Exam 1 Flashcards

1
Q

What is the normal MAP? What happens when it is lowered?

A

70-110

if <68, blood starts to shut to the brain and kidneys

if <65 blood starts to shunt to heart with decreased perfusion to brain and kidneys

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2
Q

What is cerebral perfusion pressure?

A

pressure needed to ensure blood flow to the brain

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3
Q

What is the normal cerebral perfusion pressure? What happens when it is lower than normal?

A

60-100mmHg

<50, ischemia and neuron death

<30, ischemia and death

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4
Q

What is the normal intracranial pressure?

A

5-15

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5
Q

What happens when ICP increases?

A

MAP will need to increase to maintain CPP

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6
Q

What are clinical manifestations of increased ICP for infants

A

fontanels are tense/bulging

cranial sutures are separated/split

increased occipital frontal head circumfrence

distended scalp veins

altered response to pain

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7
Q

What are clinical manifestations of increased ICP for adults/adolexcents/children?

A

change in mental status (early sign)

headache

vomiting

change in pupils or vision

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8
Q

What are later manifestations of increased ICP?

A

severely decreased LOC

decreased sensory response to painful stimuli

alterations in pupil size and reactivity (nonreactive, uneven, large/blown)

cheyne-stokes respirations

decreased/altered motor response to commands

decerbrate or decortiate posture

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9
Q

What is the cushing’s triad? Why does this occur?

A

increased systolic bp with widening pulse pressure

bradycardia

altered respirations

body compensating to increased ICP

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10
Q

What can occur when the brainstem is compressed?

A

hypothalamus produces and pituitary secretes ADH causing:

SIDAH: high levels of ADH causing hyponatremia and hypoosmolarity can lead to low urine output, increased body weight, muscle cramping, pain, weakness

Diabetes insipidus: deficiency of production or secretion of ADH or a decreased renal response to ADH resulting in fluid/electrolyte imbalances caused by increased urine output and plasma osmolarity

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11
Q

What is herniation?

A

last stage of progression of increased ICP before death where the brain tissue is forcibly shifted downward (area of less pressure) causing death of brain stem

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12
Q

What are nursing interventions for those with increased ICP

A

HOB at 30

temperature control

nutriton

eliminate or minimize noise

suction secretions prn

avoid activities that may increase ICP (hip flexion to decrease risk of increasing intrabdominal pressure)

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13
Q

What medications can be given for increased ICP?

A

mannitol: IV osmotic diuretic which will cause 1. plasma expansion to reduce hematocrit and blood viscosity to increase CBF and cerebral O2
2. osmotic effect to cause fluid movement from tissues into blood vessels to decrease total brain fluid content

hypertonic saline solution: produces movement of water out of brain cells into vessels

both are often used together

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14
Q

What is the nursing assessment for ICP?

A

mental status

glasgow coma scale (eye opening, best verbal response, best motor response)

pupil reaction (doll’s eyes (eyes stay fixated as the head moves))

cranial nerves

motor strength and response

vital signs

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15
Q

What are the classifications of the glasgow coma scale?

A

mild = 13-15
moderate = 9-12
severe = 3-8

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16
Q

What is a concussion? Typical signs?

A

sudden, transient mechanical head injury with disruption of neural activity

brief disruption in LOC (not always)
amnesia about the event
headache

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17
Q

What medications can be given for concussion?

A

acetaminophen for headache

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18
Q

What is focal injury?

A

localized area of injury consisting of lacerations, contusions, hematomas, and cranial nerve injuries that can be minor to severe

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19
Q

What is latent TB versus TB disease?

A

latent: asymptomatic, +TST, CXR will be normal, sputum tests will be negative, not contagious

disease: symptomatic, +TST, CXR may be abnormal, sputum tests may be positive, contagious

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20
Q

What are clinical manifestations of TB disease?

A

cough lasting 3 weeks or more

coughing up blood or sputum

angina

weakness and fatigue

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21
Q

What are complications of TB?

A

miliary TB: widespread of TB bacteria to distant organs that will be fatal if not treated

pleural TB: unilateral, exudative pleural effusion, empyema (pus in pleural cavity)

organ involvement due to TB disease manifestations

22
Q

What diagnostic tests are there for TB?

