GERIATRICS + Stroke Medicine Flashcards
What does the internal carotid artery branch off to supply?
branches off to create the Anterior cerebral artery, as well as posterior communicating artery to join the circle of Willis
After this the ICA continues on as the Middle cerebral artery, which supplies the lateral portions of the cerebrum.
What does the middle cerebral artery supply?
· MIDDLE CEREBRAL ARTERY—(huge artery) supplies majority of lateral surface of the hemisphere and deep structures of anterior part of cerebral hemisphere.
What does the anterior cerebral artery supply?
· ANTERIOR CEREBRAL ARTERY (supplies and runs over Corpus Callosum and supplies Medial aspects of Hemispheres (anteromedial aspects of the cerebrum)
Outline the pathology behind an ischaemic stroke of atherosclerotic origin
Basically formation of atherosclerotic plaque
Irritants damage the endothelium, damage becomes a site for atherosclerosis
A plaque forms, made of fats, cholesterol, proteins, calcium and immune cells encased in a fibrous cap.
If cap ruptures, (interestingly smaller plaques are more dangerous as they have weaker caps that are more prone to being ruptured), then
Soft core is thrombogenic and platelets adhere to the exposed collagen, creating a clot, Known as an Atherothromboembolism
Outline the pathology behind an ischaemic stroke of emboli origin.
Blood clot from elsewhere in the body, typically from atherosclerosis or from the heart
Cardiac emboli from AF, MI or infective endocarditis 🡪 blood stasis, forming a blood clot.
Only emboli in the systemic circulation/aka left side of heart can cause an embolic stroke.
Emboli in right side of heart will go to the lung, *unless a patient has a Septal defect- they can travel through the septal defect and go up to brain
Outline the pathology behind an ischaemic stroke due to shock. What are watershed infarcts
A rapid drop in blood pressure/perfusion to brain means that areas in the brain furthest from arterial blood supply - Known as Watershed zones Can undergo infarction.
Watershed infarcts are unique ischemic lesions which are situated along the border zones between the territories of the major cerebral arteries.
Causes of ischaemic strokes - Where are the “Watershed zones” of the brain?
- Cortical border zone infarction: border of ACA/MCA and MCA/PCA
- Internal border zone infarction: borders of penetrating MCA branches,orborders of the deep branches of the MCA and ACA (resulting in deep white matter infarction)
Name some risk factors for a stroke
- Hypertension
- Age: the average age for a stroke is 68 to 75 years old
- Smoking
- Diabetes
- Hypercholesterolaemia
- Atrial fibrillation
- Vasculitis
- Family history
- Haematological disease: such as polycythaemia, Sickle cell anaemia
- Medication: such as hormone replacement therapy or the combined oral contraceptive pill
What are the clinical manifestations of a stroke in the anterior cerebral artery?
1. Lower limb weakness and loss of sensation to the lower limb.
2. Gait apraxia (unable to initiate walking).
3. Incontinence.
4. Drowsiness.
Decrease in spontaneous speech.
Contralateral hemiparesis (weakness of one side of the entire body) and sensory loss with lower limbs > upper limbs
What are the clinical manifestations of a stroke in the middle cerebral artery?
Contralateral hemiparesis with upper limbs > lower limbs
Facial drop
sensory loss with upper limbs > lower limbs
Homonymous hemianopia
Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere; patients fail to be aware of items to one side of space
Aphasia: if affecting the ‘dominant’ hemisphere (the left in 95% of right-handed people) as Brocas/Wernickes areas supplied by MCA)
Aphasia is the medical term for full loss of language, while dysphasia stands for partial loss of language.
What is a homonymous hemianopia?
a visual field defect involving either the two right or the two left halves of the visual fields of both eyes.
What are the clinical manifestations of a ischaemic stroke in the vertebral basilar arteries?
- Cerebellarsigns
- Reduced consciousness
- Quadriplegiaorhemiplegia
quadriplegia,
disturbances of gaze and vision,
lockedin syndrome (aware, but unable to respond
What is the first line investigation to do for a stroke, what would you see?
CT scan ASAP
Distinguishes ischaemic from haemorr
hypoattenuation (darkness) of the brain parenchyma
loss of grey matter-white matter differentiation, and sulcal effacement - a space or cavity has been obliterated by the external application of mass effect.
hyperattenuation (brightness) in an artery indicates clot within the vessel lumen
What are some other investigations you would do for a Stroke
- ECG:assess for AF, MI
-
Bloods:
- Screen for risk factors includingHba1c, lipids, clotting screenand rule out stroke mimics such ashypoglycemia and hyponatraemia
- In younger patients, consider ESR, autoantibody and thrombophilia screen (ESR raised in vasculitis)
- CT angiogram (CTA):identifies arterial occlusion and should be performed in all patients who are appropriate for thrombectomy
- MRI head:MRI is an alternative to non-contrast CT head; MRI is more sensitive but CT is safer and easier to obtain
What is the management for an Ischaemic stroke?
