Module 10 Sensory/Skin Flashcards

1
Q

Tx: Headaches

A

Test:Always start w/less invasive/strong med

•Aspirin
•Acetaminophen (Tylenol)
•NSAIDS
•Muscle relaxants
•Caffeine containing analgesics
•Antiseizure meds: topiramate (Topamax) (*dont D/C abruptly can cause seizures and kidney stones (drink water!!) . Takes 2-3 months to kick in.)
•Triptans (sumatriptan, Imitrex)
•B-Blockers (if Pt has low BP, don’t give!)
•Botox

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2
Q

Nursing management: Headaches

A

•stress coping strategies
•relaxation, exercise (yoga), socialization
•massages, moist hot packs
•avoid common triggers

Most important = tx pain, coping, avoid triggers by keeping a log to figure out what’s causing the headaches

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3
Q

What are the 5 degenerative disorders in this module?

A

•Multiple Sclerosis (MS)
•Parkinson’s disease
•myasthenia Gravis (MG)
•Amyotrophic lateral sclerosis (ALS)
•Huntington’s disease

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4
Q

MS overview

A

•Disseminated demyelination of nerve fibers (myelin sheaths) of brain & spinal cord

Exact cause is unknown, believed to be genetic, environmental exposure(extreme temps or infection)

Higher in women 30-35 age of onset. Can try to slow it down and manage symptoms & quality of life

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5
Q

Clinical manifestation: MS

A

test 1st symptoms often related to vision (blurred or double vision. Red/green distortion. Possible blindness in one eye)
•gradual: weeks-months
•extreme weakness/paralysis (worst case)
•numbness & tingling
•lhermitte’s sign (shock down extremities)
•other problems: speech impairment, hearing loss, tremors, nystagmus (involuntary eye movements), ataxia (coordination/imbalance)

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6
Q

Clinical signs cont. (MS)

A

•constipation(more common) / diarrhea
•spastic bladder OR flaccid bladder (may have to straight cath themselves)
•sexual problems (psychosocial, anxiety, decreased libido/sensation)
•cognitive issues (forgetful, reading comprehension)
•emotional changes

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7
Q

Dx studies (MS)

A

•No definite test for MS
•H&P play a big role
•MRI/CSF analysis (increased immunoglobulin)

•to be Dx, Pt must have evidence of :
-2 inflammatory demyelimating lesions in at least 2 areas of CNS
-damage or attack occurring at different times
-all other dx ruled out

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8
Q

Drug Therapy (MS) 58.13 1370 know for test

A

no cure, only management of Symptoms. Starting therapy early helps pt’s
•start w/ immunomodular drugs (B-interferons)
•immunosuppressants, monoclonal antibody, corticosteroids, anticholinergics, muscle relaxants, nerve conductor enhancers

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9
Q

Alternate Nursing management (MS)

A

•Surgery
•dorsal column electrical stimulation
•PT: exercise (decreases spasticity, coordination, retrains unaffected muscles to act for impaired ones, WATER EXERCISE* (both sides)

GOALS: maintain ADL’s, muscular functions. Each goal is dependent on Pt’s symptoms/problems

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10
Q

Patient/family teaching (MS)

A

•teach about triggers
•coping w/Walker wheel chair, home safety)
•good balance & exercise & rest, healthy diet.
•minimize caffeine (may be a trigger, if on test it says eliminate it’s wrong**)
•teach meds
•self- catheterization (if needed)

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11
Q

Parkinson’s overview

A

•chronic, progressive neurodegenerative disorder characterized by :
-bradykinesia (slow movement)
-rigidity (stiffness)
-tremor at rest
-gait changes (shuffling)

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12
Q

Parkinson’s etiology

A

Degeneration of dopamine-producing neurons in the substantia Nigra of midbrain

Not hereditary but thought that certain genetic risk could interplay w/environmental factors :
-exposure to well water
-high dairy
-pesticides
-industrial chemicals
-drug induced (street or meds)
-TBI

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13
Q

Clinical manifestations (Parkinson’s) Test*

A

TRAP:
T:remor (often 1st sign, may go
Unnoticed by others, worsens w/stress)
R:igidity (increased resistance to passive ROM, jerky quality -cogwheel-, slow movement)
A:kinesia (absence or loss of voluntary muscle movement -blinking, swinging arms, swallowing, expressions, drooling, shuffling)
P:ostural instability (unable to stop themselves from propulsion. Pull test. Can’t control movement may hurt spouse in sleep!)

May have speech problems

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14
Q

Dx studies (Parkinson’s)

A

There’s not one specific test for Parkinson’s.

