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UKMLA Prep > Medicine of older adult 👵🏼 > Flashcards

Medicine of older adult 👵🏼 Flashcards

Condition and presentation

1
Q

Alzheimer’s disease

A
  • Most common form of dementia
  • progressive neurodegenerative disorder that leads to cognitive decline, memory impairment, and a range of behavioural and psychological symptoms.
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2
Q

Epidemiology of Alzheimer’s disease

A
  • common in older patients
  • More common in women than men
  • genetic association (APOE e2,3,4)
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3
Q

Pathophysiology of alzheimer’s

A
  • accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature
  • disruption of neural communication
  • abnormal tau protein accumulates, forming neurofibrillary tangles; nutrients cant be transported
  • neurotransmitter imbalance
  • neural loss and brain atrophy
  • inflammatory response
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4
Q

Risk factors for alzheimers

A
  • APOE gene
  • advancing age
  • family hx
  • poor lifestyle (lack of exercise, drinking, smoking)
  • CVD risk
  • low attainment at school
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5
Q

Features of Alzheimer’s disease

A
  • Memory Impairment
  • Language Impairment:
  • Executive Dysfunction:
  • Behavioural Changes:
  • Psychological Symptoms:
  • Disorientation:
  • Loss of Motor Skills
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6
Q

Investigations for Alzheimer’s

A
  • FBC, TFT and U+Es (rule out underlying delirum
  • PET scan and MRI to identify brain atrophy
  • CSF to identify biomarkers associated with alzheimers.
  • cognition assessment- MOCA, MMSE, 10 pojnt scale
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7
Q
A
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8
Q

Managment of Alzheimer’s

A
  • Non-pharmalogical (CBT, brain enrichment)
  • family and patient education
  • **cholinesterase inhibitors **(e.g. donepezil)
  • N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. memantine), may be prescribed to manage cognitive symptoms.
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9
Q

Charles Bonnet syndrome

A
  • complex, vivid visual hallucinations generally in individuals with significant vision loss.
  • Commonly associated conditions include age-related macular degeneration, glaucoma, and cataract.
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10
Q

Signs and symptoms of Charles Bonnet syndrome

A
  • well-formed, vivid, elaborate, and often stereotyped visual hallucinations in a partially sighted person.
  • The imagery can be varied, including groups of people or children, animals, and panoramic countryside scenes.
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11
Q

Investigations of Charles Bonnet syndrome

A
  • Clinical presentation and patient history.
  • Neurological and ophthalmic examinations
  • FBC, U+E
  • CBS hallucinations may persist despite treatment of underlying eye conditions
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12
Q

What is the managment of CBS?

A
  • education and reassurance
  • optimise eye sight
  • Medication can be used to ease symptoms rather than cure it.
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13
Q

Drugs used in managment of CBS

A

Atypical Antipsychotics:
* Risperidone (brand name Risperdal)
* Quetiapine (brand name Seroquel)
* Olanzapine (brand name Zyprexa)

Selective Serotonin Reuptake Inhibitors (SSRIs):
* Sertraline (brand name Zoloft)
* Citalopram (brand name Celexa)
* Escitalopram (brand name Lexapro)

Antiepileptic Drugs:
* Gabapentin (brand names Neurontin, Gabapentin)
* Pregabalin (brand name Lyrica)
* Levetiracetam (brand name Keppra)

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14
Q

Constipation

A

infrequent bowel movements, hard stools, excessive straining, tenesmus and sometimes necessitating manual evacuation.

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15
Q

Rome IV criteria for

A
  • Fewer than three bowel movements per week
  • Hard stool in more than 25% of bowel movements
  • Tenesmus in more than 25% of bowel movements
  • Excessive straining in more than 25% of bowel movements
  • A need for manual evacuation of bowel movements
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16
Q

Primary constipation

A
  • no organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles
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17
Q

Secondaryconstipation

A

due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction

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18
Q
A
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19
Q

Risk factors of constipation

A
  • Advanced age
  • Inactivity
  • Low calorie intake
  • Low fibre diet
  • Certain medications
  • Female sex
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20
Q

2WW criteria for constipation

A
  • Constipation (or diarrhoea) with weight loss
  • 60 and over.
  • Consider an urgent, direct access CT scan, or an urgent ultrasound scan if CT is not available, to rule out pancreatic cancer
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21
Q

Bedside investiagtions for Secondary constipation

A
  • PR exam
  • Stool culture – MC&S, ova,cysts,parasites
  • FIT testing (if accompanied with new rectal bleeding and signs suggestive of colorectal cancer), faecal calprotectin
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22
Q

Constipation-what blood tests to do?

