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CBL Year 2 > Headache > Flashcards

Headache Flashcards

1
Q

Which reflex regulates MAP by adjusting cardiac output and total peripheral resistance

A

baroreceptor reflex

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2
Q

if a patient has a blood pressure of 120/80 how would you estimate their MAP

A

MAP = 1/3 pulse pressure + diastolic pressure
1/3 (120-80) +80
13.3 +80
93.3 mmHg

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3
Q

what does CPP stand for

A

cerebral perfusion pressure

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4
Q

what does ICP stand for

A

intracranial pressure

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5
Q

how is ICP measured

A

by inserting a pressure transducer into brain parenchyma or a catheter into the lateral ventricle

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6
Q

what can a fall in cerebral perfusion pressure lead to

A

can result in cerebral ischaemia and eventually neuronal death

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7
Q

how is intracranial pressure measured

A

by inserting a pressure transducer into the brain parenchyma or a catheter into the lateral ventricle

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8
Q

what does the munro Kellie doctrine state

A

is that the sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two.

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9
Q

Some examples of the blood brain barrier and diseases that can affect it

A

eclampsia - makes the membrane more permeable and so results in pulmonary oedema
Meningitis - makes it more permeable to toxins and some antibiotics
HIV virus - thought to cross the barrier by hiding in monocytes to cause encephalitis

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10
Q

equation for CPP (Cerebral perfusion pressure)

A 
CPP = MAP - ICP 
MAP = 1/3 pulse pressure + diastolic
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11
Q

in the context of trauma what can a decrease in MAP and increase in ICP result in

A

a catastrophic decrease in CPP

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12
Q

relationship between hyper/hypocapnia and cerebral perfusion

A

Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF.

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13
Q

what is the cerebral metabolic rate

A

The cerebral metabolic rate of oxygen (CMRO2) is the rate of oxygen consumption by the brain, and is thought to be a direct index of energy homeostasis and brain health.

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14
Q

What is autoregulation and how does it affect cerebral blood flow and ICP?

A

Autoregulation of cerebral blood flow is the ability of the brain to maintain relatively constant blood flow despite changes in perfusion pressure

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15
Q

how does a headache occur (nerves)

A

The headache occurs when the 5th cranial (trigeminal) nerve is stimulated. This nerve sends impulses (including pain impulses) from the eyes, scalp, forehead, upper eyelids, mouth, and jaw to the brain.

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16
Q

cerebral venous thrombosis (in terms of headache)

A

Cerebral venous thrombosis (CVT) is an uncommon cerebrovascular disease presenting with a remarkably wide spectrum of signs and mode of onset. In all series, headache is the most frequently occurring symptom at any time, present in over 80% of cases,1 and it is also the commonest initial symptom.

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17
Q

what is anopsia (aka anopia)

A

also known as blindness, is the absence of vision due to either a structural defect of the eye(s) or the lack of the eye(s) completely.

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18
Q

what is a scotoma

A

a partial loss of vision or blind spot in an otherwise normal visual field.

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19
Q

what does it mean if pupils are equal and reactive to light

A

that shining a light into the eye causes constriction of the ipsilateral pupil (direct reflex) and of the contralateral pupil (consensual reflex)

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20
Q

where is CSF produced

A

produced by the choroid plexus mainly in the lateral ventricles of the brain
(around 500mls a day)

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21
Q

composition of CSF

A

few cells

lower protein and glucose concentrations than in plasma

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22
Q

Brief description of CSF fluid flow

A
  • through foramen of munro to third ventricle
  • through aqueduct of Slyvius to the fourth ventricle
  • through foramina of Luschka (lateral) and foramen of Magendie (midline) into the cisterna magna behind medulla and under the cerebellum
  • Cisterna magna is continuous with subarachnoid space
  • CSF flows upward over the brain and is reabsorbed by arachnoid granulations into venous sinus blood
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23
Q

Cushioning function of the CSF

A

brain and CSF have almost identical specific gravity
brain floats and is cushioned by CSF
minor blows to head cause skull and brain to move simultaneously so it doesn’t get bashed against a hard surface