-Diagnose off of pt’s hx and clincial features
-to diagnose it require the presence of TRAP & confirmation of PD (positive response to antiparkinsonian meds)

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15
Q

Drug therapy (Parkinson’s) *test

A

Primary : levopoda (effectiveness may decrease over time therefore may be used in combo with Other drugs)

Antiviral
Anticholinergic
MOA-B
Meds also give to tx dementia & depression

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16
Q

Surgical therapy (Parkinson’s)

A

For severe cases where meds aren’t working and motor skills decrease

-deep brain stimulation
-Ablation (destroy tissue that produces abnormal chemical or electrical impulses causing symptoms )
-transplantation (fetal neural tissue into basal ganglia, not as common)

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17
Q

Nursing management/teaching (Parkinson’s)

A

Pg. 1376
Nutrition: 6 small meals a day, cut it in small pieces and let them take their time eating, look for dysphasia, bradykinesia, aspiration, if on levapoda save all protein for dinner meal

•promote physical activity (constipation issues, PT, OT)

•caregiver teaching to help promote ADL’s
•teach depression & anxiety coping skills

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18
Q

Myasthenia Gravis (MG)

A

• an autoimmune disease at the neuromuscular junction, marked trifluctuating weakness of certain skeletal muscle groups
• weakness increases with use. It is suggested that the auto antibody production starts in the thymus because thymuc hyperplasia and tumor are common with MG.

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19
Q

Clinical manifestations (Myasthenia Gravis) Test

A

** Fluctuating weakness of skeletal muscles. 1st muscle involved is usually ocular. ***

• other muscles involved muscles used to chew, swallow, speak and breathe.

• no sensory or reflexes lost- muscle atrophy is rare

• 20% will stay in facial region. Not every patient will look the same or have the same symptoms.

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20
Q

Complications (MG)

A

• MG symptoms may be exacerbated by stress, trauma, weather extremes, beta-blockers, and antibiotics

• Myasthenic crisis: acute worsening of muscle weakness, especially in areas that affects swallowing or breathing, airway infections.

•may become a medical emergency (respiratory intubation supplies ready. Need RT to be there!)

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21
Q

Diagnostic studies (MG)

A

Can be confirmed w/diagnostic testing
-H&P
-EMG (single fiber EMG for confirming**) slow to respond shows muscle fatigue
-Tensilon test (injection)
-CT scan to evaluate thymus after Dx (tumor, hyperplasia)

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22
Q

Drug therapy (MG)

A

• anticholinesterase drugs most successful long term
• corticosteroids (alternating days-prednisone- long-term use= Cushing’s)
•immunosuppressants (azathioprine=imuran)
•plasmapheresis(short term improvement) & IV immunoglobulin G

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23
Q

Nursing management (MG)

A

•H&P
•thorough drug/medication hx
•assess muscle strength, swallow, speech, cough, and gag reflex
•nutrition : smaller meals, semi-solid foods, someone watching/helping them
•coping skills, how it’s effecting their daily life

24
Q

ALS overview

A

•Rare, progressive neuromuscular disorder marked by loss of motor neurons. Linked to Pt: white males 55-75. Prognosis 2-5 years

•motor neurons in the brain stem & spinal cord gradually degenerate for unknown reasons. No transport signals to muscles

25
Q

Clinical Manifestation (ALS)

A

Progressive muscle weakness & atrophy (classic sign)

•common initial “limb onset” (tripping, stumbling)
•Bulbar onset (speech, swallowing)
•pain, sleep disorders, constipation
•spasticity & hyperreflexia
•drooling, esophageal reflux
•emotional instability (depression, anxiety intellect still intact)

26
Q

Tx (ALS)

A

•Riluzole can slow progression
•Edaravone

-facilitate communication, diversional activity
•reduce aspiration risk, watch for respiratory insufficiency
•moderate endurance-type exercises to reduce ALS spasticity**
•pain control from muscle weakness

  • advanced directives /code status
    -family support, coping
    -Tx possible depression
27
Q

Huntington’s Disease overview

A

•progressive, Degenerative brain disorder
•deficiency of neurotransmitter Ach & GABA, opposite symptoms of Parkinson’s
•GENETICALLY TRANSMITTED, autosomal dominant disorder
•asymptomatic w/family hx can get genetic testing

-higher in women 30-50
-50% chance of passing to children
-family planning/adoption

28
Q

Clinical manifestations (Huntington’s disease)

A

•Prognosis 10-30 years
•Movement disorder marked by abnormal & excessive involuntary movements (chorea)
-writhing, twisting, aspiration, malnutrition risk to speech, chewing, swallowing, gait deterioration, ambulation becomes impossible
•Psychiatric symptoms present early (manic anxiety, depression social decline)
•cognitive deterioration is variable: perception, memory, attention and learning
•2 causes of death: pneumonia and suicide

