Test 5 Flashcards
rheuamtoid arthritis
chronic systemic autoimmune disease causing inflammation of connective tissue in the synovial joint
- has remission and exacerbations
autoimmune, but could be due to enviroment, or from infections
-triggers formation of IgG immunoglobulins
first phase: rheumatoid synovitis, lymphocytes, and plasma cells increase
next: cartilage is damaged
then: inflammatory response, more damage
clinical manifestations of RA
-subtle onset
joint pain and swelling, fatigue, anorexia, weight loss, stiffness, limited ROM, stiffness after inactivity, signs of inflammation, deformities (ulnar drift, swan neck, boutonniere, hallux valgus)
possible nodules, depression, sjogren’s syndrome, fractures, decreased grip
RA diagnostics and meds
POS RHEUMATOID FACTOR
ANA
crp
esr
x ray
aspiration of synovial fluid
meds
DMARDS (ex- sulfasalazine)
- drink fluids, use sunscreen, get eye exams
BMR
- end in umab
- dont get live vaccines
- get PPD before starting
-report bleeding, bruising
Immunosuppressants
ex- methotrexate - causes bone marrow suppression and hepatotoxicity
antitumor necrosis meds
ex- etanercept
plan activities around morning stiffness
GOUT
non systemic inflammation of joints from elevated uric acid that collects in them, typically from disturbed purine metabolism
periods of remission and exacerbations
sudden onset, swelling and severe pain, low grade fever, tophi
most commonly affects big toe
could lead to kidney damage
foods not to eat for gout
avoid foods with purines: alcohol, caffeine, shellfish, beef
tophi
visible deposits of sodium urate crystals
diagnostics and care for gout
INCREASED URiC ACID LEVELS
x-ray
wbc
esr
synovial aspiration
Meds-
**colchicine- for acute attack. take with food to avoid GI upset
probenecid- reduce uric acid. take w food to avoid Gi upset
**allopurinol- for prevention. blocks formation of uric acid
sulfinpyrazone- reduce uric acid. take w food to avoid Gi upset
systemic lupus erythematosus (SLE)
multisystem autoimmune disease affecting skin, jointsm serous membranes, renal, hematologic, and neuro
unknown etiology, could be from hormones
meds could trigger
SLE clinical manifestations
could be mild to severe
butterfly rash
vascular skin lesions
photosensitivity
oral/nasopharyngeal ulcers
lung disease
dysrhythmias
coagulation disorders
anemia
increased risk for infection
pericarditis
kidney damage
alopecia
arthritis
SLE care
Diagnostics- ANA, anti ANA, ANTI smith, UA, SBS, CRP
treat symtoms
DMARDS, BMR topicals, NSAIDS
fibromyalgia
chronic central pain syndrome with widespread fatigue, pain, muscle weakness.
May feel “burning” pain and tenderness
patients may experience depression, migraines, overwhelmed, anxiety, restless leg syndrome, IBS, decreased memory
Diagnostics- 11-18 different pain locations, 3 months widespread pain
Meds- Lyrica, gabapentin, anti anxiety
patients should try exercise, relaxation, diet changes, massage, heat and cold.
they need to find out what exacerbates it
opioids don’t help this disease, only non opioids
sjogren’s syndrome
autoimmune disease that targets moisture producing exocrine glands such as in nose, throat, airways, and eyes creating dryness.
Also affects glands in stomach, pancreas and intestines
may be triggered from viral or bacterial infection, or genetic and environment.
lymphocytes attack and damage the lacrimal and salivary glands
sjogren’s syndrome clinical manifestations
dryness overall..
dry eyes- blurred , photosensitivity
dry mouth- most concerning, airway and choking issues. could have taste changes and be thirsty, mouth sores
dry skin
vaginal dryness
joint and muscle pain
thyroid issues
sjogren’s syndrome diagnostics and care
Diagnostics- Schirmer’s test for tear production, salivary gland function
Meds- eye drops, pilocarpine for dry mouth
increase humidity for airways
moisten food with sauces, eat more creamy foods, high calorie drinks, finely chop foods.
