test 4 Flashcards
polycystic kidney disease
cysts on kidneys from mutations in genes
no cure
most common hereditary and autosomal deficit
*prevent infection of urinary tract
acute kidney injury
sudden onset
reversible but could lead to CKD
-commonly caused by acute tubular necrosis from shock
diagnosed by elevated BUN, creatine, K, and possible oliguria
primary cause of death is infection
chronic kidney disease
onset- months to years
irreversible
later stages will require dialysis
diagnosis- uremia/anuria, HTN
cardio issues is most common cause of death
also called chronic renal failure
BUN in kidney disorders
elevated
creatine in kidney disorders
elevated
glomerular filtration rate (GFR) in kidney disorders
low
potassium in kidney disorders
elevated
hemoglobin and hematocrit in kidney disorder
low
RBC in kidney disorders
decreases (less erythropoietin being made)
phosphorus in kidney disorders
elevated
magnesium also increases
calcium in kidney disorders
low
sodium in kidney disorders
low
risk factors for CKD
age over 60
heart issues
diabetes
ethnicity (Af amer, native amer)
HTN
Family hist
PKD
peritoneal dialysis
In peritoneal (stomach), done at home, higher risk for infection
hemodialysis
Artery and vein put together, cleaning blood and replacing. done at clinic about 3x weekly
Check for bruit and thrill, it should feel this way
benign prostatic hyperplasia (BPH)
Enlargement of prostate gland, disruption of urine outflow
- difficulty urinating
- decreased flow
-urinary frequency
BPH risk factors
aging
obesity
lack of physical activity
alcohol use
erectile dysfunction
smoking diabetes
family history
inflammatory urinary symtoms
from inflammation or infection
nocturia
urgency
frequency
dysuria
bladder pain
incontinence
obstructive urinary symptoms
from enlarged prostate
weak stream
difficulty initiating
diagnostics and care for BPH
rectal exam
urinalysis and culture
prostate specific antigen (PSA)
BUN, creatine
post void residual (ultrasound)
Drugs - 5a reductase inhibitors, a-adrenergic receptor blockers
TURP- surgery to remove prostate
Erectile dysfunction
inability to attain or maintain a erection for satisfactory sexual function
in younger people its from substance abuse, stress and anxiety
in older people its from chronic medical issues
treatments
erectogenic drugs- phosphodiesterase inhibitors, such as sildenafil (viagra). sex therapist, VEDs, penile implants
risk factors of ED
Diabetes, vascular disease, surgery, meds, trauma, chronic illness, stress, depression
reduced blood flow to penis
osteomyelitis
Infection of bone, bone marrow
microorganisms enter the blood causing inflammation and pressure - bone cant expand, leading to ischemia - infection spreads, blood flow is compromised - results in bone death from ischemia.
dead bone forms a sequestrum that is difficult for WBC and antibiotics to reach
can form a chronic sinus tract which can drain purulent drainage (late symptom)
what typically causes osteomyelitis
staphylococcus
direct entry osteomyelitis
Trauma, open wound, fracture, surgery, diabetes injuries
indirect entry osteomyelitis
from infection
ischemia
decreased blood flow
necrosis
dead tissue
local clinical manifestations of osteomyelitis
constant bone pain that worsens w activity and is relieved by rest
swelling, tenderness and warmth
limited ROM
if goes untreated or doesnt work, could lead to systemic clinical manifestations
systemic clinical manifestations of osteomyelitis
fever
night sweats
chills
restlessness
nausea
malaise
drainage (late sign)
acute vs chronic osteomyelitis
acute- less than 1 month, same S&S
chronic- longer than a month or doesn’t respond to antibiotic therapy
- can be from inadequate therapy or exacerbations
- scar tissue forms which makes it hard for antibiotics to penetrate
- could lead to sepsis, septic arthritis, fractures
diagnostics for osteomylelitis
wound culture and sensitivity
WBC count
ESR
CRP
x-ray
CT/MRI
radionuclide bone scans
osteomyelitis nursing care
assess past history, signs of infection, ROM
dressing changes
monitor labs
Prevention is key! prevent extra infections and foot drop
osteomyelitis wound care
get rid of dead tissue- debridement
dry dressings
saline/antibiotic
wet to dry
wound vac
Dress one dressing at a time, wash hands, change gloves, then move to next- avoid cross contamination
diagnostic test to tell if something is systemic
blood culture
osteomyelitis meds
antibiotics- Vancomycin, gentamycin, ceftriaxone, cefazolin
-long term use: ototoxicity, nephrotoxicity, neurotoxicity, allergy development, c-diff
***Start on antibiotic as soon as get wound culture, even if there Is no results
NSAIDs
opioids
Muscle relaxants- baclofen, cyclobenzaprine (these are addictive and make you drowsy)
gentamycin med alert
assess dehydration before starting, ensure proper kidney function, monitor levels
fluoroquinolone med alert
may cause tendinitis, tendon rupture
