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3rd YEAR ALL REVISION > everything for summative > Flashcards

everything for summative Flashcards

1
Q

define placenta praevia

A

when the placenta is over the internal cervical os

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2
Q

what are the 3 main causes of antepartum haemorrhage?

A

placenta praaevia

placental abruption

vasa praevia

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3
Q

management of placenta praevia?

A

corticosteroids given between 34 and 35+6 weeks gestation

planned c-section

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4
Q

what is vasa praevia?

A

where the fetal vessels are within the fetal membranes and travel across the internal cervical os.

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5
Q

risk factors for vasa praevia?

A

low lying placenta

multiple pregnancy

IVF pregnancy

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6
Q

management of vasa praevia?

A

corticosteroids given from 32 weeks gestation to mature fetal lungs

elective c-section

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7
Q

what is placental abruption?

A

when the placenta separates from the wall of the uterus during pregnancy

the site of attachment can bleed extensively after the placenta separates

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8
Q

risk factors for placental abruption?

A

previous abruption

pre-eclampsia

trauma

multiple pregnancy

fetal growth restriction

multigravida

increased maternal age

smoking/cocaine use

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9
Q

presentation of placental abruption?

A

sudden onset severe abdominal pain that is continuous

vaginal bleeding

shock

fetal distress on CTG

‘woody’ abdomen on palpation

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10
Q

features of ectopic pregnancy?

A
  • shoulder tip pain
  • missed period
  • constant lower abdo pain in right of left iliac fossa
  • vaginal bleeding
  • cervical motion tenderness
  • dizziness/syncope
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11
Q

how is ectopic pregnancy investigated

A

transvaginal USS - gestational sac containing a yolk sac or fetal pole may be seen in Fallopian tube

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11
Q

how is ectopic pregnancy investigated

A

transvaginal USS - gestational sac containing a yolk sac or fetal pole may be seen in Fallopian tube

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12
Q

what are the criteria for expectant management of ectopic pregnancy?

A
  • follow up needs to be possible
  • enraptured
  • adnexal mass < 35mm
  • no visible heart rate
  • no pain
  • hCG level < 1500 IU/l
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13
Q

what are the criteria for management of ectopic with methotrexate?

A
  • hCG must be < 5000 IU/l
  • confirmed absence of intrauterine pregnancy on USS
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14
Q

criteria for surgical management in an ectopic pregnancy?

A
  • pain
  • adnexal mass > 35mm
  • visible heartbeat
  • hCG levels > 5000 IU/l
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15
Q

what is a polymorphism?

A

any variation in the human genome that has a population frequency of greater than 1%

OR

any variation in the human genome that does not cause a disease in its own right. It may however, predispose to a common gene.

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16
Q

what is a mutation?

A

a gene change that causes a genetic disorder

OR

any heritable change in the human genome

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17
Q

what is the percentage of Down syndrome recurrence if you have a child with Down syndrome?

A

approx 1% if child has primary trisomy 21

higher if caused by Robertsonian translocation

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18
Q

what is the percentage of Down syndrome recurrence if you have a child with Down syndrome?

A

approx 1% if child has primary trisomy 21

higher if caused by Robertsonian translocation

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19
Q

name the condition with genome 47 XY + 18

A

Edward Syndrome

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20
Q

name the condition with genome 45X

A

Turner syndrome

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21
Q

what is the first line chromosome test?

A

array CGH - it is genome wide and can find polymorphisms

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22
Q

Which treatment is used in HER2 positive breast cancer?

A

Trastuzamab

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23
Q

Which treatment is used in chronic myeloid leukaemia?

A

Imatinib - Philadelphia chromosome

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24
Q

what are Mendelian disorders?

A

diseases that segregate in families in the manner predicted by Mendel’s Laws.

a disease that is caused by a change in a single gene.

