Final Exam Quizlet Flashcards
hypovolemia
loss of water AND electrolytes
hypovolemia defining characteristics
confusion, combative, coma
tachycardia/pnea
irritable
dizzy, weak, fever
orthostatic hypotension
increased hct, BUN, and Na+
decreased hgb
hypovolemia interventions and assessments
monitor Na+, urine specific gravity, osmolality, vitals, I&Os, abd girth, daily weight
salt free foods
IV fluids
replace lost fluids over 48h
skin care and O2
hypervolemia
sodium and water retention
defining characteristics of hypervolemia
confusion, disoriented, convulsion, coma
increased BP
decreased BUN, hct, sodium, specific gravity
SOB, tachypnea, dyspnea, weak, crackles, pleural effusion, pulmonary edema, peripheral edema, ascites, polyuria, weight gain
hypervolemia interventions and assessments
monitor ABG, resp status, response to diuretics, rate of IV therapy, abd girth for ascites, strict I&Os, weight
restrict sodium and fluid intake, administer diuretics as prescribed, O2 therapy, elevate HOB
hypervolemia interventions and assessments
monitor ABG, resp status, response to diuretics, rate of IV therapy, abd girth for ascites, strict I&Os, weight
restrict sodium and fluid intake, administer diuretics as prescribed, O2 therapy, elevate HOB
resp acidosis risk factors
hypoventilation (COPD, PNA, atelectasis)
resp depression (barb or sedative, Guillain-barre)
resp arrest
resp acidosis clinical manifestations
neurological (coma, drowsy, disoriented)
cardio (hypotension, tachy)
resp (shallow, dyspnea, tachy, brady)
muscular (weak, tremors)
GI (N/V/D)
resp alkalosis risk factors
hyperventilation, anxiety, salicylates, disease states, mechanical overventilation, hypermetabolic states, acute hypoxia, pulmonary disease, anemia, hypotension
resp alkalosis clinical manifestations
neurologic: hyporeflexia, disoriented, weak, coma
muscular: tetany, hyperreflexia
respiratory: hyperventilation, dyspnea, tachypnea
cardiac: syncope, chest pain, EKG changes
diaphoresis
metabolic acidosis risk factors
cardiac arrest, ASA overdose, excess production of acids (DKA, lactic)
inadequate loss of acids (uremia)
excess loss of base (diarrhea)
metabolic acidosis clinical manifestations
neurologic: hyporeflexia, disoriented, weak, coma
GI: n/v/d, abdominal pain, dehydration
Cardiac: peripheral edema, weak pulse, hypotension
respiratory: hyperventilation
metabolic acidosis nursing interventions
treat underlying cause (diarrhea, DKA)
monitor K+ levels, neurologic status
provide mechanical ventilation
dialysis as ordered
metabolic alkalosis risk factors
loss of acids (vomit, excess gastric suctioning)
base or buffer imbalance (K+ deficit, excess NaHCO3 intake)
disease states (cushings, kidney)
multiple transfusions
over correction of acidosis
metabolic alkalosis clinical manifestations
neurologic: confusion, stupor, coma
GI: anorexia, nausea, vomiting
MS: weakness, tetany, paresthesia
hyperreflexia, tremors, cramps
respiratory: hypoventilation, cyanosis
potassium important info
NEVER IM OR IV PUSH/BOLUS
never on empty stomach
diuretics cause what
K+/Na+ loss
5 pain stimulating substances
histamine
bradykinin
acetylcholine
potassium
prostaglandins
3 pain controlling substances
enkephalins, endorphins, serotonin
acute pain
SYMPATHETIC nervous system responses
related to specific injury
protective pain
pt restless, anxious
goes away within 3 months
distinct starting point and cause
chronic pain
PARASYMPATHETIC
adaptation response
6 months+
chronic pain treatment
decrease time loss from work
increase quality of relationships
decrease anxiety
superficial pain
in cutaneous area
mild to moderate pain with sympathetic manifestations (rapid, shallow, respirations)
deep somatic pain
felt below the cutaneous area
both sympathetic and parasympathetic
ex. tendons, ligaments, bones, blood vessels, nerves
visceral pain
can have superficial or deep somatic pain that localized
confined to a specific area
referred pain
felt in a part of the body other than where the pain was produced
a type of visceral pain
usually originates in one organ but felt in the skin
intractable pain
severe pain
resistant to treatment and any of the usual relief measures
pt usually referred to neurologist
breakthrough pain
acute exacerbation of pain that is transitory
ex. pt given q4 hours but experiences pain in between the doses
still must be treated
cancer-related pain
progression of cancer
can be caused by treatment
acute or chronic
large dose of pain meds
not PRN, around the clock
adaption response
vitals are normal, no symptoms
only discuss pain if asked
sleepiness, shifting away or guarding, facial expressions, withdrawing from socialization
NSAIDS do what
block prostaglandins in PERIPHERY
acetaminophen does what
blocks prostaglandins in CNS
analgesic adjuvants
anticonvulsants and anti anxiety
pain management WHO ladder
mild-moderate: nonopioids like ASA, NSAIDS, paracetamol
mod-severe: mild opioids (codeine), with or without nonopioids
severe: strong opioids (morphine) with or without non opioids
pain meds effective within how long
30-60 min
elderly nursing responsibilities (drugs)
more sensitive
monitor opioid doses, titrate down
reduced sensory perception and metabolism
PCA
Patient is getting a continuous dose every hour, but is allowed to get a bolus infusion every 15 minutes if they need more relief.
