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
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.
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).
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.
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.
6
Q
What drugs are ototoxic?
A
Aminoglycosides
Furosemide
Aspirin
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).
8
Q
Receptive Dysphasia
A
Difficulty comprehending speech
Damage to the Wernicke Area at the back of the temporal lobe
9
Q
Expressive Dysphasia
A
Difficulty producing speech
Damage to the broca area at the front of the temporal lobe
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.
11
Q
Time coding
A
Firing of action potentials synchronise, the timing between firing is used to identify frequency (only over 3Hz)
12
Q
What is the innervation of the Vestibular Apparatus?
A
Vestibulo-portion of CNVIII
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.
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.
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.
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).
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.
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.
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.
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
21
Q
Causes of Conductive Hearing Loss
A
Infection
Foreign Bodies - tumour, wax
Anatomical Abnormalities
Otosclerosis
22
Q
Causes of Sensioneural Hearing Loss
A
Ageing Noise induced Hereditary Disease - Tumours Head Trauma Drug Damage
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
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.
25
Describe pure tone audiometry
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
26
Describe the results of pure tone audiometry which would show conducive deficit
10dB gap between the conductive and sensioneural lines
| Lines plateau at around 60dB.
27
Describe the results of pure tone audiometry which would show sensioneural deficit
No gap between the 2 lines
| Steady decline with both lines with increasing frequency.
28
Describe different levels of hearing impairment
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
29
Describe ways to effectively communicate with patients with hearing impairments
```
Ensure good lighting on face
Pick a quiet area
Use hand gestures
Use facial expressions
Speak clearly
Use BSL
```
30
Describe ways to identify if a patient has hearing problems
```
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
```
31
Describe the viral life cycle
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)
32
Give examples of routes of viral transmission
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
33
What arbovirus does not use a vector for transmission?
Rabies
34
What is horizontal and vertical viral transmission?
Horizontal - between members of the same generation
| Vertical - between mother - fetus
35
Define pathogenicity
the severity of a disease caused by a virus
36
Define pathogenicity factors
the factors that allow a virus to cause a disease e.g. immune evasion, host cell entry method, replication
37
Define virulence
the severity of disease caused by a strain of the same virus
38
Define localised and generalised infections
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
39
Methods of prevention of viral infections
```
Good surveillance
Quarantine/Isolation of infected individuals
Vaccinations
Lifestyle changes
Vector control of arboviruses
Pre exposure Prophylaxis - HIV
Post exposure prophylaxis - Rabies/HIV
```
40
HCV Treatment
Acute:
Monitor for spontaneous recovery
Chronic:
Weekly Pegylated Interferon A (inhibits replication and increases host antiviral response)
Oral Ribovirin daily - stops viral RNA synthesis
41
HBV Treatment
Acute:
Supportive treatment
Chronic:
Weekly pegylated Interferon A (inhibits replication and increases host antiviral response)
Oral antiviral (tenofovir/entecevir) - inhibits HBV DNA polymerase
42
HSV Treatment
Oral Aciclovir or Valaciclovir
Aciclovir - activated by thymidine kinase (viral enzyme)
Valaciclovir - pro drug - increased bioavailability but more expensive
43
VZV Treatment
```
Children = self resolving
Adults = oral acyclovir/valaciclovir
```
44
CMV Treatment
CMV = problematic in transplant patients
| Ganaciclovir - inhibits viral DNA polymerase
45
Influenza Treatment
Vaccine - >65, Pregnant or 2 weeks post-partum women
Tamiflu (oral oseltamivir) = neuraminidase inhibitor
OR Z
Zanamivir (relenza)
46
What 9 viruses can be treated with antivirals?
