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Phase 3a Emily > Geriatrics (+ stroke) > Flashcards

Geriatrics (+ stroke) Flashcards

1
Q

What does the internal carotid artery branch off to supply?

A

branches off to create the Anterior cerebral artery, as well as posterior communicating artery to join the circle of Willis

After this the ICA continues on as the Middle cerebral artery, which supplies the lateral portions of the cerebrum.

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2
Q

What does the middle cerebral artery supply?

A

MIDDLE CEREBRAL ARTERY—(huge artery) supplies majority of lateral surface of the hemisphere and deep structures of anterior part of cerebral hemisphere.

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3
Q

What does the anterior cerebral artery supply?

A

ANTERIOR CEREBRAL ARTERY (supplies and runs over Corpus Callosum and supplies Medial aspects of Hemispheres (anteromedial aspects of the cerebrum)

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4
Q

Outline the pathology behind an ischaemic stroke of atherosclerotic origin

A

Basically formation of atherosclerotic plaque:

Irritants damage the endothelium, damage becomes a site for atherosclerosis

A plaque forms, made of fats, cholesterol, proteins, calcium and immune cells encased in a fibrous cap.

If cap ruptures, (interestingly smaller plaques are more dangerous as they have weaker caps that are more prone to being ruptured),

then
Soft core is thrombogenic and platelets adhere to the exposed collagen, creating a clot,
= Known as an Atherothromboembolism

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5
Q

Outline the pathology behind an ischaemic stroke of emboli origin.

A

Blood clot from elsewhere in the body, typically from atherosclerosis or from the heart

Cardiac emboli from AF, MI or infective endocarditis 🡪 blood stasis, forming a blood clot.

Only emboli in the systemic circulation/aka left side of heart can cause an embolic stroke.

Emboli in right side of heart will go to the lung, *unless a patient has a Septal defect- they can travel through the septal defect and go up to brain

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6
Q

Outline the pathology behind an ischaemic stroke due to shock. What are watershed infarcts

A

A rapid drop in blood pressure/perfusion to brain means that areas in the brain furthest from arterial blood supply - Known as Watershed zones Can undergo infarction.

Watershed infarcts are unique ischemic lesions which are situated along the border zones between the territories of the major cerebral arteries.

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7
Q

Causes of ischaemic strokes - Where are the “Watershed zones” of the brain?

A
  1. Cortical border zone infarction: border of ACA/MCA and MCA/PCA
  2. Internal border zone infarction: borders of penetrating MCA branches,orborders of the deep branches of the MCA and ACA (resulting in deep white matter infarction)
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8
Q

Define: stroke

A

rapidly developing clinical signs of focal disturbance of cerebral function lasting more than 24 hrs or leading to death with no apparent cause other than a vascular origin

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9
Q

Name some risk factors for a stroke

A
  • Hypertension
  • Age: the average age for a stroke is 68 to 75 years old
  • Smoking
  • Diabetes
  • Hypercholesterolaemia
  • Atrial fibrillation (ischaemic)
  • Vasculitis
  • Family history
  • Haematological disease: such as polycythaemia, Sickle cell anaemia
  • Medication: such as hormone replacement therapy or the combined oral contraceptive pill
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10
Q

What risk factors in young people increase likelihood of stroke?

A
  • patent foramen ovale
  • polycystic kidney disease (cause perianeurysms > SAH)
  • AVMs arteriosus venous malformations
  • vasculitis
  • thrombophilias
  • sickle cell
  • cocaine use > severe hypertension
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11
Q

What is the Oxford stroke Bamford classification?

A

categorises stroke based on initial presenting symptoms + signs

  1. total anterior circulation stroke (TACS)
    all 3 of the following:
    - unilateral weakness of face, arm and leg
    - homonymous hemianopia
    - higher cerebral dysfunction (dysphasia visuospatial)
  2. partial anterior circulation stroke (PACS)
    2 of the following:
    - unilateral weakness of face, arm and leg
    - homonymous hemianopia
    - higher cerebral dysfunction (dysphasia visuospatial)
  3. lacunar syndrome
    ONE of the follwoing
    - pure sensory stoke
    - pure motor stroke
    - sensori-motor stroke
    - ataxic hemiparesis
  4. Posterior circulation syndrome (POCS)
    ONE of the following
    - cranial nerve palsy + contralateral motor/sensory deficit
    - bilateral motor/sensroy deficit
    - conjugate eye movement disorder
    - cerebellar dysfunction
    - isolated homonymous hemianopia or cortical blindness
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12
Q

What are the clinical manifestations of a stroke in the anterior cerebral artery?

A

Lower limb weakness and loss of sensation to the lower limb.
2. Gait apraxia (unable to initiate walking).
3. Incontinence.
4. Drowsiness.
Decrease in spontaneous speech.

Contralateral hemiparesis (weakness of one side of the entire body) and sensory loss with lower limbs > upper limbs

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13
Q

What are the clinical manifestations of a stroke in the middle cerebral artery?

A

(big artery so can cause weakness all along one side)

Contralateral hemiparesis with upper limbs > lower limbs
Facial drop
sensory loss with upper limbs > lower limbs

Homonymous hemianopia

Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere; patients fail to be aware of items to one side of space

Aphasia: if affecting the ‘dominant’ hemisphere (the left in 95% of right-handed people) as Brocas/Wernickes areas supplied by MCA)
Aphasia is the medical term for full loss of language, while dysphasia stands for partial loss of language.

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14
Q

Posterior circulation infarction

A
  • ipsilateral cranial nerve palsy and a contralateral motor sensory deficit
  • conjugate eye movements disorder
  • cerebellar disfunction
  • crossed signs
  • isolated homonymous hemianopia
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15
Q

Wallenberg and weber syndrome

A

Wallenberg = occlusion of PICA
DANVAH
Dysphasia
Ataxia
Nystagus
Vertigo
anaesthesia
horners

Weber’s = occlusion of paramedic of posterior cerebral artery
‘Web in my eye’

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16
Q

What is a homonymous hemianopia?

A

a visual field defect involving either the two right or the two left halves of the visual fields of both eyes

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17
Q

Lacunar infarction

A
  • occlusion of deep penetrating arteries
  • affects a small volume of sub cortical white matter
    (don’t present with cortical features)
  • pure motor hemiparesis
  • ataxic hemiparesis
  • clumsy hand and dysarthria
  • pure hemisensory
  • mixed sensorimotor
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18
Q

What are the clinical manifestations of a ischaemic stroke in the vertebral basilar arteries?

A
  • Cerebellar signs
  • Reduced consciousness
  • Quadriplegia or hemiplegia
  • disturbances of gaze and vision,
  • locked in syndrome (aware, but unable to respond)
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19
Q

What is the first line investigation to do for a stroke, what would you see?