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24
Q

metabolic function of CSF

A
  • helps ,maintain a constant environment for brain cells
  • drains unwanted metabolites from venous blood
  • transports hormones from one side of the brain to the other
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25
Q

three (basic) causes of increased ICP

A
  • Increase in brain volume : localised space occupying lesion (tumour, abscess), generalised brain oedema (hyponatremia, hypertensive encephalopathy)
  • increase in blood volume: Intracerebral, subdural bleeding, vasodilation due to hypercapnia, decreased venous draining due to thrombosis , cough, head down tilt
  • increase in CSF volume: hydrocephalus, meningitis
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26
Q

describe idiopathic intracranial hypertension

A
  • cause unknown
  • headaches worse on coughing or sneezing
  • examination is normal apart from papilloedema
  • refer to neurologist
  • requires CT/MRI to exclude other causes of increase ICP
  • lumbar puncture to measure opening pressure
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27
Q

brief description of hydrocephalus

what is non communicating due to? what is communicating due to?

A
  • accumulation of CSF resulting in an increase in ICP
  • Non communicating would be due to blockage somewhere between foramen of munro and foramina of Luschka and Magendie
  • communicating would be due to failure to drain via the arachnoid granulations
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28
Q

features indicating rising ICP

A
  • headache due to stretch receptors and nociceptors around intracranial vessels and with the dura mater, worse in the morning
  • nausea and vomiting due to pressure on vomiting centres in brain stem
  • visual disturbances due to raised pressure around the optic nerve
  • seizure
  • decreased level of consciousness from drowsy to eventual deep coma
  • abnormal posturing ( decorticate and decerebrate)
  • Cushing response
  • Brain death when ICP exceed CPP
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29
Q

what is papilloedema

A

Papilledema is swelling of your optic nerve, which connects the eye and brain. This swelling is a reaction to a buildup of pressure in or around your brain that may have many causes.

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30
Q

Describe oculomotor palsy (CNIII)

A

A complete third nerve palsy causes a completely closed eyelid and deviation of the eye outward and downward. The eye cannot move inward or up, and the pupil is typically enlarged and does not react normally to light.

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31
Q

what does uncal herniation cause/what is it

A

herniation of part of the temporal lobe over the tentorium cerebelli and it causes ipsilateral CN III (oculomotor) palsy and a blown pupil

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32
Q

warning with doing a lumbar puncture in ICP

A

do not perform an LP in a patient with raised ICP unless they have idiopathic intracranial pressuree

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33
Q

describe decorticate posturing

A

indicates severe brain injury
flexor response spontaneously or in response to pain
M3 on glasgow coma scale
damage to upper midbrain
an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight.

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34
Q

describe decerebrate posturing

A

indicates severe brain injury
extensor response spontaneously or in response to pain
M2 on Glasgow coma scale
damage to upper pons

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35
Q

describe Cushing response/ reflex

A
  • attempts to raise MAP to increase CPP and CBF
  • triggered by brainstem ischaemia due to increase in ICP
  • indicates that death may be imminent unless ICP reduced
  • sympathetic activation causes a rise in TPR and hence increase in MAP and systolic pressure
  • In response to increase in MAP the baroreceptor reflex causes a bradycardia through increased vagal parasympathetic tone
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36
Q

Cushings triad (in context of a head trauma)

A
  • Decreased heart rate
  • increased systolic blood pressure
  • disordered breathing pattern with pattern of alternating apnoea and sighing

-get immediate senior help from anaesthetist, intensivist and neurosurgeon to decrease ICP

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37
Q

what is mononuclear vision loss and where is the lesion located

A

Loss of vision in one eye

Lesion is in optic nerve (right after the eye)

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38
Q

what is bitemporal hemianopia and where is the lesion located

A

visual loss of half in both eyes
For example: loss of left half in left eye and right half in right eye
lesion is in the optic chiasm - where the optic nerves meet

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39
Q

what is contralateral hemianopia and where is the lesion located

A

visual loss of half in both eyes
for example: loss of half left in left eye and half left in right eye
lesion can be in the optic tract ( after optic chiasm) or optic radiations

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40
Q

another name for idiopathic intracranial pressure

A

pseudotumour cerebri

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41
Q

difference between intracranial and intracerebral

A

The former refers to all bleeding occurring within the skull, while the latter indicates bleeding within the brain parenchyma.

