GERIATRICS Flashcards
DELIRIUM
What is delirium?
- Transient, acute syndrome characterised by disturbance of consciousness, perception, sleep-wake cycle, emotion + cognition
- Acute confusional state, fluctuates in severity, usually reversible
DELIRIUM
what are the causes of delirium?
PINCH ME –
- Pain
- Infection (UTI, pneumonia, septicaemia)
- Nutrition (thiamine, B12 + folate deficiency)
- Constipation (faecal impaction)
- Hydration (dehydrated)
- Metabolic/medication
- Environment/electrolytes (changes in environment, hyper/hypo Ca2+, Na+, K+)
DELIRIUM
What are some metabolic/medication causes of delirium?
- Hyper/hypo thyroid + glycaemia
- Hypercortisolaemia
- Substance misuse
- Withdrawal (incl. delirium tremens)
- Opioids, anticholinergics, Parkinson’s meds, steroids, BDZs, interactions
DELIRIUM
What are some other causes of delirium?
- Urinary retention, vascular events (CVA, MI)
DELIRIUM
Who are high risk patients that require screening on admission?
- > 65y, men, previous delirium
- Pre-existing cognitive deficit (dementia, PD, stroke)
- Sensory impairment (hearing/visual)
- Significant illness (hip #, cancer)
- Poor nutrition
- Hx of alcohol excess
DELIRIUM
What are the 2 sub-types of delirium?
Which is more dangerous?
- Hyperactive = agitated/aggressive, hallucinations, delusions, wandering + restless
- Hypoactive = withdrawn, quiet, lethargic, lacks concentration, slow
- Hypoactive as less likely to be recognised
DELIRIUM
What is the ICD-10 diagnostic criteria for delirium?
- Impaired consciousness + inattention (poor conc, memory deficit, “clouding of consciousness”)
- Perceptual OR cognitive disturbance (agitation, hallucinations > Lilliputian)
- Acute onset + fluctuating course (often worse at night = sundowning)
- Evidence it may be related to a physical cause
DELIRIUM
What are some other/non-specific features of delirium?
- Disinhibition
- Falls
- Loss of appetite
- Labile mood
DELIRIUM
What is a suitable screening tool for delirium?
4AT (≥4 = likely) –
- Alertness
- AMT4 (age, DOB, hospital name, year)
- Attention (list months backwards)
- Acute change or fluctuating course
DELIRIUM
What other cognitive tools can be used in the assessment of delirium/dementia?
- GP-COG (GP assessment of cognition)
- 6-CIT (6-item cognitive impairment test)
- AMT (abbreviated mental test)
- MOCA (Montreal Cognitive Assessment, <26/30)
- MMSE
- ACE-III
DELIRIUM
What general investigations would you do/enquiry about in a patient with delirium?
- Full physical exam
- Vitals (?sepsis), ECG
- Check if passed stools
- Check nutritional + hydration status
- Confusion screen
DELIRIUM
What is a confusion screen?
- FBC, B12 + folate, U+Es, Ca2+, ?phosphate, TFTs, LFTs, glucose, INR + clotting, blood + urine cultures, ?CRP/ESR
DELIRIUM
What other investigations or referral could you consider other than bloods?
- CXR or CT head if indicated
- Referral to memory clinic or old age psychiatrist
DELIRIUM
What is the mainstay of delirium management?
- Identify + treat cause with sufficient nutrition, hydration + mobilisation
- Maximise orientation + make environment safe + comforting
DELIRIUM
How should a patient be managed in the first instance?
Conservative de-escalation
- Talk to pt + listen to them
- Quiet bay or side room
- Big clocks, calendars, same staff members for orientation
- Family visits + personal belongings (pictures)
- Tx sensory impairments (glasses, hearing aids)
- Prevent ward changes
- Sleep hygiene (promote night sleep, not daytime)
DELIRIUM
Sometimes conservative de-escalation is inadequate and medications may be required. What are some options?
- Short-term antipsychotics – haloperidol 0.5mg or olanzapine
- Short-acting BDZ like lorazepam 0.5mg (caution may exacerbate confusion + over sedate)
- Long-acting BDZ if withdrawing (chlordiazepoxide, diazepam)
DEMENTIA
What is dementia?
- Syndrome of acquired, chronic, global impairment of higher brain function in an alert patient, which interferes with ability to cope with daily living
DEMENTIA
What are the 2 types of dementia and where is affected?