A

CT scan ASAP
- non-contrast
- Distinguishes ischaemic from haemorrhagic

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20
Q

Define hyperattenuation and hypo attenuation

A

hypoattenuation
- (darkness) of the brain parenchyma
loss of grey matter-white matter differentiation, and sulcal effacement

hyperattenuation
- (brightness) in an artery indicates clot within the vessel lumen

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21
Q

What are some other investigations you would do for a Stroke?

A
  • ECG: assess for AF, MI
  • ECHo (endocarditis/thrombus)
  • Carotid doppler USS (carotid stenosis)
  • Bloods:
    (FBC, ESR, Lipid, glucose, clotting screen, LFTs)
    Screen for risk factors including Hba1c, lipids, clotting screen and rule out stroke mimics such as hypoglycemia and hyponatraemia
    In younger patients, consider ESR, autoantibody and thrombophilia screen (ESR raised in vasculitis)
  • CT angiogram (CTA): identifies arterial occlusion and should be performed in all patients who are appropriate for thrombectomy
  • MRI head:MRI is an alternative to non-contrast CT head; MRI is more sensitive but CT is safer and easier to obtain
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22
Q

Management: ischaemic stroke

A
  • maintain stable blood glucose levels, hydration status and temp (Nil by mouth = struggle to swallow)
  1. thrombolysis = alteplase
    - <4.5hrs of symptoms onset and haemorrhage excluded on imaging
    (but can do up to 9hrs IF CT shows an area of brain tissue is salvageable
    OR from ‘wake up’ stroke’ form 9 hrs after the mid point of sleep)
    - bolus and infusion
    (do even if not seen clot on CT)

Thromboectomy
- mechanical recanalisation of culprit vessel
- do if can’t do thrombolysis
- up to 24hrs post stroke onset if imaging shows salvageable brain tissue

  1. Aspirin 300mg for 2 weeks
  2. Prophylaxis
    - lifelong clopidogrel 75mg
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23
Q

What are some complications of thrombylysis ?

A

Bleeding anywhere,
- especially in the brain haemorrhagic stroke,
NEVER FOR HAEMORRHAGIC STROKE
- and in the urinary tract - so try to avoid catherising patients who have just had thrombolysis
-

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24
Q

What are the contraindications to thrombolysis?

A

ABCDEFG
A - anticoagulation
B - BP >185/110
C - CNS procedure/ cranial trauma/ recent stroke 3/12
D - diathesis (ACTIVE BLEEDING)
E - endocarditis, every major surgery/surgery last 2/52
F - former history of ICH at any time
G - glucose <3 or >10, GI bleed,

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25
Q

What are complications of stroke you will have to manage?

A
  • DVT risk = stockings, flowtrons
  • pressure sores = from immobility
  • nil by mouth due to poor swallowing
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26
Q

What are the long term lifestyle management for stroke?

A
  • stop smoking
  • exercise
  • good diet
  • alcohol cessation
  • driving advice = 1 month normally, 6-12 months for HGVs
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27
Q

What is the treatment for small strokes?

A

Dual anti platelet
75mg of aspirin + clopidogrel

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28
Q

medical secondary prevention management

A
  • antiplatelets = aspirin +/or clopidogrel then clopidogrel for lifelong
  • anticoagulation
    = prevent blood clots in a low pressure system
    CHADVASc for stroke
    ORBIT score for risk of bleeding
  • hypertension
    Acute : risk of hypo perfusion
    Chronic: long term blood pressure targets of <130/80
  • diabetes
  • cholesterol
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29
Q

Major sign of haemorrhage stroke

A

sudden severe headache

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30
Q

Management: haemorrhage stroke

A
  1. ABCDE
  2. blood pressure
  3. bleeding tendency
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31
Q

What are some conditions that are stroke mimics?

A
  • seizures
  • SOL
  • migraine
  • metabolic (hypoglycaemia or hyponatraemia)
  • functional neurological disorder (hoover’s sign)
  • vestibular neuritis/ other causes of vertigo
  • spinal cord/peripheral nerve/ cranial nerve lesions
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32
Q

What are the reversal medications of anticoagulation?

A

Warfarin reversal
= beriplex and vitamin K

Heparin = portamine

Apixaban/riavroxaabn = beriplex

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33
Q

What is the difference between bell’s palsy and a stroke?

A

Bell’s
LMN lesion
can’t crease forehead
onset hours -days
treat with steroids

stroke
- sudden onset
- forehead spring
- UMN lesion
- treat with thrombolysis

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34
Q

What is a TIA?

A

Sudden onset focal neurological deficit.

Older definition:
symptoms of a stroke that resolve within 24 hours.

New definition:
transient neurological dysfunction secondary to ischaemia without infarction.
Either time based or tissue based

DOES NOT CAUSE ACUTE INFARCTION

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35
Q

What are the symptoms of a TIA in the internal carotid artery?

A

Depends on the site of the TIA:

ACA - weak/numb contralateral leg

MCA - weak/numb contralateral side of body, face drooping w/forehead spared, dysphasia (temporal)

PCA -Homonymous hemianopia: visual field loss on the same side of both eyes
Hemisensory loss
Amaurosis fugax

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36
Q

What are the symptoms of a TIA in the vertebral/ basilar arteries?

A

Diplopia – double vision
Vertigo
Vomiting
Choking and dysarthria
Ataxia
Hemisensory loss

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37
Q

TIA scoring - what score can help stratify which patients are at a higher risk of a stroke following a TIA?

A

ABCD2 score – risk score of strokes (max score is 7)

A – Age – > 60 (1 point)
B – Blood pressure (at presentation), 140/90 or more (1 point)

C – Clinical features: Unilateral weakness (2 points), Speech disturbance without weakness (1 point)

D – Duration, 60 minutes or longer (2 points), 10-59 minutes (1 point)
D – Presence of diabetes (1 point)

High risk:
ABCD2 score of 4 or more, AF is present, More than TIA in one week or a TIA whilst on anti-coagulation

Low risk:
None of the above
Present more than a week after their last symptoms have resolved

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38
Q

investigations: TIA

A
  1. The Face Arm Speech Time Test (FAST test): check for/ ask about facial weakness, arm weakness, speech difficulty
  • ECG: rule out AF as an underlying cause
  • Auscultation: listen for carotid bruit
  • Bloods:
    PT time/INR - in case thrombolytic therapy is needed
    To exclude hypoglycaemia/hyponatraemia
    FBC – looking for polycythaemia
  • CT scan - Request an urgent CT scan of the head
  • Carotid doppler – look for stenosis
  • CT angiography – look for stenosis
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39
Q

Acute Management: TIA

A
  1. Immediate management
    Aspirin 300mg
    Refer to specialist – to be seen within 24h of symptom onset
  2. Antiplatelet therapy
    Standard treatment is Aspirin 75mg daily
    With modified-release Dipyridamole
    OR Clopidogrel daily
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40
Q

What procedure can be done for a TIA?