Maintain stable blood glucose levels, hydration status and temperature
Blood pressure should not be lowered too much during a stroke because this risks reducing the perfusion to the brain.
- Thrombolysis: alteplase given if < 4.5 hours of symptom onset and haemorrhage excluded on imaging
Aspirin 300mg for 2 weeks
Prophylaxis - Lifelong clopidogrel (75mg, an Antiplatelet)
What are some complications of thrombylysis ? What is the treatment for small storkes
Small strokes - Dual antiplatelet, of 75mg of Aspirin and Clopigerel
Complications of thrombolysis -
Bleeding anywhere, especially in the brain haemorrhagic stroke, and in the urinary tract - so try to avoid catherising patients who have just had thrombolysis
What is a TIA?
Sudden onset focal neurological deficit.
Older definition:
symptoms of a stroke that resolve within 24 hours.
New definition:
transient neurological dysfunction secondary to ischaemia without infarction.
Either time based or tissue based
DOES NOT CAUSES ACUTE INFARCTION
What are the symptoms of a TIA in the internal carotid artery?
Depends on the site of the TIA:
ACA - weak/numb contralateral leg
MCA - weak/numb contralateral side of body, face drooping w/forehead spared, dysphasia (temporal)
PCA -Homonymous hemianopia: visual field loss on the same side of both eyes
Hemisensory loss
Amaurosis fugax
What are the symptoms of a TIA in the vertebral/ basilar arteries
Diplopia – double vision
Vertigo
Vomiting
Choking and dysarthria
Ataxia
Hemisensory loss
TIA scoring - what score can help stratify which patients are at a higher risk of a stroke following a TIA?
ABCD2 score – risk score of strokes (max score is 7)
A – Age – > 60 (1 point)
B – Blood pressure (at presentation), 140/90 or more (1 point)
C – Clinical features: Unilateral weakness (2 points), Speech disturbance without weakness (1 point)
D – Duration, 60 minutes or longer (2 points), 10-59 minutes (1 point)
D – Presence of diabetes (1 point)
High risk:
ABCD2 score of 4 or more, AF is present, More than TIA in one week or a TIA whilst on anti-coagulation
Low risk:
None of the above
Present more than a week after their last symptoms have resolved
What are the primary investigations for a TIA
The Face Arm Speech Time Test (FAST test): check for/ ask about facial weakness, arm weakness, speech difficulty
- ECG: rule out AF as an underlying cause
- Auscultation: listen for carotid bruit
- Bloods:
- PT time/INR - in case thrombolytic therapy is needed
- To exclude hypoglycaemia/hyponatraemia
- FBC – looking for polycythaemia
CT scan - Request an urgent CT scan of the head
Carotid doppler – look for stenosis
CT angiography – look for stenosis
What is the management for a TIA?
Immediate management
Immediate loading dose: Aspirin 300mg
Refer to specialist – to be seen within 24h of symptom onset
Antiplatelet therapy
Standard treatment is Aspirin 75mg daily
With modified-release Dipyridamole
OR Clopidogrel daily
What is the acute management for a TIA?
What procedure is done?
- Antiplatelet:initiallyaspirin 300mg - the first-line, immediate management, if aspirin not appropriate, give an Clopidergol
REFER TO STROKE SPECIALIST*
Carotid endarterectomy:surgical procedure to remove the blockage, Done within 2 weeks stenosis of > 70% on Doppler is an indication for urgent endarterectomy
What further managment can you provide for a TIA, after the acute antiplatelets?
A High intensity Statin - atorvastatin : 20-80 mg orally once daily
An anticoauglant for AF - eg A low molecular weight heparin eg dalteparin, or
A direct thrombin inhibitor or factor Xa inhibitor - rivaroxaban
Give aspirin 300mg OD for 2wks, then switch to clopidogrel 75mg OD.
What are the main complications of a TIA?
How can you distinguish between a TIA and a Stroke?
Increased risk of stroke
Increased risk of underlying CVD
You cant distinguish until after recovery
TIA Sx resolve usually within/<24 hours
Stroke Sx last more than 24 hours
What are the subtypes of haemorrhagic stroke?
Intracerebral: bleeding within the brain parenchyma
Subarachnoid: bleeding into the subarachnoid space, between the pia mater and arachnoid mater of the meninges
Intraventricular: bleeding within the ventricles; prematurity is a very strong risk factor in infants
An intracerebral haemorrhage that involves just the brain tissue is called an intraparenchymal haemorrhage, whereas if the blood extends into the ventricles of the brain which store cerebrospinal fluid, it’s called an intraventricular haemorrhage.
What are the main aetiologies of a primary haemorrhagic stroke?
Hypertension
- Arteriovenous malformations: blood vessels that directly connect an artery to a vein. Over time these abnormal vessels dilate and can rupture
- Vasculitis
- Vascular tumours - aka Haemangioma
Cerebral amyloid angiopathy: a degenerative disease where abnormal protein deposits in the walls of arterioles making them less compliant
Head trauma
How can a haemorrhagic stroke be secondary to an ischaemic stroke?