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25
Q

name the headache:
- bilateral
- band-like pattern around the head
- pressing/tightening
- mild/moderate, non-disabling
- no nausea or vomiting
- attacks last 30 minutes to 7 days

A

tension headache

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26
Q

name the headache:
- unilateral (often bilateral)
- pulsating.throbbing
- moderate/severe
- disabling
- nausea/vomiting/photophobia/phonophobia
- attacks last hours to days

A

migraine

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27
Q

name the headache:
- always unilateral
- excruciating, stabbing, burning
- very severe
- restlessness, no aggravation by physical activity
- conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, ptosis
- attacks last 15 minutes to 3 hours

A

cluster headache

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28
Q

management of tension headache?

A
  • basic analgesia
  • reassurance
  • relaxation techniques
  • hot towels
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29
Q

name the headache:
- facial pain
- lasts few seconds to hours
- electricity-like shooting pain
- attacks worsen over time
- can be triggered by cold weather, spicy food, caffeine, citrus fruits

A

trigeminal neuralgia

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30
Q

what is the treatment for trigeminal neuralgia?

A

Carbamazepine

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31
Q

acute management of migraines?

A
  • paracetamol
  • triptans (serotonin receptor agonists)
  • NSAIDs
  • anti-emetics
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32
Q

which medications are used in the prophylaxis of migraines?

A
  • propranolol
  • topiramate (teratogenic)
  • amitriptyline
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33
Q

what does normal pressure hydrocephalus show on MRI?

A

Ventriculomegaly without sulcal enlargement

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34
Q

why can’t the COCP be taken with history of migraines?

A

there is a significantly increased risk of ischaemic stroke

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35
Q

what are the driving rules after a first seizure?

A
  • must inform DVLa
  • will have to be seizure free for 6 months before applying to have licence reinstated
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36
Q

what additional step needs to be considered when administering IV phenytoin for a seizure?

A

cardiac monitoring

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37
Q

first line management for myoclonic seizures in males?

A

sodium valproate

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38
Q

first line management for myoclonic seizures in females?

A

Levetiracetam

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39
Q

1st line investigation for MS?

A

MRI with contrast

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40
Q

how does normal pressure hydrocephalus present?

A
  • urinary incontinence
  • gait abnormality
  • dementia
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41
Q

what is the management of an acute MS relapse?

A

high dose steroids - oral or IV methylprednisolone for 5 days

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42
Q

which artery has caused the stroke based on this presentation:
- contralateral hemiparesis
- sensory loss with upper extremity affected more
than lower
- contralateral homonymous hemianopia
- aphasia

A

Middle cerebral artery

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43
Q

general red flags for back pain?

A
  • failure to improve after 4-6 weeks of conservative therapy
  • night pain or pain at rest that won’t go away
  • progressive motor/sensory deficit
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44
Q

cancer red flags back pain?

A
  • age > 50
  • unintended weight loss
  • history of cancer
  • pain at night and in recumbency
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45
Q

what symptoms does a stroke affecting the left MCA give?

A

dysphasia

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46
Q

what symptoms does a stroke of the right MCA give?

A

sensory/visual inattention/neglect (right MCA)

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47
Q

which arteries make up the PCA?

A

2 vertebral arteries and a basilar artery

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47
Q

what arteries does the posterior circulation of the brain comprise of?

A

2 vertebral arteries and a basilar artery

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48
Q

which artery supplies the occipital cortex?

A

PCA

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49
Q

what symptoms does a stroke affecting the PCA give?

A

hemiparesis/hemisensory loss

ataxia

dysarthria

vertigo, diplopia, facial nerve palsy, tongue palsy, dysphasia

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50
Q

symptoms/signs of total anterior circulation syndrome?

A

Hemiplegia involving at least 2 of:

  • face, arm and leg +/- hemisensory loss
  • homonymous hemianopia
  • cortical signs (dysphasia, neglect etc)
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51
Q

how long after a stroke can thrombolysis be used?

A

up to 4.5 hours after onset of symptoms

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52
Q

how is blood pressure lowered in ICH to prevent haematoma expansion?