A

mantoux TB skin test (TST): cannot distinguish between active and latent but can indicate presence of antibodies (if 10-15mm reading)

interferon-gamma release assays: measures immune response to TB, if negative would indicate no latent or active TB, can indicate presence of antibodies

sputum: collected over 3 consecutive days, only test to determine between latent and active

CXR: for visualization of active TB

23
Q

How can community spread of TB be prevented?

A

direct observation therapy where the nurse will directly observe the pt comply with medications

24
Q

What is bacille calmette-guerin (BCG) vaccine?

A

vaccine for TB that is recommended in countries or settings with high incidence of TB, may cause a false +TST

25
Q

What are the drugs used to treat active TB?

A

RIPE: rifampin, isoniazid, pyrazinamide, ethambutol

26
Q

How long is the treatment for active TB? for latent TB?

A

6 to 9 mo

3, 4, or 6-9

27
Q

What are the drugs used for latent TB?

A

rifampin and isoniazid

28
Q

What are the manifestations of osteoarthritis compared to rheumatoid arthritis?

A

OA:
“wear and tear disease”
can be seen asymmetrically
NO systemic involvement
pain is primary symptom and reason for seeking care, early stages: pain relief with rest, late stages: pain at rest and/or with barometric pressure, disability, joint stiffness after period of rest
commonly involves weight-bearing joints
Heberden’s nodes (distal finger joints due to osteophytes and loss of joint space, red, swollen, and tender
Bouchard’s nodes (proximal finger joints are red, swollen, and tender)

RA:
chronic and systemic
pannus formation is most common indicator
fatigue, anorexia, weight loss
general stiffness after activity and in the morning
joint stiffness of especially small joints (“spindle fingers”, “zig-zag”, subluxation)
has a precipitating event
systemic manifestations: rheumatoid nodules, cataracts and vision loss, muscle fiber degeneration, nodules in heart and lungs, Sjogren’s syndrome (diminished lacrimal or salivary secretions), felty syndrome (enlarged spleen with low WBC = risk of infection), hand deformities and decreased grasp strength, depression

29
Q

What are the nursing interventions for osteoarthritis?

A

rest and joint protection
heat
cold (for acute flare ups)
nutrition
exercise to reduce weight on joints
avoid smoking
transcutaneous electrical nerve stimulation (TENS)
complementary and alternative therapies
administer pain medications such as acetaminophen or topical applications, NSAIDs if necessary
prepare client for corticosteroid injections into joints
position joints in function position and avoid flexion of knees and hips
immobilize the affected joint with a splint or brace until inflammation subsides
encourage adequate rest

30
Q

What are nursing interventions for rheumatoid arthritis?

A

pharmacologic: DMARDs (cornerstone treatment to slow disease progression and decrease risk of joint erosion and deformity), biologic response modifiers (slows disease progression), tumor necrosis factor inhibitors (reduce inflammation and stop disease progression)

physical mobility: preserve joint function, provide ROM exercises, balance rest and activity, splints may be used during acute inflammation to prevent deformity, prevent flexion contractures, apply heat or cold, encourage consistency with exercise, avoid weight-bearing on inflammed joints

self care: assess need for assistive devices such as rasied toilet seats, work with OT, instruct pt in alternative strategies for providing ADLs

fatigue: identify factors that may contribute to fatigue, monitor signs for anemia and administer iron, folic acid, and vitamins, monitor for medication related blood loss through stool, instruct pt to conserve energy by pacing activities and obtaining assistance when possible

31
Q

What are risk factors for osteoporosis?

A

increased age
family hx
low weight and BMI
late menarche, early menopause, low endogenous estrogen levels
lifestyle (smoking, inadequate amounts of weight bearing activity, excessive alcohol intake, nutrtional)

ethnicity (highest to lowest risk):
asians, native alaskan indian, native american
white, non-hispanic women
hispanic groups
white men and african american women
african american men

32
Q

What are manifestations of osteoporosis?

A

low BMD
increase risk of fx

33
Q

What are the screening recommendations for osteoporosis?

A

hx of risk factors
height: historical height loss of 6cm or more is consistent with diagnosis

34
Q

How can osteoporosis be managed?

