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Gerontological Nursing > Exam 2: Gero Lecture 6 > Flashcards

Exam 2: Gero Lecture 6 Flashcards

1
Q

Describe acute illness.

A

Occurs suddenly and often without warning
Stroke, myocardial infarction, hip fracture, infection

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2
Q

Describe chronic illness.

A

Managed rather than cured
Always present but not always visible
Most common chronic condition in persons over 65 is arthritis, followed by hypertension

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3
Q

What is the preventive phase, definitive phase, crisis phase, and acute phase of chronic illness trajectory?

A

Preventive phase (pre-trajectory)
No S/Sx

Definitive phase (trajectory onset)
S/Sx & diagnosis PRESENT

Crisis phase
Life-threatening situation

Acute phase
Active illness requiring hospitalization

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4
Q

what is the stable, unstable, downward, and dying phase of chronic illness trajectory?

A

Stable phase
Controlled illness course/symptoms

Unstable phase
Not controlled but not requiring/desiring hospitalization

Downward phase
Progressive decline

Dying phase
Immediate weeks/days/hours before death

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5
Q

what are the key points of chronic illness trajectory framework?

A

Majority of health problems in late life are chronic
Chronic illnesses
Acute phase of illness management
Other phases of management
Maintaining stable phases is central in managing chronic illness
Primary care nurse is the coordinator of multiple resources needed to promote quality of life along the trajector

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6
Q

What is frailty?

A

Incidence increases with age
Normal age-related decreases in reserve capacity are depleted and not able to compensate
Combination of geriatric syndromes

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7
Q

regarding frailty: The formal diagnosis is made in the presence of at least three of the following:

A

Unintentional weight loss
Self-reported exhaustion
Weak grip strength
Slow walking speed
Low activity

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8
Q

What are CV diseases?

A

HTN
HF

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9
Q

what is HTN?

A

HTN is a complex disease with a core defect of vascular dysfunction that leads to target organ damage.

HTN is the MOST COMMON chronic condition in people > 65 yo.

In short: 60 yrs or older
BP is OK if LESS THAN 150 SBP OR 90 DBP

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10
Q

what are the HTN interventions?

A

Weight reduction (5-20 mmHg reduction)
DASH diet (8-14 mmHg reduction)
Lower sodium intake (2-8 mmHg reduction)
Increase physical activity (4-9 mmHg reduction)
EtOH in moderation (2-4 mmHg reduction)

LOSE WEIGHT!

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11
Q

what is HF?

A

Most common cause for hospitalization, re-hospitalization, and disability for those over 65 yo
Heart cannot keep up with workload of the heart
Results in insufficient oxygen delivery to body

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12
Q

what is the HF etiology?

A

Results from damage from hypertension and CHD
Ventricles ENLARGE and DILATE  Results in weaker muscle

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13
Q

what is HF also related to?

A

(weakens the heart muscles)
EtOH abuse
Drug abuse
Chronic hyperthyroidism
Valvular disease
Some chemotherapy medications
Radiation therapy near heart (breast cancer, for example)

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14
Q

What happens with LHF?

A

pump failure to body
SBP –> decreased contractility can’t squeeze
DBP –> decreased filling can’t relax
think DYSPNEA

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15
Q

What happens with RHF?

A

pump failure to lungs
results from left side failure
think EDEMA – but also ascites

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16
Q

what happens with congestive HF? (acute decompensated)

A

swelling, edema, fluid in lungs (pulmonary edema)
must remove fluid

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17
Q

what are the CV interventions?

A

Complete assessment of all risk factors and existing disease
lifestyle changes
Medication regimen tailored to specific disease process and patient needs
Focus on symptom management and prevention of exacerbations of disease

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18
Q

What are the CV drugs?

A

ACE (captopril, etc.)
ARB (losartan, etc.)
Diuretics (loop and K+ diuretics, thiazide)
B-Blocker (-lol, etc.)

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19
Q

What is the action for ACE’s and ARB’s?

A

vasodilation –> reduces the cardiac preload and post load improving

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20
Q

What is the action of diuretics?

A

reduce fluid retention

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21
Q

what is the action of B-Blockers?

A

improve contractility of heart muscles

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22
Q

What is neuro-Parkinson’s disease?