A

IV labetalol or IV GTN

(BP > 150mmHg)

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53
Q

what is gliosis?

A

an astrocytic response to CNS injury

  • astrocyte hyperplasia and hypertrophy
  • nucleus enlarges and becomes vesicular and the nucleolus Is prominent
  • cytoplasmic expansion with extension of ramifying processes
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54
Q

what do microglia do in response to injury?

A

proliferate and are recruited through inflammatory mediators

form aggregates around areas of necrotic and damaged tissues

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55
Q

what is seen macroscopically 12-24 hours after a stroke?

A

red neuron, oedema (cytotoxic and vasogenic) with generalised cell swelling

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56
Q

where do intracerebral haemorrhages most commonly occur?

A

basal ganglia

thalamus

cerebral white matter

cerebellum

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57
Q

what is the most common cause of subarachnoid haemorrhage?

A

rupture of a berry aneurysm

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58
Q

risk factors for subarachnoid haemorrhage?

A
  • female
  • smoking
  • hyperT
  • drugs
  • PKD
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59
Q

what is hydrocephalus ex vacuo (seen in Alzheimer’s)?

A

dilatation of the ventricular system and a compensatory increase in CSF volume secondary to a loss of brain parenchyma

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60
Q

what is the most common brain tumour in children?

A

Pilocytic astrocytoma

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61
Q

what is the definition of MS?

A

an autoimmune demyelinating disorder characterised by distinct episodes of neurological deficit, separated in time, and which correspond to spatially separated foci of neurological injury.

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62
Q

what does MS show in a CSF sample?

A

IgG oligoclonal bands

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63
Q

clinical features of MS?

A

optic neuritis

motor or sensory deficit in trunk and limbs

spasticity

bladder dysfunction

cranial nerve signs

ataxia

nystagmus

internuclear ophthalmoplegia

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64
Q

what are the differences between active and inactive plaques?

A

active plaques
- perivascular inflammatory cells
- microglia
- ongoing demyelination
- yellow/brown with an ill-defined edge

inactive plaques
- gloss
- little remaining myelinated axons
- oligodendrocytes and axons reduced in number
- grey-brown well-demarcated
- classically situated around lateral ventricles

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65
Q

which genes are linked to Alzheimer’s?

A
  • APP
  • Presenilin 1 (chromosome 14) and 2 (chromosome 1)
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66
Q

macroscopic findings in Alzheimer’s?

A
  • cortical atrophy
  • frontal, temporal and parietal lobe atrophy
  • widening of sulk
  • narrowing of gyri
  • dilatation of ventricles
  • brainstem and cerebellum normal
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67
Q

microscopic features of Alzheimer’s?

A
  • neurofibrillary tangles
  • extensive neuronal loss with associated astrocyte proliferation
  • neuritic plaques
  • amyloid angiopathy
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68
Q

how does Lewy bodies dementia present?

A
  • hallucinations
  • fluctuating levels of attention/cognition
  • REM sleep behaviour disorder
  • memory is affected a lot later than in
    Alzheimer’s
  • fluctuation in severity of condition on a day-to- day basis
  • features of Parkinsonism may be present at onset or emerge shortly after
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68
Q

how does Lewy bodies dementia present?

A
  • hallucinations
  • fluctuating levels of attention/cognition
  • REM sleep behaviour disorder
  • memory is affected a lot later than in
    Alzheimer’s
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69
Q

what are the pathological features of Lewy bodies dementia?

A

degeneration of the substantial nigra

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70
Q

what are the macroscopic features of Lewy body dementia?

A

pallor in the substantial nigra, where pigmented dopaminergic neurones run

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71
Q

what are the microscopic features of Lewy body dementia?

A
  • loss of pigmented neurone
  • reactive gliosis
  • spread of Lewy bodies from brainstem to cortex
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72
Q

How is Huntington’s disease inherited?

