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3A > Geriatrics and stroke medicine > Flashcards

Geriatrics and stroke medicine Flashcards

1
Q

What are the tow arteries that supply the brain?

A

Internal carotid
Vertebral arteries

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2
Q

Recap - Outline the main roles of the
a) Frontal lobe
b) Temporal Lobe
c) Parietal Lobe
d) occipital lobe

A

Frontal - decision making, movement, executive function, personality.

Temporal - hearing (primary auditory cortex), memory and language, smell, facial recognition

Parietal - Sensory info

Occipital lobe - Vision

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3
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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4
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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5
Q

After entering the cranium through the foramen magnum, what branches does the vertebral artery give off? What do the 2 vertebral arteries then go on to do?

A

Give off Spinal arteries, supply the entire length of spine

Gives off The Posterior Inferior cerebellar artery - supplies cerebellum

also gives off a menigeal branch

But after this two vertebral arteries converge to form the basilar artery

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6
Q

What arteries branch off the basilar artery?

A

Superior cerebellar artery (SCA)
Anterior inferior cerebellar artery (AICA) - Both to supply the cerebellum
The Pontine arteries

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7
Q

What does the posterior cerebral artery go on to supply? What is it a branch of?

A

Supplies occipital lobe, posteromedial temporal lobes, midbrain, thalamus,

It is the terminal branch of the basilar arteries,

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8
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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9
Q

What is a stroke?

A

An acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology

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10
Q

What are the two types of stroke?

A

Two kinds of stroke are ischaemic (85%) and haemorrhagic (15%)

The two types of ischaemic events in the brain are a Cerebral infarction (an ischaemic stroke) or a Transient ischaemic attack (TIA)

a TIA is not considered to be an actual stroke

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11
Q

What are the different causes of an ischaemic stroke?

A
  • Cardiac: atherosclerotic disease, AF, Embolism due to septal abnormality
  • Vascular: aortic dissection, vertebral dissection
  • Haematological: hypercoagulability such as antiphospholipid syndrome, sickle cell disease, polycythaemia
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12
Q

What are the different causes of haemorrhagic strokes?

A

Intracerebral: bleeding within the brain parenchyma:
- Trauma
- Cerebral amyloid
- Hypertension

Subarachnoid: bleeding between the pia and arachnoid matter
- Trauma
- Berry aneurysm
- Arteriovenous malformation

Intraventricular: bleeding within the ventricles

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13
Q

What are the risk factors for having a stroke?

A
  • Hypertension
  • Smoking
  • AF
  • Vasculitis
  • Medication
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14
Q

If the anterior cerebral artery is affected in a stroke where in the body will this present?

A

Feet and legs

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15
Q

If the middle cerebral artery is affected in a stroke where in the body will be affected?

A
  • Hands and arms
  • Face
  • Language centres in dominant hemisphere
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16
Q

What are the symptoms of a anterior cerebral artery stroke?

A

Contralateral hemiparesis and sensory loss more commonly affects the lower limbs

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17
Q

What are the symptoms of a middle cerebral artery stroke?

A
  • Contralateral hemiparesis and sensory loss with upper limbs more affected
  • Homonymous hemianopia
  • Aphasia: if the affecting dominant hemisphere 95% of right handed people this is the left side
  • Hemineglect syndrome if affecting non-dominant hemisphere patients won’t be aware of one side of their body
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18
Q

What are the symptoms of a posterior cerebral artery stroke?

A
  • Contralateral homonymous hemianopiawithmacular sparing
  • Contralateral loss of pain and temperature due to spinothalamic damage
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19
Q

What are the symptoms of a vertebrobasilar artery stroke?

A
  • Cerebellar signs
  • Reduced consciousness
  • Quadriplegia or hemiplegia
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20
Q

What is Weber’s syndrome and what are the symptoms of it?

A
  • A midbrain infarct that leads to oculomotor palsy and contralateral hemiplegia
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21
Q

What are the symptoms of lateral medullary syndrome (posterior inferior cerebellar artery oculsion)

A
  • Ipsilateral facial loss of pain and temperature
  • Ipsilateral Horner’s syndrome miosis (constriction of the pupil), ptosis (drooping of the upper eyelid), and anhidrosis (absence of sweating of the face)
  • Ipsilateralcerebellar signs
  • Contralateralloss of pain and temperature
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22
Q

What is used to classify stokes and how does it do it?

A

The Bamford classification and it categorises strokes based on the area of circulation affected

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23
Q

What are the different classifications in the Bamford classification?

A
  • Total anterior circulation stroke
  • Partial anterior stroke
  • Lacunar stroke
  • Posterior circulation stroke
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24
Q

What is a TACS?

A

Total anterior circulation stroke

Blood vessel= anterior or middle cerebral artery

Criteria: all of
- Hemiplegia
- Homonymous hemianopia
- Higher cortical dysfunction

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25
Q

What is a PACS?

