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Case 16 Flashcards

1
Q

What is the structure of the middle ear?

A

Ossicles - Malleus, Incus and Stapes - amplify sound waves by 18x, connects to oval window
Stapedus Muscle - connects to stapes and controls sound wave amplitude
Tensor Tympani muscle - connects to the malleus and dampens down loud noises e.g. thunder, chewing
Pharyngo-tympanic membrane - connects the nasopharynx and middle ear

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2
Q

What is the structure of the external ear?

A

The pinna - funnels sounds into the ear canal for localisation and externalisation
External Auditory Meatus - lined with squamous epithelium, inner third is comprised of collagen and has hairs - secretes waxy cerebrum
outer 2 thirds consists of bone.

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3
Q

What is the structure of the inner ear?

A

Scala Vestibuli and Scala media are separated by the reissner’s membrane
Scala Media and Scala tympani are separated by the basilar membrane (organ of corti).
Scala Media contains endolymph (low Na, high K).
Scala Vestibuli and Tympani contain perilymph (high Na, low K).

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4
Q

Describe the process of sound transduction

A

Inwards stapes movements amplifies sound signals into the oval window to enter the cochlea. Inwards movements creates pressure gradient pushing down on the basilar membrane and causing fluid to be pushed out of the round window via the Scala tympani.
High frequency waves displace the BM at the base
Low frequency waves displace the BM at the apex.
Outwards stapes movement equilibrates the pressure and causes fluid to move back into the round window.

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5
Q

Describe the role of sterocillia on inner and outer hair cells

A 
Bending towards the tallest stereocillia induces depolarisation. 
In IHC (1 row), depolarisation causes release of NT and activates the cochleo-vestibular nerve. 
In OHC (3 rows), depolarisation causes prestin to be activated which amplifies basilar membrane movement.
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6
Q

What drugs are ototoxic?

A

Aminoglycosides
Furosemide
Aspirin

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7
Q

What is the auditory pathway?

A

The cochlea nerve transmits signals from the cochlea to the cochlear nucleus (between the medulla and pons), then to the colliculus and then to the auditory cortex = Herschels gyrus (temporal lobe).

Superior Olive uses sound frequency and intensity from both ears to localise sounds.

Contralateral auditory input. (L ear to R auditory Cortex).

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8
Q

Receptive Dysphasia

A

Difficulty comprehending speech

Damage to the Wernicke Area at the back of the temporal lobe

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9
Q

Expressive Dysphasia

A

Difficulty producing speech

Damage to the broca area at the front of the temporal lobe

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10
Q

Place Coding

A

Tonotopic organisation of sound frequencies within the auditory cortex of where action potential originated.
High frequencies at the posterior end of the cochlea
Low frequencies at the anterior end.

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11
Q

Time coding

A

Firing of action potentials synchronise, the timing between firing is used to identify frequency (only over 3Hz)

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12
Q

What is the innervation of the Vestibular Apparatus?

A

Vestibulo-portion of CNVIII

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13
Q

Role of the Otolith Organs

A

To detect straight line acceleration and changes in head angle.
Consist of the Utricle (horizontal) and Saccule (vertical) which contain sensory epithelium called macula.
Changes in gravity drag the gelatinous cap with otolith fragments to cause bending of stereocillia.

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14
Q

Role of the Semicircular Canals

A

3 Perpendicular Canals - Lateral, Superior and Posterior
Detect rotational acceleration
1) Head and canal rotates whilst the fluid remains stationary - essentially opposite rotation. Cupulla and stereocillia bend = depolarisation.
2) Fluid catches up and both canal and fluid rotate in the same direction. Upright cupola and stereocillia
3) Head and canal stop rotating - cupola and stereocillia bend backwards = hyperpolarisation.

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15
Q

How do the otolith organs control balance?

A

Input from the otolith organs via CNVIII to the lateral vestibular nucleus - inputs to the cerebellum and limb motor neurones.

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16
Q

How do the semi circular canals control balance?

A

Input from the SC canals via CNVIII to the medial vestibular nucleus - inputs to the head and neck motor neurones and to the extra-ocular motor neurones (III, IV, VI).

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17
Q

What is the vestibulo-occular reflex?

A

Stabilising the eyes so they point in the same direction by compensating for head movement with counter rotation of eyes via the medial and lateral rectus eye muscles.

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18
Q

What is nystagmus?

A

Physiological response to external movement with slow gradual eye movement in the opposite direction followed by rapid flick back.

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19
Q

What is pathological nystagmus?

A

Jerky eye movements without external movement which cause vision loss and are due to brainstem or vestibular lesions.

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20
Q

What is Meniere’s Disease?

A

failure of the end-lymphatic duct to regulate end-lymphatic pressure.
Symptoms:
Incapacitating vertigo, Tinnitus, distorted hearing, fluctuating LF hearing loss, nausea, sensation of pressure in ear

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21
Q

Causes of Conductive Hearing Loss

A

Infection
Foreign Bodies - tumour, wax
Anatomical Abnormalities
Otosclerosis

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22
Q

Causes of Sensioneural Hearing Loss

A 
Ageing
Noise induced
Hereditary 
Disease - Tumours
Head Trauma 
Drug Damage
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23
Q

Describe Rinne’s Test and it’s purpose

A

Purpose - To see if AC>BC
Place the vibrating tuning fork behind ear on mastoid process and check patient can hear.
Move the tuning fork in front of the ear and ask which is loudest.

