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NSG > NUR326 Exam 4 > Flashcards

NUR326 Exam 4 Flashcards

1
Q

synovial/diathrodial joint

A

any joint that allows movement

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2
Q

subchrondral bone plate

A

under the cartilage
bone just underneath the cartilage

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3
Q

articular cartilage

A

covers the bone of the joint, provides a smooth, slippery surface that allows free movement of a joint

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4
Q

synovium

A

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

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5
Q

joint capsule

A

surrounds the joint
unties articulating bones

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6
Q

three phases of bone healing

A
  1. inflammatory - hematoma forms
  2. reparative - fibrous cartilage and ossification
  3. remodeling - healing is complete
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7
Q

osteoarthritis

A

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

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8
Q

RF of osteoarthritis

A

aging, obesity, history of playing sports, history of trauma, heavy occupational work, misalignment

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9
Q

etiology of OA

A

stress is applied to joints, degeneration of cartilage, osteoblasts are activated which lead to bony spurs, narrows joint space, becomes a chronic disease

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10
Q

osteophytes

A

small bony projections that develop on the rim of the bone adjacent to cartilage loss
hallmark in OA**

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11
Q

OA symptoms

A

deep aching joint pain, relieved with rest
pain during cold weather
stiffness in the mornings
popping during motion
joint swelling
altered gait
limited ROM

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12
Q

herbeden’s nodes

A

swellings at the distal interphalangeal joint (OA)

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13
Q

bouchard’s nodes

A

proximal interphalangeal joint (OA)

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14
Q

pharmacotherapy for OA

A

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

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15
Q

NSAID MOA

A

reduce the production of prostaglandin
causes an increase in ulcer development
contraindicated with a history of ulcers

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16
Q

cautions with NSAIDS

A

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

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17
Q

OA dietary supplements

A

glucosamine sulfate - maintains cartilage health
chondroitin sulfate - slows cartilage breakdown

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18
Q

degenerative disk disease (DDD)

A

degeneration of the lumbar and cervical spine
causes pain, motor weakness, and neuropathy

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19
Q

S/S of DDD

A

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

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20
Q

commonalities between rheumatoid arthritis and systemic lupus erythematous

A

inflammatory conditions that result in pain, limitation of movement, destruction or erosion of joints, ligaments, or muscles
autoimmune orgin
systemic, not local

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21
Q

rheumatoid arthritis (RA)

A

systemic autoimmune disease that is type III hypersensitivity
inflammation of the synovium

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22
Q

RA etiology

A

not fully understood, genetic link, women 40-60, and tobacco use

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23
Q

RA pathogenesis

A

autoimmune attack against the synovial tissue
immune cells are activated and they produce rheumatic factor - attacks against the body, destroys cartilage

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24
Q

pannus

A

type of vascularized scar tissue, able to get nutrients but also contains inflammatory cells
causes bone erosion, bone cysts, and fissure development
in RA

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25
Q

CM of RA

A

early - vague
late - bilateral pain, stiffness, motion, limitation, inflammation
advanced - deformity and disability, joint subluxation

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26
Q

RA systemic involvement

A

fatigue, malaise
rheumatoid nodules, sjogren’s sydrome

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27
Q

systemic lupus erythematous (SLE)

A

autoimmune inflammatory disease that affects many organ systems, has acute flare ups, and is unpredictable
autoimmune attack against the body’s own DNA

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28
Q

two types of lupus

A

discoid - targets skin
systemic - targets internal organs

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29
Q

SLE predisposing factors

A

genetics, female, age 20-40, African American, environmental triggers, allergies to antibiotics, hormonal factors, and tobacco use

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30
Q

SLE pathogenesis

A

b-lymphocytes are hyperactive and productive autoantibodies
antinuclear antibody*
forms immune complexes
inflammatory response destroys the tissue

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31
Q

SLE CM

A

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

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32
Q

SLE Flares

A

exacerbations and remissions
warning signs of flares: fatigue, pain, headache
prevention: recognize warning signs and avoid triggers

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33
Q

sjogren syndrome

A

autoimmune destruction of any moisture producing gland
lacrimal gland
salivary gland

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34
Q

methotrexate

A

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

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35
Q

hydrochroroquine

A

SLE RA
antiinflammatory
slows progression when used with another DMARD
rare SE - retinopathy