- Used for cancer pain and post op pain
-Morphine/ Hydromorphone
cancer treatment considerations
biopsy
neutropenic precautions
hospice
chemo
internal radiation
chemo
3 kinds of biopsy
excision
incision (large tumor where part are removed for analysis)
needle biopsy (tissue samples from mass are aspirated)
neutropenic precautions
no flowers/fresh fruit/raw veggies
wear mask, gown, gloves
avoid crowds
keep door closed
disposable equipment used
hospice
6 months or less to live
chemo
systemic intervention
antineoplastics (kills cancer cells)
Primary, adjuvant, or neoadjuvant
Given VAD (larger veins in chest, implanted in chest, dressing changed every 48 hours), or a PICC
MONITOR NEUTROPHILS
chemo side effects
finger numbness, bone marrow suppression (MONITOR FOR 100 DAYS), n/v, anorexia, GI disturbance, alopecia, mucositis (culture lesions), stomatitis, loss of libido, impotence
internal radiation
brachytherapy
sealed/unsealed source
radioactive device in patient
brachytherapy
device in pt so radiation is in continuous contact with tumor
pt is radioactive while device is in them
strict bedrest with bathroom privileges, low residue diet, antidiarrheals, urinary catheter
internal radiation safety standards
distance, time, shielding
avoid handling if dislodged
6 feet away at all times except essential care
30 min/8 hours
give meds at same time as assessments
pt alone in room
internal radiation systemic side effects
nausea, fatigue, myelosuppression (thrombocytopenia, leukopenia, anemia)
internal radiation localized effects
stomatitis, dysgeusia (altered taste sensation), xerostomia (dry mouth)
cancer excision surgery
tumor is small and excised
removed entirely and sent to lab for examination
paliative surgery
done when cure is not possible to improve quality of life
microcytic anemia
iron deficiency
megaloblastic anemia
folic deficiency
pernicious anemia
B12 deficiency
hypoproliferative anemia
underproduction of RBCs by bone marrow
hemolytic anemia
increased destruction of RBCs
RES destroys RBCs
hgb levels and clini manifestations
mild: 10-12
asymptomatic, fatigue
moderate: 6-10
fatigue, dyspnea, palpitations, tachy, diaphoresis on exertion
severe: below 6
chronic fatigue, severe symptoms, peripheral edema
anemia diagnostics
history and physical CBC
reticulocyte count
coag screening (INR, PT, PTT)
bone marrow aspiration
INR/PT
warfarin
PTT
heparin
iron deficiency anemia (microcytic) risk factors
blood loss
hemorrhoids
menstruating and pregnant
adolescents, children, infants
microcytic anemia nursing care
diet rich in eggs, meat, leafy greens, liver (best source), vit C
minimal milk, fiber, soy, coffee, tea
supplemental iron (rinse, straws)
Z track injections
monitor for dark tarry stools (can indicate internal bleeding)
avoid antacids
folate deficiency anemia risk factors
does not affect nervous system
alcohol
seizure meds
genetics (crohns, celiac)
infants
megaloblastic anemia treatment
oral/dietary supplements (folic acid from diet, vit B12)
treat underlying condition
decrease alcohol
S&S of megaloblastic anemia
decreased appetite
irritable, fatigue, diarrhea, glossitis, pallor
B12 deficiency (pernicious anemia) diet
meat, fish, fortified cereal, tofu
pernicious anemia risk factors
decreased b12/malabsorption
ileal resection
crohn’s disease
gastrectomy
hereditary lack of intrinsic factor
vegans
autoimmune
anything harming gastric lining
pernicious anemia symptoms
slow onset
decreased mental status (peripheral neuropathy)
glossitis (beefy red tongue)
mood swings
decreased CO
decreased RBC, hgb. hct
vitiligo and greying hair
pernicious anemia diagnosis
schilling test
PO administration
small dose of radioactive vit B12
if urine is radioactive, it means they have enough B12 so it’s being excreted, which is good
pernicious anemia management
Vit B12 injections
never orally if caused by gastrectomy
cyanocobalamin (IM or nasal spray), monthly, response within 24-48 hr, within 72 hr RBC and reticulocyte count increases
iron supplements
o2 administration
blood transfusions
erythropoietin injections twice a week until iron stores are replenished
aplastic anemia
normocytic and normochromic erythrocytes (normal size and heme content, low in number)
bone marrow hypoplasia: incomplete RBC development
bone marrow aplasia: lack of RBC development
pancytopenia: BM suppression, decreased RBC, WBC, PLT
aplastic anemia risk factors
congenital
idiopathic
idiosyncratic (drug reaction)
acquired (myelotoxins)
autoimmune infections: epstein barr
aplastic anemia causes
altered stem cell: inhibits division
altered BM (replaced by fat)
aplastic anemia S&S
pancytopenia
petechia (low PLT)
purple/red spots
purpura (bleeding under skin)
retinal hemorrhage
hypoxia
anemia S&S
aplastic anemia care
immediate withdrawal of offending agent