A

Carotid endarterectomy:
surgical procedure to remove the blockage,
Done within 2 weeks stenosis of > 70% on Doppler is an indication for urgent endarterectomy

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41
Q

Long term management: TIA

A
  • Statin = atorvastatin 20-80mg OD
  • Anticoagulant for AF
    e.g. low molecular weight heparin e.g. dalteparin
    OR
    direct thrombin inhibitor
    OR
    factor Xa inhibitor rivaroxaban
  • Give aspirin 300mg OD for 2wks then switch to 75mg clopidogrel OD
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42
Q

What are the main complications of a TIA?
How can you distinguish between a TIA and a Stroke?

A

Increased risk of stroke
Increased risk of underlying CVD

You cant distinguish until after recovery
TIA Sx resolve usually within/<24 hours
Stroke Sx last more than 24 hours

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43
Q

What are the subtypes of haemorrhagic stroke?

A

Intracerebral: bleeding within the brain parenchyma

Subarachnoid: bleeding into the subarachnoid space, between the pia mater and arachnoid mater of the meninges

Intraventricular: bleeding within the ventricles which stop CSF; prematurity is a very strong risk factor in infants

Intraparenchymal haemorrhage: An intracerebral haemorrhage that involves just the brain tissue

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44
Q

What are the main aetiologies of a primary haemorrhagic stroke?

A
  • Hypertension
  • Arteriovenous malformations: blood vessels that directly connect an artery to a vein. Over time these abnormal vessels dilate and can rupture
  • Vasculitis
  • Vascular tumours - aka Haemangioma
  • Cerebral amyloid angiopathy: a degenerative disease where abnormal protein deposits in the walls of arterioles making them less compliant
  • Head trauma
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45
Q

How can a haemorrhagic stroke be secondary to an ischaemic stroke?

A

Ischaemia causes brain tissue death.

If there is reperfusion, there’s an increased chance that the damaged blood vessel might rupture. Bleeding into dead tissue is called haemorrhagic conversion.

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46
Q

Outline the pathology that a haemorrhagic stroke leads to.

A

pool of blood which increases pressure in the skull and puts direct pressure on nearby tissue cells and blood vessels

downstream tissue from bleed are also deprived of oxygen-rich blood. Healthy tissue can die from both the direct pressure and the lack of oxygen

Increased ICP can also lead to
CSF obstruction, - Hydrocephalus
Midline shift
Tentorial herniation

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47
Q

What are some general clinical manifestations of a haemorrhagic stroke?

A

Similar to an ischaemic stroke - brain region specific
- Headache
- Weakness
- Seizures
- Vomiting
- Reduced consciousness

  1. Anterior or middle cerebral artery stroke: numbness and sudden muscle weakness.
  2. Broca’s area or Wernicke’s area stroke: slurred speech or difficulty understanding speech, respectively.
  3. Posterior cerebral artery stroke: vision disturbances.
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48
Q

Investigations: intercranial haemorrhage

A
  1. Request an immediate non-contrast CT scan of the head
    - will see hyperattenuation (brightness), suggesting acute blood, often with surrounding hypoattenuation (darkness) due to oedema
  2. Angiography: visualise the exact location of haemorrhage
  3. Check FBC and clotting
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49
Q

Management: intercranial haemorrhage

A
  1. Consider intubation, ventilation and ICU care if they have reduced consciousness
  2. Correct any clotting abnormality - STOP ANTICOAGULANTS IF PT IS ON THEM
  3. Correct severe hypertension but avoid hypotension
    Craniotomy, or stereotactic aspiration
  4. Drugs to relieve ICP - IV MANITOL
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50
Q

Treatment for intracerebral haemorrhagic stroke - How does mannitol work?

A

elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma

Mannitol hinders tubular reabsorption of water and enhances excretion of sodium and chloride by elevating the osmolarity of the glomerular filtrate.

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51
Q

What are the 3 main causes of a Subarachnoid Haemorrhage?

A
  1. Trauma
  2. Atraumatic cases are referred to as spontaneous SAH - often due to a saccular cerebral (Berry) Aneurysm - 70-80% of SAH cases
  3. Arteriovenous malformation(AVM) - abnormal connections between artery and vein can dilate and cause rupture - 15% of SAH cases

Can be Idiopathic

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52
Q

Outline the pathophysiology behind a subarachnoid haemhorrage.

A

Rupture of blood vessel - leads to a rise in ICP,

Pressure on healthy tissues can make them die, as well as brain tissue not getting blood it needs due to bleed - Ischaemia

Vessels being bathed in a pool of blood can cause vasospasm - will further reduce the supply of blood flow to the brain

Also can irritate the meninges, which can lead to scarring which can obstruct CSF outflow ==> Hydrocephalus

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53
Q

What are some signs of a Subarachnoid haemhorrhage?

A
  • Neck stiffness
  • Budzinski’s Sign - Flexion of neck = Flexion of Knees
  • Kernig sign - Knee cannot be fully extended with hip flexed at 90 degrees
  • Focal neurological deficit - eg if affecting Posterior cerebral artery - Oculomotor palsy
  • Increased BP
  • ‘Thunderclap’ headache
  • Meningism: photophobia and neck stiffness - due to Meningies irritation
  • Vision changes
  • Nausea and vomiting
  • Speech changes
  • Seizures
  • Papilledema
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54
Q

What are some differentials for a subarachnoid haemorrhage?

A

Migraine
Meningitis
Corticol vein thrombosis
Carotid/vertebral artery dissection

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55
Q

Investigations: SAH

A
  1. Urgent Non Contrast CT head
    ASAP
    Detects >95% of SAH in first 24 hours - Subarachnoid and/or intraventricular blood, hyperdense areas in the subarachnoid space
    “Star” shaped sign - or hyerdense blood in the gyri - as blood is not in the brain tissue, but on top of the pia mata
  2. ECG - Arrhythmias and ischaemic changes, Prolonged QTc, ST segment/T-wave abnormalities.
  3. Lumbar puncture – if CT normal but SAH still suspected
    Findings - RBCs or xanthochromia (yellow pigmentation due to degradation of haemoglobin to bilirubin)
  4. Electrolytes - Moderate hyponatraemia
  5. ABG – to rule out hypoxia
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56
Q

Non-surgical management: SAH

A

Immediately refer to neurosurgeon

  1. Nimodipine - Ca2+ antagonist, (CCB) Reduces vasospasm and therefore cerebral ischaemia
  2. Re-examine CNS often
  3. IV fluids -Maintain cerebral perfusion
    Ventricular drainage for hydrocephalus
  4. IV mannitol + head elevation (30°) + intubation with hyperventilation = If features of raised intracranial pressure
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57
Q

Surgical management: SAH

A
  1. endovascular coilingo f the aneurysm
    - reduces blood circulation to the aneurysm inserting one or more microsurgical detachable platinum wires, into the aneurysm until there is no more blood flow occurring. Usually enter through leg.
  2. surgical clipping via craniotomy
    - opening in the skull is created to reach the aneurysm. Then small metal clip on the neck (opening) of the aneurysm to obstruct the flow of blood.
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58
Q

Define: Extradural/ Epidural Haemorrhage

A

A bleed ABOVE the dura mater, between the outer endosteal of the dura and the skull.