Positive Test = AC>BC - Normal hearing or Conductive deficit
Negative Test = BC>AC - Sensioneural Deficit

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24
Q

Describe Weber’s test and it’s purpose

A

Place the vibrating fork in the midline of the forehead and ask patient to describe where they can hear it - L or R ear, equally, or centrally.
Purpose - to identify sensioneural deficit

Normal = Hearing equally or centrally

Positive Rinne’s and sound head in one ear = sensioneural - sound head in the good ear

Negative Rinne’s and sound heard in one ear = conductive - sound heard in the bad ear.

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25
Q

Describe pure tone audiometry

A

Patient wear headphones with an oscillator which sits on the mastoid process behind the ear, and listens to different frequencies.
A (frequency X axis and loudness on Y axis) graph is created with a sensioneural and conductive line

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26
Q

Describe the results of pure tone audiometry which would show conducive deficit

A

10dB gap between the conductive and sensioneural lines

Lines plateau at around 60dB.

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27
Q

Describe the results of pure tone audiometry which would show sensioneural deficit

A

No gap between the 2 lines

Steady decline with both lines with increasing frequency.

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28
Q

Describe different levels of hearing impairment

A

Mild - Struggle to understand speech in noisy environments
Moderate - Use of hearing aid
Severe - Use of hearing aid and lip reading
Profound - Use of hearing aid and lip reading and BSL/finger spelling

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29
Q

Describe ways to effectively communicate with patients with hearing impairments

A 
Ensure good lighting on face
Pick a quiet area
Use hand gestures
Use facial expressions
Speak clearly 
Use BSL
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30
Q

Describe ways to identify if a patient has hearing problems

A 
Asking you to repeat often 
Speaking loudly themselves
Complains you aren't speaking loud enough
Pointing to their ears
No reaction to loud noises
Uses BSL
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31
Q

Describe the viral life cycle

A

1) Attachment to host cell membrane using surface proteins
2) Host Cell entry
3) Replication using host genome
4) Assembly
5) Release (Enveloped viruses take portion of host cell membrane)

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32
Q

Give examples of routes of viral transmission

A

Respiratory - inhalation, fingers to RT, via conjunctiva
Feacal - Oral - contaminated water or food, aerosol droplet of vomit
Sexual
Mechanical - blood transfusions, via skin/mucosa abrasions
Urine
Conjunctiva

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33
Q

What arbovirus does not use a vector for transmission?

A

Rabies

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34
Q

What is horizontal and vertical viral transmission?

A

Horizontal - between members of the same generation

Vertical - between mother - fetus

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35
Q

Define pathogenicity

A

the severity of a disease caused by a virus

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36
Q

Define pathogenicity factors

A

the factors that allow a virus to cause a disease e.g. immune evasion, host cell entry method, replication

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37
Q

Define virulence

A

the severity of disease caused by a strain of the same virus

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38
Q

Define localised and generalised infections

A

localised - infection at the site of entry e.g. norovirus at GI epithelium
generalised - infection at a site far from entry e.g. measles, mumps, rubella

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39
Q

Methods of prevention of viral infections

A 
Good surveillance 
Quarantine/Isolation of infected individuals 
Vaccinations
Lifestyle changes
Vector control of arboviruses 
Pre exposure Prophylaxis - HIV
Post exposure prophylaxis - Rabies/HIV
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40
Q

HCV Treatment

A

Acute:
Monitor for spontaneous recovery
Chronic:
Weekly Pegylated Interferon A (inhibits replication and increases host antiviral response)
Oral Ribovirin daily - stops viral RNA synthesis

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41
Q

HBV Treatment

A

Acute:
Supportive treatment
Chronic:
Weekly pegylated Interferon A (inhibits replication and increases host antiviral response)
Oral antiviral (tenofovir/entecevir) - inhibits HBV DNA polymerase

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42
Q

HSV Treatment

A

Oral Aciclovir or Valaciclovir
Aciclovir - activated by thymidine kinase (viral enzyme)
Valaciclovir - pro drug - increased bioavailability but more expensive

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43
Q

VZV Treatment

A 
Children = self resolving
Adults = oral acyclovir/valaciclovir
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44
Q

CMV Treatment

A

CMV = problematic in transplant patients

Ganaciclovir - inhibits viral DNA polymerase

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45
Q

Influenza Treatment

A

Vaccine - >65, Pregnant or 2 weeks post-partum women
Tamiflu (oral oseltamivir) = neuraminidase inhibitor
OR Z
Zanamivir (relenza)

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46
Q

What 9 viruses can be treated with antivirals?

