Paeds - Skin, Infectious diseases, Neuro, Psych Flashcards
(331 cards)
1
Q
What is eczema
A
-Chronic atopic condition causes by defects in the normal skin barrier
-leading to inflammation in the skin due to allergens and bacteria entering the gaps in the skin barrier
2
Q
What does atopic mean
A
Where there is evidence of IgE antibodies
3
Q
Presentation of eczema (5)
A
-dry, red, itchy skin
-flexor surfaces, face and neck particularly sore
-episodic with flare ups
-thickening of the skin (lichenification)
-excoriation - removal of the skin
4
Q
Pathophysiology of eczema
A
-eczema is caused by defects in the barrier that the skin provides.
-Tiny gaps in the skin barrier provide an entrance for irritants, microbes and allergens that create an immune response
-resulting in inflammation and the associated symptoms.
5
Q
How does eczema of darker skin present
A
-may also effect the extensor surfaces
-patches of hyper and hypo pigmentation
6
Q
DDX of eczema (5)
A
Psoriasis
Seborrhoeic dermatitis
Fungal infections
Contact dermatitis
Scabies
7
Q
Management of eczema for maintenance
A
Create artificial barriers
-emollients - E45 used as much as possible and after washing - lotions, creams, gels, sprays
-soap substitutes
-bandages
Avoid triggers
- hot bathes
- cold weather
- dietary products - food diaries can help
- washing powders
- stress
Topical steroids
8
Q
Steroid ladder for eczema
A
Mild - hydrocortisone 0.5%, 1% and 2.5%
Moderate - clobetasone butyrate 0.05% (eumovate)
Potent - betamethasone valerate 0.1% (betnovate)
Very potent - clobetasol propionate 0.05% (dermovate)
9
Q
What may be used if topical corticosteroids fail in eczema
A
Topical calcineurin inhibitors
-tacrolimus
-pimecrolimus
10
Q
When would you use each topical calcineurin inhibitors
A
Tacrolimus - aged 2+ with moderate to severe disease to avoid skin atrophy and other adverse side effects from steroids
Pimecrolimus - aged 2-16 with moderate disease on face and neck to avoid skin atrophy and other adverse affects from steroids
11
Q
Common topical steroid side effects
A
-redness
-stinging and burning
-skin atrophy (thinning)
-acne
-hyperpigmentation
12
Q
What are the common organisms that cause nfection from eczema skin breakdown (3)
A
- s.aureus
- herpes simplex virus (HSV-1)
- varicella zoster virus
13
Q
Tx of s.aureus skin infection from eczema
A
-Oral Flucloxacillin
-If severe may require IV abx
14
Q
Presentation of eczema herpeticum
A
-widespread, vesicular rash (Fluid filled)
-punched out erosions left after vesicles burst
-fever
-lethargy
-irritability
-reduced oral intake
-lymphadenopathy
15
Q
Investigations of eczema herpeticum
A
Viral swabs of the vesicles
16
Q
Treatment of eczema herpeticum
A
Aciclovir
17
Q
Complications of eczema herpeticum
A
-In immunocompromised can be life threatening
-Bacterial superinfection
18
Q
What is stephens johnson syndrome
A
-disproportional immune response causing epidermal necrosis
-resulting in blistering and shedding of the top layer of the skin - less than 10% of body surface area affected
19
Q
Cause of Stephen Johnson syndrome
A
Medications
-anti epileptics
-allopurinol
-antibiotics
-NSAIDs
Infections
- herpes simplex
- mycoplasma pneumonia
- cytomegalovirus
- HIV
20
Q
Clinical presentation of Stephen Johnson syndrome
A
Start with:
Fever
Sore throat
Sore eyes
Itchy skin
Then develop
Purple/red rash
Blistering leaving raw tissue
Shedding of lips
Ulceration of eyes
21
Q
Mx of Stephen Johnson syndrome
A
-medical emergency supportive care -
Antiseptic
Analgesia
Nutritional care
Iv fluids - prevent dehydration from skin loss
Ointments for corneal blistering
Tx
Steroids - reduce inflammation
Immunoglobulins
Immunosuppressants - TNF inhibitors e.g infliximab to reduce inflammation
22
Q
Complications of stephens johnson syndrome
A
Secondary infection: The breaks in the skin can lead to secondary bacterial infection, cellulitis and sepsis
Permanent skin damage: damage to skin, hair, nails, lungs and genitals.
Visual complications: eye involvement can range from sore eyes to severe scarring and blindness.
23
Q
What is urticaria
A
Small itchy lumps that appear on the skin
24
Q
Pathophysiology of urticaria
A
-Release of histamine and pro inflammatory chemicals by mast cells
causing dermal oedema due to vessel dilatation
-may be part of an allergic reaction in acute urticaria
-may be part of autoimmune reaction in chronic urticaria
25
Causes of acute urticaria (6)
Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)
26
What is Chronic idiopathic urticaria
Recurrent episodes of chronic urticaria without a clear underlying cause or trigger.
27
What is chronic inducible urticaria and give some examples
episodes of chronic urticaria that can be induced by certain triggers, such as:
Sunlight
Temperature change
Exercise
Strong emotions
Hot or cold weather
Pressure (dermatographism)
28
What is autoimmune urticaria
Chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.
29
Management of urticaria
Antihistamines
-Fexofenadines (chronic)
-Oral steroids for severe flares
Problematic cases
-LRTA
-Cyclosporins
30
What is allergic rhinitis
-IgE mediated type 1 hypersensitivity reaction to environmental allergens Causing a response in nasal mucosa
31
Three types of allergic rhinitis
Seasonal e.g hay fever
Perennial (year round) e.g house dust mite
Occupational - associate with work or school
32
Presentation of allergic rhinitis
-Runny, blocked and itchy nose
-Sneezing
-itchy, red and swollen eyes
33
How do you diagnose allergic rhinitis
-based on a history - FHX of atopic triad
-skin prick testing for pollen, dust mites etc
34
Triggers for allergic rhinitis
Tree pollen or grass - seasonal symptoms (hay fever)
House dust mites and pets - persistent symptoms, worse in dusty rooms at night
Pets - persistent symptoms when the pet or their hair, skin or saliva is present
Mould
35
Management of allergic rhinitis
- AVOID the trigger - e.g dust mite allergy change pillows regularly and good ventilation
-oral antihistamines taken prior to exposure
-nasal corticosteroid sprays - fluticasone taken regularly
36
Examples of non sedating antihistamines (3)
Cetirizine
Loratadine
Fexofenadine
37
Examples of sedating oral antihistamines
Chlorphenamine
Promethazine
38
Correct nasal spray technique
- use opposite hand for whichever side nostril it is
-aim slightly outward from nasal septum
- DONT sniff as soon as you spray, but after
- shouldn’t taste it at the back of their mouth
39
What is anaphylaxis
Severe type 1 hypersensitivity reaction causing compromisation of the airways, breathing or circulation
40
How does a anaphylactic reaction occur - pathology
-IgE stimulates mast cells to rapidly release histamine and pro inflammatory chemicals - mast cell degranulation
-compromising airways and breathing and circulation
41
Give 6 Presentations of anaphylaxis
-Urticaria
-Itching
-Angio-oedema, with swelling around lips and eyes
-Abdominal pain
-SOB
-wheeze
-lightheadedness
-swelling of the larynx
42
How to manage anaphylaxis
A- airway is it secure
B – Breathing: Provide oxygen if required. Salbutamol can help with wheezing.