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42
Q

difference between extradural, subdural and subarachnoid

A

extradural is on the outside of the natural covering of the brain (‘dura mater’)
subdural is on the inner surface of the dura
subarachnoid is under the arachnoid layer

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43
Q

stroke vs infarct

A

stroke is the sudden onset neurological onset whereas an infarct is what causes the stroke

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44
Q

what is an incidentaloma

A

victim of medical imaging technology

find something even when not looking for it

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45
Q

Saccular (berry) aneurysm

A

Berry (saccular) aneurysms are the most common type of intracranial aneurysm, representing 90% of cerebral aneurysms. Generally speaking, there is a ballooning arising from a weakened area in the wall of a blood vessel in the brain.

Saccular aneurysms are rounded berrylike outpouchings that arise from arterial bifurcation points, most commonly in the circle of Willis

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46
Q

Charcot-Bouchard aneurysm

A

Charcot-Bouchard aneurysms are minute aneurysms (microaneurysms) in the brain that occur in small penetrating blood vessels with a diameter that is less than 300 micrometers. The most common vessels involved are the lenticulostriate branches (LSA) of the middle cerebral artery (MCA).

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47
Q

examples of a intraparenchymal haemorrhage

A

stroke

contusion

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48
Q

clinical features of an intraparenchymal haemorrhage

A

Non-traumatic intraparenchymal hemorrhages typically present with a history of sudden onset of stroke symptoms including a headache, nausea, vomiting, focal neurologic deficits, lethargy, weakness, slurred speech, syncope, vertigo, or changes in sensation

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49
Q

clinical features of subarachnoid hemorrhage

A

A subarachnoid hemorrhage is bleeding in the space between your brain and the surrounding membrane (subarachnoid space). The primary symptom is a sudden, severe headache. The headache is sometimes associated with nausea, vomiting and a brief loss of consciousness.

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50
Q

clinical features of a subdural haemotoma

A 
Headache that doesn't go away. ...
Confusion and drowsiness.
Nausea and vomiting.
Slurred speech and changes in vision.
Dizziness, loss of balance, difficulty walking.
Weakness on one side of the body.
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51
Q

pathophysiology of a subdural haematoma

A

Bleeding in a SDH occurs from tearing of the bridging veins that cross from the cortex to the dural venous sinuses, which are vulnerable to deceleration injury. This subsequently leads to accumulation of blood between the dura and arachnoid and results in a gradual rise in intracranial pressure (ICP).

looks like a crescent shape on a CT

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52
Q

clinical features of a Extradural haematoma

A

typical symptoms of EDH include headache, nausea/vomiting, confusion and reduced level of consciousness. Typical clinical signs of EDH include confusion, cranial nerve deficits, motor or sensory deficits of the limbs, hyperreflexia, spasticity, upgoing plantar reflex and Cushing’s triad

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53
Q

pathophysiology of extradural haematoma

A

As the volume of blood leaking from the damaged blood vessel into the extradural space increases, it begins to strip the outer layer of the meninges, the dura mater, away from the skull. This often leads to the lemon-shaped haematoma, which is visible on CT and MRI imaging

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54
Q

clinical features of concussion

A

headache or “pressure” in head.
Nausea or vomiting.
Balance problems or dizziness, or double or blurry vision.
Bothered by light or noise.
Feeling sluggish, hazy, foggy, or groggy.
Confusion, or concentration or memory problems.
Just not “feeling right,” or “feeling down”.

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55
Q

clinical features of cerebral brain thrombosis

A

Patients with cerebral venous thrombosis (CVT) present with a remarkably wide spectrum of signs and symptoms. Most common are headaches (> 80%), seizures (approximately 40%), hemiparesis (approximately 40%), altered consciousness (15-20%), and papilledema (20-30%) [1–3].

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56
Q

what causes cerebral brain thrombosis

A

Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome. Obesity. Low blood pressure in the brain (intracranial hypotension) Inflammatory bowel disease like Crohn’s disease or ulcerative colitis.