Ischaemia causes brain tissue death.
If there is reperfusion, there’s an increased chance that the damaged blood vessel might rupture. Bleeding into dead tissue is called haemorrhagic conversion.
Outline the pathology that a haemorrhagic stroke leads to.
pool of blood which increases pressure in the skull and puts direct pressure on nearby tissue cells and blood vessels
downstream tissue from bleed are also deprived of oxygen-rich blood. Healthy tissue can die from both the direct pressure and the lack of oxygen
Increased ICP can also lead to
CSF obstruction, - Hydrocephalus
Midline shift
Tentorial herniation
What are some general clinical manifestations of a haemorrhagic stroke?
Similar to an ischaemic stroke - brain region specific
- Headache
- Weakness
- Seizures
- Vomiting
- Reduced consciousness
- Anterior or middle cerebral artery stroke: numbness and sudden muscle weakness.
- Broca’s area or Wernicke’s area stroke: slurred speech or difficulty understanding speech, respectively.
- Posterior cerebral artery stroke: vision disturbances.
What are some manifestations that can point to a haemorrhagic stroke, over ischaemic?
Pointers to haemorrhage:
Sudden loss of consciousness
Severe headache
Meningism- the clinical syndrome of headache, neck stiffness and photophobia, often with nausea and vomiting - can be caused by raised ICP
Coma
Will only cause a headache when there is pressure on the meninges!!
These are unreliable, a CT scan is needed for differentiation
What are the investigations for a intercranial haemorrhage?
Request an immediate non-contrast CT scan of the head - will see hyperattenuation (brightness), suggesting acute blood, often with surrounding hypoattenuation (darkness) due to oedema
- Angiography: visualise the exact location of haemorrhage
- Check FBC and clotting
What is the management for an intercranial haemorrhage?
- Consider intubation, ventilation and ICU care if they have reduced consciousness
- Correct any clotting abnormality - STOP ANTICOAGULANTS IF PT IS ON THEM
Correct severe hypertension but avoid hypotension
Craniotomy, or stereotactic aspiration
Drugs to relieve ICP - IV MANITOL
Treatment for intracerebral haemorrhagic stroke - How does mannitol work?
elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma
Mannitol hinders tubular reabsorption of water and enhances excretion of sodium and chloride by elevating the osmolarity of the glomerular filtrate.
What are the 3 main causes of a Subarachnoid Haemorrhage?
- Trauma
-
Atraumaticcases are referred to asspontaneousSAH - often due to a saccular cerebral (Berry) Aneurysm - 70-80% of SAH cases
Arteriovenous malformation(AVM) - abnormal connections between artery and vein can dilate and cause rupture - 15% of SAH cases
Can be Idiopathic
Outline the pathophysiology behind a subarachnoid haemhorrage.
Rupture of blood vessel - leads to a rise in ICP,
Pressure on healthy tissues can make them die, as well as brain tissue not getting blood it needs due to bleed - Ischaemia
Vessels being bathed in a pool of blood can cause vasospasm - will further reduce the supply of blood flow to the brain
Also can irritate the meninges, which can lead to scarring which can obstruct CSF outflow ==> Hydrocephalus
What are some signs of a Subarachnoid haemhorrhage?
- Neck stiffness
- Budzinski’s Sign - Flexion of neck = Flexion of Knees
- Kernig sign - Knee cannot be fully extended with hip flexed at 90 degrees
- Focal neurological deficit - eg if affecting Posterior cerebral artery - Oculomotor palsy
- Increased BP
‘Thunderclap’ headache
- Meningism: photophobia and neck stiffness - due to Meningies irritation
- Vision changes
- Nausea and vomiting
- Speech changes
-
Seizures
Papilledema
What are some differentials for a subarachnoid haemorrhage?
Migraine
Meningitis
Corticol vein thrombosis
Carotid/vertebral artery dissection
What investigations would you do for a subarachnoid haemorrhage?
urgent Non Contrast CT head
ASAP
Detects >95% of SAH in first 24 hours - Subarachnoid and/or intraventricular blood, hyperdense areas in the subarachnoid space
“Star” shaped sign - or hyerdense blood in the gyri - as blood is not in the brain tissue, but on top of the pia mata
ECG - Arrhythmias and ischaemic changes, Prolonged QTc, ST segment/T-wave abnormalities.
Lumbar puncture – if CT normal but SAH still suspected
Findings - RBCs or xanthochromia (yellow pigmentation due to degradation of haemoglobin to bilirubin)
Electrolytes - Moderate hyponatraemia
ABG – to rule out hypoxia
What is the non surgical management for a subarachnoid haemorrhage?
