Phase 3A Medicine > COTE > Flashcards

COTE Flashcards

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1
Q

Define polypharmacy

A

being prescribed more than FOUR medications

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2
Q

Define pharmacodynamics

A

how the DRUG interacts with the body

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3
Q

Define pharmacokinetics and the four subtypes

A

how the BODY affects the drug

  • Absorption
  • Distribution across body compartments
  • Metabolism
  • Excretion
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4
Q

What can polypharmacy result in?

A
  • Increased risk of SEs
  • Risk of drug-drug interaction
  • Therapeutic cascade (as a result of SEs misinterpreted as a new medical condition)
  • Risk of meds not being thoroughly reviewed
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5
Q

Why is polypharmacy more common in the elderly?

A
  • Frailty
  • Communication problems
  • Co-morbidities
  • Prescribing for SEs
  • Changes in pharmacokinetics:
    - Increased % body fat
    - Decreased % body water and serum albumin
    - Results in increased distribution of fat-soluble
    drugs and decreased distribution of water-soluble
    drugs
  • Decreased metabolism with age
  • Increased kidney problems (reduced GFR -> reduced excretion of drugs excreted by kidneys, e.g. Digoxin
  • Decreased liver volume and enzyme activity (hepatic metabolism of many drugs decreased so the dose should be adjusted to reduce risk of toxicity)
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6
Q

Complications of polpharmacy?

A
  • Increased morbidity and mortality
  • Increased hospital stay lengths
  • Reduce compliance
  • Risk of adverse effects and drug-drug interactions
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7
Q

Define inappropriate prescribing

A
  • prescribing a CI drug
  • prescribing for inappropriate dose or duration
  • prescribe drug likely to adverseley effect prognosis
  • not prescribe a drug that could improve outcomes
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8
Q

how to avoid polypharmacy?

A
  • Regular medication reviews
  • Combining medications
  • Take a thorough history
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9
Q

Define osteoporosis

A

Progressive loss of bone mass associated with change in bone micro-architecture

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10
Q

What is bone remodelling

A
  • A normal process continually taking place within bone.
  • An essential process that allows bone to adapt to stressors and repair microdamage.
  • The net product of bone formation and resorption.
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11
Q

What are the stages of bone remodelling?

A
  • Activation of osteoclasts from circulating precursor cells - medicated by RANK ligand (NF-kB)
  • Aggregation and adherence of osteoclasts to regions fo active bone resorption on trabecular plates
  • OsteoClastic breakdown of bone matrix -> releasing CALCIUM, MINERALS and ACTIVE GROWTH FACTORS
  • OsteoBlastic deposition of OSTEOID with subsequent MINERALISATION as CALCIUM and PHOSPHATE is deposited
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12
Q

What happens in post-menopausal women?

A
  • Shift towards RESORPTION, leading to net bone loss
  • Osteoclasts function in less regulated manner -> perforating through trabecular plate
  • No framework for osteoblast activity and structural integrity is lost
  • Loss of connectivity between trabecular plates is typical of microstructural changes seen in OP
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13
Q

Name an OP risk tool and what it calculates

A

FRAX: 10-year fracture risk

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14
Q

What are the risk factors for primary osteoporosis?

8

A
  • Female
  • Previous fragility fracture
  • Maternal history of hip fracture
  • Current smoker
  • Alcohol intake > 3 units/day
  • Glucocorticoids > 3 months > 5mg/day
  • Low calcium and vitamin D deficiency
  • Low BMI (<19)
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15
Q

What are the causes of secondary osteoporosis?

5

A
  • Rheumatoid arthritis
  • Chronic malabsorption/malnutrition (e.g. coeliac)
  • Hyperthyroidism/Hyperparathyroidism
  • Premature menopause (< 45yrs)
  • Chronic liver disease
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16
Q

What investigations might you do if suspected osteoporosis?

A
  • Bloods: FBC/UE/LFT/TFT/Calcium/Phosphate/VitD/PTH/Coeliac serology/myeloma screen
  • DEXA Scan: GOLD STANDARD - measures BMD standard deviation from norm.
    T-score = average 25yr old; -2.5 = OP
    Z-score = age-matched score
  • Whole spine XR
  • Bone turnover markers: serum C-terminal telopeptide (CTX levels)
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17
Q

Pharmacological management for OP? Important things to consider?