A

Full blood count (may show an anaemia), U+Es (including calcium), TFTs

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23
Q

Constipation imaging

A
  • Abdominal x-ray if suspicious of a secondary cause of constipation such as obstruction (may reveal faecal loading)
  • Barium enema if suspicious of impaction or rectal mass
  • Colonoscopy if suspicious of lower GI malignancy
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24
Q

Managment of constipation

A
  • lifestyle changes
  • laxatives
    1. Bulk forming laxative
    2. osmotic laxative
    3. stimulant laxative
    4. stool softners
    5. enemas
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25
Q

Acute confusional state

A
  • Is a frequent condition, primarily observed among elderly individuals.
  • It manifests through symptoms such as disorientation, hallucinations, inattention, memory problems, mood or personality changes, and disturbed sleep.

aka delirium

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26
Q

Pre-disposing factors for ACS

A
  • age > 65 years
  • background of dementia
  • significant injury e.g. hip fracture
  • frailty or multimorbidity
  • polypharmacy
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27
Q

Multifactoral events which can lead to ACS

A
  • infection: particularly urinary tract infections
  • metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
  • change of environment
  • any significant cardiovascular, respiratory, neurological or endocrine condition
  • severe pain
  • alcohol withdrawal
  • constipation
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28
Q

Features of ACS

A
  • memory disturbances (loss of short term > long term)
  • may be very agitated or withdrawn
  • disorientation
  • mood change
  • visual hallucinations
  • disturbed sleep cycle
  • poor attention
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29
Q

ACS managment

A
  • Treat the underlying cause
  • Haloperidol 0.5 mg as the first-line sedative
  • Parkinson patients may need to be weaned off medications
  • if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred
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30
Q

Olazapine side effects

A
  • weight gain
  • increased appetite
  • sedation
  • dry mouth
  • Ortostatic hypertension
  • Extrapyrimidal symptoms
  • constipation
  • dry mouth
  • elevated liver enzyme
  • WCC change
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31
Q

Dementia with Lewy bodies (DLB)

A

rogressive, complex condition, accounting for approximately 10-15% of dementia cases.

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32
Q

Featured of DLB

A
  • Fluctuating cognition: Changes in attention and alertness may occur.
  • Parkinsonism: Rigidity, bradykinesia, and postural instability are common.
  • Visual hallucinations: Patients often experience complex and recurrent visual hallucinations.
  • High sensitivity to neuroleptics: These drugs can induce or worsen parkinsonism.
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33
Q

LBD vs Dementia

A

if cognitive impairment and parkinsonism develop <1 year of each other, it is likely LBD.

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34
Q

DLB investigations

A
  • Dopamine transporter (DaT) scan: This can help distinguish DLB from other types of dementia.
  • Neuropsychological testing: To assess cognitive functioning and fluctuations.
  • Electroencephalography (EEG): Although not diagnostic, a slowing background rhythm may be seen in DLB.
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35
Q

Managment of DLB

A
  • Non-pharmacological interventions: These include cognitive stimulation, physical therapy, and occupational therapy.
  • Supportive care: As DLB is a progressive disorder, palliative and end-of-life care considerations are essential.
  • Medications: Cholinesterase inhibitors can help manage cognitive symptoms. However, caution is required with antipsychotic medications due to neuroleptic sensitivity.
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36
Q

Complications of DLB

A
  • Rapid disease progression: Compared to other dementias, DLB may progress more rapidly.
  • Severe neuroleptic sensitivity: This can lead to severe parkinsonism and potential neuroleptic malignant syndrome, a life-threatening neurological disorder.