transfusions
radiotherapy
bone marrow transplant
bone marrow aspiration/biopsy
TB
reportable, communicable, inflammatory, destructive disease
spread from person to person via inhalation of infected droplet nuclei
TB risk factors
homeless, malnutrition, overcrowded areas, health care workers, immune dysfunction, alcoholism, children under 3, elderly, certain geographic areas, men double the rate of women
TB microorganism characteristics
aerobic
acid fast
reproduces slowly in the body
destroyed by heat, sun, and pasteurization
TB sensitization
1st time individual is infected= develops a sensitivity reaction
occurs 2-10 weeks after primary infection
positive reaction to tuberculin skin tests
TB infected individuals
residual remains dormant in lungs
asymptomatic
partial destruction of most organisms can occur
may reactivate later when resistance is decreased
can be triggered by mental and physical stress, oncology, inadequate drug treatment
TB skin test
people with HIV may get false negative, contraindicated in BCG vaccine patients
reliable
appearance of a “wheal”, induration area read within 48-72 hours
10mm or more is positive reaction
TB converters
someone who develops a positive skin test, negative test converted to positive
high risk for developing TB
placed on INH preventative therapy for 6-12 months
quantiFERON-TB gold test
preferred to those with BCG
results in 24-36 hours
negative test means no latent or active TB
TB sputum culture
confirms diagnosis
3 specimen on consecutive days
negative TB test
no longer contagious
contagious until treated
TB patient room
isolated
negative pressure until negative sputum culture
wear mask for 3 weeks
TB management
treatment for 6-12 months
primary resistance TB
one or more line of anti TB agents
secondary (acquired) resistance
resistance to one or more anti TB agents and undergoing therapy
multi-drug resistance TB
resistance to 2+ agents like INH and rifampin
first line TB drugs
INH and rifampin
pyrazinamide (PZA, for active TB)
ethambutol (myambutol)
TB interventions
teach regimen and side effects, importance of compliance
prevention of spread
what to avoid with INH
high protein, high calorie, high calcium diet with iron and B6 supplements
5 foods to avoid with INH
tuna, red wine, aged cheese, soy sauce, yeast extract
asthma incidence, etiology, risks
allergy, esophageal reflux, male, genetics, elderly, urban areas, ethnicity
asthma clinical manifestations
wheezing, chest tightness, dyspnea, SOB, no wheezing if blocked, cough, tachycardia, diaphoresis, anxiety, panic, mood changes, hyperventilation
bronchodilators
increases smooth muscle relaxation
no effect on inflammation
increase fluid intake
take 5 min before other inhaled drugs
monitor HR
methylxanthines
long acting
theophylline
dilates bronchi, used when other drugs ineffective
can build up and become toxic
cholinergic agonists
intermediate acting
ipratropium
watch for increased HR
anti inflammatory drugs asthma
corticosteroids
long acting, local or systemic
pulmicort/flovent/azmacort= most common
significant S/E= delayed wound healing, personality changes, fluid retention, taper doses, rinse mouth
asthma complications
pneumonia, atelectasis, hypoxemia, respiratory acidosis, respiratory failure, emphysema, chronic hypoxia, chronic bronchitis, asthmaticus
COPD
emphysema and chronic bronchitis
symptoms of COPD
worsening breathlessness upon exertion, leads to breathlessness at rest
COPD etiology and risk factors
smoking, alpha 1-antitrypsin deficiency, air pollution, occupational exposure, infection
clinical manifestations of COPD
distended neck veins, right ventricular enlargement, lower sternal pulsations, GI disturbance, weight loss, dependent edema, metabolic and resp acidosis, pulmonary hypertension, hypoxia, fatigue, weak, enlarged/tender liver, bounding pulse, warm cyanotic extremities, cough
oxygen therapy for COPD
heated, humidified system
clear secretions
monitor liter flow and effectiveness with pulse ox., oxygen toxicity and oxygen induced hypoventilation, skin breakdown, anxiety
teach at home use
COPD complications
pulmonary hypertension, cardiac dysrhythmias, pneumonia, atelectasis, pneumothorax, bronchospasm, RF
emphysema
increased ventilatory “dead space”, hyperinflation of the lung, loss of elasticity, increased mucus, destruction of alveolar walls, alveoli collapse, spontaneous pneumothorax, chest tube for re-expansion of lung
caused by smoking, genetics, pollution
emphysema clinical manifestations
severe SOB at rest
PaO2 level below 40mmHg
chronic productive cough
barrel chest
wheezing, crackles, rhonchi
diminished breath sounds
tachypnea
hypoxia
hypoxemia
hypercapnia
fatigue
anorexia
PVD
stasis of blood in lower extremities from damage or obstruction (raise them)
