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Geriatrics Flashcards

1
Q

What is the definition of an Ischaemic stroke?

A

A sudden onset focal or global neurological deficit of vascular aetiology which lasts more than >24 hours or leads to death(or with evidence of infarction on imaging).

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2
Q

What are the main causes of an Ischaemic Stroke?

A
  • Large Vessel Atherosclerosis (50%)
  • Intracranial small vessel atherosclerosis (25%)
  • Cardio-embolic (AF) (20%)
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3
Q

What are the risk factors for an ischaemic stroke?

A
  • older age
  • male sex
  • family history of ischaemic stroke
  • Previous stroke or TIA
  • hypertension
  • smoking
  • diabetes mellitus
  • atrial fibrillation.

Weaker risk factors: hypercholesterolaemia, obesity, poor diet, oestrogen-containing therapy, and migraine

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4
Q

What are the clinical features of a stroke?

A
  • Limb weakness
  • Facial weakness
  • Dysphasia (speech disturbance)
  • Visual field defects
  • Sensory loss
  • Ataxia and vertigo (posterior circulation infarction)

Stroke symptoms are usually asymmetrical

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5
Q

What is the first line investigation for someone presenting with a stroke?

A

Non-contrast Head CT Scan with 1 hour of attending hospital

(very sensitive to haemmorhagic, but will appear normal in the first few hours of an ischaemic stroke)

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6
Q

What is the most sensitive test for confirming an ischamic stroke?

A

Diffusion Weighted MRI

Only done if the diagnosis is unclear

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7
Q

What are some post-acute ischaemic stroke investigations?

A
  • Bloods (Glucose, TFTs)
  • Carotid ultrasound (critical carotid artery stenosis)
  • ECG (for Atrial Fibrillation)
  • CT/MR angiography (intracranial and extracranial stenosis)
  • Echocardiogram (if a cardio-embolic source is suspected)
  • Vasculitis and Thrombophilia screens (in young patients)
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8
Q

What are some post-acute Haemmorhagic stroke investigations?

A

Serum toxicology screen

(sympathomimetic drugs (e.g. cocaine) are a strong risk factor)

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9
Q

What is the acute management of an ischaemic stroke?

A

Once a head CT has ruled out haemorrhage:

Thrombolysis with Alteplase (tissue plasminogen activator) if patients present within 4.5 hrs of symptom onset. (Assuming there are no contraindications)

Mechanical Thrombectomy in patients with an anterior circulation stroke (+ selected posterior circulation strokes) providing they have good baseline function.

  • Procedure must begin within 5 hours of known onset
  • Must be a proximal intracranial large vessel occlusion

300mg Aspirin for 2 weeks started immediately if thrombolysis not offered. Or 24hrs after thrombolysis.

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10
Q

Give some contraindications for thrombolysis

A
  • Recent head trauma
  • GI or intracranial haemorrhage
  • Recent surgery
  • Clotting disorders
  • Acceptable BP, platelet count, and INR
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11
Q

HALTSS

What are the key steps for secondary stroke prevention?

A
  • Hypertension - Anti-hypertensive therapy should be initiated 2 weeks post-stroke.
  • Antiplatelet therapy - Clopidogrel (75 mg once daily) or warfarin (in patients with a stroke secondary to AF); started 2 weeks post-stroke.
  • Lipid-lowering therapy - High dose Atorvastatin (20-80mg) once nightly.
  • Tobacco - smoking cessation
  • Sugar - Diabetes Screen
  • Surgery - Carotid endarterectomy in patients with ipsilateral carotid artery stenosis
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12
Q

What are some stroke differential diagnoses?

A
  • Hypoglycaemia
  • Drugs / Alcohol
  • Seizure
  • Migraine
  • Bell’s Palsy
  • Tumour / Space occupying lesion
  • Meningitis / Encephalitis
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13
Q

What is a Total Anterior Circulation Infarct (TACI) defined by?

A
  • Contralateral hemiplegia or hemiparesis, AND
  • Contralateral homonymous hemianopia, AND
  • Higher cerebral dysfunction (e.g. aphasia, neglect)

A TACI involves the anterior AND middle cerebral arteries on the affected side.

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14
Q

What is a Partial Anterior Circulation Infarct (PACI) defined by?

A
  • 2 of the factors for a TACI OR
  • Higher cerebral dysfunction alone.

A PACI involves the anterior OR middle cerebral artery on the affected side.

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15
Q

What is a Posterior Circulation Infarct (POCI) defined by?

A
  • Cerebellar dysfunction, OR
  • Conjugate eye movement disorder, OR
  • Bilateral motor/sensory deficit, OR
  • Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR
  • Cortical blindness/isolated hemianopia.

A POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).

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16
Q

What is a Lacunar Infarct defined by?

A

involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

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17
Q

What are the 4 Posterior Stroke Syndromes?

A
  • Basillar Artery Occlusion - Causes locked in syndrome, loss of consciousness or sudden death
  • Wallenberg’s syndrome (lateral medullary syndrome)
  • Lateral pontine syndrome - Caused by occlusion of the anterior inferior cerebellar artery
  • Weber’s syndrome/ Medial Midbrain Syndrome - Caused by occlusion of the paramedian branches of the upper basilar and proximal posterior cerebral arteries
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18
Q

Define Locked in Syndrome

A

It’s Quadriparesis with preserved consciousness and ocular movements.

Its caused by Basillar Artery Occlusion

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19
Q

What is the clinical presentation of Lateral Pontine Syndrome?

A

Symptoms are similar to Wallenberg’s (see above), but:
Ipsilateral: facial paralysis and deafness

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20
Q

What is the clinical presentation of Weber’s Syndrome?

A

It causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.

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21
Q

What is the definition of a Haemorrhagic Stroke?

A

A cerebrovascular event that occurs when the wall of a blood vessel in the brain weakens and ruptures.

This rupture causes bleeding in the brain, leading to haematoma formation and consequently neuronal injury.

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22
Q

What is the clinical presentation of a Sub-arachnoid Haemmorhage?

A
  • Severe “Thunderclap” Headache
  • Vomiting
  • May have seizures
  • May have loss of consciousness
  • May have CN3 and CN6 Nerve palsy

Meningitis Mimics:

  • Neck Stiffness and Photophobia
  • Kernig’s sign
  • Brudinski’s sign
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23
Q

What are the risk factors for a haemorrhagic stroke?

A
  • Age
  • Male sex
  • Family history of haemorrhagic stroke
  • Haemophilia
  • Cerebral amyloid angiopathy/hypertension
  • Anticoagulation therapy
  • Illicit sympathomimetic drugs (e.g. cocaine and amphetamines)
  • Vascular malformations (younger patients)

Weaker RFs include: NSAIDs, Heavy alcohol use and
Thrombocytopenia

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24
Q

What is the epidemiology of haemorrhagic strokes?

A

They make up 15% of all strokes (the other 85% being ischaemic)

  • Increasing prevalence with age
  • More common in men
  • Intra-cerebral haemorrhages more common in Asians.

Three quarters are intra-cerebral haemmorhages and the rest are sub-arachnoid.

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25
Q

What are the causes of a Haemorrhagic Stroke?

A
  • Cerebral Amyloid Amyopathy (CAA): where beta peptide deposits in the walls of small blood vessels making them weak.
  • Hypertension
  • Aneurysms
  • Arteriovenous Malformations (AVM)
  • Trauma
  • Blood thinning medication
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26
Q

What is the clinical presentation of Wallenberg’s Syndrome?

A
  • Ipsilateral: facial pain and temperature loss
  • Contralateral: limb/torso pain and temperature loss
  • Ataxia, nystagmus
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27
Q

Describe Kernig’s Sign

A

The patient is positioned lying on their back with both the hip and knee flexed at 90 degrees.

The examiner then attempts to extend the patient’s knee. If the patient experiences pain and resistance to knee extension, especially when attempting to straighten the leg, it is considered a positive Kernig’s sign.

This sign suggests meningeal irritation or inflammation.

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28
Q

Describe Brudinski’s Sign

A

The examiner gently flexes the patient’s neck forward toward the chest while the patient is lying on their back.

If the patient involuntarily flexes their hips and knees in response to neck flexion, it is considered a positive Brudzinski’s sign.

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29
Q

What is the general clinical presentation for a haemorrhagic stroke?

A
  • Severe headache
  • Altered consciousness, ranging from drowsiness to coma
  • Vomiting
  • Focal neurologic signs
  • Seizures
  • Hypertension
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30
Q

What investigations should be done when a haemorrhagic stroke is suspected

A

Non-Contrast Head CT - Is first line and diagnostic

MRI of the head - Can help identify underlying causes

MR Angiogram or Digital Substraction Angiography - Helps to identify vascular abnormalities that could have caused the bleed

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31
Q

What is the management for a haemorrhagic stroke?

A

After a head CT:

Surgical:

  • Burr Hole Craniotomy (for Subdural haemorrhage)
  • Surgical Clipping or endovascular coiling (for Subarachnoid haemorrhage)

Pharmacological

  • Hypertensive control
  • IV Fluids - To maintain cerebral perfusion
  • Nimodipine 60mg for 3/52 (CCB) - Reduces cerebral artery spasm (subarachnoid)
  • IV Mannitol - Reduces Intra-cranial pressure (Sub and extradural)
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32
Q

What is the definition of a TIA?

A

A sudden-onset transient focal neurological deficit with vascular aetiology, where typically, symptoms resolving in less than 1 hour.

It’s caused by focal brain, spinal chord or retinal ischaemia without evidence of acute infarction.

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33
Q

What are the risk factors for a TIA?

A
  • Increased age
  • Male sex
  • hypertension
  • diabetes mellitus
  • high cholesterol
  • atrial fibrillation and carotid stenosis
  • smoking,
  • History of past TIAs / Strokes or cardio-embolic events.
  • Family history of cardiovascular disease / stroke
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34
Q

What are the clinical features of a TIA?

A

Sudden onset neurological deficits (Most resolving within 1 hour)

  • Speech difficulty (dysphasia)
  • Arm or leg weakness
  • Sensory changes
  • Ataxia, vertigo or loss of balance
  • Visual disturbances: Homonymous hemianopia, diplopia or Amaurosis Fungax
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35
Q

What is Amaurosis Fungax?

A

The sudden painless loss of vision in 1 eye

Caused by an emboli passing into the retinal, ophthalmic or ciliary artery; causing temporary retinal hypoxia.

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36
Q

What are some differential diagnoses for a TIA?

A

Ischaemic Stroke

Haemorrhagic Stroke

Migraine with Aura

Focal Motor Seizures

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37
Q

What is the main diagnostic investigation for a TIA?

A

Diffusion Weighted MRI Scan

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38
Q

What other investigations are recommended for a TIA?

A
  • Blood Tests (glucose, lipid profile, clotting factors, LFTs, TFTs, CRP/ESR)
  • Carotid Ultrasound
  • Echocardiogram (looking for cardiac thrombus)
  • ECG looking for AF
  • Consider 24 Hour Tape (looking for paroxysmal AF)
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39
Q

What is the management for a TIA?

