Medicine of older adult 👵🏼 Flashcards

Condition and presentation (121 cards)

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
Acute confusional state
* 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
26
Pre-disposing factors for ACS
* age > 65 years * background of dementia * significant injury e.g. hip fracture * frailty or multimorbidity * polypharmacy
27
Multifactoral events which can lead to ACS
* 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
28
Features of ACS
* memory disturbances (loss of short term > long term) * may be very agitated or withdrawn * disorientation * mood change * visual hallucinations * disturbed sleep cycle * poor attention
29
ACS managment
* 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
30
Olazapine side effects
* weight gain * increased appetite * sedation * dry mouth * Ortostatic hypertension * Extrapyrimidal symptoms * constipation * dry mouth * elevated liver enzyme * WCC change
31
Dementia with Lewy bodies (DLB)
rogressive, complex condition, accounting for approximately 10-15% of dementia cases.
32
Featured of DLB
* **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.
33
LBD vs Dementia
if cognitive impairment and parkinsonism develop <1 year of each other, it is likely LBD.
34
DLB investigations
* **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.
35
Managment of DLB
* **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.
36
Complications of DLB
* **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. ## Footnote ``
37
Trimethoprim and renal function
* 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
38
Psychotic features (3)
- hallucinations (e.g. auditory) - delusions - thought disorganisation - agitation/aggression - neurocognitive impairment (e.g. in memory, attention or executive function) - depression - thoughts of self-harm
39
thought disorganisation
- alogia: little information conveyed by speech - tangentiality: answers diverge from topic - clanging - word salad: linking real words incoherently → nonsensical content
40
conditions linked with psychosis
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
41
auditory hallucinations in schizophrenia
- two or more voices discussing the patient in the third person - thought echo - voices commenting on the patient's behaviour
42
examples of thought disorders
- thought insertion - thought withdrawal - thought broadcasting
43
Passivity phenomena:
- bodily sensations being controlled by external influence - actions/impulses/feelings - experiences which are imposed on the individual or influenced by others
44
Delusional perceptions
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'
45
features of scizophrenia
- 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
46
5 key principles of the MCA
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
47
Risk factors of BHP
- 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
48
voiding symptoms (obstructive): (BHP)
weak or intermittent urinary flow straining hesitancy terminal dribbling incomplete emptying
49
BHP storage symptoms (irritative)
urgency frequency urgency incontinence nocturia
50
Post micturition BHP
dribbling
51
complications of BHP
urinary tract infection retention obstructive uropathy
52
International Prostate Symptom Score (IPSS)
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
Assessment of BPH
- Urine dip - U&Es - PSA - urinary frequency chart -IPPS
54
Managment of BPH
- 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
alpha-1 antagonists e.g. tamsulosin, alfuzosin
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
5 alpha-reductase inhibitors e.g. finasteride
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
risk factors of urinary incontinence
advancing age previous pregnancy and childbirth high body mass index hysterectomy family history
58
inital investigations of urinary incontinence
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
Managment of UI
- 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
Stress incontinence managment
- pelvic floor training - surgical procedures - duloxetine
61
Duloxetine
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
Nocturnal enuresis managment
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
delirium predisposing factors
age > 65 years background of dementia significant injury e.g. hip fracture frailty or multimorbidity polypharmac
64
precipitating effects for delirium
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
features of delirium
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
Managment of delirium
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
Managment of Lewy body dementia
both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer's. Avoid neuroleptics
68
features of Lewy body dementia
progressive cognitive impairment parkinsonism visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
69
diagnosis of Lewy body demenita
usually clnical - PET scan be used
70
factors that predispose to pressure sores
malnourishment incontinence: urinary and faecal lack of mobility pain (leads to a reduction in mobility)
71
Managment of pressure sores
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
how many grades of the waterlow score is there?
4
73
waterlow grade 1
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
Waterlow grade 2
Partial thickness skin loss involving epidermis or dermis, or both. The ulcer is superficial and presents clinically as an abrasion or blister
75
Waterlow grade 3
Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
76
Waterlow grade 4
Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss
77
Managment of malnutrition
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
Features of pulmonary oedema of CXR
- 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
What is this showing?
