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Geries Flashcards

1
Q

What is benign paroxysmal positional vertigo characterized by

A

sudden onset dizziness and vertigo triggered by changes in head position

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2
Q

How long do the BPPV episodes last

A

10/20 seconds

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3
Q

How is BPPV diagnosed and explain this method 1

A

positive Dix Hallpike manouevre: have the patient sit up and hold their head 45 degrees in one direction. Quickly lower them down to supine and ensure their head dips to 30 degrees past the couch and observe for 30 seconds for nystagmus. This should be repeated for the other side too. Positive test is pt experiences vertigo on this test (rotary nystagmus may or may not be seen but is not a necessary factor)

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4
Q

How is BPPV managed? 4

A
  1. usually spontaneous resolves
  2. Epley manouevre
  3. teaching pts exercises for vestibular rehabilitation eg Brandt Daroff exercises
  4. medication betahistamine can be given but does not always work
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5
Q

What indicates delirium over dementia 3

A
  1. acute onset
  2. fluctuation of symptoms eg worse at night
  3. abnormal perceptions eg illusions/ delusions
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6
Q

What are the causes of delirium 8

A

PINCH ME
pain
infection (UTI/ pneumonia )
nutrition (low)
constipation
hydration (low)
medication (eg benzos)
environment + electrolytic

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7
Q

What are the features of delirium 5

A

disordered thinking
clouded consciousness/ cognition
can have visual complex hallucinations
less than 6 months
disturbed sleep wake cycle
(DLC)

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8
Q

What are the types of delirium 3 and explain each

A

hyperactive: agitation with hallucinations
hypoactive: withdrawn plus reduced GCS
mixed

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9
Q

What are the investigations for delirium 5

A
  1. bloods: FBC, U&E, TFTs, LFTs, glucose, blood cultures
  2. ECG
  3. consider urine dip + MSU (dip not sensitve over 65 so send straight for a MSU)
  4. sputum culture/ CXR
  5. screening with 4 AT
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10
Q

What is 4AT screening for and explain it

A

delirium

  1. alertness
  2. AMT4 (abbreviated mental test: age, dob, name, place)
  3. attention (states months in reverse order)
  4. acute (whether this is a recent change of mental state in the past 2 weeks)
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11
Q

What is the management for delirium

A

to orient:
reduce noise, have same staff, family visitors

agitation:
verbally calm, then IM haloperidol

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12
Q

What medications can trigger delirium 5

A

TCA
opiates
steroids
levodopa
alcohol/ substance withdrawl

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13
Q

What investigations must be done after an elderly fall

A

Bedside tests: BP, blood glucose, urine dip, ECG
Bloods: FBC, UE, LFT, bone profile
Imaging: x-ray of injured limbs, CT head if hit head
4 4 2

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14
Q

What are the NICE guidelines for those with a falls history or at falls risk 3

A
  1. assess gait + balance: do turn 180 test or timed up and go test
  2. multidisciplinary assessment for patients over 65 with 2+ falls in past year with either of them requiring medical treatment and poor results in 1. test
  3. if they do not meet the criteria for a multidisciplinary treatment then annual review
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15
Q

name some risk factors for falling

A
  1. polypharmacy
  2. vision problems
  3. MSK- gait disturbances eg parkinsons/ lower limb weakness
  4. postural hypotension (ACEi/ beta blockers/ CCB)
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16
Q

What medications can increase the risk of falls 5

A
  1. nitrates (due to postural hypotension)
  2. beta blockers (due to postural hypotension)
  3. opiates
  4. ACE inhibitors (due to postural hypotension)
  5. antidepressants (due to postural hypotension)/ antipsychotics
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17
Q

What is the score for osteoporosis

A

T >-2.5 on Dexa Scan

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18
Q

What is dementia

A

progressive decline in cognitive function in alert pts for over 6 months

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19
Q

What are the two subcategories of dementia and examples for each 4, 3

A

cortical: grey matter
alzheimers (mc- 60%)
frontotemporal
vascular
lewy body

subcortical: white matter
parkinson
huntington
alcohol related dementia

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20
Q

What is the pathophysiology of Alzheimers

A

beta amyloid plaques
(tau protein neurofibrillary tangles) widespread in cortex

axon damage and decreased Acetylcholine transmission

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21
Q

What are the symptoms of alzheimers

A

4 As
aphasia
agnosia (familiar objects/ voices)
amnesia in gradual decline
apraxia

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22
Q

What is the pathophys of vascular dementia and symptoms

A

stroke leading to cortical infarct
same 4 As of alzheimers but more severe in a stepwise decline