Muscular dystrophy
group of genetic disorders characterized by progressive SYMMETRIC wasting of SKELETAL muscle
- can’t make dystrophin
causes gradual loss of strength, increasing disability
- no evidence of neuro involvement
-Duchenne is most common type
diagnostics and care for MD
genetic testing DMD gene mutation
muscle enzymes
Electromyogram
muscle fiber biopsy
ECG for cardiac dysrhythmias
no definite therapy to stop progression, corticosteroids can help, as well as gene therapy, stem cell therapy, PT, orthotic jacket
trach or vent may be needed in future
*proper nutrition needed
*dysrhythmias are most common cause of death in this
localized back pain
patient can pinpoint where
diffuse back pain
back pain over a large area
radicular low back pain
comes from nerve; sciatica
referred back pain
in lower back but can be caused by something else; such as kidney
chronic low back pain
3 months or longer
causes of low back pain
degenerative conditions such as arthritis
osteoporosis
metabolic bone disease
weakness from scar tissue due to prior injury
chronic strain from obesity, pregnancy, posture
congenital spine issues
nursing management : back pain and post op back surgery
back pain
- past med hist
-assess mobility and reflexes
diagnostics- CT, MRI, XRAY- fractures, swelling
-refer to PT
educate on body mechanics, sleeping positions, weight
-NSAIDS, Corticosteroids if needed
Post op
-assess for CSF leakage (headache is sign)
-assess surg site, bowel & urinary function
patient education, ensure pt in right position for post op
osteoporosis
chronic, progressive, metabolic deterioration of bone tissue. causes bone fragility
manifestations
- could be in any bone, common in hip, spine, wrist
- back pain
- fractures
- weakness
- loss of height from spinal fracture
- kyphosis (dowagers hump)
typically not diagnosed until 25-40% calcium loss
- deca scan
- bone mineral density (BMD) test
mineral to look at in blood for bone formation
calcium and phosphorus
osteoblast
build bone
osteoclast
break down bone
osteoporosis risk factors and treatment
risk factors
- menopause, IBD/malabsorption, kidney disease, RA, alcoholism
meds can cause- corticosteroids, antiseizure, antacids, heparin, chemo
treatment
vitamin D, calcium, bisphosphonates, human PTH, selective estrogen receptor modulator (SERM)
osteoarthritis
decreased lubrication of joints, causing bones to rub together. sometimes forms bone spurs
-Slow progression
*noninflammatory of synovial joints
not normal part of aging, usually happens by age 40
- can be from repetitive work/sports movements, obesity, menopause, previous injury
clin manifestations
- joint pain, loss of function, referred pain, crepitation, stiffness (usually feels better after movement), red swollen joints
diagnosed by MRI, XRAY, CT bone scan
avoid repetitive movements
NSAIDs, tylenol, hot showers can help
ankylosing spondylosis (marie-strumpell disease)
chronic progressive disease affecting the spine
- begins w synovis (joint inflammation), moves to fibrosis, then ankylosis which causes fusion of spine, “bamboo spine”
s&s
- pain and stiffness
- kyphosis
- iritis (inflammation of eye) or uveitis - could lead to vision loss
- decreased resp function - diaphragm can’t fully move
diagnosed by x ray
decrease pain, increase mobility, get vaccinations
treatment- corticosteroids, PT, analgesics, anti inflammatories
pagets disease
enlargement of bones, bone deformities. Unknown cause. More common in men over 50
- osteoblast and osteoclast not working in unison
- genetic identification of bone destruction
- leads to fragile expanding bones
S&S
compression of nerve
constipation/loss of appetite
pain from fractures, deformed bones
overgrowth in head causing headache
weakness, fatigue
provide pain relief, encourage rest, prevent falls
monitor calcium
meds to prevent- calcitonin, etidronate disodium, alendronate, bisphosphonates
osteomalacia
decalcification of bones, leading to porosity and softening of bones
caused by inadequate intake, absence of sunlight exposure, malabsorption, chronic renal disease
s&s
- bone pain and tenderness
- muscle weakness
- bowed legs (later sign)
- kyphosis
diagnosed by xray
- pain relief, safety, rest, body alignments, sunlight, vit D/ca
meds- glucosamine, chondrotin
foods w vitamin D
milk, eggs, enriched cereals, bread
why is osteoporosis more common in women
less calcium, less bone mass, menopause
what 2 diseases is diabetes often accompanied with
HTN, hyperlipidemia
what is diabetes characterized by
hyperglycemia related to abnormal insulin production, impaired insulin utilization, or both
complications of diabetes
stroke
heart disease
blindness
end stage renal disease
lower limb amputations
what does insulin do? what makes it
allows for glucose to get into cells
made by beta cells
what ethnicites are more at risk for diabetes
american indian, hispanic, blacks
type I diabetes
pancreas cannot make insulin.
