid sedating meds d/t increases sensitivity and increased sedation effects (may cause myxedema coma)
mxedema coma
rare but serious disorder caused by low thyroid hormone production; can be precipitated by illness, withdrawal of thyroid meds, anesthesia, surgery, hypothermia, sedatives
myxedema assessment
hypotension, bradycardia, hypothermia, hyponatremia, hypoglycemia, gen edema, resp fail, coma
myxedema interventions
maintain patent airway, asp. precautions, IV fluids, levothyroxine IV, glucose IV, corticosteroids, assess temp/blood pressure/mental status/ electrolytes/glucose, keep pt warm
hypoparathyroidism
hyposecretion of parathyroid hormone by parathyroid gland; can occur following thyroidectomy that removes parathyroid tissue
hypoparathyroidism assessment
hypocalcemia, hyperphosphatemia, numbness/tingling in face, muscle cramps in extrem., abdominal cramping, + trosseaus or + chvosteks, signs of overt tetany, hypotension, anxiety, irritability, depression
CATS for signs of hypocalcemia
convulsions, arrhythmias, tetany, stridor and spasms
hypoparathyroidism interventions
monitor VS, monitor for hypocalcemia and tetany, seizure precautions, emergency trach set O2 and suction at bed, increase calcium intake (calcium gluconate IV, high calcium low phos diet, vit d supps), admin phosphate binding agents to excrete via GI, encourage medic alert bracelet
cholecystitis
inflammation of the gallbladder; acute or chronic; majority of acute cases are calculous cholecystitis
acalculous cholecystitis
inflammation without obstruction by gallstones
manifestations of cholecystitis
pain, tenderness, rigidity of RUQ; may radiate to midsternal area or right shoulder; accompanied by N/V if acute
jaundice types
pre-hepatic- excessive breakdown of RBC overwhelms liver ability to process bilirubin; hepatic- livers impaired ability to process bilirubin, occurs in hepatitis cirrhosis and drug induced liver injury; post-hepatic- obstructive, blocked bile flow from liver to intestine that commonly occurs with gallstones tumors and bile duct disorders
signs and symptoms of jaundice
yellowing of skin/eyes, dark urine d/t excess bilirubin excretion, pale/clay colored stool d/t lack of bilirubin in GI tract, pruritis; may include symptoms of hepatomegaly, splenomegaly, abd pain, fatigue/weakness, cognitive changes, and bleeding
ascites manifestations
increased abdominal girth, rapid weight gain, SOB
ascites nursing interventions
negative sodium balance to reduce fluid retention (2g), administration of diuretics and monitoring fluid/electrolyte balance, prepare for paracentesis (up to 5-6L removed)
transjugular intrahepatic portosystemic shunt
cannula threaded through portal vein by transjugular route and placed between portal circulation and hepatic vein; decreases sodium retention and prevents recurrence of fluid accumulation that would result in ascites
hepatic encephalopathy
accumulation of ammonia and other toxic metabolites in blood d/t hepatic insufficiency and portosystemic shunting; early signs are mental changes and motor disturbances; late signs are constructional ataxia, asterixis and fetor hepaticus
assessment of hepatic encephalopathy
EEG, changes in LOC, potential seizures, fetor hepaticus, monitor fluid electrolyte and ammonia levels
4 stages of hepatic encephalopathy
- normal level of consciousness with periods of lethargy and euphoria, reversal of day night sleep patterns; 2. increased drowsiness disorientation, inappropriate behavior, mood swings, and agitation; 3. stuporous, difficult to rouse, sleeps most of time, marked confusion, incoherent speech; 4. comatose, may not respond to painful stimuli
managing hepatic encephalopathy
eliminate precipitating cause, lactulose to reduce serum ammonia, IV glucose to minimize protein catabolism, protein restriction, reduction of ammonia from GI tract via suction enema and oral antibx, discontinue sedatives analgesics and tranquilizers, monitor or treat complications/infections