A

calcium supplements (avoid usage with renal injury or risk of kidney stones)
weight bearing exercise

pharmacologic:
calcitonin
raloxifene (selective estrogen receptor modulator with common adverse effects: hot flashes and leg cramps and serious adverse effects; increase risk of blood clots)
bisphosphonates: suppresses osteoclast bone reabsorption, DC does not result in cessation of action, must be taken with water and on an empty stomach, avoid taking with calcium

35
Q

What are the risk factors for breast cancer?

A

age 50 and older
gender (predominantly women)
genetic: BRCA1 and BRCA2
hormone usage, especially post-menopausal usage
family hx
personal hx
menstrual hx: early menarche (before 12), late menopause (after 45)
full term pregnancy after 30
nulliparity
atypical epithelial hyperplasia of breast tissue
breast denisty: more connective than fatty tissue makes it harder to see masses on mammograms
weight and obesity after menopause due to fat cells storing estrogen
ionizing radiation
alcohol consumption

36
Q

What is inflammatory breast cancer? Pathophysiology?

A

rare rapid development of breast cancer making the affected breast red, swollen, tender
occurs when cancer cells block lymphatic vessels and skin covering breast

37
Q

What is paget’s?

A

rare breast cancer that starts at the nipple and extends to areolar

38
Q

What is phyllodes tumor?

A

breast tumor that rapidly grows in leaf-life pattern but rarely metastasize

39
Q

What are clinical manifestations of breast cancer?

A

nontender lump in breast that typically is found in upper outer quadrant
abnormal nipple discharge
rash around nipple area
nipple retraction
dimpling of skin
change in nipple position
usually painless
Peau d’orange: skin becomes thick and pitted with a texture and appearance similar to orange peel
infiltration, dimpling

40
Q

What is the nurse’s role in the stages of end of life?

A

denial: be supportive and listen
anger: don’t take anger personally, help pt maintain autonomy as much as possible
bargaining: listen, do not give false hope
depression: listen, refer to spiritual leaders if wanted
acceptance: honor wishes, simplify environment, peaceful environment

41
Q

What are nursing interventions for end of life care?

A

pain: proactively prevent

respiratory: elevated HOB, pace activities throughout day, administer oxygen as needed

constipation: proactively prevent with increase fluids, fiber, possible stool softener

poor nutritional intake: may need to simulate appetite, at an increase fall risk

42
Q

What is left sided heart failure?

A

blood backs up into lungs
likely to lead to right sided HF
can be systolic or diastolic dysfunction: systolic leads to low ejection fraction and decreased perfusion to organs, diastolic leads to ventricle not filling completely (decreased stroke volume) with blood but with a normal ejection fraction

43
Q

What are the clinical manifestations of left sided heart failure?

A

DROWNING
dyspnea
rales (crackles)
orthopnea (dyspnea upon lying down)
weakenss
nocturnal paroxysmal dyspnea
increased HR
nagging cough
gaining weight

44
Q

What is right sided heart failure?

A

congestion of blood in the heart causing back up in the venous system and tissues

45
Q

What are the signs and symptoms of right sided heart failure?

A

SWELLING
swelling of legs, hands, liver, abdomen
weight gain
edema (pitting)
large neck veins (JVD)
lethargy
irregular HR (afib)
nocturia
girth of abdomen increased

46
Q

What are the major pharmaceutical therapies for heart failure? Side effects?

A

ACE inhibitors - prils
side effects: dry, nagging cough, hypotension, hyperkalemia, renal insufficiency

ARBs - sartans
side effect: hyperkalemia

47
Q

How are diuretics used in heart failure?

A

symptom management by promoting excretion of sodium and water

48
Q

What are the classes of lupus drugs?

A

NSAIDs
anti-malarial
corticosteroids
immunosuppressives
anticoagulants
B lymphocyte stimulator
topical immunomodulators

49
Q

What is the pathophysiology of lupus?

A

multi-system inflammatory and autoimmune disease that affects the skin, joints, serous membranes (pleura, pericardium), renal, hematologic, and neurologic

50
Q

What are the clinical manifestations of lupus?

A

dermatologic: butterfly rash over cheeks, vascular skin lesions

musculoskeletal: pain in multiple joints, morning stiffness

cardiopulmonary: pleurisy (inflammation of pleural), tachypnea, inflammation of heart

renal: glomerulonephritis progressing into end stage renal disease

neurologic: peripheral neuropathy, cognitive problems, mood disorders, headache

hematologic: thrombocytopnea (increased risk of infection)