lube for vaginal dryness
skin lotion
avoid salty, acidic or spicy foods.
enucleation
removal of eye
sclera
fibrous outer coat of eye
choroid
middle vascular layer of eye
retina
middle nerve in eye
what is cornea responsible for
refraction
what are eye lens responsible for
accomodation and focus
what is iris responsible for
controlling amount of light
what does retina do
perception of color (cones) and light (rods)
normal aging of eye
- cornea thickening and flattening- can cause astigmatism
- lens thickens, increases IOP- glaucoma risk
- Lens opacity- cataracts
- retina degeneration- decreases visual acuity and color perception
- lacrimal gland issues
- iris rigidity
common manifestations of eye issues
redness, pain, burning
edema
increased tearing
headache
N/V
squinting
visual disturbances
accommodation disorders
refractive errors
caused by irregular corneal curve, focusing power of lens, or eye length
light doesn’t hit eye correctly
main symptom is blurred vision, but could cause pain, eye strain, or headaches
treated w surgery or lenses
myopia
nearsightedness. cant see far away
hyperopia
farsightness. trouble seeing near. light focuses behind retina
presbyopia
farsightedness due to aging. reading glasses needed
astigmatism
Irregular cornea curvature causing light rays to bend unequally
visual impairment management
Worry about safety? Can they see? Do they need glasses to see?
care- Glasses and contacts most common, but could have laser surgery, bifocals
Know if patient has contacts, some meds cause contacts to stick to eye, such as chemo, or if patient is unconscious take contact out to avoid damage and infections
Hordeolum
Stye- infectious sebaceous gland in lid margin. Use warm compress 4x daily
Conjunctivitis
inflammation of conjunctiva.
Bacterial- pink eye- pus, itchy- contagious
viral- tearing, feeling of something in eye
-treated w eye drops
Keratitis
inflammation of cornea. Need to Clean eye with baby shampoo could be from herpes simplex, ulcers, parasites, fungus
Chalazion
chronic inflammatory granuloma of sebaceous gland on lid. blocked oil gland
Strabismus
inability to focus both eyes simultaneously. Usually from eye muscle issue, may need eye muscle surgery. Causes double vision
Keratoconus
cornea budges outward
are corneal transplants safe
yes- no vascularity involved
nursing management of extraocular disorders
find out if its contagious
warm/cool compress
hand washing
retinopathy
damage to retina. Common in diabetics and HTN pts
Retinal detachment
separation of retina and epithelium behind, fluid can build up and if untreated will cause blindness.
Risk factors- Age, myopia, trauma.
Symptoms- Photophobia, floaters, curtain closing
Requires surgery
age related macular degeneration (ARMD)
most common cause of irreversible vision loss in people over 60. due to normal aging process of retina.
Risk factors- age , hereditary, ethnicity, smoking, HTN, poor nutrition
cataracts
opacity within lens. Happens with age but can happen earlier in patients with DM.
risk factors- light exposure, age, DM, meds (like steroids), trauma
s&s
decreased vision
abnormal color perception
glare
pupil looks cloudy
phacoemulsification
Most common surgical procedure in US- removes cataracts
pupils need to be dilated, pain and anti inflammatory eye drops gave before surgery, surgeon admins med that breaks lens up, it gets vacuumed, then replaced with another lens.
Post op- shield to sleep - stops from eye rubbing, avoid pressure on front of face such as no bending, bearing down or lifting weights. Eye drop anti inflam. and antibiotic, avoid bright lights
**Patient has to have eye appt 24 hours after surgery so eye pressure can be assessed
complications- hemorrhage, increased eye pressure
glaucoma
Increases intraocular eye pressure, putting pressure on optic nerve and could cause blindness over time.
We want to slow the progression of loss of eyesight. Aqueous pressure flows in and out to balance pressure, but with glaucoma this is a issue
symptoms: blurry vision, halos, loss of vision, headache, pain, N/V
Treatment:
open angle- beta blockers, motics, adrenergic agonists.
eye drops preferred- but could still cause systemic effects, monitor BP and HR
angle closure- surgery
care- drops, no lifting, avoid tightness on neck
types of glaucoma
angle closure- sudden onset, emergency. surgery typically needed. usually from bulging lens
open angle- slow onset. from aging, hereditary, retinal issues
rinne test
compares bone to air conduction with tuning fork.
