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Head And Neck > PBL 6 - Haematomas > Flashcards

PBL 6 - Haematomas Flashcards

1
Q

Which arteries supply the brain?

A

Vertebral arteries

Internal carotid arteries

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2
Q

Draw a diagram of the arterial blood supply of the brain.

A

See poster.

Include:

  1. Aortic arch and branches
  2. Internal carotid arteries
  3. Vertebral arteries
  4. Basilar artery
  5. Circle of Willis
  6. Posterior cerebral artery (and communicating)
  7. Middle cerebral artery
  8. Anterior cerebral artery (and communicating)
  9. Ophthalmic artery
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3
Q

What are the 4 branches of the vertebral arteries? These branch off before the vertebral arteries fuse to become the basilar artery.

A
  1. Meningeal branch
  2. Anterior spinal artery
  3. Posterior spinal artery (x2)
  4. Posterior inferior cerebellar artery (x2)
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4
Q

What are the 4 branches of the basilar artery?

A
  1. Anterior inferior cerebellar arteries (x2)
  2. Pontine arteries (several)
  3. Superior cerebellar arteries
  4. Posterior cerebral arteries (x2) - join circle of Willis
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5
Q

Where do the internal carotid arteries enter the cranial cavity?

A

Carotid canals

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6
Q

What are the 4 branches of the internal carotid arteries?

A
  1. Ophthalmic arteries
  2. Posterior communicating artery
  3. Middle cerebral arteries
  4. Anterior cerebral arteries
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7
Q

What is the venous drainage of the brain?

A
  1. Superior sagittal sinus
  2. Inferior sagittal sinus
  3. Straight sinus
  4. Transverse sinuses
  5. Sigmoid sinuses
  6. Cavernous sinuses
  7. Superior/inferior petrosal sinuses
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8
Q

What do venous sinuses of the brain drain into, and where does this exit the cranial cavity?

A

Internal jugular vein (via the sigmoid sinus)

Leaves cranial cavity via jugular foramen

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9
Q

Which 2 structures run through the cavernous sinuses?

A 
Internal carotid artery
Abducens nerve (CN 6)
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10
Q

Which 4 structures run through the walls of the cavernous sinuses?

A 
Oculomotor nerve (CN 3)
Trochlear nerve (CN 4)
Ophthalmic nerve (V1)
Maxillary nerve (V2)
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11
Q

Discuss the clinical significance of the cavernous sinuses.

A
  1. Receive venous drainage from emissary veins, which can carry infection into the brain
  2. Have many nerves etc. running through the walls of the sinuses, which can be damaged during inflammation of the sinuses
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12
Q

List the 4 folds of the cranial dura mater.

A

Falx cerebri
Tentorium cerebelli
Falx cerebelli
Diaphragma sellae

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13
Q

Describe the blood supply of the dura mater.

A

Anterior meningeal arteries
a. Origin: ethmoidal arteries

Middle and accessory meningeal arteries
a. Origin: maxillary artery

Posterior meningeal artery
a. Origin: ascending pharyngeal artery

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14
Q

What is the clinical significance of the middle meningeal artery?

A

Passes across the pterion - the very thin, easily fracture part of the skull where the frontal, parietal and temporal bones meet

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15
Q

Describe the pathway of the middle meningeal artery.

A
  1. Enters cranium via the foramen spinosum (lateral to the sella turcica)
  2. Divides into the anterior and posterior branches
    a. Anterior - passes vertical tot he vertex of the skull; passes over pterion
    b. Posterior - passes posterosuperiorly; supples region of middle cranial fossa
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16
Q

What are arachnoid granulations, and what is their function?

A

Growths of arachnoid mater into the venous sinuses (formed by arachnoid villi)

Function: reabsorption of CSF into venous blood

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17
Q

List the 12 cranial nerves.

A
  1. Olfactory
  2. Optic
  3. Oculomotor
  4. Trochlear
  5. Trigeminal
  6. Abducens
  7. Facial
  8. Vestibulocochlear
  9. Glossopharyngeal
  10. Vagus
  11. Spinal accessory
  12. Hypoglossal
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18
Q

For each cranial nerve, state whether their function is motor, sensory, or both.

A
  1. Sensory
  2. Sensory
  3. Motor
  4. Motor
  5. Both
  6. Motor
  7. Both
  8. Sensory
  9. Both
  10. Motor
  11. Motor
  12. Motor
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19
Q

What is the function of the trochlear nerve?