A

autosomal dominant pattern
Huntington gene on chromosome 4p - mutated with increase in CAG repeats

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73
Q

what are the macroscopic findings in Huntington’s disease?

A

Atrophy of the basal ganglia; caudate nucleus; putamen

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74
Q

what are the microscopic findings of Huntington’s disease?

A

simple neuronal atrophy of striata neurones of the basal ganglia

pronounced astrocytic gloss

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75
Q

what are the macroscopic findings of frontotemporal dementia?

A

extreme atrophy of the cerebral cortex in frontal and later in temporal lobes

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76
Q

what are the microscopic findings of frontotemporal dementia?

A

Pick’s cells (swollen neurons)

Intracytoplasmic filamentous inclusions - Pick’s bodies

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77
Q

management for idiopathic tension headache?

A

weight loss and acetazolamide

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78
Q

which spinal columns are affected in subacute combined degeneration of the spinal cord?

A

dorsal columns and lateral corticospinal tracts

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79
Q

what class of medications should be avoided in patients taking SSRIs?

A

triptans - risk of serotonin syndrome

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80
Q

management of delirium tremens?

A

admit to hospital

long-acting Benzos - Chlordiazepoxide, Diazepam

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81
Q

what would a patient with bullimia’s ECG look like?

A

Hypokalaemia - first degree heart block, flattened T waves, tall P waves

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82
Q

when should a patient under 25 who has been started on an SSRI be reviewed?

A

after 1 week

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83
Q

features/symptoms of mania?

A

lasts for at least 7 days

elevated mood, increased activity and grandiose ideas of self-importance.

causes severe functional impairment in social and work setting

likely to require hospital admission

can present with psychotic symptoms

84
Q

features/symptoms of hypomania?

A

lasts for < 7 days

persistent mild elevation of mood, increased energy and activity

increased sociability, talkativeness and over-familiarity

Increased sexual energy

Decreased need for sleep

can be high functioning and doesn’t impair functional capacity in social or work setting

doesn’t exhibit any psychotic symptoms

85
Q

features of anorexia nervosa?

A

reduced BMI

bradycardia

hypotension

enlarged salivary glands

86
Q

physiological abnormalities associated with anorexia nervosa?

A

hypokalaemia

Low FSH, LH, oestrogen and testosterone

raised cortisol and growth hormone

impaired glucose tolerance

87
Q

what are the first rank symptoms of schizophrenia?

A

auditory hallucinations

thought disorders

passivity phenomena

delusional perceptions

88
Q

mechanism of action of Mirtazapine?

A

noradrenergic and specific serotonergic antidepressant

increases release of neurotransmitters by blocking alpha 2 adrenoreceptors

89
Q

long-term side effects of ECT?

A

apathy

anhedonia

concentration difficulties

loss of emotional responses

difficulty learning new information

90
Q

risk factors for developing BPD?`

A

prenatal exposure to Toxoplasma gondii

premature birth < 32 weeks gestation

childhood maltreatment

postpartum period

cannabis use

91
Q

characteristics of bipolar I ?

A

the person has experienced at least 1 episode of mania

92
Q

characteristics of bipolar II ?

A

the person has experienced at least 1 episode of hypomania but never an episode of mania.

they must have also experienced at least 1 episode of major depression.

93
Q

what medication is added if lithium is not effective in the long-term management of BPD?

A

sodium valproate (NOT IN PREGNANCY OR WOMEN OF CHILDBEARING AGE)

94
Q

side effects of lithium?

A

increased thirst

increased volume and frequency of urination

tiredness

weight gain

fine tremor

95
Q

side effects of lithium toxicity?

A

confusion

drowsiness

visual problems

loss of appetite

difficulty speaking

seizures

excessive thirst + urination

(risk of toxicity is decreased by taking their dose at the same time every day and regular attending to have their blood tested)

96
Q

what are the signs of lower motor neurone disease?

A

muscle wasting

reduced tone

fasciculations

reduced reflexes

97
Q

what are the signs of upper motor neurone disease?