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59
Q

Where is the most common site for an extradural haematoma? Why is this?

A

Pterion
= where the frontal, parietal, temporal and sphenoid bones join together

  • relatively thin
  • located right above the middle meningeal artery
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60
Q

What are some symptoms of an extradural haemorrhage

A
  • Head injury
  • Reduced GCS: loss of consciousness after the trauma due to concussion
  • There might be a LUCID INTERVAL after initial trauma if there is a slower bleed. This is followed by rapid decline. ==> Therefore, if suspect a fracture/bleed in head injury, they need a scan!

Headaches
Vomiting
Confusion
Seizures
Pupil dilation if bleeding continues
May be focal neurological symptoms e.g. muscle weakness, hemiparesis, abnormal plantar reflex (upgoing plantar) or sensory problems

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61
Q

Investigations: extradural haematoma

A

CT scan
– shows biconvex hyperdense haematoma that is adjacent to the skull
- Blood forms rounded/biconvex shape as the tough dural attachments to the skull keep it more localised
- Don’t cross suture lines

Skull X-ray
– may be normal or show fracture lines crossing the course of the middle meningeal artery
- Skull fracture increases the extradural haemorrhage risk so do an urgent CT on anyone with suspected skull fracture

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62
Q

If a pupil is fixed and dilated , what is effected?

A

Edinger-Westphal nucleus disrupts the normal regulation of pupil size by interfering with the parasympathetic innervation, as well as the occulomotoro nerve

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63
Q

What are the main causes for a subdural haematoma?

A

Rupture of bridging veins, usually caused by:

  • Brain atrophy: in the elderly the brain shrinks in size which means that the bridging veins are stretched across a wider space where they are largely unsupported
  • Alcohol abuse: caused the wall of the veins to thin out, and make them more likely to break.
  • Trauma/ injury e.g.
  • Falls
  • Shaken baby syndrome
  • Acceleration-deceleration injury: speeding on the road and then suddenly slamming the brakes
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64
Q

What are some clinical manifestations of a subdural haematoma?

A
  • Reduced GCS: loss of consciousness right after the injury or in the ensuing days to weeks as the haematoma increases in size.
  • Headaches
  • Vomiting
  • Seizures
  • Sometimes there can be focal neurological symptoms e.g. muscle weakness, unequal pupils, hemiparesis or sensory problems
  • Confusion
  • May fluctuate
    Insidious physical & intellectual slowing
  • Personality change
  • Unsteadiness

They often cannot remember the traumatic injury as it was long ago

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65
Q

Investigations: subdural haemorrrhage

A

Immediate NON CONTRAST CT head to establish the diagnosis.
- Shows clot and midline shift.

Bleeding is between the dura and arachnoid so subdural haematomas follow the contour of the brain and form a crescent-shape and cross suture lines. This is different to an epidural haemorrhage!

Check FBC and clotting

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66
Q

What would you see on a non contrast CT head for someone with a:

  1. Acute Subdural haematoma
  2. Chronic subdural haematoma
  3. Acute on chronic haematoma
A
  1. Acute subdural haematoma: hyperdense mass = looks “more white” than the surrounding healthy brain tissue
  2. Chronic subdural haematoma: hypodense masses = “less white” than the surrounding brain tissue.
  3. Acute on chronic bleeding: combination of hyperdense and hypodense, seen in individuals who have a rebleed in the bridging veins after a chronic haematoma has already formed.
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67
Q

Define: Benign paroxysmal positional vertigo (BPPV)

A

Common cause of recurrent episodes of vertigo triggered by head movement

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68
Q

Presentation: benign paroxysmal positional vertigo (BPPV)

A

certain head movements can trigger attacks e.g. turning over in bed
- symptoms settle after 20-60s
- asymtpomatic between attacks
- does not cause hearing loss or tinnitus

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69
Q

What is the cause of BPPV?

A
  • caused by crystals of calcium carbonate called otoconia that become displace into the semicircular canals
  • MC in posterior semicircular canal
  • displaced by viral infection, head trauma, ageing or unknown cause
  • crystals disrupt normal flow of endolymph through the canals, confusing the vestibular system
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70
Q

What is the Dix-Hallpike manoeuvre?

A

Used to diagnose BPPV

Involved moving patients head in a way that moves endolymph through the semicircular canals and triggers vertigo in patient with BPPV

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71
Q

What is the Epley manoeuvre?

A

To treat BPPV

  • move crystals in the semicircular canal intra position that does not disrupt endolymph flow
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72
Q

What are Brandt-Daroff exercises?

A

can be performed by the patient at home to improve symptoms of BPPV

  • sit on edge of bed, and lying sideways, from one side to the other, while rotating the head slightly to face the ceiling
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73
Q

Define: delirium

A

Acute, transient and reversible state of confusion, caused by organise causes

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74
Q

What are the two types of delirium?

A
  1. hyperactive delirium
    - agitation
    - delusions
    - hallucinations
    - wandering
    - aggression
  2. Hypoactive
    - lethargy
    - slowness with everyday tasks
    - excessive sleeping
    - inattention
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75
Q

What is the cause of delirium?

A

CHIMPS PHONED

Constipation
Hypoxia
Infection
Metabolic disturbance
Pain
Sleeplessness
Prescriptions
Hypothermia/pyrexia
Organ dysfunction (hepatic or renal impairment)
Nutrition
Environmental changes
Drugs (over the counter, illicit, alcohol and smoking)

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76
Q

Investigations: delirium

A
  • abbreviated mental test score
  • bloods: FBC< LFTs, Calcium, B12, folate, glucose, blood culture
  • urinalysis
  • Imaging = CT head, CXR
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77
Q

Management: delirium

A
  • identify and treat underlying cause
  • supportive management in hospital
  • take steps to prevent future episodes w.g. drugs that predicate delirium, observe them for early signs
78
Q

define: dementia

A

irreversible, progressive decline and impairment of more than on aspect of higher brain function (concentration, memory, language, personality, emotion)

This occurs without impairment of consciousness

79
Q

Name 3 types of Dementia

A

Alzheimer’s.
Vascular.
Lewy Body

80
Q

Give 3 differential diagnoses for dementia.

A

Old age.
Depression.
Physical health problems e.g. DM, hypothyroid, vitamin deficiencies.
delirium

81
Q

What is the main investigative screening tool used for dementia?