29
Q

Tx: Huntington’s disease

A

Med to improve movement:
-Tetrabenazine (can worsen depression)

•psychiatric disorders: SSRI’s (Zoloft)

•High caloric Diet 4000-5000 cals/day
-moving so much and burning calories

•End of life planning/code status
•counseling/support

30
Q

Guillain-Barre Syndrome overview

A

Short-term, goes away, can recover within a year

•autoimmune process that occurs a few weeks after a viral or bacterial infection, exact cause unknown
•most common type: acute inflammatory demyelination polyneuopathy (AIDP) (don’t need to know different types)
•following infection/surgery/trauma edema and inflammation, segmental loss of myelin sheath, slows down signals to muscles, muscle denervation & atrophy

31
Q

Clinical Manifestations (GB)

A

**Ascending, rapidly progressive, symmetrical weakness of limbs
**1st sign weakness, paranesthesia & hypotonic of lower limbs
**watch for symptoms begins in lower and progresses up. Emergency intubation/breathing problems need RT!!)

•Reflexes weak or absent
•ANS dysfunctions (orthostatic hypotension, incontinent, sweating, bladder/bowel problems)
•cranial nerve involvement
•muscle pain often at night

32
Q

Complications (BG)

A

Respiratory Failure (be ready with intubation supplies, RT needs to be notified)
•respiratory infection (not breathing adequately for gas exchange)

•UTI
•Paralytic ileus
•VTE/PE
•nutritional deficiencies

33
Q

Dx studies (GB)

A

•H&P shows clinical features of progressive weakness. More than 1 limb AND decreased or absent reflexes
•labs: LFT, Creatinine
•CSF analysis done to rule out other disorders
•EMG and nerve conduction studies done after 2 weeks

34
Q

Nursing management /TX (GB)

A

•Supportive Tx
•vent if necessary
•immunomodulating tx
•asses respiratory and cardiac function a lot***
•assess nutritional status, bowel sounds, gag reflex look for drooling
•refer to PT,OT, speech therapy

35
Q

GUILLIAN BARRE RECOVERY

A

•most recover spontaneously right before 30 days
• 80% will walk independently 6 months/full recovery 1 year
•older Pt’s take longer to heal and have longer tx
•dependent on virus or bacterial infection (antibiotics)

36
Q

Functions of the integumentary system

A

•Composed of: skin, hair, nails, and certain glands
•Serves to protect the underlying body
•Barrier against bacteria and viruses
•Prevents excess water loss
•Sends signals to brain related to pain, heat, cold, touch, pressure, and vibration
•Vitamin D is made in the epidermis

37
Q

Integumentary assessment

A

•Allergies (lotion, latex, dressings, nickel, dyes/detergents)
•Medical History, including meds!
•Subjective Data (skin routine/hygiene)
•Objective (rash, wounds, lesions, moles)

38
Q

variations of assessment in light and dark skin

A

Pg 405

Dark skin: look at lips, mucus membranes, palms/soles of feet, sclera, fingernails

39
Q

Gerontological changes in integumentary

A

•Skin:Decreased subcutaneous fat, degeneration of elastic folds, collagen stiffener, decreased sebaceous glands, increased capillary fragility and permeability

•Hair: Decreased melanin, decreased oil and density, decreased estrogen levels

•Nails: Decreased peripheral blood supply, increased keratin, decreased circulation

See table 22.1: ”Gerontological Assessment Differences”, page 398

40
Q

Dx studies for integumentary

A

1.assess 2.diagnose 3.treat

Stains and cultures: for bacterial, fungal, and viruses (don’t need to know different biopsies)
•Biopsy:
•punch
•excisional
•incisional
•shave
•Woods lamp (black light)

41
Q

Bacterial infections

A

•Predisposing factors (obesity, diet/nutrition, hygiene, diabetes, corticosteroids)

•Most common:
•Furuncle/ Furunculitis
•Folliculitis
•Carbuncle
•Cellulitis
•Impetigo

•How do we prevent skin infections: keep skin clean, dry, Pt teach diet and weight and diabetes control

42
Q

Cellulitis overview

A

•Inflammation of the subcutaneous tissues. Primary= injury secondary= happened because of something else

•S&S: hot, tender, erythematous, and edematous area with diffuse borders, chills, malaise, and fever, inflammation

•Treatment: Moist heat, immobilization, and elevation Antibiotics (may need IV abx if severe)

•If untreated may progress to gangrene

43
Q

Viral infections overview

A

Very hard to tx on skin

•Skin lesions common in viral infections

•Most common:
•Herpes simplex (HSV) type I (oral) or II (genital)
•Herpes zoster (Shingles)
•Plantar warts (caused by HPV): on bottom of foot, grows inward, cone shaped with black dots.
•Verruca vulgaris (also caused by HPV) flesh colored papule, painful