A

increased tone or spasticity

brisk reflexes

upping plantar responses

98
Q

which medication is used in motor neurone disease to slow the progression of it?

A

Riluzole

99
Q

what is the pathophysiology of Parkinson’s?

A

Progressive reduction of dopamine in the basal ganglia (produced in the substantial migration) leads to disorders of movement.

100
Q

what is the classic triad of features in Parkinsons?

A

resting tremor

rigidity

bradykinesia

101
Q

which medications is given in Parkinson’s to treat symptoms?

A

Levodopa - synthetic dopamine given orally to boost dopamine levels.

usually paired with Carbidopa or Benserazide

102
Q

what are the side effects of Levodopa?

A

dystonia

chorea

athetosis

103
Q

what is the mechanism of action of Entacapone?

A

inhibit the catechol-o-methyltransferase enzyme which metabolises levodopa in the body and the brain.

taken with levodopa.

104
Q

what is the main side effect of dopamine gnosis’s (Carbergoline, Pergolide etc)

A

pulmonary fibrosis

105
Q

which type of tumour is linked to myasthenia gravis?

A

thymomas

106
Q

how does myasthenia gravis present?

A

diplopia

ptosis

weakness in facial movements

swallowing difficulty

fatigue in jaw while chewing

slurred speech

progressive weakness with repetitive movements

107
Q

how is myasthenia gravis diagnosed?

A

presence of ACh-R antibodies

presence of MuSK antibodies

presence of LRP4 antibodies

CT or MRI thymus gland - used to look for thymoma

108
Q

name the type of aphasia:

  • speech non-fluent, laboured and halting
  • comprehension normal
  • repetition is impaired
A

Broca’s aphasia

due to lesion in inferior frontal gyrus - supplied by superior division of left MCA

109
Q

when can investigations be commenced for infertility?

A

for couples who have been trying to conceive for 1 year after frequent (every 2 -3 days), unprotected sexual intercourse.

110
Q

when can couples have an early referral for infertility investigations?

A
  • if the woman is aged 36 or over

OR

  • there is a known cause of infertility

OR

  • there is a history of predisposing factors
111
Q

what investigations are done in primary care to assess male infertility?

A
  • semen analysis
  • chlamydia screen
112
Q

what investigations are done in primary care to assess female infertility?

A
  • mid-luteal progesterone - to assess whether the woman is ovulating
  • FSH and LH - to assess ovarian function
  • chlamydia screen
113
Q

what are the 2 types of urinary incontinence?

A

stress and urge

114
Q

how is urge incontinence caused?

A

overactivity of the detrusor muscle of the bladder

(AKA overactive bladder)

115
Q

describe urge incontinence

A

suddenly feeling the urge to pass urine, having to rush to the bathroom and not arriving before urination occurs.

116
Q

how is stress incontinence caused?

A

weakness of the pelvic floor and sphincter muscles which allows urine to leak at times of increased pressure on the bladder.

117
Q

describe stress incontinence

A

urinary leakage when laughing, coughing or surprised

118
Q

what is overflow incontinence?

A

when there is chronic urinary retention due to an obstruction to the outflow of urine.
results in an overflow of urine and the incontinence occurs without the urge to pass urine.

more common in men

119
Q

risk factors for urinary incontinence?

A
  • increased age
  • post-menopausal
  • increased BMI
  • previous pregnancies and vaginal deliveries
  • pelvic organ prolapse
  • pelvic floor surgery
  • neuro conditions such as MS
  • cognitive impairment and dementia
120
Q

how is urinary incontinence investigated?

A
  • bladder diary
  • urine dip
  • post-void residual bladder volume
  • urodynamic testing
121
Q

management of stress incontinence?

A

avoid caffeine, diuretics and overfilling bladder

avoid excessive or restrictive fluid intake

weight loss

pelvic floor exercises - for at least 3 months before surgery

  • surgery
  • duloxetine
122
Q

management or urge incontinence?