A

ACE-III screening tool

82
Q

Dementia: what 5 cognitive domains does the ACE-III screening tool assess?

A

Attention.
Memory.
Fluency.
Language.
Visiospatial.

83
Q

What drugs can be used in the treatment of dementia?

A
  1. Acetylcholinesterase inhibitors e.g. Donepezil, Rivastigimine, galantamine
    (mild to moderate dementia)
  2. NMDA antagonist e.g. Memantine.
    (used for contraindications for AChE inhibitors + more severe dementia)
  3. RF reduction in vascular dementia is important too
84
Q

What are the features of Alzheimer’s dementia?

A
  • Progress steadily
  • amyloid plaques and neurofibrillary tangles
  • main presentation = memory loss
  • > 60 yrs old
85
Q

What genes put you at risk of AD?

A

APP and presenilin genes (PSEN1, PSEN2)
- APP on chromosome 21, so increased risk for people with down syndrome

alleles of apolipoprotein E4 = not as good at clearing beta plaques

86
Q

What are some of the symptoms of AD?

A
  1. Agnosia- can’t recognise things
  2. Apraxia can’t do basic motor skills
  3. Aphasia speech difficulties

Cognitive impairment
Agitation and emotional lability
Depression and anxiety
Sleep cycle disturbance: Motor disturbance: wandering is a typical feature of dementia

87
Q

Investigations: alzheimer’s

A

Full blood count
Urea and electrolytes
Liver function tests
Inflammatory markers (e.g., CRP and ESR)
Thyroid profile
Calcium
HbA1c
B12 and folate

MRI - by specialist to exclude structural pathology

CT head
- brain looks smaller
- atrophy in fronto-temporal regions

88
Q

What is the diagnostic criteria for AD?

A

Functional ability: inability to carry out normal functions

Impairment in 2 or more cognitive domains

Differentials excluded

89
Q

What is the definitive diagnosis for AD?

A

Brain biopsy after autopsy

90
Q

What are the features and RF of vascular dementia?

A

2nd MC
RF:
MC in males
after stroke
hypertension

presentation:
- stepwise progress
(period of stability, before acute decline progression)
- main affects white matter areas
- cognitive impairment = mood distrubances and disorders

91
Q

What are the features of Lewy body dementia?

A

> 50 yrs old

Presentation:
- rapidly progresses, death MC in first 7 yrs
- fluctuating cognitive impairment
- visual hallucinations
- dementia symptoms 12 months before motor symptoms
- Parkinson like symptoms

Investigation:
DaT scan

92
Q

What are the causes of Lewy body dementia?

A
  • Spherical Lewy body alpha-synuclein proteins deposited in the brain
    (also present in Parkinson’s)
93
Q

What is pseudo-dementia?

A

Cognitive impairments secondary to a mental illness e.g. depression/anxiety.

94
Q

What is the difference between dementia and pseudodementia?

A

dementia - make up answers

pseudo dementia
- answer ‘don’t know’
- impairments in excessive functioning and attention

95
Q

What is frontotemporal dementia?

A

A neurodegenerative disorder characterised by focal degeneration of the frontal and temporal lobes.

  • MC <65 yrs early onset

It is a heterogenous condition with various subtypes e.g., Pick’s disease

96
Q

What are the genes associated with FTD?

A
  • C9ORF72 gene: found on chromosome 9. MC cause
  • MAPT (microtubule associated protein)- found on chromosome 17
  • Granulin precursor(GRN): found on chromosome 17.
97
Q

What are the frontal lobe effects of FTD?

A

Personality and behaviour change:
- Disinhibition
- Loss of empathy
- Apathy
- Hyperorality(e.g. dietary changes, attempt to consume non-edible products, eat beyond satiety)
- Compulsive behaviour(e.g. cleaning, checking, hoarding)

98
Q

What are the temporal lobe effects of FTD?

A

Language problems:
- Effortful speech
- Halting speech
- Speech sound errors
- Speech apraxia
- Word-finding difficulty
- Surface dyslexia or dysgraphia: mispronouncing difficult words (e.g. yacht)

99
Q
A
100
Q

How would you diagnose FTD?

A

Diagnosis based on cognitive assessment

Imaging:
MRI: exclude other pathology; indicates changes in the frontal and temporal lobes

Definitive diagnosis = brain biopsy after a person has died

101
Q

What are the pharmacological treatments for FTD?

A

Serotonin reuptake inhibitors (SSRI) = used for difficult behavioural symptoms. Have been shown to decrease disinhibition, anxiety, impulsivity and repetitive behaviours.

Atypical anti-psychotics = can help with agitation and behavioural symptoms.

102
Q

Aetiology: frontal lobe syndrome

A
  • head injury
  • cerebrovascular event
  • infection
  • neoplasm
  • degenerative disorders e.g. Pick’s disease
103
Q

presentation: Frontal lobe syndrome

A

“He’s not the father I know”

Symptoms: Decreased lack of spontaneous activity, Loss of attention, Perseveration

Signs: Neglect (right-sided brain lesions typically neglect the left hemispace)

104
Q

Investigations: Frontal lobe syndrome

A

Bloods – B12 levels, TFTs, serology for syphilis and antinuclear antibodies

Consider MRI/CT scanning

105
Q

Management: Frontal Lobe syndrome

A

General supportive care sharing some principles with dementia care

106
Q

What are the causes of falls in the elderly?

A

I HATE FALLING

  • Inflammation (joints)
  • Hypotension
  • Arrhythmia
  • Tremor
  • Equilibrium (balance issues, drug induced or other causes)
  • Foot pain
  • Auditory/Visual impairment
  • Leg length discrepancy
  • Lack of conditioning
  • Illness
  • Nutrition poor
  • Gait problems
107
Q

What disorders contribute to risk of falls?

A

Blood pressure regulation
- anaemia
- arrhythmias
- COPD
- dehydration
- infections
- diabetes
- heart disorders

Central processing
- delirium
- dementia
- stroke

Gait
- arthritis
- foot deformities
- muscle weakness

108
Q

What are signs of a cardiac cause of falls?

A
  • chest pain
  • palpitations
  • sweating
  • no stimulus
  • arrythmia
  • low BP
  • on exertion
  • while lying down
  • known PMH or FH
109
Q

What medications contribute to the risk of falls?

