Geriatrics Flashcards
WHat is a stroke?
•(cerebrovascular accident – CVA) = Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24hoyrs or leading to death, with no apparent cause other than of vascular origin. sudden interruption in the vascular supply of the brain.
What is a transient ischaemic attacks?
•TIA – Transient ischemic attack – sudden onset of focal neurologic symptoms and/or sign lasting typically <1hours, brought on by transient decrease in blood flow. Causes are same eg, atherothromboemboiusm, cardioembolism, hypervsicosity, vasculitis. Check not hypoglycaemia, migraine aura, focal epilepsy etc. Do bloods, lipids CXR, ECG, doppler, poss angiography, C. Control RFs, antiplatelet drugs, anticoag factor, carotid endarectomy qithin 2w possible. Driving stopped for at least 1m. ABDE score for emergency referral (age, BP, clinical, duration symptoms, diabetes).
SYmptoms and signs of a stroke
•Symptoms + Signs: Sudden onset, Motor weakness (face/arm/leg weakness or sensory loss), loss coordination, speech problems (dysphasia-understanding/generation language, dysarthria, dysphonia), swallowing problems, visual field defects (homonymous hemianopia), balance problems. Dynamic phenomenon. Loss of function. Mostly UMN lesion but these symptoms aren’t immediate– so tone usually increases but this is gradual, brisk reflexes, clonus,
Cerebral hemisphere infarct symptoms
– Contralateral hemiplegia (flaccid then spastic), contralateral sensory loss, homonymous hemianopia, dysphasia
Brainstem infarct symptom
•– may result in more severe symptoms including quadriplegia and lock in syndrome.
Haemorrhages - signs/symptoms generally
•more likely to have decrease in level of consciousness, headache, nausea and vomiting.
Ischaemi vs haemorrhagic stroke
What is this
Intracerebral ahemorrhage
WHta is a TACI?
- Total anterior circulation infarct
- Invovles ACA + MCA
- Unilateral hemiapresis and/or hemisensory loss of face/arm/leg
- Homonymous hemianopia
- Higher cognitive dysfunction eg, dysphasia
PACI
- Partial anterior ciruclation infarcts
- Smaller arteries of anterior circulation
- 2 of:
- Unilateral hemiapresis and/or hemisensory loss of face/arm/leg
- Homonymous hemianopia
- Higher cognitive dysfunction eg, dysphasia
Lacunar infarct
- Involves perforating arteries aroudn internal capsule, thalamus and basal gnaglia
- 1 of following:
- Unilateral weakness (and/or sensory deficity) of face and arm, arm and leg or all three
- Pure sensory stroke
- Ataxis hemiparesis
Posteiror ciruclation infarct:
Vertebrobasillar arteries
1 of following:
- Cerebellar of brainstem syndromes
- Loss of consciousness
- Isolated homohymous hemianopia
Symptoms of anterior cerebral artery stroke
Contralateral hemiparesis and snesory loss, lower extremity >upper
Symptoms middle cerebral artery stroke
- Contralateral hemiparesis and sensory loss, upper extremity> lower.
- Contralateral homonymous hemianopia, aphasia
Posterir cerebral artery stroke symptoms
Contralateral homonymous hemianopia wit muscular sparing. Visual agnosia
Webers syndrome (branches of posterior cerebral artery that supply midbrain)
Ipsilateral CN III palsy
Contralateral weakness of upper an dlower extremities
Posterior inferior cerebellar artery stroke (lateral medullar syndrome, wallenberg syndrome)
Ipsilateral: facial pain and temp loss
Contralateral limb/torso pain and temp looss
Atai, nystagmus
Anterior inferior cerebellar artery (lateral pontine syndrome) stroke symtpoms
SYmptoms similar to Wallenbers but ipsilateral facia apralyis and deafness
- Ipsilateral: facial pain and temp loss.
- Contralateral limb/torso pain and temp loss.
- Ataxia, nystagmus
Retinal/opthalmic artery stroke
Amaurosis fugac
Basilar artery storke symptoms
Locked in syndrome
Investigations in stroke
- CT first - see if ischaemic or haemorrhagic
- MRI might be later for diagnostic
- Also - ECG, CXR, Bloods etc. Can do carotid imaging (carotid USS) to see if need carotid endararterectomy
- Acute ischaemic stroke - may show areas of low density in grey and white matter which can take time. Also could show hyperdense atery sign corresponding with artery cot
- Acute haemorrhagic stroke - hyperdense material (blood) surrounded by lower densoty (oedema)
Subarachnoid vs subdural vs epidural on CT
Management of strokes
•Management: maintain homeostasis (blood glucose, bp), screen swallow, ct/mri within 1hour, antiplatelets, thrombolysis, thrombectomy. .
•Ischaemic – thrombolysis if criteria met. Within 4.5 presentation, no previous ICH, uncontrolled hypertension, pregnant etc. Once hemorrhagic excluded then 300mg aspirin ASAP and continue antiplatelet therapy.
•TIA = <24h. Give aspirin 300mg immediately unless contraindicated (if taking anticoag etc or exclude haemorrhage). If has had more than 1 TIA or cardioembolic source or severe carotid stenosis then discuss admission with storke specialist. If within last 7days suspected then urgen assess with stroke Dr within 24hrs and if more than a week ago then specialist assessment within 7days if possible with stroke Dr
•Haemorrhagic stroke – neurosurgical consultation. Most not suitable for surgery. So supportive Tx. Anticoags and antithrombotics should be stopped to minimize bleeding. If anticoagulated then reverse as quickly as possible and try reduce BP (evidence)
Primary vs secondary prevention in strokes
- Primary - look for and treat HTN, DM, Hyperlipiedmia, cardiac disease, af
- Secondary - control RFs, mainly lower cholesterone, BP. Antiplatelets after stroke. Bleeding scores.
