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NLM2 > Clinical > Flashcards

Clinical Flashcards

1
Q

Some organisms that commonly cause meningitis?

A

Viruses: Herpes, EBV

Bacteria

Fungi e.g. Toxoplasma

Helminths

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2
Q

Fatality rate for bacterial meningitis?

A

10-30%

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3
Q

Main types of bacterial meningitis?

A

Meningococci, Hib, pneumococcus

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4
Q

Signs of meningitis? (get some)

A

Severe headache, neck stiffness, fever, vomiting, confusion, brudzinski’s sign, rash, bruising

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5
Q

Difference in the analysis of CSF in bacterial and viral meningitis?

A

Bacterial has neutrophils and viral lymphocytes

Glucose in bacterial is low, in viral it is normal

Protein is higher in bacterial too

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6
Q

Steps of meningococcal infection?

A

Colonise nasopharynx

Invade epithelial cells

Enter circulation and either/both the CSF and the bloodstream (septicaemia)

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7
Q

Treatment for ALS? How effective?

A

Riluzole, 3 month increase in survival

non-invasive ventilation improves quality of life

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8
Q

How might an axonal injury arise?

A

Traumatic brain injury - direct cut of the axon

MS - inflammatory lesion

Stroke - ischaemic injury

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9
Q

How is regeneration different in the PNS to the CNS?

A

Schwann cells in PNS produce high levels of growth factors, and a permissive environment for repair is created

An inhibitory environment is created in the CNS, by the glia

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10
Q

What is basilar invagination?

A

Upwards herniation of the margins of the foramen magnum into the posterior cranial fossa

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11
Q

What is cephaloceles?

A

Extracranila extensions of the parenchyma or meninges through skull defect

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12
Q

What protein aggregates in many neurodegenerative disorder most naotably in lewy bodies in AD?

A

Aβ (amyloid beta)

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13
Q

How does Aβ contribute to age determined macular degeneration?

A

Induces complement activation and this recruits inflammatory factors

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14
Q

Types of neurotransmission?

Which are dysfunctional?

A

Classical

Spillover - activation of adjacent receptors (dysfunction)

Exocytosis occuring away from membranes defined as active zones (dysfuntion)

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15
Q

What three things often contribute to neurodegeneration?

A

BBB dysfunction

Neuroinflammation (Abeta)

Neurotransmission dysfunction

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16
Q

Viruses that cause meningitis?

A 
Herpes
Mumps
Polio
Japanese encephalitis
HIV
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17
Q

Viruses that cause encephalitis?

A

Herpes
Rabies
west nile virus
Japanese encephalitis

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18
Q

Common 5 types of Herpes viruses?

A

HHV - 1 + 2
HHV 3 - chicken pox/shingles

HHV 4 - EBV (glandular fever)
HHV 5 - cytomegalovirus

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19
Q

What is herpes Zoster?

A

When the virus establishes a life-long latent infection in the dorsal root ganglia, and can be reactivated

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20
Q

How and where do HHV 1 and 2 often infect, anatomically

A

They travel from peripheral nerves to the dorsal root ganglia, can travel back down peripheral nerves to reactivate

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21
Q

What commonly causes sporadic encephalitis?

A

HHV1 (95%)

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22
Q

What can be used to treat Herpes, especially in encephalitis?

A

Acyclovir

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23
Q

What is osteomyelitis?

A

Infection of bone tissue

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24
Q

Main three mechanisms of osteomyelitis infection?

A

Haematogenous - from blood

Direct inoculation

Contiguous - from adjacent soft tissue infection

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25
Q

Clinical features of septic arthritis?

A

Acute (mostly)

Pain

Fever

Movement limited

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26
Q

Two types of Septic arthritis?

Causes?

A

Chronic:

  • TB
  • Fungi
  • Lyme disease

Acute/viral

  • Rubella/vaccine
  • mumps
  • Hep B
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27
Q

What is a prion? (in prion disease)

A

An infection that is solely protein based, encoded by your own disease

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28
Q

Is there an infammatory response in prion disease?

A

Nope

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29
Q

What does prion disease cause?

A

Rapid neurodegeneration and death in avg. 1 year, due to accumulation of prion proteins in the brain

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30
Q

Three main types of primary headaches?

A

Tension-headache

Migraine

Cluster headaches

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31
Q

Who normally gets tension-headaches?

A

All ages

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32
Q

Who normally gets migraines?

A

Teen - young adult

Female

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33
Q

Who normally gets cluster headaches?