A

Beta-blockers (bradycardia)

Diabetic medications (hypoglycaemia)

Antihypertensives (hypotension)

Benzodiazepines (sedation)

Antibiotics (intercurrent infection)

110
Q

Investigations: falls

A

bedside
- lying and standing BP
- urine dipstick
- ECG
- cognitive screening
- blood glucose

Bloods
- urea + electrolytes
- LFTs
- bone profile

Imaging
- CXR
- CT head
- Echo

111
Q

Management: falls

A
  • Gait = Physiotherapy
  • Visual problems = Eye test and ensure wears glasses
  • Hearing difficulties = Remove earwax
    Hearing assessment
  • Medications review = Reduce unnecessary medication
  • Alcohol intake = Alcohol cessation advice
    Alcohol service referral
  • Cognitive impairment = Referral to a psychiatric team
  • Postural hypotension = Review medication, Improve hydration
  • Continence
    = Treat or rule out infections
    Continence assessment
  • Footwear
    Ensure good fitting footwear
  • Environmental hazards
    Turn on lights
    Take up rugs
112
Q

How do you diagnose postural hypotension?

A
  • A drop in systolic BP of 20mmHg or more (with or without symptoms)
  • A drop to below 90mmHg on standing even if the drop is less than 20mmHg (with or without symptoms)
  • A drop in diastolic BP of 10mmHg with symptoms (although clinically much less significant than a drop in systolic BP).
113
Q

What are the causes of postural hypotension?

A
  • dehydration
  • medication
  • Parkinsons
  • diabetes
  • Addisons
114
Q

Investigations: postural hypertension

A
  • lying and standing BP
  • tilt testing
  • ECG
  • echo
115
Q

Define: carotid sinus syndrome

A

hypersensitive baroreceptors in carotid
- cause syncope when pressure put on carotid

116
Q

Define: frailty

A

State of increased vulnerability resulting from ageing-associated decline in functional reserve,
Across multiple physiological systems,
Resulting in compromised ability to cope with everyday or acute stressors

117
Q

investigations: frailty

A
  • gait speed
  • self-reported health status
  • PRISMA-7 questionnaire
118
Q

What are the causes of urinary incontinence?

A

Age-related changed: reduced total bladder capacity, reduced bladder contractile function, reduced ability to postpone voiding, atrophy of vagina and urethra, loss of pelvic floor and urethral sphincter musculature, hypertrophy of prostate

Comorbidity: reduced mobility, medication, constipation, impaired cognition

Reversible: UTI, delirium, drugs, constipation, polyuria, urethral irritability, prolapse, bladder stones and tumours

Environmental: Bed Bound, Toilet Too Far/Hard To Access

119
Q

Investigations: urinary incontinence

A
  • Symptoms (stress, urgency, obstructive), bladder diary
  • Examination: vaginal, rectal, neuro
  • Urinalysis and midstream urine
120
Q

Management: urinary incontinence

A

Depends on cause

Urge
- bladder retraining
- overactive bladder (anticholinergic) > oxybuytnin or mirabegnon

Stress
- pelvic floor exercises
- duloxetine

BPH
- finasteride or tamsulosin

121
Q

What are the indications for a catheter with urinary incontinence?

A
  • symptoms of urinary retention
  • obstructed outflow
  • deteriorating renal function
  • acute renal failure
  • intensive care
122
Q

What are the complications of catheterisation?

A
  • blockage
  • bypassing
  • infection
123
Q

What are the causes of faecal incontinence?

A
  • MC faecal impaction or neurogenic
  • haemorrhoids
  • rectal prolapse
  • tumours
  • IND
  • drugs
124
Q

Management: faecal incontinence

A
  • Treat constipation
  • Neurological: toilet at appropriate time, planned evacuation (loperamide)
  • Overflow incontinence: rehydrate, enema (phosphate agent), complete colonic washout, manual evacuation, laxatives
  • Prevention: once or twice weekly enema
125
Q

What are the risk factors for constipation?

A
  • advanced age
  • inactivity
  • low calorie intake
  • low fibre diet
  • medications
  • female
126
Q

What are signs and symptoms of constipation?

A
  • infrequent bowel motions (<3 per week),
  • difficultly passing bowel motions,
  • tenesmus (frequent urge to go to the loo without being able to go) - 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
127
Q

What are the causes of constipation?

A
  • Dietary e.g. inadequate fibre intake, inadequate fluid intake
  • Behavioural e.g. inactivity, avoidance of defecation
  • Electrolyte disturbance e.g. hypercalcaemia
  • Drugs, particularly opiates, calcium channel blockers and some antipsychotics
  • Neurological disorders e.g. spinal cord lesions, Parkinson’s disease, diabetic neuropathy
  • Endocrine disorders e.g. hypothyroidism
  • Colon disease e.g. stricture, malignancy
  • Anal disease e.g. anal fissure, proctitis
128
Q

Management: constipation

A

Depends on cause
- lifestyle,
- laxatives
* Bulk = ispaghula husk, methylcellulose,
* Stool softeners = docusate sodium,
* Osmotic laxative = lactulose, macrogol,
* Stimulant laxatives = senna, bisacodyl

129
Q

What is osteoporosis/osteopenia?

A

Osteoporosis is a condition where there is a reduction in the density of the bones.

Osteopenia refers to a less severe reduction in bone density than osteoporosis. Reduced bone density makes bone less strong and more prone to fractures.

130
Q

What are risk factors for osteoporosis?

A

SHATTERED

S - Steroid use (can increase cortisol = ⬆️ bone resorption + osteoblast apoptosis)
H- Hyperthyroidism, hyperparathyroidism (⬆bone turnover)
A- Alcohol and tobacco use (poisons osteoblasts)
T- Thin = not exercising/using skeleton enough
T- Testosterone decrease
E- early menopause- oestrogen is protective
R- renal or liver failure
E- Erosive/inflammatory bone disease
D- dietary e.g., reduced Ca2+, malabsorption, diabetes

131
Q

Pathophysiology of osteoporosis

A

Reduced bone strength + fall = fracture

reduced bone strength caused by:
- reduced bone mineral density
- reduced bone quality (reduced bone turnover + architecture)

132
Q

How can a fall in levels of oestrogen cause bone mass to decrease?

A

Oestrogen deficiency leads to an increased rate of bone loss. It is key to the activity of bone cell receptors found on osteoblasts, osteocytes, and osteoclasts.

It is thought that osteoclasts survive longer in the absence of oestrogen and there is an arrest of osteoblastic synthetic architecture

resorption > formation

133
Q

How can glucocorticoids cause a reduction in bone mass?

A
  • They cause an increased turnover of bone.
  • Prolonged use can result in reduced turnover state however the synthesis is affected resulting in bone mass reduction
134
Q

How does trabecular archictecture change with ageing?

A

Decrease in trabecular thickness, more pronounced for non load-bearing horizontal trabeculae

Decrease in connections between horizontal trabeculae (falls put more strain on vertical so preserve vertical connections more)

Decrease in trabecular strength and increased susceptibility to fracture

135
Q

What is the symptom of osteoporosis and where is this most likely to occur?

A

There is an increased frequency of fractures.

The most common ones include, vertebral crush fracture, and those of the distal wrist (Colles’ fracture) and proximal femur

136
Q

What is the FRAX tool?