A

HBV, HCV, HSV. VZV, CMV, Influenza, RSV, HPV, HIV

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47
Q

What is the structure of HSV

A

Double stranded enveloped DNA virus (fried egg virus)

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48
Q

HSV Lifecycle

A
  1. Primary Infection (1st HSV infection) or Initial infection (1st HSV-2 infection in prior HSv-1 infected individual)
  2. Latency - in sympathetic neurone ganglion
  3. Reactivation (due to stress, cold, menstruation, immunosuppression)
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49
Q

HSV Epidemiology and Transmission

A

Epidemiology
80% HSV-1 and 20% HSV-2 seroprevalence
Most infections occur by 5yo

Transmission
Mucosal contact
HSV-1 = Kissing
HSv-2 = Sexual contact

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50
Q

HSV Clinical Symptoms

A

Oral HSV-1 Herpes
Primary - asymptomatic/gingivostomatitis
Reactivation - asymptomatic/cold sores

Genital Herpes (HSV-1/2)
Primary - Severe gentialia blistering - can require hospitalisation
Reactivation - milder blistering or asymptomatic

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51
Q

HSV Management

A

Symptom relief

Antivirals - Aciclovir/Valaciclovir

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52
Q

HSV Diagnosis

A

PCR by lesion swab or CSF

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53
Q

VZV Pathogenesis

A

Infection occurs at respiratory mucosa/conjunctiva
Replication at the lymph node
Primary vireamia - replication in liver and spleen
Secondary Vireamia - skin dissemination
Chicken Pox (varicella)
Latency Period (Dorsal root ganglion)
Shingles (Zoster)

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54
Q

Varicella Epidemiology and Clinical Features

A

Peak age = 5yo around winter/spring - 90% household attack rate
Infectious from 2 days before rash till full crusting of vesicles
Diagnostic criteria - centripetal rash - range of macules - papules - vesicles - pustules

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55
Q

Zoster Epidemiology and Clinical Features

A

25% get shingles with increasing incidence over 50
infectious from day rash appears to fully crusting of vesicles
Diagnostic criteria - rash in 1 dermatome

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56
Q

Otitis Externa Clinical Symptoms

A

Localised - follicle - furuncle
Diffuse
Malignant (rare) - locally destructive

Symptoms - ear pain, discharge and bleeding, redness of pinna, AEM, tympanic membrane, irritability in children

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57
Q

Otitis Externa Causes

A

Bacterial
Localised - S.aureus
Diffuse - S.aureus/H.influenzae

Fungal -
Candida albicans/aspergillus

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58
Q

Otitis Externa Treatment

A

Bacterial - Flucloxacillin

Fungal Spray - Clotrimazole/Acetic Acid

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59
Q

Otitis Media Symptoms

A 
(With effusion = Glue ear)
Hearing loss
Not commonly ear pain
fever/general malaise 
perforation (rare)
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60
Q

Otitis Media Causes

A

Bacterial:
Strep pyogenes/Strep pneumoniae/H.influenzae/M.catarrhalis

Viral:
RSV/rhinovirus/adenovirus/ influenza

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61
Q

Otitis Media Treatment

A

Only treat with antibiotics if systemically unwell:
Amoxicillin (5-7 day course)

Children with recurrent infections - Gromit - stabilises pressures on either side of the tympanic membrane to prevent infection recurring

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62
Q

Clinical Symptoms of Labrynthitis/Vestibular Neuritis

A

Incapicitating vertigo
Dizziness
Nausea

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63
Q

Causes of Labrynthitis/Vestibulr Neuritis

A

Most commonly viral (HSV-1 after a URTI)

Bacterial case = more severe

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64
Q

Sinusitis and it’s clinical symptoms

A

Inflammation of the paranasal sinuses

Discoloured Nasal Discharge 
Pain/tenderness under eyes/nasal bridge
Coughing 
Pain in teeth 
Frontal Headaches
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65
Q

Causes of Sinusitis

A

Commonly viral:
RSV/parainfluenza/rhinovirus

Bacterial (secondary infection)
Strep pnuemoniae, S.aureus, M.cattarhalis, H.infleunzae

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66
Q

Sinusitis Treatment

A

Only if systemically unwell (bacterial) - Phenoxymethylpenecillin

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67
Q

Throat Infections:

Acute Pharyngitis and Tonsillitis Definition

A

A.P = Inflammation of part of the throat behind the soft pallete
Tonsillitis - Inflammation of the tonsils

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68
Q

Throat Infection Causes

A

Viral - 85-95% adult (and children>5) throat infections
70% of child infections
Rhinovirus/influenza/corona/EBV

Bacterial:
Most common - Group A BH Strep (Strep Pyogenes)
H.influenzae

Fungal:
Candida albicans - pharyngitis
Neisseria gonorrhae - Gonococcal Pharyngitis

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69
Q

Quinsy Causes

A

Unilateral tonsilar abscess after tonsillitis
Strep pyogenes
S.aureus
H. influenzae

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70
Q

Causes and Treatment of Quinsy

A

Unilateral tonsillar abscess secondary to tonsillitis

Bacterial causes:
Strep.pyogenes/S.aureus/H/influenzae

Treatment - Specialist - IV antibiotics (risk of sepsis)