Normal is hearing air conduction longer
Conductive hearing loss is hearing bone conduction longer
Sensorineural is when both are reduced
Weber test
helps determine if both ears here equally, or if one side is worse than other
common auditory issue clinical manifestations and diagnostics
pain, fever, headache, discharge, personality change, dizziness, vertigo, tinnitus
diagnostics- tuning fork, audiogram
common auditory issue clinical manifestations and diagnostics
pain, fever, headache, discharge, personality change, dizziness, vertigo, tinnitus
diagnostics- tuning fork, audiogram
presbycusis
hearing loss due to aging
otitis externa
Inflammation of ear canal; swimmer ear. Could be bacterial or fungal. First sign is usually pain. Apply warm compress and ear drops
otitis media
infection of middle ear
Otosclerosis
hereditary where spongy bone develops in middle ear and bones cant make sound as needed, resulting in conductive loss. Typically bilateral. Eardrum may appear reddish due to vascular and bone changes
Meniere’s disease
vertigo, tinnitus, fluctuating sensual hearing loss. Onset is typically between 30-60
Change positions slowly because if not could cause vertigo
benign paroxysmal positional vertigo (BPPV)
vertigo, nausea, nystagmus, loss of balance. No real hearing loss. Intermittent, can be corrected by maneuvers. Unknown cause. Accounts for 50% vertigo cases.
Acoustic neuroma
Benign tumor affecting cranial nerve- unilateral progressive sensorineural hearing loss, tinnitus, sensation in ear canal, intermittent vertigo.
Often requires surgery and can lead to facial paralysis
conductive hearing loss
from inner or middle ear
can be from fluid, wax, eardrum issues
treatment can be meds, surgery, hearing aid
bone conduction implant can help
sensorineural or perceptive hearing loss
problem within cochlea or pathway to auditory cortex
caused by trauma, aging, ototoxic meds, DM, meniere’s disease
cochlear implants can help
presbycusis falls under this
skin function
protection, regulator of temp, water, electrolytes
skin layers
Epidermis- outer layer
Dermis- middle layer, sweat glands, hair follicle, nerves and sebaceous gland,
Subcut tissue- inner layer, fat cells
what causes most skin bacterial infections
staphylococcus aureus
strep A and B
treated with antibiotics
impetigo
Very contagious. Could affect kidneys. Bacterial infect
common in kids
looks like peanut butter crusting on face
folliculitis
hair follicle infection from bacteria
cellulitis
Skin infection usually caused by staph A
common in hospitals
common viral skin infections
herpes simplex
herpes zoster (shingles)- AIRBORNE also, reactivates from chicken pox
verruca vulgaris (warts)
Plantar warts- on bottom of feet
treated with antivirals
common skin infestations (worms, bugs, insects)
bee/wasp stings- need to get stinger out
bed bugs
pediculosis (lice)- may take a few treatments, contagious
scabies- contagious. skin precautions needed. very itchy
Ticks- bullseye rash; could lead to lyme disease
common benign dermatologic conditions
acne
moles
psoriasis- use UV light, topical steroids
seborrheic keratosis- non cancerous skin growth
acrochordons- skin tags
lipoma- fatty lump
lentigo- pigmented macule
common skin fungal infections
candidiasis- yeast
tinea corporis- ringworm
tinea cruris- jock itch
tinea pedis- athlete’s foot
tinea unguium- nail fungus
common allergic skin conditions
allergic contact dermatitis
urticaria-hives
drug reactions
atopic dermatitis
vesicle
small fluid filled sac
macule
flat, non palable
nodule vs papule
both are elevated, palpable lesions
nodule is larger than papule
GERD (gastroesophageal reflux disease)
chronic damage to mucosa from stomach acid getting into lower esophagus, causing irritation and inflammation.