A

bladder retraining - for at least 6 weeks

anticholinergic medication - oxybutynin, tolterodine and solifenacin

mirabegron

invasive procedures where medical treatment fails

123
Q

how does the combined oral contraceptive pill work?

A

mimics the luteal phase of the menstrual cycle, leading to inhbiition of the hypothalamic-pituitary-gonadal axis.

this prevents the release of LH and FSH needed for ovulation.

thickens the cervical mucus and thins the endometrium

124
Q

how often is the contraceptive injection given?

A

every 12 weeks

125
Q

how does the IUS work?

A

thins the endometrium to prevent implantation

thickens the cervical mucus to prevent sperm passage

126
Q

what are the most common reasons for he insertion of the Mirena coil?

A

contraception (5 years)

menorrhagia (5 years)

endometrial protection for women on HRT (4 years)

127
Q

how many days after unprotected sex can the copper coil be used?

A

5 days

128
Q

how long after taking levonorgestrel for emergency contracpetioncan the COCP or OCP be taken?

A

immediately after

129
Q

how long after unprotected sex can levonorgestrel be used as emergency contraception?

A

72 hours

130
Q

how long after taking Ulipristal (EllaOne) for emergency contraception can the pill be taken?

A

5 days after

131
Q

in which patient groups should Ulipristal be avoided in?

A

patients with severe asthma

132
Q

management of bacterial vaginosis?

A

Metronidazole orally or by vaginal gel

(clindamycin is the alternative)

133
Q

what investigations are done for BV?

A
  • vaginal pH using swab and pH paper
  • charcoal vaginal swab for microscopy - shows ‘clue cells’ on microscopy
134
Q

which organism normally causes BV?

A

gardnerella vaginalis

135
Q

how does trichomoniasis present?

A

50% asymptomatic

frothy, yellow-green vaginal discharge - may have fishy smell

itching

dysuria

dyspareunia

balanitits

examination of cervix - strawberry cervix

136
Q

management of trichomoniasis?

A

Metronidazole

137
Q

management of gonorrhoea?

A

single dose of IM ceftriaxone 1g - if sensitivities unknown

single dose of oral ciprofloxacin 500mg - if sensitivities are known

138
Q

how does gonorrhoea present?

A
  • odourless purulent discharge, possible green or yellow
  • dysuria
  • pelvic pain (females)
  • testicular pain/swelling in males
139
Q

which results are typically seen in PCOS?

A

raised testosterone

low sex hormone binding globulin (SHBG)

raised LH

normal FSH

140
Q

what is the management of atrophic vaginitis?

A

topical oestrogen cream

141
Q

what is the first line management of uterine prolapse?

A

vaginal pessary

142
Q

where is progesterone produced?

A

corpus luteum

143
Q

what are the three phases of the uterine cycle?

A

proliferative phase

secretory phase

menstrual phase

144
Q

management of eclampsia?

A

magnesium sulphate

145
Q

what is the management of placental abruption when the foetus is alive, < 36 weeks and not showing signs of distress?

A

admit and administer steroids

146
Q

first line management of nausea and vomiting in pregnancy?

A

cyclizine

147
Q

how long after giving birth do women need to start using contraception again?

A

21 days

148
Q

which type of cancer causes pain on drinking alcohol?

A

Hodgkin’s lymphoma

149
Q

what is the most common cause of vitamin B12 deficiency?

A

presence of anti-intrinsic factor antibodies

150
Q

how is a definitive diagnosis of sickle cel disease made?

A

haemoglobin electrophoresis

151
Q

what is seen on a blood film with DIC?

A

schistocytes

152
Q

what does the Factor V Leiden mutation result in?

A

resistance to action of protein C

153
Q

what are some causes of immune-mediated decreased platelet survival?

A
  • idiopathic thrombocytopenia purpura
  • SLE
  • rheumatoid arthritis
  • sarcoidosis
  • anti-phospholipid syndrome
154
Q

what are some non-immune causes of decreased platelet survival?

