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Nursing > Adult Health Exam 4 (musculoskeletal & male reproductive disorders) > Flashcards

Adult Health Exam 4 (musculoskeletal & male reproductive disorders) Flashcards

1
Q

how many bones in body

A

206

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2
Q

what are osteoblasts vs osteoclasts?

A 
blast = builders
clast = remodelers
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3
Q

osteocytes

A

mature bone

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4
Q

what are the 5 diff types of bones

A

Long bones, short bones, flat bones, irregular bones, sesamoid bones

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5
Q

what is compact bone vs spongy bone

A

Compact bone (cortical): dense and looks smooth

Spongy bone (cancellous): small lattice-like pieces called trabeculae

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6
Q

what are the 2 types of marrow and what do they contain

A

Red marrow consists mainly of hematopoietic tissue

Yellow marrow consists mostly of fat cells

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7
Q

how does estrogen affect bones?

A

Estrogen–induces chemical in osteoclasts that causes self destruction

Impact of menopause–decreases bone

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8
Q

How do calcitonin and TFH affect bone growth

A

Calcitonin & TSH = inhibit osteoclastic activity, stops remodeling process

-anterior pituitary promotes bone growth

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9
Q

how does parathyroid hormone affect bone growth

A

Parathyroid hormone = promotes activity for osteoblastic activity

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10
Q

how does GH affect bone growth

A

Growth hormone = facilitate bone growth until adult bone is reached

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11
Q

muscle strength is measured on what scale

A

0-5

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12
Q

what are lab studies associated with bone probs

A
  • Calcium (norm: 8.8-10.3 mg/dL)
  • Phosphorus (3-4.5 mg/dL) is inversely proportionate to Ca
  • Vitamin D
  • Calcitonin + Parathyroid
  • Estrogen stimulates osteoblasts
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13
Q

what are imaging studies for bone issues?

A

XR, CT, MRI, arthrogram, DEXA (bone mineral density scan), bone scan, EMG, arthroscopic exam arthroscopy, arthrocentesis

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14
Q

What is a DEXA scan?

A
  • Considered the “Gold Standard” for osteopenia/osteoporosis diagnosis
  • No prep required
  • Obtain height/weight
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15
Q

what happens to MSKL system with age

A
  • Bone remodeling…
  • Decrease in muscle fxn, mass & strength (sarcopenia)
  • Decrease in motor neurons
  • Decrease in joint/ligament/tendon flexibility and increase in stiffness
  • Kyphotic posture
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16
Q

What are the ACCESS risk factors for osteoporosis

A 
A: alcohol 
C: corticosteroids
C: low calcium 
E: estrogen low
S: smoking 
S: sedentary lifestyle
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17
Q

what is pathophys for osteoporosis and s/sx

A

Bone resorption activity is greater than bone rebuilding activity
Osteoclasts > osteoblasts

s/sx
“Silent” disease…
Dowager’s hump
Pathologic fracture

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18
Q

how to diagnose osteoporosis?

A
  • Bone density tests: DEXA Scans
  • –Osteopenia vs osteoporosis
  • Quantitative computed tomography

prevention is key

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19
Q

what are nutritional changes for osteoporosis?

A
  • -Calcium + vitamin D supplements (1st line PREVENTION!)
  • -Recommended Calcium dosing for adults > 51: 1200mg/day
  • -Recommended Vitamin D dosing: 800-1000iu
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20
Q

what meds for osteoporosis

A

Ca, vitD biphosphonates (fosamax), calcitonin, estrogen agonist/antagonist, parathyroid, dual acting bone agent, monoclonal

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21
Q

Calcium & vitamin D for osteoporosis

A

Ca dosing for adults >51 = 1200mg/day
Recommended Vitamin D dosing = 800-100 iu
Administration considerations = need together

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22
Q

Bisphosphonates for osteoporosis

A

Oral (Fosamax; risedronate; ibandronate)

  • -Fosamax = take on empty stomach w full glass of water, sit up for 30 min afterwards, SE is destruction of jaw bone
  • or monthly IV
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23
Q