C – Circulation: Provide an IV bolus of fluids
D – Disability: Lie the patient flat to improve cerebral perfusion
E – Exposure: Look for flushing, urticaria and angio-oedema
Then THREE medications
-intramuscular adrenaline - repeated after 5 minutes if no improvement
-antihistamines - such as cetirizine
-steroids - usually IV hydrocortisone
43
What should happen after an anaphylactic event (3)
-period of assessment and observation - due to BIPHASIC reactions can occur
-measure serum mast cell tryptase within 6 hours of event
-educate and follow up with child and family - about allergy and how to manage, teach BLS and epi pen administration
44
When are epi pens given in anaphylaxis
- TO ALL CHILDREN AND ADOLESCENTS with anaphylactic reactions
-children with generalised reactions but with certain risk factors
45
What are some risk factors that mean that those with only generalised allergic reactions get adrenaline auto injectors (5)
- asthma needing inhaled steroids
-poor access to medical treatment e.g location
- adolescents
- nut or insect sting allergies which are higher risk
-significant co morbidities such as CVD
46
Steps to use an adrenaline auto injector
The first step is to confirm the diagnosis of anaphylaxis.
Prepare the device by removing the safety cap on the non-needle end. There is a blue cap on EpiPen and a yellow cap on Jext.
Grip the device in a fist with the needle end pointing downwards. The needle end is orange on EpiPen and black on Jext. Do not put your thumb over the end, because if the device is upside down you will inject your thumb with adrenalin and could risk losing it.
Administer the injection by firmly jabbing the device into the outer portion of the mid thigh until the device clicks. This can be done through clothing.
Remove the device and gently massage the area for 10 seconds.
Phone an emergency ambulance. A second dose may be given (with a new pen) after 5 minutes if required.
47
What are petechiae
Less than 3mm, non blanching, red spots caused by burst blood vessels
48
What are purpura
3-10mm, non blanching, red/purple macules, papules created by leaking of blood vessels
49
DDX of non blanching rashes
-Meningococcal septicaemia
-henoch schonlein purpura
-Idiopathic thrombocytopenic purpura (ITP)
-acute leukemias
-Haemolytic uraemic syndrome
-viral illness
-NAI
50
Management of non blanching rash
URGENT referral and investigation
-definitive Mx dependent on cause
51
Name 6 Non blanching rash Investigations
FBC
U+E
CRP
ESR
Coag screen
Blood culture
LP
BP
urine dipstick
Meningococcal PCR
52
Why FBC for non blanching rash investigation
-can detect anemia which can suggest leukemia or HUS
-can detect low white cells which can suggest leukemia
-low platelets can suggest ITP/HUS
53
Why LP for people with non blanching rash
To diagnose meningitis or encephalitis
54
Why urine dipstick investigation for non blanching rash
Proteinuria and haematuria can suggest HSP with renal involvement
Or Haemolytic uraemic syndrome
55
What a Kawasaki disease
Systemic, medium vessel vasculitis affecting young children typically under 5 years
56
What demographic is kawasakis more common in
Asian children, typically boys - Japanese and Korean
57
Presentation of kawasakis disease (7)
-**persistent high fever for more than 5 days**
- red maculopapular rash
-skin peeling on palms and soles
-strawberry tongue
-cracked lips
-cervical lymphadenopathy
-bilateral conjunctivitis
58
What investigations would you do for suspected kawasakis (6)
FBC - anaemia, leukocytes is and thrombocytosis
LFT - hypoalbuminemia
Inflammatory markers - ESR/CRP raised
Inflammatory markers - ESR raised
Urinalysis - shows raised WBC
ECHO - can show coronary artery pathology
59
How does kawasakis progress throughout its course
Acute phase - child most unwell with fever, rash and lymphadenopathy
Subacute phase - acute Sx settle - desquamation (skin shedding) and arthralgia (joint pain) occurs. Coronary aneurysms may form
Convalescent stage - remaining sx settle and blood tests return to normal
60
How long does each phase of kawasakis last
Acute: 1-2 weeks
Subacute: 2-4 weeks
Convalescent: 2-4 weeks
61
Management of kawasakis
High dose aspirin - to reduce thrombosis
IVIG - reduce coronary artery aneurysm risk
Follow up with echo to monitor
62
Why is aspirin rarely given in children
Risk of Reye’s syndrome - causes swelling of liver and brain
63
What is reye syndrome
Condition causing swelling in liver and brain
- aspirin can cause this in children due to damaging mitochondria
64
What is meningitis
Inflammation of the lining of the brain and spinal cord usually due to viral or bacterial infection
65
What is meningococcus
A gram negative diplococcus of Nisseria meningitidis
66
What is meningococcal septicaemia
Meningococcus bacterial infection in the bloodstream
67
Most common causes of bacterial meningitis in children (2)
-Nisseria meningitidis (meningococcus)
-streptococcus pneumoniae (pneumococcus)
68
Most common cause of meningitis in neonates and how is it spread to the neonate
Group B strep - usually contracted form birth that live in mothers vagina
69
Sx of meningitis
Classic triad
-**fever
-neck stiffness
-altered mental state**
-vomiting
-headache
-photophobia
-seizures
70
When would you order a lumbar puncture as part of the meningitis investigations
-Children under 1 month
-1-3 months with fever and are unwell
-under 1 year with unexplained fever
71
What two tests are used to look for meninges irritation
Kernigs test - flex one hip and knee at 90 degrees, and then slowly straighten the knee - will produce spinal pain or some resistance
Brudzinski test - lift their neck off the bed and flex chin to their chest - causes involuntary flexion of their hips and knees
72
Mx of bacteria meningitis in the community
- urgent stat injection of IM or IV BENZYLPENECILLIN prior to hospital transfer
- if Penecillin allergy transfer to hospital is still the priority
73
Hospital management of meningitis
-Lumbar puncture if there is time, but skip if patient acutely unwell
-blood test for meningococcal PCR
-give ABX
- under 3 months - cefotaxime plus amoxicillin
- above three months - ceftriaxone
74
What is given for under 3 month babies in meningitis
Cefotaxime plus amoxicillin
75
Why is amoxicillin given in under 3 month babies with suspected meningitis
To cover listeria contracted during pregnancy
76
What Abx is given in addition to the usual in meningitis if there is a risk of pneumococcal infection that is Penecillin resistant
Vancomycin
77
Why might steroids be used in bacterial meningitis
To reduce the severity of hearing loss and neurological damage
-dexamethasone 4 times daily for 4 days over 3 months
78
What do you give for meningitis post exposure prophylaxis
Single dose of ciprofloxacin give ASAP
79
Most common causes of viral meningitis
Herpes simplex virus
Varicella zoster virus
80
How is viral meningitis treated
-Supportive tx
-Aciclovir
81
Complications of meningitis
-Hearing loss
-Seizures and epilepsy
-Cognitive impairment and learning disability
-Memory loss
-Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity
-death
82
Where is a LP inserted
L3-4 invertebral space
83
What virus causes chickenpox
Varicella zoster virus (VSV)
84
Presentation of chicken pox
-widespread red papules progress to vesicles (fluid filled) and crust over
-fever
-itch
-fatigue and malaise
85
How is chickenpox spread
-highly contagious through direct contact with the lesions