A

Superior oblique muscle (looks up and medial)

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20
Q

What is the function of the abducens nerve?

A

Lateral rectus muscle (looks lateral)

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21
Q

How do you test the function of the optic nerve?

A

Test 5 aspects of sight:

  1. Acuity
  2. Colour
  3. Fields
  4. Reflexes
  5. Fundoscopy
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22
Q

How do you test the function of the vestibulocochlear nerve?

A

Rinne’s test

Weber’s test

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23
Q

How do you test the function of the glosspharyngeal nerve?

A
  1. Test the gag reflex

2. Touch the arches of the pharynx

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24
Q

How do you test the function of the vagus nerve?

A
  1. Test pharyngeal muscles:
    a. Ask patient to speak - observe uvula while saying “aaah”
    b. Check that the uvula is central
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25
Q

How do you test the function of the spinal accessory nerve?

A
  1. Test the sternocleidomastoid

2. Test the trapezius

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26
Q

How do you test the function of the hypoglossal nerve?

A
  1. Observe tongue for muscle wasting or fasciculations
  2. Ask patient to stick their tongue out
    a. Deviation to one side indicates weak muscles on that side
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27
Q

What is the difference between primary and secondary brain injuries?

Give some examples of each.

A

PRIMARY: immediate response to initial injury
Examples:
—Focal lesions (contusion, haemorrhage)
—Diffuse injuries (concussion, diffuse axonal injury)

SECONDARY: processes resulting from initial injury
Examples:
---Brain oedema
---Infection
---Ischaemia
28
Q

List different types of brain injury.

A

Focal:

  1. Scalp lesions
  2. Skull fractures
  3. Intracranial bleeds/space occupying lesions
    a. Contusions
    b. Extradural haematoma
    c. Subdural haematoma
    d. Subarachnoid haematoma
  4. Intracerebral haematoma

Diffuse:

  1. Concussion
  2. Diffuse axonal injury
  3. Diffuse vascular injury
29
Q

What are the consequences of contusions?

A
  1. Depends on size/location/related cerebral oedema
  2. Subarachnoid haematoma
  3. Cognitive defects
  4. Motor defects
  5. Secondary brain injury, e.g.
    a. Brain oedema
    b. Increased IC pressure
30
Q

What are the causes of extradural haematomas?

A
  1. Arterial bleeding (usually middle meningeal artery)

2. Skull fracture

31
Q

Describe the pathophysiology of extradural haematomas.

A
  1. Arterial bleeding causes rapid expansion of the extradural haematoma
  2. This causes compression of the brain
  3. This may cause brain herniation:
    a. Midline shift
    b. Cerebral hemisphere forced through tentorium cerebelli
    c. Cerebellum forced through tentorium cerebelli (this compresses the brainstem)
32
Q

Describe the appearance of the following on CT imaging:

a) Extradural haematoma
b) Subdural haematoma
c) Subarachnoid haematoma

A

Extradural haematoma - lens shaped

Subdural haematoma - crescent shaped

Subarachnoid haematoma - following the sulci/gyri of the brain

33
Q

What are the clinical features of an extradural haematoma?

A
  1. Brief period of unconsciousness
  2. Lucid period
  3. Rapid deterioration
  4. Focal symptoms relating to damaged area of brain, e.g.
    a. Ipsilateral pupil dilation
    b. Contralateral hemiparesis
  5. Increased ICP
34
Q

What are subdural haematomas caused by?

A
  1. Venous bleeding
35
Q

Describe the classification of subdural haematomas.

A

Acute - symptoms within 24 hours of injury

Subacute - symptoms within 2-10 days of injury

Chronic - symptoms seen several weeks after injury

36
Q

Describe the pathophysiology of subdural haematoma.

A
  1. Venous bleeding causes slow expansion of the haematoma
  2. Subdural haematoma is more common in older people due to:
    a. Brian shrinking - this stretches the veins
    b. Encapsulation of haematoma - due to fibroblast activity
    c. Collection of fluid exerts osmotic pressure, drawing fluid from the subarachnoid space
37
Q

Describe the clinical features of subdural haematomas.

Consider differences between acute and chronic subdural haematomas.

A
  1. Slow onset
  2. Acute subdural:
    a. More rapid
    b. Severe oedema
    c. Uncontrollably high ICP
    d. Loss of consciousness
    e. Decerebrate posturing
    f. Usually no lucid period
  3. Chronic subdural:
    a. Decreased consciousness level
    b. Drowsiness
    c. Confusion
    d. Headache
    e. Apathy
38
Q

What are the clinical features of subarachnoid haematomas?