Calcitonin for osteoporosis

A

made by thyroid, inhibits osteoclasts, can give as SQ injection, take vit d supp too

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24
Q

Estrogen agonist/antagonist for osteoporosis (evista)

A

preventative & treats osteoporosis, SE are risk for DVT

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25
Q

Parathyroid hormone for osteoporosis

A

protective factor against hormone regulated bone loss, SQ inj

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26
Q

Dual-acting bone agent for osteoporosis

A

decrease osteoclast, incr osteoblast activity, balance bone turnover

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27
Q

Monoclonal (denosumab/Prolia), Evenity for osteoporosis

A

inhibit osteoclastic activity, reducing bone reabsorption, last option med, SQ injection 2x/year, SE decrease serum calcium (do not give if low)

Evenity = new dual action monoclonal antibody, inhibits osteoclasts and increases osteoblast activity for severe osteoporosis —do not use if hx of MI/stroke

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28
Q

patient education for osteoporosis

A 
Take medication as prescribed
Weight reduction
Adequate Calcium and vitamin D supplementation 
Exercise
Avoid: alcohol, smoking
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29
Q

osteoarthritis

A

Progressive disease of articular cartilage (diarthrodial joints with synovial membrane)

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30
Q

risk factors for osteoarthritis

A

Risk factors =

Age
Female
Obesity (weight loss of 10% increases function of joint by 30%)
Occupation, manual labor
Poor diet = cartilage deteriorates from enzymes or nutrition

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31
Q

Articular Cartilage and involvement in osteoarthritis

A

-Chondrocytes make white smooth cartilage→ yellow & opaque with rough edges & softens. As it thins bones get closer

–causes central loss of cartilage, subchondral bone becomes more dense, osteophytes (bone spurs, classic sign*) develop

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32
Q

s/sx of osteoarthritis

A
  • Localized joint s/sx = pain, swelling
  • Asymmetrical
  • Pain in AM, with weather changes, activity
  • Eventually, pain all the time
  • Loss of ROM (knee lock), cracking
  • Bouchard’s nodules = at proximal, RED
  • Heberden’s nodes = at distal osteophytes
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33
Q

what are bouchards nodules

A

proximal, red, osteoarthritis

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34
Q

what are heberdens nodes

A

at distal osteophytes, osteoarthritis

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35
Q

what is ESR for osteoarthritis indicative of

A

ESR (erythrocyte sedimentation rate) will be normal/elevated = indicates inflammation

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36
Q

what does increased CRP in osteoarthritis mean?

A

Increased CRP high sensitivity = indicates blood vessel injury, predictive test

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37
Q

what does osteoarthritis synovial fluid look like?

A

turbid, cloudy

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38
Q

how to determine RA vs osteoarthritis

A

Draw lab for rheumatoid factor to determine, negative = osteoarthritis; positive = RA

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39
Q

what is management for OA

A
  • Conservative: phys therapy, NSAIDs, corticosteroid injections
  • Prevent OA through exercise, weight bearing and wt loss
  • GOAL = decrease pain, maintain mobility
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40
Q

what meds for OA

A
  • -Tylenol, 4g/day max = Can also impact BG levels and cause fake low
  • -NSAIDS = Considerations = careful with older, liver/renal insufficiency, higher risk for GI bleed (dark, tarry stools),
  • -COX-2 inhibitors
  • -Corticosteroid injections
  • -Opioids–sparingly
  • -Lidocaine patches
  • -Glucosamine
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41
Q

what are different surgeries for OA

A
  • -Debridement
  • -Arthroplasty = resurface joint
  • -Osteotomy = correct deformity by cutting bone, alter joint stress
  • -Arthrodesis = fusion of joint
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42
Q

Sequence of progression of OA 6 steps

A

1 - Incongruity in joint surfaces leads to reduction in motion
2 - Osteophytes (bone spurs) form at joint margins
3 - Cartilage becomes softer and less elastic
4 - Erosion of articular surfaces
5 - Joint cartilage becomes yellow and granular
6 - Joint space narrows

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43
Q

joint replacement dx criteria

A

Dx = based on deformity, tissue destruction, loss of function

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44
Q

what are complications of hip, knee surgeries?