A

Partial anterior circulation stroke

Blood vessel= anterior or middle cerebral artery
Criteria is any two of:
- Hemiplegia
- Homonymous hemianopia
- Higher cortical dysfunction

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26
Q

What is a lacunar stroke?

A

Blood vessel= perforating arteries

Criteria: there is no higher cortical dysfunction or visual field abnormality and there is one of:
- Pure hemimotor or hemisensory loss
- Ataxic hemiparesis
- Pure sensorimotor loss

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27
Q

What is a PCS?

A

Posterior circulation stroke

Blood vessel= Posterior cerebral or vertebrobasilar artery
Criteria:
- Cerebellar syndrome
- Isolated homonymous hemianopia
- Loss of consciousness

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28
Q

What is used to identify strokes in hospital?

A

Recognition of Stroke in the Emergency Room (ROSIER) scale.

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29
Q

What are the criteria for the ROSIER scale?

A
  • Loss of consciousness
  • Seizure activity

New, acute onset of:
- Asymmetric facial/arm/leg weakness
- Speech disturbance
- Visual field defect

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30
Q

When would a stroke be possible using the ROSIER scale and what would happen as result?

A

A stroke is possible if they have any of the criteria and hypoglycaemia has been excluded

WOULD REQUIRE URGENT NON-CONTRAST CT
- Aspirin 300mg stat (after the CT)

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31
Q

What are the initial investigations for a stroke?

A

Non Contrast CT of head

ECG- to asses for AF
Bloods to look for hyponatremia/hypoglycaemia
Carotid doppler

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32
Q

What is the gold standard test for a stroke?

A

Diffusion weighted MRI is more sensitive but harder to obtain

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33
Q

What are the differentials for a stroke?

A
  • Hypoglycaemia
  • Hyponatremia
  • Hypercalcaemia
  • Uraemia
  • Hepatic encephalopathy
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34
Q

What is the treatment for a ischaemic stroke?

A
  • Antiplatelets Aspirin given as soon as possible once haemorrhagic stroke is excluded
  • Thrombolysis: alteplase- given within 4.5 hours of symptom onset
  • Thrombectomy must score > 5 on NIH Stroke Scale/Score (NIHSS) and pre-stroke functional status < 3 on the modified Rankin scale
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35
Q

What should be performed before thrombectomy?

A

CT angiogram (CTA): identifies arterial occlusion

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36
Q

What is given for the prevention of ischaemic strokes?

A
  • Clopidogrel an antiplatelet
  • High dose statin
  • Carotid stenting
  • Manage underlying risks
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37
Q

What are the driving rules after a stroke?

A
  • Must not drive for 1 month after a stroke and can’t drive a HGV for 1 year after a stroke
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38
Q

What is a TIA?

A
  • A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction.
  • It usually resolves within 24 hours
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39
Q

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

A

ACA: weak numb contralateral leg

MCA: 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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40
Q

What are the investigations for a TIA?

A
  • Auscultation: listen for carotid bruit
  • CT scan: request an urgent CT scan of the head
  • Carotid doppler- look for stenosis
  • CT angiography- look for stenosis
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41
Q

What is the management for a TIA?

A
  • First line antiplatelet initially with aspirin 300mg
  • Carotid endarterectomy: surgery to remove blockage of >70% on doppler
  • Manage cardiovascular risk
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42
Q

What is a crescendo TIA?

A

Where there are two or more TIAs within a week. It carries a high risk of a stroke

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43
Q

How many people who have a TIA will go on to have a stroke?

A

10% within 3 months

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44
Q

What are the two categories a haemorrhagic stroke can be split into?

A
  • Intracerebral where the bleeding occurs within the cerebrum
  • Subarachnoid when bleeding occurs between the pia and arachnoid matter
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45
Q

What can cause an intracerebral haemorrhage?

A
  • Hypertension causing atherosclerosis and microaneurysms called bouchard aneurysms
  • ** Arteriovenous malformations** blood vessels that directly connect an artery to a vein
  • Vasculitis/Vascular tumours
  • Secondary to an ischaemic stroke- ischaemia causes brain tissue death. If there is reperfusion there’s an increased chance that the damaged vessel might rupture
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46
Q

What are the risk factors for developing an intracerebral stroke?

A
  • Head injury
  • Hypertension
  • Aneurysm
  • Brain tumour
  • Anticoagulant
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47
Q

Describe the pathophysiology of an intracerebral haemorrhage?

A
  • Once blood starts to spew from vessel it creates a pool of blood which increases pressure in the skull and outs pressure on nearby cells and vessels. This can lead to brain herniation
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48
Q

What is the presentation of an intracerebral haemorrhage?