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57
Q

define meningism

A

irritation of the meninges

-typically causes neck stiffness, photophobia and headache

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58
Q

define meningitis (presents with, caused by, which one is fatal)

A

inflammation of the meninges

  • typically presents with fever, headache and meningism
  • can be caused by bacteria, virus, fungi, parasites, non infective causes
  • bacterial meningitis is fatal
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59
Q

define encephalitis

A

inflammation fo the brain parenchyma

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60
Q

what is meningio-encephalitis

A

inflammation of the brain substances and parenchyma

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61
Q

what is a cerebral abscess

A

focal collection within the brain parenchyma, which can arise as a complication of a variety of infections, trauma or surgery

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62
Q

what are the meninges

A

three connective tissue membranes that ensheath the CNS

  • dura mater
  • arachnoid mater
  • pia mater
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63
Q

2 functions of the meninges

A
  • provide a support framework for the cerebral and cranial vasculature
  • acting with CSF to protect CNS from mechanical damage
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64
Q

viral CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)

A 
appearance - usually clear/turbid
opening pressure - normal
WBC - high, usually high lymphocyte
glucose - high glucose
protein - high
microbiology - usually sterile
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65
Q

bacterial CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)

A 
appearance - turbid/purulent
opening pressure - normal/elevated
WBC - high, mainly polymorphs
glucose - low
protein - high
microbiology - organism on gram stain
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66
Q

tuberculosis CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)

A 
appearance - turbid/viscous
opening pressure - normal/elevated
WBC - high, mainly lymphocytes
glucose - low
protein - high 
microbiology - positive Ziehls - Nielson stain
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67
Q

subarachnoid haemorrhage CSF analysis (appearance, opening pressure, WBC count, glucose, protein, microbiology)

A 
appearance - blood stained (yellow)
opening pressure - elevated
WBC - normal/slightly increased
glucose - normal
protein - increased
microbiology - sterile
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68
Q

effects of meningitis

A
  • disrupts blood brain barrier
  • increases entry of water soluble antibiotics
  • raised ICP
  • cerebral oedema
  • increased CPP
  • can lead to CSF obstruction and hydrocephalus
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69
Q

most common causes of meningitis in the UK

A

Neisseria Meningitidis

Streptococcus pnuemoniae

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70
Q

risk factors for community acquired meningitis

A
  • > 65 age
  • splenectomy
  • complement deficiency
  • alcohol excess
  • HIV
  • diabetes mellitus
  • travel to endemic areas (Africa, Mecca)
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71
Q

two physically demonstrable symptoms of meningitis.

A

Kernig sign: Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.
Brudzinski’s sign: Position the patients supine and passively flex their neck. This test is positive if this manoeuvre causes reflex flexion of the hip and knee.

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72
Q

contraindications to a lumbar puncture

A
  • signs suggestive of raised ICP
  • shock
  • extensive or spreading purpura
  • after convulsions stabilised
  • clotting abnormalities
  • local superficial infection at site of LP
  • respiratory insufficiency
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73
Q

signs of raised ICP

A
  • reduced or fluctuating levels of consciousness
  • relative bradycardia and hypertension
  • focal neurological signs
  • abnormal posture or posturing
  • unequal, dilated, or poorly responsive pupils
  • abnormal “dolls eye” movement
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74
Q

where is LP preferentially performed

A

L4,5 or L3,4

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75
Q

what do you treat suspicion of meningiococcal infection with

A

benzylpenicillin or ceftriaxone

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76
Q

at what age is a meningiococcoal infection highest

A

<5 years or 15-19

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77
Q

bacterial meningitis symptoms

A
  • fever
  • headache(typically over hours)
  • rash (peticheal/blotchy)
  • neck stiffness
  • confusion
  • vomiting
  • shock
78
Q

glass test

A

for meningitis
Press the side of a clear glass firmly against the skin.
Spots/rash may fade at first.
Keep checking.
Fever with spots/rash that do not fade under pressure is a medical emergency.
Do not wait for a rash. If someone is ill and getting worse, get medical help immediately.

