Passmed geriatrics Flashcards

1
Q

acute confusional state predisposing fx

A

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

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2
Q

acute confusional state precipitating fx

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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3
Q

clinical fx acute confusional state

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may be very agitated or withdrawn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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4
Q

how to manage acute confusional state
- non medical
- medical

A

tx underlying cause - ie, constipation
modify environment - side room
1st line for delirium - haloperidol or olanzapine, except in parkison’s - reduction of parkinson meds and if require urgent tx then atypical antipsychotics (quetiapine, clozapine)

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5
Q

non pharmacological mx of alzheimer’s

A

activities to promote wellbeing
cognitive stimulation therapy
group reminiscence therapy and cognitive rehab

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6
Q

pharmacological mx of alzheimer’s

A

acetylcholinesterase inhibitors - donepezil, galantamine, rivastigmine
2nd line - memantine (NMDA receptor antagonist) - used when intolerant of 1st line, as an add on in severe, or monotherapy in severe

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7
Q

mx non cognitive sx of alzheimer’s

A

NO ANTIDEPRESSANTS
antipsychotics used if risk of harming themselves, agitation, hallucination, delusions

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8
Q

other tx options of alzheimer’s

A

donepezil

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9
Q

donepezil c/i and adverse effect

A

in pts with bradycardia
s/e - insomnia

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10
Q

alzheimer’s risk fx

A

increasing age
family history of Alzheimer’s disease
5% of cases are inherited as an autosomal dominant trait
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome

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11
Q

macroscopic changes in alzheimer’s

A

widespread cerebral atrophy, particularly involving the cortex and hippocampus

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12
Q

microscopic change alzheimer’s

A

cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
hyperphosphorylation of the tau protein

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13
Q

biochemical changes alzheimer’s

A

a deficit of acetylcholine from damage to an ascending forebrain projection

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14
Q

define neurofibrillary tangles and how affect in AD

A

paired helical filaments are partly made from a protein called tau
tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
in AD are tau proteins are excessively phosphorylated, impairing its function

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15
Q

factors favouring delirium over dementia

A

acute onset
impairment of consciousness
fluctuation of symptoms: worse at night, periods of normality
abnormal perception (e.g. illusions and hallucinations)
agitation, fear
delusions

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16
Q

order of prev in dementia types

A

1.alzheimers
2. vascular
3. lewy body

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17
Q

assessment tools for dementia

A

10-point cognitive screener (10-CS), 6-Item cognitive impairment test (6CIT)

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18
Q

other ways to assess dementia but not NICE recommended

A

abbreviated mental test score (AMTS), General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE)

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19
Q

MMSE score indicated dementia

A

24 or less /30

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20
Q

dementia ix

A

blood screen to exclude reversible causes - FBC, UE, LFT, calcium, ESR/CRP, TFT, vit B12, folate
neuroimaging - subdural haematoma, normal pressure hydrocephalus

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21
Q

rare causes of dementia

A

Huntington’s
CJD
Pick’s disease (atrophy of frontal and temporal lobes)
HIV (50% of AIDS patients)

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22
Q

ddx dementia

A

hypothyroidism, Addison’s
B12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates

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23
Q

what parts of body involve normal gait

A

The neurological system - basal ganglia and cortical basal ganglia loop.
The musculoskeletal system (which must have appropriate tone and strength).
Effective processing of the senses such as sight, sound, and sensation (fine touch and proprioception).

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24
Q

risk fx for falling

A

Lower limb muscle weakness
Vision problems
Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson’s disease etc)
Polypharmacy (4+ medications)
Incontinence
>65
Have a fear of falling
Depression
Postural hypotension
Arthritis in lower limbs
Psychoactive drugs
Cognitive impairment