Complications of infarct
- Haemorrhagic transformation
- Malignant MCA syndrome - cerebral oedema so need hemicraniotomy
- Seizure
- DVT/PE
- Aspiration pneumonia
- Pressre sores
- Spasticity
- Pain
- Increased falls risk
- Continence problems
- Depression
Thrmbolysis in stroke management
- Aspirin and anticoag treatment
- Thrombectomy - For ischemic stroke (clot in big artery). Intervention neuroradiological procedure. After confirm stroke <6h with NIHSS>6 CT head excludes other things and CTA confirms large vessel occlusions… Normally thrombolysis unless contra-indication. Before. Femoral access. Try aspiration to suck out clot or stentriever
-
Thrombolysis isn’t always good – risk of bleeding in haemorrhage hence time cut off. SO <4.5hrs when <80, 03hrs >80, no haemorrhage/infarct on CT. There is scoring system.
- Contraindications = BP consistent >180/105, stroke<3m/any ICH, surgery or bleed<3wks, (blood sugar really low/high, warfarin and INR>1.4), platelets <100. 15-2)% eligible.
•
RFs for falls
- CV RFs - dehydration, blood loss, medication, cardiac arrhythmias, postural hypotension
- Confusion - delirium, dementia, alcohol and drugs, brain injury patholgoy
- Medications
- Postural instability
- Visual problems
- BPPV
Cause and RFs for pressure sores
- Cause = Pressure and/or shear forces over a bony prominence in the presence of a number of RFs (mostly immobility).
- RFs = Alzheimer’s, CVD, DM, COPD, Hip fracture, HF. DVT, limb paralysis, lower limb oedema, malignancy, Parkinson’s, RA, UTIs
Braden risk scale for pressure sores
•sensory perception, moisture, activity, mobility, nutrition, friction/shear.
Pressure sore - ulcer assessment
Cause, site, dimensions, age, exudate, signs inflamm, pain, wound appearance, surrounding skin, undermining/tracking (fistula), odour.
Management and complications of pressure sores
- Mx = Adequate pressure redistribution (pressur even), good nutrition, appropriate wound mx. Refer if extensive superficial or high grade. Repositioning, treat concurrent conditions, support usrfaces, pain relief, infection control.
- Complications – Cellulitis, joint infections (can damage cartilage and tissue), bone infections (osteomyeltitis- can reduce function of joints and limbs). Cancer (long term non helaing like marjolins ulcers -> SCC), sepsis.
Surgery and elderly - why is this more complicated
- In the frail – multicomponent intervention, frailty is significant risk factor for complications in elective + emergency surgical patients.
- Post op delirium – common + underdiagnosed + delays rehan
- Post-op pain – underappreciated in elderly (particularly those with cognitive disorders. Anesthetists should administer opioid sparing analgesia where possible.
- Elderly should be assumed to have capacity to make own decisions.
- Ass of anaethetists greta britian and Ireland aimed to give guidelines on peri-op care of elergy.
Types of incontinence
- Stress incontinence – urine leaks as pressure put on bladder like during exercise, cough, sneeze, laughing.
- Urge incontinence – sudden need to urinate and cant hold urine long enough to get to toilet. May be in DM, Alzheimer’s, Parkinson’s, MS, stroke
- Overflow incontinence – small amounts urine leak from bladder that’s always full. Eg , enlarged prostate blocking urethra. Diabetes AND spinal cord injuries can cause this.
- Functional incontinence – in those who have normal bladder control. Just have problem getting to toilet from arthritis or other disorders that mean you can move quick.
Invetsigations in incontinence and management
- Ix = physical exam, history, urine + blood samples, examine inside bladder with cystoscope, fill bladder with warm fluid and use cystoscope to check how much can hold before leaking, order bladder US to check fully emptying each void, keep diary.
-
Mx =
- Bladder control training (Pelvic muscle exercise, urinary suppression-distraction and time voiding and extend).
- Medical – medications, vaginal estrogen cream (urge/stress), bulking agents (help close bladder opening), medical devices (catheter).
- Biofeedback (sensory to make aware of signals), electrical nerve stimulation, surgery.
- Behavior + lifestyle – loose weight, stop smoking, choose water, no to alcohol, prevent constipation.
DNA CPR - and how made
- DNACPR – Do not attempt CPR but can still have other forms active treatment
- On specific form, kept in medical records. Can have short period or no end date. Not legally binding unless advance decision to refuse treatment. If not have DNACPR then best interest decision but speak to important people to you or mental capacity advocate, MDT team.
- Might also have lasting power attorney document.
- Advanced decision/directive is essentially a living will, it is a signed legal dated document which involves patient detailing which treatments they wish to refuse. Must have been made when patient was “sound mind” and must be completed in presence of witness who must also sign and date document.
- Doctor decides in advance – even if don’t agree. If they think it would cause physical or psychological harm, but you should have chance to understand what it is and why they don’t think suitable. Individual basis, can ask for second opinions. Cant demand one if not deemed to be in best interest.
- Use when patients medical condition puts them at risk of having life threatening event or deterioration. When CPR would be deemed not successful due to condition (most successful when reversible cause)/ when they wish for one).
- In hospital – on nerve centre of not for resus (NFR) or yellow at front of notes. Medical decision with patient’s opinion but not legally binding till advanced directive. Cantdemand it but can refuse. Ignroe if DNACPR for cancer but go into cardiac arrest for different reason like procedure then can do CPR.
Adnvanced decision
- Advanced decision to refuse treatment, legally binding. To ensure individuals can refuse specific treatments that they do not want to have in the future
- Must be: valid (when they had capacity), must be applicable (specific to medical circumstances), made when over 18 + fully informed, not made under influence or people, must be written down, signed and witnessed.
- Can not refuse basic care etc or treatment for MHcondition if sectioned.
ADvanced statement
- Statement of wishes and care preferences. Allows individual to make general statements about wishes, beliefs, feeligns, values and how these influence their preferences.
- Not legally binding but must be taken into consideration when naking best interest decisions
- Religious, spiritual views, food preferences, infoabout daily routine where you would like to becared for, any people you would like to beconsulted when best interest decisions made (not same power as lasting power of attorney)
DNACPR convo
- Should be had at earliest opportunity
- Assess knowledge of patient, ’how much do they know’. If they don’t know much this may mean you will need to ‘break the bad news’.