A
  • Vitamin D supplements for all with fracture/at risk
  • Calcium supplements (dependent on base levels and diet)
  • Bisphosphonates:
    o Ensure no serious dental issues -> can cause osteonecrosis of the jaw
    o CI if CrCl < 30mL/min
    o PO alendronic acid if probability > 1% (unless GORD/PUD)
    o IV zoledronic acid if probably > 10%, or if oral not tolerated or CI (Oral can be difficult to take as have to take first thing and remain standing for 30 mins)
    o Risk of atypical femur fracture so monitor BMD
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18
Q

Lifestyle management for OP?

A
  • Weight-bearing and muscle-strengthening exercises
  • Falls prevention
  • Smoking cessation and alcohol avoidance
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19
Q

Define syncope

A

Transient loss of consciousness due to transient global cerebral hypoperfusion characterised by rapid onset, short duration and complete recovery

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20
Q

Epidemiology of syncope?

A
  • Incidence rises over 70yrs of age

- Men are more likely to have a cardiac cause

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21
Q

Syncope differentials?

A

Loss of consciousness:

  • Epilepsy
  • Metabolic disorders (hypoxia/hypoglycaemia)
  • Intoxication
  • Vertebrobasilar TIA

Without LOC:

  • Cataplexy
  • Drop attacks
  • Falls
  • Pseudosycnope
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22
Q

Types of cardiac syncope?

A 
Bradycardic:
- Sinus node disease
- Atrioventricular disease
Tachycardic:
- Supraventricular
- Ventricular
Drug-induced:
- Antiarrhythmics
- Antianginals
- Antiemetics
- Antipsychotics
- Inotropes
Cardiac:
- Acute MI
- Hypertrophic cardiomyopathy
- Pericardial disease/tamponade
- Congenital abnormalities
Others:
- Pulmonary embolus
- Severe pulmonary HTN
- Acute aortic dissection
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23
Q

Treatment for cardiac syncope?

A
  • Stop any drugs that may exacerbate arrhythmias
  • Sinus node disease/AV defects -> cardiac pacing
  • Ventricular tachycardia -> cardiac catheter ablation/IUD
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24
Q

Define orthostatic hypotension

A

Within 3 mins of standing:

  • Systolic BP drop of 20mmHg (with or without symptoms)
  • OR a drop to below 90mmHg on standing even if the drop is less than 20mmHg (with or without symptoms)
  • OR diastolic drop of 10 mmHg with symptoms

Occurs as a consequence of impaired vasoconstriction due to chronic impairment of autonomic sympathetic activity