Autoimmune disease
type II diabetes
pancreas cannot make enough insulin, or cells are resistant
can be prevented with good diet and staying active
gestational diabetes
occurs during pregnancy. BG usually returns to normal after birth.
Higher risk for developing diabetes in future
type I diabetes symptoms
- usually develops in younger ages, quickly
weight loss
polyuria
polydipsia
ketones in urine (ketoacidosis)
polyphagia
weakness
fatigue
type II diabetes symptoms
-progressive onset, adults
obesity- lifestyle related
polyuria
polydipsia
polyphagia
fungal infections/yeast infections
slow healing wounds
vision changes
meds and issues that could cause diabetes
corticosteroids
thiazides
phenytoin
atypical antipsychotics
cushing syndrome
hyperthyroidism
recurrent pancreatitis
cystic fibrosis
hemochromatosis
parenteral nutrition
hemoglobin A1C
avg blood sugar over past 3 months
good is between 4% to 8%
rapid acting insulin
onset 10-30 mins
peak- 30 mins-3 hours
duration 3-5 hours
ex- insulin humalog
short acting insulin
onset 30 mins-1 hour
peak 2-5 hours
duration 5-8 hours
clear
regular insulin
intermediate acting insulin
onset 1.5-4 hours
peak 4-12 hours
duration 12-18 hours
cloudy
NPH insulin
long acting insulin
onset 0.8-4 hours
peak- none
duration 16-24 hours
glargine (lantus)
metformin
oral drug
most effective 1st line treatment for type II diabetes
reduces glucose production
enhances insulin sensitivity
improves glucose transport
may cause gas/bloating and diarrhea
must hold before and after IV contrast
rare comp- lactic acidosis
sulfonylureas
increases insulin production from pancreas, increases cellular sensitivity to insulin
adverse- hypoglycemia possible
ex- glipizide, glyburide
diabetes diet
Complex carb- brown rice, lean protein, non starch veggies- broccoli
limit alcohol
exercise and diabetes
30 mins day/5 days weekly- aerobic activity
resistance training 3x weekly for type II
Avoid exercise if hyperglycemic WITH KETONES IN URINE
hyperglycemia symptoms
excessive hunger, excessive thirst, weakness, frequent urination, nausea,
blurred vision, sores not healing properly, sleepiness after eating
hypoglycemic symptoms
hunger
shakiness
fast HR
anxiety
sweating
dizziness
blurred vision
weakness
headache
irritability
diabetic ketoacidosis
usually occurs in type 1 diabetics
high blood glucose, muscle and lipid cells starved for glucose due to lack of insulin. Cells start using fat as a source of energy. liver cells produce ketones, making urine acidic. Could lead to coma or death.