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36
Q

difference in RA and SLE

A

RA - focus on joints
SLE - multisystem

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37
Q

gouty arthritis

A

urate crystals in the synovial fluid
acute painful inflammation

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38
Q

chronic tophaceous gout

A

advanced stage
tophi - white nodules composed of urate crystals

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39
Q

uric acid

A

waste product of purine metabolism
contains nitrogen, excreted in urine
sources: red meat, organ meat, seafood

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40
Q

predisposing factors of gout

A

male, genetics, diet, obesity, diuretic therapy and kidney insufficiency

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41
Q

pathogenesis of gouty arthritis

A

elevated uric acid levels, uric acid accumulates in body fluids, forms urate crystals, deposition in or around joints, inflammation, gouty arthritis

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42
Q

CM of gouty arthritis

A

intense pain, commonly in big toe, worst in early morning
inflammation
fever
malaise

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43
Q

complication of gouty arthritis

A

urate kidney stones

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44
Q

pharmacotherapy for gouty arthritis

A

acute - NSAIDS, corticosteroid therapy, colchicine
prophylactic - allopurinol, colchicine, probenecid

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45
Q

allopurinol

A

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

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46
Q

colchicine

A

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

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47
Q

probenecid

A

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

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48
Q

what is the relationship between bone mass, age, and sex?

A

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

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49
Q

osteopenia vs osteoporosis

A

osteopenia - low bone mass
osteoporosis - porous bone

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50
Q

osteopenia

A

thinning of trabecular matrix of the bone before osteoporosis

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51
Q

osteoporosis

A

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

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52
Q

osteoporosis RF

A

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

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53
Q

FRAX

A

prediction tool for assessing individual risk of fracture
used to provide treatment guidelines
calculates a 10 year risk score of a hip fracture

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54
Q

osteoporosis patho

A

bone resorption from osteoclasts
bone formation from osteoblasts
failure to make new bone or increased resorption or BOTH

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55
Q

osteoporosis CM

A

early - none
late - fractures, pain, loss of height, stooped posture

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56
Q

3 most common fractures caused by osteoporosis

A

hip
wrist
vertebrae

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57
Q

hip fracture complications

A

death
high lifetime risk
requires hospitalization
mortality up to 40%
may cause them to need a caretaker

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58
Q

hip fx RF

A

age >65, female, hx osteoporosis or falls

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59
Q

clinical presentation of a hip fx

A

sudden onset of hip pain before or after a fall
inability to walk
severe groin pain
tenderness
externally rotated effected leg
shortened extremity

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60
Q

osteoporosis prevention pharm

A

calcium supplement
vitamin D supplement
exercise

61
Q

alendronate

A

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

62
Q

raloxifene

A

“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

63
Q

calcitonin-salmon

A

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)

64
Q

causes of fractures

A

traumatic, fatigue, pathologic

65
Q

open vs closed fracture

A

open - penetrates skin
closed - does not break skin

66
Q

transverse fracture

A

straight line across bone

67
Q

spiral fracture

A

twisting break along bone

68
Q

longitudinal fracture

A

up and down the bone

69
Q

oblique fracture

A

diagonal fracture

70
Q

comminuted fracture

A

more than one fracture line and more than two fragments

71
Q

impacted fracture

A

crushed
caused by jumping from height

72
Q

greenstick fracture

A

thinning of bone and breaking off
more likely in kids

73
Q

stress fracture

A

small break due to repeated stressor on the bone

74
Q

avulsion

A

fracture of the patella

75
Q

PED CM of fractures

A

Pain
Edema
Deformity

76
Q

complications of fractures

A

delayed healing
bone growth impairment
compartment syndrome
fat embolism syndrome

77
Q

RF for delayed bone healing

A

infection
smoking
malnutrition

78
Q

malunion

A

improper alignment

79
Q

nounion

A

no healing for 4-6 months post-fracture

80
Q

compartment syndrome

A

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”

81
Q

CM of compartment syndrome

A

extreme pain
very quick process
check for pulse distal to the cast*

82
Q

fat embolism syndrome

A

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

83
Q

osteomyelitis

A

an acute or chronic pus producing (pyogenic) infection of a bone
usually from bacteria (staphylococcus aureus)