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25
what establish from falls hx
Where was the patient when they fell? When did they fall? Did anyone else see the patient fall? (collateral history) What happened? Were there any associated features before/during/after Why do they think they fell? Have they fallen before? Systems review Past medical history (especially issues related to balance/sight/gait) Social history
26
meds that cause postural hypotension
nitrates diuretics anticholinergics antidepressants beta blockers L-Dopa ACEi
27
meds that cause falls due to other mechanisms
benzo antipsychotics opiates anticonvulsants codeine digoxin other sedatives
28
ix when someone falls
Bedside tests - Basic observations, blood pressure, blood glucose, urine dip and ECG Bloods - Full Blood Count, Urea and Electrolytes, Liver function tests and bone profile Imaging- X-ray of chest/injured limbs, CT head and cardiac echo
29
nice cks mx of falls to assess risk
Identify all individuals who have fallen in the last 12 months. As per above identify why they are at risk. For those with a falls history or at risk complete the 'Turn 180° test' or the 'Timed up and Go test'.
30
pts >65 when require MDT assessment
>2 falls in the last 12 months A fall that requires medical treatment Poor performance or failure to complete the 'Turn 180° test' or the 'Timed up and Go test'
31
3 types of frontotemporal lobar degeneration
Frontotemporal dementia (Pick's disease) Progressive non fluent aphasia (chronic progressive aphasia, CPA) Semantic dementia
32
common fx of frontotemporal lobar dementia
Onset before 65 Insidious onset Relatively preserved memory and visuospatial skills Personality change and social conduct problems
33
pick's disease clinical fx
personality change impaired social conduct hyperorality disinhibition increased appetite perseveration
34
pick's disease macroscopic changes
Focal gyral atrophy with a knife-blade appearance Atrophy of the frontal and temporal lobes
35
microscopic changes pick's disease
Pick bodies - spherical aggregations of tau protein (silver-staining) Gliosis Neurofibrillary tangles Senile plaques
36
avoid in pick's disease
AChE inhibitors or memantine
37
CPA clinical fx
non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.
38
semantic dementia clinical fx
fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer's memory is better for recent rather than remote events.
39
pathological fx in lewy body dementia
alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
40
clinical fx lewy body dementia
progressive cognitive impairment typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson's disease, where the motor symptoms typically present at least one year before cognitive symptoms cognition may be fluctuating, in contrast to other forms of dementia in contrast to Alzheimer's, early impairments in attention and executive function rather than just memory loss parkinsonism visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
41
how lewy body dementia diagnosed
clinical SPECT - single proton emission computed tomography
42
lewy body dementia mx
acetylcholinesterase inhibitors - donepezil, rivastigmine memantine neuroleptics avoided - can develop irreversible parkinsonism
43
definition of multimorbidity
The presence of two or more long-term health conditions, including: Defined physical or mental health conditions, learning disabilities, symptom complexes such as chronic pain, sensory impairments and alcohol or substance misuse
44
prevalence of comorbidity
higher in females combined mental and physical is more common in younger adults socioeconomic deprivation
45
most common comorbid conditions
HTN pain DM hearling loss depression anxiety IBS chronic pain prostate disorders thyroid disorders CAD
46
risk fx comorbid conditions
Increasing age Female sex Low socioeconomic status Tobacco and alcohol usage Lack of physical activity Poor nutrition and obesity
47
complications comorbid conditions
decreased QoL increased treatment burden mental health issues polypharmacy carers welfare
48
how frailty assesed
evaluation of gait speed, self-reported health status, or the PRISMA-7 questionnaire: The PRISMA-7 involves questions considering the age, sex, health problems, assistance required and walking aid use of the patient
49
mx of comorbid conditions
optimising care offer alternative f/u reduce no of high risk meds Consider a 'bisphosphonate holiday' in those taking bisphosphonates for longer than three years as there is no consistent evidence of continued benefits after this point. Discuss stopping bisphosphonates after 3 years and include patient choice, fracture risk and life expectancy in the discussion. STOPP/START tool individualised management plan education Use the action plan to follow up with the patient at agreed points: NHS England recommends a yearly review of all medications for people aged over 65, however, medications should be reviewed periodically to ensure that patients are being informed, given adequate laboratory tests and that treatments are optimised
50
define pressure ulcers
develop in patients who are unable to move parts of their body due to illness, paralysis or advancing age. They typically develop over bony prominences such as the sacrum or heel
51
risk fx of pressure ulcers
malnourishment incontinence lack of mobility pain (leads to a reduction in mobility)
52
risk of pressure score how assessed
The Waterlow score is widely used to screen for patients who are at risk of developing pressure areas. It includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.
53
grading of pressure ulcers