- Cortical dementias affect the cerebral cortex
- Subcortical dementia affect the basal ganglia + thalamus
DEMENTIA
How does cortical dementia present?
Give some examples.
- Memory impairment, dysphasia, visuospatial impairment (apraxia), problem solving + reasoning deficit
- AD, lewy-body, frontotemporal
DEMENTIA
How does subcortical dementia present?
Give some examples
- Psychomotor slowing, impaired memory retrieval, depression/apathy, executive dysfunction, personality change, language preserved
- PD, Huntington’s, alcohol-related + AIDS
DEMENTIA
How does delirium differ from dementia for…
i) deterioration?
ii) course?
iii) consciousness?
iv) thought content?
v) hallucinations?
i) Rapid (hours-days) + usually reversible vs. slow (months-years) + not reversible
ii) Acute + fluctuating vs. insidious + progressive
iii) Clouded vs. alert
iv) Vivid, complex + muddled vs impoverished
v) V common, visual vs. in 1/3rd, auditory/visual
DEMENTIA
What are some diagnostic features of dementia?
- Multiple cognitive deficits (memory, orientation, language, reasoning)
- Resulting impairment in ADLs (washing, dressing)
- Clear consciousness
- Other common Sx include behavioural + psychological Sx of dementia (BPSD), sleep issues (insomnia, daytime drowsiness, nocturnal restlessness)
DEMENTIA
What are behavioural + psychological symptoms of dementia (BPSD)?
What causes them?
- Heterogenous group of non-cognitive symptoms + behaviours seen in dementia
- Same causes as delirium
DEMENTIA
How does behavioural + psychological symptoms of dementia (BPSD) present?
- Anxiety/depression, agitation, psychosis (may think nurses out to get them), disinhibition
DEMENTIA
What are some general investigations for dementia?
- Full Hx + collateral with full physical exam + MSE
- Check for reversible causes with confusion screen ± CXR ± CT head
DEMENTIA
What might a MMSE score indicate in dementia?
MMSE (/30) –
- 21–26 = mild, 14–20 = mod, 10–14 mod-severe, <10 = severe cognitive impairment
DEMENTIA
What type of imaging may be used in dementia?
- SPECT to differentiate between Alzheimer’s + frontotemporal
- DaTscan shows ‘comma’ in normal but 2 dots in Lewy body + Parkinson’s dementia at the basal ganglia
DEMENTIA
What biological treatment can be used in dementia?
- Bio = risperidone for agitation (apart in Lewy-Body)
DEMENTIA
What social treatment can be used in dementia?
- OT assessment to remain independent (pendent, labels on cupboards, key safe, carers, handrails)
- Physio assessment
- Encourage family visits + photos
- Animal/pet therapy, music, arts + crafts
- Care plans + advanced directives before worsens
- Services – Dementia UK, Alzheimer’s society, Age UK, admiral nurses
ALZHEIMER’S DISEASE
What is the pathophysiology of Alzheimer’s disease?
- Accumulation of beta-amyloid peptide plaques which result in degeneration of cerebral cortex with cortical atrophy + loss of acetylcholine.
ALZHEIMER’S DISEASE
What is the onset of Alzheimer’s disease like and why?
- Insidious onset dementia due to generalised deterioration of the brain
ALZHEIMER’S DISEASE
What are the causes of Alzheimer’s disease?
- Unknown but most common type of dementia
ALZHEIMER’S DISEASE
What genes have been implicated to…
i) familial early-onset Alzheimer’s?
ii) late onset Alzheimer’s?
i) APP gene, presenilin 1 + 2 (autosomal dominant)
ii) Apolipoprotein E (ApoE)
ALZHEIMER’S DISEASE
What are some risk factors for Alzheimer’s?
- CVD = HTN, DM, hypercholesterolaemia, smoking
- FHx
ALZHEIMER’S DISEASE
What is the clinical presentation of Alzheimer’s
4As of Alzheimer’s –
- Amnesia (recent memories poor, disorientation about time)
- Apraxia (unable to button clothes, use cutlery)
- Agnosia (unable to recognise body parts, objects, people)
- Aphasia (later feature, mixed receptive/expressive)
Insidious + progressive course of short-term memory loss Sx in early disease
ALZHEIMER’S DISEASE
On CT/MRI head in Alzheimer’s disease, what are the macroscopic pathological changes?
Diffuse cerebral atrophy (shrunken brain), increased sulcal widening, enlarged ventricles
ALZHEIMER’S DISEASE
What is the management of Alzheimer’s?