79
Q

what to give neonates in bacterial meningitis

A

cefotaxime plus amoxicillin

80
Q

what to give children over 3 months in bacterial meningitis

A

cefotaxine or ceftriazone

81
Q

what to give adults (18-60) in bacterial meningitis

A

cefotaxime or ceftriazone

82
Q

what to give adults over 60 in bacterial meningitis

A

ceftotaxime or ceftriazone
PLUS
amoxicillin or ampicillin

83
Q

acute complications of meningitis

A

septic shock
subdural empyema
seizures
cerebral venous sinus thrombosis

84
Q

chronic complications of meningitis

A 
deafness - especially in children
learning difficulties
behavioural problems 
epilepsy
visual disturbances
85
Q

follow up for probable or confirmed bacterial meningitis

A

should be followed up within 6 weeks of hospital discharge

86
Q

brief description of viral meningitis

(what percentage of cases does it cause? what viruses cause it? is meningism present? symptoms?

A
  • causes 50-80% of cases
  • enterovirus and herpesvirus (herpes simplex and varicella zoster), HIV
  • mild onset
  • meningsm less prominent
  • fever not always present
  • rash in varicella zoster and genital ulcers in herpes simplex
  • non specific symptoms
87
Q

Herpes simplex encephalitis description

affects what lobe
what do you treat it with

A

neurological emergency
affects temporal lobe
treat with IV acyclovir

88
Q

pathogenesis of cerebral abscesses (direct, haematogenous, other)

A

direct spread: ears, sinuses, dental infections (single abscesses)
haematogenous: bacteraemia associated brain abscesses (multiple abscesses)
following penetrating trauma or neurosurgery

89
Q

conditions that can lead to bacteraemia associated brain abscesses (haematogenous causes)

A

infective endocarditis
lung abscess, empyema
pelvic infections
pulmonary aterio-venous malformations

90
Q

clinical features of cerebral abscesses

A 
headache
fever
confusion
seizure
focal neurology
91
Q

how to diagnose a cerebral abscess

A

CT/MRI brain, aspiration/drainage of abscess and send for microscopy, culture and sensitivity (MC&S), echocardiogram
LP is contraindicated in patients with focal neurology signs/symptoms

92
Q

treatment of a cerebral abscess

A

surgical drainage of the abscess
empirical antibiotic treatment
treatment duration (4-6 weeks)

93
Q

Key infections to be aware of in HIV patients with a low CD4 count (4 things)

A

cryptococcal meningitis (fungal meningitis)
cerebral toxoplasmosis (causes cerebral abscesses)
tuberculosis
progressive multifocal leukoencephalopathy (destroys cells that produce myelin)

94
Q

How to diagnose tuberculoma (radiograph)

A

discrete enhancing lesions of the brain surrounded by oedema (can be single or multiple)

95
Q

how to diagnose tuberculoma (CSF)

A

if no evidence of raised ICP

  • very high protein and normal glucose with pleocytosis
  • acid fast bacilli (AFB) on Ziehl-Neelsen stain and culture
96
Q

how do diagnose cerebral malaria

A

thick and thin blood films x 3
rapid diagnostic tests
FBC (platelets), LFTs, BM

97
Q

what is acute rhinosinusitis

A

symptomatic inflammation of the nasal cavity and paranasal sinuses

98
Q

most common cause of acute rhinosinusitis

A

viral infection

99
Q

viral sinusitis (when does it resolve, treatment)

A

resolves in 7-10 days

treatment: analgesia, intranasal glucocorticoids

100
Q

symptoms of acute rhinosinusitis

A

frontal headache and nasal symptoms PLUS at least 2 of:

  • nasal blockage
  • rhinorrhea/discharge
  • loss of smell
  • facial pressure/tenderness
101
Q

three key clinical features of meningitis

A

fever, headache and neck stiffness

102
Q

describe features of a migraine

A 
bad headache
nausea
photophobia
phonophobia (sound)
osmophobia (odours)
lasts 3-72 hours 
women > men
103
Q

describe features of a cluster headache

A 
severe side locked headache
lasts 30-90 mins
unilateral tearing
unilateral red eye
unilateral nasal stuffiness
pain behaviour
circadian
circannual
men more likely than women
104
Q

describe features of temporal arteritis (giant cell arteritis)

