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Phase 3a - Arun&Erin > Paeds - Skin, Infectious diseases, Neuro, Psych > Flashcards

Paeds - Skin, Infectious diseases, Neuro, Psych Flashcards

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

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2
Q

What does atopic mean

A

Where there is evidence of IgE antibodies

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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

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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.

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5
Q

How does eczema of darker skin present

A

-may also effect the extensor surfaces
-patches of hyper and hypo pigmentation

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6
Q

DDX of eczema (5)

A

Psoriasis
Seborrhoeic dermatitis
Fungal infections
Contact dermatitis
Scabies

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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

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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)

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9
Q

What may be used if topical corticosteroids fail in eczema

A

Topical calcineurin inhibitors
-tacrolimus
-pimecrolimus

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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

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11
Q

Common topical steroid side effects

A

-redness
-stinging and burning
-skin atrophy (thinning)
-acne
-hyperpigmentation

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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
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13
Q

Tx of s.aureus skin infection from eczema

A

-Oral Flucloxacillin
-If severe may require IV abx

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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

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15
Q

Investigations of eczema herpeticum

A

Viral swabs of the vesicles

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16
Q

Treatment of eczema herpeticum

A

Aciclovir

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17
Q

Complications of eczema herpeticum

A

-In immunocompromised can be life threatening

-Bacterial superinfection

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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

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19
Q

Cause of Stephen Johnson syndrome

A

Medications
-anti epileptics
-allopurinol
-antibiotics
-NSAIDs

Infections
- herpes simplex
- mycoplasma pneumonia
- cytomegalovirus
- HIV

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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

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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

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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.

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23
Q

What is urticaria

A

Small itchy lumps that appear on the skin

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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

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25
Q

Causes of acute urticaria (6)

A

Allergies to food, medications or animals
Contact with chemicals, latex or stinging nettles
Medications
Viral infections
Insect bites
Dermatographism (rubbing of the skin)

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26
Q

What is Chronic idiopathic urticaria

A

Recurrent episodes of chronic urticaria without a clear underlying cause or trigger.

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27
Q

What is chronic inducible urticaria and give some examples

A

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)

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28
Q

What is autoimmune urticaria

A

Chronic urticaria associated with an underlying autoimmune condition, such as systemic lupus erythematosus.

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29
Q

Management of urticaria

A

Antihistamines
-Fexofenadines (chronic)

-Oral steroids for severe flares

Problematic cases
-LRTA
-Cyclosporins

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30
Q

What is allergic rhinitis

A

-IgE mediated type 1 hypersensitivity reaction to environmental allergens Causing a response in nasal mucosa

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31
Q

Three types of allergic rhinitis

A

Seasonal e.g hay fever

Perennial (year round) e.g house dust mite

Occupational - associate with work or school

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32
Q

Presentation of allergic rhinitis

A

-Runny, blocked and itchy nose
-Sneezing
-itchy, red and swollen eyes

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33
Q

How do you diagnose allergic rhinitis

A

-based on a history - FHX of atopic triad
-skin prick testing for pollen, dust mites etc

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34
Q

Triggers for allergic rhinitis

A

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

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35
Q

Management of allergic rhinitis

A
  • 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

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36
Q

Examples of non sedating antihistamines (3)

A

Cetirizine
Loratadine
Fexofenadine

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37
Q

Examples of sedating oral antihistamines

A

Chlorphenamine
Promethazine

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38
Q

Correct nasal spray technique

A
  • 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
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39
Q

What is anaphylaxis

A

Severe type 1 hypersensitivity reaction causing compromisation of the airways, breathing or circulation

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40
Q

How does a anaphylactic reaction occur - pathology

A

-IgE stimulates mast cells to rapidly release histamine and pro inflammatory chemicals - mast cell degranulation

-compromising airways and breathing and circulation

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41
Q

Give 6 Presentations of anaphylaxis

A

-Urticaria
-Itching
-Angio-oedema, with swelling around lips and eyes
-Abdominal pain
-SOB
-wheeze
-lightheadedness
-swelling of the larynx

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42
Q

How to manage anaphylaxis

A

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

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43
Q

What should happen after an anaphylactic event (3)

A

-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

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44
Q

When are epi pens given in anaphylaxis

A
  • TO ALL CHILDREN AND ADOLESCENTS with anaphylactic reactions

-children with generalised reactions but with certain risk factors

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45
Q

What are some risk factors that mean that those with only generalised allergic reactions get adrenaline auto injectors (5)

A
  • 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

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46
Q

Steps to use an adrenaline auto injector

A

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.