Immediately refer to neurosurgeon
Nimodipine - Ca2+ antagonist, (CCB) Reduces vasospasm and therefore cerebral ischaemia
Re-examine CNS often
IV fluids -Maintain cerebral perfusion
Ventricular drainage for hydrocephalus
If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol
What is the surgical management for a subarachnoid haemorrhage?
first-line endovascular coilingof the aneurysm -reduces blood circulation to the aneurysm inserting one or more microsurgical detachable platinum wires, into the aneurysm until there is no more blood flow occurring. Usually enter through leg.
Second-line issurgical clippingvia craniotomy - opening in the skull is created to reach the aneurysm. Then small metal clip on the neck (opening) of the aneurysm to obstruct the flow of blood.
Define what an Extradural/ Epidural Haemorrhage is.
A bleed ABOVE the dura mater, between the outer endosteal of the dura and the skull.
Where is the most common site for an extradural haematoma? Why is this?
The most common site where the frontal, parietal, temporal and sphenoid bones join together, CALLED THE PTERION ===>
This section of the skull is relatively thin and it’s located right above the middle meningeal artery.
What are some symptoms of an extradural haemorrhage
Head injury
- Reduced GCS: loss of consciousness after the trauma due to concussion
- There might be a lucid interval after initial trauma if there is a slower bleed. This is followed by rapid decline. ==> Therefore, if suspect a fracture/bleed in head injury, they need a scan!
- Headaches
- Vomiting
- Confusion
- Seizures
- Pupil dilation if bleeding continues
- May be focal neurological symptoms e.g. muscle weakness, hemiparesis, abnormal plantar reflex (upgoing plantar) or sensory problems
What investigations would you do for a extradural haematoma?
CT scan – shows biconvex hyperdense haematoma that is adjacent to the skull:
Blood forms rounded/biconvex shape as the tough dural attachments to the skull keep it more localised - Don’t cross suture lines
Skull X-ray – may be normal or show fracture lines crossing the course of the middle meningeal artery
Skull fracture increases the extradural haemorrhage risk so do an urgent CT on anyone with suspected skull fracture
If a pupil is fixed and dilated, what is affected?
An affixed and dilated pupil usually indicates a problem with the parasympathetic innervation of the eye, often due to an issue affecting the oculomotor nerve or its associated pathways, or the nucleus that controls this, the Edinger-Westphal nucleus
This can be caused by various conditions such as brain injury, brain haemorrhage, uncal herniation, or an aneurysm pressing on the oculomotor nerve.
What are the main causes for a subdural haematoma?
Rupture of bridging veins, usually caused by:
- Brain atrophy: in the elderly the brain shrinks in size which means that the bridging veins are stretched across a wider space where they are largely unsupported
- Alcohol abuse: caused the wall of the veins to thin out, and make them more likely to break.
-
Trauma/ injury e.g.
- Falls
- Shaken baby syndrome
- Acceleration-deceleration injury: speeding on the road and then suddenly slamming the brakes
What are some clinical manifestations of a subdural haematoma
- Reduced GCS: loss of consciousness right after the injury or in the ensuing days to weeks as the haematoma increases in size.
- Headaches
- Vomiting
- Seizures
- Sometimes there can be focal neurological symptoms e.g. muscle weakness, unequal pupils, hemiparesis or sensory problems
Confusion
May fluctuate
Insidious physical & intellectual slowing
Personality change
Unsteadiness
They often cannot remember the traumatic injury as it was long ago
What is the investigations for a Subdural haemorrhage?
- Immediate NON CONTRAST CT head to establish the diagnosis. Shows clot and midline shift.
Bleeding is between the dura and arachnoid so subdural haematomas follow the contour of the brain and form a crescent-shape and cross suture lines. This is different to an epidural haemorrhage!
Check FBC and clotting
What would you see on a non contrast CT head for someone with a
Acute Subdural haematoma
Chronic subdural haematoma
Acute on chronic haematoma
- Acute subdural haematoma: hyperdense mass = looks “more white” than the surrounding healthy brain tissue
- Chronic subdural haematoma: hypodense masses = “less white” than the surrounding brain tissue.
- Acute on chronic bleeding: combination of hyperdense and hypodense, seen in individuals who have a rebleed in the bridging veins after a chronic haematoma has already formed.
What is the management of subdural haematoma?
IV mannitol - reduce ICP
Burr hole / Craniotomy to relieve pressure
Craniotomy a large opening in the skull is created to evacuate the haematoma and relieve the associated mass effect.
What would you give in the management of a stroke in someone with AF?
Warfarin/DOAC, it’s superior to aspirin in Atrial fibrillation / mural thrombus
Warfarin blocks one of the enzymes (proteins) that uses vitamin K to produce clotting factors. This disrupts the clotting process, making it take longer for the blood to clot
DOAC - eg rivaroxaban inhibit Thrombin
What is seen in Wernicke’s Aphasia?
What artery is blocked in wernickes aphasia?
history of fluent, yet confused speech.
Wernicke’s aphasia can be caused by a blockage in the inferior division of the left Middle Cerebral Artery
Therefore, a patient with Wernicke’s aphasia will talk fluently. However, the content will not make sense.
What is seen in Brocas Aphasia?
