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Phase 3a > Geratology > Flashcards

Geratology 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)
  • 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
  • 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

It can be any of:

  • A pure motor stroke
  • Pure sensory stroke
  • Sensorimotor stroke
  • Ataxic hemiparesis
  • Dysarthria-clumsy hand syndrome.

A LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.

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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

Its the same as Wallenberg’s Syndrome, but with additional involvement of pontine cranial nerve nuclei.

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

What are the risk factors for a haemmorhagic 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 haemmorhagic strokes?

A

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

  • Increasing prevalence with age
  • More common in men
  • Intra-cerebral haemmorhages 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 Horner’s syndrome
  • Ipsilateral loss of pain and temperature sensation on the face
  • Contralateral loss of pain and temperature sensation over the contralateral body.
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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 haemmorhagic 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 haemmorhagic stroke is suspected

A

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 haemmorhagic 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
  • or without a clear cause
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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

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?

A

The Dix-Hallpike Manoeuvre

It involves moving the patient’s head in a way that moves endolymph through the semicircular canals and triggers vertigo in patients with BPPV.

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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.

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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
  • Dementia
  • Previous History of Delirium
  • Significant Co-morbidities
  • 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)
Prescriptions
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 infection screen
  • Confusion Screen (including bloods and urinalysis)
  • Imaging (possibly Head CT/MRI, Chest XRay or ultrasound of the abdomen depending on scenario)
  • ECG
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55
Q

What blood tests are involved in Confusion Screen?

A
  • 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)
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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
  • 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

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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59
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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60
Q

What are some causes of Reversible Dementia?

A
  • Depression
  • B12 and Folate Deficiency
  • Hypothyroidism
  • Normal Pressure Hydrocephalus (NPH)
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61
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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62
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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63
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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64
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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65
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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66
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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67
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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68
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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69
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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70
Q

What are the first line investigations for Alzheimer’s Disease?

A

History - Cognitive decline questionnaire (MMSE)
Examination - Neurological Exam
Blood tests - Confusion Screen

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71
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 scan
CSF Analysis

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72
Q

What is the management of Alzheimer’s Disease?

A

Non-pharmacological:
* Psychological interventions
* cognitive stimulation therapy
* occupational therapy

Pharmacological:
* Cholinesterase inhibitors (rivastigamine, galantamine, and donpezil) in mild-moderate dementia
* Memantine (NMDA inhibitor) in severe dementia

There is no curative treatment

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73
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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74
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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75
Q

What are the main causes of vascular dementia?

A

The primary cause is ischemic or hemorrhagic 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)
  • cerebral autosomal dominant arteriopathy with subcortical infarcts
  • leukoencephalopathy
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76
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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77
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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78
Q

What are some differentials for vascular dementia?

A

Alzheimer’s disease

Lewy body dementia

Frontotemporal dementia

Normal pressure hydrocephalus

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79
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.

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

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80
Q

What is the diagnostic investigation for vascular dementia?

A

MRI Head - To identify vascular changes or infarcts

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81
Q

What is the management of vascular dementia?

A

symptomatic treatment
* Cognitive enhancers like cholinesterase inhibitors or memantine.
* Management of neuropsychiatric symptoms

Detection and address of CV risk factors
* E.g. hypertension, diabetes, hyperlipidaemia and smoking

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82
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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83
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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84
Q

What is the clinical presentation of frontotemporal dementia?

A

Personality changes

Language impairments
Varying from mild problems with word finding to severe aphasia.

Cognitive decline
Although memory may be relatively preserved in the early stages, executive function is frequently impaired

Motor abnormalities
Some patients may develop features of motor neurone disease, including muscle weakness and dysarthria.

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85
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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86
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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87
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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88
Q

What is the management for frontotemporal dementia?

A

Non-Pharmacological
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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89
Q

Define Dementia with Lewy Bodies

A

It’s a type of 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.

It tends to progress more rapidly compared to other dementias.

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90
Q

Where in the brain do Lewy Bodies accumulate?

A

The Substantia nigra, Paralimbic, and Neocortical areas.

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91
Q

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

A

Parkinson’s Disease

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92
Q

What are the clinical features of Dementia with Lewy Bodies?

