GERIATRICS + Stroke Medicine Flashcards

Question 1

Q

What does the internal carotid artery branch off to supply?

Answer

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.

Question 2

Q

What does the middle cerebral artery supply?

Answer

A

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

Question 3

Q

What does the anterior cerebral artery supply?

Answer

A

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

Question 4

Q

Outline the pathology behind an ischaemic stroke of atherosclerotic origin

Answer

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

Question 5

Q

Outline the pathology behind an ischaemic stroke of emboli origin.

Answer

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

Question 6

Q

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

Answer

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.

Question 7

Q

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

Answer

A

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

Question 8

Q

Name some risk factors for a stroke

Answer

A

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

Question 9

Q

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

Answer

A

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

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

Question 10

Q

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

Answer

A

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.

Question 11

Q

What is the associated effects of a stroke/lesion affeccting the posterior cerebal artery?

Answer

A

Contralateral (aka opposite side) homonymous hemianopia with macular sparing
Visual agnosia

Question 12

Q

What is the associated effects of a stroke/lesion affeccting the branches of the posterior cerebral artery that supply the midbrain?

What is this known as?

Answer

A

Weber’s syndrome

Ipsilateral CN III palsy - “down and out” eyelid, ptsosis (eyelid drooping) and fixed dilation due to parasympathetic fibers being effected, diplopia

Contralateral weakness of upper and lower extremity

Question 13

Q

What is the associated effects of a stroke/lesion affeccting the Posterior inferior cerebellar artery

What is it known as?

Answer

A

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

(ipsilateral facial symptoms and the contralateral body symptoms (chess-board distribution))

known as lateral medullary syndrome, Wallenberg syndrome

no facial paralysis or hearing loss

Question 14

Q

What is the associated effects of a stroke/lesion affeccting the Anterior inferior cerebellar artery (lateral pontine syndrome)

Answer

A

Symptoms are similar to Wallenberg’s (PICA lesion), so get
Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

(ipsilateral facial symptoms and the contralateral body symptoms (chess-board distribution))

but also get
Ipsilateral: facial paralysis and deafness

Question 15

Q

What is an lacunar stroke and what are the symptoms of it?

Answer

A

A lacunar stroke is a type of ischemic stroke caused by the blockage of small arteries that supply deep brain structures, such as the basal ganglia, thalamus, or brainstem. It results in small, localized areas of damage.

often Pure motor stroke: Weakness in one side of the body (face, arm, leg).

Question 16

Q

What is a homonymous hemianopia?

Where are the lesions most likely to be?

Answer

A

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

**the contralateral optic tract or radiation/cortex

Question 17

Q

How do total anterior circulation infarcts present, and what is affected?

What about partial

Answer

A

Total anterior circulation infarcts (TACI, c. 15%)
involves middle and anterior cerebral arteries
all 3 of
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

are presentPartial anterior circulation infarcts (PACI, c. 25%)
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of the above criteria are present

Question 18

Q

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

Answer

A

Cerebellarsigns
Reduced consciousness
Quadriplegiaorhemiplegia

quadriplegia,
disturbances of gaze and vision,
lockedin syndrome (aware, but unable to respond

Question 19

Q

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

Answer

A

CT scan ASAP
Distinguishes ischaemic from haemorr

hypoattenuation (darkness) of the brain parenchyma
loss of grey matter-white matter differentiation, and sulcal effacement - a space or cavity has been obliterated by the external application of mass effect.
hyperattenuation (brightness) in an artery indicates clot within the vessel lumen

Question 20

Q

What are some other investigations you would do for a Stroke

Answer

A

ECG:assess for AF, MI
Bloods:
- Screen for risk factors includingHba1c, lipids, clotting screenand rule out stroke mimics such ashypoglycemia and hyponatraemia
- In younger patients, consider ESR, autoantibody and thrombophilia screen (ESR raised in vasculitis)
CT angiogram (CTA):identifies arterial occlusion and should be performed in all patients who are appropriate for thrombectomy
MRI head:MRI is an alternative to non-contrast CT head; MRI is more sensitive but CT is safer and easier to obtain

Question 21

Q

What is the management for an Ischaemic stroke?

Answer

A

Maintain stable blood glucose levels, hydration status and temperature

Blood pressure should not be lowered too much during a stroke because this risks reducing the perfusion to the brain.

Thrombolysis: alteplase

Aspirin 300mg for 2 weeks

Prophylaxis - Lifelong clopidogrel (75mg, an Antiplatelet)

If clopidogrel is contraindicated or not tolerated, give aspirin 75mg for secondary prevention following stroke

Question 22

Q

What are some conidtions/criteria that need to be met when giving thrombolysis?

Answer

A

given if < 4.5 hours of symptom onset and haemorrhage excluded on imaging, or for Patients who present 4.5-9 hours after symptom onset, or with ‘wake-up stroke’ should still be considered for thrombolysis if they have imaging evidence of potential to salvage brain tissue.

Question 23

Q

What are some complications of thrombylysis ? What is the treatment for small storkes

What is an important CI in it?

