NUR326 Exam 4 Flashcards
synovial/diathrodial joint
any joint that allows movement
subchrondral bone plate
under the cartilage
bone just underneath the cartilage
articular cartilage
covers the bone of the joint, provides a smooth, slippery surface that allows free movement of a joint
synovium
space between two articulating bones
synovial membrane that is the inner lining of the cavity
secretes synovial fluid that lubricates the joint surfaces and removes debris
joint capsule
surrounds the joint
unties articulating bones
three phases of bone healing
- inflammatory - hematoma forms
- reparative - fibrous cartilage and ossification
- remodeling - healing is complete
osteoarthritis
degeneration of joints caused by aging and stress
obesity and age increase risk
commonly effects: cervical spine, lumbar spine, hip, knee, hand, first metatarsal phalangeal joint, and spared joints
RF of osteoarthritis
aging, obesity, history of playing sports, history of trauma, heavy occupational work, misalignment
etiology of OA
stress is applied to joints, degeneration of cartilage, osteoblasts are activated which lead to bony spurs, narrows joint space, becomes a chronic disease
osteophytes
small bony projections that develop on the rim of the bone adjacent to cartilage loss
hallmark in OA**
OA symptoms
deep aching joint pain, relieved with rest
pain during cold weather
stiffness in the mornings
popping during motion
joint swelling
altered gait
limited ROM
herbeden’s nodes
swellings at the distal interphalangeal joint (OA)
bouchard’s nodes
proximal interphalangeal joint (OA)
pharmacotherapy for OA
focus on pain management and reduce swelling
mild to moderate pain: tylenol, topical capsaicin, NSAIDS
moderate to severe pain: NSAIDS, tylenol + tramadol, opioids, steroid injections
NSAID MOA
reduce the production of prostaglandin
causes an increase in ulcer development
contraindicated with a history of ulcers
cautions with NSAIDS
may effect kidney function
risk for GI bleed - contraindicated with ulcers, use with caution for those with a history of GI bleeds or current anticoag therapy
OA dietary supplements
glucosamine sulfate - maintains cartilage health
chondroitin sulfate - slows cartilage breakdown
degenerative disk disease (DDD)
degeneration of the lumbar and cervical spine
causes pain, motor weakness, and neuropathy
S/S of DDD
lumbar - pain in lower back that radiates to back of leg, pain in butt or thighs, pain worsens when sitting/bending/ lifting/twisting
numbness/tingling/ weakness in legs
foot drop
cervical - chronic neck pain that radiates to shoulders and down the arms, numbness or tingling in the arm or hand, weakness
commonalities between rheumatoid arthritis and systemic lupus erythematous
inflammatory conditions that result in pain, limitation of movement, destruction or erosion of joints, ligaments, or muscles
autoimmune orgin
systemic, not local
rheumatoid arthritis (RA)
systemic autoimmune disease that is type III hypersensitivity
inflammation of the synovium
RA etiology
not fully understood, genetic link, women 40-60, and tobacco use
RA pathogenesis
autoimmune attack against the synovial tissue
immune cells are activated and they produce rheumatic factor - attacks against the body, destroys cartilage
pannus
type of vascularized scar tissue, able to get nutrients but also contains inflammatory cells
causes bone erosion, bone cysts, and fissure development
in RA
CM of RA
early - vague
late - bilateral pain, stiffness, motion, limitation, inflammation
advanced - deformity and disability, joint subluxation
RA systemic involvement
fatigue, malaise
rheumatoid nodules, sjogren’s sydrome
systemic lupus erythematous (SLE)
autoimmune inflammatory disease that affects many organ systems, has acute flare ups, and is unpredictable
autoimmune attack against the body’s own DNA
two types of lupus
discoid - targets skin
systemic - targets internal organs
SLE predisposing factors
genetics, female, age 20-40, African American, environmental triggers, allergies to antibiotics, hormonal factors, and tobacco use
SLE pathogenesis
b-lymphocytes are hyperactive and productive autoantibodies