A
  • Fluctuating cognition
  • Parkinsonism
  • Visual hallucinations
  • High sensitivity to neuroleptics (antipsychotics)
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93
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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94
Q

What are some differentials of Dementia with Lewy Bodies?

A

Alzheimer’s disease

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

Vascular dementia

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95
Q

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

A

Careful History and clinical examination (Diagnosis is primarily clinical)

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

Neuropsychological testing
Assess cognitive functioning and fluctuations.

Electroencephalography (EEG)
A slow background rhythm may be shown (although not diagnostic)

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96
Q

What is the management for Dementia with Lewy Bodies?

A

Pharmacological
Cholinesterase inhibitors can help manage cognitive symptoms (but caution needs to be taken with antipsychotics due to neuroleptic sensitivity)

Non-Pharmacological
Cognitive stimulation
Physical therapy
Occupational therapy

Supportive Care
Palliative and end-of-life care considerations (due to its progressive nature)

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97
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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98
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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99
Q

Describe the epidemiology of Parkinson’s

A

Prevalence increases with age

More common in males

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100
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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101
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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102
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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103
Q

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

A

Autonomic dysfunction
Leading to constipation, symptomatic orthostasis (postural hypotension), and erectile dysfunction

Olfactory loss

Sleep disorders
e.g. REM behavioural disorder

Psychiatric features
depression, anxiety, and hallucinations

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104
Q
A
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105
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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106
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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107
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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108
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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109
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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110
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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111
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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112
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
113
Q

What is the pathophysiology of Osteoporosis?

A

Osteoporosis occurs due to imbalanced bone remodelling where there is increased osteoclast compared to osteoblast action.

This imbalance results in decreased peak bone mass. And causes changes in the bone architecture including thinning of the cortical bone as well as a decrease in trabecular thickness and a decrease in connections between the horizontal trabeculae.

114
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).

115
Q

What is the diagnostic investigations 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

116
Q

What does the FRAX Score estimate?

A

The 10-year probability of a major osteoporotic fracture.

117
Q

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

A

10%

118
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
119
Q

What is the pharmacological management of Osteoporosis?

A

Bisphosphonates

e.g.
Alendronate 70 mg once weekly (oral)
Risedronate 35 mg once weekly (oral)
Zoledronic acid 5 mg once yearly (intravenous)

120
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.

121
Q

What are the side effects of Bisphosphonates?

A

Reflux 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

122
Q

What is this wrong with this X-Ray?

A

Intra-Capsular Neck of Femur Fracture

123
Q

What are the 2 types of NOF Fracture?

A

Intracapsular Fractures
Occur within the joint capsule. They are further subdivided into displaced and non-displaced fractures. Displaced fractures carry a high risk of avascular necrosis due to possible disruption of the blood supply to the femoral head.

Extracapsular Fractures
Occur outside the joint capsule and include intertrochanteric and subtrochanteric fractures. They have a better prognosis due to a lower risk of avascular necrosis.

124
Q

What is the epidemiology of NOF Fractures?

A

Prevalence increases with age
More common in Females

125
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.

126
Q

What causes NOF Fractures

A
  • Fall onto side in the elderly
  • High energy trauma like car accidents in the young
127
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
128
Q

What are the differentials for a NOF Fracture?

A

Intertrochanteric Fracture

Pelvic Fracture

Hip Dislocation

129
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

130
Q

What is the management of a NOF Fracture?

A

Cannulated Screw Fixation
Used for non-displaced intracapsular fractures

Dynamic Hip Screw (DHS)
Usually used for stable, extracapsular fractures. It involves the insertion of a single large screw into the femoral head, combined with a side plate fixed to the femoral shaft.

Hemiarthroplasty
Involves replacing the femoral head and neck with a prosthesis. It’s performed for displaced intracapsular fractures in older patients with lower activity levels, as these fractures have a high risk of non-union and avascular necrosis.

Total Hip Arthroplasty (THA)
Involves the replacement of both the femoral head and the acetabulum with prosthetic components. It’s used for displaced intracapsular fractures in younger, more active patients or older patients with pre-existing osteoarthritis.

131
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.

132
Q

What’s wrong with this X-Ray

A

Tibial Shaft Fracture

133
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)
134
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
135
Q

What are some differentials for a Tibial Shaft Fracture?

