General Medicine (including COTE) Flashcards
Renal causes of hypovolaemic hyponatraemia
Diuretics - thiazide + loop diuretics
Mineralocorticoid insufficiency e.g. Addison’s
Osmotic diuresis e.g. low glucose, urea
Nephropathy
Causes of euvolaemic hyponatraemia
SIADH
Abnormal ADH release e.g. hypothyroidism,
Psychogenic polydipsia
Other - high water, lower solute intake e.g. anorexia nervosa
Hypovolaemic causes of hyponatraemia
GI losses - diarrhoea, vomiting, pancreatitis
Skin losses - sweating, burns
Renal losses - diuretics, nephropathy
Other - Addison’s disease, sepsis
Hypervolaemic causes of hyponatraemia
Failures (heart, liver, renal)
Nephrotic syndrome
Clinical features of hyponatraemia
Headache
Confusion
N+V
Lethargy
Irritability
Seizures/LOC/Coma
Often asymptomatic
Outcome of urine tests in SIADH
High urine osmolality
High urine sodium
(Low serum sodium)
Management of SIADH
Stop offending medication if relevant (usualyl diuretics)
Fluid restriction
Tolvaptan - ADH receptor blocker
Potential complication of treating severe hyponatraemia too quickly
Central pontine myelinolysis (osmotic demyelination syndrome)
Medications that most commonly cause hyponatraemia
Diuretics - especially thiazide + loop diuretics
SSRIs esp citalopram
Antipsychotics e.g. haloperidol + phenothiazines
Carbamazepine
PPIs
ACE inhibitors
Blood tests in confusion screen
FBC: WCC for infection
CRP (infection)
U+Es (Uraemia + hyponatraemia)
Bone profile (hyper/hypocalcaemia)
B12/Folate (deficiency)
TFTs (hypothyroid)
Glucose
LFTs (hepatic encephalopathy)
Coagulation/INR (intracranial bleed)
What indicates a significant postural drop in hypotension
> 20 systolic drop
10 diastolic drop
Within 3 minutes from lying to standing
Post-ACS medications
Block An ACS
- Beta blocker
- ACEi
- Aspirin
- Clopidogrel
- Statin
Risk factors for dementia
Genetics - family history
Insulin resistance e.g. T2DM
Atherosclerosis
Hypothyroidism
Depression
History of head injury
HIV
PD
DSM-IV criteria for dementia
Decline in memory and learning (on tests)
One of:
- Aphasia
- Apraxia
- Agnosia
- Reduced executive function
Symptoms interfere with functioning
Gradual onset + continual decline
No known organic cause
Not due to delirium
Not due to mental health disorder e.g. depression
Differential diagnosis of dementia
Normal reduced cognition of advanced age
Delirium
Depression
Drug abuse/side effect
Medical disorders
Medical disorder differentials of dementia
Anaemia
Hypothyroidism
Cerebral tumours/metastases
Syphilis (neurosyphilis)
Amyloidosis
Creutzfeldt-Jakob disease
Poor nutrition
Features of Lewy-body dementia
Progressive cognitive impairment - persistent memory dysfunction not apparent in early stages
Cognition may be fluctuating, with lucid periods
Parkinsonism (typically develops after cognitive impairment)
Visual hallucinations (may have other symptoms e.g. delusions)
Depression + sleep disturbance
Pathology of Lewy-body dementia
Alpha-synuclein cytoplasmic inclusions (Lewy bodies)
In the substantia nigra, paralimbic + neocortical areas
Management of Lewy body dementia
Acetylcholinesterase inhibitors e.g. donepezil, rivastigmine
or Memantine (NMDA receptor amtagonist)
Medications to be avoided in Lewy body dementia
First generation antipsychotics - may develop irreversible parkinsonism
e.g. haloperidol
Risk factors for Alzheimer’s disease
Increasing age
FHx
5% cases inherited autosomal dominant
Caucasian ethnicity
Down’s syndrome
Apoprotein E allele E4
Macroscopic pathological changes in Alzheimer’s disease
Widespread cerebral atrophy
Particularly cortex + hippocampus
Microscopic pathological changes in Alzheimer’s disease
Cortical plaques due to deposition of type A-beta-amyloid protein
Intraneuronal neurofibrillary tangles
Caused by abnormal aggregation of the tau protein
Pharmacological management of Alzheimer’s disease
Acetylcholinesterase inhibitors e.g. donepezil, rivastigmine, and galantamine - for mild to moderate disease
2nd line: memantine (NMDA receptor antagonist)
- Moderate AD if intolerant of, or acetylcholinesterase inhibitors contraindicated
- Add on in moderate or severe
- Monotherapy in severe disease
Contraindications/side effects of donepezil
Relatively contraindicated in bradycardia
Adverse effects include insomnia
What is Pick’s disease
Dementia caused by localised atrophy of the frontal and temporal lobes
Blood tests done in a patient with suspected dementia to exclude reversible causes
FBC
U+E
LFTs
Calcium
Glucose
ESR/CRP
TFTs
Vitamin B12 + folate levels
Features of frontotemporal dementia/Pick’s disease
Personality change
Impaired social conduct
Hyperorality
Disinhibition
Increased appetite
Perseveration behaviours
More common in patients under 65
Memory problems tend to occur later
Macroscopic changes in Pick’s disease/FTD
Atrophy of the frontal and temporal lobes
Microscopic changes in Pick’s disease/FTD
Pick bodies - spherical aggregations of tau protein
Gliosis
Neurofibrillary tangles
Senile plaques
Assessment tool for frailty status
PRISMA-7
What is frailty
State of impaired homeostasis –> increased vulnerability to minor stressor events
Elements of PRISMA-7 assessment
Age
Sex
Health problems
Help at home
Mobility
Social support
What is multimorbidity
The presence of two, or more, long-term health conditions