A
  1. Slow onset

2. Similar to subdural haematoma

39
Q

Define concussion.

A

A temporary disturbance in brain function as a result of trauma

40
Q

Describe the clinical features of concussion.

A
  1. Headache
  2. Possible loss of consciousness
  3. Retrograde amnesia
  4. Anterograde amnesia
  5. Irritability
  6. Insomnia
  7. Poor concentration/memory
41
Q

Describe the complications of concussion.

A
  1. Chronic traumatic encephalopathy
    a. “A progressive degenerative disease of the brain caused by repetitive brain trauma”
    b. Clinical features:
    - –Loss of executive function
    - –Poor memory
    - –Alzheimer-like symptoms
  2. Second impact syndrome
    a. “Rapid and severe brain swelling with often catastrophic results, caused by a second concussion occurring before a first one has properly healed”
    b. Clinical features:
    - –Cerebral congestion and oedema
    - –Death
42
Q

Define diffuse axonal injury.

A

A brain injury in which damage is in the form of extensive lesions in white matter tracts, occurring over a widespread area

43
Q

Describe the pathophysiology of diffuse axonal injury.

A
  1. Shearing forces on axons make them change character to become brittle
  2. The force of trauma makes them snap
  3. Further axon damage:
    a. Release of excitatory neurotransmitters - excitotoxicity
    b. Axon stretching - axons snap
44
Q

Define diffuse vascular injury.

A

A brain injury in which there are many small haemorrhages

45
Q

Describe the clinical features of diffuse vascular injury.

A
  1. Death (DVI is incompatible with life)
46
Q

Describe the 4 main mechanisms of brain injury.

A
  1. Hypoxia
  2. Ischaemia
  3. Oedema
  4. Increased intracranial pressure
47
Q

What’s the difference between hypoxia and ischaemia?

A

Hypoxia - “deprivation of oxygen with maintained blood flow”

Ischaemia - “deprivation of oxygen due to interrupted or greatly reduced blood flow”

48
Q

List the clinical features of hypoxia.

Differentiate between chronic and acute hypoxia.

A

Chronic hypoxia:

  1. Fairly well tolerated
  2. Listlessness
  3. Drowsiness
  4. Impaired problem solving

Sudden and severe hypoxia:

  1. Unconscioiusness
  2. Convulsions
  3. Cardiac arrest
  4. Ischaemia
49
Q

Describe the pathophysiology of ischaemia.

A
  1. Decreased blood flow means insufficient oxygen and glucose is delivered to the brain
  2. Waste products are not removed from the brain
  3. Laminar necrosis occurs - short, creeping segments of necrosis within and parallel to the cerebral cortex
  4. Consequences of ischaemia:
    a. Excitotoxicity
    b. Free radical formation
    c. Mitochondrial injury
    d. Activation of apoptosis
50
Q

Describe the clinical features of ischaemia.

A
  1. Infarction of brain tissue
  2. Diffuse brain dysfunction
  3. Unconsciousness (within seconds)
  4. Death
51
Q

Which areas of the brain are most vulnerable to ischaemia?

A

Watershed areas, i.e. on the border between areas of blood supply

52
Q

In what sort of conditions will the brain be damaged by excitatory neurotransmitter release?

A
  1. Stroke
  2. Hypoglycaemic injury
  3. Trauma
  4. Chronic degenerative disorders
53
Q

Describe the pathophysiology of excitotoxicity due to ischaemia.

A
  1. In prolonged ischaemia, metabolic depletion of ATP causes the release of glutamate
  2. Glutamate causes influx of Ca2+ into brain cells (via NMDA channels)
  3. Excess intracellular Ca2+ activates the calcium cascade, which causes:
    a. Release of intracellular enzymes causing protein breakdown
    b. Free radical formation
    c. Lipid peroxidation
    d. DNA fragmentation
    e. Mitochondrial injury
    f. Nuclear breakdown
    g. Cell death
54
Q

What are the 2 types of cerebral oedema? What causes each of these?

A
  1. Vasogenic
    a. Blood-brain barrier dysfunction allows water/proteins to move into the interstitial space from the blood)
  2. Cytotoxic
    a. Increased intracellular fluid volume, e.g. due to:
    - –Dysfunction of the Na+/K+ ATPase pump
    - –Build up of lactic acid (causing extracellular acidosis)
    b. Rupture of cells due to cellular oedema
55
Q

What are the clinical features of the 2 types of cerebral oedema?