A

Immediate assessment (ideally within 24 hrs of symptoms) and referral to the TIA clinic

Lifestyle modification

  • Regular exercise
  • Smoking cessation
  • Healthy Diet

Control of vascular risk factors

  • Hypertension (ACE inhibitor (e.g. ramipril), or ARB (e.g. candesartan)
  • Diabetes
  • Dyslipidaemia (start statin e.g. simvastatin 40mg)

Antiplatlet Therapy

  • Immediate Aspirin 300mg
  • Patients with a High risk TIA or Low risk stroke (according to NIHSS <4) may be started on Dual antiplatelet Therapy (DAPT)
    • Aspirin + Clopidogrel 75mg

No driving until seen by specialist

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40
Q

What is the definition of Benign Paroxysmal Positional Vertigo (BPPV)

A

Is a condition characterised by sudden, episodic attacks of vertigo induced by changes in head position.

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41
Q

What is the pathophysiology of Benign Paroxysmal Positional Vertigo?

A

It’s caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals.

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.

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42
Q

What are the causes of Benign Paroxysmal Positional Vertigo?

A

The calcium carbonate crystals can be displaced by:

  • viral infection
  • head trauma
  • ageing
  • Idiopathic
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43
Q

What are the clinical features of Benign Paroxysmal Positional Vertigo?

A
  • Vertigo attacks provoked by specific head movements (like turning the head to one side while in bed or looking upwards)
  • Episodes of rotational vertigo lasting between 30 seconds to 1 minute
  • Recurrent episodes, often resolving naturally over weeks to months before re-occurring wekks-months later
  • Patients are asymptomatic between attacks

There is no hearing loss or tinnitus

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44
Q

What are some differential Diagnoses for BPPV?

A

Meniere’s disease
episodic vertigo, tinnitus, hearing loss, and sensation of fullness in the ear

Vestibular neuritis
sudden onset severe vertigo, nausea, and imbalance lasting for several days

Labyrinthitis: vertigo
hearing loss, and tinnitus

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45
Q

What is the main diagnostic test for BPPV?

What is the observed finding?

A

The Dix-Hallpike Manoeuvre

  • Rapidly lower the patient to the supine position with an extended neck
  • A positive test recreates the symptoms of benign paroxysmal positional vertigo
  • Rotatory nystagmus
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46
Q

What is the management for BPPV?

A

The Epley Manouvre

This aims to move the detached otoliths out of the semicircular canal and back to the utricle where they originate.

Vestibular Rehabilitation with Brandt-Daroff exercises can be done by the patient at home

Betahistine medication is often prescribed but has limited effectiveness

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47
Q

What is the definition of Delirium?

A

It’s an acute and fluctuating disturbance in attention and cognition causing a confusional state.

Often accompanied by a change in consciousness.

It is typically reversible and frequently seen in the elderly.

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48
Q

What is the epidemiology of Delirium?

A

The prevalence increases with age, severity of illness and the presence of pre-existing cognitive impairment.

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49
Q

What factors may predispose someone to Delirium?

A
  • Old Age
  • Underlying Cognitive Impairment (Dementia)
  • Previous History of Delirium
  • Frailty or multimorbidity
  • Polypharmacy
  • Sensory Impairment
  • Change of Environment
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50
Q

PHONED CHIMPS

What are the main causes of Delirium?

A

Pain
Hypothermia/Pyrexia
Organ dysfunction (renal or hepatic impairment)
Nutrion
Environmental changes
Drugs and alcohol (OTC, illicit, Anti-cholinergics, Opiates, Anti-convulsants)

Constipation
Hypoxia
Infection
Metabolic disturbance (Electrolyte imbalance, Endocrinological issues, Wernicke’s Encephalopathy)
Polypharmacy
Sleep deprivation

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51
Q

WHERE THE F AM I

What is the clinical presentation of Delirium?

A

Where: Disorientation

Thought disorganisation
Hallucinations
Energy Changes: Can by hyperactive or hypoactive

Fluctuating

Acute and Altered sleep
Memory problems

Inattention

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52
Q

What are the features of Hyperactive and Hypoactive Delirium?

A

Hyperactive:

  • Agitated
  • Hallucinations
  • Restless
  • Aggressive

Hypoactive:

  • Withdrawn/Drowsy/Excessive sleeping
  • Calm and Quiet
  • Slowness with everyday tasks
  • Poor concentration/inattention
  • Reduced appetite

Delirium may present as a mixed picture containing features of both or fluctuate between the two. Hypoactive delirium is very hard to pick up

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53
Q

What are some differential diagnoses of Delirium?

A
  • Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.
  • Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.
  • Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.
  • Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.
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54
Q

What initial investigations should be done for Delirium?

A
  • Comprehensive physical examination and history
  • Abbreviated Mental Test Score (AMTS)
  • Confusion Screen (including bloods and urinalysis and imaging)
  • Imaging (possibly Head CT/MRI, Chest XRay or ultrasound of the abdomen depending on scenario)
  • ECG
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55
Q

What tests are involved in a Confusion Screen?

A

Blood Tests:

  • FBC (infection, anaemia, malignancy)
  • U&Es (hyponatraemia, hypernatraemia)
  • LFTs (liver failure with secondary encephalopathy)
  • Coagulation/INR (intracranial bleeding)
  • TFTs (hypothyroidism)
  • Calcium (hypercalcaemia)
  • B12 + folate/haematinics (B12/folate deficiency)
  • Glucose (hypoglycaemia/hyperglycaemia)
  • Blood cultures (sepsis)

Urinalysis:

  • UTI is a very common cause of delirium in the elderly

Imaging Studies:

  • CT Head: if concerned about intracranial bleeding, stroke, ischaemia or abscess
  • Chest X-ray: If concerned about pneumonia or pulmonary odema
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56
Q

What is the non-pharmacological management of Delirium?

A
  • Providing an environment with good lighting
  • Maintaining a regular sleep-wake cycle
  • Regular orientation and reassurance
  • Ensure patients pain is controlled
  • Use same staff
  • Put patients in side room where there is less noise
  • Ensuring the patient’s glasses and hearing aids are used if needed
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57
Q

What pharmacological management can be used for delirium?

A

Treat underlying cause of Delirium

Small doses of haloperidol or olanzapine/Lorazepam/Midazolam.

To be used with caution and only in patients who are extremely agitated and present a danger to themselves or others

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58
Q

Give some differences between delirium and dementia?

A

Delirium

  • Acute
  • Fluctuant
  • Reversible
  • Often have sleep disturbance/consciousness fluctuation
  • Underlying pathology/cause

Dementia:

  • Progressive
  • Constant
  • Irreversible
  • Typically unaltered sleep patterns (in early stages)
  • Brain dysfunction
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59
Q

What is Dementia Syndrome?

A

Decline in memory with impairment of at least one other cognitive function such as skilled movements, language or executive function.

  • A progressive condition which usually requires progressive cognitive decline for >6 months to be diagnosed.
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60
Q

What are the main types of Dementia?

A
  • Alzheimer’s Disease (accounts for 60-80% of cases)
  • Vascular Dementia
  • Lewy Body Dementia
  • Fronto-temporal Dementia
  • Mixed Dementia
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61
Q

What are some causes of Reversible Dementia?

A
  • Depression
  • B12 and Folate Deficiency
  • Hypothyroidism
  • Normal Pressure Hydrocephalus (NPH)
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62
Q

What is BPSD and give some examples?

A

Behavioural and Psychological Symptoms of Dementia

  • Psychosis: Hallucinations and Delusions
  • Excitation: Agitation and Aggression
  • Mood Disorders: Depression, Apathy, Emotional withdrawal, Anxiety
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63
Q

What is one of the best non-pharmacological treatments for dementia?

A

Cognitive Stimulation Therapy

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64
Q

Define Alzheimer’s Disease

A

Alzheimer’s disease is a chronic, neurodegenerative disorder characterised by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain.

This leads to the deterioration of cognitive function, memory loss, and various behavioural and psychological symptoms.

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65
Q

What is the Epidemiology of Alzheimer’s Disease?

A

Increasing prevalence with age
Women more commonly affected than men
APOE Gene

Alzheimer’s is the most common cause of dementia (>50%)

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66
Q

What is the pathophysiology of Alzheimer’s Disease?

A

Amyloid Plaques: The accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature. These abnormal protein deposits are believed to disrupt neuronal communication, trigger inflammation, and ultimately lead to cell death.

Tau Tangles: Inside nerve cells, abnormal tau protein accumulates, forming neurofibrillary tangles.

Neuronal Loss and Brain Atrophy: As the disease progresses, significant neuronal loss occurs, particularly in brain regions responsible for memory and cognitive function, such as the hippocampus and the cerebral cortex.

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67
Q

Give some risk factors for Alzheimer’s Disease

A

Age: Advanced age is the most significant risk factor >65yrs

Genetic Predisposition: apolipoprotein E (APOE) gene, Down’s syndrome

Family History: Having a first-degree relative with Alzheimer’s disease

Cardiovascular Risk Factors: Conditions like hypertension, diabetes, obesity, and hypercholesterolemia

Lifestyle Factors: Physical inactivity, smoking, and a diet high in saturated fats may contribute to increased risk.

Traumatic Brain Injury: A history of head injuries, particularly repeated concussions, has been linked to a higher risk of developing Alzheimer’s disease.

Low Educational Attainment: Lower levels of education may be associated with an increased risk.

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68
Q

What are some clinical features of Alzheimer’s Disease?

A

Memory Impairment

Language Impairment

Executive Dysfunction - impaired planning, organisation, and activities of tasks

Behavioural Changes

Psychological Symptoms

Disorientation

Loss of Motor Skills

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69
Q

Give some examples of behavioural changes you may see in Alzheimer’s Disease?

A

Agitation
Aggression
Apathy
Mood swings
Irritability

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70
Q

Give some examples of Psychological symptoms you may see in Alzheimer’s Disease?

A

Hallucinations
Delusions
Paranoia (in later stages)

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71
Q

What are some differential Diagnoses for Alzheimer’s Disease?

A

Vascular Dementia
Lewy Body Dementia
Frontotemporal Dementia
Mild Cognitive Impairment (MCI)
Normal Age related Decline

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72
Q

What are some Screening tests for Dementia?

A
  • Six Item Cognitive Impairment Test (6CIT)
  • 10-point Cognitive Screener (10-CS)
  • Mini-Cog
  • General Practitioner Assessment of Cognition (GPCOG)
  • Montreal Cognition Assessment (MoCA)
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73
Q

What are the investigations for Dementia?

A

Screening assessment

Required to exclude physical cause before referral

  • Confusion screen (Bloods, Urine, Imaging)

Referral to Memory Clinic

  • Addenbrooke’s Cognitive Examination-III (ACE-III)
  • < 88/100 suggests possible dementia
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74
Q

What areas are assessed in the Addenbrookes Cognitive Examination III?

A
  • Attention
  • Memory
  • Language
  • Visuospatial function
  • Verbal fluency

Scored out 100

  • < 88 suggests possible dementia
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75
Q

What are the diagnostic investigations for Alzheimer’s Disease?