A 
age > 50 years
tender scalp
thick, ropey temporal arteries
fever
weight loss
night sweats
raised inflammatory markers
likely to go blind
steroid and biopsy asap
105
Q

describe features of acute glaucoma

A 
headache 
vomiting
eye pain
rock hard eye
blurred vision
mild dilated pupil
get optician to measure eye pressure
106
Q

features of a tension headache

A

most common type of primary headache

mild, featureless headache

107
Q

features of analgesic headache

A

painkillers (particularly opiates) can transform episodic migraines into chronic featureless dull headache
avoid paracetamol or NSAIDs more than 15 days/month
avoid opiates, analgesic compounds more than 10 days/month

108
Q

features of trigeminal neuralgia

A

Episodes of severe, shooting or jabbing pain that may feel like an electric shock. Spontaneous attacks of pain or attacks triggered by things such as touching the face, chewing, speaking or brushing teeth. Attacks of pain lasting from a few seconds to several minutes. Pain that occurs with facial spasms.

109
Q

some common things headache might be due to

A 
dehydration
alcohol - hangover
influenza
high altitude
high pressure
hyponatraemia
110
Q

what can you test for when you do a lumbar puncture?

A 
opening pressure
microscopy, culture and sensitivity (MC&S)
viruses (PCR)
protein
glucose (paired serum)
oligoclonal bands (paired serum)
flow cytometry
cytology
neurodegenerative biomarkers
111
Q

why would you test flow cytometry when doing a lumbar puncture

A

checks for haematological cancer

112
Q

why would you test raised lactate when doing a lumbar puncture

A

for mitochondrial disease

113
Q

diagnostic indications for a lumbar puncture

A

suspected neurological infection
suspected subarachnoid haemorrhage
suspected neuroinflammatory disease
suspected CNS malignancy

114
Q

therapeutic indications for a lumbar puncture

A

suspected raised intracranial pressure secondary to IIH

intrathecal administration of drugs (methotrexate)

115
Q

complications of a lumbar puncture

A

post LP headache (reduced with atraumatic / non cutting needle)
pain
bleeding (spinal haematoma)
infection
damage to surrounding structures
cerebral herniation (only in cases on raised ICP but. not IIH)
failure of procedure

116
Q

anatomical landmarks for an LP

A

left lateral position
between L3/4 or L4/5
line between both posterior superior iliac crests
go in at a 15 degree angle (aim to hit umbilicus)

117
Q

what anatomical landmarks makes the pop sound when performing an LP

A

ligamentum flavum

only push 1/2 cm in further to obtain CSF

118
Q

in bad cases of IIH what would be done after multiple LPs

A

shunting

119
Q

describe multiple sclerosis

A
  • demyelinating autoimmune disease
  • damage to the insulating cover of nerve cells of brain and spinal cord
  • characterised by: lesions “plaques” in the CNS, inflammation, destruction of myelin sheaths of neurons
120
Q

how to diagnose MS

A

clinical presentation alone (If 2+ relapses and signs)
clinical presentation and MRI
clinical presentation and CSF

121
Q

what would you see in the CSF of someone with MS

A

oligoclonal bands of IgG on electrophoresis

122
Q

2 most common organisms that cause meningitis

A

neisseria meningitidis

streptococcus pnuemoniae

123
Q

why is CSF examined in a subarachnoid haemorrhage

A

RBC (must be high in all tubes to distinguish from trauma)

xanthochromia (presence of bilirubin)

124
Q

xanthochromia and subarachnoid haemorrhage

A

can be seen in patients with jaundice, high CSF protein or carotene addiction

125
Q

3 headaches in the context of domestic violence

A

tension headache
migraine
traumatic brain injury

126
Q

what do you typically treat tension headaches with (generally speaking)

A

analgesics/ tricyclics

127
Q

what do you typically treat migraines with

A 
analgesics
triptans
amitriptyline 
topiramate
propranolol
candesartan
128
Q

what do you typically treat cluster headaches with

A

sumatriptan
oxygen
verapamil
lithium

129
Q

what do you typically treat trigeminal neuralgia with

A

carbamezapine

130
Q

stepwise approach to migraine treatment

A

Step 1 : over the counter analgesics, NSAIDs
step 2: Triptans
Step 3: combination treatment of triptans with NSAIDs +/- antiemetic (prochlorperazine, metoclopramide)