A
  • medications - heparin, carbamazepine, ibuprofen etc
  • splenomegaly
  • haemolytic uraemic syndrome
  • HELLP syndrome
    -thrombotic thrombocytopenic purpura
155
Q

symptoms of thrombocytopenia?

A

spontaneous bruising or excessive bruising as a result of minor injury

bleeding gums

epistaxis which may be excessive, frequent and prolonged

GI bleeding

genitourinary bleeding

menorrhagia

156
Q

what are the clinical findings of thrombocytopenia?

A

petechiae (< 2mm)

purpura (0.2-0.1mm)

found on skin and oral mucosa

157
Q

what are the 3 layers of the cerebellar cortex?

A

molecular layer (outer)

Purkinje cell layer (middle)

granule cell layer (inner)

158
Q

what side of the body will signs appear in a cerebellar hemisphere lesion?

A

ipsilateral side

159
Q

which symptoms does a unilateral cerebellar hemispheric lesion cause?

A

disturbance of limb coordination

intention tremor

unsteady gait

160
Q

which symptoms do bilateral cerebellar lesions cause?

A

slowed, slurred speech

bilateral incoordination of the arms

staggering, wide bed gait

161
Q

what symptoms does a midline lesion of the cerebellum present with?

A

disturbance of postural control

162
Q

which 3 arteries supply the cerebellum?

A

superior cerebellar artery

anterior inferior cerebellar artery

posterior inferior cerebellar artery

163
Q

what are the functions of the basal ganglia?

A

facilitate purposeful movements

inhibit unwanted movements

help maintain posture and muscle tone

164
Q

what symptoms do lesions of the basal ganglia cause?

A

affect the contralateral side of the body

changes in muscle tone

dyskinesias

tremor

chorea

myoclonus

165
Q

what is the pathology behind Huntington’s disease?

A

progressive degeneration of the basal ganglia and cerebral cortex

166
Q

what are the signs/symptoms of normal pressure hydrocephalus?

A
  • abnormal gait
  • urinary incontinence
  • dementia
167
Q

investigations for normal pressure hydrocephalus?

A

Lumbar puncture

lumbar drain test

168
Q

management of normal pressure hydrocephalus?

A

VP shunt

medium-low or low-pressure valve

169
Q

management of idiopathic intracranial hypertension?

A

weight loss

carboanhydrase inhibitors - Actetazolamide, Topiramate

diuretics

CSF diversion

interventional radiology

170
Q

pathway of CSF secretion?

A

choroid plexus (lateral ventricles) > ventricular system > subarachnoid space (Magendie and Luschka) > venous system (arachnoid granulations)

171
Q

how is CPP calculated?

A

MAP - ICP = CCP

172
Q

what effect does CO2 have on arterioles?

A

increased CO2 - vasodilation

decreased CO2 - vasoconstriction

173
Q

what is the normal ICP for adults?

A

7-15 mmHg

174
Q

early signs of raised ICP?

A

decrease level of consciousness

headache

pupillary dysfunction +/- papilloedema

changes in vision

nausea and vomiting

175
Q

late signs of raised ICP?

A

coma

fixed, dilated pupils

hemiplegia

bradycardia

hyperthermia

increased urinary output

176
Q

medical management of raised ICP?

A

diuretics (mannitol, hypertonic saline, furosemide)

barbiturate coma

anti-epileptics

177
Q

which type of visual defect would a lesion in the left temporal lobe present with?

A

right superior homonymous quadrantinopia

(PITS)

178
Q

which type of visual field defect would a lesion of the right parietal lobe present with?

A

left inferior homonymous quadrantinopia

179
Q

management of cluster headache?

A

subcutaneous sumatriptan

100% oxygen

180
Q

clinical features of brown-sequard syndrome?