A

Once reversible courses of confusion are eliminated and dementia is still suspected:

  • Brain imaging - MRI or PET scanmay show brain atrophy or presence of amyloid plaques
  • CSF Analysis may be used to detect specific biomarkers associated with AD
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76
Q

What are some important measures to put in place following a diagnosis of dementia?

A
  • Lasting Power of Attorney
  • Advanced decisions
  • Planning future care
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77
Q

What is the management of Alzheimer’s Disease?

A

Non-pharmacological:

  • Cognitive Stimulation Therapy
  • Psychological interventions
  • Activities to promote wellbeing (walking)
  • occupational therapy

Pharmacological:

  • First line: Acetylcholinesterase inhibitors (rivastigamine, galantamine, and donpezil) in mild-moderate dementia
  • Second line: Memantine (NMDA inhibitor) in severe dementia

Treatment of BPSD

  • Antidepressants (SSRIs)
  • Antipsychotics (risperidone)
  • Benzodiazepines (in acute crisis)
    There is no curative treatment
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78
Q

Define Vascular Dementia

A

Vascular dementia is an umbrella term denoting a collection of cognitive impairment syndromes caused by cerebrovascular disease.

These syndromes include stroke-related vascular disease, subcortical vascular dementia, and mixed dementia (a combo of alzheimer’s and vascular)

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79
Q

What is the epidemiology of Vascular Dementia?

A

Increasing prevalence with age
More common in men
Risk higher in people with cardio risk factors

Its the second most common type of dementia (15-20%)

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80
Q

What are the main causes of vascular dementia?

A

The primary cause is ischemic or haemorrhagic cerebrovascular disease, which leads to brain damage.

Various different vascular events or conditions can lead to vascular dementia including:

  • multi-infarct and single-infarct dementia
  • subcortical vascular dementia (known as Binswanger’s disease)
  • (CADASIL) Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
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81
Q

What are the Risk Factors for vascular dementia?

A

They mirror those of stroke and CVD:

  • hypertension
  • diabetes mellitus
  • hyperlipidemia
  • smoking
  • atrial fibrillation
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82
Q

What is the clinical presentation of vascular dementia?

A

It’s characterised by a progressive, stepwise deterioration in cognition.

This typically occurs over a span of several months to years.

Patients may present with a history of strokes.

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83
Q

What are some differentials for vascular dementia?

A

Alzheimer’s disease

Lewy body dementia

Frontotemporal dementia

Normal pressure hydrocephalus

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84
Q

What are the first line investigations for vascular dementia?

A

Comprehensive history and examination

Cognition screening - MMSE (Mini-Mental State Examination) or MoCA (Montreal Cognitive Assessment)

Medication review - to exclude medication-induced cognitive impairment.

MRI Scan show white matter changes

Exclusion of reversible organic causes - like vitamin B12 or folic acid deficiency, hypothyroidism, or normal pressure hydrocephalus.

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85
Q

What is the diagnostic investigation for vascular dementia?

A

MRI Head - To identify vascular changes or infarcts

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86
Q

What is the management of vascular dementia?

A

Detection and address of CV risk factors

  • hypertension, diabetes, hyperlipidaemia and smoking

symptomatic treatment

  • Tailored to the individual
  • Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
  • Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
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87
Q

What is the definition of frontotemporal dementia?

A

Frontotemporal dementia is a heterogeneous group of neurodegenerative disorders characterised by progressive atrophy of the frontal and/or temporal lobes of the brain.

Leading to impairments in behaviour, personality, language, and motor functions.

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88
Q

What are the 3 recognised types of Frontotemporal Dementia?

A
  • Frontotemporal Dementia (Picks Disease)
  • Progressive Non Fluent Aphasia
  • Semantic Dementia
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89
Q

What is the epidemiology of frontotemporal dementia?

A

It’s one of the most common forms of early onset dementia.
Typically develops in peoples’ 60s and 70s

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90
Q

What are some common features of Frontotemporal lobar dementias?

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change, disinhibition, language impairment and social conduct problems

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91
Q

What are the macroscopic and microscopic findings of Picks disease?

A

Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.

Macroscopic changes seen in Pick’s disease include:

  • Atrophy of the frontal and temporal lobes

Microscopic changes include:

  • Pick bodies - spherical aggregations of tau protein (silver-staining)
  • Gliosis
  • Neurofibrillary tangles
  • Senile plaques
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92
Q

What is the clinical presentation of frontotemporal dementia?

A

Personality change and impaired social conduct.

Other common features:

  • Hyperorality
  • Disinhibition
  • Increased appetite
  • Perseveration behaviours.

Language impairment is another common feature

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93
Q

What sort of personality changes may someone with frontotemporal dementia exhibit?

A

Patients often exhibit disinhibited behaviour and apathy early on.

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94
Q

What are some differentials for frontotemporal dementia?

A

Alzheimer’s disease

Vascular dementia

Creutzfeldt-Jakob disease
Rapidly progressive dementia with neurological signs like myoclonus, ataxia, and visual disturbances. Periodic sharp wave complexes on EEG are suggestive.

Primary progressive aphasia
Characterised by gradual, insidious decline in language abilities with relative preservation of other cognitive functions.

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95
Q

How is frontotemporal dementia diagnosed?

A

Neuroimaging (like CT and MRI)
Would show atrophy of frontal and/or temporal lobe

Genetic Testing
Used in cases where an inherited form of FTD is suspected

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96
Q

What is the management for frontotemporal dementia?

A

Non-Pharmacological
Cognitive Stimulation Therapy
Counselling
Behaviour modification strategies
Caregiver support
Speech and language therapy
Physiotherapy
Occupational therapy

Pharmacological
SSRIs and Antipsychotics to control behavioural symptoms

There is no curative treatment

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97
Q

Define Dementia with Lewy Bodies

A

It’s a type of rapidly progressive dementia caused by deposits of an abnormal protein (alpha-synuclein) forming cytoplasmic inclusions known as Lewy bodies within brain cells.

These aggregates disrupt normal cell functioning and eventually lead to neuronal death.

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98
Q

Where in the brain do Lewy Bodies accumulate?

A

Abnormal protein (alpha-synuclein) forming cytoplasmic inclusions known as Lewy bodies within brain cells.
Accumulate in:

  • Substantia nigra
  • Paralimbic
  • Neocortical areas.
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99
Q

What other neurological condition is Dementia with Lewy Bodies associated with?

A

Parkinson’s Disease

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100
Q

What are the clinical features of Dementia with Lewy Bodies?

A
  • Fluctuating cognition compared to other forms of dementia
  • REM sleep disorder (often the initial symptom)
  • Parkinsonism
  • Recurrent Visual hallucinations
  • High sensitivity to neuroleptics (antipsychotics)
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101
Q

What will neuroleptics (antipsychotics) do in someone with dementia with Lewy Bodies?

A

They can induce or worsen parkinsonism

They can also cause neuroleptic malignant syndrome

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102
Q

What are some differentials of Dementia with Lewy Bodies?

A

Alzheimer’s disease

Parkinson’s disease dementia
It shares many symptoms with DLB, but Parkinson’s disease dementia tends to start with motor symptoms year before cognitive decline.

Vascular dementia

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103
Q

What are first line investigations may be done in Lewy Body Dementia?

A

Careful History and clinical examination (Diagnosis is primarily clinical)

CT/MRI Head May be normal or show cortical atrophy

Dopamine transporter (DaT) scan
Can help distinguish DLB from other types of dementia.

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104
Q

What is the management for Dementia with Lewy Bodies?

A

Pharmacological

  • AchE inhibitors (Donepazil, Rivastigmine) and Memantine can be used
  • Neuroleptics should be avoided due to the risk of irreversible parkinsonism

Non-Pharmacological

  • Cognitive stimulation therapy
  • Physical therapy
  • Occupational therapy

Supportive Care

  • Palliative and end-of-life care considerations (due to its progressive nature)
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105
Q

Why are neuroleptic medications not used in Lewy Body Dementia?

A

Due to the high risk of developing irreversible parkinsonism

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106
Q

Define Parkinson’s Disease

A

It’s a condition where there is a progressive reduction in dopamine in the basal ganglia, leading to disorders of movement.

The symptoms are characteristically asymmetrical, with one side of the body affected more.

The typical patient is an older man, around 70 years old, with a gradual onset of symptoms.

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107
Q

What is the classic triad of Parkinsonism?

A

Resting tremor (a tremor that is worse at rest)

Rigidity (resisting passive movement)

Bradykinesia (slowness of movement)

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108
Q

Describe the epidemiology of Parkinson’s

A

Prevalence increases with age

More common in males

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109
Q

What is the most likely cause of Parkinson’s disease?

A

The accumulation of Lewy Bodies within the dopaminergic cells of the substantia nigra of the basal ganglia; leading to their neuronal death and the reduction of dopamine.

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110
Q

Name some risk factors for Parkinson’s

A

Family History
Male Sex
Increasing Age

Being a non-smoker - Smoking reduces the risk of Parkinson’s

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111
Q

What are the motor characteristics of Parkinson’s?

A

Triad of Parkinsonism
Bradykinesia
Asymmetric 3-5Hz “pill-rolling” tremor
Lead pipe rigidity

This can manifest in a Parkinsonian gait
(small, shuffling steps, slowness of movement, especially on initiation and turning, flexed posture, and asymmetric tremor)

Other features:

  • Hypomimic facies
  • Cogwheeling when testing tone
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112
Q

What are some non-motor characteristics of Parkinson’s?

A

Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Postural instability (increasing the risk of falls)
Constipation
Erectile Dysfunction
Cognitive impairment and memory problems

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113
Q

What are some Parkinson’s-Plus Syndromes?

A
  • Multiple System Atrophy - Presents with early autonomic dysfunction and postural instability compared to PD
  • Lewy Body Dementia - Early and prominent cognitive dysfunction before parkinsonism traits. (Visual Hallucinations)
  • Progressive Supranuclear Palsy
  • Corticobasal Degeneration
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114
Q

What are some differential Diagnoses for Parkinson’s Disease?

A
  • Benign Essential Tremor
  • Multiple System Atrophy (MSA): Very prominent autonomic dysfunction, early postural instability, poor response to levodopa
  • Dementia with Lewy Bodies (DLB): Early and prominent cognitive dysfunction, visual hallucinations, fluctuating cognition
  • Progressive Supranuclear Palsy (PSP): Early gait instability and falls, vertical gaze palsy, prominent axial rigidity
  • Corticobasilar Degeneration: May have predominant apraxia, aphasia and ‘alien hand’ syndrome
  • Wilson’s Disease: May be associated with signs of liver disease
  • Dementia Pugilistica: Secondary to repeated head trauma
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115
Q

What are the investigations for Parkinson’s Disease?

A

Parkinson’s disease is primarily a clinical diagnosis, supported by positive response to treatment trials.

An absolute failure to respond to 1-1.5g of levodopa daily almost excludes a diagnosis of idiopathic Parkinson’s disease.

Other investigations such as MRI Head or a Dopamine Transporter Scan (DaT scan) can be considered in atypical cases.

The NICE guidelines recommend that the diagnosis is made using the UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria

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116
Q

What is the Management of Parkinson’s Disease?