A

Fibular Fracture

Compartment Syndrome

Sprain or Sprain

136
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

137
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

138
Q

What is the definition of Heart Failure?

A

Also known as congestive heart failure (CHF) or congestive cardiac failure (CCF)

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

139
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

140
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.

141
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.

142
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)
143
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).

144
Q

What are the common causes of Systolic HF?

A
  • Ischaemic heart disease
  • Dilated cardiomyopathy
  • Myocarditis
  • Infiltration (haemochromatosis or sarcoidosis)
145
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).

146
Q

What are the causes of Diastolic HF?

A
  • Uncontrolled chronic hypertension
    (significant left ventricular hypertrophy reduces filling of the left ventricle)
  • Hypetrophic cardiomyopathy
  • Cardiac tamponade
  • Constrictive pericarditis
147
Q

Whats the difference between Acute and Chronic HF?

A

Acute HF is either new onset HF symptoms or an acute deterioration in a patient with known chronic HF.

Chronic HF in comparison progresses much slower and may take years to develop.

148
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.

149
Q

What are the clinical features of left heart failure?

A

Symptoms

  • Fatigue
  • Shortness of breath on exertion
  • 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.

150
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.

151
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).

152
Q

What are the clinical features of Right Heart Failure?

A

Symptoms

  • Fatigue
  • Ankle swelling
  • Weight gain
  • Abdominal swelling and discomfort
  • Anorexia and nausea

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

153
Q

What is the most common cause of right heart failure?

A

Left Heart Failure

154
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

155
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)

156
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.

157
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).

158
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.

159
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.
160
Q

What is the diagnostic investigation for HF?

A

Transthoracic Echocardiogram

161
Q

What other investigations should be carried out for HF?

A

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

162
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

163
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.
164
Q

What is the pharmacological management of Heart Failure?

A

A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated

B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated

A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)

L – Loop diuretics (e.g., furosemide or bumetanide)

ARB (e.g. Candesartan) is used if intolerant to ACE-I
Consider Hydralazine if intolerant to both ARB and ACE-I

Other medications:
* Hydralazine and a nitrate for Afro-Caribbean patients.
* Ivabradine if in sinus rhythm and impaired EF.
* Digoxin = useful in those with AF.

165
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

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

166
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
167
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

168
Q

What are the risk factors for Constipation?

A

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

169
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

170
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
171
Q

Give some red flag symptoms for GI malignancy

A

Weight loss
Loss of appetite
Abdominal mass
Dark stool

172
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

173
Q

What investigations should be done for Constioation?

A
  • 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
174
Q

What is the management for Constipation?

A

It depends on the underlying cause and may involve:

  • Exclusion of underlying causes including colorectal cancer
  • Lifestyle modifications such as dietary improvements and increased exercise
  • 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

If laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary.

175
Q

What are the different types of Urinary Incontinence?

A

Stress incontinence
Urge incontinence
Overflow incontinence
Mixed incontinence

176
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.

177
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

178
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.
179
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.

180
Q

What are the risk factors for Urge Incontinence?

A

Recurrent urinary tract infections
High BMI
Advancing age
Smoking
Caffeine

181
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)

182
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,

183
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.

184
Q

What is Mixed Incontinence?

A

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

185
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.

186
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)
187
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.

188
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

189
Q

What is the definition of Malnutrition?

A

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

Classification using BMI:
17-18.5 - mild malnutrition.
16-17 - moderate malnutrition.
<16 - severe malnutrition.

190
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.
191
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.

192
Q

What are some differentials for malnutrition?

A

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

193
Q

How can malnutrition be managed in the elderly?

A
  • General nutritional advice
  • Use of Supplements
  • 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
194
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

195
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…

196
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.

197
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.

198
Q

What is the definition of Hypothermia?

A

A core body temperature of < <35°C

199
Q

How is Hypothermia classified?

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, respiratory depression, reduced consciousness and may cease to shiver.

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

200
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)
201
Q

How is Hypothermia managed?

A
  • 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.

202
Q

What are the risk factors for hypothermia?