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71
Q

Epiglottitis Causes

A

Inflammation of the epiglottis
Bacterial Causes:
H.influenzae/BH A,B,C Streptococci - strep.pneumoniae

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72
Q

Explain the patterns of viral disease

A

Acute - short, lived, self resolving e..g flu
Subclinical - asymptomatic e..g polio
Persistent and chronic - acute/subclinical infection not resolved by host immune system e.g. Hep B
Latent - dormant virus that persistently reinfects e..g HSV
Slowly Progressive - take many year to manifest e..g SSPE

73
Q

Describe different incubation periods

A

IP = time period between exposure and onset of disease/symptoms

short - <7 days (localised)
moderate - 7-21 days e.g.influenza
long - months e.g. Hep A
very long - years e.g.HIV

74
Q

Define Generation time

A

Time period between exposure and an individual being infectious

75
Q

Define Reproduction Number (Ro)

A

The number of infections in a susceptible population caused by one virally infected individual

76
Q

Define vaccine

A

a biological preparation consisting of an attenuated or killed form of a microbe, it’s toxins or surface proteins which initiate an immune response

77
Q

What are the ideal properties of a vaccine?

A 
Only require few immunisations 
broadly protective 
cheap
stable 
few side effects 
induces effective immunity 
prevents disease transmission (Horizontal or vertical)
78
Q

Otitis Externa Causes

A

Bacterial
Localised - S.aureus
Diffuse - S.aureus/H.influenzae

Fungal -
Candida albicans/

79
Q

Otitis Externa Treatment

A

Bacterial - Flucoxacillin

Fungal - spray - clotrimazole/acetic acid

80
Q

Otitis Media Clinical Features

A

Hearing loss
Some ear pain (not common)
Perforation (rare)
fever

81
Q

Otitis Media Causes

A 
Bacteria:
Strep.pyogenes
strep.pneuomoniae
H.influenzae
M.catarhallis 
Viral:
RSV
Rhinovirus
Adenovirus
Influenza
82
Q

Otitis Media Treatment

A

Amoxicillin (only if systemically unwell = bacterial)

83
Q

Vestibular Neuritis/Labrynthitis Clinical Symptoms

A

Incapacitating Vertigo
Dizziness
Nausea and Vomiting

84
Q

Vestibular Neuritis/Labrynthitis Causes

A

More commonly viral than bacterial

85
Q

Sinusitis Clinical Symptoms

A

Inflammation of the sinuses

Tenderness under eyes and nasal bridge
Discoloured nasal discharge Frontal headaches
Tooth pain
Coughing

86
Q

Sinusitis Causes

A

Viral (more common)
RSV
Rhinovirus
Parainfluenza

Bacterial
Strep.pneuomoniae
H.influenzae
M.cattarhalis 
S.aureus
87
Q

Sinusitis Treatment

A

Phenyoxymethylpenecillin - only if systemically unwell

88
Q

Throat Infections Causes

A

Pharyngitis - inflammation of the part of that behind the soft pallete
Tonsilitis - inflammation of the tonsils

Causes 
Viral 
95% adult and children > 5yo, 70% children < 5yo
Rhinovirus
Influenza
Corona virus 
Parainfluenza 
EBV

Bacterial
Group A BH Strep - Strep pyogenes
H.influenzae

Fungal
Candida albicans - pharyngitis
Neisseria gonorrhae - Gonococcal pharyngitis

89
Q

Throat infection Treatment

A

FeverPAIN
Score 4/5 = 65% liklihood of Strep pyogenes
Phenoxymethylpencillin

90
Q

Epiglottitis Causes

A

Inflammation of the epiglottis
Causes
Streptococci - Strep pneumoniae
H.influenzae

91
Q

Viral Disease Patterns

A

Acute - short lived, self resolving e.g. Flu
Subclinical - asymptomatic e..g Polio
Persistent and Chronic - Acute or subclinical infections to controlled by the host immune system e.g. HepB
Latent - Dormant viruses which reinfect often e.g. HSV
Slowly progressive - take many years to manifest e.g. SSPE

92
Q

Incubation period

A

the time period between viral exposure and onset of symptoms of disease

93
Q

Generation time

A

time period between viral exposure and an individual being infectious

94
Q

Reproduction number

A

number of infections in a susceptible population caused by one virally infected individual

95
Q

Vaccine Definition and Ideal qualities

A

a biological preparation of an attenuated or killed form of. amicorbe, it’s toxins, or surface proteins which initiates an immune reponse

Qualities
Induces effective immunity 
requires few immunisations 
Cheap
Stable 
Few side effects 
Prevents disease transmission
Broadly effective
96
Q

Describe the 2 effector mechanisms of vaccines

A

B cells
Initiates replication and activation of long lived B cells (germinal centre of the lymph node) which produce IgG antibodies and plasma cells and activation of short lived B cells (medullary cord of Lymph node) which produce IgM antibodies.
B memory cells are also produced

T cells
Initiates activation of CD8 Lymphocytes - cytotoxic T cells and release of antiviral cytotoxins to kill virally infected cells.
T memory cells are also produced.