- No cure, does not improve life expectancy but thought to slow rate of decline + allow functioning at higher level
- AChEi (donepezil, rivastigmine) for mild–mod
- NMDA antagonist (memantine) for mod–severe
VASCULAR DEMENTIA
What causes vascular dementia?
- Any type of vascular disease affecting blood vessels of brain
VASCULAR DEMENTIA
What is the clinical presentation of vascular dementia?
- Stepwise deterioration with short periods of stability then suddenly decline
- Patchier cognitive impairment than Alzheimer’s
- Focal neuro signs if caused by stroke
VASCULAR DEMENTIA
What would a CT head show in vascular dementia?
- ≥1 areas of cortical infarction (white on CT), may show micro-infarcts
VASCULAR DEMENTIA
What is the management of vascular dementia?
Not reversible but prevent further decline –
- Lifestyle (lose weight, healthy diet, stop smoking + alcohol)
- Atorvastatin 80mg if high cholesterol
- Optimise co-morbidities (HTN, DM)
- Aspirin or clopidogrel (75mg OD)
LEWY-BODY DEMENTIA
What is the pathophysiology of Lewy-Body dementia?
- Presence of Lewy bodies (protein deposits) in the basal ganglia + cerebral cortex, typically presents between 50–80y
LEWY-BODY DEMENTIA
What condition is Lewy-Body dementia closely associated to?
- Parkinson’s disease (25% of PD patients will develop)
LEWY-BODY DEMENTIA
What is the clinical presentation of Lewy-Body dementia?
- Fluctuating onset, progression, cognition + consciousness
- Vivid visual hallucinations (small children, animals)
- Parkinsonism (tremor, stooped + shuffling gait, hypomimia)
- Frequent falls
- REM sleep behaviour disorder (sleep walking, aggression) commonly precedes other Sx
- Rapid decline more so than other types
LEWY-BODY DEMENTIA
What is the management of Lewy-Body dementia?
- Conservative management
- AChEi used in mild–mod (rivastigmine 1st line), memantine last resort
- SENSITIVE to antipsychotics, can make worse + lead to neuroleptic malignant syndrome
FT DEMENTIA
What are 2 common features in frontotemporal (FT) dementia?
- Early personality changes + relative intellectual sparing.
FT DEMENTIA
What causes FT dementia?
- Unknown, younger mean age of onset
- Can be due to neurosyphilis (typically causes frontal lobe Sx such as aggression + personality change), associated with MND
FT DEMENTIA
What are the
i) frontal lobe symptoms
ii) temporal lobe symptoms
iii) generic features
of FT dementia?
i) Euphoria, disinhibition, personality changes + emotional blunting
ii) Speech disturbances (progressive non-fluent aphasia, may end up mute), expressive dysphasia
iii) Insidious onset with poor insight, amnesia not as severe as Alzheimer’s
FT DEMENTIA
What is the management of FT dementia?
- No specific treatment
- SSRIs may help behavioural symptoms
MILD COG IMPAIRMENT
What is mild cognitive impairment?
- Cognitive impairment without functional impairment (ADLs minimally affected)
FALLS
What is a fall?
- Event that results in unintentionally coming to rest at a lower level, usually the floor
FALLS
What are some neurological causes of falls?
- Stroke
- PD or other movement disorders (Huntington’s)
- Visual impairment
- Peripheral neuropathy or myopathy
FALLS
What are some cardiovascular causes of falls?
- Vasovagal or situational syncope
- Postural hypotension
- MI, arrhythmias
- Dehydration or shock
FALLS
What are some iatrogenic causes of falls?
- BDZs (sedative so impairs coordination)
- Polypharmacy (combination of drugs + interactions)
- Anti-hypertensives (ACEi, CCB, beta-blockers, diuretics)
- Anti-depressants + anti-psychotics
FALLS
What are some power causes of falls?
- Inactivity > muscle weakness
- Dizziness/loss of balance or proprioception (vertigo)
- Pain/MS > osteoarthritis
FALLS
What are some environmental causes of falls?
- Loose rugs
- Pets
- Furniture
- Unstable footwear
- Poor lighting
FALLS
What are some other causes of falls?
- Infection or sepsis
- Delirium
- Incontinence
- Hypoglycaemia
- Alcohol (intoxication, neuropathy, Korsakoff’s or Wernicke’s)
FALLS
What parts of the history are important when assessing falls?