What artery is blocked in Brocas aphasia?
causes non-fluent speech. Patients often have word-finding difficulties. However, comprehension remains intact.
Broca’s area is within the frontal lobe = often affected by infarction of the left superior division of middle cerebral artery.
What is Benign paroxysmal postional vertigo?
common cause of recurrent episodes of vertigo triggered by head movement. It is a peripheral cause of vertigo, meaning the problem is located in the inner ear rather than the brain
What is the presentation of Benign Paroxysmal postional vertigo?
It is more common in older adults.
A variety of head movements can trigger attacks of vertigo. A common trigger is turning over in bed. Symptoms settle after around 20 – 60 seconds, and patients are asymptomatic between attacks. Often episodes occur over several weeks and then resolve but can reoccur weeks or months later.
BPPV does not cause hearing loss or tinnitus.
What is the pathophysiology behind BPPV? What is thought to cause it?
BPPV is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal.
The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.
They may be displaced by a viral infection, head trauma, ageing or without a clear cause.
How do you diagnose BPPV? Outline how to do it
The Dix-Hallpike manoeuvre:
It involves moving the patient’s head in a way that moves endolymph through the semicircular canals and triggers vertigo in patients with BPPV.
In patients with BPPV, the Dix-Hallpike manoeuvre will trigger rotational nystagmus and symptoms of vertigo. The eye will have rotational beats of nystagmus towards the affected ear (clockwise with left ear and anti-clockwise for right ear BPPV).
How do you carry out the Dix Hallpike manoeurve to diagnose BPPV?
To perform the manoeuvre:
The patient sits upright on a flat examination couch with their head turned 45 degrees to one side
Support the patient’s head to stay in the 45 degree position while rapidly lowering the patient backwards until their head is hanging off the end of the couch, extended 20-30 degrees
Hold the patient’s head still, turned 45 degrees to one side and extended 20-30 degrees below the level of the couch
Watch the eyes closely for 30-60 seconds, looking for nystagmus
Repeat the test with the head turned 45 degrees in the other direction
What manourve do you do to treat BPPV? Outline how ot do it
Epley Manoeuvre
- Sit upright w head turned 45 degrees to one side (eg right)
- Lie down as quickly as you can, w head still turned 45 degrees (to right) - wait for a minute or so
- Turn your head to 45 degrees other side (eg left) keeping your head down and hanging over the edge of your bed.
- Turn to lie on your left hand side, not moving your head, rotate head again 45 degrees again to the left so you are facing floor
- Slowly sit up, tilting your head down to tuck chin to chest
What is delirium? name some factors of it
First described more than 2500 years ago, delirium, derived from the Latin word delirare (deviate from a straight track), is an acute, fluctuating syndrome of altered attention, awareness and cognition caused by an underlying condition or event in vulnerable people
Disturbance of consciousness , with reduced ability to focus or shift attention.
Changes in cognition or development of perceptual disturbance not better accounted for by pre-existing or evolving dementia.
Disturbance develops over a short period of time and fluctuates over the course of the day.
What are some common causes and risk factors of Delirium?
Risk factors >65y, dementia/previous cognitive impairment, hip fracture, acute illness, psychological agitation (eg pain).
Causes
* Surgery/post-GA.
* Systemic infection: pneumonia, UTI, malaria, wounds, IV lines.
* Intracranial infection or head injury.
* Drugs/drug withdrawal: opiates, levodopa, sedatives, recreational.
* Alcohol withdrawal
* Metabolic:uraemia,liver failure,Na+or glucose, Hb,malnutrition(beriberi,p268).
* Hypoxia: respiratory or cardiac failure.
* Vascular: stroke, myocardial infarction.
* Nutritional: thiamine, nicotinic acid, or B12 deficiency
How can delirium be divided?
Delirium can be divided into three subtypes:
hperactive delirium: a subtype of delirium characterised by people who have heightened arousal and can be restless, agitated or aggressive
hypoactive delirium: a subtype of delirium characterised by people who become withdrawn, quiet and sleepy
mixed
hypoactive and mixed delirium can be more difficult to recognise
What are the 6 main precipitants of delirium?
PINCH ME
Pain
Infection
Nutrition
Co-morbidities
Hydration
Medication
Environment
+ bladder
What are some investigations you would do for delirium
Look for the cause (eg UTI, pneumonia, MI): do FBC, U&E, LFT, blood glucose,
ABG, septic screen (urine dipstick, CXR, blood cultures); also consider ECG, malaria
films, LP, EEG, CT.
Think about causes - be vigilant for constipation
What are the diagnostic tools used in assessing patients for delirium?
AMT
Abbreviated Mental Test - a score of 6 or less implies a mental impairment 10 questions in total
- What is your age
- What is the time
- Can you remember an address (42 West Street)
- What’s the year
- Name of hospital you’re in?
- Can you recognise the role of two different people ? (eg nurse, doctor)
- What year did WW1 begin ?
- What is your DOB?