97
Q

Properties of Live Vaccine

A

Injected route, few doses, no adjuvant, long term immunity, good T cell response, mild side effects

98
Q

Properties of inactivated vaccine

A

injection (killed virus/toxins, viral like particle, polysaccharide), requires adjuvant (enhances immune response), short term immunity, weak T cell response, SE - pain at site of injection

99
Q

Vaccination Schedule at 8 weeks

A 
Diptheria
Tetanus 
Polio
Whooping Cough 
H Influenza B 
Hep B
PCV
Rota Virus 
Men B
100
Q

Vaccination Schedule at 1 year

A

MMR

Men C

101
Q

Vaccination Schedule at 12/13 years

A

HPV

102
Q

Vaccination Schedule at 14

A

Men ACWY

Triple Booster

103
Q

Vaccine Risks/Side effects

A 
Muscle and Joint pain 
Headaches
Site of injection pain 
mild fever 
fatigue 
anaphylaxis
104
Q

Measles

A 
Respiratory Transmission
10 day Incubation Period 
Ro - 18 days 
Prodromal Symptoms - 2-4 days
Kopliks spots and maculopapular rash

Infectious from onset of prodrome to 4 days after rash disappears

105
Q

Complications of Measles

A

Diarrhoea
Susceptible to opportunistic infections - pneumonia, otitis media
CNS complications -Encephalitis, SSPE
Death

106
Q

Rubella and its complications

A

Respiratory Transmission
Mild disease in adults, clinical features - maculopapular rash and lymphadenopathy

Infectious from 1 wk before onset till 4 days after rash disappears

Pregnancy Complications - CRS
>12 wks - Fetal Malformations
13-16wks - Sensioneural Hearing Loss

107
Q

Mumps

A

Respiratory Transmission

Clinical Features
Parotiditis
Fever

Complications:
Swollen testicles (1 in 4)
Viral Meningitis (1 in 10)
Encephalitis

108
Q

MMR Vaccine Scandal and its consequences

A

1 year, Booster at 3 years 4 months

Scandal with Andrew Wakefield about MMR vaccine causing autism - reduced uptake in MMR vaccine in 2000s resulting in increased MMR incidence worldwide from 2017 - teenagers travelling etc increases spread

109
Q

Reporting Notifiable Infectious Diseases

A

Every medical practitioner has a statuary duty to report any suspected diagnosis of a notifiable disease (Do not wait for Lab confirmation)

All labs must report confirmation of NI diseases

Report via notification form to HPT officer - who report to PHE within 3 days

Important to report to:
Trace the source
Reduce spread and incidence
Early detection

110
Q

Role of HPT

A

HPT role to respond to:
Infectious diseases
Chemical radiation and hazards
Major emergencies

Importance:
Disease surveillance
Implement and monitor national action plans locally
Reduce infection spread

111
Q

Layers and Function of Meninges

A

Meninges - 3 membranous layers surrounding the brain and spinal cord

Function - to provide structural support and with CSF to protect CNS structures from mechanical damage

Dura Mater - outer fibrous double membrane tightly adhered to bone, separates to contain the sinus
Arachnoid Mater - thin translucent looser membrane
Pia Mater - thin translucent membrane which is tightly adhered to the sulci and gyri of the brain

112
Q

Dural Extensions

A

Tentorium cerebelli - seperaes the cerebellum from the rest of the brain
Falx cerebri - divides the cerebrum into 2 hemispheres
Falx cerebelli - divides the cerebellum into 2 hemispheres within the great longitudinal fissure

113
Q

Differences between the meninges around the spinal cord and the brain

A

Has an Epidural Space
Denticulate ligament - bilateral thickening of the pia mater
Filum Terminale - thick extension of the pia mater from the conus medullaris to the coccyx

114
Q

Blood Supply of the meninges

A

Anterior Meningeal Artery - Anterior Ethanoid artery - Ophthalmic Artery - Internal Carotid

Middle Meningeal Artery - Maxillary Artery - External Carotid Artery

Posterior Meningeal Artery - Ascending Pharyngeal Artery - External Carotid Artery

115
Q

Clinical Importance of the Middle meningeal artery

A

Lies underneath the pterion bone (thinnest and most fragile bone) - head trauma can cause it to fracture which can rupture the middle meningeal artery and cause an epidural bleed

116
Q

Clinical Importance of the Meningeal Spaces

A

Potential Epidural/Extradural Spaces
Subdural Space
Subarachnoid Space

Blood will collect in these spaces if there is a bleed

117
Q

Meningeal Innervation

A

Trigeminal Nerve (CNV) - 1st division - Ophthalmic Nerve

118
Q

Describe the Venous Sinuses

A 
No valves - blood flows in either direction - allows infection spread
Located within the dura mater 
Cavernosus Sinus - contains multiple cranial nerves:
occulomotor - extrinsic eye muscles
trochlear - oblique eye muscles
ophthalmic - eyeball
maxillary - nasal cavity, sinuses 
abduceris - eye lateral rectus muscle
119
Q