A

Female over 30

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34
Q

Common causes of raised Intracranial pressure?

A

Space occupying lesions

CSF blockage leading to hydrocephalus

Idiopathic intracranial hypertension

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35
Q

Causes of secondary headaches?

A

Raised ICP

Vascular

Meningitis/encephalitis

Giant cell arteritis

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36
Q

Types of hearing loss?

A

Conductive

Sensorialneural

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37
Q

Common causes of conductive hearing loss?

A

Otitis media
Otosclerosis
Trauma

38
Q

Types of otitis media?

causes?

A

Supprative (pus-producing)
- Viral (90%)

non-supprative
- glue ear

39
Q

What is cholesteatoma?

A

Erosion/rotting of middle ear/mastoid

40
Q

Treatment for otoslerosis?

A
  • hearing aid

- stapedectomy

41
Q

What is acoustic neuroma?

A

Benign tumour of vestibular nerve?

42
Q

two types of vestibular disorders?

A

Central = brainstem + cerebellum

Peripheral = inner ear or vestibulocochlear nerve

43
Q

What is BPPV?

A

Benign paroxysmal positional vertigo

Caused by substances in the vestibular apparatus

cured through a epley movement

44
Q

Three main causes of recurrent vertigo?

A

BPPV

Vestibular migraine

Movement provoked pathologies

45
Q

What do NK cells recognise on cell surface membranes?

A

Glycoproteins

46
Q

Raised intracranial pressure symptoms?

A

Headache

Nausea and Vomiting

Pupilloedema

reduced consciousness

47
Q

Common causes of raised intracranial pressure?

A

Expanding mass

increase in CSF/water content/blood volume

48
Q

What can lead to cerebral vasodilatation?

A

Increased PaCO2
Decreased PaO2
Decreased pH

Decreased cerebral perfusion pressure

49
Q

Types of hydrocephalus?

A

Communicative (absorption issue)

non-communicative (blockage)

50
Q

Types of cerebral drains?

A

Subarachnoid

Intraventricular

Intraparenchymal

Epidural

51
Q

Treatment options for raised intracranial pressure?

A

Heads up

Venous drainage (e.g. central line)

Sedation

Hyperventilation

CSF drainage

Mannitol

52
Q

Roles of the parietal, temporal, frontal and occipital association cortexes?

A

Parietal AC: attending to stimuli

Temporal AC: recognising stimuli

Frontal AC: planning responses

Occipital AC: recognising visual stimuli

53
Q

What is neglect syndrome, what area of the brain is damaged?

A

When the left visual field is completely ignored by patients

Damage to the right parietal lobe

54
Q

Why is neglect syndrome always caused by damage to the right parietal lobe and not the left?

A

The left visual field only has connections to the right parietal lobe, but the right visual field has connections to left and right

55
Q

What is agnosia?

Two types?

A

Agnosia: inability to recognise things

Somatosensory: The inability to recognise objects by touch

Prosopagnosia: Inability to recognise faces

56
Q

What is apraxia, two categories?

A

Conditions involving damage to the prefrontal cortex

Ideomotor:

  • inability to execute learned purposeful movements

Conceptual apraxia:

  • inability to complete multistep actions in the correct order
57
Q

What is aphasia, the two categories, and where is damaged in those categories?

A

Aphasia is damage to areas of speech

Expressive is inability to produce the correct speech = motor (broca’s area)

Receptive aphasia = sensory (wernicke’s area)

58
Q

Three types of learning/conditioning?

A

Classical conditioning - association of one thing with another causing one response to be linked to a new stimulus

Operant conditioning - Using both positive and negative reinforcement (negative reinforcement is NOT punishment but the removal of a negative thing, e.g. less hunger)

Social learning theory - complex learning requiring high amounts of cortical functioning

59
Q

Two types of long-term memory?

A

Procedural - cognitive perceptual and motor skills

Declarative - facts

60
Q

Three levels of encoding of memories?

A
  1. Structural (how it looks) - not encoded very well
  2. Phonemic (how it sounds) - encoded intermediately well
  3. semantic (what it means) - encoded very well
61
Q

Types of forgetting?

A

Failure to encode

Decay

Retrieval failure: can’t find memory cue

motivated forgetting: repressed memories

interference: confusion with other memories

62
Q

Two categories of myelopathies?

A

Compressive

Non-compressive

63
Q

Examples of a compressive myelopathy?