Answer

A

Small strokes - Dual antiplatelet, of 75mg of Aspirin and Clopigerel

Complications of thrombolysis -
Bleeding anywhere, especially in the brain haemorrhagic stroke, and in the urinary tract - so try to avoid catherising patients who have just had thrombolysis

A blood pressure exceeding 185/110 mmHg is an absolute contraindication to thrombolysis in acute ischaemic stroke. Lowering it below this threshold is crucial before considering thrombolysis to mitigate the risk of intracerebral haemorrhage.

Question 24

Q

What is a TIA?

Answer

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 CAUSES ACUTE INFARCTION

Question 25

Q

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

Answer

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

Question 26

Q

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

Answer

A

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

Question 27

Q

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

Answer

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

Question 28

Q

What are the primary investigations for a TIA

Answer

A

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

Question 29

Q

What is the management for a TIA?

Answer

A

Immediate management
Immediate loading dose: Aspirin 300mg
Refer to specialist – to be seen within 24h of symptom onset

Dual Antiplatelet therapy
Standard treatment is Aspirin 75mg daily
With modified-release Dipyridamole
OR Clopidogrel daily

Dont give aspirin if history of GI issues for risk of bleeding, NICE advises just clopipedergrel

Question 30

Q

What is the acute management for a TIA?

What procedure is done?

Answer

A

Antiplatelet:initiallyaspirin 300mg - the first-line, immediate management, if aspirin not appropriate, give an Clopidergol

REFER TO STROKE SPECIALIST*

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

Question 31

Q

What further managment can you provide for a TIA, after the acute antiplatelets?

Answer

A

A High intensity Statin - atorvastatin : 20-80 mg orally once daily

An anticoauglant for AF - eg A low molecular weight heparin eg dalteparin, or
A direct thrombin inhibitor or factor Xa inhibitor - rivaroxaban

Give aspirin 300mg OD for 2wks, then switch to clopidogrel 75mg OD.

Question 32

Q

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

Answer

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

Question 33

Q

What are the subtypes of haemorrhagic stroke?

Answer

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; prematurity is a very strong risk factor in infants

An intracerebral haemorrhage that involves just the brain tissue is called an intraparenchymal haemorrhage, whereas if the blood extends into the ventricles of the brain which store cerebrospinal fluid, it’s called an intraventricular haemorrhage.

Question 34

Q

What are the main aetiologies of a primary haemorrhagic stroke?

Answer

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

Question 35

Q

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

Answer

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.

Question 36

Q

Outline the pathology that a haemorrhagic stroke leads to.

Answer

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

Question 37

Q

What are some general clinical manifestations of a haemorrhagic stroke?

Answer

A

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

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

Question 38

Q

What are some manifestations that can point to a haemorrhagic stroke, over ischaemic?

Answer

A

Pointers to haemorrhage:

Sudden loss of consciousness
Severe headache
Meningism- the clinical syndrome of headache, neck stiffness and photophobia, often with nausea and vomiting - can be caused by raised ICP
Coma

Will only cause a headache when there is pressure on the meninges!!

These are unreliable, a CT scan is needed for differentiation

Question 39

Q

What are the investigations for a intercranial haemorrhage?

Answer

A

Request an immediate non-contrast CT scan of the head - will see hyperattenuation (brightness), suggesting acute blood, often with surrounding hypoattenuation (darkness) due to oedema

Angiography: visualise the exact location of haemorrhage
Check FBC and clotting

Question 40

Q

What is the management for an intercranial haemorrhage?

Answer

A

Consider intubation, ventilation and ICU care if they have reduced consciousness
Correct any clotting abnormality - STOP ANTICOAGULANTS IF PT IS ON THEM

Correct severe hypertension but avoid hypotension
Craniotomy, or stereotactic aspiration

Drugs to relieve ICP - IV MANITOL

Question 41

Q

Treatment for intracerebral haemorrhagic stroke - How does mannitol work?

Answer

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.

Question 42

Q

What are the 3 main causes of a Subarachnoid Haemorrhage?

Answer

A

Trauma
Atraumaticcases are referred to asspontaneousSAH - often due to a saccular cerebral (Berry) Aneurysm - 70-80% of SAH cases
Arteriovenous malformation(AVM) - abnormal connections between artery and vein can dilate and cause rupture - 15% of SAH cases

Can be Idiopathic

Question 43

Q

Outline the pathophysiology behind a subarachnoid haemhorrage.

Answer

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

Question 44

Q

What are some signs of a Subarachnoid haemhorrhage?

Answer

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

Question 45

Q

What are some differentials for a subarachnoid haemorrhage?

Answer

A

Migraine
Meningitis
Corticol vein thrombosis
Carotid/vertebral artery dissection

Question 46

Q

What investigations would you do for a subarachnoid haemorrhage?

Answer

A

urgent Non Contrast CT head
ASAP
Detects >95% of SAH in first 24 hours - Subarachnoid and/or intraventricular blood, hyperdense areas in the subarachnoid space
“Star” shaped sign - or hyerdense blood in the gyri - as blood is not in the brain tissue, but on top of the pia mata

ECG - Arrhythmias and ischaemic changes, Prolonged QTc, ST segment/T-wave abnormalities.

Lumbar puncture – if CT normal but SAH still suspected
Findings - RBCs or xanthochromia (yellow pigmentation due to degradation of haemoglobin to bilirubin)

Electrolytes - Moderate hyponatraemia
ABG – to rule out hypoxia

Question 47

Q

What is the non surgical management for a subarachnoid haemorrhage?