Longitudinal Fissure

A

divides the brain into 2 hemispheres

120
Q

Central Sulcus

A

divides frontal and parietal lobe

121
Q

Lateral fissure

A

divides frontal, parental and temporal lobe from the occipital lobe

122
Q

Parieto-occipital fissure

A

Divides parietal and occipital lobe

123
Q

Transverse fissure

A

Separates the occipital lobe and the cerebellum

124
Q

Cauda Equina

A

Extension of the Sarah, coccygeal, spinal and lumbar nerves.
Birth - L2/3
Adults - L1

125
Q

Conus Medullaris

A

Termination of the spinal cord

126
Q

Clinical Consideration of the Cavernosus Sinus

A

Easy infection spread due to no valves and dense connections - developing thrombi can compress nerves within the cavernosus sinus to cause palsy

127
Q

Connections between the ventricles

A

Lateral and 3rd = Interventricular foramen

3rd and 4th = Cerebral Aqueduct

128
Q

Importance and location of the 2 ventricular apertures/foramen

A

Median Aperture (of Magendie) and the 2 lateral aperture (of Luschka) - allow CSF to flow from the 4th ventricle to the Sub arachnoid space

129
Q

Where are there most likely to be ventricular obstructions?

A

Connections between the ventricles - interventricular duct, cerebral aqueduct, median and lateral apertures

130
Q

Cells involved in the BBB

A

Endothelial cells surround the blood vessels and have specific transport proteins on their surface and tight gap junctions between the cells to provide a physical barrier.

Astrocytes (glial cells) have end feet that wrap around the endothelial cells. Their function is to:
Provide a safe immunological environment
Provide adequate pH and nutrients for neurones
Provide structural support

131
Q

CSF Production and Circulation

A

30% of the CSF is produced by the ependymal cells in the ventricle walls (all 4).
The choroid plexus produces 70% of the CSF and is specialised tissue made up of ependymal cells.

Circulation
Lateral Ventricles - interventricular foramen - 3rd ventricle - cerebral aqueduct - 4th ventricle - apertures to the sub arachnoid space/spinal cord and tissue - reabsorbed via arachnoid granulations into the blood - reabsorbed into the dura mater sinuses via the sub arachnoid villi to recirculate (occurs due to the higher CSF cooled osmotic pressure than the blood, and due to the lower hydrostatic pressure in the sub arachnoid space than the sinuses)

132
Q

Lumbar Puncture Method

A

Extract a CSF sample from the cauda equina - nerves are seperated which reduces risk of nerve damage.

133
Q

Lumbar Puncture Diagnostic Use

A 
Normal = Clear appearance
Bacterial = Cloudy, low glucose, high protein
Viral = Cloudy/clear, normal glucose, normal/high protein 
TB = Slightly cloudy, viscous, low glucose, high protein
134
Q

Meningitis and it’s clinical Symptoms

A

Inflammation of the leptomeninges (Sub arachnoid and Pia Mater) of the brain and spinal cord.

Clinical Symptoms usually non-specific and vague at first - rapidly progress and require hospital admission within 24 hours. 
Symptoms:
Seizures
Altered Mental State
Headaches 
Fever
Stiff neck 
Back rigidity 
Photophobia 
Non blanching rash (trunk, wrists, arms)
135
Q

Meningococcal Meningitis

A

Non blanching petechial rash on trunk, backs of arms and wrists very suggestive of meningococcal meningitis.

Meningitis symptoms and symptoms of sepsis

136
Q

Bacterial causes of Meningitis

A 
Neonates
Strep agalactae (most common)
Strep pneumoniae
E coli 
Listeria Monocytogenes

Children
Strep pneumoniae
Neisseria meningitides
H influenzae

Adults
Strep pneumoniae
Neisseria meningitides

Elderly 
Strep pneumoniae 
Neisseria meningitides
H influenzae
Listeria monocytogenes
137
Q

Bacterial and Viral Meningitis Treatment

A

Treatment
Suspect Meningitis and NB rash present = Parenteral Benzylpenecillin and call 999 for immediate hospital admission

Suspect meningitis and no NB rash = Call 999 for immediate hospital admission
IPD or H.I.b = cefotaximine

Viral meningitis is clinically indistinguishable from bacterial - treat the same.

138
Q

Viral Meningitis Causes

A

Less severe and more common than bacterial
HSV-1/2
HIV
EBV
Non-polio virus (coxsackle or echoviruses)

139
Q

Meningitis Epidemiology

A

Reduced incidence in Men A, B, C and Y due to MenB and MenACWY vaccines

Increasing incidence of MenW - difficult to recognise as unusual symptoms so often goes unrecognised and without treatment rapidly progresses to death.