A
  • Sudden headache
  • Weakness
  • Seizure
  • Vomiting
  • Reduced consciousness
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49
Q

What are the investigations for a intracerebral haemorrhage?

A
  • CT/MRI to confirm size and location of the haemorrhage
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50
Q

What is the management for a intracerebral haemorrhage?

A
  • Correct severe hypertension but avoid hypotension
  • Drugs to relieve intercranial pressure mannitol
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51
Q

What are the surgeries that can be performed for an intracerebral haemorrhage?

A
  • Craniotomy part of the skull bone is removed to drain any blood and relieve pressure
  • Stereotactic aspiration: aspirate off blood and relieve intracranial pressure guided by a CT scanner. Good for bleeding that is located deeper in the brain
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52
Q

What can cause SAH?

A
  • Trauma is a key factor
  • Atraumatic cases are referred to as spontaneous SAH
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53
Q

What are the most common causes of spontaneous SAH?

A
  • Berry aneurysm- they account for 80% of cases.
  • Arise at points of bifurcation within the circle of Willis: the junction between the anterior communicating and anterior cerebral artery
  • They are associated with **PKD, coarction of the aorta, and connective tissue disorders (Marfan)
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54
Q

What are the risk factors for having a SAH?

A
  • Cocaine use
  • Sickle cell anaemia
  • Connective tissue disorders
  • Neurofibromatosis: tumours form on your nerve tissues
  • PKD
  • Alcohol excess
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55
Q

What can occur as a result of a subarachnoid haemorrhage?

A
  • Blood vessels that are bathing in a pool of blood can start to intermittently vasoconstrict. If this occurs in the circle of Willis it will reduce the supply of blood flow to the brain causing further injury
  • Over time blood in the subarachnoid space can irritate the meninges and cause inflammation which leads to scarring of the surrounding tissue. The scar tissue can obstruct the normal outflow of CSF causing fluid to build up leading to hydrocephalous
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56
Q

What are the signs of a SAH?

A
  • 3rd nerve palsy: if the aneurysm occurs in posterior communicating artery
  • 6th nerve palsy a non-specific sign which indicates raised intercranial pressure
  • Reduced GCS
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57
Q

What are the symptoms of a SAH?

A
  • Thunderclap headache
  • Neck stiffness
  • Photophobia
  • Vision changes
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58
Q

What are the initial investigations for SAH?

A
  • FBC
  • Serum glucose
  • Clotting screening
  • Urgent non-contrast CT of the head. Blood will cause hyperattenuation (this means becoming more dense on CT will show as white) in the subarachnoid space
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59
Q

What tests would you perform if the CT is negative but a SAH is still suspected?

A
  • Lumbar puncture: will show RBCs or or xanthochromia (yellow pigmentation due to degradation of haemoglobin to bilirubin)
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60
Q

What is given to prevent vasospasm in SAH?

A

Nimodipine is a CCB and prevents vasospasms

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61
Q

What is the management to stop the bleeding?

SAH

A
  • first-line is endovascular coilingof the aneurysm;
  • second-line is surgical clippingvia craniotomy
  • If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol
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62
Q

What are the complications of a SAH?

A
  • Rebleeding 22% risk at one month
    • Vasospasm: accounts for 23% of deaths; at highest risk for the first 2-3 weeks after SAH; treated with (induced) hypertension,hypervolemia andhaemodilution (triple-H therapy).
  • Hydrocephalus: acutely managed with external ventricular drain (CSF drainage into an external bag) or a long-term ventriculoperitoneal shunt, if required
  • Seizures: seizure-prophylaxis is often administered (e.g. Keppra)
  • Hyponatraemia: commonly due to syndrome of inappropriate antidiuretic hormone secretion (SIADH)
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63
Q

What is a subdural haemorrhage?

A

Bleeding below the dura matter

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64
Q

Who is most likely to suffer from a SDH?

A
  • Elderly
  • Alcoholics
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65
Q

What can cause a SDH?

A
  • Brain atrophy: in the elderly the brain shrinks in size meaning the bridging veins are stretched across a wider space
  • Alcohol abuse causes the walls of the veins to thin out making them more likely to break
  • Trauma/injury: falls, shaken baby syndrome, acceleration-deceleration injury
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66
Q

What is a haematoma and how do they cause issues?

A

The collection of blood that forms as a result of a haemorrhage

As damaged bridging veins are under low pressure, the bleeding can be slow causing a delayed inset of symptoms as the haematoma gradually increases in size

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67
Q

What is an acute SD haematoma?

A

One that causes symptoms within 2 days

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68
Q

What is a subacute SD haematoma?

A

One that causes symptoms between 3-14 days

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69
Q

What is a chronic SD haematoma?

A

One that causes symptoms after 15 days

70
Q

What are the symptoms of a SDH?

A
  • Reduced GCS
  • Headaches
  • Vomiting
  • Seizures
71
Q

What does a subdural haematoma look like on a CT scan?