primary cause- incompetent lower esophageal sphincter (LES)
Symptoms- heart burn (pyrosis), dyspepsia, pain, discomfort, regurgitation, resp issues such as wheezing, coughing, sore throat
GERD complications
esophagitis- inflammation. Repeated esophagitis may lead to scar tissue, stricture, and dysphagia
barrett’s esophagus (BE)- Metaplasia of stomach cells into esophagus, cells release acid. increases risk for cancer
respiratory bronchospasm, laryngospasm, aspiration
dental erosion
diagnostics for GERD and hiatal hernia
endoscopy with biopsy
barium swallow (esophagram)
motility studies- looks for nerve damage
pH monitoring
GERD management
small meals
avoid alcohol, caffeine, smoking
upright position 2-3 hours after eating
avoid eating 2-3 hours after meals
weight reduction
elevate head of bed
surgery if meds dont work
proton pump inhibitors (PPI)
decreases HCL secretion and irritation
- best for healing esophagitis and decrease strictures
-take before meal
long term use could cause decreased bone density, b12 deficiency, magnesium deficiency
for GERD, duodenal ulcer, esophagitis
names: omeprazole, rabeprazole
H2 receptor blocker
decreases HCL secretion and irritation
available in many different forms
Only effective in 50% cases. PPI to cure ulcer, H2 to prevent
names: Cimetidine, famotidine (pepcid)
take before meals
prokinetics
increase gastric emptying and motility
adverse effects- CNS (anxiety, hallucinations), extrapyramidal (tremor, dyskinesia)
for gastroparesis, chronic constipation
names: Prucalopride, prycalopride, metoclopramide
antacids
neutralize acid; provides quick relief for mild, intermittent symptoms. Short duration
give 2 hours after meals
use w caution in renal patients, HTN, cirrhosis
For GERD
names:Aluminum hydroxide, calcium carbonate (tums)
hiatal hernia
herniation of part of the stomach into the esophagus through opening in diaphragm.
- caused by weakened muscle in diaphragm and esophagogastric opening or intra abdominal pressure
symptoms- heartburn, dyspepsia, regurgitation, resp symptoms,chest pain
conservative- reduce intra abdominal pressure
surgery- reduce hernia, optimize LES pressure
hiatal hernia complications
GERD, esophagitis, ulcers, hemorrhage, stenosis, strangulation, aspiration
surgeries for GERD, or hiatal hernia
nissen fundoplication- uses sutures
LINX reflux management system- uses magnets to strengthen LES
Peptic ulcer disease (PUD)
Erosion of GI mucosa from HCL acid and pepsin
typically happens in: lower esophagus, stomach, duodenum, or post op gastrojejunal anastomosis
may be classified by location.. gastric, duodenal
pain is a priority nursing diagnosis
types of hiatal hernia
sliding hiatal hernia- most common
rolling/paraesophageal hernia- more concerning. Blood flow issue
acute vs chronic PUD
acute- superficial erosion and minimal inflammation
chronic- erosion of muscular wall with formation of fibrous tissue
gastric ulcers
more prevalent in females older than 50
increased obstruction
increased mortality
high recurrence = increased cancer risk
burning 1-2 hours after meals, if penetrating, increased pain w food
risk factors- H. pylori, NSAIDs, bile reflux
duodenal ulcer
most common- 80% of peptic ulcers
common in men age 35-45
at risk: COPD, cirrhosis, pancreatitis, hyperparathyroidism, CRF patients
from H. pylori
high HCL secretion
usually will occur, disappear and then reoccur again
burning 2-5 hours after meal. pain relief w antacids and food
PUD risk factors and diagnostics
risk factors
-H. Pylori
->oral-oral or fecal-oral route, more common in blacks and hispanics
-NSAID use/corticosteroid/anticoagulants
-alcohol/smoking
-caffeine
-stress
diagnostics
EGD- sedated
tissue specimen to test for H pylori
barium contrast
CBC, liver enzymes, amylase, stool sample
PUD management
decrease gastric acidity
No NSAID or ASA for 4-6 weeks unless with PPI, h2 receptor
endoscopic evaluations
cytoprotective drug therapy- dont give w antacid
avoid tigerring food
PUD complications
hemorrhage, most common in duodenal
perforation- most lethal. contents spill into peritoneal cavity
severe abdominal pain. board like abdomen, bowel sounds absent, shock. If untreated could lead to bacterial peritonitis- sepsis -> Antibiotics, NS, LR, albumin 5%
gastric outlet syndrome- edema, inflammation, pylorospasm, or scar tissue cause obstruction in distal stomach and duodenum. Gas and bloating occur later. Treated by decompressing with NGT, fluid and electrolytes, balloon dilation
signs of shock
hypotension (could be from losing volume), tachycardia, sweaty, pallor
gastritis
inflammation of gastric mucosa
could be acute or chronic, diffuse or local
chronic is typically from H. pylori
patho- HCl and pepsin diffuse into mucosa resulting in tissue edema, disruption of capillary walls with loss of plasma into gastric lumen and possible hemorrhage
Risk factors- NSAIDs, female over age 60, history of PUD, anticoagulation therapy, corticosteroid use, digoxin, alendronate
symptoms include heaviness, pain, heartburn, N/V
what does bile do and where does it get excreted
break down fat.