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23
Q

What is the pathophys of lewy body dementia

A

deposits of proteins (lewy body) in basal ganglia and cortex

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24
Q

What are the symptoms of lewy body dementia 4 and the triad

A
  1. REM sleep disorder
  2. vivid visual hallucinations
  3. parkinsoniam after neuro sx
  4. fluctuating consciousness + cognition

cognitive fluctaution
parkinsonism
hallucinations

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25
Q

What is the pathophys of frontotemporal dementia and symptoms

A

pick body deposition in frontal and temporal lobes

frontal: apathy, mood disorder, decreased executive function eg sleep, hyperphagia)
temporal: trouble with grammer

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26
Q

What can be a precursor to dementia

A

MCI (mild cognitive impairment)

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27
Q

What are the investigations for dementia 5

A
  1. 10-CS cognitive questionnaire (involves orientation questions (year, month, date) and animal naming task) 6–7 indicates possible cognitive impairment, and 0–5 indicates probable cognitive impairment (lower the score, the more concerning)
  2. bloods to rule out other causes: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels
  3. MRI head
  4. SPECT for FTD, alzheimers and LBD (LBD= 2 dots for basal ganglia
  5. Alzheimers measure amyloid beta and tau protein in CSF
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28
Q

What are the results of the 4 dementia types in MRI head

A

alzheimers: diffuse cortical and hippocampal atrophy, sucal widening and increased size of ventricles (micro level= tau + beta amyloid plaques + decreased ach axons)

FTD: F+T deposits and atrophy (micro level= pick bodies- U+Tau proteins)

Vascular: 1+ white cortical infarct- extensive white infarcts

Lewy body dementia: cortical deposits with basal ganglia deposits or normal (micro level= U + alpha S proteins)

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29
Q

What is the treatment for dementia types

A

alzheimers:
1. ACHase inhibitors eg rivastigmine/ donepezil
2. NDMA eg memantine (but side effects dizziness, headaches, SOB)

FTD: SSRI, antipsych

vascular: statins and aspirin to reduce vascular risk factors

lewy body: ACHase inhibitors eg like alzheimers

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30
Q

What medications should not be given in certain types of dementia and why (2)

A

never give antipsychotics to alzheimers due to increase risk of death

never give ACHase inhibitors to FTD pts as this worsens their sx

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31
Q

What are the features of pseudodementia 4

A

pseudodementia= treatable conditions that mimic dementia- MC is depressed pt
replied to questions with ‘i dont know’
normal MMSE
typically with recent bereavement

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32
Q

What is postural hypotenstion

A

10mmHg diastolic drop in BP sitting to standing which is not resolved in 3 mins OR 20+mmHS systolic

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33
Q

What is the pathophysiology of postural hypotension

A

impaired neuro-cardiac baroreceptors reflex

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34
Q

What are the causes of postural hypotension 6

A

CV: HF, MI, AF
Neuro: parkinsons
iatrogenic: BP lowering meds eg CCB/ ACEi/ diuretics
other: addisons

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35
Q

investigations for postural hypotension 3

A
  1. lying and standing blood pressure
  2. ECG
  3. review meds
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36
Q

What is the management for postural hypotension and any SEs

A
  1. conservative= increase water intake and stand up slow
  2. off licence meds= fludrocortisone (mineralocorticoid) but SE of fluid retention/ oedema
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37
Q

What are the types of incontinence and explain what causes each

A

Stress Incontinence: weak pelvic floor and sphincter muscles (linked with previous pregnancies)
Urge Incontinence: overactivity of detrusor muscle of bladder
Mixed incontinence: combination of stress and urge incontinence

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38
Q

What are the investigations for incontinence 4

A
  1. bladder diaries should be completed for a minimum of 3 days
  2. vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles (‘Kegel’ exercises)
  3. urine dipstick and culture
  4. urodynamic studies
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39
Q