- Collateral Hx
- Circumstances (timing, physical environment)
- Sx before + after fall
- Previous falls, #, syncope or near misses
- PMH for co-morbidities
- Functional performance (assess ADLs)
FALLS
What clinical examinations would you perform?
- CVS (LSBP, HR + rhythm, murmurs esp. AS)
- MSK (assess footwear, joints for deformity + stiffness)
- Neuro (identify stroke, peripheral neuropathy, ?Parkinson’s)
FALLS
What investigations would you do for someone presenting with a fall?
- FBC, B12 + folate, U+Es, Ca2+, phosphate, glucose, TFTs, vitamin D
- 24h ECG, ECHO if ?cardiac cause
- Head-up tilt table testing if unexplained syncope with normal ECG + no structural heart disease
FALLS
What are some complications of a long-lie following a fall?
- Pressure ulcers
- Dehydration
- Rhabdomyolysis
- Hypothermia
FALLS
What is rhabdomyolysis?
- Skeletal muscle breakdown due to traumatic, chemical or metabolic injury
FALLS
What can cause rhabdomyolysis?
- Crush injuries
- Prolonged immobilisation following a fall
- Prolonged seizures
- Hyperthermia
- Neuroleptic malignant syndrome
FALLS
How may rhabdomyolysis present?
- Urine may be dark (‘Coca-Cola urine) + urinalysis +ve to Hb but without RBCs
FALLS
What is the management of rhabdomyolysis?
- Measure U+Es, creatinine, CK levels + monitor urine output
- Supportive with IV fluids, correct electrolytes, ?temporary dialysis
FALLS
How can falls be prevented in a hospital setting?
- Treat infection, dehydration + delirium actively
- Stop incriminating drugs or avoid staring them
- Provide good quality footwear + access to walking aid
- Keep a call bell close to hand
- Good lighting
FALLS
How can fall frequency be reduced?
- Drug review to reduce meds that can increase risk
- Strength + balance training with physio (Tai Chi)
- Walking aids
- Environmental assessment + mods by OT
- Ensure vision optimised with glasses
FALLS
How can adverse consequences from falls be reduced?
- Osteoporosis detection + treatment
- Alarms such as pullcord or pendant alarms to summon help
- Supervision via visits from carers, family, neighbours
POSTURAL HYPOTENSION
What is the pathophysiology of postural hypotension?
- When standing, gravity causes blood to pool in legs + abdo which decreases BP as less blood circulating back to heart
- Normally, baroreceptors near heart + carotid arteries sense this lower BP + send signals to brain to signal heart to beat faster, pump more blood, cause vasoconstriction + stabilise BP
- In postural hypotension, something interrupts this mechanism
POSTURAL HYPOTENSION
What are some iatrogenic causes of postural hypotension?
Diuretics, anti-hypertensives, antidepressants, polypharmacy
POSTURAL HYPOTENSION
What are some other causes of postural hypotension?
How common is it?
- Blood loss, dehydration + shock
- Occurs in 30% of patients >70y
POSTURAL HYPOTENSION
How may postural hypotension present?
- Postural light-headedness, dizziness, blurred vision
- Weakness, fatigue, palpitations + headache may be present
POSTURAL HYPOTENSION
What investigations would you do to diagnose postural hypotension?
Lying + standing blood pressure
- Abnormal drop in BP of ≥20/10mmHg within 3 minutes of standing (<20/10 is physiological)
Investigate medical causes (FBC, U+Es, B12 + folate, TFTs, LFTs, CRP/ESR, ECG)
POSTURAL HYPOTENSION
What is the conservative management of postural hypotension?
- Drinks lots of water
- Avoid alcohol
- Compression garments (stockings)
- Stand slowly, elevating head of the person’s bed
POSTURAL HYPOTENSION
What is the pharmacological management of postural hypotension?
- Med review + stop causative agent
- Fludrocortisone (raises BP by raised Na+ levels + affecting blood volume) but can cause uncomfortable oedema
- Midodrine (when cause if autonomic dysfunction) but can cause retention, itchy scalp + paraesthesia
PRESSURE ULCERS
What is an ulcer?
- Open sore caused by a break in the skin or mucous membrane which fails to heal
PRESSURE ULCERS
How rapidly can a new pressure ulcer develop?
- 2h of tissue ischaemia sufficient for subsequent development of ulcer + there’s a considerable lag between ischaemic insult + resting ulcer
PRESSURE ULCERS
What are 4 contributing factors to pressure ulcer development?
- Pressure
- Shear
- Friction
- Moisture
PRESSURE ULCERS
Explain how pressure causes pressure ulcers.