Answer

A

Immediately refer to neurosurgeon

Nimodipine - Ca2+ antagonist, (CCB) Reduces vasospasm and therefore cerebral ischaemia

Re-examine CNS often

IV fluids -Maintain cerebral perfusion
Ventricular drainage for hydrocephalus

If features of raised intracranial pressure: consider intubation with hyperventilation, head elevation (30°) and IV mannitol

Question 48

Q

What is the surgical management for a subarachnoid haemorrhage?

Answer

A

first-line endovascular coilingof the aneurysm -reduces blood circulation to the aneurysm inserting one or more microsurgical detachable platinum wires, into the aneurysm until there is no more blood flow occurring. Usually enter through leg.

Second-line issurgical clippingvia craniotomy - opening in the skull is created to reach the aneurysm. Then small metal clip on the neck (opening) of the aneurysm to obstruct the flow of blood.

Question 49

Q

Define what an Extradural/ Epidural Haemorrhage is.

Answer

A

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

Question 50

Q

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

Answer

A

The most common site where the frontal, parietal, temporal and sphenoid bones join together, CALLED THE PTERION ===>
This section of the skull is relatively thin and it’s located right above the middle meningeal artery.

Question 51

Q

What are some symptoms of an extradural haemorrhage

Answer

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

classic history is patient who initially loses, briefly regains and then loses again consciousness after a low-impact head injury - the lucid interval

Question 52

Q

What investigations would you do for a extradural haematoma?

Answer

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

Question 53

Q

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

Answer

A

An affixed and dilated pupil usually indicates a problem with the parasympathetic innervation of the eye, often due to an issue affecting the oculomotor nerve or its associated pathways, or the nucleus that controls this, the Edinger-Westphal nucleus

This can be caused by various conditions such as brain injury, brain haemorrhage, uncal herniation, or an aneurysm pressing on the oculomotor nerve.

Question 54

Q

What are the main causes for a subdural haematoma?

Answer

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

Question 55

Q

What are some clinical manifestations of a subdural haematoma

Answer

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

Question 56

Q

What is the investigations for a Subdural haemorrhage?

Answer

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

Question 57

Q

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

Acute Subdural haematoma
Chronic subdural haematoma
subacute

what is the timeframe for chronic subdrual haematoma, and subacute haematoma

Answer

A

Acute subdural haematoma: hyperdense mass = looks “more white” than the surrounding healthy brain tissue
Chronic subdural haematoma: hypodense masses = “less white” than the surrounding brain tissue.
subacute subdural haemorrhage is visualised as an isodense crescent-shaped collection. time frame is 1-2 weeks

Time frame for chronic SD haematoma - several weeks-months of confusion, fluctuating cognition, recurrent falls, and focal neurological deficits.

Question 58

Q

What is the management of subdural haematoma?

Answer

A

IV mannitol - reduce ICP
Burr hole / Craniotomy to relieve pressure

Craniotomy a large opening in the skull is created to evacuate the haematoma and relieve the associated mass effect.

A decompressive craniectomy is the management choice for symptomatic acute subdural haemorrhage. This is a more invasive surgery than a burr hole procedure and is not necessitated in most cases of chronic subdural haemorrhage

Burr hole evacuation is the most likely operation to be done for symptomatic chronic subdural bleeds

Question 59

Q

What would you give in the management of a stroke in someone with AF?

Answer

A

Warfarin/DOAC, it’s superior to aspirin in Atrial fibrillation / mural thrombus

Warfarin blocks one of the enzymes (proteins) that uses vitamin K to produce clotting factors. This disrupts the clotting process, making it take longer for the blood to clot

DOAC - eg rivaroxaban inhibit Thrombin

Question 60

Q

What is seen in Wernicke’s Aphasia?

What artery is blocked in wernickes aphasia?

Answer

A

history of fluent, yet confused speech.
Wernicke’s aphasia can be caused by a blockage in the inferior division of the left Middle Cerebral Artery

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

Question 61

Q

What is seen in Brocas Aphasia?

What artery is blocked in Brocas aphasia?

Answer

A

causes non-fluent speech. Patients often have word-finding difficulties. However, comprehension remains intact.

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

Question 62

Q

What is Benign paroxysmal postional vertigo?

Answer

A

common cause of recurrent episodes of vertigo triggered by head movement. It is a peripheral cause of vertigo, meaning the problem is located in the inner ear rather than the brain

Question 63

Q

What is the presentation of Benign Paroxysmal postional vertigo?

Answer

A

It is more common in older adults.

A variety of head movements can trigger attacks of vertigo. A common trigger is turning over in bed. Symptoms settle after around 20 – 60 seconds, and patients are asymptomatic between attacks. Often episodes occur over several weeks and then resolve but can reoccur weeks or months later.

BPPV does not cause hearing loss or tinnitus.

Question 64

Q

What is the pathophysiology behind BPPV? What is thought to cause it?

Answer

A

BPPV is caused by crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. This occurs most often in the posterior semicircular canal.

The crystals disrupt the normal flow of endolymph through the canals, confusing the vestibular system. Head movement creates the flow of endolymph in the canals, triggering episodes of vertigo.

They may be displaced by a viral infection, head trauma, ageing or without a clear cause.