urine and feces
what does the liver do
removes potentially toxic byproducts of certain meds like tylenol, statins
metabolizes nutrients from food to produce energy
helps body fight infection by removing bacteria from blood
produce substances that regulate blood clotting
stores vitamins, minerals and sugar
produces most protein needed by body
produces bile, which digest fat and absorbs vitamins
causes of hepatitis
Viral (most common)
Alcohol
Drug-Induced
Chemicals
Autoimmune diseases
Metabolic problems
Fatty liver disease
hep A
RNA virus transmitted by fecal-oral. by eating contaminated food or water
there is a vaccine for this, no treatment
- not chronic
symptoms can be mild to acute
practice good hand hygiene
pos anti- HAV or IgM= active
IgG- shows previous infection
hep B
DNA virus Transmitted through blood or bodily fluids (Blood, semen, saliva)
there is a vaccine
drug choices- alpha interferon, peginterferon
can be acute or chronic
screen for pos antigen/antibodies
get blood screened and have good hygiene
hep C
RNA virus Transmitted through blood-blood contact
NO vaccine
drugs- direct acting antivirals
avoid sharing needles, razzors, etc
acute or chronic
acute- asymptomatic
chronic- liver damage
screen for pos hep B antibody
virus will never go away but symptoms will, make sure to tell partners
hep D
defective RNA virus from contact with infected blood, but only occurs in people already infected with hep B
Hep B vaccine, none specific for D
drug- interferon
avoid sharing of needles, razors, etc
hep E
RNA virus transmitted through contaminated food or water, fecal-oral
no vaccine
no treatment
avoid drinking from potentially unsafe source
Clinical manifestations for hepatitis
fever
fatigue
headache
loss of appetite
unexplained weight loss
dark urine
jaundice
pale colored stool
abdominal pain
N/V
hepatomegaly
lymphadenopathy
splenomegaly
acute typically last 1-6 months
systemic manifestations of hep B
Rash, angioedema, arthritis, fever, malaise, cryoglobulinemia, glomerulonephritis, vasculitis
cryoglobulinemia
Presence of abnormal proteins in blood
acute vs chronic hepatitis
acute
large numbers of hepatocytes are destroyed, but liver cells can regenerate after infection
chronic
chronic infection can cause fibrosis of liver then progress to cirrhosis
acute vs chronic hepatitis
acute
large numbers of hepatocytes are destroyed, but liver cells can regenerate after infection
chronic
chronic infection can cause fibrosis of liver then progress to cirrhosis
hepatitis convalescent phase
begins as jaundice is disappearing
- last weeks to months
- causes malaise and easy fatigability
- liver is still enlarged but spleen reduces back to normal
most people typically recover but a lot of hep C and some of hep B patients may get chronic hepatitis
diagnostics for hepatitis
antibody/antigen panels
LFT- AST and ALT
bilirubin elevated
Alk phos elevated
enlarged liver and spleen
liver biopsy
care for hepatitis
acute A and B are typically just supportive care and only treated if severe (just B)
acute C needs antivirals
chronic hep B- interferons
eat well balanced diet, high in calories, vitamin supplements (especially D), no alcohol
liver cirrhosis
end stage liver disease
not many symptoms early on
late stages- jaundice, portal htn, peripheral edema , ascites
possible spider angiomas, hematologic issues, endocrine issues, neuropathies
issues with ascites
worry about breathing as it could become labored
think about dehydration from vascularity
Monitor for hyperkalemia
Bacterial peritonitis
hepatic encephalopathy
neuropsychiatric manifestation of liver disease