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25
Types of orthostatic syncope?
``` Drug-induced: - Antihypertensives - Diuretics - Vasodilators - Phenothiazides - Antidepressants Primary autonomic failure: - Pure autonomic failure - Parkinsons (w/autonomic failure) - Multi-system atrophy - Dementia with lewy bodies Secondary autonomic failure: - Diabetes mellitus - Amyloidosis - Spinal cord injury - Uraemia Volume depletion: - Haemorrhage - Diarrhoea - Vomiting - Dehydration ```
26
Management of orthostatic syncope?
Discontinue any offending medication if possible Lifestyle modifications: - Increase fluid intake - Counter manoeuvres - Compressions stockings Pharmacological: - Fludrocortisone (mineralocorticoid - increases plasma vol) - Midodrine (alpha-antagonist - increases BP)
27
Define reflex syncope?
Transient loss of consciousness due to inappropriate cardiovascular response of vasodilation or bradycardia, cerebral hypoperfusion Most common cause of syncope!
28
Types of reflex syncope?
``` Vasovagal: - Emotional stress (fear/pain) - Orthostatic stress Situational: - Post-prandial - Post-micturition - Cough/sneeze - Post-exercise - Playing a wind instrument - Weight lifting Carotid sinus syndrome ```
29
Describe carotid sinus syndrome
- Ventricular pause of > 3 seconds and a fall in systolic BP of > 50 mmHg following carotid sinus massage - Disease of the autonomic nervous system - Hypersentivie baroreceptors: o Cause dilation and drop in BP o Bradycardia o Collapse - A form of REFLEX syncope - Rare before 40 yrs - Diagnosis with tilt table and carotid massage - 3 types: o Cardioinhibitory o Vasodepressor o Mixed
30
Treatment of reflex syncope?
- Physical counter manouevres (knees crossed) at suspected time --> increases BP - Cardioinhibitory carotid sinus syndrome -> cardiac pacing may be beneficiary
31
Describe sinus sick syndrome
- Usually cause by sinus node fibrosis - Sinus node becomes dysfunctional and in some cases slows to the point of sinus bradycardia or sinus pauses - Diagnose with history, ECG and carotid sinus massage
32
Describe vascular steal syndrome
- Subclavian artery stenosis - Means you can't get blood from subclavian (due to stenosis), so blood is 'stolen' from the Circle of Willis instead - Leads to collapse
33
What is the STOPP tool?
The Screening Tool of Older Person Prescriptions - For patients over 65 yrs Aims to: - Improve the appropriateness of prescription - Reduce the occurrence of adverse events - Reduce drug costs
34
What is the START tool?
The Screening Tool to Alert doctors of the Right Treatment | - Looks at which medications should be used for certain conditions on patients 65 yrs and older
35
Which medications may cause urinary incontinence and how might they present?
- Alcohol: Polyuria, frequency, delirium - ACE-I: Cough and stress incontinence - Anticholinergic: Urinary retention and overflow - Diuretic: Polyuria, frequency, urgency - Opiates: delirium, sedation, constipation and urinary retention - Tricyclic antidepressants: Urinary retention and overflow
36
Define stress incontinence
- Sphincter weakness - Detrusor pressure causes closing press of urethra - Involuntary leakage on effort or exertion
37
What are the causes of stress incontinence?
- Menopause (low oestrogen) - Radiotherapy - Pelvic surgery - Congenital weakness - Vaginal prolapse - Post-prostatectomy in men
38
How might stress incontinence present?
- When cough/laugh/lift/exercise/movement | Must exclude overactive bladder via CYSTOMETRY
39
How would you manage stress incontinence?
- PELVIC FLOOR EXERCISES= 1ST LINE - Lifestyle changes: smoking cessation, weight loss, reduced caffeine intake - Vaginal cones Medication: DULOXETINE Surgery: mid-urethral sling insertion with tension-free vaginal tape (TVT)
40
Define overactive bladder
Urgency +/- urge incontinence, usually with frequency or nocturia, in the absence of proven infection - Involuntary detrusor muscle bladder contractions during filling phase - May be spontaneous or provoked
41
What are the causes of overactive bladder?
- Mostly IDIOPATHIC - Neurogenic: Parkinsons, MS, stroke, spinal cord injury - Infective: UTI - Bladder outlet obstruction
42
Management of overactive bladder?
- FIRST LINE = BLADDER TRAINING - Lifestyle measures (smoking/caffeine/weight loss) - Pelvic floor exercises Medication: - ANTICHOLINERGICS (Tolteridine/Solifenacin/Oxybutynin) - B3 adrenoreceptor agonists (Mirabegron) Others: - Intravaginal oestrogens - Intradetrusor botox injections - Sacral nerve stimulation
43
Presentation of overactive bladder?
- Urgency, frequency, nocturia, key-in-door, hand washing, sexual intercourse - Childhood enuresis is common (involuntary urination) - Urine dairy will find the frequent passage of small vols of urine, particularly at night