Different breathing (kouzmal)- body is trying to excrete extra acid
Fruity smelling breath
hyperosmolar hyperglycemic nonketotic syndrome (HHNS)
usually occurs in type II diabetes
high blood sugar increases urination, if these liquids arnt replaced, the individual can become severely dehydrated
- can be from impaired thirst mechanism or inability to get fluids
High BG can lead to altered mental status, confusion, seizures, coma or death
what is given to hypoglycemic patients
Glucose tab or gel if conscious in hospital
if unconscious, 50% dextrose
if somewhere else, give hard candy
assessing resp
lung sounds, breaths/min, effort of breathing, cough, o2 sat, nailbed, color, dyspnea, SOB, history, pain, tracheal deviation
acute vs chronic resp illness skin color
acute- cyanotic, pallor
chronic- grey
6 Ps of dyspnea
1- Pulmonary bronchial constriction- asthma or anaphylaxis
2- Possible foreign body
3- Pulmonary embolus
4- Pneumonia
5- pump failure
6- pneumothorax
tuberculosis
infectious disease caused by mycobacterium tuberculosis
- most common in lungs, but can affect brain, kidney, joints
*This must be reported to CDC if positive
why does drug resistance occur in TB
incorrect prescribing
Lack of case management- follow up
non adherence- compliance
TB risk factors
homeless
resident of inner city neighborhood
foreign born persons
living or working in institutions
poverty- bad access to health care
IV drug users
immunosuppressants (cancer, HIV)
leading cause of death of HIV patients
TB
How does TB spread
airborne particles- can stay in air for minutes to hours since they’re small
- sneezing, breathing, talking, singing, coughing
transmission requires close, frequent, or prolonged exposure
- Based on how many organisms fly out
Concentration- how much space?
Length of time of exposure
Immune system of person exposed
TB pathophys
Primary- active
Latent- not causing issues
Reactivated- had it in body but randomly became active
When TB is inhaled, it may go latent and lodge in bronchioles and alveoli until possibly reactivating. If caught, we still treat to avoid it going active
- only 5-10% will develop active TB
TB is aerophilic (oxygen loving) that is why it is most common in lungs
TB pathophys
Primary- active
Latent- not causing issues
Reactivated- had it in body but randomly became active
When TB is inhaled, it may go latent and lodge in bronchioles and alveoli until possibly reactivating. If caught, we still treat to avoid it going active
- only 5-10% will develop active TB
TB is aerophilic (oxygen loving) that is why it is most common in lungs
symptoms of TB
active
- dry cough that will become productive
- weight loss
- low-grade fever
- night sweats
- malaise
- dyspnea and hemoptysis (bloody sputum) are late symptoms
- pleuritic pain
- adventitious breath sounds
latent
No symptoms, positive PPD test
immunocompromised and TB
less likely to have a fever and other signs of infection
PPD skin test won’t have as big as a reaction- smaller bump >5mm are considered positive
TB diagnostics
purified protein derivative (PPD)- positive = induration, palpable, raised hardened area at injection site. Must be >15mm induration in not compromised people
Two step test
blood test
chest x-ray (may appear normal, can’t use as only diagnoses)
3 consecutive sputum cultures (Not negative for TB until all 3 test are negative)
- examines acid fast bacteria (AFB)
-results can take up to 8 weeks, start therapy until results are back
care for TB
infectious for first 2 weeks of treatment- wear mask, avoid crowds
Four drug regimen
-Isoniazid
-rifampin (rifadin)
-pyrazinamide - dont take when pregnant
-ethambutol
These drugs will be taken for 6-9 months, and they must be taken in front of hospital staff daily. Avoid alcohol with these and monitor liver levels
does latent TB need treatment
yes to avoid it becoming active
TB vaccine
BCG
causes PPD skin test to be positive
- not in US unless needed for select induviduals
goals for TB
COMPLIANCE
prevention
normal pulmonary function
hospital care for TB
airborne isolation room with negative airflow (airflow goes outside), 6-12 airflow exchanges/hour
healthcare workers wear HEPA masks (N95)
only visors who have been in contact with patient already can visit in hospital
- screen these patients to make sure they dont have it
restrictive lung diseases
breathing in has been effected.