A
  • The very elderly or the very young.
  • Those who are chronically ill, especially with cardiovascular disease.
  • People who are malnourished.
  • People who are exhausted.
  • Those intoxicated with alcohol or drugs.
  • People with cognitive impairment - eg, in Alzheimer’s disease.
  • Those with underlying medical conditions (e.g. hypothyroidism, stroke, severe arthritis, Parkinson’s disease).
203
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.

204
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.

205
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.
206
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
  • Unwise, unsafe or dangerous decisions does not mean that person does not have capacity.
  • All treatment given to a person who lacks capacity must be in the patients best interests
  • Anything done for a person who lacks capacity must be done in the least restrictive way possible
207
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

208
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

209
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

210
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

211
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
212
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

213
Q

What are the problems with Polypharmacy?

A
  • Managing multiple medications can be expensive, difficult to track, and hard to manage. Especially in those who have little mobility and are homebound.
  • It increases the risk of drug side effects
  • Increases the risk of drug interactions
214
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

215
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.

216
Q

Name some risk factors for pressure ulcers

A
  • Dementia
  • Diabetes
  • Recent Hip fracture and surgery
  • Limb Paralysis
  • Malignancy
217
Q

Describe the European Pressure Ulcer Advisory Panel grading system

A

Grade 1: Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness can also be used

Grade 2: partial-thickness skin loss involving epidermis, dermis, or both. The ulcer is superficial and presents as an abrasion or blister.

Grade 3: Full-thickness skin loss involving damage to, or necrosis of, subcutaneous tissue that may extend down to, but not through, underlying fascia.

Grade 4: Extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures, with or without full-thickness skin loss. Extremely difficult to heal and predisposes to fatal infection.

218
Q

What is the management of a pressure ulcer?

A

Healing is slow, but as long as the patient has adequate pressure redistribution, good nutrition and appropriate wound management, the ulcer will heal in most cases.

  • Repositioning of the patient
  • Pressure-relieving support surfaces
  • Local wound management using modern wound dressings
  • Pain relief with paracetamol … NSAIDs are not used as they can increase peripheral oedema
  • Infection control
219
Q

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

A

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

They can cause pain, tenderness or bleeding and grow over weeks or months.

SCCs sometimes metastasise, which can be fatal.

220
Q

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

A
  • Family history or previous history
  • Some genetic syndromes
    e.g. Xeroderma Pigmentosum, an autosomal recessive condition that reduces the ability of the body to repair UV damage to DNA.
  • Pale skin/light hair
  • High levels of sun or UV exposure
    e.g. through occupation, sunburn, or use of sun-beds

*Immunosuppression: where HPV viruses are thought to play a key role

  • Chronic inflammation
    e.g. a Marjolin ulcer
  • Predisposing lesions
    Pre-malignant lesions that occur due to sun damage
  • Actinic (solar) keratosis
    Appear as scaly, keratotic, rough lesions, either plaques or papules.
  • Bowen’s Disease:
    (intraepidermal SCC)
  • Smoking
  • Old age and male sex
221
Q

What is the clinical presentation of a Squamous Cell Carcinoma?

A
  • Skin appears keratinised, scaly, irregular nodules. On occasion, the keratin may be so developed that it forms a horn or a plug.
  • They may be ulcerating, and have an everted edge
  • Often in sun exposed areas.
  • The lesions may be polypoid
  • The lesion is usually slow growing, over months
  • Any complications are usually from local invasion; distant metastasis is rare, but can occur
  • Pain, tenderness, and bleeding may be present
222
Q

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

A

Punch biopsy

223
Q

What is the Diagnostic Investigation for a Squamous Cell Carcinoma?

A

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

224
Q

When is a SCC classed as high risk?

A
  • 2cm+ diameter
  • Location on the ear, lip, face, hands, feet, or genitals
  • Elderly or immunosuppressed
  • Histological features: thicker than 2mm, poor differentiation, blood or nerve involvement, invasion of subcutaneous tissue
225
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
226
Q

What is the definition of Pseudodementia?

A

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

227
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
228
Q

How is Pseudodementia investigated?

A

Comprehensive cognitive assessments and psychiatric evaluations.

229
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.

230
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.

231
Q

What causes Charles Bonnet Syndrome?