-infected droplets from a cough or a sneeze
86
Complications of chickenpox (6)
-bacterial superinfection
-dehydration
-necrotising fasciitis
-conjunctival lesions
-pneumonia
-encephalitis
-shingles
-DIC
87
What does the reactivation of VSV lead to (2)
Shingles
Ramsay hunt syndrome
88
What is Ramsay hunt syndrome
Occurs when there is a shingles outbreaks that affects the facial nerve near one of the ears causing hearing loss and facial paralysis
89
Mx of chicken pox
-usually self limiting
-Aciclovir in immunocompromised patietns/ those at greater risk such as adolescents
-Chlorphenamine for itching
-avoid school
90
How is chickenpox in a pregnant mother around delivery time managed
-varicella zoster immunoglobulins
-Aciclovir
91
What is a bacterial superinfection
A second bacterial infection superimposed by the earlier one typically by another bacterial agent
92
Symptoms of chickenpox
Fever
Malaise
Feeding problems
Vomiting/diarrhoea
Headache
Rash
93
how to diagnose chickenpox
-usually clinical due to presence of fluid filled rash
-viral polymerase chain reaction
94
What is fetal varicella syndrome and how is it characterised
An intrauterine infection of varicella zoster characterised by one or more of :
-skin scarring
-hypoplasia of limbs (incomplete development)
-neurological disorder e.g learning difficulties
-eye disorder e.g cataracts
In the baby
95
What organism is measles caused by
Measles morbillivirus
96
What is the classic presentation of measles
-Fever
-coryzal symptoms
-conjunctivitis
Followed by exanthem - widespread rash
97
Which groups are at increased risk of measles (3)
Children less than 1year old
Pregnant
Immunocompromised patients
98
How is measles spread (2)
Person to person contact
Airborne droplets of respiratory secretions
99
Incubation period of measles
6-21 days
100
What does incubation period mean
time from acquisition of the pathogen to development of symptoms
101
Pathophysiology of measles
-virus replicates locally
-then spreads to regional lymph nodes
-spreads to other immune cell sites and around the the body
-leading to symptoms
102
How long are people infective for when they have measles
5 days before rash appearance
4 days after rash appearance
103
What are the four stages of measles infection
Incubation period
Prodromal period
Period of exanthem
Period of recovery
104
What is the prodromal period of measles
- lasts 2-4 days
Characterised by:
Fever
Malaise
Anorexia
Conjunctivitis
Coryza: runny nose, sore throat, nasal stuffiness
Cough
105
What are Koplik spots
-usually occur 48 hours before exanthem
- white/grey lesions that have a red base
-typically located on buccal mucosa
106
What is the period of exanthem in measles
The development of a widespread erythema to us rash starting on the face then moving down
107
What type of rash occurs in measles
maculopapular, blanching rash that may become non-blanching in the later stages.
108
Diagnostic tests for measles
- antibody testing:
IgM - initial response - main diagnostic method
IgG - long lasting
Viral PCR - samples of blood/ throat
109
Mx of measles
-usually self limiting
Supportive
-rest and fluid
-analgesia
-antipyretic
-avoid work and school
-notify the health protection team as is a notifiable disease
110
Complications of measles
Diarrhoea
Mesenteric lymphadenitis - abnormal lymph nodes
Secondary infections (e.g. otitis media, gastroenteritis, **pneumonia**)
Keratitis - inflammation of cornea
Myocarditis
Neurological (e.g. encephalitis, acute disseminated encephalomyelitis, subacute sclerosis panencephalitis)
111
What is the vaccination programme for measles
-combines measles mumps and rubella (MMR)
-given at 1 and 3 years
112
What is encephalitis
Inflammation of the brain due to either autoimmune or infective causes
113
What the most common cause of encephalitis
Viral infection via Herpes simplex virus (HSV)
114
Most common cause of encephalitis in neonates
HSV-2 from Genital herpes contracted during birth
115
What viruses other than HSV can lead to encephalitis
-VSV
-CMV
-EBV
-enterovirus
-adenovirus
-influenza
-measles, mumps, rubella
-polio
116
Presentation of encephalitis in children
Fever
Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
117
How to diagnose encephalitis
-LP for CSF sample and viral PCR testing
-CT scan if LP contraindicated
-MRI scan after the LP to visualise the brain
-EEG
-HIV testing recommended in patients with encephalitis
-swabs of throat and vesicles for causative organisms
118
Contraindications for a LP (3)
GCS below 9
Heamodynamically unstable
Active seizures
119
Management of encephalitis in children
Antivirals:
Aciclovir - treats HSV and VSV
Ganciclovir treats CMV
Repeat LP - to ensure successful treatment
120
Give 6 Complications of encephalitis (10)
Lasting fatigue
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance
121
What is impetigo
A superficial bacterial skin infection usually caused by staph aureus due to a break in the skin allowing them to enter
122
What are the two classifications of impetigo
Bullous or non bullous
123
What is non bullous impetigo
-usually occurs around the mouth and nose
-lesions that release exudate, but do not cause systemic symptoms or make child feel unwell
124
How to treat impetigo
-antiseptic cream (**1% H202**) 1st line
-topical fusidic acid
-Abx - oral flucloxacillin for widespread or severe impetigo
-patients told to not touch the lesions and stay off school until lesions go away for 48 hrs
125
What is bullous impetigo patholophysiology
- ALWAYS caused by staphylococcus aureus bacteria
- s.aureus produces epidermolytic toxins that break down the skin proteins
-leads to fluid filled vesicles forming on skin which burst leaving a GOLDEN CRUST that are painful and itchy
126
What is bullous impetigo
- impetigo that always caused by s.aureus
- lead to painful itchy areas
- leads to systemic symtoms like fever, diarrhoea when lesions are widespread
127
What is scalded skin syndrome
- a severe superficial blistering skin disorder which causes outmost skin layer (epidermis), due to exotoxin release from specific strains of staph. Aureus
128
How do you confirm diagnosis of impetigo
Swabs of the vesicles
129
Tx of bullous impetigo
-Abx - s. Aureus usually with Flucloxacillin either orally/ IV
130
Complications of impetigo
Cellulitis - if infection gets deeper
Sepsis
Scarring
Post strep glomerulonephritis - if strep pyogenes
Scalded skin syndrome
Scarlet fever
131
What organism causes whooping cough
Bordetella pertussis
132
Presentation of whooping cough
Starts with :
-coryzal symptoms
-low grade fever
-mild dry cough
Develops into:
-paroxysmal cough - recurring attacks of coughing
- loud inspiratory whoop
133
Diagnosis of whooping cough (2)
- nasal swab with PCR testing
-antipertussis toxin immunoglobulin G test - tested in oral fluid (5-16) / blood (17+)
134
Management of whooping cough
- supportive care
abx
- macrolides e.g erythromycin within first 21 days
- Vulnerable patients - co- trimoxazole
- vulnerable close contacts given prophylactic antibiotics
135
What is HIV
A retrovirus that causes progressive immunodeficiency making the patient increasingly vulnerable to opportunistic infections
136
What is AIDS
a state of immunodeficiency that results from infection with HIV
137
What is the CD4 count for someone to have AIDS
Less than 200
138
What are the different types of HIV
HIV-1: most common strain, found worldwide.