What is the management for incontinence 1,3,3

A

lifestyle: weight loss, smoking cessation, reduce alcohol and caffeine intake

for urge incontinence
1. refer for bladder retraining (gradually increasing the intervals between voiding over 6 weeks)
2. medications
-> first line oxybutynin (muscarinic) NOT FOR ELDERLY (rfx falls)
-> mirabegron (beta 3 agonist- bladder relaxant) NOT FOR HTN pts
3. botox for cases that have not responded to two meds

for stress incontinence:
1. referral for pelvic floor muscle trains (8 contractions performed 3 x daily for 3 months)
2. duloxetine (increases muscle tone of urethra for women who do not want surgery)
3. surgical management

for mixed- treat the most dominant incontinence type

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40
Q

What is the definition of malnutrition according to NICE 3

A
  1. BMI of 18.5 or less
  2. unintentional weight loss greater than 10% within the last 3-6 months; or
  3. a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months

2 or more of the above

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41
Q

How is malnutrition screened?

A

MUST score involves:
BMI, recent weight loss, acute disease
to calculate overall risk of malnutrition

if low risk (0), no action
medium risk (1), observe
high risk (2+), commence nutritional care pathway starting with food/ food supplement eg fortisip trial for 4 weeks then calculate MUST score again. BUT BE CAREFUL OF REFEEDING SYNDROME

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42
Q

Define hypothermia and 3 stages with features

A

Hypothermia is defined as a core body temperature of <35°C and is classified as follows:

mild (32°C to 35°C): characterised by tachycardia, tachypnoea, vasoconstriction and shivering

moderate (28°C to 32°C): may have cardiac arrhythmias, hypotension, respiratory depression, reduced consciousness and may cease to shiver

severe (<28°C): markedly reduced consciousness/coma, apnoea, arrhythmia, fixed and dilated pupils

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43
Q

What are the ECG signs seen in hypothermia 3

A

-> Bradycardia and bradyarrhythmias e.g. sinus bradycardia

-> Osborne Waves (‘J waves’) = positive deflection at the J point between the end of the QRS and beginning of the ST segment

-> prolonged all interveals eg QRS, QT, PR etc

44
Q

What is the mx for hypothermia 3

A
  1. warming the patient by covering with a warm blanket
  2. warm drinks
  3. Passive warming may be supplemented by intravenous administration of warmed fluids and application of warm air (e.g. using a Bair-Hugger)
45
Q

What is hyperthermia value and symptoms 4

A

above an acceptable core body temp of 38.3

lack of sweating
faintness
confusion
hyperpyrexia
muscle rigidity/ heat cramps

46
Q

What happens in malignant hyperthermia, characteristic and cause and tx 2

A

excessive release of calcium from skeletal muscle
autosomal dominant
antipsychotics and anaesthetic agents

Tx:
dantrolene (prevents Ca+ release)
cooling blankets and drinks

47
Q

What can indicate non accidental injury 3

A
  1. delayed presentation
  2. injury doesn’t match story or child’s development
  3. injuries on sites not commonly exposed to trauma eg genitals
48
Q

What is the management for non accidental injury? 3

A
  1. skeletal survery (head, chest, pelvis, upper and lower limbs)
  2. CT head on day of presentation and opthamology review if head trauma for retinal haemorrhages
  3. immediately first thing to do is contact the safeguarding lead to get child protection services and social workers involved
49
Q

What are pressure sores? and most common areas to get them

A

Tissue damage caused by prolonged pressure or friction
sacrum

50
Q

What are the risk factors for pressure sores? 3 How is this risk assessed?

A

immobility
increasing age
chronic illnesses that impair healing eg diabetes/ peripherla vascular disease

Waterlow score
>10 risk
>15 high risk
>20 very high risk

51
Q

What are the features of pressure sores 4

A

skin changes
pain at site
swelling and warmth around area

52
Q

What is the grading for pressure sores

A

Stage 1 - non-blanching redness
Stage 2 - partial thickness- shalow ulcer with pink wound bed
Stage 3 - full thickness skin loss- fat can be visibale but bone/tendon/muscle not exposed
Stage 4 - full thickness tissue loss- bone /tendon/muscle exposed
Unstageable: depth unknown due to top being covered

53
Q

What is the ix for pressure sores

A

only if signs of infection then swab sent off for MC+S

54
Q

What is the mx for pressure sores 3

A
  1. reducing pressure on affected areas through repositioning, specialised mattresses, and cushions.
  2. wound cleaning and dressing
  3. analgesia