A

Cervical spondylosis

Tumour

Epidural abscess

Trauma

Central cord syndrome

64
Q

Examples of non-compressive myelopathies?

A

Acute: vascular infarction

Sub-acute: MS/HIV, EBV

Chronic:

hereditary spastic paraperesis
MND
Tumour
Copper/B12 deficiency
MS
HIV, syphilis
65
Q

Process of positive adjustment in patients with a long-term-condition

A
  1. Diagnosis
  2. Adjustment process
  3. Adjustment outcome
66
Q

Stages of change in a patient?

A

Precontemplation

Contemplation

Preperation

Action

Maintenance/relapse

67
Q

Common classifications of dementia?

A

Dementia with lewy bodies (15%)

Vascular (20%)

Alzheimers (60%)

68
Q

Classification of dementia diagnosis?

A

Progressive decline in memory and other cognitive abilities > 6 months

69
Q

Common features of dementia?

A

Apraxia/Aphasia

Cognitive decline

70
Q

treatment for dementia?

A

AchEI - Donepezil

Memantine - stabilises glutamatergic neurotransmission

71
Q

rare causes of dementia?

A

FTD - frontotemporal dementia

Huntingtons

CJD

72
Q

Possible modes of genetics of dementia

A
  1. Autosomal dominant, every generation has it
  2. Familial dementia: one or more relative has it
  3. Sporadic: out of the blue
73
Q

Details of autosomal dominant genetic inheritance of dementia?

A

Early onset, APP gene thought to be the cause

APOE gene also implicated

74
Q

What are the functions of the reticular formation?

A

Ascending pain pathways

Integrative functions

75
Q

What are the parasympathetic nuclei and their outputs?

A

Edinger westphal - Ciliary

Superior salivatory - Facial - Pterygopalatine ganglion and submandibular gland

Inferior salivatory - Glossopharyngeal - Otic

76
Q

How does the corneal reflex work?

A

The efferent limb from each eye is the facial nerve, they then synapse on the MLF which connects the efferent limb to the afferent limb (trigeminal nerve)

77
Q

If the corneal reflex arc is transected at the afferent limb what is lost?

A

Both corneal reflexes of the eye are lost

78
Q

If the corneal reflex is transected in the efferent limb on the direct side what is lost?

A

The direct response is lost but the consensual is still present.

79
Q

What travels in the DLF (dorsal lateral fasciculus)?

A

The reticulospinal tract.

80
Q

The process of the pupillary light reflex?

A

Afferent limb - optic nerve

Efferent limb - occulomotor nerve

Optic nerve - Pretectal nuclues (PAG) - Edinger westphal nucleus (PAG) - Occulomotor nerve - Ciliary ganglion

81
Q

Why do both pupils restrict even when light is shone into only one?

A

The pretectal nucleus sends fibres to both edinger westphal nuclei

82
Q

When might the pupillary reflex be absent?

A

MS

Uncal herniation

Horners syndrome

83
Q

What are the two eye movements transmitted by the MLF?

A

Circadic movements - one thing to another e.g. words (voluntary)

Smooth Pursuit movements - watching a moving object (involuntary)

84
Q

What type of cortex covers most of the human brain, how many layers does it have?

A

Neocortex - 6 layers

85
Q

What is cell layer 4 and 5 for in the neocortex, what is larger in the PMC and PSC?

A

Cell layer 4 is for inputs - larger in the PSC

Cell layer 5 is for output - larger in the PMC

86
Q

What would a lesion to the right parietal association cortex commonly cause?

A

Contralateral neglect syndrome (left hemineglect)

87
Q

What is the definition of agnosia/aphasia/ataxia/apraxia/amnesia?

A

Agnosia - inability to recognise things

Aphasia - deficits in speech

Ataxia - inability in coordination

Apraxia - deficits in planning of motor actions

Amnesia - memory deficits

88
Q

Two forms of apraxia?

A

Ideomotor - can’t execute learned movements voluntarily

Conceptual - can’t execute multistep actions in the right order

89
Q

Two types of aphasia, what is damaged in each?

A

Expressive - damage to brocas area - slow laboured monotonous speech

Receptive - damage to wernickes - fluent speech with the wrong words, unaware of the mistakes being made, unable to read

90
Q

What area is damaged in prosopagnosia?

A

Fusiform gyrus in the temporal lobe

91
Q

What is a depressive episode defined as?

A

2 of the following:

  • Pervasive low mood
  • reduced energy
  • Reduced interest and enjoyment

For 2 weeks

NLM2 (14 decks)

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