HIV-2: less common, it was first identified in 1986 in West Africa where it remains largely restricted. Is slower in course than HIV 1
139
How does HIV-1 work
-carries a glycoprotein-120 which attaches to CD4 receptor on T-helper cells
-HIV then enters the helper cells and has reverse transcriptase allowing RNA to go to DNA
-this viral DNA is incorporated into the host cells own genome catalysed by HIV enzyme integrase
-allows the HIV to produce viral proteins and replicate
-it can then go on and Infect other cells
140
Routes of transmission for HIV
-sexual transmission
Anal
Vaginal
Oral
-vertical transmission
In utero
Breast feeding
-Contaminated needles
Sharing needles
-Contaminated blood products and organs
141
Three stages of HIV
Acute - Asx or flu like symtoms ( fever, sore throat, malaise)
Chronic - around 6 months - tend to be Asx
AIDS - patients present with Malaise and fatigue, weight loss and opportunistic infections
142
Give some examples of some AIDS defining illnesses
Neoplasms
-non Hodgkin’s lymphoma
-cervical cancer
Bacterial
-recurrent pneumonia
-mycobacterium tuberculosis
-mycobacterium avium complex
Viral
-CMV
-HSV
-progressive multi focal leukoencephelopathy
Fungal
-PCP
-candidiasis
-cryptococcosis
Parasitic
-cryptosporidiosis
-cerebral toxoplasmosis
143
What are the investigations for testing for HIV
HIV antibody screen - tests exposure to HIV virus
HIV viral load - tests directly for HIV in the blood
144
When might HIV viral load be undetectable in a patient who has HIV
When a patient is on antiretroviral therapy
145
When should babies who have HIV positive parents be tested
HIV viral load test at 3 months - check for exposure during birth
HIV antibody test at 24 months -to assess whether they have contracted HIV since their 3 month viral load e.g from breastfeeding
146
Why might the antibody test be positive for HIV in infants who don’t have HIV
This is due to HIV maternal antibodies that have crossed the placenta during pregnancy.
147
Tx for HIV (4)
-Antiretroviral therapy (ART) to suppress the HIV infection
-Normal childhood vaccines, avoiding or delaying live vaccines if severely immunosuppressed.
-Prophylactic co-trimoxazole (Septrin) for children with low CD4 counts, to protect against pneumocystis jirovecii pneumonia (PCP)
-Treatment of opportunistic infections
148
What does antiretroviral therapy consist of
Give an example
- two nucleoside reverse transcriptase inhibitor (NRTIs)
- plus either a protease inhibitor, integrase inhibitor or non nucleoside reverse transcriptase inhibitor
E.g
Tenefovir- DF and emtricitabine (2xNRTIs)
Plus
Atazanavir
149
What are the target measurements for viral load and CD4 count in testing
-viral load - <50 copies of viral genome/ ml blood
-CD4 count - >350 two readings a year apart
150
What is PrEP
Pre exposure prophylaxis usually:
-Tenofovir Disoproxil / emtricitabine
151
Who should PrEP be given to
-people who inject drugs
-trans, homosexual men and heterosexual people who have condomless sex especially ANAL
152
What monitoring do patients with PrEP need
HIV test - 3 monthly
STI screening - 3 monthly
Renal function - based on age and eGFR
153
How do NRTIs work and Give some examples of NRTIs for HIV (4)
Tenofovir disoproxil fumarate
Abacavir
Emtricitabine
Lamivudine
154
Side effects of tenefovir disoproxil fumarate
-renal failure
-osteoporosis
155
Lamivudine side effects
Pancreatitis
156
Emitricitabine side effects
Hyperpigmentation of palms of hand and soles of feet
157
Examples of NNRTIs, and whats the main problem with them
Efavirenz
Nevirapine
- resistance to these drugs
158
Examples of integrase inhibitors for HIV
Give some complications of them
Dolutegravir
Raltegravir
Can cause weight gain, psychiatric illness, insomnia
159
Protease inhibitor examples and side effects
Atazanavir
Darunavir
Lopinavir
-hyperlipidaemia, insulin resistance and hepatotoxicity.
160
Signs and symptoms of rubella
Prodrome - mild illness with low grade fever
Exanthematous - maculopapular rash starting on the face then over the body
Lymphadenopathy around ears and base of skull
Petechiae on soft palate
161
How to diagnose rubella
Serology - rubella IgM
162
Management of rubella
Supportive - fluid and rest
Prevention: immunisation with MMR
163
Complications of rubella (4)
-arthritis
-myocarditis
-encephalitis
-thrombocytopenia
-deafness if baby gets it from birth
164
What is hand, foot and mouth disease caused by
Coxsackie A virus
enterovirus (rarely)
165
Complications of hand foot and mouth disease
Dehydration
Bacterial superinfection
Encephalitis
166
Mx of HFM disease
Supportive - fluid, analgesia (paracetamol)
Should resolve within 10 days
Avoid sharing towels ad bedding as contagious
167
How can HFM disease be spread (4)
- direct contact with cough or sneeze
- direct contact of fluid from blisters
- faeco oral transmission
- vertical transmission
168
Signs and symptoms of HFM disease (7)
Blistering red spots on hand, feet and mouth
Fever
Malaise
Decreased appetite
Cough
Abdo pain
Myalgia
169
What are causes of toxic shock syndrome
Toxin-producing staphylococci or streptococci
170
Signs and symptoms of toxic shock syndrome
- high fever
-Vomiting and diarrhoea
-shock and hypotension
-altered conscious level
-myalgia
-skin rash - diffuse macular rash
-desquamation of palms and soles
171
Treatment for toxic shock syndrome (3)
IV Antibiotics against staphylococci and streptococci. **Clindamycin often added to flucloxacillin**
IV immunoglobulin
IV fluids and resuscitation
172
What is toxic shock syndrome
Bacterial infection release toxins into the bloodstream that spread to body organs causing multi systemic symptoms
173
What is nikolsky sign
Nikolsky sign is where very gentle rubbing of the skin causes it to peel away. This is positive in SSSS.