A

DVT, PE, Wound site infection, wound site infection, joint dislocation

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45
Q

pain meds pre/post arthroplasty

A

Pre op = nausea, stool softeners

Post op = pain meds, beta blockers, normal meds, antithrombotics

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46
Q

what are the 6 Ps for assessing for distal limb function/clot

A

polar, pallor, pain, pulselessness, paralysis, paresthesias

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47
Q

What is pagets disease

A

bone disease

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48
Q

risk factors for pagets disease

A

Risk factors =

Genetics
measles as child 
Male 
Older than 50
Caucasian, european descent (dutch, british)
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49
Q

pathophys of pagets

A

accelerated bone remodeling

  • Osteoblasts enlarged
  • Osteoclasts overactive
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50
Q

where are the deformities of pagets usually

A

commonly skull, femur, tibia, pelvic bones, vertebrae

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51
Q

what does a radiographic exam for pagets look for

A

can for hot spots (weak spots)

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52
Q

what enzyme is elevated with pagets

A

Elevated ALP = enzyme made by bone cells, especially w overproducing bone cells

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53
Q

what meds for pagets

A 
NSAIDs
COX2
calcitonin
bisphosphonates
denosumab
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54
Q

what does calcitonin do for pagets

A 
Calcitonin = first line, decreases osteoclast activity, helps with collagen breakdown
SE = flushing :/
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55
Q

what are biphosphonates for pagets for

A

Bisphosphonates = helps with bone pain, decrease osteoclast activity

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56
Q

what does denosumab do for pagets

A

Denosumab = Monoclonal–inhibit osteoclastic activity, reducing bone reabsorption, last option med, SQ injection 2x/year, SE decrease serum calcium (do not give if low)

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57
Q

what are 2 surgical tx for pagets

A

Joint replacement

Spinal decompression

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58
Q

what is prognathism with pagets

A

Skeletal changes (deformities) → enlargement of mandible joint (prognathism)

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59
Q

what other body issues come with pagets

A

hearing loss, fractures, bone deformities

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60
Q

what is rheumatoid arthritis

A
  • -Chronic systemic autoimmune disease of joints, has remissions and exacerbations
  • -RA characterized by synovitis and joint deformity
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61
Q

risk factors for RA

A
  • Female
  • Smoking leads to autoimmunity
  • bacterial/viral infection that leads to autoimmunity
62
Q

what is the cause of RA

A

–Presence of antigens to T cells triggers immune response → cytokine release + attack cartilage→ synovial fluid damaged → ↑ synovial fluid→ impaired movement + pain!

–Autoimmunity happens = RA has autoantibodies (RF)

63
Q

what are the 4 stages of RA

A
  1. Inflammation = synovitis after enzyme activation
  2. Pannus formation = granulation tissue (MOST DESTRUCTIVE ELEMENT OF RA)
  3. Fibrous ankylosis = tough fibrous
  4. Bony ankylosis = calcification of fibrous connective tissue causes bones to be fused and immobilized. Fixation of joint
64
Q

what are the s/sx of RA

A
  • -Stiff in AM, inflamed joints, spongy deformed joints bilaterally (ulnar deviation, swan neck, boutonniere deformities, toe bunions)
  • -Systemic itis = synovitis, episcleritis, scleritis, pleuritis (lung pleura), pericarditis
  • -Rheumatoid nodules = extra articular, subQ, non tender nodes, can be in lung or eye
  • -Sjorgren syndrome
65
Q

what is sjorgren syndrome

A

Sjogren’s syndrome = dry eyes keratoconjunctivitis sicca, dry mouth xerostoma, dry vagina

66
Q

what are lab tests to dx RA

A
  • -CBC–will see anemia typically
  • -ESR (acute/chronic) and CRP increased–used to monitor response to tx
  • -+ RA factor = supports dx of RA
  • -ANA = antinuclear antibody = measures antibodies that destroy tissue (greater titer = more inflammatory)
  • -Anti CCP (cyclic citrullinated peptides)
  • -Synovial fluid analysis & tissue biopsy = Synovial fluid is turbid in RA
67
Q

what is the priority time frame to treat RA. what is the goal?