131
Q

what pathways does paracetamol work on

A

effects on prostaglandin production

on serotenergic, opioid, nitric oxide, and cannabinoid pathways

132
Q

3 main properties of NSAIDs

A

analgesic
anti-inflammatory
anti - pyretic

133
Q

how do NSAIDs work

A

they inhibit prostaglandin synthesis on COX enzymes (COX1 and COX2)

134
Q

3 main classifications of NSAIDs

A

carboxylic acids
enolic aicd
cox II inhibitor

135
Q

what are naproxen and ibuprofen examples of

A

NSAIDS - carboxylic acid - propanoic acid

136
Q

examples of cox II inhibitor NSAIDs

A

celecoxib

valdecoxib

137
Q

Triptan medication

what type of drug are they, what are they designed to do

A

5HT agonists

designed to stop headaches once they have come on for migraines and cluster headaches

138
Q

prescribing triptans and monitoring use

A

should be taken early during a migraine but not during the aura
do not repeat if not responding to first dose
avoid using for more than 10 days a month (can lead to medication overuse headache)

139
Q

four medications for prophylaxis of migraines (from lecture)

A

tricyclic antidepressants
topiramate
candesartan
propanolol

140
Q

examples of tricyclic antidepressants

A 
amitriptyline
amoxapine
imipramine
trimipramine 
protriptyline
141
Q

mechanism of tricyclic antidepressants (TCA’s) in prophylaxis of headaches

A

inhibit reuptake of noradrenaline and serotonin (5HT)

142
Q

how does topiramate work

A

blocks voltage gated sodium and calcium channels
inhibits excitatory glutamate pathways
enhances effect of GABA
inhibits carbonic anhydrase activity

143
Q

how does candesartan work (in relation to prophylaxis of headaches)

A

it is an angiotensin II receptor antagonist (ARB - antihypertensive)
inhibits vasoconstriction by blocking the stimulation of AT1 receptors in vascular smooth muscle
(inhibits excessive cerebral vasoconstriction)

144
Q

analgesics and other meds given to people with tension type headaches

A 
analgesics include - paracetamol, NSAIDs, opioids (codeine)
tricyclic antidepressants (TCD)
145
Q

description of a cluster headache

A

thunderclap headache
sharp, burning or piercing sensation on one side of the head , often felt around the eye, temple and face, tends to occur on the same side for each attack
restless and agitated during attacks because pain is so intense, usually rocking, pacing, or banging their head against the wall

146
Q

acute treatment for a cluster headache

A

oxygen - breathing 100% o2 at minimum of 12L/min

triptans - sumitriptan (nasally or IV)

147
Q

prophylaxis for cluster headaches

A

first line is verapamil (Ca channel blocker)
corticosteroids (inappropriate for long term use)
lithium carbonate

148
Q

another name for medication overuse headache

A

rebound headahce

149
Q

true/false

medication overuse headache only occurs in people with a history of a primary headache

A

true

150
Q

treatment for medication overuse headache

A

abrupt withdrawal or tapering down of medication

151
Q

when is inpatient withdrawal therapy recommended for people with medication overuse headache

A

patients overusing opioids, benzodiazepines, or barbituates

152
Q

what drug has moderate evidence of prophylactic treating of migraines in patients with medication overuse headaches as well

A

topiramate

153
Q

2 latest treatments for migraines

A

botox

monoclonal antibodies

154
Q

describe what is meant. by a primary tumour CNS

A

originates from cell types native to the brain

155
Q

describe what is meant by a secondary tumour CNS

A

derived from cells that have spread (metastasised) from somewhere else in the body

156
Q

symptoms of brain tumours

A 
changes in mood
personality changes
cognitive decline
nausea
projectile vomiting
decreased appetite
visual problems
speech problems
ataxia
157
Q

clinical symptoms of a frontal brain tumour

A 
personality changes
behavioural or emotional changes 
inappropriate behaviour
impaired judgement
loss of vision
primitive reflexes
158
Q

clinical symptoms of a occipital brain tumour

A

visual loss

visual hallucinations

159
Q

clinical symptoms of a temporal brain tumour

A

personality changes
auditory hallucinations
complex partial seizures
memory difficulties

160
Q

clinical symptoms of a parietal brain tumour

A

receptive aphasia (if on left side)
spatial disorientation (if on right side)
impaired speech
lack of recognition