174
What is Staphylococcal Scalded Skin Syndrome
A condition caused by a s.aureus that produces epidermoltyic toxins
When on there is a skin infection it causes the skin to break down
175
Mx of SSSS
-IV antibiotics - oxacillin or vancomycin (MRSA)
-fluid and electrolyte balancing
-topical emollient
-dressings
176
Treatment of candid alibicans infection
Oral or topical nystatin, fluconazole.
177
Investigations for Candida albicans
Skin scrapings for microscopy and culture.
178
Predisposing factors to candida albicans (4)
Moist body folds
Treatment with broad spec Abx
Immunosuppression
Diabetes mellitus
179
What is severe combined immunodeficiency (SCID)
A severe cause of immunodeficiency due to a combination of different genetic disorders resulting in absent/dysfunctional T and B cells
180
SCID presentation
-persistent diarrhoea
-failure to thrive
-opportunistic infections - CMV, chickenpox, pneumocystis jiroveci
-unwell after live vaccinations such as the BCG or MMR
-omen syndrome
181
What is omen syndrome
Autosomal recessive syndrome that causes SCID due mutation in RAG1/2 that codes for important T and B cells
182
Management of SCID (4)
- treat underlying infections
- immunoglobulin therapy
-patient put in sterile environment
-heamopoetic stem cell transplantation
183
What is epilepsy
A Conditon where there is a tendency to have seizures
184
What are seizures
transient episodes of abnormal electrical activity in the brain.
185
What is a generalised tonic clonic seizure
Where there is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) movements.
186
What signs are usually accompanied with tonic clonic seizures (4)
tongue biting
incontinence
groaning
irregular breathing
187
Mx of tonic clonic seizures
1st line - sodium valporate
2nd line - lamotrigine or carbamazepine
188
What happens after a generalised tonic clonic seizure
A post ictal period
-confusion
-drowsiness
-patient is irritable
189
What are focal seizures
Seizures that start at the temporal lobe, and then can go on to become generalised
190
How can focal seizures present (4)
Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot
191
Mx of focal seizures
Reverse of tonic clonic
1st line - lamotrigine or carbamazepine
2nd - sodium valproate or Levatiracetam
192
What are abscence seizures
A type of seizure that is characterised by the patient becoming blank, staring into space, and have no recollection of the incident
193
Mx of absence seizures
First line: ethosuximide
Or sodium valproate
194
What are atonic seizures
Seizures where there are Brief lapses in muscle tone usually last no longer than 3 minutes
195
What condition may atonic seizures indicate
Lennox gastaut syndrome - a childhood onset epilepsy syndrome
196
Tx for atonic seizures
First line: sodium valproate
Second line: lamotrigine
197
What are myoclonic seizures
sudden brief muscle contractions where the patient usually remains awake
198
Mx of myoclonic seizures
First line: sodium valproate
Other options: lamotrigine, levetiracetam or topiramate
199
What is west syndrome
A rare disorder starting at around 6 months characterised by clusters of full body spasms
200
Tx for west syndrome (2)
Prednisolone
Vigabatrin - for infantile spasms
201
Investigations for seizures
Electroencephalogram (EEG)
MRI of the brain
Additional:
ECG - excludes heart problems
Blood electrolytes - Na,K, Ca, mg
Blood glucose- rule out hypoglycaemia
Blood and urine cultures and LP - rule out meningitis and encephalitis and sepsis
202
When should other pathology be considered for seizures in children e.g tumours (3)
-the first seizure is under 2 years
-focal seizures
-no response to 1st line anti epileptic
203
What advice is given to children with seizures
Take showers rather than baths
Be very cautious with swimming unless seizures are well controlled and they are closely supervised
Be cautious with heights
Be cautious with traffic
Be cautious with any heavy, hot or electrical equipment
204
Sodium valproate side effects (4)
**Teratogenic**- don’t give to girls
Liver damage and hepatitis
Hair loss
Tremor
205
Carbamazepine side effects
-Agranulocytosis
-Aplastic anaemia - body fails to make enough RBC
-Induces the P450 system so there are many drug interactions
206
Phenytoin side effects (3)
-Folate and vitamin D deficiency
-anaemia (folate deficiency)
-Osteomalacia (vitamin D deficiency)
207
Ethosuximide side effects (2)
Night terrors
Rashes
208
Lamotrigine side effects
Stevens-Johnson syndrome or DRESS syndrome. These are life threatening skin rashes.
Leukopenia
209
What is the management of when someone is having a seizure
- put patient in a safe area
-place in recovery position if possible
-put something soft under head
-remove obstacles that could injure
-make a note of start and end point
-call ambulance if lasting more than 5 minutes or is their 1st
210
What is the definition of status epilepticus
A seizure that either:
-lasts longer than 5 minutes
Or
-2 or more episodes without regaining consciousness
211
Mx of someone with status epilepticus in hospital
**ABCDE**
-secure airway
-give high conc oxygen
-assess cardiac and resp function
-check blood glucose levels
-Gain IV access (cannula)
-IV lorazepam repeated after 10 minutes if seizure continues
-IV phenytoin
212
Medical options for status epilepticus in the community (2)
Buccal midazolam
Rectal diazepam
213
What are febrile convulsions
type of seizure that occurs in children with a high fever.