muscle pumping action during activity is not sufficient to help pump blood to the heart
venous insufficiency nursing care
thigh high stockings when awake
elevate legs above heart when sleeping (and for 4 min 4x/day)
avoid crossing legs, prolonged sitting or standing
daily walks
no warm soaks, avoid topical therapy, high cal and protein diet
clinical manifestations PVD
reddish blue discoloration
muscle cramps
increased pain w ambulation
dilated superficial veins w edema
mild ankle swelling
heaviness, erythema, lipodermatosclerosis, stasis dermis/ulcers
S&S arterial insufficiency
claudication numbness and tingling, decreased or absent pulses bilaterally, pale elevated leg and dusky/red when dependent, cool, absent or mild edema, dry skin, ulcers on toes and gangrene
S&S of venous insufficiency
feeling of fullness with prolonged sitting or standing
difficult to find pulse
cyanotic on dependency
warm
edema present
moist skin
superficial ulcers with gangrene
PE risk factors
venous stasis, HRT, fracture (fat embolus)
PE S&S
chest pain
tachy
dyspnea
dry cough
blood tinged sputum
petechiae
hypotension
low grade fever
PE treatment
monitor for bleeding in urine or tarry stool, teeth brushing
anticoags
complete bed rest
HTN guidelines
lower SBP <140, diastolic <90
based on 2+ BP readings taken on 2+ separate occasions with HCP
essential (primary) htn
no known cause
associated w obesity, smoking, family hx, sodium or alcohol, stress, ethnicity, gender
secondary HTN
specific disease states (identifiable causes such as kidney disease or meds)
malignant HTN
severe increase in BP with rapid progression
ages 30-50
systolic may be 200+
pulmonary HTN
vasoconstriction of pulmonary arterial circulation creates high pulmonary artery BP
poor tissue perfusion, hypoxemia, may get right sided HF
isolated systolic HTN
mostly seen in older adults
systolic >140, diastolic normal
more energy needed for circulation
HTN urgency
high BP
no evidence of organ damage
fast acting oral agents, normalize BP within 24-48h
HTN emergency
BP >180/120
damage to organs
IV vasodilators reduce BP by 25% within 1 hour
gradual reduction over 6 hours
type 1 DM
insulin dependent
S&S of type 1 DM
3 Ps
weight loss
fatigue
frequent infections
muscle wasting/cramps
ketosis (fruity breath)
type 2 diabetes
functioning pancreas
risks of type 2 DM
obesity, inactivity, heredity, sedentary lifestyle, genetics, above 50, hx of high BP, fatigue, decreased energy, frequent infections
hypoglycemia clinical manifestations
glucose below 60
give OJ, honey, hard candy
JUICE, STARCH, PROTEIN
TIRED: tachy, irritable, restless, excessive hunger, diaphoresis/depression
assess glucose, urine, mental changes, N/V/D
DKA
dehydration, hypovolemic shock, lactic acidosis, slow onset, fruity breath, tachy, hypotension, acidosis, high blood sugar, hyperkalemia
D: diuresis, delirium, dizzy, dehydrated
K: kussmaul/ketone breath
A: abd pain
DKA treatment
dehydrate with NS, reverse shock, restore potassium, administer insulin
monitor blood sugar and urine (ketones and proteins)
HHNS
only in type 2 DM
urine test + for glucose but - for ketones
no acidosis
glucose from 600-3000
give fluid and electrolytes with insulin
rapid acting insulin times
onset: 5-15
peak: 30-60
duration: 2-4h
rapid insulin examples
lispro (humalog), aspart (novolog), glulisine
given with meals and can be IV
short acting insulin times
onset: 30-60 mins
peak: 2-3h
duration: 4-6h
30-60 min before a meal and can be IV
intermediate insulin times
onset: 2-4h
Peak: 4-12h
duration: up to 12h
given after food
intermediate insulin examples
novolin L and novolin N
Long acting insulin times
onset: 1-6h
no peak or duration
DO NOT MIX
diabetes and exercise
exercise for 20-45 min, 3x/day
complex carbs to prevent hypoglycemia
diabetes diet
10-20% protein
20-30% fat (10% sat)
50-60% carbs
DM diagnosis
fasting glucose >126 (NPO 8-12h)
glucose tolerance: check glucose q3h, nothing but water and the drink
postprandial: >200, check 2h after meal
HbA1c: >6.5% (goal is <7%)
diabetes foot care
properly fitting, non restrictive shoes
avoid prolonged sitting, standing, crossing legs, walking barefoot, open toed shoes
inspect feet daily using a mirror
cut nails straight across after bath/shower
avoid lotion between toes, dry thoroughly
microvascular complications of DM
diabetic retinopathy (control glucose and BP)
nephropathy
neuropathic complications of DM
mononeuropathy
polyneuropathy
autonomic neuropathy
nerves become edematous, myelin sheath becomes damaged, nerves become damaged
feet and lower limbs become numb, ache, or throb
can cause impotence or decreased libido
macrovascular complications of DM
CAD
CVD
HTN
PVD
infections from immobilized WBC, usually in mouth, feet, bladder, female genitals, causes gingivitis