antinuclear antibody*
forms immune complexes
inflammatory response destroys the tissue
SLE CM
fatigue, photosensitivity, butterfly rash, fever, weight changes, unusual hair loss, periorbital edema
nephritis*
the more organs involved, the more CM and the worse the prognosis
SLE Flares
exacerbations and remissions
warning signs of flares: fatigue, pain, headache
prevention: recognize warning signs and avoid triggers
sjogren syndrome
autoimmune destruction of any moisture producing gland
lacrimal gland
salivary gland
methotrexate
first line therapy for SLE and RA
immunosuppressive
SE - GI, bone marrow suppression, shortened life expectancy
11 BBW
folic acid supplementation is necessary*
teratogenic, no alcohol
contact HCP with signs of infection
hydrochroroquine
SLE RA
antiinflammatory
slows progression when used with another DMARD
rare SE - retinopathy
difference in RA and SLE
RA - focus on joints
SLE - multisystem
gouty arthritis
urate crystals in the synovial fluid
acute painful inflammation
chronic tophaceous gout
advanced stage
tophi - white nodules composed of urate crystals
uric acid
waste product of purine metabolism
contains nitrogen, excreted in urine
sources: red meat, organ meat, seafood
predisposing factors of gout
male, genetics, diet, obesity, diuretic therapy and kidney insufficiency
pathogenesis of gouty arthritis
elevated uric acid levels, uric acid accumulates in body fluids, forms urate crystals, deposition in or around joints, inflammation, gouty arthritis
CM of gouty arthritis
intense pain, commonly in big toe, worst in early morning
inflammation
fever
malaise
complication of gouty arthritis
urate kidney stones
pharmacotherapy for gouty arthritis
acute - NSAIDS, corticosteroid therapy, colchicine
prophylactic - allopurinol, colchicine, probenecid
allopurinol
antigout agent
inhibits the production of uric acid
used for prophylaxis
SE - rash
interacts with hypoglycemic agents and warfarin
take with food or milk if it causes GI irritation
monitor urine uric acid and serum glucose
takes 2-6 weeks to improve
monitor PT/INR if on warfarin
colchicine
anti gout agent
inhibits leukocyte infiltration and disrupts cell division
for gout flares and prophylaxis
SE - GI (if this happens stop administration**, could be the first sign of toxicity)
contraindicated in renal disease
avoid grapefruit, alcohol, and B12 vitamins
many other drug interactions
probenecid
uricosuric agent
inhibits the reabsorption of uric acid in the kidneys
treats hyperuricemia with gout
SE - GI, dizziness, headache, kidney/liver impairment
many drug interactions
what is the relationship between bone mass, age, and sex?
women have later bone mass in early postmenopausal years
women don’t start with as much bone mass
women lose more bone mass than men
osteopenia vs osteoporosis
osteopenia - low bone mass
osteoporosis - porous bone
osteopenia
thinning of trabecular matrix of the bone before osteoporosis
osteoporosis
bone mineral density of 2.5 SD below peak bone mass
measured with DEXA scan
low bone mass, micro-architectural deterioration, increased bone fragility, susceptible to fracture
osteoporosis RF
age, female, history of fractures as an adult, family history, low body weight, smoking, alcoholism, steroid therapy and immune suppressive drugs
thin and small frame, lack of weight bearing exercises, lacking vitamin D and calcium, eating disorders, gastric bypass, lack of estrogen and testosterone, excess caffeine
FRAX
prediction tool for assessing individual risk of fracture
used to provide treatment guidelines
calculates a 10 year risk score of a hip fracture
osteoporosis patho
bone resorption from osteoclasts
bone formation from osteoblasts
failure to make new bone or increased resorption or BOTH
osteoporosis CM
early - none
late - fractures, pain, loss of height, stooped posture
3 most common fractures caused by osteoporosis
hip
wrist
vertebrae
hip fracture complications
death
high lifetime risk
requires hospitalization
mortality up to 40%
may cause them to need a caretaker
hip fx RF
age >65, female, hx osteoporosis or falls