140
Q

Lyme disease

A

Bacterial CNS Infection - Borrelia Burgdorferi
Transmitted via tick to human

Stage 1 (localised) - erythema migrans at site 3-36 days days after bite

Stage 2 (disseminated):
neurological disorders (borrelia neurosis)
unilateral/bilateral facial palsy
meningitis/meningism 
mild encephalitis
141
Q

Viral Encephalitis Causes

A

HSV-1/2
EBV/CMV
VZV
Measles/Mumps

142
Q

HSE

A

HSE - HSV-1 in adults and children, HSV-2 in children < 3months
Most common in age extremities

Clinical Symptoms:
Altered consciousness 
Focal/generalised seizures
Raised intracranial pressure
Psychological symtoms 
Focal neurological symptoms

Treatment
Immediate treatment on suspicion of IV aciclovir 10-20 days

143
Q

Rabies Tranmission and Clinical Symptoms

A

enveloped negative sense ssRNA virus

Transmitted via an animal to human by saliva from bites/scratches

2-10 day period of non-specific symptoms after infection

3 weeks to 19 years for disease to manifest from periphery to the CNS

Clinical Symptoms 
Aggressive (Furious - 80%)
Paralysis (Dumb - 20%)
Excessive salivation
Seizures
Cranial and cerebral nerve dysfunction
Death
144
Q

Rabies Treatment and Prevention

A

Supportive treatment only once symptoms appear

Prevention
Post exposure prophylaxis - after immediate exposure to prevent virus taking hold
Highly effective vaccine

145
Q

Brain/Intracranial Abscess Causes and Treatment

A

Polymicrobrial cause:
S.aureus
Strep
Listeria species

Treatment:
Ceftriaxone
S.aureus - Metrondiazole and varimycin
Ampicillin or chloramphenicol
Surgical removal
146
Q

Japanese encephalitis cause

A

leading cause of viral encephalitis in Asia

flavivirus - enveloped positive sense ssRNA virus closely related to west nile virus and St Louis encephalitis virus

147
Q

Symptoms of Japanese Encephalitis

A

Majority - asymptomatic
Prodrome - fever, headache, D and V
Neurological syndrome - midl confusion - agitation - coma

148
Q

Tension Type Headache - Timing, Character, Triggers, Impact

A

Primary Headache
Lasts 30 mins - 7 days
Episodic < 15 days
Chronic > 15 days

Character
Tight band 
Squeezing pressure
Bilateral 
Neck Pain

Triggers
Stress
Anxiety
Depression

Impact
Mild - affect daily activities

149
Q

Types of Migraine

A

Migraine with Aura
Migraine without Aura
Migraine with aura and no headache

150
Q

Character of Migraine

A 
1. Prodrome
Fatigue
Irritability 
Depression
Food cravings
Difficulty concentrating
Stiff neck 
Variable in different individuals but same for each person each time
  1. Aura
    Fortification (zig zag lines)
    Scotoma - partial loss of vision in normal field
    Geometric patterns
    numbness/paraesthesia/speech, motor difficulties
  2. Headache
    Pulsating - severe
    Unilateral
    Associated with nausea or photo/phonophobia
  3. Postdrome
    Patient feels washed out
151
Q

Migraine Timing, Triggers and Impact

A

Timing:
4hrs - 3days - usually adolescent onset

Triggers:
Cheese/Chocolate
Lack of/too much sleep
Dehydration
Pre-menstrual 
Skipped meals

Impact:
Severe - need to go to sleep in dark room

152
Q

Cluster Headaches Timings, Character, Triggers and Impact

A

Timings:
30 mins - 3hrs usually at night
Wakes patient from sleep

Character:
Unilateral severe pain behind one eye
Rapid onset
Ipsilateral autonomic symptoms at same eye - nasal congestion, eye watering, facial sweating

Triggers:
Alcohol
Lack of Sleep
Impact - very severe, disports sleep, and affects work/school

153
Q

List types of Primary Headache

A 
Tension Type
Cluster
Migraine 
Sexual
Stabbing 
Cough
Thunderclap
Hypnic
Hemicrania continua
154
Q

How are secondary headaches diagnosed

A

Evidence of a condition which is known to cause headaches
Headaches resolved when underlying condition is resolved
Headaches correspond with timing of the underlying condition

155
Q

Sub Arachnoid Haemorrhage Causes

A

Bleeding into the sub arachnoid space

Causes:
Rupture of a berry aneurysm in the circle of willis (anterior cerebral, anterior choroidal, posterior cerebral arteries).

Blood acts as an irritant and bleeding causes an increase in intracranial pressure

156
Q

Sub Arachnoid Haemorrhage Clinical Features

A

Explosive thunderclap headache (worst headache ever within moments)
Occipital location
Meningism signs
Sentinal bleeds

157
Q

Giant Cell Arteritis Clinical Features

A

Medium and large artery vasculitis - commonly temporal but can affect any division of carotid artery

headache location at site of artery affected - commonly occipital or temporal

Jaw claudication
Amaurosis fugax - partial vision loss (can be permanent)
Scalp tenderness
Generally unwell - tired/stiff joints

158
Q

Raised Intracranial Pressure Clinical Features

A

Triad of headache, nausea nd vomiting and papilloedema
Altered mental state due to upper brain stem distortion
Generally worse in morning and when coughing

Late signs - Raised BP, wide pulse pressure and bradycardia

159
Q

Raised intracranial pressure causes

A

Space occupying lesion - tumour, heamatoma, abscess

1) direct pressure on brain
2) raising intracranial pressure
3) increased brain instability - seizures

Intracranial infection
Menigism triad - headache, neck stiffness, photophobia
Encephalitis triad - headache, fever, personality change