- . Name the current Monarch or PM
- Count backwards from 20 to 1
DSM-5 (diagnostic and statistical manual of mental disorders)
What is the management for delirium
As well as identifying and treating the underlying cause, aim to:
* Reorientate the patient: explain where they are and who you are at each encounter.
Hunt down hearing aids/glasses. Visible clocks/calendars may help.
* Encourage visits from friends and family.
* Monitor fluid balance and encourage oral intake . Be vigilant for constipation.
* Practise sleep hygeine
* Review medication and discontinue any unnecessary agents. Only use sedation if the
patient is a risk to their own/other patients’ safety (never use physical restraints).
Consider haloperidol and lorazepam as sedatives if patients are very agitated
Define frailty
a clinical state of increased vulnerability and reduced ability to cope with everyday/acute stressors resulting from aging-associated decline in reserve and function across multiple physiological systems.
What are the acute presentations of frailty? (also known as frailty syndromes)
falls
sudden reduced mobility
new or accelerated state of confusion (delirium)
acute change in continence
sensitivity to a new medication
What are the most common comorbidities contributing to frailty? 5+
stroke
CHD
Diabetes Mellitus
Alzheimer’s Disease
urinary problems
depression
visual loss
hearing and visual impairment
falls
What are the 5 elements of a comprehensive Geriatric assessment?
FEMPS
Functional ability - Mobility, balance, ADL
Environment - House of residence, equipment, safety features
Mental Health - Cognition/Mood
Physical Health -
Optimise Comorbidities
Medication review, frailty status
Social Circumstances - Former/informal carers, and Power of Attorney status
Outline the four steps in the comprehensive Geriatric assessment process.
- assessment.
- Writing a problem list: this should cover all five domains, with prioritization.
- Management planning: for each problem, a management plan should be proposed.
- Goal setting: for each management plan, a treatment goal is established.
An example of such a goal would be an improvement in measures of postural sway following gait and balance exercise within 4 weeks.
What are the major risk factors for falls in the elderly? (not explicit conditions, more general stuff)
age 80+
female
low weight
previous fall
polypharmacy/medications (commonly benzodiazepines, antidepressents, bp-lowering drugs, anticonvulsants)
cognitive impairment
orthostatic hypotension
vision problems
chronic health conditions affecting mobility
environmental risk factors
lack of assistive devices in the bathroom
loose throw rugs
low level lighting
obstacles on the walking path
slippery outdoor conditions
What are some common medical conditions that can increase the risk of falls in the elderly?
Osteoporosis
Arthritis
Neurological disorders: Conditions like Parkinson’s disease, multiple sclerosis, or neuropathy can impair balance and coordination.
Cardiovascular conditions: Heart disease, low blood pressure, irregular heart rhythms, aortic stenosis.
Vision problems
Medication side effects
Cognitive impairment: Conditions like dementia or Alzheimer’s disease can impair judgment and increase the risk of falls.
Dehydration
What are some risk factors for patients that can lead to oesteoporosis?
SHATTERED
Steroid (prednisolone use) – SSRIs, GnRH analogues
(goserelin)
Hyperthyroidism, hypercalciuria and hyperparathyroidism + Cushing’s
Alcohol and tobacco
Thin – BMI < 18.5, T1DM
Testosterone ↓ - ↑ bone turnover, hypogonadism turner’s/Klinefelter
Early menopause – ↑ bone turnover, premature ovarian failure
Renal or liver failure
Erosive/inflammatory bone disease – RA/myeloma
Dietary calcium ↓ or malabsorption, T1DM
Strength training can increase bone mass, so protective
What are some symptoms of oesteoporosis? What are the most common sites of fractures for someone with oesteoporosis?
Asymptomatic condition with the exception of fractures
Common fragility fractures include vertebral crush fracture and those of the distal wrist (Colles’ fracture) and proximal femur.
may also see Thorasic Kyphosis (hunching over)
What screening tool can you use in osteoporosis?
FRAX = fracture risk assessment tool
Predicts the risk of a fragility fracture over the next 10 years. Usually the first step of assessment and is done on patients at risk of osteoporosis
BMI, co-morbidities, smoking, alcohol and family history +/- bone mineral density
- It gives results as a percentage 10 year probability of a:
- Major osteoporotic fracture
- Hip fracture
What T scoring on a DEXA scan would be indicative of
Better than reference
No evidence of oesteoporosis
Osteopenia (offer lifestyle advice)
Osteoporosis
T-score
>0 BMD = is better than the reference.
0 to -1 = BMD is in the top 84%: no evidence of osteoporosis.
-1 to -2.5 = Osteopenia. Risk of later osteoporotic fracture. Offer lifestyle advice.
-2.5 or worse = Osteoporosis. Offer lifestyle advice and treatment Repeat DEXA in 2yrs.
What are some other treatment options for osteoporosis?
Hormone replacement therapy should be considered in women that go through menopause early.
Raloxifene - Selective oestrogen receptor
Teriparatide - recombinant PTH, increases bone formation
Describe what heart failure is.