44
Q

Herpes simple virus

A

•Type I: Oral
•Type II: Genital
•Contagious by fluids and respiratory droplets

*stay away from intimate contact, very contagious

•S&S: Painful local reaction, single or group vesicles, systemic symptoms

•Tx: Soothing moist compression, petroleum jelly to lesion, antiviral (acyclovir (Zovirax), valacyclovir (Valtrex

45
Q

Herpes Zoster (shingles) overview

A

•Activation of the varicella-zoster virus
Very painful & contagious. Immunecompromised pt more at risk

•S&S: Linear distribution along a dermatome or grouped vesicles and pustules (look like chickenpox). Usually on trunk, face, and lumbosacral areas.

•Tx: skin care & hygiene
Topical: wet compress, silver sulfadiazine (Silvadene) to rupture vesicles
•Systemic: antivirals (”virs” like HSV) within 72 hours to prevent postherpetic neuralgia

46
Q

Candidiasis overview

A

•Fungal infection cause by Candida albicans
•Appears in warm, moist areas such as groin, submammary folds, oral mucosa
•Can be caused by immunosuppression (HIV, chemo, radiation, organ transplant)
•Can present in mouth, vaginal, and skin

47
Q

Candidiasis S/S & Tx

A

•Mouth :(oral thrush)

•Vagina: vaginitis with red, edematous, painful vaginal wall, white patches. Discharge and pruritis. Pain during urination and intercourse.

•Skin: popular erythematous rash with pinpoint satellite lesions around edges.

•Tx: Antifungals (“zole”): fluconazole, ketoconazole, vaginal suppositories, oral lozenges

48
Q

What are the 3 big infestations/bites in this module?

A

•bedbugs
•Lyme disease (ticks)
•scabies

49
Q

Bed bugs S/S & Tx

A

S&S: wheal surrounded by vivid flare, firm urticaria transforms into persistent lesions. SEVERE pruritis (itching)

•Chlorocyclohexane: treat mattress and bedding. Pest control.

•Tx: Usually only require management of pruritis symptom. Antihistamines or topical corticosteroids

50
Q

Lyme disease S/S & Tx test

A

•S&S: spreading, ringlike rash 3-4 weeks after bite.
•Warm, itchy or painful rash
•Flu-like symptoms
•**Cardiac arrhythmias*, arthritic, and neuro manifestations (late): can be deadly!

•Tx: Tx symptoms, may use oral or IV abx (doxycycline) can become septic

51
Q

Scabies S/S & Tx TEST

A

May appear 48 hours- 30 days

•S&S: Severe itchy, common between fingers/toes, genitalia, axillary folds, wrists, not common on face.

•Tx: 5% permethrin topical lotion: 1 overnight app then another 1 week later.
•Tx all family members
•Cover personal items for 5 days, launder clothes/linen with bleach
•Abx if secondary infection

52
Q

Allergic skin problems

A

•Contact Dermatitis from irritants : (jewelry, perfume, detergent)
•Delayed reaction, sometimes 2-7 days after contact
•Occurs after 1 or more exposures

•Atopic Dermatitis (eczema)
•Genetically influenced, chronic, relapsing
•Associated with allergic rhinitis and asthma
•Often triggered by environmental influence
•Most common in kids

53
Q

Eczema Tx

A

•Tx: Moisturize, try to use preservative, non-perfumed/dyes products, non-scented lotions. Don’t take hot showers
•Topical meds
•Corticosteroids
•Abx for secondary infection

54
Q

Psoriasis overview

A

•Chronic autoimmune problem, very common. Effects normally 15-35y/o while males

•Presentation can vary depending on stage (acute to chronic) Acute: Bright red, oozing vesicles.

•Subacute: Scaly, red to brown plaques.

•Chronic: Thickening skin, potential hypo/hyperpigmentation

55
Q

Psoriasis Tx

A

Tx:
•Topical: Corticosteroids
•Systemic: Methotrexate, immunosuppressants

•Goal is to improve quality of life
•Can be emotionally and physically disabling (TEST QUESTION)
•Depression common

56
Q

Levadopa

A

Class: dopamine precursor used in management of Parkinson’s disease

*dont DC abruptly
*effectiveness may decrease over time so a combo may be used (other drugs!)

From book alert:
-Monitor for signs of dyskinesia
- side effects of nausea, vomiting, lightheadedness
-stress to pt’s that effects may be delayed for several weeks to months
-teach patient or caregiver to report any uncontrolled movement of face eyelids, mouth, tongue, arms, hands, or legs, mental changes, palpitations, and difficulty urinating
-do not give with food because protein reduces absorption**