44
Investigations for incontinence?
- Urine dipstick and urinlaysis (UTI check) - MSU - FVC (freq-vol chart): urine diary - ePAQ questionnaire - Post-void bladder scan - Residual urine (RU): USS or in/out catheter - Urodynamics: detrusor activity
45
Causes of bladder outflow obstruction (BOO)?
- Phimosis - Stricture - STD - Trauma - Blood clot - Calculi - BPH - Cancer of prostate/bladder - Cancer of cervix/colon
46
Define delirium
A state of mental confusion that develops quickly and usually fluctuates in intensity
47
What are the four key features of delirium?
- Disturbance of consciousness - Changes in cognition or development of perpetual disturbance - Disturbance develops over a short period of time and fluctuates over the course of a day - History supports an underlying medical condition, medication withdrawal or intoxication
48
Risk factors for delirium
- Dementia - Multiple comorbidities - Physical frailty - Older age - Sensory impairments, e.g. visual
49
Investigations for delirium?
- White cell count/CRP - Electrolytes - LFTs - TFTs - Glucose - CXR - Urinalysis - ECG - Serum calcium, B12, folate - Specimen cultures
50
Precipitating factors for delirium?
- Drug initiation - Medical illness - Systemic infection - Metabolic derangement - Surgery - Pain - Brain disorders (stroke/seizures) - Systemic organ failure
51
Examination in delirium?
- Mini Mental State (MMS) - Montreal cognitive assessment (MoCA) - Addenbrooke's cognitive exam (ACE-R) - The confusion assessment method (CAM): o Acute onset and fluctuating course o AND inattention o AND disorganised thinking OR altered level of consciousness
52
Differentials of delirium?
- Dementia - Focal neurological syndromes, e.g. WE, frontal lobe lesion - Non-convulsive status epilepticus - Primary psychiatric illness
53
Management fo delirium?
Treat the underlying cause: - Drug review for polypharmacy - Pain: simple analgesia - Constipation: laxatives - Infection: antibiotics - Correct electrolytes Manage the environment: - Involve family - Clock and calendars - Soft lighting - Sleep hygiene - Correct any sensory impairment - Keep them mobile and active - Avoid multiple moves - Minimise provocation (loud noises) Monitor: - Vital Signs - Bowel habits - Nutrition and hydration - Pressures areas - Electrolytes - Response to antibiotics - Re-explore diagnosis if not improving Sedation: - Haloperidol or Lorazepam (PO/IM) - NOT haloperidol in Parkinson's/Lewy Body dementia (extra-pyramidal side effects) - Only used if all other options exhausted
54
Types of delirium?
Hyperactive: - Heightened arousal - Sensitive to surroundings - verbally and physically aggressive - Restless - Carphologia (pulling straw from mud wall) - Wandering and disorientated - Unable to follow complex commands Hypoactive: - Confused with depression - More common - Reduced psychomotor activity Or can be mixed!
55
Causes of delirium?
D: Drugs, Dehydration, Dementia E: ELectrolyte disorders, Epilepsy L: Lack of drugs (withdrawal), Lungs, Liver, Lack of sleep, Low O2 I: Infection, e.g. UTI/pneumonia R: Reduced sensory input, Renal failure, Retention I: Injury or Intercranial damage, Ictal U: Unfamiliar environment, Uraemia, Undernutrition M: Myocardial/pulmonary, Metabolic, Metastases
56
Differences between delirium and dementia? (6)
Delirium: - Acute onset (vs. progressive) - Altered consciousness (vs. no altered consciousness) - Inattention and distractability (vs. no disorder of alertness) - Underlying medical cause (vs. none) - No interference with ADLs (vs. interference) - No memory decline (vs. memory decline)
57
Definition of dementia per DSM
Impairment of memory, PLUS ONE: - Language impairment - Agnosia (inability to recognise people/objects) - Apraxia (difficult expressing, or doing certain activities) - Impairment of executive function ALSO: impairment in functioning, present for > 6 months, no other medical/psych explanation
58
Alzheimer's
- Most common (62%) - Caused by BRAIN DEGENERATION - MACROscopic changes: atrophic brain, parituclarly the hippocampus, and enlarged ventricles - MICROscopic changes: amyloid plaques, neurofibrillary tangles (abnormal protein deposition) - Genetics: APP, PSEN-1 and -2, APDE, Down's syndrome
59
Vascular dementia
- 2nd most common (17%) - Problems with blood supply, e.g. stroke/atherosclerosis - 3 types: Multi-infarct, subcortical vascular, post-stroke dementia - Generally SUDDEN ONSET, stepwise deterioration - Increased risk: smoking, high-fat diet, diabetes, HTN
60
Mixed dementia
10% will have a mix of AD and VaD
61
Lewy-body dementia
- Fluctuations in cognition - Early visual hallucinations - Associated with PARKINSONS - Lewy bodies in the brain cortex and BASAL GANGLIA - LBD and Parkinson's disease dementia (PDD) have the same pathology BUT LBD presents within 2yrs of motor symptoms, where as PDD is later