high lipids when glucose is high
high bad fats
complications of insulin administration
local: rash at site
systemic: hives
lipodystrophy: disturbance of fat metabolism with insulin absorption
lipoatrophy:loss of fat w dimpling
lipohypertrophy: fibro-fatty masses at site with scarring
hyperthyroidism
fine tremors, heat intolerance, many loose stools daily, diaphoresis, warm moist skin (salmon color), palpitations, rapid pulse at rest
hyperactive DTR, increased appetite, insomnia, weakness, nervous, restless, emotional hyperexcitability, irritable, apprehensive, rapid speech
nursing care of hyperthyroidism
monitor SE of meds, S&S of thyroid crisis, place in private room with cold temp, stimulus should be avoided
hypothyroidism
subnormal temp, intolerance to cold, decreased metabolism, dry skin with course, thick, pale, carotene look, thick and brittle nails, hair thins, hypotension and bradycardia, weight gain, paresthesia of fingers, hypoventilation, expressionless face, apathy, large tongue, slow speech, drooling, large goiter
hypothyroidism nursing care
provide high bulk, low calorie diet
administer cathartics/stool softeners
after replacement check for signs of hyperthyroidism
encourage med alert bracelet
prevent myxedema coma
education pt on infection reporting & importance of medication
medication effects not seen for at least 2 weeks, monitor for levothyroxine SE
subtotal thyroidectomy
5/6 part of the thyroid gland is removed
prolonged remission
remaining gland is sutured to trachea
total thyroidectomy
for thyroid cancer
lifelong HRT
thyroid surgery
done for children, adolescents, pregnant women, who cannot tolerate PTU or those who have large goiters causing esophageal compression
risky, may cause nerve damage or hemorrhage
preop management
euthyroid for 2-3 months
to decrease size and vascularity of gland
given thioamide 4-6 weeks before surgery
postop pt teaching thyroid surgery
coughing and deep breathing
support neck
no talking
lifelong HRT
on empty stomach, 30 min before meals
postop management thyroid surgery
monitor for hypocalcemia
airway humidification
suctioning
restrict visitors
increase cals, protein, and carbs
small, frequent meals
weight, intake and output
thyroid storm
life threatening
sudden surge of large amounts of thyroid hormone in blood (abrupt)
high fever (106º), severe agitation, confusion, n/v/d, malignant exophthalmos, dyspnea, coma, vascular collapse
cholelithiasis
calculi in the gallbladder
gallstones composition (pigment: 25%, cholesterol: 75%)
biliary colic with obstruction of cystic duct
stone may retreat or pass
cholelithiasis diagnostics
ultrasonography, cholecystography, endoscopic retrograde cholangiopancreatography, PCT, MRI, blood test, X-ray
cholelithiasis treatment
ERCP and PTC (removal of stones) and extracorporeal lithotripsy to dissolve stones
NG tube
nutrition: low fat
avoid alcohol, gas forming foods, fried foods
drug therapy: antibiotics, lipid/cholesterol lowering drugs, antispasmodics, analgesics
cholecystectomy
surgical procedure to remove gallbladder
cholelithiasis postop care
assess, monitor vitals, O2 sat, skin care, biliary drainage, t-tub or NG tube, pain control, I&O, encourage activity
low fat diet, ideal weight, limit pregnancies
report fever, jaundice, pruritus, dark urine, pale stools
dumping syndrome
food rapidly enters jejunum
vasomotor disturbances
within 10-30 minutes after eating
vertigo, tachy, syncope, sweating, pallor, palpitations, N/D, weakness
dumping syndrome pt teaching
small frequent meals
avoid drinking with meals
high protein, high fat, low carb, low fiber (dry diet)
antispasmodics
lying down after meals
GERD
Backflow of gastric contents into the esophagus
incompetent LES and inflamed esophageal mucosa
mucus and saliva are protective factors
GERD risk factors
unknown cause
pressure zones, weight gain, obesity, pregnancy, lying flat, spicy food, high fat foods, caffeine, carbonation, chocolate, chewing tobacco, elderly
NSAIDs and stress increase gastric acid
clinical manifestations of GERD
dyspepsia
pain after activities/meals, supine position, radiates to the back of neck or jaw (confused with angina), walking
esophageal spasm/odynophagia
intermittent dysphagia
acid regurgitation
water brash
eructation
distended abdomen
GERD diagnosis
barium swallow, esophagoscopy, esophageal biopsy, cytology, gastric secretions, acid tests
medical management of GERD
mild- antacids, work in 30 minutes to increase gastric pH, avoid mg antacids
persistent- histamine receptor antagonists, reduce gastric secretions, take 1 hr before or after antacid
severe- cholinergic drugs (reglan) increases LES pressure and gastric emptying, taken before meals
PPIs (nexium) suppress gastric secretions
GERD nursing interventions
small frequent slow meals
chew!