ALL pressure sores, regardless of grading require wound dressing, analgesia and a nutritional assessment

55
Q

What medications can cause postural hypotension 7

A
  1. morphine
  2. TCA amytryptyline
  3. Ace inhibitors
  4. Beta blockers
  5. nitrates
  6. loop/ thiazide diuretics
  7. antiparkinsonian drugs eg levodopa
56
Q

What are the 5 giants of geries

A

instability
immobility
impaired cognition
iatrogenesis
incontinence

57
Q

What is osteoporosis and pathophys

A

T score > -2.5 on DEXA scan

destruction of horizontal trabeculae, causing a decrease of BMD

58
Q

What are the causes of osteoporosis

A

SHATTERED
steroids
hyperthyroidism
alcohol/ smoking
thin
testosterone low
early menopause
renal/ liver failure
erosive bone disease (RA)
drugs (methotrexate, lithium, warfarin)

59
Q

What are the most common pathological fractures with osteoporosis 3

A

colles (falling on outstretched hand= radius fracture)
NOF (external rotation and shortened leg)
compression fracture of spine (widow stoop)

60
Q

What are the ix for osteoporosis

A
  1. bloods (FBC, U/E, bone profile, LFT)
  2. xray of fracture
  3. DEXA scan
61
Q

What is a DEXA scan and Z score

A

DEXA= (t score)compares BMD to healthy 30 year old
z score= compares BMD to someone of same demophraphic

62
Q

What do the DEXA scan results mean

A

-1 to -2.5 osteopenia
-2.5 or worse osteoporosis

63
Q

How can osteoporosis be risk stratified and actions

A

FRAX score (10 year fracture risk)
<10 low risk, DEXA/ follow up in 5 years
10-19 mod risk, offer DEXA and consider tx
20+ high risk do DEXA and give tx

64
Q

What is management for osteoporosis 4

A
  1. lifestyle: increase dietary calcium, sunlight exposure for vit D, calcium supplements (ADCALD3)
  2. bisphosphonates (inhibit osteoclasts) eg alendronate 70mg PO or IV zolendronate 5mg yearly
  3. denosumab (human monocloncal antibody which inhibits RANK L) 2 x yearly SC injection
  4. oestrogen containing HRT

you have to be BOLD with osteoporosis management

65
Q

What does advanced care planning involve

A

allows patient to place care plans for the future for when they may lack capacity
eg respect forms and appointing LPA (lasting power of attorney)

66
Q

Explain the IMCA

A

NHS appoints for non lasting of attorney patients who can inquire about medical decision but cannot make these on the patient behalf

67
Q

Explain Lasting power of attourney

A

appointed to make decisions on behalf of patient without capacity eg financial and health decisions
This is regulated by the office of public guardians

68
Q

Explain an advanced statement vs an advanced decision

A

statement: written statement detailing treatment preferences should they lack capacity in the future eg wanting to pass away at home, wanting vegan food only etc

Advanced decision” This only involves refusing treatment, not demanding it and does not encompass refusing basic treatment like food and painkillers

69
Q

Explain a court appointed deputy

A

if patient has no LPA and there is a dispute over best interests so an application is made the court for a temporary decision maker

70
Q

What are DOLS (deprivation of liberty safeguard)

A

patient not allowed to leave, placed in a 24 hours supervised residence in the situation of a DOLS assessment and pt lacks capacity/ risk to self or others
-> only in care homes/ hospital

71
Q

What is the main complication of hip fractures

A

avascular necrosis as the blood supply to femoral head is via femoral neck (where fracture ocurs)

72
Q

What are the features of a hip fracture 3

A
  1. pain
  2. shortened and externally rotated leg
  3. may or may not be able to weight bear
73
Q

What is the grading system for hip fractures and what is the exception

A

The Garden system:

Type I: Stable fracture (not fractured all the way through the neck)
Type II: Complete fracture but undisplaced (fractured through but not broken off)
Type III: Displaced fracture, usually rotated and angulated, but still has boney contact (fractured through, broken off slightly)
Type IV: Complete boney disruption (fractured through, broken off completely)