Capillary pressures >35mmHg compress capillaries + cause ischaemia
PRESSURE ULCERS
Explain how friction causes pressure ulcers.
Rubbing skin decreases integrity
PRESSURE ULCERS
What score is used to screen for risk of pressure ulcer development?
Waterlow score
PRESSURE ULCERS
What are the different grades for pressure ulcers?
- 0 = skin hyperaemia
- I = non-blanching erythema with intact skin
- II = broken skin or blistering (epidermis ± dermis only)
- III = full-thickness skin loss involving damage/necrosis of subcutaneous tissue
- IV = extensive loss, destruction/necrosis of muscle, bone, joint or tendon
- Unstageable = depth unknown, base of ulcer covered by debris
PRESSURE ULCERS
What are some investigations for pressure ulcers?
- FBC (WCC), cultures
- CRP/ESR
- Swabs for MC&S if infected
- XR for bone involvement (?osteomyelitis)
PRESSURE ULCERS
How can pressure ulcers be prevented?
- Keep pt as mobile as possible
- Repositioning (6h or 4h in high risk)
- Pressure redistributing mattress + chair and friction reduction (heel support, cushions)
- Barrier creams as moist environment promotes healing
- Regular skin assessment
PRESSURE ULCERS
What is involved in a skin assessment?
- Check for areas of pain + discomfort, skin integrity at pressure areas
- Colour changes
- Variations in heat, firmness + moisture (incontinence, oedema, dry/inflamed skin)
PRESSURE ULCERS
What is the management of pressure ulcers?
- Pain relief
- Refer to tissue viability nurse
- Empirical Abx then matched with sensitivities if signs of infection
- Wound dressing (gels to soften, hydrogels often seaweed based for cavities)
- Debridement with scalpel, maggots or topical streptokinase for grade 3/4
MALNUTRITION
What is malnutrition?
- State in which a deficiency of energy, protein ± other nutrients causes measurable adverse effects on the body’s form, composition, function + clinical outcome
MALNUTRITION
What patients are at risk of malnutrition?
- Eaten little/nothing for >5d (or likely to do so)
- Poor absorptive capacity
- High nutrient losses
- Increased nutritional needs from causes such as catabolism
MALNUTRITION
What are the 3 broad categories of causes of malnutrition?
- Inadequate nutritional intake
- Increased nutrient requirements
- Inability to utilise ingested nutrients (malabsorption)
(Or a combination)
MALNUTRITION
What can cause inadequate nutrient intake?
Reduced appetite,
pain,
dysphagia,
starvation,
unfamiliar foods,
mood
MALNUTRITION
How is malnutrition defined?
- BMI <18.5kg/m^2
- Unintentional weight loss >10% in last 3–6m
- BMI <20kg/m^2 AND unintentional weight loss >5% in last 3–6m
MALNUTRITION
What investigations would you do in someone with malnutrition?
- U+Es, LFTs + ECG prior to commencing feedings
- Serum albumin often marker of nutrition (can be inaccurate)
MALNUTRITION
What are the components of MUST?
- BMI = 18.5-20 (1), <18.5 (2)
- Hx of weight loss = 5-10% (1) ≥10% (2)
- Acutely unwell or likely to have no intake >5d (2)
MALNUTRITION
What are some consequences of malnutrition?
- Impaired immunity, wound healing + recovery from illness
- More hospital admissions, prolonged stays + refeeding syndrome
- Loss of muscle mass (falls, more chest infections, decreased mobility)
- Micronutrient deficiencies (selenium, zinc, Fe anaemia, vitamin D = osteomalacia)
MALNUTRITION
What is the impact of the consequences from malnutrition?
- Lead to poorer prognosis
- Reduced QOL
- Greater healthcare needs
MALNUTRITION
What is the overall principle for the management of malnutrition?
- Food first – if the gut works, use it
- Snacks, nourishing drinks, food fortification (add full-fat cream to mashed potato)
MALNUTRITION
What is the second line management of malnutrition?
What are they?
Who overviews this care and what is their role?
- Oral nutritional supplements (ONS)
- Liquid/powder/semi-solid with macro + micronutrients (milkshake, semi-solid, soup)
- Registered dietician Ax to take into account nutritional requirements, taste + texture preferences, suitability (vegan, halal), volume consideration (fluid restriction), cost into account > tailored prescription
MALNUTRITION
What is the role of a dietician?