A

It gives a prediction of the risk of a fragility fracture over the next 10 years

It involves the inputting of information such as age, BMI, co-morbidities, smoking, family history and if done you can enter a bone mineral score from a DEXA scan

137
Q

What do the results of the FRAX tool give?

A

It gives the result as a percentage probability of a:

  • Major osteoporotic fracture
  • Hip fracture
138
Q

What is used to assess bone mineral density?

A

DEXA scan

139
Q

What is a DEXA scan and what does it measure?

A

It stands for dual-energy x-ray absorptiometry.
- low radiation dose

It assess how much radiation is absorbed by the bones indicating how dense the bone is.
- measures important fracture sites

The measurement is usually taken from the Hip
(lumbar spine, proximal femur + distal radius MC)

140
Q

What are the T and Z scores of a DEXA scan and which one is more clinically relevant?

A

T-score: represents the number of standard deviations compared with the mean for a healthy young adult

Z-score: represents the number of standard deviations the bone density falls below a person for their age

T-score is more relevant

141
Q

What do the different T-scores represent?

A

More than -1 = Normal

-1 to -2.5 = Osteopenia

Less than -2.5 = Osteoporosis

Less than -2.5 plus a fracture = Severe Osteoporosis

142
Q

What is the management for someone who has had a FRAX score without a DEXA scan?

A

Low risk- reassure
Medium risk- offer DEXA scan and recalculate the risk with the results
High risk: offer treatment

143
Q

What are some lifestyle management/light treatment for mild osteoporosis/osteopenia?

A
  • Activty and exercise
  • Weight control
  • Reduce alcohol/stop smoking
  • calcium supplementation with vitamin D = in patients at risk of fragility fractures with an inadequate intake of calcium.
144
Q

What is the first line treatment for someone at high risk of a fracture?

A

Bisphosphonates - they interfere with osteoclast activity reducing their activity
E.g.
Alendronate 70mg once weekly
Riseronate 35mg once weekly
Zoledronic acid 5 mg once yearly (intravenous)

145
Q

What are the side effects of bisphosphonates?

A

Reflux and oesophageal erosions.
They are taken 30 minutes before food to prevent this

Osteonecrosis of the jaw and external auditory canal

146
Q

How should people be monitored who have osteoporosis or who are at risk of getting it?

A

Low risk patients should have a follow up within 5 years

Patients being treated should have a repeat FRAX and DEXA after 3-5 years and a treatment holiday if BMD has improved (this is 18months to 3 years of treatment before a repeat assessment)

147
Q

Define: malnutrition

A

State in which a deficiency of energy, protein, and/or other nutrients causes measurable adverse effects on the body’s form, composition, function and clinical outcome.

148
Q

What are the two types of malnutrition?

A
  1. Acute malnutrition: a brief period of inadequate nutrition that is most commonly in relation to an acute illness with a high inflammatory state, such as pneumonia, and results in muscle wasting and rapid weight loss.
  2. Chronic malnutrition: inadequate nutrition that lasts longer than three months. Often secondary to social, behavioural, and economic factors in addition to illness-related causes.
149
Q

What are the causes of malnutrition?

A
  • Decreased nutrient intake (starvation),
  • Increased nutrient requirements (sepsis or injury),
  • Inability to utilise ingested nutrients (malabsorption)
150
Q

What are the risk factors for malnutrition?

A
  • chronic illnesses,
  • the elderly
  • living in supported accommodation
  • drinking excessive amounts of alcohol over a prolonged period.
  • Being hospitalised for extended periods of time
  • Problems with dentition, taste or smell
  • Polypharmacy
  • Social isolation and loneliness
  • Mental health issues including grief, anxiety and depression
  • Cognitive issues including confusion
151
Q

How to diagnose malnutrition?

A
  • BMI <18.5 kg/m2
  • unintentional weight loss >10% last 3-6 months
  • BMI <20kg/m2 AND unintentional weight loss >5% within 3-6mths
152
Q

What are the clinical features of malnutrition?

A
  • High susceptibility or long durations of infections
  • Slow or poor wound healing
  • Altered vital signs including bradycardia, hypotension, and hypothermia
  • Depleted subcutaneous fat stores
  • Low skeletal muscle mass
153
Q

What is refeeding syndrome?

A

Metabolic disturbances as a result of reintroduction of nutrition to patients who are starved/severely malnourished

154
Q

What are the biochemical features of referring syndrome?

A
  • hypophosphataemia
  • hypokalaemia
  • thiamine deficiency
  • abnormal glucose metabolism
155
Q

What are the complications of malnutrition?

A
  • Impaired immunity (increased risk of infections)
  • Poor wound healing
  • Growth restriction in children
  • Unintentional weight loss, specifically the loss of muscle mass
  • Multi-organ failure
  • cardiac failure
  • Death
156
Q

Management: malnutrition

A
  • Monitor blood biochemistry, - Commence re-feeding with guidelines ,
  • Recognise electrolytes (phosphate, K+, Mg),
  • Monitor glucose and Na levels,
  • Supportive care,
  • Refer to nutritional support team/dietician
157
Q

What are the risk factors for pressure sores?

A
  • Malnourishment,
  • Incontinence,
  • Lack of mobility,
  • Pain (leads to a reduction in mobility)
158
Q

How to assess the risk of pressure sores?

A

Water low score:
includes a number of factors including body mass index, nutritional status, skin type, mobility and continence

159
Q

What are prevention methods for pressure sores?

A

Barrier creams
Pressure redistribution
Repositioning
Regular skin assessment

160
Q

Management: Pressure sores

A

Moist wound environment encourages ulcer healing:
- Hydrocolloid dressings and hydrogels
- Surgical debridement
- antibiotics only if there are signs of infection

161
Q

What is the classification for pressure sores?

A

Grade 1 – non-blanching erythema with intact skin

Grade 2 – partial thickness skin loss involving epidermis, dermis or both (abrasion/blister)

Grade 3 – full-thickness skin loss involving damage/necrosis of sub-cut tissue

Grade 4 – extensive loss, destruction/necrosis of muscle, bone or support structures

Unstageable – depth unknown, base of ulcer covered by debris

162
Q

Define: polypharmacy

A

When a patient has 4+ medications

163
Q

What is the START tool?

A

Suggests medications that may provide additional benefits
i.e., proton pump inhibitors for gastroprotection in patients on medications increasing bleeding risk

164
Q

What is the STOPP tool?

A

Used to assess which drugs can be potentially discontinued in elderly patients undergoing polypharmacy

165
Q

How is capacity assessed?

A

Ability to understand the information relevant to the decision, Retain the information , Weigh up the information, Communicate the decision

166
Q

What are the key parts of the mental capacity act?