214
What are the two type of febrile convulsions
Simple
Complex
215
What are simple febrile convulsions
Generalised tonic clonic seizures - last less than 15 minutes and only occur ONCE during the illness
216
When can a febrile convulsion be described as a complex febrile convulsions (3)
- when they consist of a partial or focal seizure
-last more than 15 minutes
-occur multiple times during the same febrile illness
217
DDX of febrile convulsion
-epilepsy
-meningitis, encephalitis
-space occupying lesion in the brain
-syncope episode
-electrolyte abnormality
-**trauma NAI**
218
Mx of a febrile convulsion
1st - manage the underlying source of infection With analgesia
-paracetemol
-ibuprofen
2nd - reassure parents if simple febrile convulsion
If complex febrile convulsion then further investigations needed
219
What do febrile convulsion increase the chance of developing in the future
Epilepsy
220
What is global developmental delay
- a child who is displaying slow development in all the domains of development
221
What are the domains of development (5)
Gross motor
Fine motor
Cognitive
Speech and language
Social
222
What diagnosis could be indicated in those with global development delay (5)
Down’s syndrome
Fragile X syndrome
Fetal alcohol syndrome
Rett syndrome
Metabolic disorders
223
What may gross Motor domain delay indicate (5)
-cerebral palsy
-ataxia
-myopathy
-spina bifida
-visual impairment
224
What conditons may fine motor delay indicate (5)
-dyspraxia
-Cerberal palsy
-muscular dystrophy
-visual impairment
-congenital ataxia
225
What conditions may a language delay indicate
-hearing impairment
-learning disability
-neglect
-autistic
-cerebral palsy
-specific social circumstances - such as multi language household
226
What may a social delay indicate
-Emotional and social neglect
-Parenting issues
-Autism
227
Examples of gross motor activities
Use of larger muscle groups:
-walking
-pushing
-pulling
-running
228
Examples of fine motor tasks
Use of hands to do complex tasks
-eat
-draw
-play
-write
229
What are examples of cognitive skills
-learning
-understanding
-problem solving
230
Give 6 features of ADHD
-very short attention span
-quickly moving from one activity to the other
-losing interest in a task
-constantly moving or fidgeting
-impulsive behaviour
-disruptive/rule breaking
231
What are the frameworks for ADHD diagnosis (2)
DSM-V
ICD-11
232
What drugs can you give for ADHD in children (3)
1st line - methylphenidate (Ritalin)
2.lisdexafemtamine/ dexamfetamine
3.atomoxetine
233
What is autistic spectrum disorder
Refers to a range of people affected by a deficit in social interaction,
communication and
flexible behaviour
234
Risk factors for ADHD
-FHx
-low birth weight/pre term
-other neurodevelopement disorders (Autism)
-people with epilepsy
-adults with a mental health condition
235
In which circumstance should you refer to cardiology before starting ADHD meds?
-patient has history of cardiac pathology
-symptoms suggestive of cardiac pathology e.g HTN, SOB
-history of sudden death in 1st degree family member under 40 suggesting a cardiac disease
236
What are the three subtypes of ADHD
Combined presentation
Predominantly inattentive presentation
Predominantly hyperactive-impulsive presentation
237
What are ADHD hyperactivity and impulsivity symptoms
Fidgety
Unable to sit still
Runs about or climbs
Noisy
Talks excessively
Difficulty waiting in line
Interrupts
238
ADHD inattention symptoms
-careless mistakes
-difficulty sustaining attention
-difficulty listening
-difficulty organising
-loses things
-easily distracted by own thoughts
-forgetful
239
What is anorexia nervosa
-eating disorder characterised by the restriction of energy intake resulting in low body weight and fear of weight gain
240
Most prevalent age for anorexia nervosa
13-18 years old
241
Risk factors for anorexia nervosa
-female gender
-age- adolescents
-FHx of eating disorders
-previous critics about weight and eating
-low self esteem
-obsessive personality
-history of sexual abuse
242
symptoms of anorexia nervosa
-restriction of intake
-low body weight
-body dysmorphia
-rapid weight loss
-intense fear of weight gain
-aggressive weight loss techniques e.g vomiting
-withdrawals from social settings
243
What are some clinical features of anorexia nervosa
-excess weight loss
-amenorrhoea
-lanugo hair - fine soft and brittle
-hypokalaemia
-hypertension
-changes in mood and depression
-solitude
-cardiac complications - arrhythmia, sudden cardiac death
244
Investigations for anorexia nervosa
-ECG - for arrhythmia, prolonged QT
-blood sugar - hypoglycaemia
-blood tests - FBC, LFT, renal function, thyroid function to check for aneamia and thyroid dysfunction
245
Management of anorexia nervosa
mostly managed in the community
- talking therapy
- supervised weight gain
- family originated help
-CBT for eating disorder
If more servers then in urgent care/hospital
-nasogastric tubes feeding
-fluid intake
-daily ECG
-sedation if resisting feed
246
What is re feeding syndrome
Fatal complication when malnourished patients receive sudden intake in calorific intake resulting in electrolyte imbalance and fluid retention
247
What is the scoff questionaire
A tool used to help identify an eating disorder
- 2 or more indicate bulimia or anorexia
S- do you make yourself **sick** because you feel too full
C – Do you worry you have lost **Control** over how much you eat?
O – Have you recently lost more than **One stone** (6.35 kg) in a three-month period?
F – Do you believe yourself to be **Fat** when others say you are too thin?
F – Would you say **Food** dominates your life?
248
What are some examinations done on people with anorexia
Vital signs - bradycardia, hypothermia and postural hypotension
Sit up, squat- stand test - assess difficulty lower the score worse it is
249
What is bulimia Nervosa
A cycle of recurrent episodes of binge eating followed by inappropriate compensatory behaviours to avoid weight gain.