- Only qualified HCP that assesses, Dx + Tx nutritional + dietary issues
- Advice on therapeutic diets, appropriate feeding methods, identifies + advises on managing refeeding syndrome
MALNUTRITION
If ONS fails, what two options for feeding are there and what is the difference?
- Enteral feeding = direct feeding into gut via tube in the stomach, duodenum or jejunum
- Parenteral feeding = IV access (often peripheral inserted central catheter, PICC line or central line) where gut feeding is inaccesible or unable to absorb sufficient nutrients
MALNUTRITION
What are the 4 different types of enteral feeding?
- Nasogastric tube = feeds into the stomach, can be inserted at ward level, short-term use (<30d)
- Nasojejunal tube = feeds into jejunum, radiologically guided, short-term (<60d)
- Percutaneous endoscopic gastrostomy (PEG) = long-term enteral nutrition
- Post-pyloric/percutaneous endoscopic jejunostomy = long-term enteral nutrition
MALNUTRITION
How do you confirm NG tube position on insertion?
- Check pH aspirate to (<5.5),
- XR confirmation second line
MALNUTRITION
What are the indications for PEG?
- Dysphagia (stroke, head + neck surgery, neuro conditions)
- Cystic fibrosis (high nutritional requirements)
- Oral nutrition intake inadequate + likely long-term
MALNUTRITION
What are the indications for PEJ/surgical JEJ?
- Delayed gastric emptying
- Upper GI/pancreatic surgery
- High risk of aspiration or severe acute pancreatitis
MALNUTRITION
What are the advantages of enteral feeding?
- Preserves gut mucosa + integrity (NG/NJ),
- improves nutritional status,
- inexpensive compared to parenteral nutrition
MALNUTRITION
What are the indications for parenteral feeding?
- Inadequate absorption (short bowel syndrome)
- GI fistula
- Bowel obstruction
- Prolonged bowel rest
- Severe malnutrition
- Significant weight loss ± hypoproteinaemia when enteral therapy not possible
MALNUTRITION
What are the advantages of parenteral feeding?
- Easily tolerated
OSTEOPOROSIS
What is osteoporosis?
- Systemic skeletal disease characterised by low bone mass + micro-architectural deterioration of bone tissue with consequent increase in bone fragility + susceptibility to fracture
OSTEOPOROSIS
What are 2 factors that are important in determining likelihood of an osteoporotic fracture?
- Propensity to fall leading to trauma
- Bone strength
OSTEOPOROSIS
What makes up bone strength?
- Bone mineral density
- Bone size
- Bone micro-architecture
- Bone mineralisation
OSTEOPOROSIS
What happens to the bone micro-architecture in osteoporosis?
- Trabecular thickness decreases, especially in the horizontal plane, meaning fewer connections between trabecular + so overall decrease in trabecular strength
OSTEOPOROSIS
What is the pathophysiology of osteoporosis?
- Imbalance between modelling + resorption
- Inadequate formation of new bone during remodelling occurs
- Excessive bone resorption (PTH can trigger this as RANK-ligand binds to RANK activating osteoclasts)
OSTEOPOROSIS
What are 2 important components in calcium homeostasis?
- Vitamin D
- Parathyroid hormone (PTH)
OSTEOPOROSIS
What is the role of vitamin D?
- Increased Ca2+ absorption in gut + released from bone
OSTEOPOROSIS
What is the role of PTH?
- Released from chief cells of parathyroid gland in response to low serum Ca2+ detected by Ca2+ sensor cells
- Increased osteoclast activity, increased intestinal Ca2+ absorption, vitamin D activation + renal tubule reabsorption of Ca2+
OSTEOPOROSIS
What are 2 important factors in osteoporosis development/primary causes?
- Increasing age
- Post-menopause as oestrogen is protective
OSTEOPOROSIS
What are the secondary causes/risk factors for osteoporosis?
SHATTERED
- Steroids
- Hyper/hypothyroid
- Alcohol/smoking
- Thin (low BMI)
- Testosterone low (F)
- Early menopause
- Renal/liver failure
- Relatives (FHx)
- Erosive bone disease (RA)
- Dietary Ca2+ low
OSTEOPOROSIS
What is the clinical presentation of osteoporosis?
- Develops asymptomatic where # often first sign at common sites
- Distal radius = Colles’ # (fall on outstretched arms)
- Proximal femur (neck of femur)
- Vertebrae leading to shorter + stooped posture (lumbar, thoracic > kyphosis aka widow’s stoop)
- Hip