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 Grade 2 Partial thickness skin loss involving epidermis or dermis, or both. The ulcer is superficial and presents clinically as an abrasion or blister Grade 3 Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. Grade 4 Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss
54
mx of pressure ulcers
moist wound environment - hydrocolloid dressings and hydrogels avoid soap only swab wound and give abx if evidence of surrounding infection consider referral to tissue viability nurses may require surgical debridement
55
vascular dementia define
a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease
56
epidemiology vascular dementia
Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia. Incidence increases with age
57
main subtypes of vascular dementia
Stroke-related VD – multi-infarct or single-infarct dementia Subcortical VD – caused by small vessel disease Mixed dementia – the presence of both VD and Alzheimer’s disease
58
risk fx of vascular dementia
History of stroke or transient ischaemic attack (TIA) Atrial fibrillation Hypertension Diabetes mellitus Hyperlipidaemia Smoking Obesity Coronary heart disease A family history of stroke or cardiovascular
59
how can VD be inherited in rare cases
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.
60
clinical fx of vascular dementia
Several months or several years of a history of a sudden or stepwise deterioration of cognitive function Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms The difficulty with attention and concentration Seizures Memory disturbance Gait disturbance Speech disturbance Emotional disturbance
61
how diagnosed vascular dementia
clinical fx formal screen for cog impairment medical review to exclude medication cause MRI scan - infarcts and white matter changes
62
criteria for vascular dementia
NINDS-AIREN criteria: Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event established using clinical examination and neuropsychological testing Cerebrovascular disease defined by neurological signs and/or brain imaging A relationship between the above two disorders inferred by: the onset of dementia within three months following a recognised stroke an abrupt deterioration in cognitive functions fluctuating, stepwise progression of cognitive deficits
63
general mx of vascular dementia
address cardiovascular risk fx
64
non pharmacological tx of vascular dementia
cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
65
pharmacological tx of vascular dementia
no specific tx AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies. There is no evidence that aspirin or statins are effective
66
Reflex syncope definition
loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery
67
Types of reflex syncope
Vasovagal Situational - cough, micturition, GI Carotid sinus syncope
68
Vasovagal syncope clinical fx
Triggered by emotion, pain, stress Warm prior to loss of consciousness Brief myoclonus jerks can occur during uncomplicated 1-2 mins duration Prolonged fatigue in post octal is suggestive of other cause
69
Orthostatic syncope causes
primary autonomic failure: Parkinson's disease, Lewy body dementia secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia drug-induced: diuretics, alcohol, vasodilators volume depletion: haemorrhage, diarrhoea
70
Cardiac syncope causes
arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular) structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy others: pulmonary embolism
71
Syncope ix
cardiovascular examination postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic ECG for all patients other tests depend on clinical features patients with typical features, no postural drop and a normal ECG do not require further investigations
72
Malnutrition how common
10% in more than 65 yr olds
73
Malnutrition mx
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
74
1st line ix for stroke
NON CONTRAST CT
75
Stroke
See neuro flash cards
76
First line laxatives for constipation
bulk-forming laxative first-line, such as ispaghula
77
2nd line mx for constipation
Osmotic - macrogol
78
Causes of hypercalcaemia
Primary hyperparathyoidism Malignancy - s.c.c lung cancer, bone mets, myeloma, sarcoidosis, vitamin D intoxication acromegaly thyrotoxicosis Milk-alkali syndrome drugs: thiazides calcium-containing antacids dehydration Addison's disease Paget's disease of the bone usually normal in this condition but hypercalcaemia may occur with prolonged immobilisation
79
Clinical fx of hypercalcaemia
bones, stones, groans and psychic moans' corneal calcification shortened QT interval on ECG hypertension
80
ECG changes in hyperkalaemia
tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole
81
Causes of hyperkalaemia
acute kidney injury drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin** metabolic acidosis Addison's disease rhabdomyolysis massive blood transfusion Food Beta blockers if renal impairment LMWH
82
Mx of severe hyperkalaemia
IV calcium gluconate: to stabilise the myocardium insulin/dextrose infusion: short-term shift in potassium from ECF to ICF other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium
83
Ways to reduce hyperkalaemia including medications
stop exacerbating drugs e.g. ACE inhibitors treat any underlying cause lower total body potassium calcium resonium loop diuretics dialysis
84
Causes of hypernatraemia
dehydration osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma diabetes insipidus excess IV saline
85
Hypocalcaemia causes
vitamin D deficiency (osteomalacia) chronic kidney disease hypoparathyroidism (e.g. post thyroid/parathyroid surgery) pseudohypoparathyroidism (target cells insensitive to PTH) rhabdomyolysis (initial stages) magnesium deficiency (due to end organ PTH resistance) massive blood transfusion acute pancreatitis
86
Mx of hypocalcaemia
severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes intravenous calcium chloride is more likely to cause local irritation ECG monitoring is recommended further management depends on the underlying cause
87
Hypocalcameia clinical fx
tetany: muscle twitching, cramping and spasm perioral paraesthesia if chronic: depression, cataracts ECG: prolonged QT interval Trousseau's sign carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
88
Hypokalamia with alkalosis causes
vomiting thiazide and loop diuretics Cushing's syndrome Conn's syndrome (primary hyperaldosteronism)
89
Hypokalaemia wirh acidosis causes
diarrhoea renal tubular acidosis acetazolamide partially treated diabetic ketoacidosis
90
Hypomagnesaemia causes
drugs diuretics proton pump inhibitors total parenteral nutrition diarrhoea may occur with acute or chronic diarrhoea alcohol hypokalaemia hypercalcaemia e.g. secondary to hyperparathyroidism calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle metabolic disorders Gitleman's and Bartter's
91
Clinical fx of hypomagnesia
paraesthesia tetany seizures arrhythmias decreased PTH secretion → hypocalcaemia ECG features similar to those of hypokalaemia exacerbates digoxin toxicity
92
Tx of hypomagneasamia
<0.4 mmol/L or tetany, arrhythmias, or seizures intravenous magnesium replacement is commonly given. an example regime would be 40 mmol of magnesium sulphate over 24 hours >0.4 mmol/l oral magnesium salts (10-20 mmol orally per day in divided doses) diarrhoea can occur with oral magnesium salts
93
Low sodium blood, high urinary sodium causes
Sodium depletion, renal loss (patient often hypovolaemic) diuretics: thiazides, loop diuretics Addison's disease diuretic stage of renal failure Patient often euvolaemic SIADH (urine osmolality > 500 mmol/kg) hypothyroidism
94
Low serum and urine sodium causes
Sodium depletion, extra-renal loss diarrhoea, vomiting, sweating burns, adenoma of rectum Water excess (patient often hypervolaemic and oedematous) secondary hyperaldosteronism: heart failure, liver cirrhosis nephrotic syndrome IV dextrose psychogenic polydipsia
95
Acute hyponatraemia wirh severe sx tx
Patients with acute, severe (<120 mmol/L) or symptomatic hyponatraemia require close monitoring, preferably in an HDU or above setting. Hypertonic saline (typically 3% NaCl) is used to correct the sodium level more quickly than would be done in patients with chronic hyponatraemia.
96
Complication of tx of hyponatrameia
Osmotic demyelination syndrome (central pontine myelinolysis) can occur due to over-correction of severe hyponatremia pathophysiology: thought to develop secondary to astrocyte (and possibly oligodendrocyte) apoptosis astrocytes and oligodendrocytes (cells of the glial syncytium) are crucial for normal myelination chronic hyponatraemia → loss of osmotically active organic osmolytes (such as myoinositol, glutamate, glutamine) from astrocytes. These provide protection against cerebral oedema
97
What considered in ‘best interests’
1. Whether the person is likely to regain capacity and can the decision wait. 2. How to encourage and optimise the participation of the person in the decision. 3. The past and present wishes, feelings, beliefs, values of the person and any other relevant factors 4. Views of other relevant people
98
LPA what
The Act allows a person to appoint an attorney to act on their behalf if they should lose capacity in the future, replacing the current Enduring Power of Attorney (EPA)
99
LPA what decisions make
life-sustaining treatment if the LPA specifies that
100
Advance decision define
can be drawn up by anybody with capacity to specify treatments they would not want if they lost capacity. They may be made verbally unless they specify refusing life-sustaining treatment (e.g. Ventilation) in which case they need to be written, signed and witnessed to be valid. Advance decisions cannot demand treatment
101
1st line for osteoposis
Alendronate
102
drugs to be aware of in older persons
NSAIDS – not use systemically in older pts, with kidneys and sodium levels. Can be used in short term, PPI cover. Topical better Oral hypoglycaemics – gliclazide – risk of hypoglycaemia Antidepressants – SSRI carry risk of hyponatraemia and postural hypotension. Adjust dose, eg: half dose of citalopram Benzodiazepines and z drugs – confusion, cog impairment, falls. Can used short term and regular reviews Anticoagulation – dose appropriate, check indication Opioids – can cause CNS depression, confusion, falls, constipation. Short term use and regular reviews
103
older age affects in terms of drug
creatinine clearance reduced must be adjust for bmi
104
prescription cascade
treat side effects from each new drug introduced rather than consider new sx is a side effect and change medication
105
comprehensive geriatric assesment
see PP
106
anticholinergic burden
risk of falls and cognitive impairment dry mouth blurred vision contipation urinary retention
107
lots of meds
dosette box blister pack carousel tablet dispenser - audible reminder
108
cant see med box
speaking labels or large print
109
eye drops
opticare to assist
110
dementia hx
progression of sx home safety and accidents
111
further ix for dementia
mention cognitive tests
112
osteoporosis mx
alendronate vid d and calcium - combo
113
bppv dix hallpike positive findings
a positive test recreates the symptoms of benign paroxysmal positional vertigo rotatory nystagmus latency, torsional geotropic nystagmus, fatigue, habituation
114
meniere's patho
endolymph
115
bppv patho
caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal. They may be displaced by a viral infection, head trauma, ageing or without a clear cause. The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.
116