84
Q

RF for osteomyelitis

A

recent trauma
DM (poor circulation)
hemodialysis
IV drug use
splenectomy
PVD

85
Q

direct osteomyelitis contamination

A

open wound from open fracture, gunshot, puncture, surgery, or insertion of metal plates

86
Q

hematogenous (indirect) contamination of osteomyelitis

A

from the bloodstream, usually in the long bones, those under 16 have the highest risk
*most common type

87
Q

hematogenous contamination patho

A

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

88
Q

what is the problem when pressure within the bone increases to that of arterial blood flow?

A

local arteries collapse
no oxygen, nutrition, immune cell, or antibiotics supply
results in impaired healing

89
Q

CM osteomyelitis

A

local - tenderness, warmth, redness, wound drainage, restricted movement
spontaneous fractures
systemic - spiking fevers, positive blood culture, leukocytosis

90
Q

pharm for osteomyellitis

A

obtain a culture
give a broad spectrum abx (naficillin, cefazolin, vancomycin)
start bacteria specific therapy when culture returns

91
Q

complications of osteomyelitis

A

chronic osteomyelitis
local spread of infection
reduced limb or joint function

92
Q

4 phases of the cell cycle

A

G1 - cell prepares to make DNA
S - 2 separate chromosomes arise
G2 - DNA synthesis ceases
M - cell divides
Go - resting phase

93
Q

what is an example of a non-cancerous cell that divides rapidly?

A

GI epithelial cells lining the GI tract

94
Q

undifferentiated stem cells

A

can be triggered to enter the cell cycle and produce parent cells

95
Q

parent cells

A

continue to divide and reproduce (blood, skin, liver cells)

96
Q

well-differentiated cells

A

do not normally divide and reproduce (neurons of skeletal and cardiac muscle)

97
Q

what are the 3 basic properties of cell proliferation?

A
  1. intracellular control of proliferation
  2. contact inhibition
  3. rate of cell proliferation
98
Q

cell differentiation

A

the process in which proliferating cells are transformed into different and more specialized types of cells

99
Q

apoptosis

A

cell begins to die and molecules on the cell’s surface change

100
Q

fertilized ovum

A

where all types of cells originate from

101
Q

stem cells

A

“reserve unit”
exist in a dormant state
when triggered by some event, they jump into the cell cycle and begin proliferation and differentiation

102
Q

what is the connection between stem cells and cancer cells?

A

mutations of cells at some point in the differentiation process from a stem cell to an adult cell that cancer cells are formed

103
Q

benign vs malignant

A

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

104
Q

what 3 things does the origin of cancer depend on?

A

genes, carcinogens, and promoters

105
Q

what are the 4 phases of carcinogenesis?

A
  1. initiation
  2. promotion
  3. progression
  4. metastasis
106
Q

oncogen and gas pedal analogy

A

mutated proto-oncogens cause the growth signal to be permanently “on” while tumor suppressor genes are inactivated “brake”

107
Q

tumor supressor genes

A

normally function to restrain cell growth
can become effective and lose the ability to inhibit cell growth and division, allowing cancer formation

108
Q

proto-oncogens

A

“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

109
Q

carcinogens

A

substances that cause the development of cancer
promoters - diet, alcohol, tobacco, hormones

110
Q

viral induced cancer

A

always involve the activation of growth promoting pathways or inhibition of tumor suppressors in infected cells

111
Q

endothelial growth factor

A

substance that gives cancer cells the ability to develop new blood vessels

112
Q

primary vs secondary tumor

A

primary - where it originated
secondary - due to the primary

113
Q

seeding vs implantation

A

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)

114
Q

lymphatic spread of cancer

A

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

115
Q

vascular spread of cancer

A

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)

116
Q

angiogenesis

A

tumor creates its own blood supply

117
Q

common sites for secondary tumors

A

lungs
bones
liver
brain

118
Q

lung cancer

A

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

119
Q

non small cell lung cancer vs small cell lung cancer

A

NSCLC - slow growing, majority of lung cancers
SCLC - rapidly growing tumor that metastasizes quickly