250
What is a binge
consuming an abnormally large amount of food in a relatively short period of time, which is associated with a sense of loss of control
251
In bulimia Nervosa what are some inappropriate compensatory behaviours they use to prevent weight gain (4)
Behaviours known as **PURGING**
-self induced vomiting
-misuse laxatives
-exercise excessively
-fast
252
Management of bulimia nervosa in children
- talking therapies
-psychological intervention
1. Bulimia guided focused family therapy
2. Eating disorder focused cognitive behavioural therapy
Pharmacological Tx
-high dose fluoxetine 60 mg OD (used alongside psychological therapy
Advise for self induced vomiters
-avoid acidic foods
-avoid brushing teeth right after
-rinse with non acid mouthwash after vomiting
-get a dental review
253
Management of autism
MDT approach - with dietician, paediatrician, social workers, child psychologists
Behavioural & educational interventions (e.g. high staff-to-student ratio, highly supportive teaching environment, predictability and structure)
Psychosocial interventions
Interventions for life skills (e.g. coping strategies for leisure activities, public transport and employment)
Interventions for speech and language problems (e.g. involvement of speech and language team)
Intervention for sleep disorders
Get family involved in care
254
What are the three types of autistic features seen in people with autism
Give some examples of each
Social interaction - lack of eye contact, avoids physical contact, difficult to have friends
Communication - delay in language, lack of smiling, eye contact or responding, repetitive use of phrases
Behaviour - stereotypical repetitive movements e.g hand flapping, greater interest in object and patterns than people, repetitive behaviour, anxiety around change to routine, picky with food
255
Is rubella a notifiable disease
YES
256
Scarlet fever cause
Group A strep e.g pyogenes
257
Complications of scarlet fever (4)
Otitis media
Post strep glomerulonephritis
Acute rheumatic fever
Sepsis
258
Is scarlet fever a notifiable disease
Yes
259
Features of scarlet fever
-Red, blotchy, macular rash
-sandpaper rash - on trunk first
- strawberry tongue
-sore throat
-fever
-lethargy
-cervical lymphadenopathy
-Flushed face
260
Tx of scarlet fever
Penicillin V for 10 days
Kept off school for 24 hours
261
Why do you want to avoid NSAIDs for patietns with chickenpox
Can cause bacterial superinfection
262
What is a common asscoatied risk for toxic shock syndrome in women
Leaving a tampon or menstrual cup in for too long
263
What organism causes slapped cheek syndrome/ fifth disease
-Parvovirus B19
264
Symptoms of slapped cheek syndrome
-Bright red rash on both cheeks
-fever
-headache
-cough
-sore throat
-joint pain
265
When are people with parvovirus B19 most infectious
They only are infectious 7 – 10 days before the rash appears
266
Complications of parvovirus B19 during pregnancy (4)
Miscarriage or fetal death
fetal anaemia
Hydrops fetalis (fetal heart failure)
Maternal pre-eclampsia-like syndrome
267
Investigations for parvovirus B19
-IgM to parvovirus, which tests for acute infection within the past four weeks
-IgG to parvovirus, which tests for long term immunity to the virus after a previous infection
-Rubella antibodies (as a differential diagnosis)
268
How does parvovirus cause fetal anemia & hydrops fetalis
-Parvovirus B19 infects erythroid progenitor cells in the fetal bone marrow and liver which produce RBC that are faulty and have shorter life span
-this anemia leads to heart failure (hydrops fetalis)
269
How does parvovirus cause fetal anemia
-Parvovirus B19 infects erythroid progenitor cells in the fetal bone marrow and liver which produce RBC that are faulty and have shorter life span
270
What is maternal pre eclampsia-like syndrome
-complication of severe fetal heart failure (hydrops fetalis).
It involves a triad
-hydrops fetalis,
-placental oedema
-oedema in the mother
271
Tx of parvovirus B19
Supportive treatment
-Intrauterine blood transfusion
272
What is the complications of listeriosis is pregnant women
High rate of miscarriage
Fetal death
Neonatal infection
273
How is listeria transmitted (2)
Eating unpasteurised dairy products
Eating contained processed meats
274
Mx of listeriosis
Amoxicillin
If listeria meningitis - IV amoxicillin
Pregnant woman - avoid high risk food such as blue cheese
275
Ix for suspected listeria
Blood cultures - **tumbling motility** on wet mount (random reorientation of the bacteria during moving(
CSF - raised protein
- reduced glucose
- pleocytosis - increased cell count
276
In which group of people is listeria a lot more likely to occur
Pregnant women
277
How do neonates get group B strep infection
-it may be present in the mothers bowel flora
-infants may be exposed to this during labour and therefore develop infection
278
Risk factors for group B strep infection (4)
-prematurity
-prolonged rupture of the membrane
-previous siblings having Group B strep infection
-maternal fever due to infection
279
Mx of group B strep in pregnant woman
Swabs at 35-37 weeks gestation
Intrapartum ABX prophylaxis - benzylpenecillin
280
When should a woman be given Intrapartum antibiotic prophylaxis for group B strep (4)
-detected GBS in a previous pregnancy
-previous baby with GBS diseases
-preterm labour
-pyrexia above 38 degrees
281
Risk factors for necrotising enterocolitis (6)
-low birth weight
-premature
-are on formula feeds
-respiratory distress/ assisted ventilation
-sepsis
-Patent ductus arteriosus
282
Presentation of baby with necrotising eneterocolitis
-vomiting green bile
-tender and distended abdomen
-absent bowel sounds
-blood in stool
Perforation of bowel can lead to shock symtoms like:
-loss of consciousness
-Tachypnoea
-not responding to touch
-cool skin
283
How is poliovirus transmitted (2)
Faecal-oral transmission
aerosol droplets
284
How does polio virus spread when in the body
-replicates in the small intestine and oropharynx in the mucosal cells
-then into lymph nodes and bloodstream
-then spreads to the central nervous system and replicates causes motor neurone destruction
285
Sx of poliovirus
high fevers
Vomiting
intense muscle pain
spasms and weakness,
loss of muscle reflexes
paralysis - affects upper legs and arms first
286
Dx of poliovirus (3)
-Stool sample
Throat sample
-CSF sample + PCR
287
Tx of polio
No treatment but prevention with polio vaccine either:
Supportive:
Pain medication
Bladder decompression
Respiratory support
Prevention:
Inactive poliovirus (IPV)
Oral - Live attenuated oral poliovirus (OPV)
Reduce effects of polio - GAMMA GLOBULIN
288
Risk of giving live attenuated polio virus
Can revert to paralytic polio
289
What is bulbar polio
When polio virus affects the motor nerves involved with speaking and swallowing
Leading to impaired breathing if motor nerves to the diaphragm get damaged
290
What is post polio syndrome
Decades after infection causes aging of neurones and they die
Causes extensive loss of muscle function due to collateral nerves also being affected
291
What stain is used to detect mycobacterium tuberculosis
Ziehl Nielsen stain - goes bright red as it is ACID. Fast bacteria
292
Mode of Transmission for TB
Inhalation
293
What happens when TB first enters the lung and how does it progress
Primary TB - first exposure infects alveolar macrophages
-can be Asx/ flu like sx
Then cell medicated immunity causes GRANULOMA to wall off bacteria - causes caseous necrosis (GHON FOCUS)
Spreads to lymph node - leading to GHON COMPLEX (caseating tissue)
Leads to **calcification** and scarring - Rankes complex
294
What is systemic miliary TB?
Where TB spreads into the vascular system and can infect other organs e.g KIDNEYS, MENINGES, ADRENAL GLANDS
295
How to test for TB
Tuberculin skin test/ Mantoux test - if they have EVER had disease
Inteferon gamma release assay - evidence of TB in blood
if these are positive - do a CXR to check if active TB
Sputum culture
bronchoalveolar lavage
296
Tx for TB
Active TB:
Rifampicin 6 months
Isoniazid 6 months
Pyrazinamide 2 months
Ethambutol 2 months
Latent TB:
Isoniazid and Rifampicin 3 months
297
How many samples have to be collected for TB sputum culture
3 separate samples
298
What occurs in reactivated TB
Due to aging or immunocompromised
Immune cells form caseous granulomas but with cavitation (gas filled space) usually in upper lobe as TB like aerobic condtions
The cavitation allows the TB to spread into further lung or vascular system
299
Presentation of TB
Cough
Haemoptysis (coughing up blood)
Lethargy
Fever or night sweats
Weight loss
Lymphadenopathy
Erythema nodosum (tender, red nodules on the shins caused by inflammation of the subcutaneous fat)
Spinal pain in spinal tuberculosis (also known as Pott’s disease of the spine)
300
Complications of eating disorders
Hypoglycaemia
Re feeding syndrome
Rhabdomyolysis
Osteoporosis
Arrhythmias
Seizures
301
What is henoch schonlein purpura (HSP)
An IgA vasculitis that causes a purpuric rash affecting the lower limbs and buttocks and Inflammation occurs in the affected organs due to IgA deposits in the blood vessels.