A

VASOGENIC:

  1. Focal neurogenic deficits
  2. Loss of consciousness
  3. Severely increased ICP

CYTOTOXIC:

  1. Cerebral dysfunction (e.g. coma, stupor)
  2. Cerebral infarction (e.g. necrosis)
56
Q

What is ICP? State its normal value.

A

“Pressure inside the cranium”

Normal ICP: 0-10 mmHg

57
Q

Describe the Monroe-Kellie hypothesis of ICP.

A
  1. There are 3 components of the cranium: blood, brain tissue, CSF
  2. A small increase in the volume of one component can be compensated for by decrease in volume of one/both of the others
  3. BUT this only allows for 120ml compensation
58
Q

How does the brain compensate for small increases in ICP?

A
  1. CSF is shifted to the spinal subarachnoid space via the foramen magnum
  2. Increased reabsorption of CSF
  3. Venous blood is shunted out of the brain
    a. Increased venous pressure
    b. Decreased cerebral blood volume
    c. Decreased ICP
59
Q

What is the cerebral perfusion pressure? State its normal value.

How is it measured?

A

CPP is the measure of blood perfusion to the brain, i.e. gradient between internal carotid artery pressure and subarachnoid vein pressure

Normal CPP: 70-100 mmHg

CPP = MAP - ICP

60
Q

What is the clinical significance of the CPP?

A

When the ICP becomes equal to or higher than the CPP, tissue perfusion becomes inadequate

This causes cellular hypoxia and neuronal death

61
Q

Describe the clinical features of increased ICP.

A
  1. Decreased consciousness
  2. General neurological deterioration
  3. Confusion
  4. Lethargy
  5. Obtundation
  6. Stupor
  7. Coma
62
Q

Describe the consequences of raised ICP.

A

HERNIATION

  1. Cerebral hemisphere is forced through the falx cerebri (cingulate herniation)
    a. Midline shift
    b. Ischaemia
    c. Cerebral oedema
  2. Cerebral hemispheres forced through tentorial notch of tentorium cerebelli
    a. This causes compression of the oculomotor nerve (fixed pupil dilation and eye paralysis)
  3. Pons is herniated
    a. Motor dysfunction
    b. Changes in consciousness
    c. Coma
  4. Medulla is herniated
    a. Respiratory effects and arrhythmias
    b. Decerebrate posturing
    c. Flaccidity
    d. Death

HYDROCEPHALUS

  1. Headache
  2. Vomiting
  3. May progress to herniation
  4. Seizures
63
Q

Define seizure.

A

A sudden surge of electrical activity in the brain

64
Q

Describe the Glasgow Coma Scale (GCS).

A

Eye opening (E)

  • –Spontaneous: 4
  • –To call: 3
  • –To pain: 2
  • –None: 1

Motor response (M)

  • –Obeys commands: 6
  • –Localises to pain: 5
  • –Normal flexion (withdrawal): 4
  • –Abnormal flexion (decorticate): 3
  • –Extension (decerebrate): 2
  • –None (flaccid): 1

Verbal response (V)

  • –Orientated in person/space/time: 5
  • –Confused conversation: 4
  • –Inappropriate words: 3
  • –Incomprehensible words/sounds: 2
  • –None: 1
65
Q

Discuss the use of GCS to classify brain injuries.

A

Mild: GCS 15
Moderate: GCS 9-12
Severe: GCS

66
Q

Describe the ischaemic cascade.

A
  1. Loss of blood supply creates loss of oxygen
    a. Therefore neurons can’t make enough ATP through aerobic respiration
  2. Neurons undergo anaerobic respiration
    a. This results in lactic acid build up, which disrupts the acid-base balance
    - –This damage neurons
    b. This also produces less energy
  3. Therefore the Na+/K+ ATPase cannot work
    a. Therefore Na+ builds up in the neuron, creating a high concentration
    b. This draws in H2O from the extracellular fluid
    c. This causes cytotoxic oedema
  4. The Na+/Ca2+ ATPase also can’t work
    a. Therefore Ca2+ builds up inside neuron
    b. This causes excitotoxicity
    - –Due to glutamate release
    c. This also causes activation of enzymes
    - –Lipases break down neuron’s cell membrane
    d. This also causes production of free radicals and ROS
    - –Neuron damage
  5. Build up of harmful chemicals causes damage to mitochondria of neuron
    a. Damaged mitochondria release apoptotic factors

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