62
Front-temporal dementia
- Atrophy/degeneration of frontal and temporal lobes - Marked by changes in behaviour, emotion and language before the memory - Up to 50% are thought to be inherited - Associated with MOTOR NEURONE DISEASE (MND)
63
Other types of dementia? (5)
- Huntington's disease - Alcohol-related dementia - Progressive supranuclear palsy (PSP) - Creutzfedt Jacob disease (CJD) - HIV-related cognitive impairment
64
Mild cognitive impairment
- Memory loss greater than expected for age but not affecting functioning enough to be classed as dementia - At greater risk of going onto to develop dementia, but identifying MCI can help monitoring and ability to treat earlier if dementia does develop - Some causes might be reversible, e.g. depression, physical illness
65
Risk factors for dementia
Modifiable: smoking, alcohol, obesity, low education levels, high cholesterol, atherosclerosis Non-modifiable: age, genetics, MCI
66
Investigations for dementia
- BLOODS: FBC, UE, TFTs, LFTs, glucose, lipids, B12, folate, renal function, ESR - COGNITIVE TESTS: ACE-R, MoCA, MMSE, 6-CIT, AMTS - Baseline ECG can be helpful - IMAGING: CT = 1st line, MRI/HMPoA-SPECT may be helpful for more detail
67
Management of dementia
- Evaluate capacity and discuss a Power of Attorney (PoA) - Developing routines - Drugs for challenging behaviour: LORAZEPAM and TRAZADONE - Depression is common: SSRI's (Citalopram) - Alzheimers: o Acetylcholinesterase inhibitors, e.g. RIVASTIGMINE, DONEZEPRIL o Antiglutaminergic treatment, e.g. MEMANTINE
68
Pathophysiology of Parkinsons
- Mitochondrial DNA dysfunction -> degeneration o dopaminergic neurons in the SUBSTANTIA NIGRA -> decreased supply of dopamine to the STRIATUM -> motor symptoms - Loss of neuromelanin-containing dopaminergic neurons in the substantial nigra - Presence of Lewy bodies in the basal ganglia, cortex and brainstem
69
Causes of Parkinsons?
- Idiopathic - Drugs - Trauma - Encephalopathy - Copper toxicity - Oxidative stress - Mitochondrial dysfunction
70
Clinical features of Parkinsons?
- Bradykinesia - Cogwheel rigidity - Resting tremor - Postural instability Others: depression, dementia, hypomimia, constipation, dribbling of saliva, change in taste/smell, insomnia, unexplained pain
71
Diagnosis of Parkinsons?
- Predominantly clinical - DATScan (Iolfuoane SPECT): shows dopamine supply and can distinguish between idiopathic and other causes - Histology: Lewy Bodies and loss of dark substantial nigra markings - If any of the following, consider a different diagnosis: o Incontinence from start o Dementia from the start o Symmetrical (ALWAYS worse on one side) o Early falls
72
Management of Parkinsons?
Only effective if idiopathic - Levodopa (L-dopa) = precursor to dopamine. Must give with a dopa-decarboxylase inhibitor, e.g. cobeneldopa or cocareldopa - Monoamine oxidase beta-inhibitors (MAOBs), e.g. Rasagaline, either as monotherapy or in adjunct - Catechol-O-methyl transferase (COMTs), e.g. Entacapone, as an adjunct, inhibit the breakdown of L-dopa
73
What two drugs would you not use in older patients?
- Anticholinergics: too many SEs, mainly confusion | - Dopamine agonists: would use in younger patients due to risk of therapeutic window becoming a problem (10-15yrs)
74
What four things would you think about in a Parkinson's checkup?
- Parkinsonian symptoms - Fluctuations in motor capabilities - Hallucinations - Dyskinesias
75
What might you do before treatment in Parkinson's?
- TReat depression, dementia, psychosis - Deep brain stimulation (DPS) - Surgical ablation of overactive basal ganglia
76
Name a differential for Parkinson's and how you would treat it?
- Essential tremor | - Treat with beta-blockers and Primidone
77
What are the complications from a long lie following a fall?
- Rhabdomyolysis - AKI - Dehydration - Malnutrition - Moisture lesions - Fractures - Subdural haemorrhages - Hypothermia - Feeling helpless/low self-esteem/post-fall syndrome
78
Risk factors for pressure ulcers?
- Diabetes - Pulmonary vascular disease - Malnutrition - Dehydration - History of pressure ulcers - Immobility - Incontinence - Living alone - Older age - High BMI - Sensory or cognitive impairment - Reduced blood supply
79
Pathophysiology of pressure ulcers?
1. Hard surface 2. Localised external pressure on the skin causes occlusion of the capillaries and compression of the tissues 3. Leads to reduced oxygen and nutrition to the tissues 4. Altered soft tissue hydration as the fluid is pushed away 5. Worsened by friction -> shear the skin off
80
What are common sites for pressure ulcers?
- Ischial tuberosity and sacrum - Heels - Back of the head