Garden system is only for INTRA capsular fractures

74
Q

What are the two locations of hip fractures

A

intracapsular (subcapital): from the edge of the femoral head to the insertion of the capsule of the hip joint- basically femoral head or neck
extracapsular: these can either be trochanteric or subtrochanteric (the lesser trochanter is the dividing line)

75
Q

What is the management of hip fractures for intracapsular hip fracture

A

undisplaced fracture: internal fixation

displaced: hemiarthroplasty (total hip replacement only if fully mobilising with max 1 walking stick, no cognitive impairment, and decent age for the surgery)

76
Q

What is the management of hip fractures for extracapsular hip fracture

A

stable intertrochanteric fractures: dynamic hip screw
if reverse oblique, transverse or subtrochanteric fractures: intramedullary rod

77
Q

What are the investigations of patella fracture

A
  1. AP x ray AND lateral x-ray (two views minimum required)
78
Q

How are patella fractures management

A
  1. undisplaced fractures: hinged knee brace for 2 months and weight bearing okay
  2. displaced fractures and those with loss of extensor mechanisms: tension band wire or screws, hinged knee brace for 2 months and weight bearing okay
79
Q

What is the requirement for ix suspected ankle fracture

A

Ottawa rule: states bony tenderness and unability to walk four weight bearing steps means an x-ray of foot is required as an ankle fracture is possible

80
Q

What is squamous cell carcinoma and risk factors 3

A

malignant tumour of epidermal keratinocytes in the skin

Rfx: excessive UV exposure, immunosuppression, smoking

81
Q

What are the features of squamous cell carcinomas 4

A
  1. typically on sun-exposed sites such as the head and neck or back of the hands and arms
  2. rapidly expanding painless, ulcerate nodules
  3. may have a cauliflower-like appearance
  4. there may be areas of bleeding
82
Q

What is the mx for squamous cell carcinoma 3

A
  1. Surgical excision with 4mm margins if lesion <20mm in diameter
  2. If tumour >20mm then margins should be 6mm.
  3. Mohs micrographic surgery may be used in high-risk patients and in cosmetically important sites
83
Q

What is guillain barre

A

immune mediated demyelination of PNS triggered by infection eg gastroenteritis (MC- campylobacter jejuni)

84
Q

Features of Guillain Barre 3

A

progressive weakness of all four limbs, in a ascending patter with lower extremities affected first

can have mild sensory signs eg distal paraesthesia/ back pain

lower motor neuron signs in lower limbs: hyporeflexia and hypotonia

85
Q

What are the ix for Guillain Barre 1

A

lumbar puncture: shows albuminocytologic dissociation: high protein but normal white cell count

86
Q

What is the mx for guillain barre? 3

A
  1. IV immunoglobulins
  2. plasma exchange
  3. FVC to monitor resp function
87
Q

What are the types of motor neurone disease and what is motor neurone disease

A

neuro condition with a combination of UMN and LMN signs

88
Q

Explain features of amyotrophic lateral sclerosis (MND) and inheritence

A

typically LMN signs in arms and UMN signs in legs
in familial cases there is a SOD 1 mutation on chromosome 21 responsible

89
Q

Explain features of primary lateral sclerosis (MND)

A

UMN signs only

90
Q

Explain features of progressive muscular atrophy (MND)

A

LMN signs only
affects distal muscles before proximal
carries best prognosis

91
Q

Explain features of progressive bulbar palsy (MND)

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei (affects cranial nerves 9-12) LMN
carries worst prognosis

92
Q

What are the UMN signs vs LMN 5

A
  1. Inspection
    UMN: No fasciculations or significant wasting (however there may be some disuse atrophy or contractures)
    LMN: Wasting and fasciculation of muscles
  2. tone
    UMN: Increased (spasticity or rigidity) +/- ankle clonus LMN: Decreased (hypotonia, flaccid) or normal
  3. Power
    UMN: Reduced with pyramidal pattern of weakness (extensors weaker than flexors in arms, and vice versa in legs)
    LMN: Reduced in distribution of affected motor root/nerve
  4. Reflexes
    UMN: Exaggerated or brisk (hyperreflexia)
    LMN: Reduced or absent (hyporeflexia or areflexia)
  5. Plantar reflex
    UMN: Upgoing/extensor (Babinski positive)
    LMN: Normal (downgoing/flexor) or no movement

in tone, power, reflexes we trust

93
Q

What is the mx for MND

A
  1. riluzole
  2. respiratory care (BIPAP used at night as a form of non invasive ventilation)
94
Q

What are the features of cerebellar disease

A

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia

95
Q

How do cerebellar lesions present?