In what two ways can it happen?
When the heart can’t supply enough blood to meet the body’s demands
Either by systolic Heart failure, where heart’s ventricles can’t pump blood hard enough during systole (not squeezing enough(
or by Diastolic heart failure, where or not enough blood fills the ventricles during diastole (not filling enough) (reduced preload)
What is systolic heart failiure?
What are it’s main causes?
Ejection fraction <40% (SV/EDV)
Caused by
IHD
MI
Hypertension
Cardiomyopathy
What is diastolic heart failure? What are its made causes?
Inability to relax and fill
There is reduced preload because there is abnormal filling of the LV
Ejection fraction >50%
Caused by
Constrictive pericarditis
Cardiac tamponade
Hypertension
How can left sided heart failure cause right sided heart failure?
LSHF leads to increased pulmonary blood pressure, due to fluid build up.
increased pulmonary blood pressure makes it harder for the right side to pump blood into.
In this case the heart failure would be biventricular, since both ventricles are affected.
What are some causes of Right sided heart failure?
Hypertension
Pulmonary stenosis
Lung disease (cor pulmonale)
Atrial/ventricular septal defects
What are the signs of left sided heart failure?
Signs:
Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur
What are the signs/symptoms of Right hand sided heart failure?
Raised JVP – JVP distension
Hepatomegaly/Splenomegaly
Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
Ascites
Weight gain (fluid)
blood backing up into the systemic veins in
a) Jugular vein
b) liver and spleen
c) peritoneum
d) interstitial soft tissue space - legs and sacrum
leads to what signs/symptoms in right sided heart failure?
Blood back up into jugular vein Raised JVP, – JVP distension -
b) leads to Hepatomegaly and Splenomegaly (Hepatosplenomegaly)- In extreme cases and lead to cirrhosis of liver, known as cardiac cirrhosis
c) Fluid build up in peritoneum leads to Ascites and weight gain
d) leads to Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
What are some signs of left sided heart failure?
think about what it backs up into! (left side backs up into lungs)
Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur
What could a chest Xray show for someone with heart failure
ABCDE
Recommended for all suspected HF patients
Alveolar oedema - seen in Bat wing shadowing
Kerley B Lines interstitial oedema
Cardiomegaly
Dilated upper lobe vessels of lungs (prominent upper lobe veins)
Effusions (pleural)
A normal CXR does not exclude the possibility of Heart Failure
Heart failure medication 1:What is the first medications you should give in patients with heart failure with reduced ejection fraction?
- an ACE inhibitor, like Ramipril, and Beta blockers, like Bisoprolol
Start low, progress slow! - monitor BP and heart rate
ABAL
(can consider giving an Angiotensin 2 receptor blocker eg Candesartan if intolerant of ACE-i)
Heart failure medication, with reduced
ejection fraction 2: After ACE inhibitors, and Beta blockers what other medications can you give?
A mineralocorticoid receptor antagonist - eg Spironolactone
Heart failure medication 3 - After ACE inhibitors and beta blockers and aldosterone receptor anatagonist what other medications can you give?
(In an reduced ejection fraction heart failure)
Loop Diuretic , like furoesmide
ABAL
Also a drug like Digoxin - good for arrhythmias and AF, and helps symptoms of LVSD (Left Ventricular Systolic Dysfunction.)
—> Helps strengthen heart muscle contractions
What is Cor pulmonale? What are some of its causes?
Right sided heart failure caused by chronic arterial pulmonary hypertension, due to lung diseases, Pulmonary vascular disorders, neuromuscular and skeletal diseases
Outline some of the physiology that occurs in the bowls of people as they age, that can lead to constipation
As we age:
r Peristaltic speed is reduced, leading to a slower transit time.
r Peristaltic strength is reduced due to muscle atrophy.
r Weakened connective tissue within the mucosa results in the
formation of diverticula.
r Increased sensory threshold for the urge to open bowel
Small bowl
Reduced absorption of some nutrients
Decreased motility
What are some associated symptoms of constipation?
Reduced Appetite
Delirium
Vomiting, Nausea
Abdo pain and distension
Urinary retention
Fecal incontinence
Name some different types of Laxatives
Bulking agents increase faecal mass, so stimulating peristalsis - eg Ispaghula husk, eg Fybogel
Stimulant laxatives increase intestinal
motility, so do not use in intestinal obstruction or acute colitis - eg Senna, bisacodyl tablets, sodium picosulphate
Stool softeners are particularly useful when
managing painful anal conditions, eg fissure. eg - Lactulose
Enema - used in rectal constipation - most often phosphate
Outline the pathophysiology behind urge incontinence. What things can cause it? (known as Overactive bladder)
Sudden urge to urinate because of an “overactive bladder”, followed immediately by involuntary urination
typically due to an uninhibited detrusor muscle that contracts randomly.
Usually associated with urinary tract infections. Inflammation may trigger the detrusor muscle.