``

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37
Q

Trimethoprim and renal function

A
  • lead to a transient rise in creatinine levels by reducing the creatinine excretion of the kidneys
  • Does not reflect actual eGFR
  • not reflective of AKI
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38
Q

Psychotic features (3)

A
  • hallucinations (e.g. auditory)
  • delusions
  • thought disorganisation
  • agitation/aggression
  • neurocognitive impairment (e.g. in memory, attention or executive function)
  • depression
  • thoughts of self-harm
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39
Q

thought disorganisation

A
  • alogia: little information conveyed by speech
  • tangentiality: answers diverge from topic
  • clanging
  • word salad: linking real words incoherently → nonsensical content
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40
Q

conditions linked with psychosis

A

schizophrenia: the most common psychotic disorder
depression (psychotic depression, a subtype more common in elderly patients)
bipolar disorder
puerperal psychosis
brief psychotic disorder: where symptoms last less than a month
neurological conditions e.g. Parkinson’s disease, Huntington’s disease
prescribed drugs e.g. corticosteroids
certain illicit drugs e.g. cannabis, phencyclidine

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41
Q

auditory hallucinations in schizophrenia

A
  • two or more voices discussing the patient in the third person
  • thought echo
  • voices commenting on the patient’s behaviour
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42
Q

examples of thought disorders

A
  • thought insertion
  • thought withdrawal
  • thought broadcasting
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43
Q

Passivity phenomena:

A
  • bodily sensations being controlled by external influence
  • actions/impulses/feelings - experiences which are imposed on the individual or influenced by others
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44
Q

Delusional perceptions

A

a two stage process) where first a normal object is perceived then secondly there is a sudden intense delusional insight into the objects meaning for the patient e.g. ‘The traffic light is green therefore I am the King’

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45
Q

features of scizophrenia

A
  • impaired insight
  • negative symptoms
    incongruity/blunting of affect
  • anhedonia (inability to derive pleasure)
  • alogia (poverty of speech)
  • avolition (poor motivation)
  • social withdrawal
  • neologisms: made-up words
  • catatonia
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46
Q

5 key principles of the MCA

A
  1. A person must be assumed to have capacity unless it is established that he lacks capacity
  2. A person is not to be treated as unable to make a decision unless all practicable steps to help him to do so have been taken without success
  3. A person is not to be treated as unable to make a decision merely because he makes an unwise decision
  4. An act done, or decision made, under this Act for or on behalf of a person who lacks capacity must be done, or made, in his best interests
  5. Before the act is done, or the decision is made, regard must be had to whether the purpose for which it is needed can be as effectively achieved in a way that is less restrictive of the person’s rights and freedom of action
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47
Q

Risk factors of BHP

A
  • age
    around 50% of 50-year-old men will have evidence of BPH and 30% will have symptoms
    around 80% of 80-year-old - men have evidence of BPH
    ethnicity: black > white > Asian
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48
Q

voiding symptoms (obstructive):
(BHP)

A

weak or intermittent urinary flow
straining
hesitancy
terminal dribbling
incomplete emptying

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49
Q

BHP storage symptoms (irritative)

A

urgency
frequency
urgency incontinence
nocturia

50
Q

Post micturition BHP

A

dribbling

51
Q

complications of BHP

A

urinary tract infection
retention
obstructive uropathy

52
Q

International Prostate Symptom Score (IPSS)

A

tool for classifying the severity of lower urinary tract symptoms (LUTS) and assessing the impact of LUTS on quality of life
Score 20-35: severely symptomatic
Score 8-19: moderately symptomatic
Score 0-7: mildly symptomatic

53
Q

Assessment of BPH

A
  • Urine dip
  • U&Es
  • PSA
  • urinary frequency chart
    -IPPS
54
Q

Managment of BPH

A
  • Observation
  • alpha-1 antagonists e.g. tamsulosin, alfuzosin
  • 5 alpha-reductase inhibitors e.g. finasteride
  • if there is a mixture of storage symptoms and voiding symptoms that persist after treatment with an alpha-blocker alone, then an antimuscarinic (anticholinergic) drug such as tolterodine or darifenacin may be tried
  • surgery
55
Q

alpha-1 antagonists e.g. tamsulosin, alfuzosin

A

decrease smooth muscle tone of the prostate and bladder
considered first-line: NICE recommend if moderate-to-severe voiding symptoms (IPSS ≥ 8)
improve symptoms in around 70% of men
adverse effects: dizziness, postural hypotension, dry mouth, depression