Pulmonary oedema
80
causes of decreased BNP levels
Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists
81
Causes of increases BNP levels
Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis
82
Managment of CHF
- ACE-inhibitor and a beta-blocker - second line: aldosterone antagonist - SGLT-2 inhibitors - third line must be started by a specialist.
83
CHF specialist drugs
vabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin and cardiac resynchronisation therapy
84
Important immunisation managment of CHF
- annual influenza vaccine - one-off pneumococcal vaccin those with splenic or rCHD should have vaccine every 5 years
85
Systolic dysfunction CHF
Ischaemic heart disease Dilated cardiomyopathy Myocarditis Arrhythmias
86
Diastolic dysfunction CHF link conditions
Hypertrophic obstructive cardiomyopathy Restrictive cardiomyopathy Cardiac tamponade Constrictive pericarditis
87
High output HF
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
What is the most common form of Guillain-Barré Syndrome in Europe and North America?
Acute Inflammatory Demyelinating Polyneuropathy (AIDP) ## Footnote AIDP is characterized by an immune-mediated attack on the myelin sheath of peripheral nerves.
89
What immune cells are key players in AIDP?
T-cells and macrophages ## Footnote These cells are involved in the immune-mediated attack on the myelin sheath.
90
What are the main symptoms of Acute Inflammatory Demyelinating Polyneuropathy (AIDP)?
Progressive, symmetrical ascending weakness, loss of reflexes, mild or absent sensory involvement ## Footnote Symptoms typically start in the legs and progress to the arms.
91
Which form of Guillain-Barré Syndrome is more common in Asia and associated with Campylobacter jejuni infection?
Acute Motor Axonal Neuropathy (AMAN) ## Footnote AMAN involves an immune attack on the axons of motor nerves.
92
What is the primary pathology of AMAN?
Immune system attacks axons of motor nerves directly ## Footnote Unlike AIDP, which targets myelin, AMAN targets the axons.
93
What are the symptoms of Acute Motor Axonal Neuropathy (AMAN)?
Pure motor weakness without sensory loss, absent reflexes ## Footnote Recovery may take longer than in AIDP due to the nature of axonal damage.
94
What distinguishes Acute Motor and Sensory Axonal Neuropathy (AMSAN) from AMAN?
Both motor and sensory axons are affected ## Footnote AMSAN has a worse prognosis due to extensive axonal involvement.
95
What are the main symptoms of AMSAN?
Weakness, sensory loss, absent reflexes ## Footnote Symptoms are more severe and prolonged than in AMAN.
96
What is Miller Fisher Syndrome (MFS) and its key symptoms?
A rare variant of GBS with ophthalmoplegia, ataxia, and areflexia ## Footnote MFS typically starts at the head and face and usually does not involve weakness.
97
What antibodies are linked to Miller Fisher Syndrome?
Anti-GQ1b antibodies ## Footnote These antibodies are associated with the pathology of MFS.
98
What is the Pharyngeal-Cervical-Brachial Variant of GBS characterized by?
Weakness in the neck, face, and arms with normal leg reflexes ## Footnote This variant affects specific muscle groups without impacting leg reflexes.
99
What are the features of Bickerstaff Brainstem Encephalitis?
Overlap with Miller Fisher, includes reduced consciousness and brainstem dysfunction ## Footnote This condition presents symptoms similar to MFS but with additional neurological impairments.
100
What is the key difference in pathology between AIDP and AMAN/AMSAN?
AIDP involves demyelination while AMAN/AMSAN involves axonal degeneration ## Footnote This fundamental difference affects the clinical presentation and recovery.
101
What triggers AIDP compared to AMAN/AMSAN?
AIDP is triggered by general infections; AMAN/AMSAN is specifically associated with Campylobacter jejuni ## Footnote The triggers can influence the prevalence of each form in different geographic regions.
102
How does sensory involvement differ between AIDP and AMSAN?
Sensory involvement is mild or absent in AIDP; present in AMSAN ## Footnote This distinction helps in the clinical diagnosis of the different forms.