- Offer to involve family or friends for emotional support
- ‘Warning shots’ or indicators of severity are often used to mentally prepare patients and families
- Should incorporate the patients wishes together with current medical opinions
- Should also involve possible of ceiling care
Symptoms in dying patients
- Recognizing dying: Cause of deterioration no longers responding to treatment or appropriate to treat.
- Expected: Changes in Obs, weakness + fatigue, decreased oral intake + swallow reflex, decreased blood perfusion, renal failure, incontinence/retention of urine, change in mental state (confusion, disorientation, delirium).
- Always ask the patient, family etc what they want. Transition to comfort care, stop Interventions + monitoring, treat symptoms + educate, oral and skin care. Be honest.
- Syndrome imminent death: 24hs-2wks. In early phase its bedbound, incontinent, decrease in ability and/or interest to eat or drink, cognitive changes. Then middle phase of tracheal congestion, further cognitive (slow to arouse), no oral intake. Late phase is comatose, temp instability, altered resp pattern, mottling + coole extremities, absence peripheral pulses.
End of life care - what to give for pain
- Pain: Conversion of usual daily dose of opiate analgesia to 24hour dose for use by syringe pump with 1/6 -> 1/10 of fsily dose andbreakthrough. Review every 24hours
- Morphine – first line for pain, monitor constipation and unwantedsedation
- Diamorphine, oxycodone, alfentayly (good for renal failure)
End of life care for breathlessness
•Breathlessness: May be from disease process, need therapeutic O2, morphine, midazolam
ENd of life care - for nausea and comtiing
•levomepropmazine, cyclizine, haloperidol, metoclopramide.
End of life care for restlessness and confusion
Haloperidol (not in parkinsoms), levomepromazine, midazolam .
End of life carefor repsirtory tract secretions
hyoscine hydrobromide, hyoscine butylbromide, glycopyrronium.
Common causes of falls
Usually an interaction to cause a fall. Weak muscles – affect strength + balance. From lack activity, arthritis…
- Poor balance – weak muscles, health conditions (parkinsons/stroke), S/Es, dizziness
- Dizziness – postural hypotension, inner ear probles, problems with HR/rhythm, dehydration
- Black outs, fainting etc – bradycardia, tachcyardia, Atrial fibrillation, foot problems – calluses, ingrown toenails, thicken nails, ulcers
- Mmeory loss, confusion, problem solving – cant judge risky situations
- Visio + hearing problems – spot hazard, depth perception for kerbs, cataracts, glaucoma
- Meds – psychotropics, BP lowering, sleeping tablets, anticonvulsants
- Alcohol – especially with some meds - can slow reactions
- Bladder and bowel conditions – rushing to toilet etc
Ix for falls
- Bedside = Vital signs (sepsis, bradycardia?), lying + standing BP (orthostatic hypotension), urine dipstick (infection, rhabdomyolysis), ECG (bradycardia, arrhythmias), Cogntivie screening (impairment), blood glucose (hypoglycaemia secondary to poor oral intake)
- Bloods = FBC (anaemia, infection), U&Es (dehydration, electrolyte abnormalities, rhabdomyolysis), LFTs (chronic alcohol use), bone profile (calcium abnormalities in malignancy or over supplementation)
- Imaging = CXR (pneumona), CT head (chronic or acute subdural/ stroke), ECHO (valvular heart disease (eg aortic stenosis))
- Specialist = Tilt table test, Epley maneuver (benign paroxysmal positional vertigo), Cardiac monitoring (eg 48hr tape- if no symptoms during monitoring episode in hospital).
Mx of falls
- Gait – physiotherapy
- Visual problems – Eye test. Ensure wears glasses
- Hearing difficulties – remove earwax, hearing assessment
- Meds review – reduce unnecessary medication
- Alcohol intake – Alcohol cessation advice, alcohol service referral
- Cognitive impairment – referral to psychiatric team
- Postural hypotension – review medication, improve hydration
- Continence – treat or rule out infections, continence assessment
- Footwear – Ensure good fitting footwear
- Environmental hazards – Turn on lights, take up rugs.
What is osteoporosis and rhw Risk factors
•Osteoporosis = Systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue (poor quality bone) with consequent increase in bone fragility and susceptibility to fracture
- RF = Age, sex, weight, previous fracture, parent fractured hip, current smoking, steroids, RA, alcohol 3 or more units/day, bone mineral density, secondary osteoporosis (eg T1DM, hyperthyroidism, hypogonadism, premature menopause (<45), chronic malnutrition, or malabsorption and chronic liver disease.
- Meds that worsen = SSRIs, antiepileptics, PPI, glitazones, long term heparin therapy, aromatase inhibitors eg, anastrozole
IX and assessing osteoporosis
- Ix - history and physical exam and blood cell count, sedimentation rate or CRP, serum calcium, albumin, creatinine, ALK, Liver trnasaminases, TFTs, DXA.
- Assessing = History, Exam, FRAX, DEXA
- DEXA (Dual energy Xray absorptiometry – measures Bone mineral density. Non invasive – measures at femoral neck and lumbar spine. Problematic if hip replacement as it would measure at titanium replacement.
>-1 = normal
-1 to -2.5 = osteopaenia
< -2.5 = osteoporosis
Tx osteoporosis
- Tx = Address lifestyle factors + falls risk, optimize calcium and vitamin D status, minimize risk from other medical conditions. Medications…
- Anti-catabolic: Biphosphonate (reduce osteoclasts that eat bone to reduce bone loss) eg, alendronate (oral), risedronate (oral), ibandronate (IV), zolendronate (IV). Denosumab
- Anabolic – teriparatide (PTH type drug to increase deposition of bone)
- Try prevent with good balance and vitamin D
Assessing risk in osteoporosis
- Female >/65 and male >/75 should be assessed and those young with risk fractures: previous fragility fracture, glucocorticoids, history falls, FH hip fracture, low BMI, smoking, too much alcohol..
