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CHHD > Geriatric Medicine > Flashcards

Geriatric Medicine Flashcards

1
Q

What age groups does geriatric medicine tackle

A

Over 75s

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2
Q

What changes to pharmacokinetics (how body deals with drug) can happen with age

A
  • Reduced volume of drug distribution
  • Reduced liver metabolism
  • Reduced renal blood flow and mass reduced clearance of water soluble drugs
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3
Q

What changes to the pharmacodynamics (what drug does to the body) can occur with age

A

Increased sensitivity of body to drugs

Lower doses often needed

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4
Q

AY BAWS CAN I HABE DE NOTE PLZ

A

In geriatrics never stop at a single diagnosis and always consider several co-existing conditions

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5
Q

What common things often complicate drugs administration and diagnoses in geriatric patients

A

Polypharmacy

Pre-existing disease

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6
Q

What is the atypical presentation of geriatric problems

A
  • Frequently present general deterioration, functional decline
  • Acute disease may be hidden but precipitates impairment in other systems
  • Falls, confusion, reduced mobility are likely to be medical problems in disguise
  • Different illnesses can present as one of ‘geriatric giants’
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7
Q

What are considered the ‘geriatric giants’ - symptoms of geriatric disease

A
  • Incontinence
  • Immobility
  • Instability
  • Intellectual impairment
  • Iatrogenic disease
  • Infection
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8
Q

What is osteoporosis

A

Skeletal disease with low bone mass and micro deterioration of bone tissue - more fragile and susceptible to fracture

Slow and progressive and symptomatic reduction in skeletal tissue until fracture occurs

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9
Q

What are the common fracture sites in osteoporosis and what symptoms arise with it

A

Common sites - spine, wrist, hip

Symptoms - pain, disability, loss of independence, premature death

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10
Q

Describe the aetiologies of osteoporosis

A
  • Mainly affects post-menopausal women as a result of oestrogen deficiency
  • In men 50% of cases associated with hypogonadism, corticosteroid treatment, alcohol excess
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11
Q

What are some non-modifiable risk factors of osteoporosis

A
  • Female
  • Family history of osteoporosis
  • Caucasian or asian ethnicity
  • Age > 65 years
  • Previous fragility fracture
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12
Q

What are some modifiable risk factors of osteoporosis

A
  • Low BMI
  • Smoking
  • Alcohol excess
  • Low calcium intake and vitamin D deficiency
  • Inactivity
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13
Q

What are some hormonal risk factors of osteoporosis

A
  • Menopause before age 45 years

- Male hypogonadism

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14
Q

What are some drug-related risk factors of osteoporosis

A
  • Glucocorticoids
  • Anticonvulsants
  • Cytotoxic therapy
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15
Q

What are some secondary causes of osteoporosis

A
  • Rheumatoid arthritis
  • Hyperthyroidism
  • Malabsorption
  • Chronic liver disease
  • Primary hyperparathyroidism
  • Prolonged immobilisation
  • Anorexia nervosa
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16
Q

What diagnosis methods are there for osteoporosis

A
  • Marked osteopenia on plain x-ray
  • Previous fragility fracture
  • Identification of risk factors for osteoporosis
  • Standard for diagnosis is assessment of bone mineral density by axial dual energy X-ray absorptiometry (DEXA scan)
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17
Q

What is the action of vitamin D and bone health

A
  • Regulates calcium and phosphate absorption and metabolism
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18
Q

How is most vitamin D produced

A

Through action of sunlight on skin to produce vitamin D3 - some from meat and vegetables

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19
Q

What symptoms are there for vitamin D deficiency

A

Asymptomatic, muscular aches and bone pains and osteomalacia

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20
Q

What lifestyle changes can be treatment for osteoporosis

A
  • Smoking cessation, alcohol moderation
  • Healthy balanced diet with good calcium intake
  • Appropriate sun exposure
  • Low salt intake
  • Id oral corticosteroids required low dose and use of steroid sparing agents
  • Regular weight-bring exercise
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21
Q

What pharmacological treatments are there for osteoporosis

A
  • Calcium and vitamin D supplements
  • Bisphosphonates e.g. alendronate, etidronate, risedronate
  • Raloxifene
  • Teriparatide
  • Calcitonin
  • Strontium ranelate
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22
Q

What are the effects of bisphosphonates on bone health

A
  • Reduces rate of bone turnover
  • Alendronate can cause oesophagitis and oral ulceration
  • Concern over potential MRONJ
23
Q

Why is HRT no longer used for long term osteoporosis treatment

A

Risk of breast cancer and cardiovascular disease

24
Q

Describe the features/characteristics of B/MRONJ

A
  • 90% of cases associated with cancer treatment IV BP
  • Mandible more commonly involved
  • Asymptomatic or painful
  • Multifocal presentations reported
  • Preceded by surgical intervention or extraction in 60%
  • Exposed bone - secondary infection can lead to sinuses or fistulae
25
Q

What are the indications for the use of bisphosphonates

A
  • Prevention and treatment of osteoporosis in post-menopausal women
  • Prophylaxis of corticosteroid-associated osteoporosis
  • Treatment of hypercalcaemia of malignancy
  • Management of bone metastases e.g. breast cancer
  • Management of osteolytic lesion in multiple myeloma
  • Management of Paget’s disease
26
Q

What bisphosphonates could be used for osteoporosis

A

Alendronate

Ibandronate

27
Q

What bisphosphonate would be used for pagets disease of bone

A

Risedronate

28
Q

What bisphosphonate would be used for corticosteroid associated osteoporosis

A

Etidronate

29
Q

What bisphosphonate would be used for hypercalcaemia of malignancy

A

Pamidronate

30
Q

What bisphosphonate would be used for osteolytic lesions

A

Zoledronate

31
Q

What are the clinical presentations of B/MRONJ

A
  • Delayed healing following a dental extraction or other oral surgery
  • Pain, soft tissue infection and swelling
  • Numbness, paraesthesia
  • Exposed bone
  • Non-exposed variant
32
Q