Answer 65

A

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

In patients with BPPV, the Dix-Hallpike manoeuvre will trigger rotational nystagmus and symptoms of vertigo. The eye will have rotational beats of nystagmus towards the affected ear (clockwise with left ear and anti-clockwise for right ear BPPV).

Answer 66

A

To perform the manoeuvre:

The patient sits upright on a flat examination couch with their head turned 45 degrees to one side

Support the patient’s head to stay in the 45 degree position while rapidly lowering the patient backwards until their head is hanging off the end of the couch, extended 20-30 degrees

Hold the patient’s head still, turned 45 degrees to one side and extended 20-30 degrees below the level of the couch

Watch the eyes closely for 30-60 seconds, looking for nystagmus
Repeat the test with the head turned 45 degrees in the other direction

Answer 67

A

Epley Manoeuvre

Sit upright w head turned 45 degrees to one side (eg right)
Lie down as quickly as you can, w head still turned 45 degrees (to right) - wait for a minute or so
Turn your head to 45 degrees other side (eg left) keeping your head down and hanging over the edge of your bed.
Turn to lie on your left hand side, not moving your head, rotate head again 45 degrees again to the left so you are facing floor
Slowly sit up, tilting your head down to tuck chin to chest

Answer 68

A

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.

ICD-10 criteria for delirium:
1.) Impairment of consciousness and attention
2.) Global disturbance in cognition
3.) Psychomotor disturbance
4.) Disturbance of sleep-wake cycle
5.) Emotional disturbances

Answer 69

A

Risk factors >65y, dementia/previous cognitive impairment, hip fracture, acute illness, psychological agitation (eg pain).

Causes
* Surgery/post-GA.
* Systemic infection: pneumonia, UTI, malaria, wounds, IV lines.
* Intracranial infection or head injury.
* Drugs/drug withdrawal: opiates, levodopa, sedatives, recreational.
* Alcohol withdrawal
* Metabolic:uraemia,liver failure,Na+or glucose, Hb,malnutrition(beriberi,p268).
* Hypoxia: respiratory or cardiac failure.
* Vascular: stroke, myocardial infarction.
* Nutritional: thiamine, nicotinic acid, or B12 deficiency

Answer 70

A

Delirium can be divided into three subtypes:

hperactive delirium: a subtype of delirium characterised by people who have heightened arousal and can be restless, agitated or aggressive
hypoactive delirium: a subtype of delirium characterised by people who become withdrawn, quiet and sleepy
mixed
hypoactive and mixed delirium can be more difficult to recognise

Answer 71

A

PINCH ME

Pain
Infection
Nutrition
Co-morbidities
Hydration
Medication
Environment
+ bladder

Answer 72

A

Look for the cause (eg UTI, pneumonia, MI): do FBC, U&E, LFT, blood glucose,
ABG, septic screen (urine dipstick, CXR, blood cultures); also consider ECG, malaria
films, LP, EEG, CT.
Think about causes - be vigilant for constipation

Answer 73

A

AMT
Abbreviated Mental Test - a score of 6 or less implies a mental impairment 10 questions in total

What is your age
What is the time
Can you remember an address (42 West Street)
What’s the year
Name of hospital you’re in?
Can you recognise the role of two different people ? (eg nurse, doctor)
What year did WW1 begin ?
What is your DOB?
. Name the current Monarch or PM
Count backwards from 20 to 1

DSM-5 (diagnostic and statistical manual of mental disorders)

The 4AT is a tool to quickly assess whether a patient has delirium or not. A score of 4 and above is suggestive of possible delirum +/- cognitive impairment

Answer 74

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. = first line
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

Answer 75

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.

Answer 76

A

falls
sudden reduced mobility
new or accelerated state of confusion (delirium)
acute change in continence
sensitivity to a new medication

Answer 77

A

stroke
CHD
Diabetes Mellitus
Alzheimer’s Disease
urinary problems
depression
visual loss
hearing and visual impairment
falls

Answer 78

A

treatment of unstable medical conditions and any treatable problems
reviewing drug treatment (including polypharmacy)
Phyiscal exericse
nutrional support/protein and calorie supplements
Vit D
comprehensive rehabilitation

Answer 79

A

FEMPS

Functional ability - Mobility, balance, ADL
Environment - House of residence, equipment, safety features
Mental Health - Cognition/Mood
Physical Health -
Optimise Comorbidities
Medication review, frailty status
Social Circumstances - Former/informal carers, and Power of Attorney status

Answer 80

A

assessment.
Writing a problem list: this should cover all five domains, with prioritization.
Management planning: for each problem, a management plan should be proposed.
Goal setting: for each management plan, a treatment goal is established.

An example of such a goal would be an improvement in measures of postural sway following gait and balance exercise within 4 weeks.

Answer 81

A

age 80+
female
low weight
previous fall
polypharmacy/medications (commonly benzodiazepines, antidepressents, bp-lowering drugs, anticonvulsants)
cognitive impairment
orthostatic hypotension
vision problems
chronic health conditions affecting mobility

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

Answer 82

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

Answer 83

A

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

Answer 84

A

review, lifestyle advice is often the mainstay of management. This includes 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.

Answer 85

A

a complex skeletal disease characterised by low bone density and micro-architectural defects in bone tissue, resulting in increased bone fragility and susceptibility to fracture.