A

Progressive disease – over 10-20 yrs
Think DOPAMINE – Dopamine is lost or inhibited
Dopamine regulates nerve impulses for MOTOR function
More common (slightly) in men than women
Onset approximately 60 years
Considered a terminal diagnosis

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23
Q

What is the classic TRIAD for PD? (motor dysfunction)

A
  1. cogwheel rigidity
  2. bradykinesia/dyskinesia –> ALL skeletal muscles are affected
  3. resting/non-intention tremors
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24
Q

what is associated with cogwheel rigidity?

A

Cogwheel Rigidity
Small jerking movements when affected muscles stretched
Muscle rigidity

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25
Q

what is associated with Bradykinesia/Dyskinesia?

A

Bradykinesia/Dyskinesia  ALL skeletal muscles are affected
Difficulty starting, continuing, and or coordinating movements
Shuffling
May become frozen (Akinesia)  absence of movement
Lip, jaw, tongue, etc. when asleep  you won’t see these

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26
Q

what is associated with resting/non-intention tremors?

A

Fine, rhythmic, purposeless tremors
Disappear with sleep and purposeful movements
Pills rolling, small handwriting, low monotone voice

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27
Q

what are the PD clinical signs for autonomic dysfunction?

A

Seborrhea (seb-o-REE-ik) dermatitis
Hyperhydrosis of face and neck
Heat intolerance
Postural hypotension
Constipation

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28
Q

what are the PD clinical signs for cog and psychologic dysfunction?

A

Dementia  dopamine not produced
Memory loss, lack of problem solving, decreased intellect
Anxiety  don’t understand what is going on
Depression
Sleep/wake reversal
Visual disturbances
Psychosis

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29
Q

what are some PD clinical signs?

A

Postural abnormalities (stooped posture)
Altered gait (slow start, short steps, “shuffle”)

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30
Q

What are the PD complications in late stages?

A

Complications in late stages can be fatal
Pressure ulcers
Pneumonia
Aspiration
Falls

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31
Q

what are the PD complications in PD crisis?

A

Parkinsonian Crisis – Major complication
Precipitated by emotional stress or sudden withdrawal of meds

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32
Q

What are the PD complications CMs?

A

Severe exacerbation of tremors, rigidity, and bradykinesia
Anxiety
Sweating
Tachycardia
Hyperpnea

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33
Q

what are the treatments and interventions for PD complications?

A

Treatment and interventions
Respiratory/cardiac support prn
Non-stimulating environment
Psychological supports
Restarting medications

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34
Q

what are the PD interventions?

A

Early assessment and symptom management

Surgical procedures
Ablation
Deep brain stimulation
Stem Cell transplantation (experimental phase)

Drug therapy focuses on mimicking or slowing dopamine breakdown

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35
Q

what is the PD nursing care: teach exercises?

A

lift toes when walking
widen legs while walking
small steps while looking forward
tight corner manipulation
swing arms with walking to improve balance and ROM
cary bag to counterbalance is necessary
facial exercises
read aloud
speak loudly with purpose and concentrated articulation –> watching your movement

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36
Q

what are the PD nursing interventions?

A

preservation of functional ability and quality of life
increase independence and ADLs
prevent complications and excess disability
coping mechanisms
increased socialization
support groups for pt and fam
physical therapy and balance training
increase strength and ROM
occupational therapy with adaptive equipment

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37
Q

What are the dopamine precursors and glutamine antagonist regarding PD meds?

A

Levodopa (Lardopa), carbidopa-levodopa (Sinemet), amantadine (Symmetrel)

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38
Q

what does Levodopa (Lardopa), carbidopa-levodopa (Sinemet), amantadine (Symmetrel) improve in PD?

A

Improves manifestations of motor dysfunction
Levodopa converted to dopamine in brain Carbidopa prevents conversion of dopamine in peripheral tissues = Synergistic effect
Amantadine increases CNS response to dopamine

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39
Q

what are the SE for Levodopa (Lardopa), carbidopa-levodopa (Sinemet), amantadine (Symmetrel) for PD?

A

N/V/D, arrhythmias, blurred vision, darkening of sweat and urine, dyskinesias, postural hypotension, hallucinations and vivid dreams

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40
Q

who should be avoided with levodopa?

A

Levodopa avoided in those with h/o TIA, angina, melanoma, Narrow Angle glaucoma

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41
Q

what is the client education for levodopa in PD?