A

Tx focused on Symptom control and minimising side effects:

Levodopa (combined with Decarboxylase inhibitors Carbidopa / Benserazide)

  • Co-beneldopa (levodopa and benserazide), with the trade name Madopa
  • Co-careldopa (levodopa and carbidopa), with the trade name Sinemet

COMT Inhibitors - Decarboxylase inhibitor to prevent breakdown of L-DOPA

MOA Inhibitors - Inhibit the breakdown of neurotransmitters such as dopamine and serotinin.

Dopamine Agonists - Mimic action of Dopamine

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117
Q

What is the definition of Osteoporosis?

A

Osteoporosis is a systemic skeletal disease characterised by reduced bone mass and altered microarchitecture of the bone tissue, leading to increased bone fragility and a consequent increase in fracture risk.

It is typically defined by a DEXA scan T-score of -2.5 or lower

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118
Q

What is the epidemiology of Osteoporosis?

A

Higher prevalence with increasing age

Most common in postmenopausal women and elderly men.

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119
Q

What are the 2 major risk factors for Osteoporosis?

A

Age
Female Gender

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120
Q

SHATTERED

What are the risk factors for Osteoporosis?

A

Steroid use
Hyperthyroidism, hyperparathyroidism
Alcohol and smoking
Thin (BMI<22)
Testosterone deficiency
Early menopause
Renal/liver failure
Erosive/inflammatory bone disease
Diabetes

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121
Q

What are the symptoms and signs of Osteoporosis?

A

It tends to be asymptomatic until a fracture occurs

  • Back pain, caused by a fractured or collapsed vertebra
  • Loss of height over time
  • A stooped posture
  • A bone fracture that occurs much more easily than expected
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122
Q

What is the pathophysiology of Osteoporosis?

A

Bone Mineral Density and Bone mass is reduced however the mineralisatoin of bone is unchanged in Osteoporosis.

Bone remodelling imbalance

  • Increased bone resorption from osteoclasts
  • Reduced bone formation by osteoblasts
  • Reduction in both bone mineral density and matrix density reducing bone mass.

Bones Brittle and Fragile

  • Reduced bone density and mass
  • Causes brittle and fragile bones

Increased fracture risk

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123
Q

Give some differentials of Osteoporosis?

A

Metabolic bone diseases
e.g. osteomalacia and hyperparathyroidism - presents with low bone mass and increased fracture risk.

Malignancies
e.g. multiple myeloma or metastatic disease, which can lead to pathologic fractures similar to those seen in osteoporosis.

Secondary causes of osteoporosis
e.g. Cushing’s syndrome, hyperthyroidism, and certain medications (e.g., glucocorticoids, anticonvulsants).

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124
Q

What is the Gold Standard investigation for osteoporosis?

A

DEXA Scan (Stands for Dual-Energy X-Ray Absorptiometry)

A bone mineral density T-Score of -2.5 is diagnostic of osteoporosis.

Its measured at the hip

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125
Q

What are the investigations to look for secondary causes of Osteoporosis?

A
  • History and physical examination
  • FBC
  • U&Es (serum calcium, creatinine, phosphate)
  • LFTs (ALP, transaminases)
  • TFTs
  • 25-OH vit D & 1,25-OH vit D
  • Serum testosterone & prolactin
  • Lateral radiographs of lumbar and thoracic spine
  • Protein immunoelectrophoresis and urinary Bence-Jones protein
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126
Q

What is the criteria on the Frax Score?

A
  • Age
  • Gender
  • Weight/Height
  • Previous Fracture
  • Previous Femoral neck BMD
  • Parental Hip Fracture
  • Current Smoking
  • Glucocorticoid Use
  • Rheumatoid Arthritis
  • Secondary Osteoporotic conditions
  • Alcohol use (> 3 units/day)
127
Q

What are the major Osteoporotic Risk Factors:

A
  • Glucocorticoid use
  • rheumatoid arthritis
  • alcohol excess
  • history of parental hip fracture
  • low body mass index
  • current smoking
128
Q

What are some causes of secondary osteoporosis?

A

Type I diabetes
osteogenesis imperfecta
long-standing hyperthyroidism
hypogonadism
premature menopause (<45 years)
chronic malnutrition or malabsorption disorders (IBD, Coeliac)
Chronic Kidney disease
Chronic liver disease

129
Q

What are some drugs that increase the risk of Osteoporosis?

A

Glucocorticoids

SAPGAL:

S: SSRIs
A: Antiepileptics
P: Proton pump inhibitors
G: Glitazones
A: Aromatase inhibitors (e.g., anastrozole)
L: Long term heparin use

130
Q

What are some scoring systems used to assess the probabilty of 10 year major osteoporotic fracture?

A

Q Fracture Tool (preferred by NICE)
FRAX Tool

Q Fracture tool > 10% are sent for DEXA

131
Q

What percentage risk on a FRAX Score prompts a DEXA scan?

A

10%

132
Q

What is the Algorithm for assessing a Fragility Fracture/Diagnosing Osteoporosis?

A

Step 1: Is there a history of fragility fracture?

  • No = Move on to step 2
  • Yes = Move on to step 2 if age < 50 OR perform DEXA if age > 50 OR Make clinical diagnosis if age ≥ 75

Step 2: Perform fragility fracture risk assessment (FRAX/Qfracture)

  • Low risk = Repeat risk assessment after 5 years
  • High-Intermediate risk = perform DEXA
133
Q

Who does NICE recommend should have osteoporosis risk assessed?

A
  • Anyone on long-term oral corticosteroids or with a previous fragility fracture
  • Anyone 50 and over with risk factors
  • All women 65 and over
  • All men 75 and over
134
Q

What is the 1st line management of Osteoporosis?

A

Lifestyle modification

  • Reducing risk factors like quitting smoking, improving diabetic control, reduce alcohol consumption and increasing exercise.
  • Adequate intake of vitamin D (400-800 IU), Calcium (at least 1000mg), and protein
  • Regular weight-bearing exercise
  • Use of hip protectors in nursing home patients
135
Q

What is the pharmacological management of Osteoporosis?

A

First line: Oral Bisphosphonates

  • Oral Alendronate 70 mg once weekly (oral)
  • Oral Risedronate 35 mg once weekly (oral)

1st line after NOF

  • IV Zoledronic acid 5 mg once yearly (intravenous)

Second Line:

  • Denosumab
136
Q

What is the Mechanism of Action of Bisphosphonates?

A

bisphosphonates bind to hydroxyapatite in bone, inhibiting osteoclast-mediated bone resorption

137
Q

What is the mechanism of action of Denosumab?

A

human monoclonal antibody that inhibits RANK ligand, which in turn inhibits the maturation of osteoclasts

138
Q

How should oral Bisphosphonates be taken?

A

On an empty stomach with a full glass of water.

Afterwards, the patient should sit upright for 30 minutes before moving or eating to reduce the risk of reflux and oesophageal erosions.

139
Q

What are the side effects of Bisphosphonates?

A

Reflux, Oesophagitis and oesophageal erosions

Atypical fractures (e.g., atypical femoral fractures)

Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment)

Osteonecrosis of the external auditory canal

140
Q

What is this wrong with this X-Ray?

A

Intra-Capsular Neck of Femur Fracture

141
Q

What are the 2 types of NOF Fracture?
What are the features of them?

A

Intracapsular Fractures (subcapital): edge of the femoral head to the insertion of the capsule of the hip joint

  • Occur within the joint capsule
  • Non-Displaced
  • Displaced (High risk of avascular necrosis of the femoral head)

Extracapsular Fractures

  • Occur outside the joint capsule
  • Intertrochanteric
  • Subtrochanteric fractures
  • Better prognosis due to a lower risk of avascular necrosis.
142
Q

What is the Classification system for Hip Fractures?

A

Garden System
Type I: Stable fracture with impaction in valgus
Type II: Complete fracture but undisplaced
Type III: Displaced fracture, usually rotated and angulated, but still has boney contact
Type IV: Complete boney disruption

Avascular Necrosis is a high risk in Types III and IV

143
Q

What is the epidemiology of NOF Fractures?

A

Prevalence increases with age
More common in Females

144
Q

Why does the prevalence of NOF Fractures increase with age?

A

Due to the increased prevalence of osteoporosis in the elderly.

As well as the increased prevalence of conditions like dementia, parkinson’s etc… that lower cognition and make them more likely to fall.

145
Q

What causes NOF Fractures

A
  • Fall onto side in the elderly
  • High energy trauma like car accidents in the young
146
Q

What is the clinical presentation of a NOF Fracture?

A
  • Severe pain in the hip or groin
  • Inability to bear weight on the affected leg
  • Shortening and external rotation of the affected leg
  • Swelling or bruising over the hip area
147
Q

What are the differentials for a NOF Fracture?

A

Intertrochanteric Fracture

Pelvic Fracture

Hip Dislocation

148
Q

What is the diagnostic investigation of a NOF Fracture?

A

Hip X-Ray

If unclear on X-Ray then a CT Scan or MRI

149
Q

What is the Management for an Intracapsular Hip Fracture?

what are the guidelines for the options?

A

Non-displaced Fracture:

  • internal fixation, or hemiarthroplasty if unfit.
  • Uses a Cannulated Hip Screw

Displaced Fracture:

  • NICE recommend replacement arthroplasty to all patients with a displaced intracapsular hip fracture
  • Total hip replacement is favoured to hemiarthroplasty if patients:
  • Were able to walk independently out of doors with no more than the use of a stick
  • Are not cognitively impaired and
  • Are medically fit for anaesthesia and the procedure.
150
Q

Why is a Hemi-arthroplasty preferred to a Total Hip Replacement in patients who are more frail, cognitively impaired or immobile?

A
  • Allows for early mobilisation and good pain relief which can prevent complications such as pressure sores and DVT,
  • Shorter operation time reducing perioperative risk in frail age group
  • Rehabilitation is quicker and easier
151
Q

What is the Management for an Extracapsular Hip Fracture?

A
  • stable intertrochanteric fractures: dynamic hip screw
  • if reverse oblique, transverse or subtrochanteric fractures: intramedullary device
152
Q

Why is Hemiarthroplasty done in the elderly to treat a NOF and not a Total hip Replacement?

A

Because the elderly are at an increased risk of falling and its virtually impossible to dislocate (v. hard) to dislocate a hemi.

Where a THA would dislocate a lot more easily.

153
Q

What’s wrong with this X-Ray

A

Tibial Shaft Fracture

154
Q

What can cause a Tibial Shaft Fracture?

A
  • High-energy trauma, such as motor vehicle collisions or falls from a height
  • Sports-related injuries
  • Low-energy trauma, particularly in individuals with weakened bone structure, (e.g.those with osteoporosis)
155
Q

What is the clinical presentation of a Tibial Shaft Fracture?

A
  • Severe pain in the lower leg
  • Swelling and tenderness around the injury site
  • Visible deformity if the fracture is displaced
  • Inability to bear weight on the affected leg
  • Possible open wound if the fracture is compound
156
Q

What are some differentials for a Tibial Shaft Fracture?