What are the management options of B/MRONJ

A
  • Identify patients at risk and educate
  • If surgical intervention necessary atraumatic technique
  • Stop BSP treatment, nutritional supplements, hyperbaric oxygen, chlorhexidine, systemic antibiotics
33
Q

What are the 2 main types of transient ischaemic attack and stroke

A 
Cerebral infarction (80%)
Intracerebral haemorrhage (15%) (incl. subarachnoid haemorrhage 5%)
34
Q

Describe cerebral infarction

A
  • Blockage of arterial blood supply by small vessel occlusion, artherothromboembolism e.g. from carotids or embolisation e.g. from atrial fibrillation, MI
  • results in disturbance to neuronal electrical activity (reversible) and cellular membrane integrity (irreversible)
35
Q

Describe intracerebral haemorrhage

A

Rupture of blood vessels in brain tissue -> direct neuronal injury and cerebral oedema

36
Q

What are some of the risk factors of cerebrovascular accidents

A
  • Hypertension
  • Smoking
  • Diabetes mellitus
  • Heart disease (Valvular ischaemic, atrial fibrillation)
  • Peripheral vascular disease
  • Past TIA/stroke
  • Polycythaemia
  • Carotid bruit
  • OCP
  • Hyperlipidaemia
  • Alcoholism
37
Q

How long do Transient Ischaemia Attacks last for (TIA)

A

Neurological signs and symptoms resolve within 24 hours - embolic

38
Q

What are the clinical features of Stroke/TIA

A
  • Involves sudden onset of a focal neurological deficit
  • Occasionally with further progression over hours
  • Ensuing disability relates to distribution of affected artery but collateral supplies may make this less clear
  • Difficult to distinguish ischaemic and haemorrhagic stroke clinically
39
Q

What are the clinical features of stroke/TIA in the anterior (carotid) circulation

A
  • Cortical dysfunction: dysphasia, sensory or visual inattention, hemianopia
  • Monoccular blindness
  • Unilateral weakness
  • Unilateral sensory disturbance
  • Dysarthria
  • Neuromuscular dysphagia
40
Q

What are the clinical features of stroke/TIA in the posterior (vertebrobasilar) circulation

A
  • Cranial nerve palsy
  • Ataxia/incoordination/disequilibrium
  • Diplopia
  • Bilateral visual loss
  • Unilateral/bilateral weakness or sensory disturbance
  • Dysarthria
  • Neuromuscular dysphagia
41
Q

What are the acute management options for stroke/TIA

A
  • Maintain patients airway - avoid hypoxia or aspiration
  • Monitor blood glucose (between 4-11)
  • Monitor BP - treatment of even very high BPs may be more harmful
  • Urgent CT/MRI - if thrombolysis considered, high risk of haemorrhage, unusual presentation
  • Nil by mouth
  • antiplatelet agents - once haemorrhagic stroke excluded
42
Q

What secondary prevention strats are there for stroke/TIA

A
  • Antiplatelet agents - aspirin, clopidogrel, dipyridamole
  • Anticoagulation - atrial fibrillation - warfarin
  • Risk factor management - hypertension, lipids, smoking, dietary advice - salt restriction
43
Q

AY BAWS CAN I HABE DE NOT PLZ

A

1/3 of stroke survivors will suffer a further stroke

44
Q

What is the definition of dementia

A
  • Acquired, global and progressive impairment of mental function
45
Q

Describe the presentation of dementia

A
  • Initial presentation is of memory loss over months or years
  • in later stages non-cognitive symptoms like agitation, aggression or apathy become apparent
  • May also be wandering, hallucinations, slow repetitive speech, mood disturbance
46
Q

Name some types of dementia

A
  • Alzeheimer’s disease
  • Vascular dementia
  • Dementia with Lewy Bodies
  • Fronto-temporal dementia syndrome
  • Other
47
Q

What are some rare causes of dementia

A
  • Hypothyroidism
  • Reduced vitamin B12/ folate/ thiamine (alcoholism)
  • Depression
  • Syphilis
  • Tumours
  • Parkinsons
  • HIV
  • Pellagra
48
Q

What is the most common form of vascular dementia

A

Multi-infarct dementia

49
Q

Describe multi-infarct dementia

A

Typically step-wise with periods of sudden decline interspersed with periods of relative stability

50
Q

What is the mean survival time from the onset of alzheimer’s disease

A

7 years

51
Q

Describe the presentation of alzheimer’s disease

A
  • Enduring, progressive and global cognitive impairment
  • Impaired visuospatial skill, memory, verbal abilities, planning abilities and lack of insight
  • Later - irritability, mood disturbance, behavioural change, psychosis, agnosia
  • Finally become sedentary and take no interest
52
Q

What is the cause of alzheimer’s disease

A
  • Accumulation of Beta amyloid peptide (degradation product of amyloid precursor protein)
  • Results in progressive neuronal damage, neurofibrillary tangles, amyloid plaques, loss of neurotransmitter acetylcholine
  • May also be vascular effects
53
Q

What management options are there for alzheimer’s disease

A
  • Symptoms may be magnified by unfamiliar environments or people
  • Develop routines
  • Acetylcholinesterase inhibitors e.g. done-evil, rivastigmine
  • Meticulous BP control
  • Treat depression
  • Avoid drugs which will exacerbate cognitive impairment

CHHD (27 decks)

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