56
Q

5 alpha-reductase inhibitors e.g. finasteride

A

block the conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH
indicated if the patient has a significantly enlarged prostate and is considered to be at high risk of progression
unlike alpha-1 antagonists causes a reduction in prostate volume and hence may slow disease progression. This however takes time and symptoms may not improve for 6 months
may also decrease PSA concentrations by up to 50%
adverse effects: erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

57
Q

risk factors of urinary incontinence

A

advancing age
previous pregnancy and childbirth
high body mass index
hysterectomy
family history

58
Q

inital investigations of urinary incontinence

A

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

59
Q

Managment of UI

A
  • bladder retraining (6 weeks)
    bladder stabilising drugs: antimuscarinics are first-line
    NICE recommend oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation)
    Immediate release oxybutynin should, however, be avoided in ‘frail older women’
    mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patien
60
Q

Stress incontinence managment

A
  • pelvic floor training
  • surgical procedures
  • duloxetine
61
Q

Duloxetine

A

a combined noradrenaline and serotonin reuptake inhibitor
mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced

62
Q

Nocturnal enuresis managment

A

look for possible underlying causes/triggers
constipation
diabetes mellitus
UTI if recent onset
general advice
fluid intake
toileting patterns: encourage to empty bladder regularly during the day and before sleep
lifting and waking

63
Q

delirium predisposing factors

A

age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmac

64
Q

precipitating effects for delirium

A

infection: particularly urinary tract infections
metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
change of environment
any significant cardiovascular, respiratory, neurological or endocrine condition
severe pain
alcohol withdrawal
constipation

65
Q

features of delirium

A

memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention

66
Q

Managment of delirium

A

treatment of the underlying cause
modification of the environment
haloperidol 0.5 mg as the first-line sedative
the 2010 NICE delirium guidelines advocate the use of haloperidol or olanzapine
management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
careful reduction of the Parkinson medication may be helpful
if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred

67
Q

Managment of Lewy body dementia

A

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.

Avoid neuroleptics

68
Q

features of Lewy body dementia

A

progressive cognitive impairment
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

69
Q

diagnosis of Lewy body demenita

A

usually clnical
- PET scan be used

70
Q

factors that predispose to pressure sores

A

malnourishment
incontinence: urinary and faecal
lack of mobility
pain (leads to a reduction in mobility)

71
Q

Managment of pressure sores

A

a moist wound environment encourages ulcer healing. Hydrocolloid dressings and hydrogels may help facilitate this. The use of soap should be discouraged to avoid drying the wound
wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria. The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis)
consider referral to the tissue viability nurse
surgical debridement may be beneficial for selected wounds

72
Q

how many grades of the waterlow score is there?

A

4

73
Q

waterlow grade 1

A

Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin

74
Q

Waterlow grade 2

A

Partial thickness skin loss involving epidermis or dermis, or both. The
ulcer is superficial and presents clinically as an abrasion or blister

75
Q

Waterlow grade 3

A

Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.

76
Q

Waterlow grade 4

A

Extensive destruction, tissue necrosis, or damage to muscle, bone or
supporting structures with or without full thickness skin loss

77
Q

Managment of malnutrition

A

dietician support if the patient is at high-risk
a ‘food-first’ approach with clear instructions (e.g. ‘add full-fat cream to mashed potato’), rather than just prescribing oral nutritional supplements (ONS) such as Ensure
if ONS are used they should be taken between meals, rather than instead of meals

78
Q

Features of pulmonary oedema of CXR

A
  • interstitial oedema
  • bat’s wing appearance
    upper lobe diversion (increased blood flow to the superior parts of the lung)
  • Kerley B lines
  • pleural effusion
  • cardiomegaly may be seen if there is cardiogenic cause
79
Q

What is this showing?