A
  • Fibular fracture: Typically presents with localized pain and swelling along the outer aspect of the lower leg
  • Ankle fracture: Usually associated with significant ankle pain, swelling, and instability
  • Compartment syndrome: Characterized by severe pain, paresthesia, and tenseness of the compartment involved
  • Sprain or strain: Usually less severe pain and swelling, with no obvious deformity
157
Q

What diagnostic investigations are done for a Tibial Shaft Fracture?

A

X-Ray

CT Scan in complex or comminuted fractures to guide surgical planning

158
Q

What is the management of a Tibial Shaft Fracture?

A

Immobilization
The use of a cast or splint to protect the fracture and promote healing

Pain control
Analgesics, including NSAIDs or opioids

Surgical intervention
Open reduction and internal fixation (ORIF) or Intramedullary nailing

Rehabilitation

159
Q

What is a Colles’ Fracture?

A
  • Classically follows a fall onto an outstretched hand (known as a FOOSH)
  • Distal radius fracture with dorsal displacement of fragments
  • Described as a dinner fork type deformity
160
Q

What are the features of a classic Colles’ Fracture?

A
  • Transverse fracture of the radius
  • 1 inch proximal to the radio-carpal joint
  • Dorsal displacement and angulation

Colles’: Dorsally Displaced Distal Radius –> Dinner fork Deformity

161
Q

What are the early and late complications of Colles’ Fracture?

A

Early

  • median nerve injury: acute carpal tunnel syndrome presenting with weakness or loss of thumb or index finger flexion
  • compartment syndrome
  • vascular compromise
  • malunion
  • rupture of the extensor pollicis longus tendon

Late

  • osteoarthritis
  • complex regional pain syndrome
162
Q

What is the definition of Heart Failure?

A

It’s defined the failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body.

163
Q

What is the epidemiology of Heart Failure?

A

Prevalence increases with age (avg age is 75)

Coronary artery disease, Hypertension and valvular diseases are common causes in the West

Chagas disease is a significant cause in Central/South America

164
Q

What are the ways Heart Failure can be classified?

A

Ejection Fraction (most common):

  • Reduced Ejection Fraction (HF-rEF) where EF is < 40%
  • Mildly reduced Ejection Fraction Where EF is 41-49%
  • Preserved Ejection Fraction (HF-pEF) where EF > 50%

Systolic/Diastolic Dysfunction (replaced by HF-rEF and HF-pEF)

  • HF-rEF is typically a problem with Systolic function
  • HF-pEF is typically a problem with Diastolic function

By Time:

  • Acute heart failure: Either new presentation or typically an acute exacerbation of chronic HF due to sudden LV failure and pulmonary oedema
  • Chronic heart failure

By Left/Right

Output:

  • Low-Output HF: Pump is not working to meet demands
  • High-Output HF: Pump works but demands are increased
165
Q

What is Low-Output Heart Failure?

A

Is much more common than High-Output HF

Occurs when cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body’s needs.

166
Q

What is High-Output Heart Failure?

A

It refers to a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet.

167
Q

AAPPTT

What are the main causes of high-output HF?

A
  • Anaemia
  • Arteriovenous malformation
  • Paget’s disease
  • Pregnancy
  • Thyrotoxicosis
  • Thiamine deficiency (wet Beri-Beri)
168
Q

Define Systolic HF

A

Systolic dysfunction refers to an impairment of ventricular contraction.

The ventricles are able to fill well, but the heart is unable to pump the blood sufficiently out of the ventricle due to impaired myocardial contraction during systole (reduced ejection fraction).

169
Q

What are the common causes of Systolic HF?

A
  • Ischaemic heart disease
  • Dilated cardiomyopathy
  • Myocarditis
  • Infiltration (haemochromatosis or sarcoidosis)
170
Q

Define Diastolic HF

A

Diastolic dysfunction refers to the inability of the ventricles to relax and fill normally.

Hence the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling (preserved ejection fraction).

171
Q

What are the causes of Diastolic HF?

A
  • Uncontrolled chronic hypertension
    (significant left ventricular hypertrophy reduces filling of the left ventricle)
  • Hypertrophic Obstructive Cardiomyopathy (HOCM)
  • Cardiac tamponade
  • Constrictive pericarditis
172
Q

Whats the difference between Acute and Chronic HF?

A

Acute heart failure may be a new presentation of heart failure or, may be, deterioration or ‘decompensation’ in a person with existing chronic heart failure.

173
Q

What does Left Heart Failure cause?

A

Left HF causes pulmonary congestion (pressure builds up on the Left hand side of the heart and there is back pressure to the lungs) and there is systemic hypoperfusion.

174
Q

What are the clinical features of left heart failure?

A

Symptoms

  • Fatigue
  • Shortness of breath on exertion
  • Dyspnoea
  • Orthopnoea (breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
  • Paroxysmal nocturnal dyspnoea
  • Nocturnal cough (± pink frothy sputum)

Signs

  • Tachypnoea
  • Bibasal fine crackles on auscultation of the lungs
  • Cyanosis
  • Prolonged cap refill time
  • Hypotension

Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation.

175
Q

What is Paroxysmal Nocturnal Dyspnoea?

A

Describes the experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.

They may describe having to sit on the side of the bed or walk around the room, gasping for breath. They may feel suffocated and want to open a window to get fresh air.

Symptoms improve over several minutes.

176
Q

What does Right Heart Failure cause?

A

Right heart failure causes venous congestion (pressure builds up behind the right heart) and pulmonary hypoperfusion (reduced right heart output).

177
Q

What are the clinical features of Right Heart Failure?

A

Symptoms

  • Fatigue
  • Ankle swelling
  • Weight gain
  • Abdominal swelling and discomfort
  • Anorexia (cardiac cachexia) and nausea

Signs

  • Raised JVP
  • Pitting peripheral oedema (ankle to thighs to sacrum)
  • Tender smooth hepatomegaly
  • Ascites
  • Transudative pleural effusions (typically bilaterally)
178
Q

What is the most common cause of right heart failure?

A

Left Heart Failure

179
Q

What is the New York Heart Association Classification of HF?

A

It classifies Heart Failure through the severity of symptoms. There are 4 classes:

Class I: No limitation on activity

Class II: Comfortable at rest but symptomatic with ordinary activities

Class III: Comfortable at rest but symptomatic with any activity

Class IV: Symptomatic at rest

180
Q

What the differentials of Heart Failure?

A

Chronic Obstructive Pulmonary Disease (COPD)
Both present with dyspnoea (and significant respiratory distress) and fatigue.

Acute Respiratory Distress Syndrome
Both present with shortness of breath, tachypnoea and respiratory distress. Both lead to the accumulation of fluid in the lungs and impaired gaseous exchange leading to hypoxaemia.

Renal Failure
Both present with fluid retention and peripheral overload.

Liver Failure
Both present with fluid retention and peripheral overload (especially ascites)

181
Q

How do you differentiate between HF and COPD?

A

In heart failure the shortness of breath is typically worse on lying flat (orthopnoea) and may be accompanied by paroxysmal nocturnal dyspnoea and peripheral oedema.

Shortness of breath in COPD tends to be worse with exertion and is likely accompanied with other symptoms including chronic productive cough, wheeze and a significant smoking history.

182
Q

How do you differentiate between HF and Acute Respiratory Distress Syndrome?

A

They can be distinguished by taking pulmonary capillary wedge pressures.

The underlying pathology between the two is different. Heart failure is a result of raised pressures in pulmonary capillaries, whereas ARDS is usually due to increased pulmonary capillary secondary to a large insult (e.g. pneumonia, aspiration, or trauma).

183
Q

What is the 1st line investigation for HF?

A

NT-Pro-BNP level

It’s released by the ventricles in response to myocardial stretch. It has a high negative predictive value.

184
Q

How would you interpret NT-Pro-BNP results?

A
  • 2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks.
  • 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks.
  • If <400ng/L be aware that diagnosis of heart failure is less likely.
185
Q

What is the diagnostic investigation for HF?

A

Transthoracic Echocardiogram

186
Q

What other investigations should be carried out for HF?

A

ECG
Bloods (U+Es, LFTs, TFTs, Glucose and Lipid profile)
Chest X-Ray

187
Q

ABCDEF

What will be seen on a HF Chest XRay?

A

A: Alveolar oedema (with ‘batwing’ perihilar shadowing)

B: Kerley B lines (caused by interstitial oedema)

C: Cardiomegaly (cardiothoracic ratio >0.5)

D: upper lobe blood diversion

E: Pleural effusions (typically bilateral transudates)

F: Fluid in the horizontal fissure

188
Q

What is the conservative management for HF?

A
  • Weight loss if BMI >30.
  • Smoking cessation
  • Salt and fluid restriction - improves mortality
  • Supervised exercise-based group rehabilitation programme for people with heart failure.
189
Q

What is the pharmacological management of Heart Failure?

symptom management
first line
Second line
3rd line
Other

A

Symptomatic Treatment: Loop Diuretics (furosemide, Budesonide) but have no role in mortality reduction

First Line HF Medications:

  • Beta-Blocker (Bisoprolol, Carvedilol) and ACE Inhibitor (ramipril)
  • ARB (e.g. Candesartan) is used if intolerant to ACE-I

Second Line HF Medications:

  • Aldosterone Antagonists (Spironolactone, Eplerenone)
  • Monitor potassium as Aldosterone antagonists and ACEi will cause Hyperkalaemia
  • SGLT-2 Inhibitors (Dapagliflozin) is a recommended ad on to standard care

Third Line HF Medications:

  • Ivabradine if in sinus rhythm >75/min and EF < 35%.
  • Sacubitril-Valsartan (ARNI) for EF <35% and Symptomatic on ACEi/ARB
  • Hydralazine and a nitrate for Afro-Caribbean patients.
  • Digoxin is used in patients with co-existent AF.

Other Treatments:

  • Annual Influenza Vaccine
  • One off Pneumococcal Vaccine
190
Q

What are the side effects of the heart failure meds?

Beta-Blockers
ACE-I
Spironolactone
Furosemide
Hydralazine
Digoxin

A

Beta blockers: Bradycardia, hypotension, fatigue, dizziness, ED

ACE inhibitors: Hyperkalaemia, renal impairment, dry cough, lightheadedness, fatigue, GI disturbances, angioedema

Spironolactone: Hyperkalaemia, renal impairment, gynaecomastia, breast tenderness/hair growth in women, changes in libido

Furosemide: Hypotension, hypoatraemia/kalaemia,

Hydralazine/nitrate: Headache, palpitations, flushing

Digoxin: Dizziness, blurred vision, GI disturbances

191
Q

What is constipation defined by?

A

Any or all of the following:

  • Fewer than three bowel movements per week
  • Hard stool in more than 25% of bowel movements
  • Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements
  • Excessive straining in more than 25% of bowel movements
  • A need for manual evacuation of bowel movements
192
Q

Primary Vs Secondary Constipation

A

Primary constipation:
No organic cause, thought to be due to dysregulation of the function of the colon or anorectal muscles

Secondary constipation:
Due to factors such as diet, medications, metabolic, endocrine or neurological disorders or obstruction

193
Q

What are the risk factors for Constipation?

A

Advanced age
Inactivity
Low calorie intake
Low fibre diet
Certain medications
Female sex

194
Q

What are the main causes of Constipation?