Bones become more porous due to increased breakdown

Answer 86

A

Osteopenia refers to a less severe reduction in bone density than osteoporosis.
Defined as bone mineral density 1-2.5 standard deviations below young adult mean value

Answer 87

A

SHATTERED

Steroid (prednisolone use) – SSRIs, GnRH analogues
(goserelin)

Hyperthyroidism, hypercalciuria and hyperparathyroidism + Cushing’s

Alcohol and tobacco

Thin – BMI < 18.5, T1DM

Testosterone ↓ - ↑ bone turnover, hypogonadism turner’s/Klinefelter

Early menopause – ↑ bone turnover, premature ovarian failure

Renal or liver failure

Erosive/inflammatory bone disease – RA/myeloma

Dietary calcium ↓ or malabsorption, T1DM

Strength training can increase bone mass, so protective

Answer 88

A

Joint disease e.g. RA, SLE
Hyperthyroidism and hyperparathyroidism – increased bone turnover
High cortisol – Cushing’s (increases bone resorption and induces osteoblast apoptosis)
Low oestrogen/testosterone e.g. hypogonadism, anorexia, menopause
Renal disease – decreased vitamin D
Previous fracture
Anorexia

Answer 89

A

As we age, the activity of osteoclasts increases and is not matched by osteoblasts.As such bone mass decreases.

Oestrogen is key to the activity of bone cells with receptors found on osteoblasts, osteocytes, and osteoclasts. The mechanisms are still being understood, but it appears osteoclasts survive longer in the absence of oestrogen, and there is arrest of osteoblastic synthetic architecture.

Answer 90

A

Asymptomatic condition with the exception of fractures

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

may also see Thorasic Kyphosis (hunching over)

Answer 91

A

FRAX = fracture risk assessment tool

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

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

It gives results as a percentage 10 year probability of a:
- Major osteoporotic fracture
- Hip fracture

Answer 92

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.

Answer 93

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.

Answer 94

A

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

vitamin D supplementation.

Answer 95

A

Bisphosphonates- they interfere with osteoclast activity reducing their activity.

Alendronate 70mg once weekly

Answer 96

A

Oesophagitis/Reflux and oesophageal erosions.

GI distress
Renal Toxicity
Hypocalcaemia
Oesophageal ulcers

Osteonecrosis (death of bone tissue) of the jaw and external auditory canal

Answer 97

A

Hormone replacement therapy should be considered in women that go through menopause early.

Raloxifene - Selective oestrogen receptor
Teriparatide - recombinant PTH, increases bone formation

Answer 98

A

Take 70 mg once a week in the morning, or 10mg daily and at least 30 minutes before any food

the patient should remain upright for at least half an hour after taking

Answer 99

A

When the heart can’t supply enough blood to meet the body’s demands

Either by systolic Heart failure, where heart’s ventricles can’t pump blood hard enough during systole (not squeezing enough(

or by Diastolic heart failure, where or not enough blood fills the ventricles during diastole (not filling enough) (reduced preload)

Answer 100

A

Because systemic hypertension makes it harder for the left ventricle to pump blood out into that systemic circulation.

To compensate, the left ventricle goes under hypertrophy so that the ventricle can contract with more force.

The increase in muscle mass means that there is a greater demand for oxygen and, to make things even worse, the coronaries get squeezed down by the this extra muscle so that even less blood’s delivered to the tissue.

Leads to more demand and reduced supply means that some of the ventricular muscle starts have weaker contractions—leading to systolic failure.

taken from osmosis video

Answer 101

A

The hypertrophy that is created by hypertension is concentric, which means that the new sarcomeres are generated in parallel with existing ones.

This means that heart muscle encroaches on the ventricular chamber space, resulting in less room for blood in there -> Can’t fill up as much

==> Therefore contributes to systolic but can also cause diastolic heart failure

Answer 102

A

Ejection fraction <40% (SV/EDV)
Caused by
IHD
MI
Hypertension
Cardiomyopathy

Answer 103

A

Inability to relax and fill
There is reduced preload because there is abnormal filling of the LV
Ejection fraction >50%

Caused by
Constrictive pericarditis
Cardiac tamponade
Hypertension

Answer 104

A

decreases blood flow to the kidneys,
activates the renin-angiotensin-aldosterone system, ultimately causing fluid retention.

Which fills the heart a bit more during diastole and increases preload, which increases contraction strength again by the Frank Starling mechanism.

leads to fluid retention, aka oedema

Answer 105

A

LSHF leads to increased pulmonary blood pressure, due to fluid build up.
increased pulmonary blood pressure makes it harder for the right side to pump blood into.

In this case the heart failure would be biventricular, since both ventricles are affected.