A

It will follow the contour of the brain and forms a Crescent shape and it Crosses suture lines

72
Q

What is the management for a SDH?

A

Drainage
- Small SDH are drained via a burr hole washout
- A large SDH requires a Craniotomy which is when part of the skull bone is removed
- IV Mannitol to reduce ICP

73
Q

What are the complications of raised ICP in a SDH?

A

Supratentorial herniation: cerebrum is pushed against the skull or the tentorium, can compress the arteries that nourish the brain leading to an ischaemic stroke

  • Infratentorial herniation: cerebellum is pushed against the brainstem, can compress the vital area in the brainstem that control consciousness, respiration, and heart rate
74
Q

What is an epidural haemorrhage?

A

Bleeding above the dura matter

75
Q

What is an epidural haemorrhage?

A

Bleeding above the dura matter?

76
Q

Who is an EDH most common in?

A

Young adults

77
Q

What is the most common cause of a EDH?

A

Head trauma

78
Q

Where is the most common site for a EDH to occur?

A

The Pterion which is the spot where the frontal, parietal and temporal and sphenoid bone join together.

It is a thin area of the skull and located just above the middle meningeal artery

79
Q

What happens once the meningeal artery has been torn?

A

Blood will pool between the skull and the external layer of the dura mater, separating it from the inner surface of the skull. The blood builds up between the skull and the outer layer of the dura mater but cannot cross the suture lines where the dura mater adheres more tightly.

If blood accumulates slowly, there may be a lucid interval which is when several hours pass before the onset of symptoms.

80
Q

What are the symptoms of a EDH?

A
  • Reduced GCS: loss of consciousness after the trauma due to concussion
  • There might be a lucid interval after initial trauma if there a slower bleed. This is followed by a rapid decline
  • Headaches
  • Vomiting
  • Confusion
  • Seizures
  • Pupil dilation if bleeding continues
81
Q

What shape will an EDH be on a CT scan?

A

They don’t cross suture lines and they push on the brain forming a biconvex shape

82
Q

What is the management for a EDH?

A

– Clot evacuation
- Craniotomy: part of the skull bone is removed in order to remove accumulated blood below.
- Followed by ligation of the vessel.
- IV mannitol to reduce ICP

83
Q

What is Cushing’s reflex?

A

Physiological nervous system response to increased intracranial pressure that results in Cushing’s triad of:
- Increased blood pressure
- Irregular breathing
- Bradycardia

84
Q

What is seen in Broca’s Aphasia?

A

Causes Non-fluent speech Patients often have word-finding difficulties. However comprehension remains intact

Broca’s area is within the frontal lobe so is often affected by infarction of the left superior division of the middle cerebral artery

85
Q

What is seen in Wernicke’s aphasia?

A

History of fluent yet confused speech can be caused by a blockage in the inferior division of the left middle cerebral artery

Therefore, a patient with Wernicke’s aphasia will talk fluently, however the content will not make sense

86
Q

What is delirium?

A

An acute, fluctuating syndrome of altered attention, awareness and cognition caused by an underlying condition or event in vulnerable people

Disturbance of consciousness , with reduced ability to focus or shift attention.

Changes in cognition or development of perceptual disturbance not better accounted for by pre-existing or evolving dementia.

Disturbance develops over a short period of time and fluctuates over the course of the day.

87
Q

What are some causes of delirium?

A
  • Surgery/Post GA
  • Systemic infections
  • Head injury
  • Drug withdrawal
  • Alcohol withdrawal
  • Metabolic: Liver failure, uraemia
  • Hypoxia
  • Vascular
  • Nutritional: thiamine, nicotinic acid, or B12 deficiency
88
Q

What are some risk factors for delirium?

A
  • > 65
  • Dementia
  • Hip fracture
  • Acute illness
  • Psychological agitation
89
Q

How can delirium be divided?

A

Hyperactive: People have heightened arousal so will be restless agitated or aggressive

Hypoactive: People will become withdrawn quiet and sleepy

Mixed

90
Q

What are the 6 main precipitants of delirium?

A

PINCH ME

Pain
Infection
Nutrition
Co-morbidities
Hydration
Medication
Environment

+ Bladder

91
Q

What are some investigations for delirium?

A

Look for causes
ABG FBC, U&E, LFT, blood glucose, septic screen (urine dipstick, CXR, blood cultures); also consider ECG, malaria films, LP, EEG, CT.

Think about causes - be vigilant for constipation

92
Q

What are the diagnostic tools used in assessing patients for delirium?

A

AMT
Abbreviated mental test ( a score of 6 or less implies a mental impairment)

  1. What is your age
  2. What is the time
  3. Can you remember an address
  4. What’s the year
  5. Name of hospital
  6. Can you recognise the role of two different people ? (eg nurse, doctor)
  7. What year did WW1 begin ?
  8. What is your DOB
  9. PM or monarch
  10. Count backwards for 20-1
93
Q

What is the management for delirium?