A

Dietary factors like inadequate fibre or fluid intake

Behavioural factors like inactivity or avoidance of defecation

Electrolyte disturbances like hypercalcaemia

Certain drugs like opiates, calcium channel blockers and some antipsychotics

Neurological disorders like spinal cord lesions,

Parkinson’s disease and diabetic neuropathy

Endocrine disorders such as hypothyroidism

Colon diseases like strictures or malignancies

Anal diseases like anal fissures or proctitis

195
Q

What are the main signs and symptoms of constipation?

A
  • Infrequent bowel movements (less than 3 per week)
  • Difficulty passing bowel motions
  • Tenesmus
  • Excessive straining
  • Abdominal distension
  • Abdominal mass felt at the left or right lower quadrants (stool)
  • Rectal bleeding
  • Anal fissures
  • Haemorrhoids
  • Presence of hard stool or impaction on digital rectal examination
196
Q

Give some red flag symptoms for GI malignancy

A

Weight loss
Loss of appetite
Abdominal mass
Dark stool

197
Q

What are some differentials for Constipation?

A

Irritable Bowel Syndrome (IBS)
Characterized by abdominal pain, bloating, and alternating constipation and diarrhea

Inflammatory Bowel Disease (IBD)
Presents with abdominal pain, weight loss, and bloody diarrhea

Anal fissures
Characterized by severe anal pain during and after bowel movements, and bright red blood in the stool

Hemorrhoids
Symptoms include painless rectal bleeding, anal itching, and discomfort

Colorectal Cancer
Symptoms include changes in bowel habits, rectal bleeding, and unintentional weight loss

198
Q

What investigations should be done for Constipation?

A

Clinical Diagnosis following History, examination and potentially DRE

Ix to consider if secondary cause

  • Full blood count
  • Electrolytes
  • Thyroid function tests
  • Blood glucose
  • Abdominal x-ray if suspicious of a secondary cause of constipation
  • Barium enema if suspicious of impaction or rectal mass
  • Colonoscopy if suspicious of lower GI malignancy
199
Q

What is the management for Constipation?

A

Investigate and exclude any secondary causes, consider red flag symptoms

  • Exclude any faecal impaction

Advice on lifestyle

  • increasing dietary fibre
  • ensuring adequate fluid intake
  • ensuring adequate activity levels

Pharmacological

  • First-line laxative: bulk-forming laxative first-line, such as ispaghula
  • Second-line: osmotic laxative, such as a macrogol
  • Enemas (e.g., sodium citrate) if impaction is present
200
Q

Give some examples of different types of Laxatives?

A
  • Enemas (e.g., sodium citrate) if impaction is present
  • Suppositories such as glycerol
  • Bulk laxatives such as ispaghula husk or methylcellulose
  • Stool softeners like docusate sodium
  • Osmotic laxatives like lactulose or macrogol
  • Stimulant laxatives like senna or bisacodyl
201
Q

What are the main complications of Constipation?

A
  • overflow diarrhoea
  • acute urinary retention
  • haemorrhoids
  • Delirium
  • Faecal impaction
202
Q

What are the different types of Urinary Incontinence?

A

Stress incontinence
Urge incontinence
Overflow incontinence
Mixed incontinence

203
Q

What is stress incontinence?

A

It involves leaking of urine when intra-abdominal pressure is raised, putting pressure on the bladder.

The pressure of the urine overcomes the mechanisms designed to maintain continence and it’s caused by a weakness of the pelvic floor and sphincter muscles.

Acts like coughing, laughing, sneezing or exercising can increase abdominal pressure sufficiently.

204
Q

What are some risk factors for Stress Incontinence?

A

Childbirth (especially vaginal).
Due to a combination of injury to the pelvic floor musculature and connective tissue, as well as nerve damage.

Hysterectomy

205
Q

How is Stress Incontinence managed?

A

Conservative

  • Lifestyle Advice like avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake.
  • Pelvic Floor Exercises

Medical Management

  • Duloxetine (only if conservative has failed and surgery isn’t an option)

Surgical Management

  • Incontinence pessaries (are placed transvaginally and apply pressure to the anterior vaginal wall)
  • Bulking agents (injectable materials placed at the bladder neck to improve continence).
  • Colposuspension and fascial slings
  • Mid-urethral slings are the gold standard surgical treatment of stress incontinence.
206
Q

What is Urge Incontinence

A

Urge incontinence is caused by overactivity of the detrusor muscle of the bladder.

It’s is also known as overactive bladder and the typical description is of suddenly feeling the urge to pass urine, having to rush to the bathroom and not arriving before urination occurs.

207
Q

What are the risk factors for Urge Incontinence?

A

Recurrent urinary tract infections
High BMI
Advancing age
Smoking
Caffeine

208
Q

How is Urge Incontinence managed?

A

Conservative

  • Bladder retraining (gradually increasing the time between voiding) for at least six weeks is first-line
  • Lifestyle Advice like avoiding caffeine, fizzy and sugary drinks, as well as avoiding excessive fluid intake.
  • Pelvic Floor Exercises

Medical Management

  • Anticholinergic medication (oxybutynin, tolterodine and solifenacin)
  • Mirabegron as an alternative

Surgical Management

  • Bladder Instillation (Involves the Intravesical injection of Botox can be used to paralyse the detrusor muscle)
  • Percutaneous sacral nerve stimulation (implanting a device in the back that stimulates the sacral nerves)
209
Q

What are the side effects of Anticholinergic Medication?

A

Dry mouth
Dry eyes
Urinary retention
Constipation
Postural hypotension.

Importantly they can also lead to a cognitive decline, memory problems and worsening of dementia,

210
Q

What condition is Mirabegron contraindicated in?

A

Uncontrolled hypertension

It works as a beta-3 agonist, stimulating the sympathetic nervous system, leading to raised blood pressure. Which can lead to a hypertensive crisis and an increased risk of TIA and stroke.

211
Q

What is Mixed Incontinence?

A

It’s a combination of urge incontinence and stress incontinence.

212
Q

What is Overflow Incontinence?

A

It occurs when there is chronic urinary retention due to an obstruction to the outflow of urine.

Chronic urinary retention results in an overflow of urine, and the incontinence occurs without the urge to pass urine.

213
Q

What causes Overflow Incontinence?

A
  • Underactivity of the Detrusor muscle (can be caused by neurological damage)
    OR
  • When urinary pressures are too high can be caused by constipation or prostatism)
214
Q

How is Urinary Incontinence investigated?

A

Bladder diary
Tracking fluid intake and episodes of urination and incontinence over at least three days. There should be a mix of work and leisure days.

Urine dipstick
To assess for infection, microscopic haematuria and other pathology.

Bladder Scan
To measure post-void residual bladder volume to assess for incomplete emptying

Urodynamic testing
Can be used to investigate patients with urge incontinence not responding to first-line medical treatments, difficulties urinating, urinary retention, previous surgery or an unclear diagnosis.

215
Q

What are Urodynamic Tests?

A

They’re a way of objectively assessing the presence and severity of urinary symptoms.

Tests Involved:
Cystometry measures the detrusor muscle contraction and pressure

Uroflowmetry measures the flow rate
Leak point pressure is the point at which the bladder pressure results in leakage of urine.

Post-void residual bladder volume tests for incomplete emptying of the bladder

216
Q

What is the definition of Malnutrition?

A

It’s a Nutrient deficiency state of protein, energy or micronutrients (vitamins and minerals).

NICE definition:

  • BMI < 18.5
  • Unintentional weight loss greater than 10% within the last 3-6 months
  • BMI < 20 and unintentional weight loss greater than 5% within the last 3-6 months
217
Q

What are the risk factors for Malnutrition? (in the elderly)

A
  • Living alone.
  • Institutionalisation or hospitalisation.
  • People with severe learning difficulties or mental health problems (depression, dementia).
  • Diseases that affect appetite, eating/swallowing or gastrointestinal function (gastric surgery, malabsorption,
  • Poor physical function - eg, caused by stroke and neurological disorders such as motor neurone disease).
  • Catabolic states.
218
Q

What is the clinical presentation of malnutrition?

A

Weight Loss (often insidious in adults)
Listlessness.
Increasing fatigue.
Cold sensitivity.
Non-healing wounds and severe decubitus ulcers.

219
Q

How is Malnutrition assessed?

A

MUST Score (Malnutrition Universal Screening Tool)

  • Done on admission to care/nursing homes and hospital or if there is concern
220
Q

What are some differentials for malnutrition?

A

Impaired physical function
e.g. infection, malignancy, renal or heart failure
Depression
Dementia

221
Q

How can malnutrition be managed in the elderly?

A
  • General nutritional advice
  • Dietician support if patient is high risk
  • Food first approach
  • Use of Supplements as second line taken between meals rather than instead of meals
  • Refer to Social Services - if the problem is inability to shop or prepare meals
  • Refer to Occupational Therapy - If the problem is difficulty with eating utensils
222
Q

What is the acute management for the severely malnourished?

A

Clinical Assessment
Assess for co-existing dehydration, infection, anaemia or hypoglycaemia

Correct shock and dehydration and restore electrolyte balance (feeding)

Reverse Malnutrition through artificial feeding
Without overloading cardiac, renal, GI or hepatic function

223
Q

Define Refeeding Syndrome

A

Refeeding syndrome is a serious and potentially life-threatening condition that can develop in malnourished patients when they begin to reintroduce food after a period of starvation or fasting.

It can occur with various different malnourishment backgrounds e.g. anorexia, alcoholism, prolonged fasting, etc…

224
Q

What causes Refeeding Syndrome?

A

It’s caused by the reintroduction of glucose, or sugar, into the body after a period of malnutrition or fasting.

During fasting, the body adapts to use fat and protein as its primary energy sources. When carbohydrates are reintroduced, insulin secretion resumes, leading to a shift in electrolytes which can disrupt the function of various organs.

225
Q

What is the clinical presentation of Refeeding Syndrome?

A

Low phosphate levels
muscle weakness, hemolysis, respiratory failure, and neurological symptoms like delirium and seizures.

Low magnesium levels
neuromuscular excitability, muscle weakness, and cardiac arrhythmias.

Low potassium levels
muscle weakness, paralysis, and potentially fatal cardiac arrhythmias.

Hyperglycemia
symptoms of diabetes, such as increased thirst and urination, fatigue, and blurred vision.

226
Q

What is the definition of Hypothermia?

what is the physiological response?

A

A core body temperature of < <35°C

This leads to the hypothalamus releasing TSH, ACTH and causing shivering as a process to warm the body up.

227
Q

How is Hypothermia classified?

What are the features at each stage?

A

Mild
(32°C to 35°C): characterised by tachycardia, tachypnoea, vasoconstriction and shivering

Moderate
(28°C to 32°C): may have cardiac arrhythmias, hypotension, Bradycardia, respiratory depression, reduced consciousness and may cease to shiver.