hepatic encephalopathy interventions
assess LOC changes, IOs, bodyweight, VS q4, serial daily ammonia levels and electrolytes, restricted dietary protein, GI tract suctioning, administer lactulose, monitor therapeutic response, monitor resp. status
hepatic cirrhosis
alcoholic: scar tissue characteristically surrounding portal areas; post-necrotic: broad bands of scar tissue; biliary: scarring occurs in the liver around bile ducts; hemochromatosis related; NAFLD/NASH related
compensated cirrhosis
ankle edema, firm and enlarged liver, intermittent mild fever, palmar erythema, splenomegaly, vascular spiders, vague morning indigestion
uncompensated cirrhosis
ascites, clubbing of fingers, continuous fever, epistaxis, hypotension, jaundice, muscle wasting, purpura
cirrhosis interventions
promote rest, improve nutrition, provide skin care, reduce risk of injury, monitor/manage potential complications
cirrhosis complications
bleeding/hemorrhage, hepatic encephalopathy, fluid volume excess
hepatitis A
spread via poor hand hygiene; oral-fecal route; incubates in 2-6 weeks; ill ness last 4-8 weeks; acute only, doe not progress to chronic disease
s/s of hepatitis A
asymptomatic, GI s/s, jaundice, dark urine, joint pain, fever, fatigue
managing hepatitis A
prevention via handwashing, vaccine, immunoglobulin for contacts to provide passive immunity; bed rest during acute, nutritional support
hepatitis B
transmitted via blood, saliva, vaginal secretions; is sexually transmitted; transmitted to infant at time of birth; acute and chronic result in cirrhosis and liver cancer; incubation is 1-6 months; risk factors are healthcare workers, birth, tattoo, IV drug use
signs and symptoms of hepatitis B
flu like symptoms, arthralgias, jaundice, dark urine
hepatitis B diagnostic
+HBsAG/ anti-HBs
managing hepatitis B
chronic meds: alpha interferon (subq) and antiviral agents (oral entecavir ETV + tenofovir TDF), bed rest, nutritional support, hand hygiene, vaccine of those at high risk, vaccination of infants; passive immunity for those exposed, standard precautions and infection control measures, screening of blood/blood products
hepatitis C
transmitted via IV drug use, sex, and blood transfusions prior to 1992; most common bloodborne infection; 1/3 cause liver cancer (need transplant), incubates in 15-160 days, can be acute or chronic, risk factors are healthcare workers IV drug users and multiple sexual partners
diagnostic for hepatitis C
anti-HCV (chronic)
signs and symptoms of hepatitis C
flu like symptoms, jaundice, dark urine
managing hepatitis C
antiviral meds like DAA, avoid alcohol, prevention via public health programs to decrease needle sharing, screening blood supply, safety needles for healthcare workers
hepatitis
viral- systemic viral infection causing necrosis and inflammation of liver cells with characteristic symptoms and cellular/biochemical changes; A/E: fecal-oral route; B/C: bloodborne; D: only people with B are at risk; nonviral- d/t drugs and medications
ascites
caused by portal HTN which increases capillary pressure and causes obstruction of venous blood flow; failure to metabolize aldosterone causing increasing fluid and sodium retention and intravascular fluid; decreased albumin synthesis causing decreased serum oncotic pressure; movement of albumin causes fluid shifts to peritoneal cavity; vasodilation of splanchnic circulation
GERD
backflow of gastric and duodenal contents into the esophagus; caused by incompetent lower esophageal sphincter, pyloric stenosis, motility disorder
GERD assessment
heartburn, cough, regurgitation, dysphagia, laryngitis, chest pain (may mimic MI); obtain HX and info about diet
GERD interventions
avoid food triggers, GERD friendly diet- smaller more frequent meals high in fiber alkaline and fluids, elevate HOB and encourage sitting up for 30 min following meal, medications- proton pump inhibitors and H2 receptor blockers, monitor for aspiration