81
Investigations for pressure ulcers?
- General exam and history - CRP/ESR - Swab and blood cultures - XR for bone involvement - Albumin (low will delay healing) - FBCs (anaemia will delay healing)
82
Stages of pressure ulcers?
Stage 1: Non-blanching erythema, skin in-tact Stage 2: Partial-thickness ulcer, loss of dermis, red and open Stage 3: Full-thickness ulcer, slough or eschar present, sub-cut fat visible Stage 4: Full-thickeness ulcer, slough, bone/tendon/muscle visible
83
Name two differentials of pressure ulcers and describe their presentations?
- Deep tissue injury: purple localised area of discoloured intact skin, or a blood-filled blister - Moisture lesion: redness or partial-thickness skin loss involving the epidermis, upper dermis or both
84
Management of pressure ulcers?
SSKIN! S: Support surface - pressure redistributing mattress S: Skin assessment - regularly K: Keep them moving - repositioning regime I: Incontinence and moisture - continence assessment and management N: Nutrition and hydration - particularly Vit C and protein - Stages 3-4: Tissue Viability Nurse (TVN) - Topical antimicrobial therapy: silver, honey or iodine-impregnated dressing - Systemic antibiotics if systemic sepsis or deep infection (e.g. osteomyelitis) - Hydrocolloid dressings - Last resort = debriding surgery
85
What is the MUST score?
Calculates risk of malnutrition - BMI: >20 =0; 18.5-20 = 1, <18.5 = 2 - Unplanned weight loss in last 3-6 months: <5% = 0; 5-10% = 1 - Acute illness or no nutritional intake for >5 days = 2 points ``` Score 0 = Low risk - Ensure appropriate food/drink choices, document action taken, rescreen in 3-6 months Score 1 = Medium risk - Follow MUST care pathway Score 2 = High risk - Follow MUST care pathway for medium risk - Refer to a dietician - Re-weigh monthly - Document action taken ```
86
What are the intrinsic risk factors for a fall?
- Female - Neurological disease - Cognitive decline - Visual deficit - Muscle weakness
87
What are the extrinsic risk factors for a fall?
- Walking aids - Footwear - Home hazards - Polypharmacy - Bifocals
88
What must you consider on assessment of a fall?
- Frequency of falls: >2/year is significant - Collateral history is needed - many don't remember a fall from > 3 months ago - Head-to-to systematic examination
89
Investigations post-fall?
Imperative: - ECG - Lying and standing BP Consider: - FBCs - U&Es - TFTs - Bone biochemistry - CK - Echocardiogram - Tilt table testing - 24hr tape
90
Management post-fall?
``` Physiotherapy: - Strength and balance training - Exercise programmes - Aerobic exercise Occupational therapy: - Home hazards assessment Medical review: - Medication review - Optimise medical comorbidities - Diagnose new medical conditions - Manage postural hypotension - Cognitive screening - Bone health assessment - Referral for cataracts surgery if necessary ```
91
Complications of a fall?
- Loss of confidence and a fear of falling - Serious injury - Long lie - Fragility fracture
92
What is the definition of frailty?
A medical syndrome with multiple causes and contributors that is characterised by diminished strength and endurance and reduced physiological function that increases an individuals vulnerability for developing increased dependency and/or death.
93
What is the frailty phenotype?
1. Unintentional weight loss 2. Weakness, evidenced by poor grip strength 3. Self-reported exhaustion 4. Slow walking speed 5. Low level of physical activity - -> 1 or 2 characteristics = pre-frail - -> no characteristics = robust
94
What is the frailty index?
- The more deficits accumulated, the more frail the person is and the greater the risk of detioration or death - Example = Rockwood Frailty Index Number of deficits an individual has / total number of deficits considered One limits is the data needed which doesn't allow for a rapid clinical assessment in more acute settings!
95
What are some physiological markers of frailty?
- Increased inflammation (CRP/IL6/Factor VIII/fibrinogen) - Elevated insulin and glucose in fasting state - Low albumin - Raised D-dimer and alpha-1-antitrypsin - Low vitamin D levels
96
What are some interventions for frailty?
- Physical activity (exercise programmes focussing on strength and balance in particular) - Protein-calorie supplementation - Vitamin D (100% in Vit-D deficiency but evidence inconclusive for others) - Minimise polypharmacy
97
What is investigated in a 'confusion screen'?
B12/folate: macrocytic anaemias, B12/folate deficiency worsen confusion TFTs: confusion is more commonly seen in hypothyroidism Glucose: hypoglycaemia can commonly cause confusion Bone Profile (Calcium): hypercalcaemia can cause confusion
Phase 3A Medicine
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