Head trauma/Bleed - S.A.H

160
Q

Red flag headache symptoms

A 
compromised immunity 
associated vomiting with no other cause 
Headache with seizures (SOL)
Worsening headaches
Headaches with vision loss
161
Q

NICE Guidelines for Antimigraine drugs

A

Most effective first line:
Oral triptan and oral NSAID

or Oral triptan with paracetamol

Consider antiemetic even in absence of N+V

162
Q

Migraine - Pre exposure prophylaxis

A

Consider:
If migraine treatment not working
If migraines are having severe impact
If getting medication overuse headaches

Topiramate or propanolol
(topiramate causes fetal malformations in pregnancy)

163
Q

Analgesics Clinical Use

A

Migraine treatment
NSAIDs, ibuprofen
taken at start of headache phase due to gastric stasis during migraines which prevents drug absorption

Alternative - diclofenac rectally

164
Q

Antiemetics clinical use

A

Migraine treatment
oral metoclopromazide
most useful in combination with analgesics
increases gastric emptying, reduces gastric stasis and increases drug absorption

can be given parenterally

165
Q

Triptans clinical use

A

Migraine treatment
5-HT1 receptor agonist (-triptan)
causes vasoconstriction to receive migraines
must be used in headache phase to be effective

can be even subcutaneously or as nasal spray

166
Q

Challenges of risk communication

A
  1. Different risk perceptions - different values, different risk taking/averting behaviours, values.
  2. quantifying terms differently
  3. Cognitive Bias
    Availability bias - people judge an event more if it is more available to them
    Confirmation bias - people look for confirming not non-confirming evidence of their beliefs
    Optimism bias
  4. Statistical illiteracy
167
Q

Tips for risk communication

A
  1. Use natural frequencies not percentages
  2. use positive framing
  3. use ARR rather than RRR or NNT
  4. Personalise risk information
  5. Present information in a supportive way
  6. Use decision aids
168
Q

Communication tips for shared decision making

A
  1. Provide correct amount of information - check prior knowledge, identify how much the patient wants to know, chunk and check
  2. Organise information - clear language, summarise, signpost, visual aids
  3. Check Patient ICE
  4. Share own thoughts and allow patient contribution
  5. Clarity of expression - check patient understanding and for any difference between doctor and patient beliefs
  6. Exploration - ICE and patient interpretation of information
169
Q

Principles of safeguarding children

A

Accountability - transparent actions
Empowerment - encourage victim to have input
Partnership - work with MDT
Prevention - taking action before harm can occur
Proportionality - proportional response to risk
Protection - advocate/ally for the child/family

170
Q

Early adversity consequences

A

Increased risk of injury, infectious diseases and chronic diseases
Poor mental health
Poor maternal health
Increased risky behaviours

171
Q

Child development timeline -Gross motor

A

6wks
Developing head control

3 months
Lift head - no head lag

6months
sit up with support
roll over

9months
sit without support
pull up to stand

12 months
sit independently
crawling and causing

18 months
walking and pushing toys

2 years
walk up the stairs (2 feet)
Kick a ball
walk backwards

3 years
walk up the stairs (alternate feet)
ride a tricycle
jump and stand on one foot

4 years
walk down stairs independently

172
Q

Child Development timeline - fine motor

A

6 weeks
hold objets momentarily
rolls
follow/fix on mum

3 months
hold rattle
loss of palmar reflex

6 months
hand to hand transfer
finger foo
open mouth for spoon

12 months
hold a cup
pincer grasp

18 months
stack 2 cubes
help to dress self
scribble

2 years
draw a line
take off socks and shoes

3 years
copy a circle
dress self with help

4 years
copy a cross
get dressed on own
hold a crayon correctly

5 years
draw stickmen
use a knife and fork

173
Q

Child development timeline - social and emotional

A

1 year
stranger anxiety

18 months
symbolic play

2 years
tantrums

3 years
toilet trained
sharing

4 years
parallel play

5 years
games with rules
take turns

174
Q

Child development timeline - Speech and language

A

6 weeks
smile

6 months
babble

1 year
1 - 2 words
pointing

2 years
can join 2 words

3 years
3-4 word sentences

4 years
tell past tense story
count to 20

5 years
understood by strangers
know colours/address etc

175
Q

Causes of child developmental delay

A

Gross motor
DMD
Cerebral Palsy
Dyspraxia

Fine motor/vision
muscle disorders
cerebral palsy
visual problems

Speech and language
hearing problems
autism
isolated speech and language delay

Emotional and social
Autism
neglect

176
Q

Define milestones and landmarks of development

A

Milestone - the upper limit of normal age a skill is achieved
Landmark - general feature of a development stage

177
Q

Factors influencing child development

A

Biological
prematurity
congenital defects (maternal health in pregnancy)
genetics

Pyschosocial 
Neglect
Social isolation
deprivation 
parental relationships
178
Q

How can family help child development

A 
Maintaining good child health 
positive attachments/relations
providing opportunities to practice skills
reading/singing songs
limiting screen time 
toddler groups
playing games

Flashcards (6 decks)

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