avoid hot or cold foods
don’t drink 2-3h before bed
elevate HOB 30
avoid tobacco, fatty, chocolate, caffeine
no strenuous activity after meals
bowel obstruction
impairment of forward flow of intestinal contents
high mortality rate if not treated within 24 hours
partial or complete
mechanical (blockage) or nonmechanical (paralytic ileus)
etiology of bowel obstruction
adhesions (most common), tumors, hernias, fecal impaction, strictures, narrowed blood vessels, intussusception, volvulus, ileus
bowel obstruction assessment
hiccups, last BM, fever, ribbon like stools, tachycardia, bowel sounds may be absent or decreased or increased, a mass
bowel obstruction clinical manifestations
abdominal cramps, fever, nausea with vomiting (may be orange or brown with fecal odor), hiccups, obstipation, partial obstruction, fluid and electrolyte imbalance
diagnostics for bowel obstruction
CBC, BUN and electrolytes, elevated amylase if pancreas affected, ABG abnormal, abdominal X-rays, CT scan, colonoscopy
bowel obstruction treatment
nonmechanical obstruction (NG)
mechanical obstruction (NG tube and removal of obstruction)
fluid and electrolyte replacement
pain management (avoid opioids)
antibiotics
surgery
surgical options for bowel obstructions
laparotomy if the cause is unknown (to find cause), adhesions removed, bowel resection
ulcerative colitis
starts at rectum and works way up, continuous, not deep, just first layer
inflamed mucosal lining of colon or rectum
unknown etiology
tobacco protects against development of UC (risk for Crohn’s)
LOW FIBER, LOW RESIDUE, LOW FAT DIET, high protein and calories
UC S&S
many loose stools with pus, blood, or mucus (10-20 liquid stools per day)
dehydration
intermittent tenesmus (straining)
metabolic acidosis or alkalosis
fistulas from exertion
toxic megacolon
crohn’s disease
deeper, not continuous, some lesions
inflammatory disease of the small intestine or beginning of colon
flares and remissions
healthy tissue interspersed with diseased tissue
crohn’s S&S
steatorrhea from malabsorption (frequent fatty stools, 5-6 per day)
loss of appetite
periumbilical pain
low grade fever
increased WBC
urgency, straining
ileostomy preop
psychological prep
bowel prep (neomycin)
cleaning enema
discuss post op incentive spirometry and breathing exercises
refer counseling
permanent ileostomy
terminal ileum brought out through the abdominal wall
brought into intra-abdominal pouch
drained with catheter
emptied every 2 hrs in the first 2 weeks
ileoanal anastomosis
colon and rectum removed
J pouch
colon removed leaving rectal sphincter
billroth 1
a gastroduodenostomy and involves resection of the lower portion of the stomach. offers a lower cure rate than the billroth 2
billroth 2
a gastrojejunostomy, the lower portion of stomach removed
MS
CNS (brain and spinal cord)
chronic, autoimmune, degenerative
inflamed nerve
loss of myelin (protects the nerves)
increase in oligodendrocyte (cells that produce myelin)
patches of plaque in white matter of CNS
schwann cells destroyed
MS triggers
infection, trauma, pregnancy, fatigue, stress
RRMS (relapse-remitting MS)
exacerbations and remissions
PPMS (primary progressive MS)
symptoms gradually worsen
SPMS (secondary progressive MS)
10-25 years after PPMS
no real recovery
PRMS (progressive relapsing)
escalates severely, few remission periods
MS etiology and contributing factors
unknown, age 20-40, immune system malfunction, viral, genetics, environmental
high suicide rate
maintain normal family function
MS diagnosis
history, mcdonald criteria (2 episodes one month apart), neuro symptoms (blurred vision, muscle weakness)
MRI
evoked potential
MS clinical manifestations
visual blurring, diplopia, blindness, nystagmus, oscillopsia
intentional tremors, poor condition, numbness, spasm, sensitivity to heat, fatigue, lassitude (collapse), poor memory, judgment, and reasoning
MS nursing management
relieve symptoms, mobility (ROM exercises), bladder, high fiber diet
prevent overheating
wide-based gate walk
increase fluids to relieve constipation
void every 2 hrs to prevent UTI
kegel exercises
avoid laxatives
MS meds
anticholinergics
amantadine HCL
antidepressants
beta blockers
antihistamines
muscle relaxants (baclofen)- spasticity
immunoregulatory (avonex, beta-interferon, rebif, copaxone, etc)
MG
autoimmune neuromuscular disease
acetylcholine receptors depleted
weakness (hallmark symptom) in the presence of sustained contraction
relieved with rest
low acetylcholine
MG clinical manifestations
ocular-diplopia and ptosis (drooping eyelid)
facial- dysphagia, dysphonia, mastication
larynx- dysarthria, aspiration, dysphagia
limbs- unsteady gait
weak diaphragm
MG diagnosis
tensilon test or edrophonium chloride- blocks breakdown of acetylcholine, given 2mg of tensilon injected IV. if muscle tone increases, an additional 8mg is given
no response= pt given bromide injected IV