A

first 2 years

GOAL of tx = control inflammation, decrease pain/stiffness

68
Q

what are meds for RA

A
  • -NSAIDS
  • -Glucocorticoids (prednisone) = immunosuppressant
  • -DMARDS
69
Q

what are side effects of predinsone and steroids for RA?

A
  • -Prednisone SE = mood changes, edema/retain Na which retains water, HTN, high BG, increased appetite, more susceptible to infection, moon face
  • -Oral steroids can stunt growth if taken early
70
Q

what are DMARDs for RA

A

antiRA drugs = alter immune system to slow disease process

–methotrexate, plaquenil

71
Q

what are SEs of DMARDs for RA

A

–Methotrexate = first line (SE = teratogen, oral sores (take daily folic acid), hepatotox, renal insufficiency, N/V, loss of appetite
–Plaquenil = antimalarial
SE = decrease UV light absorption, eye damage

72
Q

what are other treatments for RA

A

-Paraffin baths to ease joint pain
-heat/cold alt q15 min (warm moist best)
-ROM/ADL assistance
balance/rest/work = resist naps, causes stiffness
-Nutrition = avoid processed foods that are inflammatory, eat fresh foods
-Surgery = joint replacement, fusion, synovectomy

73
Q

what is scleroderma

A

Definition = autoimmune, t cells attack and body overproduces collagen

also called crest syndrome

74
Q

what are the 2 types of scleroderma

A 
Limited = legs, arms, face (slower process) 
Diffuse = body (fast)
75
Q

what are s/sx of scleroderma

A
  • -Waxy skin, tightening of tissues
  • -Blood vessels tighten up → increased BP
  • -Lung tissue sclerosis → poor gas exchange
  • -Organs tighten → dysphagia, renal probs, infection risk
  • -Calcium deposits on skin
  • -Raynaud’s phenomenon = spasming of small vessels
  • -Esophageal dysfunction
  • -Sclerodactylyl = thick/tightening of skin on hands/fingers
  • -Telangiectasia = dilation of capillaries causing red marks on surface of skin
76
Q

what are drugs for managing scleroderma

A
  • Calcium channel blockers for raynauds

- DMARD meds

77
Q

patient education for scleroderma

A

Protect from temp changes, avoid stressors, understand meds

78
Q

what is systemic lupus erythematosus

A

–Chronic, multisystem, autoimmune, progressive, inflammatory disorder

–affects Skin, kidneys, hematologic, CNS

79
Q

what are the 2 types of SLE

A
  • -Discoid: skin only

- -Systemic = Involves all connective tissues, Remissions and exacerbations

80
Q

Precipitating factors/triggers for SLE

A

UV light exposure
Infection
Stress

81
Q

what are risk factors for SLE

A
  • -Genetics, race (3x ↑ in Afr. Am & Nat. Am.), gender (Women 10x > men; age 20 to 40)
  • -Hormones: Worse at menarche and postpartum–estrogen enhances activity of SLE
82
Q

what is the pathophys for SLE

A

Autoantibodies complexes are produced → trigger inflammation
Immune complexes cause vasculitis → thicken intimal lining → thrombus formation → deprive organs of arterial blood and oxygen

83
Q

s/sx for SLE

A

general fatigue, weight loss, butterfly rash, alopecia, photosensitivity, polyarthralgia of hip/shoulder, pericarditis and pleuritits, nephritis, seizure activity, psychosis