A

As well as identifying and treating the underlying cause, aim to:
* Reorientate the patient: explain where they are and who you are at each encounter.
Hunt down hearing aids/glasses. Visible clocks/calendars may help.
* Encourage visits from friends and family.
* Monitor fluid balance and encourage oral intake . Be vigilant for constipation.
* Practise sleep hygeine
* Review medication and discontinue any unnecessary agents. Only use sedation if the
patient is a risk to their own/other patients’ safety (never use physical restraints).

Consider haloperidol and lorazepam as sedatives if patients are very agitated

94
Q

What is frailty?

A

A clinical state of increased vulnerability and reduced ability to cope with everyday/acute stressors resulting from aging-associated decline in reserve and function across multiple physiological systems.

95
Q

What are the acute presentations of frailty?

A

Falls
Reduced mobility
New or accelerated state of confusion
Acute change in continence
Sensitivity to new medication

96
Q

What are the most common comorbidities contributing to frailty?

A

Stroke
CHD
Diabetes
Dementia
Urinary problems
Depression
Visual loss
Falls

97
Q

What are the 5 elements of a comprehensive geriatric history?

A

FEMPS

Functional ability
Environment
Mental health
Physical health
Social circumstances

98
Q

What are risk factors for falls in the elderly?

A

Age 80
Female
Low weight
Previous fall
polypharmacy/medications (commonly benzodiazepines, antidepressants, bp-lowering drugs, anticonvulsants)
Cognitive impairment
cognitive impairment
orthostatic hypotension
vision problems
chronic health conditions affecting mobility

environmental risk factors
lack of assistive devices in the bathroom
loose throw rugs
low level lighting
obstacles on the walking path
slippery outdoor conditions

99
Q

What are some common medical conditions that can increase the risk of falls in the elderly?

A

Osteoporosis
Arthritis
Neurological disorders: Conditions like Parkinson’s disease, multiple sclerosis, or neuropathy can impair balance and coordination.
Cardiovascular conditions: Heart disease, low blood pressure, irregular heart rhythms, aortic stenosis.
Vision problems
Medication side effects
Cognitive impairment: Conditions like dementia or Alzheimer’s disease can impair judgment and increase the risk of falls.
Dehydration

100
Q

What are some ways to manage orthostatic hypotension?

A

ensuring adequate hydration and salt intake, graded standing (going from lying to sitting and sitting to standing in separate stages), compression stockings and avoiding warm and crowded environments.

101
Q

What is osteoporosis?

A

A complex skeletal disease characterised by low bone density resulting in increased bone fragility and susceptibility to fracture

Bones become more porous due to increased breakdown

102
Q

What is osteopenia?

A

A less severe reduction in bone density than osteoporosis

Defined as bone mineral density 1-2.5 standard deviations below young adult mean value

103
Q

What are some risk factors for patients that can lead to osteoporosis?

A

SHATTERED

S- Steroids
H- Hyperthyroidism
A- Alcohol and tobacco
T- Thin
T- Low testosterone
E- Early menopause
R- Renal or liver failure
E- Erosive bone disease
D- Low Dietary calcium

104
Q

How can old age and oestrogen affect bone turnover?

A

As we age the activity of the osteoclasts increases and is not matched by the osteoblasts. Therefore bone turnover decreases

Oestrogen is key to the activity of bine cells with receptors found on osteoblasts, osteocytes, and osteoclasts.

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

105
Q

What are the most common sites of fractures for someone with osteoporosis?

A

Common fragility fractures include vertebral crush fracture and those of the distal wrist (Colles’ fracture) and proximal femur.

may also see Thoracic Kyphosis *(hunching over)

106
Q

What screening tool can you use in osteoporosis?

A

RAX = fracture risk assessment tool

Predicts the risk of a fragility fracture over the next 10 years. Usually the first step of assessment and is done on patients at risk of osteoporosis

BMI, co-morbidities, smoking, alcohol and family history +/- bone mineral density

  • It gives results as a percentage 10 year probability of a:
    • Major osteoporotic fracture
    • Hip fracture
107
Q

What is the gold standard investigation you would do for suspected osteoporosis?

A

DEXA Scan (dual-energy xray absorptiometry)

Measures bone mineral density by measuring how much radiation is absorbed by the bones

Scanning Hip is best

Gives T score (main one) - number of standard deviations below the mean for a healthy young adult their bone density is.

and Z score - represent the number of standard deviations the patients bone density falls below the mean for their age.