103
Which form of Guillain-Barré Syndrome typically has a faster recovery rate?
Acute Inflammatory Demyelinating Polyneuropathy (AIDP) ## Footnote Recovery is faster in AIDP because myelin regrows more quickly than axons regenerate.
104
True or False: Reflexes are absent in both AIDP and AMAN/AMSAN.
True ## Footnote Both conditions exhibit absent reflexes in the affected areas.
105
What is the most common form of Guillain-Barré Syndrome in Europe and North America?
Acute Inflammatory Demyelinating Polyneuropathy (AIDP) ## Footnote AIDP is characterized by an immune-mediated attack on the myelin sheath of peripheral nerves.
106
What immune cells are key players in AIDP?
T-cells and macrophages ## Footnote These cells are involved in the immune-mediated attack on the myelin sheath.
107
What are the main symptoms of Acute Inflammatory Demyelinating Polyneuropathy (AIDP)?
Progressive, symmetrical ascending weakness, loss of reflexes, mild or absent sensory involvement ## Footnote Symptoms typically start in the legs and progress to the arms.
108
Which form of Guillain-Barré Syndrome is more common in Asia and associated with Campylobacter jejuni infection?
Acute Motor Axonal Neuropathy (AMAN) ## Footnote AMAN involves an immune attack on the axons of motor nerves.
109
What is the primary pathology of AMAN?
Immune system attacks axons of motor nerves directly ## Footnote Unlike AIDP, which targets myelin, AMAN targets the axons.
110
What are the symptoms of Acute Motor Axonal Neuropathy (AMAN)?
Pure motor weakness without sensory loss, absent reflexes ## Footnote Recovery may take longer than in AIDP due to the nature of axonal damage.
111
What distinguishes Acute Motor and Sensory Axonal Neuropathy (AMSAN) from AMAN?
Both motor and sensory axons are affected ## Footnote AMSAN has a worse prognosis due to extensive axonal involvement.
112
What are the main symptoms of AMSAN?
Weakness, sensory loss, absent reflexes ## Footnote Symptoms are more severe and prolonged than in AMAN.
113
What is Miller Fisher Syndrome (MFS) and its key symptoms?
A rare variant of GBS with ophthalmoplegia, ataxia, and areflexia ## Footnote MFS typically starts at the head and face and usually does not involve weakness.
114
What antibodies are linked to Miller Fisher Syndrome?
Anti-GQ1b antibodies ## Footnote These antibodies are associated with the pathology of MFS.
115
What is the Pharyngeal-Cervical-Brachial Variant of GBS characterized by?
Weakness in the neck, face, and arms with normal leg reflexes ## Footnote This variant affects specific muscle groups without impacting leg reflexes.
116
What are the features of Bickerstaff Brainstem Encephalitis?
Overlap with Miller Fisher, includes reduced consciousness and brainstem dysfunction ## Footnote This condition presents symptoms similar to MFS but with additional neurological impairments.
117
What is the key difference in pathology between AIDP and AMAN/AMSAN?
AIDP involves demyelination while AMAN/AMSAN involves axonal degeneration ## Footnote This fundamental difference affects the clinical presentation and recovery.
118
What triggers AIDP compared to AMAN/AMSAN?
AIDP is triggered by general infections; AMAN/AMSAN is specifically associated with Campylobacter jejuni ## Footnote The triggers can influence the prevalence of each form in different geographic regions.
119
How does sensory involvement differ between AIDP and AMSAN?
Sensory involvement is mild or absent in AIDP; present in AMSAN ## Footnote This distinction helps in the clinical diagnosis of the different forms.
120
Which form of Guillain-Barré Syndrome typically has a faster recovery rate?
Acute Inflammatory Demyelinating Polyneuropathy (AIDP) ## Footnote Recovery is faster in AIDP because myelin regrows more quickly than axons regenerate.
121
True or False: Reflexes are absent in both AIDP and AMAN/AMSAN.
True ## Footnote Both conditions exhibit absent reflexes in the affected areas.