HBV, HCV, HSV. VZV, CMV, Influenza, RSV, HPV, HIV
47
What is the structure of HSV
Double stranded enveloped DNA virus (fried egg virus)
48
HSV Lifecycle
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)
49
HSV Epidemiology and Transmission
Epidemiology
80% HSV-1 and 20% HSV-2 seroprevalence
Most infections occur by 5yo
Transmission
Mucosal contact
HSV-1 = Kissing
HSv-2 = Sexual contact
50
HSV Clinical Symptoms
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
51
HSV Management
Symptom relief
| Antivirals - Aciclovir/Valaciclovir
52
HSV Diagnosis
PCR by lesion swab or CSF
53
VZV Pathogenesis
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)
54
Varicella Epidemiology and Clinical Features
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
55
Zoster Epidemiology and Clinical Features
25% get shingles with increasing incidence over 50
infectious from day rash appears to fully crusting of vesicles
Diagnostic criteria - rash in 1 dermatome
56
Otitis Externa Clinical Symptoms
Localised - follicle - furuncle
Diffuse
Malignant (rare) - locally destructive
Symptoms - ear pain, discharge and bleeding, redness of pinna, AEM, tympanic membrane, irritability in children
57
Otitis Externa Causes
Bacterial
Localised - S.aureus
Diffuse - S.aureus/H.influenzae
Fungal -
Candida albicans/aspergillus
58
Otitis Externa Treatment
Bacterial - Flucloxacillin
| Fungal Spray - Clotrimazole/Acetic Acid
59
Otitis Media Symptoms
```
(With effusion = Glue ear)
Hearing loss
Not commonly ear pain
fever/general malaise
perforation (rare)
```
60
Otitis Media Causes
Bacterial:
Strep pyogenes/Strep pneumoniae/H.influenzae/M.catarrhalis
Viral:
RSV/rhinovirus/adenovirus/ influenza
61
Otitis Media Treatment
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
62
Clinical Symptoms of Labrynthitis/Vestibular Neuritis
Incapicitating vertigo
Dizziness
Nausea
63
Causes of Labrynthitis/Vestibulr Neuritis
Most commonly viral (HSV-1 after a URTI)
| Bacterial case = more severe
64
Sinusitis and it's clinical symptoms
Inflammation of the paranasal sinuses
```
Discoloured Nasal Discharge
Pain/tenderness under eyes/nasal bridge
Coughing
Pain in teeth
Frontal Headaches
```
65
Causes of Sinusitis
Commonly viral:
RSV/parainfluenza/rhinovirus
Bacterial (secondary infection)
Strep pnuemoniae, S.aureus, M.cattarhalis, H.infleunzae
66
Sinusitis Treatment
Only if systemically unwell (bacterial) - Phenoxymethylpenecillin
67
Throat Infections:
| Acute Pharyngitis and Tonsillitis Definition
A.P = Inflammation of part of the throat behind the soft pallete
Tonsillitis - Inflammation of the tonsils
68
Throat Infection Causes
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
69
Quinsy Causes
Unilateral tonsilar abscess after tonsillitis
Strep pyogenes
S.aureus
H. influenzae
70
Causes and Treatment of Quinsy
Unilateral tonsillar abscess secondary to tonsillitis
Bacterial causes:
Strep.pyogenes/S.aureus/H/influenzae
Treatment - Specialist - IV antibiotics (risk of sepsis)
71
Epiglottitis Causes
Inflammation of the epiglottis
Bacterial Causes:
H.influenzae/BH A,B,C Streptococci - strep.pneumoniae
72
Explain the patterns of viral disease
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
Describe different incubation periods
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
Define Generation time
Time period between exposure and an individual being infectious
75
Define Reproduction Number (Ro)
The number of infections in a susceptible population caused by one virally infected individual
76
Define vaccine
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
What are the ideal properties of a vaccine?