- FRAX(40-49,BMD optional)/ Q-fracture (30-99, larger group RF) for 10year risk of developing fracture
- NICE sometimes recommend BMD assessment (DEXA) before treatment which affect BM or under 40 with major RF
What is syncope and common causes
- Syncope = transient, self limited LOC, rapid onset with complete spontaneous recovery. Transient global cerebral hypoperfusion. 9Stroke is focal cerebral hypoperfusion)
- Reflex mediated syncope – mostly vasovagal syncope, also carotid sinus syncope, situation syncope at any age.
- Orhtostatic hypotension – fall SBP>20/ DBP>10 within 3mins standing. Drugs/autonomic failure
- Cardiac – arrhythmia, structural cardiac disease
How to Ix syncope
- VVS – clinical Dx, tilt test if in doubt
- OH – lying &Standing BP, SBPd rop>20, DBP drop>10
- CSS- CSM 9carotid sinus massage) for 10s (supine then upright), SBP drop>50/ asystole >3s
- Cardiogenic syncope – 12 lead EC, external/internal loop recorder, Echo, cardiac MRI
EValuation of SYncope
- Initial – loss consciousness, heart disease, important clinical features
- Ask – position, activity, predisposing factors, precipitating events
- Onset of attack – nausea, vom, abdo discomfort, feeling cold, sweat, aura, pain, blurred vision. And form eyewitnesses (tongue biting, movements, duration, skin colour).
- End of attack – sweating, cold, nausea, confusion, skin colour, injury, chest pain, palpitations
- Background – FH sudden death/ congenital arrhythmogenic hear disease/fainting, previous cardiac disease, neuro history, metabolic disorders, medication (hypotensive, antiarrhythmic, QT prolonging agents)
- Exam – sign cardiac failure/ murmur, neuro exam.
- 12 lead ECG
- Hospitalize if – significant heart disease, ECG abnormalities, syncope in exercise, severe injury, FH sudden death, syncope in supine, frequent, high suspicious cardiac arrhythmia, stroke/focal neurology
Syncope vs non syncope
Syncope: Reflex syncope (neurally-mediated)- fainting (vasovagal, carotid sinus syndrome CSS), situational), orthostatic hypotension, arrhythmias, structural cardiac or cardiopulmonary disease, cerebrovascular
Non-syncope: disorders resembling syncope without any impairment consciousness (falls, cataplexy, drop attacks, dissociative attacks), disorders with partial or complete loss of consciousness (seizure, metabolic disorders, TIA, intixification).
Delirium vs dementia
Def of dementia
- Dementia (major neurocognitive disorder): Impairment of memory and othe rhigher cortical processes such as language, leading to a progressive decline in function. DSM5:
- Cognitive decline in one or more domain
- Deficits interfere with independence in everyday activities
- Not in context of delirium
- Not better explained by another rmental disorder (eg, major depression)
- Subtype required eg, Alzheimers, PDD, Traumatic brain injury
DSM 5 Features Delirium
DSM 5 Features Delirium:
a) Disturbance of attention + awareness
b) onset short, acute change form baseline, fluctuating
c) Additional disturbance in cognition (memory, language, orientation)
d) A and C are not due to pre-existing dementia
e) History supports underlying medical condition
Lewy body dementia
- Alpha synuclein cytoplasmic inclusions (lewybodies) in substantia nigra, paralimbic and neocortical areas.
- Progressive cognitive impariements, ocngition may fluctuate, usually develops befor eparkinsonism. Visual hallucinations.
- Dx – usually clinical, SPECT used. (Dat scan) Fluctuating attention and concentration, recurrent well forme visual hallucinations, spontaneous parkinsonism.
- Mx – Ach inhibitors and memantine in alzheimers.
Vascular dementia
- Group of ysndromes of cognitive impairment caused by different mechanisms cuasing ishcameia or haemorrhage secondary to CV disease.
- Stroke related VD – milti nfarct or single infarct dementia
- Subcorticla VD – small vessel disease
- Mixed dementia - AZ + VD
- RFs – history of stroke or TIA, AF, HTN, DM, Hyperlipiaemia, smoking, obesity, coronary heart disease, FH stroke or CV.
- Rarely inherited
- Typically present with several months or several years of history of uddent or stepwise deterioration of cognitive function
- May include – Focal neuro abnormalities, difficutly with attention and concentration, seizures, memory disturbance, gait disturbance, speech disturbance, emotional disturbanve
- Dx – History = physical exam, forma screen for cognitive impairment, medical review, MRI scan (infarcts + extensive white matter changes) . NINDS-AIREN criteria
- Tx – symptomatic, address CV RFs. Only consider ACEi or memantaine if suspected mixed.
Alzheimers disease- what is it and RFs
- Alzheimer’s = Progressive degenerative disease of the brain accounting for the majority of dementia in the UK (so most common pathology)
- RFs = Increasing age, FH (amyloid precursor protein gene, SEN1, PSEN2), 5% inherited (autosomal dominant), apoprotein E allele E4, Caucasian ethnicity, downs syndrome. APOE polymporphicalleles are main determinant of sporadic. E4 allele most at risk so APOE E4
- Macroscopic = Widespread cerebral atrophy, particularly involving cortex and hippocampus.
- Microsocpic = Type A B amyloid protein (extraneuronal) and intraneuronal neurofibrillary tangles caused by abnormal aggregation of Tau protein (excessively phosphorylated so reduced bidning to micrtotubules and reduce microtubule stability).
Biochem= Deficit of Ach from damage to ascending forebrain projection.
Alzheimers features
- Amnesia – recent memories lost first
- Aphasia – word finding problems, speech muddles,disjointed
- Agnosia – recognition problems
- Apraxia – inability to carry out skilled tasks despite normal motor function
Alzheimers disease Mx
- Promote wellbeing, cognitive stimulation therapy, group reminiscence therapy + cognitive rehab
- AcheI – donepezil, galantamine, rivastigmine for mild moderate.
- Memantine (NMDA receptor antagonist) – 2nd line for moderate and intolerance or add on/singular for severe AD.
- Antidepressants, and possibly antipsychotics
- Donepezil – relatively contraindicated in aptientswith bradycardia. A/E are insomnia.
Peudodementia
(depressive dementia)
- Primarily associated with cognitive deficits in older patients with depression. Often present with self neglect and weight loss as a result.