108
Q

What T scoring on a DEXA scan would be indicative of

Better than reference
No evidence of oesteoporosis
Osteopenia (offer lifestyle advice)
Osteoporosis

A

T-score
>0 BMD = is better than the reference.
0 to -1 = BMD is in the top 84%: no evidence of osteoporosis.
-1 to -2.5 = Osteopenia. Risk of later osteoporotic fracture. Offer lifestyle advice.
-2.5 or worse = Osteoporosis. Offer lifestyle advice and treatment Repeat DEXA in 2yrs.

109
Q

What are some lifestyle managements for osteopenia/mild osteoporosis?

A

Activity and exercise
Weight control
Reduce alcohol and stop smoking
NICE recommend calcium supplementation with vitamin D - eg Calcihew-D3

vitamin D supplementation.

110
Q

What is the treatment for someone at high risk of a fracture? (specific drug name)

A

Bisphosphonates- they interfere with osteoclast activity reducing their activity.

Alendronate 70mg once weekly

111
Q

What are the die effects of bisphosphonates?

A

Oesophagitis/Reflux and oesophageal erosions.

GI distress
Renal toxicity
Hypocalcaemia
Oesophageal ulcers

Osteonecrosis of the jaw and external auditory canal

112
Q

How should you take bisphosphonates?

A

Take once a week in the morning at least 30 minuets before food

A patient should remain upright for at least 30 mins after taking

113
Q

How can hypertension cause heart failure?

A

The left ventricular wall hypertrophies (to increase the cardiac output against increased resistance)

Long term the myocytes atrophy and the ventricle will dilate as the oxygen can’t supply all of the muscle have a reduction in muscle volume, causing the complications of left ventricular dilatation and congestive heart failure

114
Q

What is systolic heart failure?

A

the inability of the heart to contract efficiently and eject adequate volumes of blood.

Ejection volume will be less than 40%

115
Q

What can cause systolic heart failure?

A

IHD, MI, Hypertension, Cardiomyopathies

116
Q

What is diastolic heart failure?

A

Reduction in the hearts compliance resulting in compromised ventricular filing

117
Q

What can cause diastolic heart failure?

A

Cardiac tamponade, Constrictive pericarditis, Hypertension

118
Q

What is left sided heart failiure?

A

The inability of the left ventricle to pump adequate amount of blood leading to pulmonary circulation congestions and pulmonary oedema

It also usually results in RHF and will have a ejection fraction of less than 40%

119
Q

What is right heart failure?

A

The inability of the right ventricle to pump adequate amounts of blood leading to systolic venous congestion and peripheral oedema and hepatic tenderness and congestion

Most commonly caused by LHF and respiratory distress such as COPD

120
Q

What is low output heart failure?

A

heart failure that results in reduced cardiac output

121
Q

What is high output heart failure?

A

Heart failure when cardiac output remains normal but there is a metabolic demand mismatch

Occurs due to reduced oxygen carrying capacity (anaemia) or increased metabolic demand

Can also be referred to as preserved ejection fraction heart failure

122
Q

What is acute heart failure?

A

Acute onset of symptom presentation.

Not always due to an acute event but often due to MI, persistent arrhythmia or mechanical event, ruptured valve or ventricular aneurysm.

123
Q

What is chronic heart failure?

A

slow symptom presentation usually due to slow progressive underlying disease. CAD and hypertension

124
Q

What is acute-on-chronic heart failure?

A

Acute deterioration of a chronic condition usually following an acute event such as anaemia, infections or arrhythmias

125
Q

What is preload?

A

The volume of blood in the ventricles just before contraction

126
Q

What is afterload?

A

The pressure at which the heart has to work to eject blood ins systole

127
Q

What is definition of heart failure?

A

Heart failure is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of the body without increasing diastolic pressure.

128
Q

What are the main causes of heart failure?

A

IHD
Hypertension
Valvular disease
Pericarditis
Arrhythmias
Cardiomyopathies
Pulmonary hypertension

129
Q

What are some causes of Right sided heart failure?

A

Pulmonary stenosis
Lung disease (cor pulmonale)
Septal defects

130
Q

What is congestive cardiomyopathy and how can it cause heart failure?

A

It is the weakening and dilation of the ventricular walls leading overstretching and reduced contractility

131
Q

What is restrictive cardiomyopathy and how can it cause heart failure?

A

It is reduced heart compliance without significant increases is muscle wall thickness leading to reduced muscle wall thickness. Reduces EDV and CO

Can be caused by sarcoidosis, amyloidosis, hemochromatosis, and endocardial fibrosis

132
Q

How do the kidneys compensate in heart failure?

A

The renin-angiotensin-aldosterone system is activated which causes fluid retention

This causes the heart to fill more during diastole increasing preload, which increases contraction strength

leads to fluid retention, aka oedema

133
Q

What are the signs of left sided heart failure?

A

Cardiomegaly (displaced apex beat)
Pulmonary oedema
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur

134
Q

What are the signs and symptoms of right sided heart failure?