```
Only require few immunisations
broadly protective
cheap
stable
few side effects
induces effective immunity
prevents disease transmission (Horizontal or vertical)
```
78
Otitis Externa Causes
Bacterial
Localised - S.aureus
Diffuse - S.aureus/H.influenzae
Fungal -
Candida albicans/
79
Otitis Externa Treatment
Bacterial - Flucoxacillin
| Fungal - spray - clotrimazole/acetic acid
80
Otitis Media Clinical Features
Hearing loss
Some ear pain (not common)
Perforation (rare)
fever
81
Otitis Media Causes
```
Bacteria:
Strep.pyogenes
strep.pneuomoniae
H.influenzae
M.catarhallis
```
```
Viral:
RSV
Rhinovirus
Adenovirus
Influenza
```
82
Otitis Media Treatment
Amoxicillin (only if systemically unwell = bacterial)
83
Vestibular Neuritis/Labrynthitis Clinical Symptoms
Incapacitating Vertigo
Dizziness
Nausea and Vomiting
84
Vestibular Neuritis/Labrynthitis Causes
More commonly viral than bacterial
85
Sinusitis Clinical Symptoms
Inflammation of the sinuses
Tenderness under eyes and nasal bridge
Discoloured nasal discharge Frontal headaches
Tooth pain
Coughing
86
Sinusitis Causes
Viral (more common)
RSV
Rhinovirus
Parainfluenza
```
Bacterial
Strep.pneuomoniae
H.influenzae
M.cattarhalis
S.aureus
```
87
Sinusitis Treatment
Phenyoxymethylpenecillin - only if systemically unwell
88
Throat Infections Causes
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
Throat infection Treatment
FeverPAIN
Score 4/5 = 65% liklihood of Strep pyogenes
Phenoxymethylpencillin
90
Epiglottitis Causes
Inflammation of the epiglottis
Causes
Streptococci - Strep pneumoniae
H.influenzae
91
Viral Disease Patterns
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
Incubation period
the time period between viral exposure and onset of symptoms of disease
93
Generation time
time period between viral exposure and an individual being infectious
94
Reproduction number
number of infections in a susceptible population caused by one virally infected individual
95
Vaccine Definition and Ideal qualities
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
Describe the 2 effector mechanisms of vaccines
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
Properties of Live Vaccine
Injected route, few doses, no adjuvant, long term immunity, good T cell response, mild side effects
98
Properties of inactivated vaccine
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
Vaccination Schedule at 8 weeks
```
Diptheria
Tetanus
Polio
Whooping Cough
H Influenza B
Hep B
PCV
Rota Virus
Men B
```
100
Vaccination Schedule at 1 year
MMR
| Men C
101
Vaccination Schedule at 12/13 years
HPV
102
Vaccination Schedule at 14
Men ACWY
| Triple Booster
103
Vaccine Risks/Side effects
```
Muscle and Joint pain
Headaches
Site of injection pain
mild fever
fatigue
anaphylaxis
```
104
Measles
```
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
Complications of Measles
Diarrhoea
Susceptible to opportunistic infections - pneumonia, otitis media
CNS complications -Encephalitis, SSPE
Death
106
Rubella and its complications
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
Mumps
Respiratory Transmission
Clinical Features
Parotiditis
Fever
Complications:
Swollen testicles (1 in 4)
Viral Meningitis (1 in 10)
Encephalitis
108
MMR Vaccine Scandal and its consequences
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
Reporting Notifiable Infectious Diseases
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
Role of HPT
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
Layers and Function of Meninges
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
Dural Extensions
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
Differences between the meninges around the spinal cord and the brain
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
Blood Supply of the meninges
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
Clinical Importance of the Middle meningeal artery
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
Clinical Importance of the Meningeal Spaces
Potential Epidural/Extradural Spaces
Subdural Space
Subarachnoid Space
Blood will collect in these spaces if there is a bleed
117
Meningeal Innervation
Trigeminal Nerve (CNV) - 1st division - Ophthalmic Nerve
118
Describe the Venous Sinuses
```
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
Longitudinal Fissure
divides the brain into 2 hemispheres
120
Central Sulcus
divides frontal and parietal lobe
121
Lateral fissure
divides frontal, parental and temporal lobe from the occipital lobe
122
Parieto-occipital fissure
Divides parietal and occipital lobe
123
Transverse fissure
Separates the occipital lobe and the cerebellum
124
Cauda Equina
Extension of the Sarah, coccygeal, spinal and lumbar nerves.
Birth - L2/3
Adults - L1
125
Conus Medullaris
Termination of the spinal cord
126
Clinical Consideration of the Cavernosus Sinus
Easy infection spread due to no valves and dense connections - developing thrombi can compress nerves within the cavernosus sinus to cause palsy
127
Connections between the ventricles
Lateral and 3rd = Interventricular foramen
3rd and 4th = Cerebral Aqueduct
128
Importance and location of the 2 ventricular apertures/foramen
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
Where are there most likely to be ventricular obstructions?
Connections between the ventricles - interventricular duct, cerebral aqueduct, median and lateral apertures
130
Cells involved in the BBB
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
CSF Production and Circulation
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
Lumbar Puncture Method
Extract a CSF sample from the cauda equina - nerves are seperated which reduces risk of nerve damage.
133
Lumbar Puncture Diagnostic Use
```
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
Meningitis and it's clinical Symptoms
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
Meningococcal Meningitis
Non blanching petechial rash on trunk, backs of arms and wrists very suggestive of meningococcal meningitis.