A

ipsilateral hemiplegia

ipsilateral loss of proprioception and vibration

contralateral loss of pain and temperature sensation

181
Q

what does the CSF in encephalitis show?

A

lymphocytosis

elevated protein

HSV, VZV or enteroviruses

182
Q

management of encephalitis?

A

IV acyclovir

183
Q

when should a CT scan be requested in head trauma?

A

skull fracture

GCS less than 15

focal neurological signs

taking warfarin

184
Q

which protein, when stained, can help detect Lewy body Dementia?

A

ubiquitin

185
Q

what happens to the caudate nucleus in huntington’s diseas

A

atrophy of caudate nucleus and loss of neurones

186
Q

what are the histopathological landmarks of frontotemporal dementia?

A

swollen neurons - Pick’s cells

filamentous inclusions - Pick’s bodies

187
Q

describe the morphology of Alzheimer’s disease on the brain

A

cortical atrophy
widened sulci
narrowed gyri
dilated ventricles

188
Q

which protein the brain can become tangled in Alzheimer’s?

A

tau protein

189
Q

which medication is used to treat cerebral oedema in patients with brain tumours?

A

Dexamethasone

190
Q

which deficits would you expect to find in subacute combined degeneration of the spinal cord?

A

loss of proprioception and vibration sensation

muscle weakness

hyper-reflexia

191
Q

which medication is used in the long term prophylaxis of cluster headaches?

A

Verapamil

192
Q

what would the investigation findings be in neuroleptic malignant syndrome?

A

raised CK

raised WCC

193
Q

how does neuroleptic malignant syndrome present?

A

hyperthermia

muscle rigidity

autonomic instability

altered mental status

194
Q

list some precipitants of a sickle crisis

A

hypoxia
dehydration
infection
cold exposure
stress
fatigue

195
Q

management of sickle crisis?

A

opiate analgesia
hydration
rest
Oxygen
antibiotics if infection
red cell transfusion if severe

196
Q

what are the 3 parameters that contractions are based on?

A

frequency

duration

intensity

197
Q

what are the 3 stages of labour?

A

cervical dilation (8-24 hours)

passage through birth canal (0-30 mins)

expulsion of placenta

198
Q

what are Braxton Hicks contractions?

A

tightening of the uterine muscles to aid body to prepare for birth

not usually felt until 2nd/3rd trimester

199
Q

what 5 parameters are assessed under the Bishops’s score?

A

effacement

dilation

firmness

position

level of presenting part

200
Q

which blood pressure reading would infer hypertension in pregnancy?

A

systolic > 140 mmHg

OR

diastolic > 90 mmHg

201
Q

what is a first degree tear?

A

tear within vaginal mucosa only

202
Q

what is a second degree tear?

A

tear into subcutaneous tissue

203
Q

what is a third degree tear?

A

laceration extends into external anal sphincter

204
Q

what is a 4th degree tear?

A

laceration extends through external anal sphincter into rectal mucosa

205
Q

what are the SSRIs of choice in breastfeeding women?

A

Sertraline or Paroxetine

206
Q

non-pharmacological management of ADHD?

A

parent training

social skills training

classroom strategies

sleep and diet changes

207
Q

pharmacological management of ADHD?

A

1st line = Methylphenidate (Ritalin)

2nd line = atomoxetine 0

3rd line = anti-depressant, anti-psychotics

208
Q

mechanism of action of methylphenidate?

A

CNS stimulant that works by improving dopamine signalling in the networks associated with executive functioning

side effects = headache, poor appetite, insomnia

209
Q

in the central dogma, which process is most likely to be affected by a mutation that changes the first base in an intron?

A

splicing

210
Q

which type of genetic sequence variant is the one most likely to cause long QT syndrome?

A

a premature stop codon in the exon 2 of a gene.

211
Q

which piece of evidence would most strongly suggest that the genetic variant in long QT syndrome is pathogenic?

A

the variant is a deletion of a single base in the exon of a gene

3rd YEAR ALL REVISION (1 decks)

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