clinical presentation of a hip fx
sudden onset of hip pain before or after a fall
inability to walk
severe groin pain
tenderness
externally rotated effected leg
shortened extremity
osteoporosis prevention pharm
calcium supplement
vitamin D supplement
exercise
alendronate
prevention and treatment of osteoporosis
binds permanently to surfaces of bones and inhibits osteoclasts
SE - GI, n/d, esophageal ulceration*
take with water
do not lie down after taking
no food, drink, calcium or vitamins for 2 hours after taking
may take a drug holiday
raloxifene
“Rail”
mimics estrogen
prevents and treats osteoporosis
reduces risk of spinal fractures by 50%
AE - hot flashes, leg cramps
take adequate calcium and vitamin D
discontinue 72 hours before prolonged immobilization
no tobacco or alcohol
teratogenic
BBW - stroke
calcitonin-salmon
bone resorption inhibitor
inhibits bone removal by osteoclasts (calcitonin)
treatment of osteoporosis
reduces spinal fractures by 30%
slows down bone loss, increases spinal bone density
can cause nasal irritation (salmon smells weird)
causes of fractures
traumatic, fatigue, pathologic
open vs closed fracture
open - penetrates skin
closed - does not break skin
transverse fracture
straight line across bone
spiral fracture
twisting break along bone
longitudinal fracture
up and down the bone
oblique fracture
diagonal fracture
comminuted fracture
more than one fracture line and more than two fragments
impacted fracture
crushed
caused by jumping from height
greenstick fracture
thinning of bone and breaking off
more likely in kids
stress fracture
small break due to repeated stressor on the bone
avulsion
fracture of the patella
PED CM of fractures
Pain
Edema
Deformity
complications of fractures
delayed healing
bone growth impairment
compartment syndrome
fat embolism syndrome
RF for delayed bone healing
infection
smoking
malnutrition
malunion
improper alignment
nounion
no healing for 4-6 months post-fracture
compartment syndrome
seen with crushing injuries, too tight of casts, long bone injuries, severe thermal burns. and animal bites
results from increased pressure within a limited amount of space
creates a “tourniquet effect”
CM of compartment syndrome
extreme pain
very quick process
check for pulse distal to the cast*
fat embolism syndrome
fat molecules in the lung after long bone fracture or major trauma that forms within 24-48 hours after injury
fat molecules from the bone marrow or traumatized tissue are released into the bloodstream, ending up in the lungs
osteomyelitis
an acute or chronic pus producing (pyogenic) infection of a bone
usually from bacteria (staphylococcus aureus)
RF for osteomyelitis
recent trauma
DM (poor circulation)
hemodialysis
IV drug use
splenectomy
PVD
direct osteomyelitis contamination
open wound from open fracture, gunshot, puncture, surgery, or insertion of metal plates
hematogenous (indirect) contamination of osteomyelitis
from the bloodstream, usually in the long bones, those under 16 have the highest risk
*most common type
hematogenous contamination patho
arterial bloodflow brings bacteria to bone
infection causes inflammation, bone destruction, and pus and edema
pressure increases
ischemia/necrosis
osteoblasts lay new bone around the old bone
infection becomes isolated
what is the problem when pressure within the bone increases to that of arterial blood flow?
local arteries collapse
no oxygen, nutrition, immune cell, or antibiotics supply
results in impaired healing
CM osteomyelitis
local - tenderness, warmth, redness, wound drainage, restricted movement
spontaneous fractures
systemic - spiking fevers, positive blood culture, leukocytosis
pharm for osteomyellitis
obtain a culture
give a broad spectrum abx (naficillin, cefazolin, vancomycin)
start bacteria specific therapy when culture returns
complications of osteomyelitis
chronic osteomyelitis
local spread of infection
reduced limb or joint function
4 phases of the cell cycle
G1 - cell prepares to make DNA
S - 2 separate chromosomes arise
G2 - DNA synthesis ceases
M - cell divides
Go - resting phase
what is an example of a non-cancerous cell that divides rapidly?