Answer 106

A

Hypertension
Pulmonary stenosis
Lung disease (cor pulmonale)
Atrial/ventricular septal defects

Answer 107

A

Signs:
Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur

Answer 108

A

Raised JVP – JVP distension
Hepatomegaly/Splenomegaly
Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed
Ascites
Weight gain (fluid)

Answer 109

A

Blood back up into jugular vein Raised JVP, – JVP distension -

b) leads to Hepatomegaly and Splenomegaly (Hepatosplenomegaly)- In extreme cases and lead to cirrhosis of liver, known as cardiac cirrhosis

c) Fluid build up in peritoneum leads to Ascites and weight gain

d) leads to Pitting oedema – sacral/leg oedema in bed-bound patients which causes a “pit” when pressed

Answer 110

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

Answer 111

A

think about what it backs up into! (left side backs up into lungs)

Cardiomegaly (displaced apex beat)
Pulmonary Oedema
3rd and 4th heart sounds
Pleural effusion
Crepitations in lung bases
Tachycardia
Reduced BP
Cool peripheries
Heart murmur

Answer 112

A

ECG
Chest X ray
BNP B-type Natriuretic Peptide levels
Echocardiogram

Answer 113

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%)

taken from almostadoctor

Answer 114

A

ABCDE
Recommended for all suspected HF patients
Alveolar oedema - seen in Bat wing shadowing
Kerley B Lines interstitial oedema
Cardiomegaly
Dilated upper lobe vessels of lungs (prominent upper lobe veins)
Effusions (pleural)

A normal CXR does not exclude the possibility of Heart Failure

Answer 115

A

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

HF - released in response to increased pressure on 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 hypervolaemia

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

Answer 116

A

ECHOCARDIOGRAM

Can confirm the diagnosis
Can calculate the ejection fraction, ventricular wall thickness etc

An ejection fraction (EF) of <40% strongly indicated heart failure
EF of 41-49% is not diagnostic, but suggestive of heart failure

Can confirm any underlying structural abnormalities – such as valve disease
Helps to stratify the type of HF present and therefore guides management

Answer 117

A

an ACE inhibitor, like Ramipril, and Beta blockers, like Bisoprolol

Start low, progress slow! - monitor BP and heart rate

ABAL

(can consider giving an Angiotensin 2 receptor blocker eg Candesartan if intolerant of ACE-i)

Answer 118

A

A mineralocorticoid receptor antagonist - eg Spironolactone

Answer 119

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

Answer 120

A

Hypertension
Heart failure
Diabetic nephropathy

eg RAMIPRIL, ENALAPRIL, PERINDOPRIL, TRANDOLAPRIL

Answer 121

A

Think - Due to reduced angiotensin II formation!! (duh)

    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

Answer 122

A

Hypertension
Diabetic nephropathy
Heart failure (when ACE-I contraindicated)

eg CANDESARTAIN, VALSARTAIN, LOSARTAN

Answer 123

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

Answer 124

A

Hypertension
Ischaemic heart disease (IHD) – angina
Arrhythmia (tachycardia)

eg AMLODOPINE, FELODIPINE, VERAPAMIL, DILTIAZEM

Answer 125

A

Ischaemic heart disease (IHD) – angina
Heart failure
Arrhythmia
Hypertension

eg BISOPROLOL, PROPRANOLOL, ATENOLOL, NADOLOL

Answer 126

A

Hypertension
Heart failure

Classes

Thiazides and related drugs (act on distal tubule)

Loop diuretics (act on loop of Henle)

Aldosterone antagonists

Answer 127

A

a) Bendroflumethiazide, hydrochlorothiazide
b) Furosemide, Bumetanide
c) Spironolactone Amiloride

Answer 128

A

Right sided heart failure caused by chronic arterial pulmonary hypertension, due to lung diseases, Pulmonary vascular disorders, neuromuscular and skeletal diseases

Answer 129

A

shortness of breath (and must say specifically at least one of; paroxysmal
nocturnal dyspnoea, orthopnoea),

Ankle swelling,

Fatigue

Answer 130

A

A diuretic, like furosemide

Answer 131

A

A diuretic, like furosemide

The previous flashcards asked about heart failure medication for when there is a reduced ejection fraction

Answer 132

A

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

Answer 133

A

Harder stools than normal
Infrequent or increased time between bowl movements
pain/difficulty passing stool

Answer 134

A

As we age:
r Peristaltic speed is reduced, leading to a slower transit time.
r Peristaltic strength is reduced due to muscle atrophy.
r Weakened connective tissue within the mucosa results in the
formation of diverticula.
r Increased sensory threshold for the urge to open bowel

Small bowl
Reduced absorption of some nutrients
Decreased motility

Answer 135

A

Chronic laxative use
Opiates - codeine, Morphine, Tramadol, opiate patches
Iron Supplements
CCB - Amlodipine, Verapamil
Anti Depressants - particularly tricyclic agents
Antipsychotics

Answer 136

A

anorectal disease (esp. if painful)
- Anal or colorectal cancer
* Fissures strictures, herpes
* Rectal prolapse

Intestinal obstruction
- Colorectal carcinoma (p618)
* Strictures (eg Crohn’s disease)
* Pelvic mass (eg fetus, fibroids)
* Diverticulosis (rectal bleeding is a
commoner presentation)

Answer 137

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
- Immobillity
- Dehydration

Answer 138

A

Reduced Appetite
Delirium
Vomiting, Nausea
Abdo pain and distension
Urinary retention
Fecal incontinence

Answer 139

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!

Answer 140

A

Bulking agents increase faecal mass, so stimulating peristalsis - eg Ispaghula husk, eg Fybogel (first line, need good hydration)

Stimulant laxatives increase intestinal
motility, so do not use in intestinal obstruction or acute colitis - eg Senna, bisacodyl tablets, sodium picosulphate

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

Enema - used in rectal constipation - most often phosphate

Answer 141

A

Urge incontinence:
Stress incontinence
Mixed incontinence:
Overflow incontinence (neurogenic bladder):

Answer 142

A

Sudden urge to urinate because of an “overactive bladder”, followed immediately by involuntary urination

typically due to an uninhibited detrusor muscle that contracts randomly.