Outline the pathophysiology behind stress incontinence. What things can cause it?
Increased abdominal pressure overwhelms the sphincter muscles and allows urine to leak out. Causes include pregnancy and exertion, like sneezing, coughing, and laughing.
- Post-prostatectomy in men
Outline the pathophysiology behind overflow incontinence. What things can cause it?
Due to either - Obstruction due to blockage in urine flow
or
Ineffective detrusor muscle. ==> Detrusor cant contract properly so the bladder doesn’t empty properly
In both cases, leads to urine build up, to the point that the bladder is so full that urine dribbles/leaks out through sphincters
Obstruction - - eg benign prostatic hyperplasia,
Ineffective detrusor = Diabetes (neurogenic bladder) Multiple sclerosis, Spinal chord injury
What tool is used to screen inpatients for malnutrition?
Outline the scoring
‘Malnutrition Universal Screening Tool’ MUST
Takes into account:
BMI
% of unplanned weight loss in the last 3-6 months
Whether the patient is acutely unwell and there has been or is likely to be no nutritional intake for more than five days
Add scores together to calculate overall risk of malnutrition
score 0 low risk Score 1 medium risk Score 2 or more high risk
Define Polypharmacy What can it lead to?
Polypharmacy is defined as being prescribed more than four medications. Over one-third of older patients are affected.
Polypharmacy can result in:
r increased risk of side-effects
r increased risk of drug– drug interactions
r a therapeutic cascade (Figure 13.2)
r increased risk of medications not being reviewed thoroughly.
r non-adherence
what is the prescribing cascade?
A prescribing cascade refers to the sequence of events in which an adverse drug event is misinterpreted as a new medical condition, leading to the addition of another, potentially avoidable, medication
Give some reasons why the risks of prescribing are greater in the elderly.
r changes in pharmacokinetics (what body does the to drug, think ADME)
r changes in pharmacodynamics (What the drug does to the body, inducing a response)
r polypharmacy
r frailty (see Chapter 5)
r communication problems
r lack of an evidence base
r guidelines being based on single-organ disease processes.
What are the 5 principles of the Mental Capacity Act?
Assume capacity – person assumed to have capacity until proven otherwise
Maximise decision-making capacity – all practical support to help a person make a decision should be given
Freedom to make seemingly unwise decisions – an apparently unwise decision in itself does not prove incapacity
Best interests – all decisions taken on behalf of the person must be in their best interests
Least restrictive option – when deciding on another person’s behalf, chose the decision that interferes the least with the person’s rights and freedom of action while still achieving goal
What questions should be asked when determining whether something is in the patients best interests?
- What are the patient’s past/present wishes or feelings relating to the decision?
- What are the patient’s values and beliefs relating to the decision?
- What are the risks/benefits of each option?
- Consider other factors e.g. future implications and safety concerns.
Should be verified with consultee ie family member or friend
Outline the two stages needed to gauge mental capacity
1 - is there impairment of or disturbance of function in a person’s brain or mind?
2 is the impairment sufficient to constitute a loss of capacity? 4 components
What are the four components around capacity to make a decision that are required in order to have capacity?
Can teh patient understand teh info required to make an decision - RECIEVE
Can they retain the info long enough to make a decision - RETAIN
Can they weigh up the info? RATIONALISE
Can they communicate the decision back RELATE BACK
4 Rs
Outline what is seen in a stage 1 and 2 pressure ulcer
Stage 1. The area looks red and feels warm to the touch. With darker skin, the area may have a blue or purple tint. - Non blanching redness!!
Stage 2. The area looks more damaged and may have an open sore, scrape, or blister.
In both, The person complains of significant pain and the skin around the wound may be discolored.
Outline what is seen in a stage 3 and 4 pressure ulcer
Stage 3. The area has a crater-like appearance due to damage below the skin’s surface. Slough is often present
Stage 4. The area is severely damaged and a large wound is present. full thickness - Muscles, tendons, bones, and joints can be involved. Infection is a significant risk at this stage.
What are the 3 most common skin cancers?
squamous-cell carcinoma, basal-cell carcinoma and melanoma
Cutaneous squamous-cell carcinoma is the second-most common cancer of the skin (after basal-cell carcinoma, but more common than melanoma)
What are some risk factors for getting a squamous cell carcinoma of the skin?
high lexposure to UV radiation
Prior scars, chronic wounds,
actinic keratosis, - is a pre-cancerous area of thick, scaly, or crusty skin
having paler skin that sunburns easily,
Bowen’s disease,
radiation therapy,
tobacco smoking,
Prior basal cell carcinoma,
HPV infection
Immunotherapy
Squamous Cell carcinoma - what is bowens Disease?
Bowen’s disease is essentially equivalent to and used interchangeably with cSCC in situ, when not having invaded through the basement membrane
What are the signs and symptoms of a squamous cell carcinoma?
SCC of the skin begins as a small nodule and as it enlarges the center becomes necrotic and sloughs and the nodule turns into an ulcer