A

Unilateral cerebellar lesions cause ipsilateral signs (symptoms on same side of lesion)

96
Q

What are causes of cerebellar dysfuncton? 4

A
  1. alcohol (chronic alcoholism can cause cerebellar atrophy)
  2. stroke (lack of blood supply to cerebellum)
  3. meds: phenytoin and carbamazepine
  4. MS
97
Q

What is the main feature of bells palsy

A

-> weakness on one side of face (due to it being a LMN facial nerve palsy, the forehead is NOT spared unlike in a stroke)

98
Q

What is the management for bells palsy 3

A
  1. oral pred within 72 hours of sx onset
  2. give pt artificial tears and eye lubricants
  3. if continues for 3 weeks, urgent referral to ENT
99
Q

What is erbs palsy

A

C5-6 damage- complication of shoulder dystocia
elbow extension, wrist and finger flexion

100
Q

What are all the CN palsies

A

2: optic tracts and radiations
3: down and out + dilated pupil
4: diplopia
6: impaired aBduction
5: weak mastication, decreased tongue sensation, decreases jaw and corneal reflexes
7: bells palsy
8: hearing loss, vertigo + balance issues
9: absent gag reflex, lack of taste posterior of tongue
10: uvula deviation contralateral to CNx lesion side (deviates to side without lesion)
11: weak SCM head turning and shrug (trapzius)
12: ipsilateral tongue deviation (deviated to side of lesion)

101
Q

What is cerebral palsy and causes (MC)

A

issues with movement and posture because of a lesion of the motor pathways whilst the brain is developing

MC antenatal: CMV/ rubella infections in utero
intrapartum: trauma/ birth asphyxia
postnatal: meningitis/ haemorrhage

102
Q

What are the features of cerebral palsy

A

motor milestones are delayed
abnormal tone (spastic)
difficulties feeding/ learning
hearing + vision (squint) issues
epilepsy
abnormal gait

MAD HEAd

103
Q

```

~~~

What are the types of cerebral palsy 4

A
  1. spastic: damage to UMN in extrapyramidal tract/ motor cortex= increased tone
    -> get tip toe walking (calf muscle tone is high so they pull tight= tip toe)
    -> get scissoring movement where inner thigh muscles are hypertonic and tight so they pull knees over midline each time they walk)
    -> same in upper limbs where elbow and wrist flexors become more active than its muscle pairs and keep arm always flexed in this position
  2. dyskinetic: damage to basal ganglia and substantia nigra= athetoid movements and oro-motor problems (basal ganglia initiates movements and inhibits unwanted movement)
    -> can go from very stiff to very floppy and vice versa
    -> twisting movements
    -> clenching and unclenching of hand
    -> symptoms get worse when stressed/ anxious and can resolve whilst sleeping
  3. ataxic: damage to cerebellum= cerebellar signs
  4. mixed
104
Q

What is the management of cerebral palsy 5

A
  1. MDT approach: PT, OT, SLT
  2. baclofen for muscle spasms
  3. for spasticity CP, botox can be done
  4. anticonvulsants
  5. PEG if indicated

my bad for asphyxiating patricia

105
Q

What is the score for stratifying frailty risk? What score indicates a frailty risk?

A

PRISMA 7
3 or more positive questions indiciate frailty

106
Q

Compare beckers and duchennes muscular dystrophy
inheritence, pathophys, sx
diagnosis

A

both= x-linked recessive mutation in dystrophin gene Xp21
beckers= non-frameshift mutation so some dystrophin
duchenne= framshift mutation= no dystrophin left, presents

sx: proximal muscle weakness so struggles to walk properly and needs support to stand up (in duchennes- compensatory bulky calf muscles)

beckers presents in children over 15, cardiac issues alongside
duchennes is from birth, more rapidly progressing, learning disabilities alongside

dx; genetic testing

107
Q

What are the four palliative care medications

A

Morphine sulfate/Oxycodone – pain and/or shortness of breath.
Midazolam – to help ease anxiety or agitation.
Glycopyrronium – to reduce resp secretions.
Levomepromazine/Haloperidol – to reduce nausea and vomiting.

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