A
  • Assume capacity – person assumed to have capacity until proven otherwise
  • Maximise decision-making capacity – all practical support to help a person make a decision should be given
  • Freedom to make seemingly unwise decisions
  • Best interests – all decisions taken on behalf of the person must be in their best interests
  • Least restrictive option – when making a decision on another person’s behalf, the alternative that achieves the necessary goal and interferes the least with the person’s rights and freedom of action must be chosen
167
Q

Define: Deprivation of Liberty

A

occurs when a person does not consent to care or treatment, for example, a person with dementia who is not free to leave a care home and lacks capacity to consent to this

168
Q

Define: Lasting power of attorney

A

A document which a person can nominate someone else to make certain decision on their behalf (for example on finances, health and personal welfare) when they are unable to do so themselves. To be valid, it needs to be registered with the Office of the Public Guardian

169
Q

Define: independent mental capacity advocate role

A

support and represent people who lack capacity and they do not have anyone else to represent them in decisions about changes in long-term accommodation or serious medical treatment. They can also be present for decisions regarding care reviews or adult protection.

170
Q

What to consider when working in someones ‘best interest’?

A

Consider:
- Whether the person is likely to regain capacity and can the decision wait
- How to encourage and optimise the participation of the person in the decision
- The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
- Views of other relevant people

171
Q

What are advanced directives?

A
  • Used to authorise or request specific procedures and refuse treatment in a predefined future situation (advance directive)
  • Advance refusals of treatment are legally binding if: The person is an adult, Was competent and fully informed when making the decision, The decision is clearly applicable to current circumstances, and There is no reason to believe that they have since changed their mind
172
Q

What are the causes of neck of femur fractures?

A
  • low energy trauma e.g. a full from standing height
  • pathological fractures e.g. tumour or infection
  • reduced bone mineral density = osteopenia and osteoporosis
173
Q

What is the classification for neck of femur fractures?

A

Garden Classification (classifies fractures according to the degree of displacement as seen on x-ray)

Stage I: incomplete fracture line or impacted fracture
Stage II: complete fracture line, non-displaced
Stage III: complete fracture line, partial displacement
Stage IV: complete fracture line, complete displacement

174
Q

What is the Pauwels classification?

A

classifies fractures according to the angle of the fracture line from horizontal:

Type I: between 0 and 30 degrees
Type II: between 30 and 50 degrees
Type III: more than 50 degrees

175
Q

What are the risk factors for a neck of femur fracture?

A
  • Age (≥65 years in women and ≥75 years in men)
  • History and risk factors of osteoporosis including menopause, amenorrhoea, smoking, excessive alcohol or caffeine intake, physical inactivity, long-term or high-dose corticosteroid use
  • Previous fragility fracture
  • History of falls
  • Poor nutrition
  • Low body mass index (<18.5kg/m2)
  • Dementia
  • Visual impairment: which increases the risk of falls and subsequently fractures
  • History of tumours (primary or secondary bone tumours, breast, bowel, prostate, kidney, lung, thyroid tumours)
176
Q

Presentation: neck of femur fracture

A
  • Pain: in the hip, groin or knee
  • Unable to weight-bear
  • Decreased or painful mobility of the affected hip
  • The affected leg is shortened, externally rotated and abducted
  • Palpation of the hip produces pain
  • The patient is unable to perform a straight leg raise (useful for discerning occult hip fractures)
  • Pain on gentle internal and external rotation of the affected leg (log roll test)
  • Soft tissue symptoms: bruising and swelling in and around the hip area
177
Q

What is the differential diagnosis of a neck of femur fracture?

A
  • Alternative fractures such as pubic ramus fractures, acetabular fractures, femoral head and femoral shaft fractures
  • Slipped capital femoral epiphysis (intermittent pain for months, pain worsens on activity)
  • Dislocated hip
  • Femoral head avascular necrosis
  • Tendonitis of any of the muscles of the hip
  • Hip bursitis
  • Osteomyelitis (fever, chills, and swelling or redness in the area)
178
Q

Investigations: neck of femur fracture

A

Investigate for underlying cause
- bloods
- urinalysis
- creatinine kinase = rhabdomyolysis

  1. X-ray - 1st line
  2. MRI - gold standard to exclude a hip fracture
179
Q

Management: neck of femur fracture

A
  1. analgesia
    - IV access for fluid resuscitation, blood transfusion, meds
  2. Surgery
    - urgent reduction and internal fixation followed by early mobilisation
180
Q

What are the complications of surgical management of neck of femur fracture?

A
  • surgical siet infection
  • post-op delirium
  • fat embolism
  • bleeding
  • nerve and vessel injury
  • muscle and ligament damage
  • leg-length discrepancies
  • soft tissue irritation
181
Q

What are the complications of non-operative management of NoF fracture?

A

Fracture displacement
Non-union or mal union
Avascular necrosis of femoral head
Venous thromboembolism
Pressure sores
Infection: pneumonia and urinary tract infections
Death

182
Q

What are the risk factors of chronic hypothermia?

A
  • ageing
  • prolonged exposure to cold temperatures
  • chronic illness e.g. diabetes, arthritis, heart conditions
  • homeless
183
Q

What are the complications of hypothermia?

A
  • irregular heartbeat
  • kidney failure
  • confusion
  • loss of consciousness
  • liver damage
  • bleeding disorders
  • breakdown of muscle tissue
184
Q

Management: hypothermia

A
  • Be gentle = jarring movements may trigger cardiac arrest
  • move the person to a warm, dry location
  • change to dry, warm clothes
  • cover in blankets
  • monitor breathing
  • give warm beverage
  • don’t apply direct heat
185
Q

What is squamous cell carcinoma?

A

DNA damage (mutation to p53 gene) from exposure to UV radiation or other damaging agents trigger abnormal changes in the squamous cells

186
Q

What does SCC of the skin look like?

A
  • scaly red patches
  • open sores
  • rough, thickened or wart like skin
  • raised growths with a central depression

can occur in the genitals too

187
Q

What are the types of SCC?

A
  1. cutaneous - top layer of skin
  2. metastatic - spread to other parts of the body
188
Q

Investigations: SCC

A
  • examination
  • skin biopsy
  • imaging test - CT or MRI
189
Q

What are the stages of SCC?

A

stage 0: cancer is only in epidermis (SCC in situ)

Stage 1: cancer is in the top and middle layers of skin (epidermis and dermis)

Stage 2: cancer is in the top + middle layers of skin and moves to target your nerves or deeper layers of skin (epidermis, dermis and subcutis)

Stage 3: cancer has spread beyond your skin to your lymph nodes

Stage 4: cancer has spread to other parts of your body

190
Q

Management: SCC

A
  • cream: imiquimod or 5-flurouracil
  • cryosurgery = freeze cancer cells
  • photodynamic therapy (PDT) = blue light to remove cancer cells
  • curettage and electrodesiccation
  • excision
  • systemic chemo
191
Q
A

Phase 3a Emily (8 decks)

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