Usually associated with urinary tract infections. Inflammation may trigger the detrusor muscle.

Answer 143

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

Answer 144

A

Due to either - Obstruction due to blockage in urine flow
or
Ineffective detrusor muscle. ==> Detrusor cant contract properly so the bladder doesn’t empty properly

In both cases, leads to urine build up, to the point that the bladder is so full that urine dribbles/leaks out through sphincters

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

Answer 145

A

Urge incontinence: frequent urination, especially at night
Stress incontinence: urinary leakage with pressure applied to the abdomen
Overflow incontinence: weak or intermittent stream or hesitancy

Answer 146

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

Answer 147

A

Avoiding caffeine, diuretics, and overfilling of the bladder
Avoid excessive or restricted fluid intake
Weight loss (if appropriate)
Supervised pelvic floor exercisesfor at least three months before considering surgery
Pessary - It is a firm ring that presses against the wall of the vagina and urethra to help decrease urine leakage.

In men after prostectomoy - use convenes

Answer 148

A

Decreased nutrient intake
Increased nutrient requirements
Inability to utilise ingested nutrients
Or combination of above

Answer 149

A

Environment/unable to cook for oneself
Meal times
Difficulty swallowing
Feeding problems
Appetite, apathy, anxiety
Pain
Medication
Radiotherapy

Answer 150

A

Acute infection/pyrexia
Inflammatory condition
Trauma
Liver disease
Wound healing
Surgery
Malignancy
Chronic infection (e.g. HIV)

Answer 151

A

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

Answer 152

A

‘Malnutrition Universal Screening Tool’ MUST

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

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

Answer 153

A

For those at high risk (score ≥2), intervention should start
immediately with dietetic input and close monitoring. Those at
medium risk (score 1) need to be monitored with food charts
for the first 3 days and then a decision is made about further
intervention

Answer 154

A

Definition
* Core temperature <35°C, but <35.5°C is probably abnormal
* Mild: 32–35°C; moderate: 30–32°C; severe: <30°C
* Fatality is high and correlates with severity of associated illness

Answer 155

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

Answer 156

A

grey complexion, with pallor and cyanosis
skin is cold to touch, both where exposed and where usually warm, for example the abdomen and axilla
confusion, drowsiness and stupor, with poor judgement
increased muscle tone, with rigidity at 32øC
shivering, until below 30øC
weakness
hypokinesia
ataxia, occasionally tremor
Initially vasoconstriction, hypertension, and tachycardia, Then myocardial suppression, hypotension, sinus bradycardia
Respiratory depression

Answer 157

A

A combination of the following modalities is usually sufficient:
* Passive external: surround with dry clothes and blankets/space
blankets
* Active external: hot air blanket (‘Bair HuggerTM’), hot water
bottle, bath
* Active internal: heated oxygen, fluid, and food
System support: maintain airway, ventilate as necessary. Good iv
access. Warm iv fluid: may need large volumes as warming causes
vasodilatation

Warm supplemental oxygen

Answer 158

A

Polypharmacy is defined as being prescribed more than four medications. Over one-third of older patients are affected.

Polypharmacy can result in:

r increased risk of side-effects
r increased risk of drug– drug interactions
r a therapeutic cascade (Figure 13.2)
r increased risk of medications not being reviewed thoroughly.
r non-adherence

Answer 159

A

A prescribing cascade refers to the sequence of events in which an adverse drug event is misinterpreted as a new medical condition, leading to the addition of another, potentially avoidable, medication

Answer 160

A

r changes in pharmacokinetics (what body does the to drug, think ADME)
r changes in pharmacodynamics (What the drug does to the body, inducing a response)
r polypharmacy
r frailty (see Chapter 5)
r communication problems
r lack of an evidence base
r guidelines being based on single-organ disease processes.

Answer 161

A

Rifampicin
Alcohol (chronic)
Phenytoin
Sulfonylureas (e.g. gliclazide)#

RAPS

Answer 162

A

Sodium valproate
Isoniazid
Carbamazepine

Macrolides
Alcohol (acute/binge)
Metronidazole

SIC MAM

Answer 163

A

The patients ability to make a decision about their care.

Answer 164

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 – an apparently unwise decision in itself does not prove incapacity

Best interests – all decisions taken on behalf of the person must be in their best interests

Least restrictive option – when deciding on another person’s behalf, chose the decision that interferes the least with the person’s rights and freedom of action while still achieving goal

Answer 165

A

Deprivation of Liberty Safeguards.

DOLS are part of the MCA, the safeguards aim to ensure that people in care homes or hospitals who lack capacity are looked after in a way that has their best interests at heart.

Answer 166

A

What are the patient’s past/present wishes or feelings relating to the decision?
What are the patient’s values and beliefs relating to the decision?
What are the risks/benefits of each option?
Consider other factors e.g. future implications and safety concerns.

Should be verified with consultee ie family member or friend

Answer 167

A

1 - is there impairment of or disturbance of function in a person’s brain or mind?