GI epithelial cells lining the GI tract
undifferentiated stem cells
can be triggered to enter the cell cycle and produce parent cells
parent cells
continue to divide and reproduce (blood, skin, liver cells)
well-differentiated cells
do not normally divide and reproduce (neurons of skeletal and cardiac muscle)
what are the 3 basic properties of cell proliferation?
- intracellular control of proliferation
- contact inhibition
- rate of cell proliferation
cell differentiation
the process in which proliferating cells are transformed into different and more specialized types of cells
apoptosis
cell begins to die and molecules on the cell’s surface change
fertilized ovum
where all types of cells originate from
stem cells
“reserve unit”
exist in a dormant state
when triggered by some event, they jump into the cell cycle and begin proliferation and differentiation
what is the connection between stem cells and cancer cells?
mutations of cells at some point in the differentiation process from a stem cell to an adult cell that cancer cells are formed
benign vs malignant
benign - glow slowly, have a well defined-capsule, non-invasive, looks like tissues from when it irises, have a low mitotic index, dividing cells are rare
malignant - grow rapidly, are not encapsulated, invade local structures and tissues, poorly differentiated (may not be able to tell what tissue it arose from), have many dividing cells, can spread distantly through blood and lymph system
what 3 things does the origin of cancer depend on?
genes, carcinogens, and promoters
what are the 4 phases of carcinogenesis?
- initiation
- promotion
- progression
- metastasis
oncogen and gas pedal analogy
mutated proto-oncogens cause the growth signal to be permanently “on” while tumor suppressor genes are inactivated “brake”
tumor supressor genes
normally function to restrain cell growth
can become effective and lose the ability to inhibit cell growth and division, allowing cancer formation
proto-oncogens
“good genes”
stimulate and regulate a cell’s movement through the cell cycle, results in cellular growth and proliferation
when mutated, they become oncogens and stimulate constant cellular proliferation and cycling
carcinogens
substances that cause the development of cancer
promoters - diet, alcohol, tobacco, hormones
viral induced cancer
always involve the activation of growth promoting pathways or inhibition of tumor suppressors in infected cells
endothelial growth factor
substance that gives cancer cells the ability to develop new blood vessels
primary vs secondary tumor
primary - where it originated
secondary - due to the primary
seeding vs implantation
seeding - erodes and sheds into body cavities and implants somewhere else (seed falls off the tree and starts growing where it lands)
implantation - direct exposure of a tumor to surrounding tissue, from one organ to the next (tree has roots)
lymphatic spread of cancer
cells become trapped in the lymph nodes
cells either die, go dormant, or proliferate
if they survive, they work their way through the lymph system
vascular spread of cancer
spreads by vascular drainage - penetrates local veins and goes through the body
first stop is often the liver because it receives blood through portal circulation before general circulation (why the liver is commonly a secondary cancer site)
angiogenesis
tumor creates its own blood supply
common sites for secondary tumors
lungs
bones
liver
brain
lung cancer
normally diagnosed late
early diagnosis is key
most prevalent in those >65 and African Americans
*cigarette smoking is the main etiology (risk increases with more smoking)
cilia are paralyzed which activates oncogens
non small cell lung cancer vs small cell lung cancer
NSCLC - slow growing, majority of lung cancers
SCLC - rapidly growing tumor that metastasizes quickly
S/S of lung cancer
cough, hemoptysis, wheeze, chest pain, dyspnea, weight loss, excessive fatigue, weakness, hoarseness, may appear as pneumonia
paraneoplastic syndrome
paraneoplastic syndrome and lung cancer
lungs secrete an excess of ACTH (cortisol)
gives the patient a tanned appearance
breast cancer: RF, S/S
RF - age >50, prolonged reproductive life, hormone replacement therapy, obesity, late childbirth, nulliparous (no pregnancies), Jewish women, and genetic mutations
S/S - single tumor, nontender tumor, firm tumor, irregular borders, commonly in the upper outer quadrant
BRCA genes
familial gene that increases the likelihood of developing breast cancer
many women choose an elective mastectomy
cervical cancer
promote screening*
RF - smoking, STD history, *HPV infection, more than two lifetime sexual partners, immunosuppression, genetics
colorectal cancer- RF, S/S
usually starts as a polyp (can be hereditary)
RF - obesity, tobacco, inactivity, insulin resistance, low fiber, high amount of animal fat, diet low in a, c, and e, ulcerative colitis, and heavy alcohol use
S/S - fatigue, weakness, weight loss, iron deficiency anemia, changes in bowel habits, melena, diarrhea, constipation, and rectal bleeding
consequences to late detection of cancer
- metastasis
- less responsive to treatment
- more debilitated by the disease
what are the strategies for success of chemo?