302
What organs are affected in HSP
skin
kidneys
gastro-intestinal tract
303
4 classic features of HSP
Purpura (100%),
Joint pain (75%),
Abdominal pain (50%)
Renal involvement (50%) IgA nephritis
304
Investigations for HSP
Exclude other pathology
FBC
Renal profile
Serum albumin
CRP
Blood cultures
Urine dipstick
BP
305
Mx of HSP
Supportive - analgesia, fluid and rest
Repeated BP and urine dip for renal complications an HTN
306
What is given to all HIV patietns with CD4 count less than 200/mm3
Co-trimoxazole to protect against pneumocystis jiroveci pneumonia
307
Causes of erythema multiforme
viruses: **herpes simplex virus (the most common cause)**
bacteria: Mycoplasma, Streptococcus
drugs: penicillin, sulphonamides, carbamazepine,
allopurinol, NSAIDs, oral contraceptive pill, nevirapine
connective tissue disease e.g. Systemic lupus
erythematosus
sarcoidosis
malignancy
308
Features of erythema multiforme
target lesions
-initially seen on the back of the hands / feet before spreading to the torso
upper limbs are more commonly affected than the
lower limbs
pruritus
309
Mode of transmission of diptheria
Respiratory -
Cough/ sneeze
Enter through Skin lesions
310
Mode of transmission of diptheria (2)
Respiratory -
Cough/ sneeze - pharyngeal diptheria
Enter through Skin lesions - cutaneous diptheria
311
Complications for diptheria
Death - psuedomembrane dislodges and causes asphyxiation
Myocarditis
Acute tubular necrosis (kidney)
Nerve demyelination:
Ocularmotor - diplopia
Diaphragmatic - breathing
312
Treatment for diptheria
Isolate patient
Macrolide e.g erythromycin
Or peneceillin G
+ Diptheria antitoxin
Vaccine 6 in 1 has diptheria
313
Dx of diptheria (3)
skin lesion or throat swab
Test for toxigenic: - ELEKS test - toxin will react with antitoxin plate and form a precipitate
PCR
314
Sx for diptheria
Low grade fever
Weakness
Malaise
Pharyngeal:
Bull neck
Sore throat
Grey leathery membrane in mouth
Cutaneous:
Shallow skin ulcers
315
Tx of Ramsay hunt syndrome
Aciclovir high dose
Prednisolone
Eye protection
316
Transmission of mumps
Respiratory droplets
317
Incubation period of mumps
14-25 days
318
Presentation of mumps
prodrome. These occur a few days before the parotid swelling:
Fever
Muscle aches
Lethargy
Reduced appetite
Headache
Dry mouth
**Parotid gland swelling, either unilateral or bilateral, with associated pain is the key feature that should make you consider mumps**
symptoms of the complications, such as:
Abdominal pain (pancreatitis)
Testicular pain and swelling (orchitis)
Confusion, neck stiffness and headache (meningitis or encephalitis)
319
Mx of mumps
Supportive - rest, fluid, analgesia
Noticeable disease so inform PHE
320
Complications of mumps (4)
Pancreatitis
Orchitis
Meningitis
Sensorineural hearing loss
321
Pathophysiology of sepsis
- **Pathogen Recognition**: Macrophages, lymphocytes, and mast cells identify invading pathogens.
- **Cytokine Release**: Cells release cytokines like **interleukins** and **tumor necrosis factor** to signal the immune system.
- **Immune Activation**: Cytokines activate other immune components, leading to further chemical release.
- **Vasodilation & Inflammation**: Chemicals like **nitrous oxide** cause blood vessels to widen, triggering body-wide inflammation.
322
What occurs in the inflammatory response during sepsis (5)
Increased Vessel Permeability: Cytokines make blood vessel linings more permeable, causing fluid leakage, oedema, and lowered blood volume.
Oxygen Delivery: Oedema around vessels creates a gap between blood and tissues, reducing oxygen supply.
Coagulation Activation: Blood clotting increases, causing fibrin buildup in vessels, impairing blood flow and oxygen delivery.
Disseminated Intravascular Coagulation (DIC): Clotting factors and platelets are consumed, causing thrombocytopenia (low platelets), bleeding, and clotting issues.
Lactate Rise: Lack of oxygen leads to anaerobic respiration in tissues, producing lactate as a waste product.
323
What is septic shock
sepsis has lead to cardiovascular dysfunction
324
Septic shock tx
IV fluids - improve the blood pressure and tissue perfusion.
If this fails
inotropes (such as noradrenalin) - stimulate the cardiovascular system and improve blood pressure and tissue perfusion.
325
Signs of sepsis children
-Deranged physical observations
-Prolonged capillary refill time (CRT)
-Fever or hypothermia
-Poor feeding
-Inconsolable or high pitched crying
-High pitched or weak cry
-Reduced consciousness
-Reduced body tone (floppy)
-Skin colour changes (cyanosis, mottled pale or ashen)
Respiratory distress (85%)
Grunting
Nasal flaring
Use of accessory respiratory muscles
Tachypnoea
Tachycardia: common, but non-specific
Apnoea (40%)
Apparent change in mental status/lethargy
Jaundice (35%)
Seizures (35%): if cause of sepsis is meningitis
Abdominal distention (20%)
Vomiting (25%)
326
What criteria should always be treated as sepsis
**Any baby under 3 months over 38 degree**
327
Immediate management of sepsis
-oxygen
-Obtain IV access (cannulation)
-Blood tests, including a FBC, U&E, CRP, clotting screen (INR), blood gas for lactate and acidosis
-Blood cultures
-Urine dipstick and MC+S
-Antibiotics 1 hour of presentation.
-IV fluids. 20ml/kg IV bolus of normal saline if the lactate is above 2 mmol/L or there is shock.
328
Most common causes for neonatal sepsis (2)
-Group B strep
-E.coli
Others:
Staphylococcus aureus
Enterococcus
Listeria monocytogenes
Viruses including herpes simplex and enterovirus
329
Risk factors for neonatal sepsis
-mother with previous group B strep infection/ has current GBS infection
-premature baby
-low birth weight
-evidence of chorioamnionitis
330
Antibiotic treatment of choice for neonatal sepsis
IV benzylpenicillin with gentamicin
331
What electrolyte imbalance is seen in anorexia nervosa
Hypokalaemia - due to vomiting and laxative use