Meningitis symptoms and symptoms of sepsis
136
Bacterial causes of Meningitis
```
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
Bacterial and Viral Meningitis Treatment
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
Viral Meningitis Causes
Less severe and more common than bacterial
HSV-1/2
HIV
EBV
Non-polio virus (coxsackle or echoviruses)
139
Meningitis Epidemiology
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
Lyme disease
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
Viral Encephalitis Causes
HSV-1/2
EBV/CMV
VZV
Measles/Mumps
142
HSE
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
Rabies Tranmission and Clinical Symptoms
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
Rabies Treatment and Prevention
Supportive treatment only once symptoms appear
Prevention
Post exposure prophylaxis - after immediate exposure to prevent virus taking hold
Highly effective vaccine
145
Brain/Intracranial Abscess Causes and Treatment
Polymicrobrial cause:
S.aureus
Strep
Listeria species
```
Treatment:
Ceftriaxone
S.aureus - Metrondiazole and varimycin
Ampicillin or chloramphenicol
Surgical removal
```
146
Japanese encephalitis cause
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
Symptoms of Japanese Encephalitis
Majority - asymptomatic
Prodrome - fever, headache, D and V
Neurological syndrome - midl confusion - agitation - coma
148
Tension Type Headache - Timing, Character, Triggers, Impact
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
Types of Migraine
Migraine with Aura
Migraine without Aura
Migraine with aura and no headache
150
Character of Migraine
```
1. Prodrome
Fatigue
Irritability
Depression
Food cravings
Difficulty concentrating
Stiff neck
Variable in different individuals but same for each person each time
```
2. Aura
Fortification (zig zag lines)
Scotoma - partial loss of vision in normal field
Geometric patterns
numbness/paraesthesia/speech, motor difficulties
3. Headache
Pulsating - severe
Unilateral
Associated with nausea or photo/phonophobia
4. Postdrome
Patient feels washed out
151
Migraine Timing, Triggers and Impact
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
Cluster Headaches Timings, Character, Triggers and Impact
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
List types of Primary Headache
```
Tension Type
Cluster
Migraine
Sexual
Stabbing
Cough
Thunderclap
Hypnic
Hemicrania continua
```
154
How are secondary headaches diagnosed
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
Sub Arachnoid Haemorrhage Causes
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
Sub Arachnoid Haemorrhage Clinical Features
Explosive thunderclap headache (worst headache ever within moments)
Occipital location
Meningism signs
Sentinal bleeds
157
Giant Cell Arteritis Clinical Features
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
Raised Intracranial Pressure Clinical Features
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
Raised intracranial pressure causes
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
Red flag headache symptoms
```
compromised immunity
associated vomiting with no other cause
Headache with seizures (SOL)
Worsening headaches
Headaches with vision loss
```
161
NICE Guidelines for Antimigraine drugs
Most effective first line:
Oral triptan and oral NSAID
or Oral triptan with paracetamol
Consider antiemetic even in absence of N+V
162
Migraine - Pre exposure prophylaxis
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
Analgesics Clinical Use
Migraine treatment
NSAIDs, ibuprofen
taken at start of headache phase due to gastric stasis during migraines which prevents drug absorption
Alternative - diclofenac rectally
164
Antiemetics clinical use
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
Triptans clinical use
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
Challenges of risk communication
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
Tips for risk communication
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
Communication tips for shared decision making
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
Principles of safeguarding children
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
Early adversity consequences
Increased risk of injury, infectious diseases and chronic diseases
Poor mental health
Poor maternal health
Increased risky behaviours
171
Child development timeline -Gross motor
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
Child Development timeline - fine motor
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
Child development timeline - social and emotional
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
Child development timeline - Speech and language
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
Causes of child developmental delay
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
Define milestones and landmarks of development
Milestone - the upper limit of normal age a skill is achieved
Landmark - general feature of a development stage
177
Factors influencing child development
Biological
prematurity
congenital defects (maternal health in pregnancy)
genetics
```
Pyschosocial
Neglect
Social isolation
deprivation
parental relationships
```
178
How can family help child development
```
Maintaining good child health
positive attachments/relations
providing opportunities to practice skills
reading/singing songs
limiting screen time
toddler groups
playing games
```