peptic ulcer disease
ulceration in mucosal wall of stomach, pylorus, duodenum, or esophagus in portion accessible to gastric secretions; erosion can extend through muscle to peritoneum; usually occurs alone and in people aged 30-60
interventions for peptic ulcer disease
monitor VS for signs of bleeding, small frequent bland meals, H2 receptor agonist or PPI to decrease gastric acid secretion, antacids to neutralize secretions, mucosal barrier protectants 1 hr before meal, prostaglandins for protecting and antisecretory actions, avoid alcohol caffeine chocolate smoking NSAIDs
peptic ulcer disease surgical interventions
gastroduodenostomy/billroth I- partial gastrectomy and remaining segment connected to duodenum; gastrojejunostomy/billroth II- partial gastrectomy and remaining segment is connected to jejunum; total gastrectomy- removal of the stomach and attach esophagus to jejunum or duodenum; pyloroplasty- enlargement of pylorus to prevent/decrease pyloric obstructing increasing gastric emptying
dumping syndrome
rapid emptying of gastric contents into the small intestine following a gastric resection
constipation
less than 3 bowel movements per week; caused by surgery, chronic laxative, immobility, diet, ignoring urge, lack of exercise
TPN
continuous administration over 24 hours or cyclical overnight through central vein/PICC; must infuse via pump; admin D10W when TPN runs dry and waiting for new bag; watch for sclerosis, phlebitis, swelling; monitor glucose
when discontinuing TPN
need evaluation by nutritionist; gradually decrease flow for 1-2 hours while increasing oral intake; change IV dressing after removal until healed; encourage PO nutrition; record IO, weight, lab results of electrolytes and glucose levels
pancreatitis
self-digestion by pancreatic enzymes; gallstone obstruct flow of pancreatic juice activating the enzymes; enzyme act. leads to vasodilation, increased permeability, necrosis, erosion, hemorrhage
causes of pancreatitis
infections, mumps complications, trauma, peptic ulcers, vascular issues, HLD, hypercalcemia, alcohol, tobacco, hereditary
interstitial edematous pancreatitis
mild common form characterized by gland enlargement due to edema; minimal organ dysfunction that resolves in 6 months; risk of shock, fluid electrolyte imbalance, sepsis
necrotizing pancreatitis
severe rare form with tissue necrosis in or around pancreas; enzymes damage blood vessels leading to bleeding and thrombosis; necrosis may extend retroperitoneal; can cause organ failure
acute pancreatitis assessment
severe abdominal pain that radiates to back that is aggravated by meals and unrelieved by antacids; abdominal guarding; rigid abdomen if peritonitis, bruising in flank (turners sign) or umbilicus (Cullens sign); n/v, fever, jaundice; hypotension, tachycardia, cyanosis, cold skin, resp. distress, hypoxia, AKI, hypocalcemia, hyperglycemia, coag issues
chronic pancreatitis manifestation
recurring severe abdominal pain and back pain, attacks become more frequent severe and longer, weight loss d/t decreased intake and malabsorption, frothy foul smelling diarrhea, calcification of gland and formation of calcium stones
diagnosing acute pancreatitis
2 of 3 following- upper abdominal pain hx, amylase/lipase elevation, typical imaging
oncological diagnosis
consists of review of systems, PE, labs, biopsies, imaging
bleeding precautions
thrombocytopenia d/t chemotherapy: <50k increased risk for bleeding, <10k increased risk for spontaneous bleeding; concern for prolonged bleeding; soft toothbrush; no flossing; no razors; hold blood thinners; low threshold for fall precautions
HIV- human immunodeficiency virus
virus that targets cells with CD4+ receptors; transmission via blood, blood products, semen, vaginal secretions, mother to child through breast milk and amniotic fluid
AIDS- acquired immunodeficiency syndrome