could be:
extrapulmonary -brain issues, meds, chest wall problems, or spinal cord issues
intrapulmonary- elasticity, diaphragm, inflammation
obstructive pulmonary issues
inability to exhale all the air out the lungs
can be from lung tissue problems, bronchial narrowing or excessive mucus production
idiopathic pulmonary fibrosis
characterized by scar tissue in the connective tissue of the lungs leading to inflammation or irritation
low survival rate
management : o2 therapy and lung transplant
sarcoidosis
chronic, multisystem, granulomatous disease of unknown cause that primarily affects lungs, but could affect others such as lymph nodes, heart, skin, eyes, etc
Treatment is to suppress inflammatory response: steroids
cystic fibrosis
autosomal recessive, multisystem disease with altered sodium and chloride ions in and out of epithelial cells causing:
1-thick secretions obstructing bronchioles, leading to air trapping
2-obstruction of pancreas
3- difficulty reproducing (reproductively)
4- GI malabsorption, obstructions
Low in sodium and water= thick mucus
signs of CF
newborn:
- meconium ileus- GI obstruction cause baby can’t poop meconium out
- resp issues
- failure to thrive/malnutrition
-steatorrhea- fatty poop, does not sink
adults:
-large, protuberant abdomen
-skinny arms and legs from malnutrition
-productive cough
-DIOS- bowel blockage
-Diabetes
sweat chloride test
for CF,
if chloride concentration is high in sweat, suspected CF
CF health complications
sinus issues
nose polyps
salty sweat
trouble breathing
abnormal pancreas function
fatty bowel movements
gallstones
trouble digesting food
enlarged heart
frequent lung infections
treatment and care for CF
pancreatic enzyme with meals, many drugs
Assess lung sounds, and PFT.
ABG in ICU and emergency cases
COPD
group of conditions with obstruction of airflow
-genetic or from environments
-3rd leading cause of death in US
emphysema
destruction of alveoli without fibrosis
Can’t get oxygen out, trying to get rid of mucus
diagnosing chronic bronchitis
2 consecutive years of 3 months or longer cough and sputum present
COPD risk factors
-cigarette smoking
-air pollution, gas, asbestos exposure
-recurring severe resp infections
-A-antitrypsin deficiency (typically allows elastin from breaking down in lungs)
-age, gender- more common in men but more women die
-socioeconomics
-asthma
air trapping
being unable to get CO2 out
chronic bronchitis
chronic inflammation. Clogged with mucus. lungs not getting oxygen well
“blue bloater”
chronic bronchitis symptoms
chronic productive cough
purulent sputum
hemoptysis
mild dyspnea
cyanosis (from hypoxia)
peripheral edema (from cor pulmonale)
crackles, wheezes
prolonged expiration
obesity (from fluid buildup)
chronic bronchitis complications
-secondary polycythemia due to hypoxemia (low oxygen=extra RBC)
-pulmonary HTN due to reactive vasoconstriction from hypoxemia
-cor pulmonale from chronic pulmonary htn (rt sided hf)
emphysema symptoms
dyspnea
minimal cough
increased minute ventilation
pink skin, purse lips
accessory muscle use (trying to get air out)
cachexia (weakness)
barrel chest (extra air)
decreased breath sounds
tachypnea
emphysema complications
-pneumothorax due to bullae
-weight loss due to work of breathing (difficulty breathing)
should you take cough suppressants to get rid of mucus in emphysema patients
no, we want them to get the mucus out
difference between asthma and copd
asthma is inflamed airways, COPD is collapsed airways with damaged alveoli
COPD diagnostics
chest xray - would show flat diaphragm
6 minute walk test
COPD assessment test (CAT)
clinical COPD questionnaire
ABG (low o2, low ph, high co2)
spirometry under 70 (normal is above 70)
COPD exacerbations
primarily from bacterial and viral infections
- COPD gets worse after each exacerbation
severity depends on use of accessory muscles and central cyanosis
Avoid sick people to help prevent
COPD exacerbations
primarily from bacterial and viral infections
- COPD gets worse after each exacerbation
severity depends on use of accessory muscles and central cyanosis
Avoid sick people to help prevent
COPD care
meds will help but disease isn’t fully reversible
Inhaled drugs are preferred
-bronchodilators
-corticosteroids (rinse mouth after inhaled to avoid thrush)
-anticholinergics
-antibiotics
-humidified oxygen (keep sat over 90%)
encourage purse lip breathing, mucus clearance devices, chest physiotherapy, huff coughing
Patient needs to stop smoking, and get vaccinations
typically only hospitalized for acute resp failure or acute exacerbations
Benefits of purse lip breathing
slows breathing down to help get rid of extra CO2
Resp acidosis
too much co2 in lungs. acid builds up. could happen with COPD patients