- ammonia cannot be converted into urea and builds to toxic levels
- affects brain
causes - LOC decline, inappropriate behavior, trouble concentrating and sleeping, asterixis (tremor like)
can occur suddenly or over time
prevent injury, promote ventilation
paracentesis
takes fluid out of abdomen region
IBS (irritable bowel syndrome)
no organic cause, relates to psychological stressors or GI infections
based on symptoms: need abdominal pain at least 1 day a week for 3 months
alteration of diarrhea or constipation
mucus in bowels
feeling of incomplete bowel movements
looser, more frequent stools
abdominal pain or bloating
no specific test- rule out other diagnostics
-stress management
dietary changes for IBS
avoid FODMAP- gluten, wheats, ryes, lactose, onions, garlic, nuts, legumes
drugs for IBS
opioid analgesics
antispasmodics
antidepressants
antidiarrheals
laxatives
IBD (inflammatory bowel disorder)
chronic, inflammation of GI tract characterized by periods of remission with exacerbations
~~autoimmune
2 types: ulcerative colitis, crohns
typically begins in teens/early adulthood, with another peak in 60s. Family history
IBD risk factors
diet, smoking, stress, NSAIDs, antibiotics, oral contraceptives, genetics
Ulcerative colitis clinical manifestation
only in colon, continuous
pain in lower left abdomen
ulcers only penetrate inner lining
bloody stool common
can have 10-20 stools a day
pain usually gets better after bowel movement
crohns disease
can occur segmented anywhere in GI tract from mouth to rectum
pain typically occurs in lower right abdominal region
ulcer penetrates through entire thickness
bleeding is uncommon but can occur
5-6 unformed stools
diagnostic for IBD
Colonoscopy (or endoscopy for crohn’s)
barium swallow
CT/MRI
stool- blood, pus, mucus, infection
Labs- crp, cbc, electrolytes
care for IBD
goals to avoid exacerbation, rest bowel
relieve symptoms and improve quality of life
drugs:
50 aminosalicylates (5 ASA)- remains remission, prevent flare ups
corticosteroids
antimicrobials
immunosuppressants
UC surgery- usually curative but only for severe cases. complications could be failure to response, fistula, hemorrhage
crohn’s surgery- won’t cure, only surgical for complications
diverticula/diverticulosis
saccular dilations or outpouching of mucosa in colon, typically from lack of fiber
more common in older adults
prevented by high fiber diet
diverticulitis
inflammation of diverticula, from when food gets stuck in these pouches.
can be diagnosed by CT with oral contrast, occult blood, enema, CBC.
allow bowel to rest
surgery can occur in recurrent cases or complications
drink fluids
avoid increased abdominal pressure
malabsorption syndrome
impaired absorption of fats, carbohydrates, proteins, minerals and vitamins
most common cause is lactose intolerance but could also be from other GI problems like IBD
symptoms include weight loss, diarrhea, steatorrhea
treatment depends on cause
celiac disease
autoimmune disease that damages small intestine mucosa, triggered by gluten (wheat, barley, rye)
-typically associated with other conditions like RA, type I DM, thyroid disease
more common in women, can occur at any age but common in childhood
consist of 3 factors- genetics, gluten ingestion, immune response
treatment is avoiding gluten
diagnosed by serologic testing, genotyping, screening, history and physical
celiac signs and symptoms
mouth ulcer and tooth erosion
diarrhea, bloating, constipation
weight loss and malnutrition
joint/muscle pain and swelling
stomach pain and nausea
brittle nails, acne, eczema
possible infertility, miscarriage and early menopause in woman