- Short duration dementia
- Equal effect on long and short term memory
- Amnesia of specific events
- Often detailed complaint about memory disturbance
- May highlight failures in aswers to questions relating to memory
- Loss social skill
- Often answer “don’t know”
- May take little effort performing tasks
Different types dementia
Causes of delirium
PINCH ME=
- Pain
- Infection
- Nutrition (or neoplasm)
- Constipation
- Hydration
- Medication
- Environment
DELIRIUMS = Drugs&Alcohol, Eyes/ears/emotional, low output state (COPD/CHF), Infection, Rectal, Ictal, Under hydration/nutrition, metabolic, subdural/slee deprivations
How to assess delerium
- History + collateral - onseny, nautrec hange, baseline, cognitive state, precipitating factors
- Examine - vital signs, conditions
- Confirm with congitive assessment
- cam/dsm-5, 4aS
- ix - Urinanalysis, sputum, FBC + Folate + Vit B12, U&E, HBA1C, LFT, Inflamm, drug levels, TFT, CXR, ECG
Parkinsons - what is it
- Parkinson’s = progressive disease of neurological system resulting from degeneration of dopamine producing neurons in the substantia nigra. Clinical signs when 80% dopamine producing neurons lost. Dopamine is a major neurochemical messenger that promotes function of basal ganglia (to orchestrate performance of well learnt, vol, semi-automatic motor and movement skills. Also contributes to cognitive processes.
- Cognitive impairment: MCI, parkinsons disease dementia, lewy body dementia, vascular dementia.
- Stages PD: Diagnostic -> Maintenance -> Complex -> Palliative
SYmptoms in parkinsons
Bradykinesia – slow movement, shuffling, difficulty initiating movement
Tremor – most at rest, worse when stressed, pill rolling
Rigidity - Lead pipe, cogwheel
- Non motor symtpoms - dementia, depresison, apathy, los s libido, anxiety
- Constipatiom, urinary incontinence, erectiel dysfunction, excessive sweating, postural hypotension, excessive salivation
- REM sleep disorder, RES, Vivid dreams, dystoni
- Pain, paraesthesia
Levodopa in parkinsons
- : Full agonist of dopamine receptors in corpus stratum
- Usually combined with decarboxylase einhibits to prevent peripheral metabolism of levodopa to dopamine . Ldopa is gold standard.
- Reduced effectiveness with time
- Unwanted S/E = Dyskinesia, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drwosiness
- If motor symptoms affecting QoL. madopar (co-beneldopa- can go to dispersible), Sinemet (co-careldopa- can be crushed), stalevo, duodopa.
- More improvement in motor symptoms and activities daily living but more motor complications and ferwer specified A/Es.
Monoamine oxidase B inhibitors in parkinsons
- rasagiline, selegeline, safinamide. Stop if unable to swallow.
- Less improvement in motor symptoms /ADL, fewer motor complications and fewer specificed adverse effects. Susceptible to falls as causes postural hypotension as possible side effect
- Inhibits breakdown of dopamine secreted by dopaminergic neurons
COMT inhibitors in pakrinsons
- Catechol-o-methyltransferase inhibitors (COMT) – entacopone, tolcapone, opicapone. Stop if cant swallow.
- COMT is enxyme involved in breakdown of dopamine, and hence may be used as adjunct to levodopa therapy. Usued in conjuction with levodopa in patients with established PD
Dopamine agonsit in parkinsons
- Convert to rotigotine patch if cant swallow with conversion alculator. Us ewith caution and titrate up if dopamine agonist naïve. Less improvement in motor symptoms + ADL, few motor complciations, more specified A/Es. Impulse control possible problem
- Bromocriptine, ropinirole, cabergoline, apomorphine. Amantadine is weak DA agonist anf NMDA eceptor channel blocker.
- Ergot derived dopamine receptor agonists (bromocriptine, cabergoline) ass with pulmonary retroperitonea and cardiac fibrosis
- Can caus eimpulse disorders. Mor elikely than levodopa to cause allucinations in older people. Also may see nasal congestion and postural hypotension.
Amantadine in parkinsons
•.- not fully understood MOA. Porbably increases dopamine release and inhibits it uptale at dopaminergic synapses. S/E are ataxia, slurred speech, confusion, dizziness, livedo reticularis.
Antimscarinics in parkinsons
•Antimuscarinics – block cholinergic receptors. Now more for drug induced pakrinsons. Help tremor and rigidity. Eg, procyclidine, benzotropine, trihexyphenidyl (benzhexol)
Flecanide - class IC Antiarrhythmic
- Strong, Fast Na channel blockers: Inhibit Na+ channels and K+ channels on atrial and ventricular myocytes and cells of purkinje fibers. Less sodium entering cell so slower depolarization and decrease in slow during phase 0.
- Tachycardia, dry mouth, urinary retention, blurred vision, constipation.
- Uses = prevent abdominal cardiac rhythms.
Beta blockers - Sympatholytic drug
- Bind to B-adrenoreceptors and block the binding of noradrenaline/adrenaline to these receptors to inhibit sympathetic effects. 1st gen- B1/B2 adrenoreceptors, 2nd gen- B1-adrenoreceptors, 3rdgen- also vasodilator actions through blocking a–adrenoreceptors.
- Uses: Hypertension, angina + MI, arrhythmias, HF
- Non-selective B1/B2 B blockers = Propranolol, timolol, nadolol
- B1-selective B blockers= atenolol, bisoprolol
- S/E = Feeling tired, dizzy, lightheaded (slows HR), cold fingers or toes, sleeping difficulties, feeling sick.
CCBs - verapamil
- Antiarrhythmic, antianginal, antihypertensive activity.
- MOA = Bind to L-type Ca2+ channels on vascular smooth muscle, cardiac myocytes + cardia nodal tissue. So cause vascular smooth muscle relaxation (vasodilation), decrease myocardial force generation, decreased HR + decreased conduction velocity within heart.
- S/E = Constipation, dizzy, fats heart beat, fatigue, flushing, headache, nausea, rash.