84
Q

damage to what organ from SLE is the number 1 cause of death of SLE

A

kidney failure

check creatinine, GFR

85
Q

what are labs for dx of SLE

A
  • -CBC: all cells are ↓= pancytopenia (especially thrombocytopenia and leukopenia)
  • -↑ ESR + CRP (again, inflammation…)
  • -ANAs against own DNA ** (most sp SLE marker)
  • -Anti-Smith antigen is most unique to SLE
  • -Low serum complement (C3, C4) = Depleted from inflammatory response
  • -Skin biopsy = shows lupus cells and inflammatory cells
86
Q

what are meds for SLE

A
  • -Corticosteroids
  • -NSAIDs
  • -immunosuppressive therapy (Cyclophosphamide (Cytoxan) and Azathioprine (Imuran) (SE= drop in CBC)
87
Q

long term management for SLE

A
  • Chronic issues = infertility from steroids, risk of immunity towards fetus and spontaneous abortion
  • Pregnancy + oral contraception
  • Prevent exacerbations/fatigue → life balance!
  • Be Sun smart: SLIP → SLOP → SLAP
  • UTD on vaccines
  • Dietary: anti-inflammatory diet
  • Assess end-organ function = Dialysis or possible need for kidney transplant
88
Q

what is Gouty arthritis

A

Arthritis of one joint by hyperuricemia = Presence of urate crystals = positive

89
Q

pathophys of gout leading to tophi

A

Abnormal purine metabolism → ↑uric acid → urate crystals → tophi develop

90
Q

what are the risk factors for gouty arthritis

A

Male only, 40-60–90% reoccur in 5 years, increases with incr BMI and age

91
Q

what are 2 types of gout

A
  • -Primary = hereditary error in metabolism of purine

- -Secondary = caused by ETOH, chemo

92
Q

what 2 things for dx of gout

A
  • -Synovial fluid aspiration shoes presence of urate crystals
  • -Uric acid in urine sample
93
Q

what are the 3 phases of gout

A
  1. Acute: Painful joint inflammation, red, tender, swelling of great toe joint (podagra)
  2. Intercritical: between attacks
  3. Chronic: pruritus, “Tophi” develop, renal calculi
94
Q

what are meds for gout

A
  • -NSAIDs
  • -glucocorticoids (acute)
  • -colchicine (for inflammation) = SE (diarrhea, n/v abd pain, take early with flares
  • -antihyperuricemics (allopurinol) = reduce urice acid levels
95
Q

what is antihyperuricemics for gout

A

Allopurinol = reduce uric acid levels

  • -SE = upset stomach
    • take 2L of water per day
    • Encourage citrus foods
96
Q

what are other managements for gout

A
  • -Wt. loss, no ETOH or purine foods, push fluids (3-4 L/day)
  • -Avoid beer, ale, wine—distilled liquor ok!
  • -Avoid soy
  • -Meds to avoid: aspirin (can increase uric acid), diuretics (can trigger attacks
  • -Support inflamed joints, bedrest, ICE
97
Q

fibromyalgia

A

Widespread PAIN triggered by a STRESSOR!

98
Q

manifestations of fibromyalgia

A
  • -Blood vessels don’t constrict leading to low BP and HR

- -Body can’t suppress cortisol → oversensitive/overreact to PAIN signals

99
Q

what may cause fibromyalgia

A

Trauma or autoimmune process

100
Q

who is affected by fibromyalgia

A

women more than men

101
Q

what med for fibromyalgia

A

pregabalin

102
Q

What are 4 symptoms of issues with the male reproductive

A
  • Pain with urination, ejaculation
  • Bleeding
  • Discharge
  • Masses
103
Q

What are 3 things to assess during exam of prostate

A
  • -Assess for inguinal hernia: stand and cough/strain
  • -Exam of rectum and prostate–draw prostate labs before invasive exam
  • -Psych assessment
104
Q

what is benign prostatic hyperplasia (BPH) pathophys

A

Pathophys = gland enlarges and pinches urethra which interferes with urine flow from the bladder

  • -Exact cause unknown, but imbalance of estrogen and testosterone could be
  • -Treatment = DHT inhibitor (slows growth by DHT hormone)
105
Q

what are s/sx of BPH

A

Difficulty urinating, increased residual urine (predisposes to UTI), urine is cloudy

FUN

  • -Frequency
  • -Urgency
  • -Nocturia
106
Q

What does the I-PSS score for BPH asess

A

I-PSS score for degree to which issues are present –emptying, urgency, nocturia, straining etc