chronic viral condition caused by human immunodeficiency virus; manifested by opportunistic infections and unusual malignancy; incubation can be 10+ years; may not be symptomatic until late in the infection
assessment for HIV/AIDS patient
malaise, fatigue, flu like symptoms, anorexia, weight loss, lymphadenopathy >3 months, leukopenia, diarrhea, night sweats, opportunistic infections, kaposi’s sarcoma
HIV stages of infection
stage 0- early, lab detectable, seroconversion, 2-12 weeks; stage 1 primary infection- CD4+ >= 500, HIV specific antibodies, flu like symptoms; stage 2 clinical latency- CD4+ 200-499 cells/mm3, asymptomatic, can still transmit, no opportunistic infections; stage 3 symptomatic infection- CD4+ <200, high viral load, opportunistic infections
diagnostic testing for HIV
antigen/antibody early as 2 weeks, HIV antibodies early as 2.5 weeks (rapid testing), Nucleic acid (RNA of virus in blood), CD4 count 500-1500is normal for non HIV (determines med therapy), plasma HIV RNA determines staging and progression
kaposi sarcoma
skinlike cancer present in individuals with HIV; most often males 60-70; elliptical-shaped cutaneous lesions; can be present on skin, anal cavity, mucosal membraneof GI tract (mouth to anus)
HIV neurological changes
HIV associated neurocognitive disorder (HAND)- subcortical neurodegenerative disease affecting 20% of those with HIV (changes in language, memory, problem solving and, psychomotor skill), peripheral neuropathy, HIV encephalopathy
rheumatoid arthritis
chronic systemic inflammatory disease, leads to destruction of connective tissue and synovial membrane within joints; exacerbated by stress and fatigue
pathology of RA
synovitis, pannus, joint disappears, bony ankylosis
manifestations of RA
years 20-60, can affect joints bilaterally, inflammation/tenderness/stiffness of joints, joint deformities, muscle atrophy, decreased ROM, spongy soft joints on palpation, constitutional symptoms like low grade fever fatigue weakness anorexia weightloss
diagnostic testing for RA
elevated ESR and/or CRP, positive rheumatoid factor, joint deterioration on imaging, synovial tissue biopsy shows inflammation
treatment for RA
NSAIDs to decrease inflammation, steroids, DMARDs (disease modifying anti-rheumatic drugs), biological response modifiers, surgery
nursing interventions for RA
increase mobility with ROM, pain management, self care by assisting with ADLs, decrease fatigue via monitoring for anemia and prescribing meds, assisting in disturbed body image
chemotherapy side effects
cytopenias, N/V/D, mucositis, alopecia, renal dysfunction, cardiotoxicity, infertility, neurotoxicity, fatigue, neutropenia
immunotherapy side effects
flu-like symptoms, hypersensitivity reaction, congestion, infection, capillary leak syndrome, pulmonary edema, myalgias, hypotension
neutropenic precautions
hand washing, washing fruits and vegetables, avoid bodies of water, gloves if gardening, avoid pet waste, dont share cups/utensils
sensory impairments in older adults
visual changes- cataracts, macular degenerations, glaucoma; auditory- presbycusis, tinnitus, earwax accumulation; cognitive changes- slower processing speed, short term memory changes, decreased multitasking ability
cataracts
clouding of the lense
macular degeneration
deterioration of the central portion of the retinag
glaucoma
increased intraocular pressure causing optic nerve damage and vision loss
nursing interventions for older adult vision losses
ensure adequate lighting, assistive magnifiers, regular eye exams
nursing interventions for auditory changes in older adults
regular hearing checks, regular cleanings, use low pitched clear speech, encourage hearing aid use
presbycusis
age related hearing loss usually to high frequency
bone health in older adults
decreased bone density; more susceptible to FX
integumentary changes in older adults
fragile skin more susceptible to temp changes, decrease subcutaneous fat