A

Age-related macular degeneration together with either a glaucoma and cataract is the most common cause.

232
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.

233
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
234
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.

235
Q

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

A
  • Falls (Instability)
  • Confusion (Intellectual Impairment)
  • Off Legs (Immobility)
  • Incontinence
  • Other specific symptoms: Chest pain, SOB, Urinary symptoms
236
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.

237
Q

What makes up a Comprehensive Geriatric Assessment?

A

Multidisciplinary approach

Focuses on determining a frail olde 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

238
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 due to significant reduction in the ability to physiologically manage these minor changes.

239
Q

What is frailty Not?

A
  • Not Irreversible
  • Not Inevitable
  • Not simply due to multiple long term conditions
240
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
241
Q

What are the 2 main models to scoring frailty?

A

Phenotype (fried criteria)

Cumulative Deficit (CFS, e-FI)

242
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
243
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.

244
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.

245
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
246
Q

What is Malnutrition?

A

A state of undernutrition

247
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
248
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)
249
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:
250
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
251
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
252
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)
253
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
254
Q

What is Parenteral Nutrtion?

A

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

255
Q

What are the indications for Parenteral Nutrition?

A
  • Inadequate absorption (eg. short bowel syndrome)
  • Gastrointestinal fistula
  • Bowel obstruction
  • Prolonged Bowel Rest
  • Severe malnutrition
256
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.

257
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
258
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.
259
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
260
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.

261
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

262
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

263
Q

What is Stage 2 AKI?

A

Increase Serum Creatinine by 2-2.9x Baseline

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

264
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

265
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.

266
Q

What are the risk factors for AKI?

A
  • Older age (e.g., above 65 years)
  • Sepsis
  • Chronic kidney disease
  • Heart failure
  • Diabetes
  • Liver disease
  • Cognitive impairment (leading to reduced fluid intake)
  • Medications (e.g., NSAIDs, gentamicin, diuretics and ACE inhibitors)
  • Radiocontrast agents (e.g., used during CT scans)
267
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

268
Q

Give some Pre-renal causes of AKI?

A
  • Dehydration
  • Hypotension (shock, Sepsis, Anaphylaxis)
  • Renal artery stenosis/obstruction
  • NSAIDs/ACEi
  • Liver/Heart failure
269
Q

Give some Renal Causes of AKI?

A
  • Acute tubular necrosis
  • Glomerulonephritis
  • Acute interstitial nephritis
  • Haemolytic uraemic syndrome
  • Rhabdomyolysis
270
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
271
Q

> DAMN

Give some examples of drugs that are nephrotoxic

A

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

272
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

273
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
274
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

275
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
276
Q

What is the Management for an AKI?

A

General Approach of ABCDE Algorithm:

A: Is the airway compromised? This is unlikely in AKI but should always be considered.

B:AKI can result in pulmonary oedema. This should be managed in section ‘B’ by sitting the patient up, giving high-flow oxygen and considering diuretics and CPAP.

C: It is imperative to asses the fluid status in a patient with AKI. This should include a clinical examination and weight. If the patient is hypovolaemic they will require intravenous fluid resuscitation; if they are fluid overloaded they will require offloading. Is there peripheral oedema suggestive of nephrotic syndrome? Do they have a murmur suggestive of infective endocarditis?

D: This is usually unaffected, but if there is neurological involvement one should have a low threshold to consider TTP as a cause. It is also important to consider whether the patient’s cognitive state may limit thair access to free water (or whether they are able to fluid restrict).

E: Are they septic? Is there a typical vascultic rash? Are there signs of systemic lupus erythematosus (SLE)?

Address Immediate Threats: Treat any life-threatening complications such as acidosis, hypovolaemia, hyperkalaemia, sepsis, and pulmonary oedema.

Identify and Treat Underlying Cause: If the cause is unclear, non-resolving, or there are indications for acute dialysis, involve nephrology early.

Monitor Patient: This includes regular observations of fluid status, including measurement of urine output (usually with a catheter) and U&Es.

Medication Review: Suspend nephrotoxic drugs and those that may worsen AKI (NSAIDs, aminoglycosides, ACE inhibitors/ARBs

277
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)

278
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

Phase 3a (11 decks)

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