107
Q

dx for BPH

A

Digital rectal exam (DRE)

Prostate sp antigen (PSA)

  • -Norm = for men less than 50 = 2.5. Over 4 needs exam
  • -May be elevated for 6 weeks post UTI–can cause false PSA reading
108
Q

2 drugs for BPH

A
  • a blockers

- 5-alpha reductase inhibitors

109
Q

How do alpha blockers

A

ALPHA BLOCKERS:

  • -ACT ON A-1 RECEPTORS
  • -SMOOTH MUSCLE RELAXATION
  • -EX: TAMSULOSIN (FLOMAX); DOXAZOSIN (CARDURA)
110
Q

how do 5 alpha reductase inhibitors work

A

5-ALPHA REDUCTASE INHIBITORS:

  • -STOPS CONVERSION OF TESTOSTERONE TO DHT
  • -EX: FINASTERIDE (PROSCAR)–also used for hairloss
111
Q

what are 3 alternative tx for BPH

A

–Saw Palmetto = USED BY OVER 2 MILLION MEN, Helps improve flow

–African Plum = IMPROVES FLOW, LESSENS NOCTURIA

–RYE GRASS POLLEN = Reduces nocturia

112
Q

what meds to avoid if you have BPH

A
  • Tranquilizers
  • OTC decongestants
  • anticholinergics
113
Q

What are 3 types of BPH surgical management

A

1st = Transurethral resection of the prostate (TURP)

2nd = transurethral incision of the prostate (TIUP or TIP)

3rd Open prostatectomy

Other = laser surgery to burn away hypertrophied tissues

114
Q

what are 3 nursing considerations for after TURP for BPH

A
  1. Subtract amount of irrigating solution for accurate I/O
  2. Older men often get confused and “pick” at catheter—need to distract
  3. Will complain of “urge to go!”
115
Q

what is TURP for BPH

A

3 way catheter tube for 3-5 days post op

–Irrigation, drain bladder, balloon

116
Q

what are other post op considerations for TURP for BPH

A
  • urinary catheter placed into bladder/cbi
  • create traction via lateral taping to patient’s abdomen or thigh to reduce risk for bleeding!
  • uncomfortable urge to void continuously
  • inform the surgeon of any bleeding!
117
Q

assessments/management for post op TURP for nurse

A

–Hemorrhage “light pink ok, ketchup no”
–Risk for DVT
fluid/electrolytes
–Meds to manage (analgesics, antispasmodics, antibiotics, stool softeners)

118
Q

when removing catheter post TURP, what to look for

A

Post catheter removal–assess for urine retention

–Keep eye on frequency, consistency, distension

119
Q

what is a TIUP/TIP for BPH

A

2nd = transurethral incision of the prostate (TIUP or TIP)

–Small to moderately enlarged prostate

120
Q

what is an open prostatectomy for BPH

A

3rd Open prostatectomy

–Large prostate with other complications like bladder damage/stones

121
Q

what is erectile dysfunction and s/sx

A
  • -Unable to achieve/maintain erection
  • -Epidemiology –increases with age
  • -Pathophy–surgery removing prostate
  • -s/sx = inability to do/retain erection
122
Q

what is dx for erectile dysfunction

A

Dx = can draw serum testosterone

123
Q

what is med for erectile dysfunction

A

–PHOSPHODIESTERASE TYPE-5 (PDE-5) INHIBITORS: (VIAGRA, LEVITRA, CIALIS)

124
Q

MOA of phosphodiesterase Type 5 inhibitors (viagra)

A

MOA: INHIBITS CGMP (SUBSTANCE THAT CAUSES SMOOTH MUSCLE RELAXATION)

125
Q

Considerations for viagra (phosphodiesterase

A
  1. Wont work without sexual stimulations
  2. Do not take with nitro or alpha blockers→ hypoT
    - -SE = facial flushing, vision changes, BP drop, headache
    - -erection for longer than 3 hours is bad
126
Q

What is MUSE for erectile dysfunction

A

Medicated urethral system for erection (MUSE)