A

Pulmonary oedema

80
Q

causes of decreased BNP levels

A

Obesity
Diuretics
ACE inhibitors
Beta-blockers
Angiotensin 2 receptor blockers
Aldosterone antagonists

81
Q

Causes of increases BNP levels

A

Left ventricular hypertrophy
Ischaemia
Tachycardia
Right ventricular overload
Hypoxaemia (including pulmonary embolism)
GFR < 60 ml/min
Sepsis
COPD
Diabetes
Age > 70
Liver cirrhosis

82
Q

Managment of CHF

A
  • ACE-inhibitor and a beta-blocker
  • second line: aldosterone antagonist
  • SGLT-2 inhibitors
  • third line must be started by a specialist.
83
Q

CHF specialist drugs

A

vabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy

84
Q

Important immunisation managment of CHF

A
  • annual influenza vaccine
  • one-off pneumococcal vaccin
    those with splenic or rCHD should have vaccine every 5 years
85
Q

Systolic dysfunction CHF

A

Ischaemic heart disease
Dilated cardiomyopathy
Myocarditis
Arrhythmias

86
Q

Diastolic dysfunction CHF link conditions

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

87
Q

High output HF

A

High-output heart failure refers to a situation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body.

88
Q

What is the most common form of Guillain-Barré Syndrome in Europe and North America?

A

Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

AIDP is characterized by an immune-mediated attack on the myelin sheath of peripheral nerves.

89
Q

What immune cells are key players in AIDP?

A

T-cells and macrophages

These cells are involved in the immune-mediated attack on the myelin sheath.

90
Q

What are the main symptoms of Acute Inflammatory Demyelinating Polyneuropathy (AIDP)?

A

Progressive, symmetrical ascending weakness, loss of reflexes, mild or absent sensory involvement

Symptoms typically start in the legs and progress to the arms.

91
Q

Which form of Guillain-Barré Syndrome is more common in Asia and associated with Campylobacter jejuni infection?

A

Acute Motor Axonal Neuropathy (AMAN)

AMAN involves an immune attack on the axons of motor nerves.

92
Q

What is the primary pathology of AMAN?

A

Immune system attacks axons of motor nerves directly

Unlike AIDP, which targets myelin, AMAN targets the axons.

93
Q

What are the symptoms of Acute Motor Axonal Neuropathy (AMAN)?

A

Pure motor weakness without sensory loss, absent reflexes

Recovery may take longer than in AIDP due to the nature of axonal damage.

94
Q

What distinguishes Acute Motor and Sensory Axonal Neuropathy (AMSAN) from AMAN?

A

Both motor and sensory axons are affected

AMSAN has a worse prognosis due to extensive axonal involvement.

95
Q

What are the main symptoms of AMSAN?

A

Weakness, sensory loss, absent reflexes

Symptoms are more severe and prolonged than in AMAN.

96
Q

What is Miller Fisher Syndrome (MFS) and its key symptoms?

A

A rare variant of GBS with ophthalmoplegia, ataxia, and areflexia

MFS typically starts at the head and face and usually does not involve weakness.

97
Q

What antibodies are linked to Miller Fisher Syndrome?

A

Anti-GQ1b antibodies

These antibodies are associated with the pathology of MFS.

98
Q

What is the Pharyngeal-Cervical-Brachial Variant of GBS characterized by?

A

Weakness in the neck, face, and arms with normal leg reflexes

This variant affects specific muscle groups without impacting leg reflexes.

99
Q

What are the features of Bickerstaff Brainstem Encephalitis?

A

Overlap with Miller Fisher, includes reduced consciousness and brainstem dysfunction

This condition presents symptoms similar to MFS but with additional neurological impairments.

100
Q

What is the key difference in pathology between AIDP and AMAN/AMSAN?

A

AIDP involves demyelination while AMAN/AMSAN involves axonal degeneration

This fundamental difference affects the clinical presentation and recovery.

101
Q

What triggers AIDP compared to AMAN/AMSAN?

A

AIDP is triggered by general infections; AMAN/AMSAN is specifically associated with Campylobacter jejuni

The triggers can influence the prevalence of each form in different geographic regions.