- Amlodipine, diltazem, felodipine
Digoxin - cardiac glycoside
Cardiac Glycosides (Digoxin):
- MOA =Increase output force of heart and decrease rate of contractions by inhibiting cellular sodium-potassium ATPase pump.
- Uses – Congestive heart failure, cardiac arrhythmias.
- S/E = Dizziness fatigue, headache, anxiety, GI upset, change in taste, blurred vision.
Warfarin
Anticoag, Vitam K antagonist
- MOA = Block function vitamin K epoxide reductase complex in liver so depletion of reduced form vitamin K which is important in clotting.
- DVT/PE, metallic heart valves…
- S.E = severe bleeding red/brown urine, black/bloody stool, severe headache,joint pain, vom/coughing up blood.
NOACs
NOAC: Novel oral anticoagulants
- Uses = prevention stroke, venous thromboembolism.
- Rivaroxaban, dabigatran (stomach upset), apixaban, edoxaban
- S/E = major bleeds
- ‘Xaban’ = direct factor Xa inhibitor
- ‘gatran’ = Direct thrombin inhibitors so prevents formation fibrin.
Drug control for AF
- Anti-arrhythmics to control AF - Flecanide, B blockers, CCBs
- Digoxin if those unsuitabe
- Cntrolling rate at which heart beats - B blockers, CCBs
- Anticoagulants - NOACS/ Warfarin
Heart Failure drugs
- ACE inhibitors
- Diuretics
- Angiotensin 2 receptor blockers
- B blockers
- Mineral corticoid receptor antagonists - spironolcatone
- Ibabradine
- Hydralazine with nitrate
- Sacubitril valsatan
- Cardiac glycosides - digoxin
- Devics
ACE inhibitors
- Inhibit ACE which stops body form angiotensin I -> Angiotensin II (important component in RAAS). Ang II is vasoconstrictor and increase bradykinin.
- Relax blood vessels and decrease blood volume so LBP and decreased O2 demand from heart
- Ramipril, captopril, enalapril
- Uses = HBP, HF
- S/E = Dry, irritating cough and can cause too low BP (-> kidney problems)
Diuretics MOA
- Use = help body get rid sodium and water. Reduced BP.
- Examples = Furosemide, bumetanide.
- MOA = Diminish sodium reabsorption at different sites in nephron so increase urinary sodium and water looses. Pass more urine and relieve ankle swelling + breathlessness caused by HF.
- 2nd class (aquaretics)- inhibit water reabsorption by blocking vasopressin receptors along collecting tubule + duct.
- S/E = Dehydration + reduced levels sodium + potassium in blood. Can reduce BP and cause dehydration symptoms.
ARBs
Angiotensin – 2 receptor blockers ARB:
- Use = HTN, HF, Valsartan post MI.
- Examples = Candesartan, losartan, valsartan. Alternative to ACEi if cough
- MOA = Block Angiotensin II receptors (AT1) on blood vessels + other tissues like heart. These involved in stimulating vascular smooth muscle contraction so dilate arteries/veins and reduce arterial pressure, preload and afterload on heart. Also down reg sympathetic adrenergic activity, promotes renal excretion NA/water, inhibit cardiac + vascular remodeling ass with chronic HTN , HF, MI
- S/E = Low BP, high levels potassium in blood
Mineralcorticoid receptor antagonists
- Use = HBP/HF. Potassium sparing diuretic in HF, npehortic syndrome, liver disease where over activation of RAS. Gynecomastia / hyperkaliemia S/E.
- Examples = Spironolactone (gynecomastia + breast tenderness + har growth women), eplerenone (sleeping diff, dizzy, headaches)
- MOA = Bind to mineralocorticoid receptor(aldosterone antagonist) inhibiting aldosterone so higher levels potassium in serum and increased sodium excretion so decreased body fluid (more urine) and lower BP. Reduce fluid around heart.
- S/E = Level of potassium can become very high (hyperkalemia ) and acute deterioration of renal function.
Ivabradine
- 1st and only Hyperpolarisation-activated cyclic nucleotide gated HCN channel blocker.
- Use = Slow heart down, useful alternative to Bblockers or alongside. Chronic heart failure.
- MOA = In isolated SA node cells, it blocks HCN pacemaker currents (If), which controls spontaneous diastolic depolarization in SA node and reg HR.
- S/E = Headaches, dizziness, blurred vision
Hydralazine with nitrate
- Use = Help relax and open up blood (improve EF)vessels. Prescribed by cardiologist for those not able to take ACEi/ARB
- MOA = Vasodilates. Afterload-preload reduction with lowering ventricular filling pressure and systemic and pulmonic vascular resistance.
- S/E = Headaches, fast heartbeat, pounding fluttering or irregular heartbeat (palpitations).
Sacubitril valsartan
Sacubitril Valsartan: Combines ARB + neprilysin inhibitor
- Use = Severe HF where heart only able to pump reduced amount O2 blood around body despite taking other meds.
- MOA = Inhibits neprilysen and blocks angiotensin II type-I receptor, increasing levels of peptides degraded by neprilysen. Inhibits release aldosterone . Relax Blood vessels to easier for heart t pump blood to your body.
- S/E = LBP, High potassium levels, kidney problems
Cardiac glycosides
- MOA =Increase output force of heart and decrease rate of contractions by inhibiting cellular sodium-potassium ATPase pump.
- Uses – Congestive heart failure, cardiac arrhythmias.
- S/E = Dizziness fatigue, headache, anxiety, GI upset, change in taste, blurred vision.
HTN Drugs
<55 = ACE i or ARB
>55 or african/caribbean = CCB
BB blokcers, CCBs, diuretics, ACEi, ARBs
OA drugs
Paracetamol, NSAIDs, opioids, steorid injections, capsaicin cream
- Lifestyle (healthy weight + exercise), medication (relieve pain), supportive therapies.
- Supportive treatment: Transcutaneous electrical nerve stimulation (numb nerve endings in spinal cord which control pain), hot or cold packs, assistive devices, manual therapy
- Surgery – joint replacement, joint fusing, adding or remove some bone around joint
- Complimentary and alternative therapies – nutritional supplements (chondroitin and glucosamine), Rubefacients (gels and creams that produce warm, reddening
Paracetamol/acetaminophen
Paracetamol/ Acetaminophen : Analgesic + Antipyretic
- Uses = Aches and pain
- MOA = Not fully established. Inhibits COX-1/COX-2 which are involved in PG synthesis (responsible for eliciting pain sensations). doesn’t inhibit in peripheral tissues. Also suggest it inhibits cox-3.