A

Raised JVP
Hepatomegaly/Splenomegaly
Pitting oedema
Ascites
Weight gain

135
Q

What are some symptoms of left sided heart failure?

A

Exertional dyspnoea
Fatigue
Weight loss
Paroxysmal nocturnal dyspnoea – attacks of severe SOB and coughing at night
Nocturnal cough – pink, frothy sputum
Orthopnoea – dyspnoea (SOB) that occurs when lying down

136
Q

What are some investigations for heart failure?

A

ECG
Chest x-ray
BNP natriuretic peptide levels
Echocardiogram

137
Q

What could you see on an ECG in someone with heart failure?

A

Should be performed on all suspected heart failure patients
May indicate the underlying cause of the heart failure such as;
Myocardial infarction/ischemia
Bundle Branch Block
Ventricular hypertrophy
Pericardial disease
Arrhythmias
Signs of previous MI - pathological Q waves

A normal ECG makes heart failure unlikely (sensitivity 89%)

138
Q

What would a chest x-ray show for heart failure?

A

ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vessels
Effusions

139
Q

What is BNP and why is it elevated in heart failure?

A

B-type Natriuretic Peptide (BNP) are peptides that cause natriuresis, diuresis and vasodilation.

HF- released in response to increased pressure on the heart

BNP signals to the body that it needs to reduce the amount of fluid in the body and help reduce the strain on the heart

They are the body’s natural defence against hypervolemia

A marker of heart failure
Released when the myocardial walls are under stress
Levels directly correlated to ventricular wall stress and severity of heart failure

RELEASED FROM THE VENTRICLES

140
Q

What is the diagnostic test for heart failure?

A

ECHOCARDIOGRAM

141
Q

What is the first medications you should give in patients with heart failure with reduced ejection fraction?

A

An ace inhibitor Ramipril and **beta blockers (bisoprolol)

Start slow and progress low

If can’t tolerate an ace inhibitor then use Candesartan Angiotensin 2 receptor blocker

142
Q

After ACE inhibitors, and Beta blockers what other medications can you give for HF?

A

A mineralocorticoid receptor antagonist - eg Spironolactone

143
Q

After ACE inhibitors and beta blockers and aldosterone receptor antagonist what other medications can you give?

A

Loop Diuretic , like furoesmide

ABAL

Also a drug like Digoxin - good for arrhythmias and AF, and helps symptoms of LVSD (Left Ventricular Systolic Dysfunction.)
—> Helps strengthen heart muscle contractions

144
Q

what are the main adverse effects of Angiotensin converting enzyme inhibitors?

A

a. Hypotension
b. Acute renal failure
c. Hyperkalaemia
d. Teratogenic effects in pregnancy

Also due to increased Kinin production

    a. Cough
b. Rash
c. Anaphylactoid reactions
145
Q

What are the main adverse effects of Angiotensin II receptor blockers? When is it contraindicated?

A

Symptomatic hypotension (especially volume deplete patients)
Hyperkalaemia
Potential for renal dysfunction
Rash
Angio-oedema

Contraindicated in pregnancy (aka not safe for pregnancy)
Generally very well tolerated

146
Q

What are the main clinical indications for diuretics?
What are the 3 classes of Diuretics often seen in treating CVD, and where do they act?

A

Hypertension
Heart failure

Classes

Thiazides and related drugs (act on distal tubule)

Loop diuretics (act on loop of Henle)

Aldosterone antagonists

147
Q

Cardiac Pharmacology - give some examples of
a) Thiazide and related diuretics
b) Loop diuretics
c) Potassium sparing diuretic

A

A) Bendroflumethiazide
B) Furosemide
C) Spironolactone

148
Q

What is Cor pulmonale?

A

Right sided heart failure caused by chronic arterial pulmonary hypertension, due to lung diseases.

Pulmonary vascular disorders, neuromuscular and skeletal diseases

149
Q

What is the first line treatment for those with heart failure and preserved ejection fraction (HFPEF)

A

A diuretic, like furosemide

150
Q

What is a key drug to be avoided in heart failure?

A

Calcium channels blockers, with the exception of Amlodipine, are generally avoided in heart failure, and verapamil in particular can worsen heart failure.

151
Q

What are some key features of constipation?

A

Harder stools than normal
Infrequent or increased time between bowel movements
Pain/difficulty passing stools

152
Q

Why as we age does constipation get worse?

A

Peristaltic speed is reduced leading to slower transit time
Peristaltic strength is reduced due to muscle atrophy
Weakened connective tissue results in the
formation of diverticula.

153
Q

What drugs can lead to constipation?

A

Chronic laxative use
Opiates: codeine
Iron supplements
CCB
Anti depressants
Antipsychotics

154
Q

What are some Anorectal diseases/Bowl obstructions that can cause constipation?