A

Weeks to months to take effect
Decrease protein intake
Avoid foods with pyridoxine
Pork, beef, avocado, beans, oatmeal
Antiemetics and PPIs/H2RA prn
Interventions to decrease postural hypotension
Teach to report increases symptoms and cardiac SEs

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42
Q

what are the PD monoamine oxidase B inhibitors (MAOB inhibitors)?

A

Selegiline (Eldepryl), rasagiline (Azilect)

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43
Q

what does Selegiline (Eldepryl), rasagiline (Azilect) do in PD?

A

Inhibits enzymes that inhibit and/or breakdown dopamine
Often used synergistically with Levodopa

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44
Q

what are the SE with selegiline and rasagiline for PD?

A

N/V, dizziness, insomnia, postural hypotension, HTN at high doses

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45
Q

what is contraindicated with selegiline and rasagiline for PD?

A

Contraindicated with Prozac and Demerol

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46
Q

what is the client education for selegiline and rasagiline for PD?

A

Take at same time each day
Report insomnia
Interventions to prevent postural hypotension
Skin exams – risk of melanoma
Avoid foods containing Tyramine

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47
Q

What is the dopamine agonists for PD?

A

Bromocriptine (Parlodel), pramipexole (Mirapex), ropinirole (Requip)

48
Q

what does Bromocriptine (Parlodel), pramipexole (Mirapex), ropinirole (Requip) do for PD?

A

mimic effects of dopamine in brain

49
Q

what is Bromocriptine (Parlodel), pramipexole (Mirapex), ropinirole (Requip) often used synergistically with in PD?

A

levodopa

50
Q

what are the SE of Bromocriptine (Parlodel), pramipexole (Mirapex), ropinirole (Requip) for PD?

A

N/V/D, arrhythmias, blurred vision, darkening of sweat and urine, dyskinesias, postural hypotension, hallucinations and vivid dreams

51
Q

what is the client edu. for Bromocriptine (Parlodel), pramipexole (Mirapex), ropinirole (Requip) in PD?

A

Same teaching as Levodopa:
Weeks to months to take effect
Decrease protein intake
Avoid foods with pyridoxine
Pork, beef, avocado, beans, oatmeal
Antiemetics and PPIs/H2RA prn
Interventions to decrease postural hypotension
Teach to report increases symptoms and cardiac SEs

Don’t stop abruptly
May cause compulsive behavior

52
Q

what is the catechol-o-methyltransferase inhibitors for PD?

A

Tolcapone (Tasmar), entacapone (Comtan)
“The Capones”

53
Q

what does Tolcapone (Tasmar), entacapone (Comtan) inhibit in PD and what is it used synergistically with?

A

Inhibit COMT, which breaks down dopamine
Used synergistically with Levodopa/Sinemet

54
Q

what does Tolcapone (Tasmar), entacapone (Comtan) interact with, what do you need to monitor, and what should not be used with it for PD?

A

Monitor LFTs
Interacts with warfarin, so monitor INR closely
Not to be used with MAOBIs

55
Q

what is the client education for Tolcapone (Tasmar), entacapone (Comtan) in PD?

A

Take with food
No ETOH or sedatives
Interventions to prevent postural hypotension
Don’t stop abruptly
Report muscle control changes, jaundice, dark urine, hallucinations

56
Q

what are the anticholinergics for PD?

A

Benztropine (Cogentin), trihexyphenidyl (Artane)

57
Q

what do Benztropine (Cogentin), trihexyphenidyl (Artane) do in PD?

A

Block the excitatory action of acetylcholine
May be used synergistically with Levodopa/Sinemet
Used early in disease or when Levodopa not tolerated
Help prevent PD symptoms of drooling, tremors, rigidity

58
Q

what should benztropine for PD not be used with?

A

Not used with any other meds with anticholinergic effects (antihistamines, TCAs, etc.)

59
Q

what are the S/S for anticholinergics for PD?

A

Assess for glaucoma S/S and photophobia

dry mouth
blurry vision
constipation
drowsiness
sedation
hallucinations
memory problems
trouble urinating
confusion
delirium
decreased sweating
decreased saliva

Long-term useTrusted Source of anticholinergics, as well as use of these drugs in older peopleTrusted Source, has been linked with an increased risk of dementia. If you’ve been prescribed one of these drugs and have concerns about this risk, be sure to talk to your doctor.

60
Q

what is the client education for anticholinergics for PD?

A

Avoid activity which promotes fluid loss
Don’t stop abruptly

61
Q

What is GERD?