- S/E = Low fever with nausea, stomach pain, loss app, dark urine, jaundice
NSAIDs
NSAIDs:
- Uses = Not for those with asthma, stomach ulcer, angina, heart attack or stroke. PPI prescribed alongside to protect stomach lining.
- Examples = Ibuprofen, naproxen. Topical (cream) onto joints.
- MOA = Reversibly inhibit COX enzymes (1/2) which inhibits prostaglandin synthesis which normally potentiates pain caused by other inflamm mediators.
- S/E = Indigestion, stomach ulcers, headaches, drowsy, dizzy, allergic reactions
Opioids
Opioid:
- Uses = Analgesia
- Examples = codeine, co-codamol (codeine + paracetamol).
- MOA = inhibit spinal nociceptive transmission. They reduce camp signaling on presynaptic nerve terminals and suppress activity of voltage gated calcium channels, which inhibits release of nociceptive transmitters
- S/E = Drowsy, nausea, constipation, resp depression
- Codeine + morphine- binds to mu-opioid receptors (involved in transmission pain through body and CNS).
Steroid injections
Steroid injections :
- Uses = Particularly painful MSK problems. LA first.
- Examples = Hydrocortisone injfections, traimcinocolon, methylprednisolone.
- MOA = Reduce inflammation by limiting capillary dilation and permeability of vascular structures.
- S/E = Cartilage damage, death nearby bone, joint infection, temporary facial flushing…
Capsaicin cream
Capsaicin Cream :
- Uses = OA in hands or knees if topical NSAIDs not helped. May burn at first as made from chillies
- MOA = Blocks nerves that send pain messages in targeted area. Should experience some pain relief within first 2 weeks of using it but up to a month to be fully effective.
- S/E = burning sensation where applied that does go, redness, itching, irritation not going.
DM - drugs used
- T1DM = Insulin – injections to control blood glucose as pancreas doesn’t make it. Long acting (basal) once/twice a day and then insulin with food or drink
- T2DM = Usually offered metformin first and if this isn’t enough then try another or combo.
S/E DM meds = bloating and diarrhea, feeling sick, weight los or weight gain, swelling, hypos.
- Metformin - biguianide
- Alpha-glucosidase inhibitors - acarbose
- Incretin mimetics - GLP-1 analogues
- Sulpnylureas
- Repaglinie (pradin) and netglinide (starlix)
- Statins
- Pioglitzone (actos)
- SGLT2-inhibtors
Metformin
Metformin : Biguanides
•MOA = Prevent liver form converting fats and amino acids to glucose. Also activate enzyme AMPK which helps cells to respond more effectively to insulin and take in glucose from blood.
Alpha-glucosidase inhibitors:Acarbose (Glucobay
•MOA = Slows down starchy food absorption after meal so blood sugar levels wont rise as fast. Competitively inhibit enzymes that convert non-absorbable carbs to simple absorbable carbs.
Incretin mimetics
Incretin mimetics: GLP-1 anlagoues
- MOA = Injection releases incretins which help you make more insulin, reduce amount sugar the liver produces and slow digestion speed. Also can reduce appetite.
- Activate GLP-1 receptors in pancreas, which leads to enhanced insulin release and reduced glucagon release- responses that are glucose dependent with consequent low risk for hypoglycaemia.
Sulphonylureas
Suphonylureas:
•MOA = Stimulate cells in pancreas to make more insulin and help insulin work more effectively. Bind to and close ATP sensitive K+ channels on cell membrane of pancreatic beta cells, which depolarizes the cell by preventing potassium from exciting.
Repaglinide and nateglinide
Repaglinide (Prandin) and nateglinide (Starlix): Pranidil glucose regulators
•Binding to channel of proteins (ATP-sensitive potassium channel) in insulin producing cells of pancreas (beta cells) so beta cells can produce more insulin
Statins
Statins:
- Helps lower bad cholesterol to help decrease risk of heart diseases in diabetes
- Competitively block active site of first and key rate limiting enzyme in mevalonate pathway, HMG-CoA so prevents substrate access and blocks HMG-COA to mevalonic acid.
Pioglitazone (Actos)
Pioglitazone (Actos): Thiazolidinediones or glitazones
- Uses = Help body use natural insulin better and protect cells in pancreas so you can produce insulin for longer.
- Bind avidly to peroxisome proliferator activated receptor gamma in adipocytes to promote adipogenesis and fatty acid uptake (peripheral not visceral fat
SGLT2-Inhibitors
SGLT2-inhibitors:
- Reduce amount sugar kidneys absorb and passes it out in urine so les sin blood.
- Inhibit SGLT2, (sodium glucose cotransporter 2) which reduces renal tubular glucose reabsorption, producing reduction in blood glucose without stimulating insulin release.
DDementia medications
- Most meds available are used to treat Alzheimer’s as this is most common form.
- Medicine to treat related conditions: Stroke, heart problems, HBP, DM, High cholesterol, chronic kidney disease, depression
- Medicines for challenging behavior (agitation, anxiety, wandering, aggression,delusions, hallucinations). Risperidone or haloperidol for aggression or extreme distress. For mod-severe and risperidone for lowest dose (up to 6wks) as serious side effects and haloperidol if other treatments not helped. Only haloperidol for vascular D. Possible antidepressants
- Alt. therapuies - gingko biloba, curcumin or coconut oil.
- Other TX – Cognitive stimulation therapy, cognitive rehab, reminiscence and life store work.