Severe
(<28°C): markedly reduced consciousness/coma, apnoea, arrhythmia, fixed and dilated pupils

228
Q

What ECG changes are seen with Hypothermia

A
  • Bradyarrhythmias e.g. sinus bradycardia, atrial fibrillation with a slow ventricular response, slow junctional rhythms and varying degrees of AV block
  • Osborne Waves (‘J waves’) = positive deflection at the J point between the end of the QRS and beginning of the ST segment
  • Prolonged PR, QRS and QT intervals
  • Shivering artefact
  • Ventricular ectopics
  • Cardiac arrest (VT, VF or asystole)
229
Q

How is Hypothermia managed?

A

Remove the patient from cold environments or cold and wet clothes

  • Passive Warming is 1st line e.g. covering the patient with a warm blanket and supplying warm drinks
  • Intravenous administration of warmed fluid
  • Application of warmed air (e.g. using a bear hugger)

Patients are at a high risk of cardiac arrest and CPR may be required.

230
Q

What are the risk factors for hypothermia?

A

General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age

231
Q

What does Article 5 of the Human Rights Act state with regards to liberty?

A

Everyone has the right to liberty and security of person.

No one shall be deprived of his or her liberty [unless] in accordance with a procedure prescribed in law.

232
Q

What are the Deprivation of Liberty Safeguards?

A

A procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm.

233
Q

What conditions must be met to allow a person to be Deprived of their Liberty?

A
  • The person must be 18 or over.
  • The person must be suffering from a mental disorder.
  • The person must be a patient in hospital or a resident in a care home.
  • The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.
  • The proposed restrictions would deprive the person of their liberty.
  • The proposed restrictions would be in the person’s best interests.
  • Whether the person should instead be considered for detention under the Mental Health Act.
  • There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.
234
Q

What are the 5 key principles of the mental capacity act?

A
  • Every adult is assumed to have capacity unless proved otherwise
  • A person must be given all practicable help to make their own decisions before they are deemed to lack capacity
  • People are allowed to make unwise or unsafe decisions
  • All treatment must be done in a patients best interests
  • Anything done must be done in the least restrictive way possible
235
Q

What are the criteria to determine if someone has capacity?

A

Understand the decision
Retain the information long enough to make the decision
Weigh up the pros and cons
Communicate their decision

236
Q

What is the Power of Attorney?

A

A legal document drawn up by a competent adult that nominates another person to make decisions on their behalf

237
Q

What is an Advance Directive?

A

It’s a medical decision made by a patient with capacity, regarding their future wishes for treatment.

It only comes into force if a patient subsequently lacks capacity

238
Q

What is the definition of Elder Abuse?

A

A single or repeated act, or lack of appropriate action, occurring within any relationship where there is an expectation of trust which causes harm or distress to an older person

239
Q

What are some risk factors for Elder Abuse?

A

Poor Physical Health

Mental Illness
Cognitive impairments (eg, dementia) or Behavioral disorders (eg, depression)

Poverty and Disruptive Living Environment

Demographic Risk Factors
More common in women, increased prevalence with increased age

240
Q

What are some Red Flags for elder abuse?

A
  • Multiple ED visits for similar injuries
  • A delay of greater than 24 hours in reporting injuries or responding to the needs of an elderly patient
  • A history of abuse
  • A patient with risk factors
241
Q

Define Polypharmacy?

A

Is a term used to describe the simultaneous use of multiple medications by a patient

Its especially common in the elderly who are more likely to have multiple chronic conditions

242
Q

What are the problems with Polypharmacy?

A
  • Increased risk of falls
  • Reduced adherence and concordance
  • It increases the risk of drug side effects
  • Increases the risk of drug interactions
243
Q

What are Pressure Ulcers / Sores?

A

They occur when skin and underlying tissues are placed under pressure that impairs blood supply, leading to tissue damage.

They’re caused by pressure and/or shear forces over a bony prominence (e.g. sacrum)in the presence of risk factors; primarily among these is immobility

244
Q

How does a pressure ulcer present?

A

They present as persistently red, blistered, broken or necrotic skin and may extend to underlying structures e.g. muscle and bone.

245
Q

Name some predisposing factors for pressure ulcers

A
  • malnourishment
  • incontinence: urinary and faecal
  • lack of mobility
  • pain (leads to a reduction in mobility)
246
Q

What is the Scoring System for Pressure Ulcers?

A

Waterlow score / Braden Scale

247
Q

Describe the European Pressure Ulcer Advisory Panel grading system

A

Grade 1: Red, intact skin.
Grade 2: Partial skin loss, looks like a blister or abrasion.
Grade 3: Full skin loss, damage down to fat layer.
Grade 4: Severe tissue damage, may involve muscle or bone.

248
Q

What is the management of a pressure ulcer?

A
  • Repositioning of the patient
  • Pressure-relieving support surfaces
  • Local wound management using moist hydrogels and hydrocolloid dressings
  • Pain relief with paracetamol (NSAIDs are not used as they can increase peripheral oedema)
  • Infection control
  • Potentially Abx if surrounding cellulitis
  • consider referral to the tissue viability nurse
  • surgical debridement may be beneficial for selected wounds
249
Q

What is the definition of a Squamous Cell Carcinoma (SCC)?

A

A SCC is a locally invasive malignant tumour of epidermal keratinocytes.

250
Q

What are the Risk Factors for developing a Squamous Cell Carcinoma?

A
  • excessive exposure to sunlight / psoralen UVA therapy
  • actinic keratoses and Bowen’s disease
  • immunosuppression e.g. following renal transplant, HIV
  • smoking
  • long-standing leg ulcers (Marjolin’s ulcer)
  • genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism
251
Q

What is the clinical presentation of a Squamous Cell Carcinoma?

A
  • Typically on sun-exposed sites such as the head and neck or dorsum of the hands and arms
  • Rapidly expanding painless, ulcerate nodules
  • May have a cauliflower-like appearance
  • There may be areas of bleeding/ulceration
252
Q

What is the first line investigation for a Squamous Cell Carcinoma?

A

Punch biopsy

253
Q

What is the Diagnostic Investigation for a Squamous Cell Carcinoma?

A

Excision Biopsy with a 4mm margin (or 6mm for high risk lesions)

254
Q

What are the good prognostic and poor prognostic features of SSQ?

A

Good Prognosis

  • Well differentiated tumours
  • < 20mm diameter
  • < 2mm deep
  • No associated diseases

Poor Pronogsis

  • Poorly differentiated tumours
  • > 20mm diameter
  • > 4cm deep
  • Immunosuppression
255
Q

What is the management of a SCC?

A
  • Its almost always treated surgically with excision using a 4mm margin (6mm in high risk lesions)
  • Sometimes Mohs Microsurgery is used
  • Radiotherapy is sometimes required
  • Lifestyle advice (use suncream)
  • Plastic surgery if the lesion is tricky to remove
256
Q

What is the definition of Pseudodementia?

A

Pseudodementia is a condition primarily associated with cognitive deficits in older patients suffering from depression

257
Q

What are the clinical features of Pseudodementia?

A
  • Short duration of symptoms mimicking dementia
  • Equal impact on long-term and short-term memory
  • Amnesia concerning specific, often emotionally charged, events
  • Detailed complaints about memory disturbances
  • Early loss of social skills in the disease progression
  • Common responses of “don’t know” to questions, rather than attempting to guess
  • Minimal effort in task performance
258
Q

How is Pseudodementia investigated?

A

Comprehensive cognitive assessments and psychiatric evaluations.

259
Q

What is the management for Pseudodementia?

A

Management primarily involves treating the underlying depressive disorder:

  • Cognitive behavioural therapy
  • Antidepressant medication

With appropriate treatment, cognitive symptoms usually improve or resolve.

260
Q

What is the definition of Charles Bonnet Syndrome?

A

It’s a medical condition characterised by complex visual hallucinations in individuals who are partially sighted or visually impaired, but otherwise cognitively healthy.

261
Q

What causes Charles Bonnet Syndrome?

A

Causes of visual impairment

  • Age related macular degeneration
  • Glaucoma
  • Cataracts
262
Q

What are some risk factors for Charles Bonnet Syndrome?

A

Advanced age
Peripheral visual impairment
Social isolation
Sensory deprivation
Early cognitive impairment

263
Q

What investigations are done to diagnose Charles Bonnet Syndrome?

A

Diagnosis mainly rests on clinical presentation and patient history.

Neurological and ophthalmic examinations can be done to rule out other potential causes of visual hallucinations.

Must occur in the absence of any other significant neuropsychiatric disturbance

264
Q

What is the management of Charles Bonnet Syndrome?

A

Involves addressing the underlying cause which may involve:

  • Addressing the visual impairment
  • Providing psycological support
  • Possible pharmacological intervention
265
Q

What is the definition of Postural Hypotension?

A

Its defined as a fall of >20mmHg in Systolic blood pressure or >10mmHg in Diastolic blood pressure within 3 minutes of standing.

266
Q

What are the Geriatric Giants in terms of how patients may present to the hospital?

A

4 Is

  • Immobility
  • Instability (falls)
  • Incontinence
  • Impaired Cognition (Delirium/Dementia)
  • Other specific symptoms: Chest pain, SOB, Urinary symptoms
267
Q

What are the main risk factors for falls in geriatrics?

A

History of falls is strongest RF

Lower limb muscle weakness
Vision problems
Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson’s disease etc)
Polypharmacy (4+ medications)
Incontinence
>65
Have a fear of falling
Depression
Postural hypotension
Arthritis in lower limbs
Psychoactive drugs
Cognitive impairment
Home trip hazzards

268
Q

What Investigations should be done for patients with Falls?

A

Assessment of Falls Risk

  • Timed Up and Go Test
  • Turn 180 degree Test

Bedside Tests

  • A-E assessment
  • Basic Observations
  • BP
  • Blood Glucose
  • Urine Dip
  • ECG

Investigations to Consider

  • Bloods: FBC, U&E, LFTs, Bone profile
  • Imaging: X-ray of chest/injured limbs, CT head, ECHO
269
Q

What interventions may be offered by specialist falls services?

A
  • Strength and balance training — most likely to benefit older community-dwelling people with a history of recurrent falls or balance and gait deficit.
  • Home hazard assessment and intervention — should be offered to older people who have received treatment in hospital following a fall.
  • Vision assessment and referral.
  • Medication review — psychotropic drugs are reviewed, with specialist input if appropriate, and discontinued if possible.
270
Q

What is Deconditioning?

A

Describes the deterioration in function that occurs in the context of an acute illness. Being stuck in hospital and bed bound causes many problems such as muscle wasting and worsening nutritional states.

This means it takes longer for them to recover and would requrie Physical and Occupational therapy input.

271
Q

What makes up a Comprehensive Geriatric Assessment?

A

Multidisciplinary approach

Focuses on determining a frail older person’s Medical, psychological and functional capabilities to enable the development of a co-ordinated and integrated plan for treatment and long term follow-up

272
Q

Define Frailty?

A

A distinct age related health state characterised by a reduction in physiological reserve resulting in adverse outcomes following minor stressor events

273
Q

What is frailty Not?

A
  • Not Irreversible
  • Not Inevitable
  • Not simply due to multiple long term conditions
274
Q

What are some factors that can prevent frailty?

A
  • Good nutrition
  • Physical activity (especially when younger)
  • Avoidance of social isolation
  • Reducing smoking and alcohol intake
275
Q

What are the 2 main models to scoring frailty?