102
Q

How does sensory involvement differ between AIDP and AMSAN?

A

Sensory involvement is mild or absent in AIDP; present in AMSAN

This distinction helps in the clinical diagnosis of the different forms.

103
Q

Which form of Guillain-Barré Syndrome typically has a faster recovery rate?

A

Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

Recovery is faster in AIDP because myelin regrows more quickly than axons regenerate.

104
Q

True or False: Reflexes are absent in both AIDP and AMAN/AMSAN.

A

True

Both conditions exhibit absent reflexes in the affected areas.

105
Q

What is the most common form of Guillain-Barré Syndrome in Europe and North America?

A

Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

AIDP is characterized by an immune-mediated attack on the myelin sheath of peripheral nerves.

106
Q

What immune cells are key players in AIDP?

A

T-cells and macrophages

These cells are involved in the immune-mediated attack on the myelin sheath.

107
Q

What are the main symptoms of Acute Inflammatory Demyelinating Polyneuropathy (AIDP)?

A

Progressive, symmetrical ascending weakness, loss of reflexes, mild or absent sensory involvement

Symptoms typically start in the legs and progress to the arms.

108
Q

Which form of Guillain-Barré Syndrome is more common in Asia and associated with Campylobacter jejuni infection?

A

Acute Motor Axonal Neuropathy (AMAN)

AMAN involves an immune attack on the axons of motor nerves.

109
Q

What is the primary pathology of AMAN?

A

Immune system attacks axons of motor nerves directly

Unlike AIDP, which targets myelin, AMAN targets the axons.

110
Q

What are the symptoms of Acute Motor Axonal Neuropathy (AMAN)?

A

Pure motor weakness without sensory loss, absent reflexes

Recovery may take longer than in AIDP due to the nature of axonal damage.

111
Q

What distinguishes Acute Motor and Sensory Axonal Neuropathy (AMSAN) from AMAN?

A

Both motor and sensory axons are affected

AMSAN has a worse prognosis due to extensive axonal involvement.

112
Q

What are the main symptoms of AMSAN?

A

Weakness, sensory loss, absent reflexes

Symptoms are more severe and prolonged than in AMAN.

113
Q

What is Miller Fisher Syndrome (MFS) and its key symptoms?

A

A rare variant of GBS with ophthalmoplegia, ataxia, and areflexia

MFS typically starts at the head and face and usually does not involve weakness.

114
Q

What antibodies are linked to Miller Fisher Syndrome?

A

Anti-GQ1b antibodies

These antibodies are associated with the pathology of MFS.

115
Q

What is the Pharyngeal-Cervical-Brachial Variant of GBS characterized by?

A

Weakness in the neck, face, and arms with normal leg reflexes

This variant affects specific muscle groups without impacting leg reflexes.

116
Q

What are the features of Bickerstaff Brainstem Encephalitis?

A

Overlap with Miller Fisher, includes reduced consciousness and brainstem dysfunction

This condition presents symptoms similar to MFS but with additional neurological impairments.

117
Q

What is the key difference in pathology between AIDP and AMAN/AMSAN?

A

AIDP involves demyelination while AMAN/AMSAN involves axonal degeneration

This fundamental difference affects the clinical presentation and recovery.

118
Q

What triggers AIDP compared to AMAN/AMSAN?

A

AIDP is triggered by general infections; AMAN/AMSAN is specifically associated with Campylobacter jejuni

The triggers can influence the prevalence of each form in different geographic regions.

119
Q

How does sensory involvement differ between AIDP and AMSAN?

A

Sensory involvement is mild or absent in AIDP; present in AMSAN

This distinction helps in the clinical diagnosis of the different forms.

120
Q

Which form of Guillain-Barré Syndrome typically has a faster recovery rate?

A

Acute Inflammatory Demyelinating Polyneuropathy (AIDP)

Recovery is faster in AIDP because myelin regrows more quickly than axons regenerate.

121
Q

True or False: Reflexes are absent in both AIDP and AMAN/AMSAN.

A

True

Both conditions exhibit absent reflexes in the affected areas.

UKMLA Prep (46 decks)

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