serum tests- antibodies to SCH receptors
electromyography (EMG)
chest x-ray (enlarged thymus gland)
MG complications
MG crisis (increase anticholinesterase)
cholinergic crisis (decrease anticholinesterase)
MG drugs
anti-cholinesterase (bromides)
immunosuppressives (prednisone, cytoxan)
plasmapheresis (removed acetylcholine receptor antibodies)
thymectomy (thymus excision)
MG nursing management
medications at exact same time
given 30-60 min before meals
given before ADL’s
cut food into small bites, sit upright
main meal= when pt is least fatigued (AM over PM)
protect eyes (sunglasses)
wear medical alert bracelet
may need artificial tears
rest periods throughout the day
parkinson’s
affects voluntary movement
chronic neurodegenerative disease, juvenile
idiopathic (unknown cause)
latrogenic (caused by drugs)
more men than women
destruction of cells in substantia nigra
DECREASED DOPAMINE
loss of control, coordination, and initiation of voluntary movement
post encephalitic parkinsonism
pt had encephalitis as a kid, developed parkinson’s symptoms as they aged
parkinson’s cardinal signs
tremors (resting, micrographia, pill-rolling)
supination/pronation
bradykinesia
rigidity
resting tremors disappear with slow, purposeful movement
propulsive gait
festination (short, shuffling steps)
hypomimia
dysphagia
rigidity of chest wall
TRAP
tremors
rigidity
akinesia
postural instability
parkinson’s teachings
high risk for falls, no rugs
firm chairs with arms
velcro/slip on shoes and clothes with buttons
rock back and forth to get up
eat sitting upright
wide based gait
raised toilet seat
parkinson’s nursing care
give semisolid foods with thickeners for dysphagia
pyridoxine, no alcohol, evenly distribute low protein
drug holiday (no stimulation room)
PT
speech pathologist for swallowing
parkinson’s diagnosis
presence of symptoms
trial of levodopa (consistent response to drug rules out parkinson’s like syndrome)
pt may have to walk around to observe for rigidity and resting tremors
levodopa for parkinson’s
only lasts 5-10 years
carbidopa for parkinson’s
combination: sinemet
gets more levodopa to the brain
non ergot derivatives
requip, mirapex
dopamine antagonist
parlodel, permax
MAOIs for parkinsons
selegiline
antivirals for parkinsons
amantadine
other 3 meds for parkinson’s
COMT inhibitors
antidepressants
antihistamines
guillian-barre
affects PNS
clinical manifestations of guillian barre
rapid onset of pain
ascending pattern
paralysis (over a few hours, lasting 1-4 weeks), paresthesia
dyskinesia
loss of DTR
respiratory paralysis (late symptom)
vocal paralysis
bladder incontinence/incomplete emptying
constipation, dizzy, cramps, BP affected
nursing management of guillian barre
ventilator, incentive spirometer, chest PT, suction to prevent aspiration, mobility, HOB15-30º. passive ROM, thigh high stockings, check bowel sounds, monitor gag reflex, TPN or G tube
refer to speech pathologist
partial (focal) seizure
simple partial (no LOC, changes in senses, aware of surroundings but can’t control, lasts 30s)
complex partial (LOC, automatism, blacks out, bizarre behavior)
generalized seizure
whole brain
tonic clonic, absence, myoclonic, atonic
myoclonic seizure
brief jerking of muscles and LOC
seizure diagnostic tests
history
EEG (within 24 hrs of seizure)
computer tomography
MRI
telemetry (brain activity monitor)
videotaping
pharm therapy for seizures
control, raise threshold, therapeutic blood level, monitor for allergies/toxicity, give meds at same time each day
switching meds: 1 med is tapered as the other is increased
phenytoin, carbamazepine, clonazepam, diazepam or lorazepam (IV), luminal (phenobarbital)
seizure pt teaching
phenytoin causes gingival hyperplasia, hirsutism, hypothermia, diplopia, BMS
avoid triggers
take meds on time and correct dose
avoid dangerous activities
wear protective headgear
lie down if experiencing aura
meticulous oral hygiene with phenytoin
wear medical alert bracelet
nursing care for seizures
assess for aura and triggers
establish/maintain airway
move objects, remain until consciousness returns
do not insert anything into mouth
turn head to the side
padded siderails on the bed
do not restrain or shout
call ambulance if seizure is longer than 10 minutes
oxygen/trach equipment at bedside
maintain saline lock for pt incase medication is needed
cast care
after swelling subsides, support extremity from underneath the palm
fingertips should NOT be pressed into cast
should not rest on hard or sharp surface before dried
cleanse pt of excess cast material
wait 30 min before weight bearing
dry plaster cast is odorless, resonant, and white, feels close to room temp
compartment syndrome
impaired blood flow within fascia
caused by external pressure (casts, splints, crushing injury, surgery, trauma)
or internal pressure (blood or fluid accumulation)
compromise in circulation, tissue death, nerve injury, ischemic-edema cycle