intermittent chemo
combo therapy
optimal dosing
regional therapy
intermittent chemo
gives chemo intermittently to allow normal cells to recover in between cycles
normal cells recover faster than cancer cells, so it strikes a balance
what is an important precaution with combination chemo therapy?
don’t want to have drugs that have overlapping toxicities, could “knock out” one part of the body
what are the “usual toxicities” of chemo?
nausea and vomiting
decreased WBC, RBC, platelets
diarrhea, alopecia, and fatigue
3 major complications of chemo
neutropenia - risk for infection
thrombocytopenia - risk for bleeding
erythrocytopenia - anemia
magic mouthwash
prescription cocktail to assist in treating stomatitis
lidocaine, mylanta, diphenhydramine, prednisolone, distilled water
*not curative
what are 3 drugs to help with chemo toxicities?
ondansetron
dexamethasone
magic mouthwash
cytotoxic agents MOA
disrupts DNA synthesis, target rapidly producing cells
cyclophosphamide
alkylating agent
nonspecific cell phase
*bladder injury plus normal toxicities and discoloration of skin and nails
methotrexate
antimetabolites
S phase specific
resemble natural metabolites
usual toxicities plus nephrotoxicity, hepatotoxicity, and abnormaltities/fatal
doxorubicin
antitumor abx
nonspecific in cell cycle phase
originates from streptomyces
usual toxicities plus cardiotoxicity
vincristine
mitotic inhibitors
m phase specific
comes from periwinkle
almost all experience peripheral neuropathy*
no bone marrow suppression in some drugs
ondansetron
blocks seretonin receptors on vagal nerve and CTZ
efficacy is improved with steroids
AE - headache, diarrhea, dizziness
promethazine
blocks dopamine receptors in the CTZ
AE - respiratory depression, drowsiness, sedation
BBW - resp depression <2 and gangrenous extraversion
biologics therapy
uses body’s immune system to kill cancer cells
many types
approved for leukemia, lymphoma, breast, bladder, brain, colon, lung, and pancreatic
biologics SE
pain, swelling soreness
flu-like
weight gain
diarrhea
risk of infection
non-self antigen
our immune system surveys the body for these foreign substances
differentiation
extent that neoplastic cells resemble normal cells both structurally and functionally
anaplasia
lack of differentiation
cellular disorganization
what types of substances are tumor markers and where can they be found?
hormones, enzymes, antigens, or genes
blood, urine, CSF, or tumor plasma membranes
*not always diagnostic of cancer
classifying cancer through the TNM system
T - tumor size
N - lymph node involvement
M - metastasis to distant organs
grades 1-3 of malignant cancers
grade 1 - cells are well differentiated
grade 2 - cells are moderately differentiated
grade 3 - poorly differentiated or anaplastic cells
4 stage cancer classification
stage 1 - confined to organ or origin
stage 2 - locally invasive
stage 3 - regional spread
stage 4 - spread to distant sites