A

Gastroesophageal reflux disease (GERD)

Goal of therapy is to prevent exacerbation of symptoms
Lifestyle and diet changes
Medication management – PPI’s
Most serious complication – Aspiration Pneumonia

62
Q

what are the symp found in elders with GERD?

A

Persistent cough, Asthma exacerbations, Laryngitis, Intermittent chest pain

63
Q

What is non-modifiable with OP?

A

female gender
northern european ancestry
advanced age
fam history of OP

64
Q

what is modifiable with OP?

A

Low birth/body weight (underweight)

Low calcium intake

Estrogen deficiency

Low testosterone

Inadequate exercise or activity

Use of steroids or anticonvulsants
Excess coffee or alcohol intake

Current cigarette smoking

65
Q

what is associated with OP stature?

A

For women, fastest overall loss of bone mineral density is 5 to 7 years immediately after menopause

66
Q

what are the OP complications?

A

Most serious health consequence of osteoporosis is morbidity and mortality resulting from falls
20-24% of adults with hip fractures die within one year
One in five will require long term care
Only 15% will be able to walk unassisted six months post fracture
Women with osteoporotic fractures have increased incidence of other major complications
Vertebral fractures often not recognized - Silent
Several new treatment options available – kyphoplasty/vertebroplasty

67
Q

what is the OP diagnosis and treatments?

A

Diagnosis
DEXA scan – dual energy-ray absorptiometry (most common)
Put feet in a “feet massager” looking machine
T-Score:
Osteopenia – diagnosis -1 to -2.5
Osteoporosis – diagnosis if greater than -2.5

USPSTF Currently (but under review):
Recommends screening women 65 and older for OP

68
Q

what are the OP interventions?

A

Weight bearing and resistance training
Adequate calcium and vitamin D intake
Education about fall prevention
Pharmacological therapy to prevent bone loss
Bisphosphonates – Teaching!! Upright for 30 min!

69
Q

what is osteoarthritis (OA)?

A

Normal soft and resilient cartilaginous lining in joint becomes thin and damaged
Joint space narrows and bones of joint rub together, causing joint destruction
Diagnosis is made clinically
Most common symptoms are stiffness with activity and pain with activity relieved by rest

70
Q

what are the most common locations for OA?

A

Neck – cervical spine
Lower back – lumbar spine
Hips
Hands
Fingers
Thumbs
Knees

71
Q

what are the OA deformities?

A

Heberden’s node – DIP – Distal Interphalangeal Joint
Only in OA

Bouchard’s node – PIP – Proximal Interphalangeal Joint
In OA and RA

72
Q

what are the OA interventions?

A

Goals of therapy are to control pain and minimize disability

Non-pharmacological therapy
Weight loss can help – 1 lb of weight places 4 lb of pressure on knees
Exercise - “Motion is the Lotion”
Strength and flexibility – support the joints
Water exercise
Physical therapy
Hot/Cold therapy – patient preference
Adaptive devices
Cane – Relieves hip pressure by 60%
Shoe lift for back pain
Knee brace for stability

73
Q

what are more OA interventions (pharm therapy)?

A

Pharmacological therapy
Acetaminophen – 4 Gram MAX/day
NSAIDs - COX2 (selective NSAID)
Joint injections – Intra-articular
Steroids - Inflammation
Hyaluronic Acid - Lubrication
Acupuncture
Surgical intervention – Knee/Hip  make sure
the surgeon is using visualization
Arthroscopy
Total Joint Replacement  take everything out

74
Q

what is rheumatoid arthritis (RA)?

A

Chronic, progressive, systemic inflammatory autoimmune disease
Primarily synovial joints
Inflammation destroys surrounding cartilage & eventually bone
Systemic
can affect any organ system i.e. vasculitis, anemia, splenomegaly, pulmonary nodules, pericarditis

75
Q

what is the RA focus of research?

A

Focus of research includes
Genetic factors
Environmental triggers in genetically vulnerable population
Hormonal triggers

76
Q

what are the RA interventions?

A

Complete physical and laboratory assessment
Pharmacological therapy
Pain management
DMARDs (disease-modifying anti-rheumatic drugs) - methotrexate
Biological response modifier - “-mab”
Exercise and physical therapy
Environmental modifications
Assistive devices

77
Q

Osteoarthritis vs. RA?