  • -Pellets in urethral which starts erection
  • -SE = urethral burning, painful erection
127
Q

what is Intervacernosal injection for erectile dysfunction

A
  • -Erection for 30-60 minutes

- -Risk for priapism –emergency

128
Q

what is a vacuum device for erectile dysfunction

A
  • -Pressure suction to cause erection

- -Cumbersome device

129
Q

what is surgical management for erectile dysfunction

A

-surgery to place an implant or penile prosthesis

–inflatable tube placed in penis; inflation bulb in scrotum

130
Q

what is pt ed for erectile dysfunction

A
  • -smoking & obesity increase ed risk
  • -ed meds should not be taken w/nitrates
  • -know med risk factors: hypoT, flushing etc
131
Q

what are risks for prostate cancer

A

Risks = race, family hx, diet, chemicals, headaches, age

132
Q

manifestations of prostate cancer

A

Manifestations = elevated PSA, trouble urinating, UTIs

133
Q

what is management for prostate cancer

A

PSA test for early detection (if PSA over 4 need follow up)
DRE = digital rectal examination
Bx = tissue staged on gleason scale, highest score = 5

134
Q

radiation–what is external beam vs brachytherapy for prostate cancer

A

Radiation

  • -External beam = outside
  • -Brachytherapy = internal (Caution = pt radioactive for period of time (2 weeks))
135
Q

how old is testicular cancer usually found in

A

15-35

136
Q

what cancer is inked to cryptorchidism

A

testicular cancer

137
Q

what are 3 ways testicular cancer spreads

A
  1. spread thru testis wall into bloodstream
  2. spread thru lymph nodes
  3. transported thru bloodstream to other organs
138
Q

what are manifestations of testicular cancer

A

Manifestations = painless mass, swelling, hardness

139
Q

how often to do testicular exam

A

once a month

140
Q

what is diagnosis for testicular cancer

A
  • -Physical assessment
  • -Ultrasonography
  • -Lab tests: Alpha-Fetoprotein (AFP); Beta human chorionic gonadotropin (hcg)
  • -Surgery for seminomas followed by radiation and/or chemotherapy
141
Q

what testicular cancer tumors are not responsive to radiation

A

Nonseminomas grow quickly and are not responsive to radiation

142
Q

what is patient ed for testicular cancer

A
  • -INFECTION
  • -CHEMO S/E
  • -NERVE DAMAGE FROM LYMPH NODE RESECTION
143
Q

how to preserve male fertility when treatment for testicular cancer is needed

A

sperm preservation/ sperm bank

144
Q

risk factors for male breast cancer

A

Risk factors = old, linked to BRCA 1&2, high alcohol, cryptorchidism, hot environments, working around gasoline

145
Q

pathophys male breast cancer

A

UNCONTROLLED GROWTH OF ABNORMAL –> CELLS IN BREAST TISSUE

MOST COMMONLY OCCURRING FORM IS DUCTAL CARCINOMA –> INVASIVE VS NONINVASIVE

146
Q

clinical manifestations of male breast cancer

A

CLINICAL MANIFESTATIONS: swelling/lump in breast tissue, dimpling, redness, discharge, peau du orange

147
Q

what hormone test done for male breast cancer to dx

A

ESTROGEN AND PROGESTERONE RECEPTOR TEST & HER2

148
Q

causes of testicular trauma

A

RESULT FROM SPORTS INJURIES, KICK TO GROIN, MOTOR VEHICLE ACCIDENTS, SELF-MUTILATION, OR FALLS AND INJURY

149
Q

pathophys of testicular trauma

A

Pathophys = TESTICULAR RUPTURE: INTEGRITY OF TUNICA ALBUGINEA IS ALTERED (HEMATOCELE), BLEEDING INTO SCROTAL WALL RESULTS IN A SCROTAL hematoma

150
Q

3 categories of testicular trauma

A
  • -blunt
  • -penetrating
  • -degloving
151
Q

treatment for testicular trauma

A
  • NSAIDs, ice, scrotal sling, bedrest 24-48 hours

- surgery

152
Q

what surgery is needed for degloving

A

skin graft

Nursing (7 decks)

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