A

Phenotype (fried criteria)

Cumulative Deficit (CFS, e-FI)

276
Q

What is the Fried Criteria of Frailty?

A

Description of a Phenotype

Frailty was defined as a clinical syndrome of 3 or more of:

  • Unintentional weight loss
  • Self-reported exhaustion
  • Weakness (grip strength)
  • Slow walking speed
  • Low physical activity
277
Q

What is the Rockwood Clinical Frailty Scale?

A

1. Very Fit: People who are active and considered “the fittest for their age”

2. Well: No active disease symptoms but they exercise often or are very active occasionally

3. Managing Well: Medical problems are well controlled but not regularly active beyond routine walking

4. Vulnerable: Not dependent on others for help but symptoms limit activities

5. Mildly Frail: More evident slowing and may require help with High order IADLs (finances, transport, heavy housework)

6. Moderately Frail: Need help with all outside activities and with keeping house. May require help with stairs and bathing but minimal assistances with dressing

7. Severely Frail: Completely dependent on personal care from whatever cause. They are however stable and not at high risk of dying within 6 months

8. Very Severely Frail: Completely dependent on care and approaching the end of life. Typically they could not recover from a minor illness

9. Terminally ill: Approaching end of life with a life expectancy of <6 months who are not otherwise evidently frail.

278
Q

What is Advance Care Planning?

A

A process of discussion about goals of care and means of setting on record preferences for care of patients who may lose capacity or communicating ability in the future.

279
Q

What may be included in Advanced Care Planning?

A
  • Legal Aspects: Advanced Directives to Refuse Treatment (ADRT) or Lasting Power of Attorney (LPoA)
  • Preferred place of care
  • Treatment options acceptable to patient and suitable for patient (ReSPECT form)
  • DNACPR decisions
  • Specific plan for complex scenarios
280
Q

How can Frailty be managed?

A

MDT Approach

  • Physiotherapy and exercise
  • Dietician for Nutritional support
  • Doctors/pharmacists for medication review of polypharmacy and care of co-morbidities
  • Occupational therapy for ADLs help and reducing falls risk
  • Social support
281
Q

What is Malnutrition?

A

A state of undernutrition

282
Q

What are some causes of Malnutrition?

A
  • Reduced Nutrient Intake (starvation)
  • Increased Nutrient Requirement (Sepsis/Injury)
  • Inability to utilise nutrients ingested (malabsorption: coeliac, IBD, IBS etc)
  • Combination of above
283
Q

What are the consequences of Malnutrition?

A
  • Reduced immune system
  • Muscle wasting leading to increased risk of falls, chest infections, reduce mobility and inactivity
  • Impaired wound healing
  • Micronutrient deficiencies (B12 deficiency causing neurological deficit)
284
Q

What is a MUST Score?

A

Malnutrition Universal Screening Tool

Scores a patient based on their:

  • BMI:
  • History of weight Loss:
  • Acute Disease Effect:
285
Q

What is the Treatment of Malnutrition?

A
  • Food first approach (unless severely malnourished): Snacks, nourishing drinks and food fortification
  • Oral Nutritional Supplements: Fortisips
  • Enteral/Parenteral Nutrition: NG tube, PEG, Parenteral feeding
286
Q

What is Enteral Nutrition? What are advantages and disadvantages?

A

Direct feeding into the gut (stomach, duodenum, Jejunum)

Advantages:

  • Preserves Gut Mucosa and Integrity
  • Improves nutritional status
  • Inexpensive compared to parenteral nutrition

Disadvantage:

  • Tolerance: nausea, satiety, bowels
  • Tube can be uncomfortable to place
  • Patient QoL
287
Q

What are some routes of Enteral Nutrition?

A

Short Term:

  • Nasogastric (NG) Tube
  • Nasojejunal (NJ) Tube

Long Term:

  • Percutaneous Endoscopic Gastrostomy (PEG)
  • Percutaneous Endoscopic Jejunostomy (PEJ)
288
Q

What are the indications for a PEG?

A
  • Dysphagia
  • Cystic fibrosis - high nutritional requirements
  • Oral nutritional intake inadequate and likely to be a long term option
289
Q

What is Parenteral Nutrtion?

A

IV feeding when the gut is inaccessible or unable to absorb sufficient nutrients to sustain nutritional status

290
Q

What are the indications for Parenteral Nutrition?

A
  • Inadequate absorption (eg. short bowel syndrome)
  • Gastrointestinal fistula
  • Bowel obstruction
  • Prolonged Bowel Rest
  • Severe malnutrition
291
Q

Define Refeeding Syndrome?

A

A serious and potentially life-threatening condition that can develop in malnourished patients when they begin to reintroduce food after a period of starvation or fasting.

292
Q

What is the Pathophysiology of Refeeding Syndrome?

A
  • A patient who is severely malnourished will be running fat stores and fat metabolism.
  • It results from a shift in use of energy stores from fat metabolism to carbohydrate metabolism.
  • This increases insulin release which results in the cellular uptake of potassium, phosphate and magnesium causing a shift in fluids and electrolytes.
  • This will result in fluid retention, cardiac arrhythmias, respiratory insufficiency and even death
293
Q

What are the clinical features of Refeeding Syndrome?

A
  • Low phosphate levels: This can lead to muscle weakness, haemolysis, respiratory failure, and neurological symptoms like delirium and seizures.
  • Low magnesium levels: This can lead to neuromuscular excitability, muscle weakness, and cardiac arrhythmias.
  • Low potassium levels: This can result in muscle weakness, paralysis, and potentially fatal cardiac arrhythmias.
  • Hyperglycaemia: This can lead to symptoms of diabetes, such as increased thirst and urination, fatigue, and blurred vision.
294
Q

What is the management of Refeeding Syndrome?

A
  • IV Pabrinex or Thiamine + Vitamin B co-strong prior to re-feeding and for the first 10 days
  • Slow introduction of nutrition to prevent fluid and electrolyte shifts
  • Daily monitoring of refeeding bloods:
    • U&Es
    • Phosphate
    • Magnesium
    • Potassium
295
Q

Define An Acute Kidney Injury (AKI)

A

Abrupt decline in kidney function that occurs within hrs to days due to a rapid decline in GFR leading to a failure to maintain fluid, electrolyte and acid-base homeostasis. It is usually (but not always) reversible.

296
Q

What are the NICE criteria for AKI

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours

Rise in creatinine of ≥ 50% in 7 days

Urine output of < 0.5ml/kg/hour for > 6 hours

297
Q

What is stage 1 AKI?

A

Increase Serum Creatinine by 1.5-1.9x Baseline

Decrease Urine output <0.5mg/kg/hr for 6-12hrs

298
Q

What is Stage 2 AKI?

A

Increase Serum Creatinine by 2-2.9x Baseline

Decrease Urine output <0.5mg/kg/hr for >12hrs

299
Q

What is Stage 3 AKI?

A

Increase Serum Creatinine by 3x Baseline

Decrease Urine output <3.5mg/kg/hr for >24hrs or during RRT

Anuria for >12 hours

300
Q

What is the Epidemiology of an AKI?

A

AKI affects 10-20% of all hospitalized patients and up to 50% of critically ill patients in intensive care.

301
Q

What are the risk factors for AKI?

A
  • Age 65 years or over
  • Chronic kidney disease
  • Other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
  • History of acute kidney injury
  • Nephrotoxic Drug use
  • Use of iodinated contrast agents within the past week
  • Illness/infection and sepsis
302
Q

How can the Causes of an AKI be classified?

A

Pre-renal: (most common) Due to inadequate blood supply reaching the kidneys reducing filtration of blood.

Renal: Where there is intrinsic disease within the kidney that leads to the reduced filtration of blood

Post renal: Caused by obstruction to the outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy

303
Q

Give some Pre-renal causes of AKI?

A
  • Dehydration
  • Hypotension (shock, Sepsis, Anaphylaxis)
  • Renal artery stenosis/obstruction
  • NSAIDs/ACEi
  • Liver/Heart failure
304
Q

Give some Renal Causes of AKI?

A
  • Acute tubular necrosis
  • Glomerulonephritis
  • Acute interstitial nephritis
  • Haemolytic uraemic syndrome
  • Rhabdomyolysis
305
Q

Give some Post renal Causes of AKI?

A
  • Kidney stones
  • Tumours (e.g., retroperitoneal, bladder or prostate)
  • Strictures of the ureters or urethra
  • Benign prostatic hyperplasia (benign enlarged prostate)
  • Neurogenic bladder
306
Q

> DAMN

Give some examples of drugs that are nephrotoxic

A

Diuretics
ACEi/ARBs/Aminoglycosides (gentamicin)
Metformin/Methotrexate
NSAIDs

307
Q

What is the pathophysiology of AKI?

A

Impaired ability of the kidneys to filter the blood.

This leads to accumulation of substances that are usually excreted:

  • Potassium ions
  • Urea
  • Fluid
  • H+ ions

Can lead to damage of the nephron and kidney

308
Q

What are the clinical features of an AKI?

A
  • Oliguria/Anuria
  • Dehydration
  • Nausea and vomiting
  • Confusion
  • Fever (sepsis)
  • Uraemia: Weakness, tremor, fatigue, nausea, vomiting, mental confusion, seizures and coma
  • Breathlessness: Combination of anaemia and pulmonary oedema secondary to volume overload
  • Acid build up - Metabolic acidosis
309
Q

What are the investigations for an AKI?

A

Blood Tests:

  • FBC
  • U&Es
  • LFTs
  • Glucose
  • Clotting
  • Bone profile
  • Creatinine Kinase (CK)
  • CRP

Arterial Blood Gas (ABG): To assess for acidosis, hypoxia and an urgent potassium level

Urinalysis:

  • Dipstick: looking for blood or protein
  • Microscopy, Culture and Sensitivities: To exclude infection
  • Urine protein:creatinine ratio

ECG: To identify Hyperkalaemia

Chest X ray: To identify pulmonary oedema if fluid overloaded

Renal Ultrasound: For Obstruction, structural kidney disease or hydronephrosis

310
Q

What is a good way to establish whether AKI is caused by pre/renal/post renal cause?

A

Urea:Creatine Ratio

  • U:Cr > 100:1 = pre-renal
  • U:Cr < 40:1 = renal
  • U:Cr 40-100:1 = Post renal
311
Q

What is the Management for an AKI?

A

Generally Supportive if haemodynamically stable

  • Ensure kidneys are perfused but not overloaded
  • Medication review and STOP nephrotoxic meds
  • Monitoring for complications (Hyperkalaemia, Uraemia, Acidosis)
312
Q

AEIOU

What are some indications for acute dialysis or haemofiltration?

A

Acidosis (severe metabolic acidosis with pH of <7.20)
Electrolyte imbalance (resistant hyperkalaemia)
Intoxication (drug overdose, poisoning)
Oedema (refractory pulmonary oedema)
Uraemia (encephalopathy or pericarditis)

313
Q

What are some complications for AKI?

A
  • Fluid overload, heart failure and pulmonary oedema
  • Hyperkalaemia which can lead to arrhythmias
  • Metabolic acidosis
  • Uraemia (high urea), which can lead to encephalopathy and pericarditis

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