A

OA:
older adults
may be unilateral (knew, hip, spine, hand
DIP AND PIP
usually NO MCP
shorter period of morning stiffness
pain with activity

RA:
women> men
symmetrical – hands and feet common
MCP and PIP
usually NO DIP
prolonged morning stiffness > 30 M
pain > with inactivity

78
Q

What is DMT1?

A

Disorder of glucose metabolism

Type I
Absolute deficiency of insulin production due to autoimmune destruction of pancreatic β cells

79
Q

what is DMT2?

A

Disorder of glucose metabolism

Type II
Combination of relative insulin deficiency and insulin resistance
Genetics, lifestyle, and aging influence development of diabetes

80
Q

what are the DM - Presentation in Older Adults?

A

dehydration
confusion, delirium
decrease visual acuity
incontinence
weight loss and anorexia (polyphagia in younger)
fatigue, nausea
delayed wound healing
parenthesis

81
Q

DM increased risk for…

A

Amputation
Peripheral neuropathy with loss of sensation
Evidence of increased pressure (redness, bony deformity)
Peripheral vascular disease (diminished or absent pedal pulses)
History of ulcers
History of amputation
Severe nail pathology

82
Q

what are the DM interventions?

A

Screening and early identification of diabetes
Prevent complications
Assessment of end organ status
Medication management
Oral agents
Insulin therapy
Assessment of self-care ability
Nutrition
Exercise
Close monitoring of residents in long-term care environment

83
Q

What are the thyroid hormones?

A

Thyrocalcitonin (calcitonin)
Tetraiodothyronine or Thyroxine (T4)
Triiodothyronine (T3)
Thyroid Stimulating Hormone (TSH)
Thyrotropin Releasing hormone (TRH)

T3 and T4 are call the “thyroid hormones”. Abnormalities of these lead to hyper and hypothyroidism

84
Q

What is associated with calcitonin?

A

Decreases calcium loss from bone
Balances Parathyroid hormone (PTH)

85
Q

what is associated with T4?

A

Produced by follicular cells if thyroid gland
T4 converted to T3 in peripheral tissues

86
Q

what is associated with T3?

A

4-5 times stronger than T4 - more potent

87
Q

what is associated with TSH?

A

Produced by pituitary gland

88
Q

what is associated with TRH?

A

Produced by hypothalmus

89
Q

what are the diagnostic studies for thyroid function?

A

Thyrotropin-releasing hormone stimulation test (TRH)
Radioactive Iodine uptake (RAI)
Thyroid scan

T3 and T4 lab values

Hormones, steroids, ASA, foods containing iodine should be avoided for 7 days before testing.

90
Q

what does the diagnostic study for TRH look like?

A

TRH injected and TSH measured to assess thyroid function

91
Q

what does the diagnostic study for RAI look like?

A

Direct test of thyroid function
Radioactive iodine absorbed by thyroid and thyroid can be visualized assessing for nodules

92
Q

what is done in a thyroid scan?

A

Similar to RAI, but iodine not used. Radioactive isotopes given orally and taken up by thyroid and visualized on scan

93
Q

what is hyperthyroidism?

A

Most severe form thyrotoxicosis
Causes
Autoimmune disorder (Grave’s disease) *most common
Multinodular goiter (Toxic goiter)
Women affected more
often, 5-7:1

94
Q

what is hyperthyroidism in elders?

A

Graves disease most common form in older adults
Also caused by toxic goiter, iodine ingestion or iodine-containing foods, contrast agents, & medications
Onset often abrupt
Thyroxine increases myocardial oxygen consumption
Increases risk for Afib and angina in person with CHD
Can cause heart failure
Most common complication – AFIB – 27% of older adults with hyperthyroidism

95
Q

what hyperthyroid symp are not seen in elders?

A

Many symptoms non-specific in older adults
Unexplained Afib
Heart failure
Constipation
Anorexia
Muscle weakness

96
Q

what hyperthyroid symp are seen in elders?

A

older adults often present w:
tachycardia
tremors
weight loss
apathetic thyrotoxicosis – slowed movement and depressed effect

97
Q

what are the hyperthyroidism meds?

A

Anti-thyroid agents – blocks thyroid hormone production
Iodides – inhibit thyroid hormone secretion
Beta Blockers – manage tachycardia, anxiety, & tremors
Radioactive Iodine (RAI) – shrinks thyroid gland

98
Q

what is associated with the anti thyroid agent?