2 is the impairment sufficient to constitute a loss of capacity? 4 components

Answer 168

A

Can teh patient understand teh info required to make an decision - RECIEVE

Can they retain the info long enough to make a decision - RETAIN

Can they weigh up the info? RATIONALISE

Can they communicate the decision back RELATE BACK

4 Rs

Answer 169

A

An Advanced Decision, short for Advanced Decision to Refuse Treatment, is a legally binding document. Its purpose is to ensure that an individual can refuse a specific treatment(s) that they do not want to have in the future.

An Advance Statement is sometimes called a “Statement of Wishes and Care Preferences”. It allows an individual to make general statements about their wishes, beliefs, feelings and values and how these influence their preferences for their future care and treatment.

An Advance Statement is not by itself legally binding, but legally must be taken into consideration when making a “best interests” decision on someone’s behalf under the Mental Capacity Act (MCA), 2005. This is because one of the criteria of the MCA is that a patient’s “wishes, feelings, beliefs and values” must be taken into consideration; an Advanced Statement provides evidence of this.

Answer 170

A

The person is an adult, and
Was competent and fully informed when making the decision, and
The decision is clearly applicable to current circumstances, and
There is no reason to believe that they have since changed their mind

Answer 171

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

Answer 172

A

Commissioned from independent organisations by the NHS and local authorities to ensure that MCA is being followed
Role of IMCA: 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.

Answer 173

A

Pressure sores are wounds that develop when constant pressure or friction on one area of the body damages the skin. Constant pressure on an area of skin stops blood from flowing normally, so the cells die, and the skin breaks down

Answer 174

A

limited movement
r sensory impairment
r malnutrition
r dehydration
r obesity
r cognitive impairment
r urinary and faecal incontinence
r reduced tissue perfusion.

The Waterlow score is widely used to screen for patients who are at risk of developing pressure areas. It includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.

Answer 175

A

Pressure ulcers cause pain and predispose to infection, which can be life-threatening

Buttocks area (on the tailbone or hips)
Heels of the feet
Shoulder blades
Back of the head
Backs and sides of the knees

Answer 176

A

Stage 1. The area looks red and feels warm to the touch. With darker skin, the area may have a blue or purple tint. - Non blanching redness!!

Stage 2. The area looks more damaged and may have an open sore, scrape, or blister.

In both, The person complains of significant pain and the skin around the wound may be discolored.

Answer 177

A

Stage 3. The area has a crater-like appearance due to damage below the skin’s surface. Slough is often present

Stage 4. The area is severely damaged and a large wound is present. full thickness - Muscles, tendons, bones, and joints can be involved. Infection is a significant risk at this stage.

Answer 178

A

Barrier creams
Pressure redistribution and friction reduction (e.g. special foam mattresses, heel support, cushions)

Repositioning (every 6 hours in normal risk; every 4 hours in high risk)

Regular skin assessment - Check for areas of pain or discomfort
Skin integrity at pressure areas
Colour changes
Variations in heat, firmness and moisture (e.g. incontinence, oedema, dry, inflammed skin)hat ma

Answer 179

A

basal-cell carcinoma, squamous-cell carcinoma and melanoma

Cutaneous squamous-cell carcinoma is the second-most common cancer of the skin (after basal-cell carcinoma, but more common than melanoma)

Answer 180

A

high lexposure to UV radiation
Prior scars, chronic wounds,
actinic keratosis, - is a pre-cancerous area of thick, scaly, or crusty skin
having paler skin that sunburns easily,
Bowen’s disease,
radiation therapy,
tobacco smoking,
Prior basal cell carcinoma,
HPV infection
Immunotherapy

Answer 181

A

Bowen’s disease is essentially equivalent to and used interchangeably with cSCC in situ, when not having invaded through the basement membrane

Answer 182

A

SCC of the skin begins as a small nodule and as it enlarges the center becomes necrotic and sloughs and the nodule turns into an ulcer

Answer 183

A

Diagnose with Biopsy

removed with surgery. A few selected cases are treated with topical medication. Surgical excision with a free margin of healthy tissue is a frequent treatment modality. Radiotherapy, given as external beam radiotherapy or as brachytherapy (internal radiotherapy), can also be used to treat cSCC.

Answer 184

A

take more time - dont make them feel rushed!

Don’t rush or jump in, talk slowly,

use simple words, and chunk up info.
use gestures and illustrations
check they’ve understood at each step
Recgonise information fatigue , one step at a time,
Ask them what help them communicate effectively - take more time

Add NHS accessable info standard

Answer 185

A

Pain
Secretion
Destress
Breathlessness
Nausea

Answer 186

A

Morphine, for breathlessness and pain

Midazolam for agitation, sub cutanelously

Answer 187

A

Secretions - Hyoscine butylbromide (Buscopan)
Buscopan works by blocking the action of acetylcholine, a chemical that stimulates glands to produce secretions. (gets rid of death rattle when pt is too weak to clear mucous from throat or airway)

Nausea - Haloperidol

haloperidol is also good for hallucinations and paranoia

Answer 188

A

According to BNF conversion tables, 10 mg of oral morphine is equivalent to approximately 5 mg of morphine given parenterally.

Buprenorphine or fentanyl are the opioids of choice for pain relief in palliative care patients with severe renal impairment, as they are not renally excreted and therefore are less likely to cause toxicity than morphine

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