161
Q

clinical symptoms of a brainstem tumour

A 
behavioural and emotional changes
difficulty speaking and swallowing
drowsiness 
headache (especially in the morning) 
hearing loss
 muscle weakness on one side of the face
endocrine abnormalities
symptoms relating to hydrocephalus if ventricles obstructed
162
Q

common sources of metastatic brain tumours

A 
lung
breast
colon
melanoma
kidney
choriocarcinoma
163
Q

uncommon sources of metastatic brain tumours

A

prostrate

gynae

164
Q

percentage of metastatic brain tumours

A

20% of all cancer patients

165
Q

what might a ragged ring on a contrast CT mean?

A

glioblastoma

metastasis

166
Q

what might a smooth ring on a contrast head CT mean?

A

abscess

167
Q

what might C-shaped lesion on a contrast head CT mean

A

demyelination

168
Q

what differentials would you have if you looked at a contrast head CT and saw a cyst with nodules

A

pilocytic astrocytoma
haemingioblastoma
PXA
ganglioma

169
Q

what do meningiomas arise form

A

arise from meningoethelial cells (arachnoid cells)

can arise anywhere in CNS where there is dura/meninges

170
Q

incidence of meningiomas

A

increases with age (most common in middle aged females)

171
Q

risk factors for developing a meningioma

A

female sex
previous radiotherapy
genetic conditions including NF2
other oestrogen dependent tumours

172
Q

common brain tumour in children

A

ependymoma

173
Q

common intraventricular brain tumours

A 
ependymoma
medulloblastoma 
neurocytoma
colloid cyst
meningioma
174
Q

common posterior fossa brain lesions

A

medulloblastoma
pilocystic astrocytoma
brain stem glioma
haemangoblastoma

175
Q

medulloblastoma

A

an embryonal tumour

represents 5% intracranial tumours

176
Q

two peak incidences of medulloblastomas

A

children and young adults (20yrs)

177
Q

what grade tumour is a medulloblastoma

A

grade 4

178
Q

how would you classify a medulloblastoma on histological appearance

A

classic
desmoplastic
excessive nodularity
large cell/anaplastic

179
Q

most common glioma in children and young adults

A

pilocytic astrocytoma

180
Q

preferential location for pilocytic astrocytomas

A

cerebellum, midline structures (thalamus, brain stem, optic chasm)

181
Q

typical brain lesions in the sella location

A

pituitary adenoma

craniopharyngioma

182
Q

what disease produces excess ACTH (adrenocorticotropic hormone.)

A

Cushings disease

can come from a pituitary adenoma

183
Q

what disease produces excess growth hormone

A

acromegaly

can come from a pituitary adenoma

184
Q

increased prolactin can cause? from what pathology

A 
gynaecosmastia (an increase in the amount of breast gland tissue in boys or men, caused by an imbalance of the hormones estrogen and testosterone. Gynecomastia can affect one or both breasts, sometimes unevenly.) 
or galactorrhea (excessive or inappropriate production of milk.)

can be caused from a pituitary adenoma

185
Q

myxopapillary ependymoma

location
incidence
clinical
imaging 
histology
A

location: exclusively in conus, cauda equina, and film terminals of spinal cord
incidence: adults most commonly affected
clinical: present with back pain
imaging: sharply circumscribed mass which is contrast enhancing
histology: elongated fibrillary processes arranged in radial pattern around vascularised mucoid fibrovascualr cores

186
Q

clinical signs of a schwannoma

A

often incidental but can produce signs of nerve compression - pain, CN VIII - hearing loss/tinnitus

187
Q

genetic NF type I brain tumours

A

schwannoma

pilocytic astrocytoma

188
Q

genetic NF type II brain tumours

A

meningiomas

189
Q

what does H&E stand for

A

haemotoxylin and eosin stain

a histochemical stain most commonly used to demonstrate tissue structure in pathology

190
Q

how can glioblastomas be diagnosed directly

A

via H&E stain

191
Q

what is IDH and why is it important

A

isocitrate dehydrogenase

found in 50-80% of astrocytomas and oligodendrogliomas

192
Q

main chemo medication used for brain tumours

A

temozolamide

CBL Year 2 (14 decks)

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