Acetylcholinesterase inhibitors
- Uses = prevent enzyme breaking down acetylcholine in brain (helps nerve cells communicate with each other)
- Donepezil (Aricept) – severe dementia. Selectively and reversibly inhibits ACHE which normally breaks down ACH
- rivastigmine (Exelon) – enhance cholinergic function through hydrolysis of cholesterase
- galantamine (reminyl)- reverisbel inhibitor ACHE and enhances intrinsic action ACH on nicotoinic receptors so increased cholinergic NT to CNS
- Also evidence for dementia with lewy bodies, parkinsons, and mixed (AD + VD)
- S/E = Nausea and loss of app (usually get better after 2w)
Memantadine
(Namenda) – NMDA Receptor antagonists
- Uses = Mod-severe alzheimers, LB dementia + alzheimers/vascular combo. Good for those who cant tolerate Achi
- MOA = Blocks effects of excessive amount of chemical in brain called glutamate by binding to NMDA receptors and stopping glutamate binding so preventing release of calcium into nerve cells
- S/E =Headaches, dizzy, constipation but only temporary usually.
Incontinence management
- Conservative – lifestyle changes (reduce caffeine, alter fluid amount, loose weight) , pelvic floor muscle training, bladder training (if urge incontinence, techniques to increase length time between feeling need and passing urine). Electrical stimulation if can’t contract pelvic floor muscles. Biofeedback (monitor how well do pelvic floor exercises), vaginal cones (to assist with pelvic floor muscle training with small weights in vagina.
- Incontinence products – pants/pads, handhled urinals, catheter, EG, device to prevent urine leakage in vagina while exercise)
- NHS continence service
Stress incontinence - duloxetine
Urge incontinence - antimuscarinics,mirabegron
Meds nocturia - Desmopressin, loop diuretic afteroon
Meds for stress incontinence
An antidepressant duloxetine can help increase muscle tone of urethra to help keep it closed. But possible side effects are nausea, dry mouth, extreme tiredness, constipation. It inhibits reuptake of serotonin and norepinephrine in CNS.
Meds for urge incontinence
- Antimuscarinics = Oxybutynin, tolterodine, darifenacin. Antagonism atmuscarinic M3 receptor at NMJ in human bladder detrusor muscle. Can lead to dry mouth, constipation, blurred vision, extreme tiredness (fatigue) and rarely cause glaucoma
- Mirabegron = If Antimuscarinics don’t help. Causes baldder to replace which helps it fill and store urine. S/E includes UTI, Fast/irregular heartbeat, palpitations, rash, itchy skin.
Meds for nocturia
- Desmopressin = Low dose version. Helps to reduce amount of urine produced by kidneys.
- Loop diuretic – late in afternoon may help. As increases production and flowurine from body so by removing excess in afternoon, it may improve symptoms at night. This isn’t licensed though.
Postural BP assessment, and brief Mx
- Have the patient lie down for 5minutes
- Measure the BP and pulse rate
- Have the patient stand
- Repeat blood pressure and pulse rate measurements after standing 1 and and 3 minutes.
A drop in BP of ≥20 mm Hg (or below 100), or in diastolic BP of ≥10 mm Hg, or experiencing lightheadedness or dizziness is considered abnormal.
Advice to stand slowly, dorsiflexing feet first before standing upright. Prevents excessive diuresis and fluid shifts than can cause suddent dop.
Fludorcortisone and midodrine (2/3rd line drig)can be used to raise it.
Progressive supranuclear palsy
- Steele Richardson Olszewski syndrome
- Parkinson plus syndrome
- Postural instability and falls – stiff broad based gait
- Impairment of vertical gaze
- Parkinsonism – bradykinesia
- Cogntivie impirmet – primarily frontal lobe dysfunctipn
- Mx – poor response to L dopa
Cerebellar syndrome
- Unilateral cerebellar lesions cause ipsilateral signs.
- DANISH:
- Dydiadochokinesia, dysmetria (past pointing)m patients may appear drunk
- Ataxia (limb, truncal)
- Nystagmus (horizontal = ipsilateral hemisphere)
- Intention tremor
- Slurred speech, scanning dysarthria
- Hypotonia
- Causes: Friederichs ataxia, ataxic telangiectasia, neoplastic, stroke, alcohol, multiple sclerosis, hypothyroidism, drugs (phenytoin / lead poisoning), paraneoplastic (eg, secondary to lung cancer)
Opiate that you can use in dialysis
Tramadol
Do not use other opiates ike morphine as respiratory depression
Ratio when converyting oral to subcut morphine
•Conversion of oral morphine -> subcut is 2:1 so half the oral dose.
Bisoprolol
•beta selective beta antagonist often sedin HF to reduce sympathetic overdrive thought to be the cause of pathologicsl heart remodellingafter cardiac stress
Amitripyline
•often used in management chronic pain, particularly neuropathic. Common side effect is constipation, which patients should be counselled on.
Fludrocortisone in orthostatic hypotension
•corticosteroid mainly for mineralcorticoid properties leading to sodium retention and effective blood volume and pressure. Indicatiosn are orthostatic intolerance and adrenal insufficiencies. Side affects are oedema due to fluid retention, hypokalaemia and supine hypertension
Constipation causes
- Dietary eg, lack fibre, lack fluid
- Behaviourla – inactivity, avoid defecation
- Electrolyte disturbances eg, hypercalcaemia
- Drugs – opiates, CCBs and some antipsychotics
- Neurologicla disorders –s pinal cord lesions,parkinsons disease, diabetic neuropathy
- Endocrine. - hypothyroidism
- Colon disease – stricture malignancy
- Anal disease eg, anal fisur,e proctitis
Consitpation management
- Exclude underlying causes
- Lifestyle modification
- Enemas if impaction eg, sodium citrae
- Supposities eg, glycerol
- Bulk laxatives eg, isphaghula hush, methlcellulose
- Stool softeners eg, docusate sodium
- Osmotic laxatives eg, lactulose, macrogol
- Stimulant laxatives eg, senna, bisacodyl.
DOLS
- Deprivation of liberty safeguard.
- Protection of rights of patients detained in a hospital or care come.
- Patients should be proven to lack in capacity andexpress a wish to leave the facility.
- Must be authorized by supervisory authorty like local authority.
- Over 18, suffering form mental disorder, patient, lack capacity, proposed restrictions would dperivethem and be in their best interests, whether MH act better and no valid decision to refuse treatment.