120
Q

S/S of lung cancer

A

cough, hemoptysis, wheeze, chest pain, dyspnea, weight loss, excessive fatigue, weakness, hoarseness, may appear as pneumonia
paraneoplastic syndrome

121
Q

paraneoplastic syndrome and lung cancer

A

lungs secrete an excess of ACTH (cortisol)
gives the patient a tanned appearance

122
Q

breast cancer: RF, S/S

A

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

123
Q

BRCA genes

A

familial gene that increases the likelihood of developing breast cancer
many women choose an elective mastectomy

124
Q

cervical cancer

A

promote screening*
RF - smoking, STD history, *HPV infection, more than two lifetime sexual partners, immunosuppression, genetics

125
Q

colorectal cancer- RF, S/S

A

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

126
Q

consequences to late detection of cancer

A
  1. metastasis
  2. less responsive to treatment
  3. more debilitated by the disease
127
Q

what are the strategies for success of chemo?

A

intermittent chemo
combo therapy
optimal dosing
regional therapy

128
Q

intermittent chemo

A

gives chemo intermittently to allow normal cells to recover in between cycles
normal cells recover faster than cancer cells, so it strikes a balance

129
Q

what is an important precaution with combination chemo therapy?

A

don’t want to have drugs that have overlapping toxicities, could “knock out” one part of the body

130
Q

what are the “usual toxicities” of chemo?

A

nausea and vomiting
decreased WBC, RBC, platelets
diarrhea, alopecia, and fatigue

131
Q

3 major complications of chemo

A

neutropenia - risk for infection
thrombocytopenia - risk for bleeding
erythrocytopenia - anemia

132
Q

magic mouthwash

A

prescription cocktail to assist in treating stomatitis
lidocaine, mylanta, diphenhydramine, prednisolone, distilled water
*not curative

133
Q

what are 3 drugs to help with chemo toxicities?

A

ondansetron
dexamethasone
magic mouthwash

134
Q

cytotoxic agents MOA

A

disrupts DNA synthesis, target rapidly producing cells

135
Q

cyclophosphamide

A

alkylating agent
nonspecific cell phase
*bladder injury plus normal toxicities and discoloration of skin and nails

136
Q

methotrexate

A

antimetabolites
S phase specific
resemble natural metabolites
usual toxicities plus nephrotoxicity, hepatotoxicity, and abnormaltities/fatal

137
Q

doxorubicin

A

antitumor abx
nonspecific in cell cycle phase
originates from streptomyces
usual toxicities plus cardiotoxicity

138
Q

vincristine

A

mitotic inhibitors
m phase specific
comes from periwinkle
almost all experience peripheral neuropathy*
no bone marrow suppression in some drugs

139
Q

ondansetron

A

blocks seretonin receptors on vagal nerve and CTZ
efficacy is improved with steroids
AE - headache, diarrhea, dizziness

140
Q

promethazine

A

blocks dopamine receptors in the CTZ
AE - respiratory depression, drowsiness, sedation
BBW - resp depression <2 and gangrenous extraversion

141
Q

biologics therapy

A

uses body’s immune system to kill cancer cells
many types
approved for leukemia, lymphoma, breast, bladder, brain, colon, lung, and pancreatic

142
Q

biologics SE

A

pain, swelling soreness
flu-like
weight gain
diarrhea
risk of infection

143
Q

non-self antigen

A

our immune system surveys the body for these foreign substances

144
Q

differentiation

A

extent that neoplastic cells resemble normal cells both structurally and functionally

145
Q

anaplasia

A

lack of differentiation
cellular disorganization

146
Q

what types of substances are tumor markers and where can they be found?

A

hormones, enzymes, antigens, or genes
blood, urine, CSF, or tumor plasma membranes
*not always diagnostic of cancer

147
Q

classifying cancer through the TNM system

A

T - tumor size
N - lymph node involvement
M - metastasis to distant organs

148
Q

grades 1-3 of malignant cancers

A

grade 1 - cells are well differentiated
grade 2 - cells are moderately differentiated
grade 3 - poorly differentiated or anaplastic cells

149
Q

4 stage cancer classification

A

stage 1 - confined to organ or origin
stage 2 - locally invasive
stage 3 - regional spread
stage 4 - spread to distant sites

NSG (12 decks)

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