A

Methimazole (Tapazole), Propylthiouracil (PTU)

99
Q

what is associated with iodides?

A

Saturated solution of potassium iodide (SSKI)

100
Q

what is associated with RAIs?

A

Most common for Graves disease
Can be used alone or prior to surgery
Absorbed by thyroid and radiation destroys tissue
Teach radiation precautions

101
Q

what is a thyroidectomy?

A

Surgical removal of part or all of thyroid
Reserved for severe case or large goiters
Review Pre-op & Post-op care

102
Q

what is a thyrotoxicosis?

A

Life-threatening
Exaggeration of hypertyroid symptoms
Treatment: Cool with ice, ↓ levels of TH, replace fluids & electrolytes, give O2, stabilize cardiac function. Avoid ASA (increases TH)

103
Q

what is hypothyroidism?

A

Women affected more often 5:1
Ages 30-60
Slow onset
Causes: Primary & Secondary
S/S: Think SLOW Metabolic

104
Q

what is hypothyroidism in elders?

A

Most frequent cause chronic autoimmune thyroiditis
Also radioiodine treatment, surgery, medications (Amiodarone), pituitary/hypothalamic abnormality

105
Q

what are the vague S/S for hypothyroidism?

A

Vague S/S – often subtle
Slowed mentation
Gait disturbances
Fatigue
Weakness
Heat intolerance

106
Q

what are the treatment and diagnosis for hypothyroidism?

A

Diagnosis
TSH, T3, T4, FT4
PE and hx; Cardiac studies to assess for complications

Treatment
Thyroid replacement therapy
Review: Levothyroxine (Synthroid)

107
Q

what is the nursing care for hypothyroidism?

A

Prevent: chilling, constipation, skin breakdown, infection
Assess: cardiac complications, edema, tachycardia, skin
Lifelong levothyroxine therapy
Warning: levothyroxine can cause digoxin toxicity

108
Q

Hypothyroidism- Myxedema Coma?

A

Rare & Life-threatening complication with HIGH mortality rate

109
Q

Hypothyroidism- Myxedema Coma causes?

A

Untreated or uncontrolled hypothyroidism
External stressors including surgery, trauma, infection, excessive exposure to cold temps

110
Q

Hypothyroidism- Myxedema Coma cms?

A

Hypothermia, Mental function ranges from depression to unconscious, Respiratory depression (hypoventilation), Hypotension, Bradycardia

111
Q

Hypothyroidism- Myxedema Coma treatment?

A

Supportive measures and stabilization of vitals
Treat underlying cause
Thyroid hormone replacement – must be slow r/t toxicity with rapid replacement

112
Q

what is prostate cancer (PC)?

A

Most common non-skin cancer in men
1 in 5 (black) & 1 in 6 (white) chance of developing
Usually detected by screening

113
Q

what are the cms of PC?

A

General urinary complaints, retention, hematuria, back pain
Cachexia, bone tenderness, lower lymphedema, adenopathy

114
Q

what are the screening for PC?

A

Screening when asymptomatic should be individualized based on personal and family history
Uncertainties, Risks, Benefits

Screening methods
Digital Rectal Exam
Prostate-Specific Antigen (PSA)

American Cancer Society
50 y/o for men at average risk who have at least a 10-year life expectancy
40 or 45 y/o for African Americans and men who have had a first-degree relative diagnosed with prostate cancer before age 65
40 y/o for men with several first-degree relatives who had prostate cancer at an early age

USPSTF
Men aged 55 to 69 years
Recommends against PSA screening in men aged 70 and older

115
Q

What are the PC diagnosis?

A

PSA
No PSA level guarantees the absence of prostate cancer.
The risk of disease increases as the PSA level increases, from about 8% with PSA levels of ≤1.0 ng/mLto about 25% with PSA levels of 4-10 ng/mL and over 50% for levels over 10 ng/mL

Digital Rectal Exam (DRE)
Examiner-dependent; serial examinations over time are best
Most patients diagnosed with prostate cancer have normal DRE results but abnormal PSA readings

Biopsy
Biopsy establishes the diagnosis
False-negative results often occur, so multiple biopsies may be needed before prostate cancer is detected

116
Q

what is the PC care?

A

Active surveillance
Watchful waiting
Radical prostatectomy (surgical removal)  will go home with a foley (teach foley care)
Radiation therapy
Hormone therapy  don’t normally have to replace male hormones

Gerontological Nursing (26 decks)

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