4-6 hr untreated= irreversible neuromuscular damage
24-48 hr, limb becomes functionless (amputation)
compartment syndrome manifestations
unrelieved ischemic pain (not controlled with analgesics)
pain with elevation (decreased arterial flow)
diminished or absent pulses distal to injury
cyanosis of extremity
tingling/paresthesia
coolness of extremity
weak
irreversible neuromuscular damage, functionless limb
osteoporosis
disrupted remodeling process
osteoclast (bone resorption)
osteoblast (bone building)
low bone mass, loss of Ca, bone deterioration, porous bone
decreased bone mineral density (peaks between ages 10-35), decreased rapidly with postmenopause
increased bone fractures- hip, vertebrae, radius
osteoporosis risk factors
female, post menopause, breastfeeding, caucasian, asian, african american, family hx, sedentary, smoking, alcohol, Ca and/or Vit D deficiency, liver disease, antithyroid med, anticonvulsant med, corticosteroids
osteoporosis pt teaching
encourage dairy, Ca supplements, Ca foods (greens, sardines, salmon with bone, broccoli)
avoid high intake of protein, sodium, caffeine
weight bearing exercises (walking or running)
Ca supplements with 6-8oz of water and food
diphosphonates to increase BMD (taken 30-60 min before meals)
osteoporosis med management
prevent loss of BMD
prevent bone resorption= hormone replacement therapy in post menopause
osteoarthritis
slowly progressive chronic-joint disease
degeneration and loss of cartilage covering synovial joint surfaces
most common form of arthritis
risk factors- middle ages, obesity, knee arthritis, sports, work injuries, repetitive joint injuries, genetics (defective cartilage or joints)
clinical manifestations of osteoarthritis
Early morning stiffness & joint pain, crepitus
Pain occurs during activity and relieved with rest
deficits in ROM
joint enlargement
heberden’s nodes (raised bony growths over distal interphalangeal joints of hand)
bouchard’s nodes (raised bony growths over proximal interphalangeal joints of hand)
total knee replacement
continuous passive motion (8hr/day)
teach s&s of infection, DVT
physical therapy
prophylactic antibiotics
total hip replacement
maintain 90º flexion of hip for 4-6 weeks
sit in straight and high chairs with arms
abduction pillow
avoid internal rotation of toes, crossing legs, twisting to reach objects, driving, tub baths, for 4-6 weeks
elevated toilet seat
complications of THR and TKR
calf and groin DVT
pulmonary embolism (prophylaxis LMW heparin)
infection (wound drainage, fever, pain, odor)
long term complications: joint stiffness, post-traumatic arthritis, avascular necrosis, nonfunctional union after fracture, malunion
arthrocentesis
surgical puncture of a joint
pin assessment and care
check every 8 hours
ice for first 24-48 hours (only one hour at a time to prevent edema)
sterile cotton tipped swab used to clean one pin at a time
buck’s traction
may be used before surgery
returns bone fragments to original position
partial weight bearing
no fowler position, joint ROM every shift
volkmann’s contracture
permanent flexion contracture of the hand at the wrist
results in a claw-like deformity of the hand and fingers
cold fingers (white or blue)
more common in children
radial pulse absent
painful restricted passive extension of fingers
fat embolism syndrome
fat globules (released from bone marrow) lodge in the pulmonary vascular bed or peripheral circulation
acute respiratory distress syndrome (ARDS)- may need mechanical ventilation
pulmonary embolus- hypotension, chest pain, fever above 105º, LOC changes
kyphosis
forward thoracic curve of spine
lordosis
inward curve of lumbar spine
amputation care
improve function and quality of life
post op- pain relief, absence of altered sensory perceptions, wound healing, acceptance of altered body image
rehabilitation
obtain prosthesis
amputation complications
hemorrhage, infection, phantom limb pain, neuroma, flexion joint contracture
pruritus
most common symptom of skin disorders
nerve endings in skin trigger itching
may indicate more serious diseases (ex. diabetes, blood disorders, liver issues)
certain meds may induce pruritus (aspirin, hormones, opioids)
pruritus nursing management
encourage pt to avoid scratching
assess for skin breakdown
apply cold compress
encourage tepid baths
use a humidifier (cool, moist environment)
medical management of pruritus
topical antipruritic agents (lidocaine and capzasin)
topical corticosteroids
oral antihistamines
melanoma
from a mole
asymmetrical
red blotchy color
diameter >6mm
can spread
melanoma care
pain, anxiety, depression, knowledge deficit
treatment is usually surgical excision of tumor and maybe chemo
psoriasis
chronic, noncommunicable skin disease
silvery plaques over elbows, knees, scalp, lower back, buttocks
no known cure
goal= slow down rapid turnover of epidermis
head lice
parasitic insects that live on the hair shaft and cause itching