A

Anorectal disease
- Cancer
- Fissures
- Rectal prolapse

Intestinal obstruction
- Colorectal carcinoma
- Strictures
- Pelvic mass
- Diverticulosis

155
Q

What are some other common disorders that can cause constipation? (metabolic/neuro)

A

Metabolic/endocrine
* Hypercalcaemia
* Hypothyroidism (rarely presents
with constipation)

Neuromuscular (slow transit from
decreased propulsive activity)
* Spinal or pelvic nerve injury (eg
trauma, surgery)
* Systemic sclerosis
* Diabetic neuropathy
- Dementia
- Immobility
- Dehydration

156
Q

What are some associated symptoms of constipation?

A
  • Reduced appetite
  • Delirium
  • Vomiting
  • Abdo pain
  • Urinary retention
  • Faecal incontinence
157
Q

What is the initial steps to take when managing constipation?

A

Before prescribing laxatives, it is important to rule out obstructive causes by careful history, abdominal examination, PR, and any appropriate investigations.

Treatment should initially focus on treating underlying causes and ensuring an adequate oral intake of fluid and fibre

Review Medications!

158
Q

What are some different types of laxatives?

A

Bulking agents crease faecal mass, so stimulating peristalsis - eg Ispaghula husk

Stimulant laxatives: increased intestinal motility so do use in intestinal obstruction or acute colitis (Senna, Bisacodyl )

Stool softeners are particularly useful when
managing painful anal conditions, eg fissure. eg - Lactulose

Enema - used in rectal constipation - most often phosphate

159
Q

What are the types of incontinence?

A
  • Urge incontinence:
  • Stress incontinence
  • Mixed incontinence:
    Overflow incontinence (neurogenic bladder):
160
Q

What causes urge incontinence?

A

Sudden urge to urinate due to an overactive bladder

Typically due to an uninhibited detrusor muscle usually associated with UTI and inflammation

161
Q

Outline the pathophysiology behind stress incontinence. What things can cause it?

A

Increased abdominal pressure overwhelms the sphincter muscles and allows urine to leak out. Causes include pregnancy and exertion, like sneezing, coughing, and laughing.
- Post-prostatectomy in men

162
Q

Outline the pathophysiology behind overflow incontinence. What things can cause it?

A

Due to either obstruction in urine flow or an ineffective detrusor muscle

This leads to urine build up to the point the bladder is so full urine dribbles/leaks out through sphincters

Obstruction - - eg benign prostatic hyperplasia,
Ineffective detrusor = Diabetes (neurogenic bladder) Multiple sclerosis, Spinal chord injury

163
Q

What is the management for urge incontinence?

A

Bladder retraining (gradually increasing the time between voiding) for at least six weeks is first-line

Anticholinergic medication, for example, oxybutynin, tolterodine and solifenacin
- B3 adrenergic agonist: mirabegron - increases BP though

164
Q

What are the 3 categories of causes of malnutrition?

A

Decreased intake
Increased requirements
Inability to utilise nutrients

165
Q

Give some factors that can affect nutritional intake, which can cause malnutrition?

A
  • Environment
  • Meal times
  • Difficulty swallowing
  • Feeding problems
  • Appetite
  • Pain
  • Medication
  • Radiotherapy
166
Q

Give some factors that can lead to an increased nutritional requirement, which can cause malnutrition

A
  • Infection
  • Trauma
  • Liver disease
  • Wound healing
  • Surgery
  • Malignancy
  • Chronic infection
167
Q

Give some factors that can lead to increasing nutritional loss, which can cause malnutrition

A

Diarrhoea
Vomiting
Bowel surgery
Pancreatic insufficiency
Inflammatory bowel disease
Losses from drains and wounds

168
Q

What tool is used to screen inpatients for malnutrition?

A

Takes into account:
BMI
% of unplanned weight loss in the last 3-6 months
Whether the patient is acutely unwell and there has been or is likely to be no nutritional intake for more than five days

Add scores together to calculate overall risk of malnutrition
score 0 low risk Score 1 medium risk Score 2 or more high risk

169
Q

What is the scoring of the MUST score?

A

-High risk intervention should start immediately

  • Medium risk need to be monitored with food charts for the first 3 days and then a decision is made about further intervention
170
Q

What are the temperature ranges for mild, moderate and severe hypothermia?

A
  • Mild: 32-35
  • Moderate: 30-32
  • Severe: <30
171
Q

What are some causes of Hypothermia? Why are older people more susceptible to hypothermia?

A

Often multifactorial.
* Illness (drugs, fall, sepsis)
* Defective homeostasis myocardial infarction
heart failure
* Cold exposure (clothing, defective temperature discrimination, climate, poverty)
- Reduced fat as we age = less insulation
inactivity
BMR slows as we age

172
Q

What is seen in hypothermia?

A

3A (11 decks)

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