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47
Q

What are petechiae

A

Less than 3mm, non blanching, red spots caused by burst blood vessels

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48
Q

What are purpura

A

3-10mm, non blanching, red/purple macules, papules created by leaking of blood vessels

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49
Q

DDX of non blanching rashes

A

-Meningococcal septicaemia
-henoch schonlein purpura
-Idiopathic thrombocytopenic purpura (ITP)
-acute leukemias
-Haemolytic uraemic syndrome
-viral illness
-NAI

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50
Q

Management of non blanching rash

A

URGENT referral and investigation
-definitive Mx dependent on cause

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51
Q

Name 6 Non blanching rash Investigations

A

FBC
U+E
CRP
ESR
Coag screen
Blood culture
LP
BP
urine dipstick
Meningococcal PCR

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52
Q

Why FBC for non blanching rash investigation

A

-can detect anemia which can suggest leukemia or HUS
-can detect low white cells which can suggest leukemia
-low platelets can suggest ITP/HUS

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53
Q

Why LP for people with non blanching rash

A

To diagnose meningitis or encephalitis

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54
Q

Why urine dipstick investigation for non blanching rash

A

Proteinuria and haematuria can suggest HSP with renal involvement
Or Haemolytic uraemic syndrome

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55
Q

What a Kawasaki disease

A

Systemic, medium vessel vasculitis affecting young children typically under 5 years

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56
Q

What demographic is kawasakis more common in

A

Asian children, typically boys - Japanese and Korean

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57
Q

Presentation of kawasakis disease (7)

A

-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

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58
Q

What investigations would you do for suspected kawasakis (6)

A

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

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59
Q

How does kawasakis progress throughout its course

A

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

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60
Q

How long does each phase of kawasakis last

A

Acute: 1-2 weeks

Subacute: 2-4 weeks

Convalescent: 2-4 weeks

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61
Q

Management of kawasakis

A

High dose aspirin - to reduce thrombosis

IVIG - reduce coronary artery aneurysm risk

Follow up with echo to monitor

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62
Q

Why is aspirin rarely given in children

A

Risk of Reye’s syndrome - causes swelling of liver and brain

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63
Q

What is reye syndrome

A

Condition causing swelling in liver and brain

  • aspirin can cause this in children due to damaging mitochondria
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64
Q

What is meningitis

A

Inflammation of the lining of the brain and spinal cord usually due to viral or bacterial infection

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65
Q

What is meningococcus

A

A gram negative diplococcus of Nisseria meningitidis

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66
Q

What is meningococcal septicaemia

A

Meningococcus bacterial infection in the bloodstream

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67
Q

Most common causes of bacterial meningitis in children (2)

A

-Nisseria meningitidis (meningococcus)
-streptococcus pneumoniae (pneumococcus)

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68
Q

Most common cause of meningitis in neonates and how is it spread to the neonate

A

Group B strep - usually contracted form birth that live in mothers vagina

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69
Q

Sx of meningitis

A

Classic triad
-fever
-neck stiffness
-altered mental state

-vomiting
-headache
-photophobia
-seizures

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70
Q

When would you order a lumbar puncture as part of the meningitis investigations

A

-Children under 1 month
-1-3 months with fever and are unwell
-under 1 year with unexplained fever

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71
Q

What two tests are used to look for meninges irritation

A

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

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72
Q

Mx of bacteria meningitis in the community

A
  • urgent stat injection of IM or IV BENZYLPENECILLIN prior to hospital transfer
  • if Penecillin allergy transfer to hospital is still the priority
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73
Q

Hospital management of meningitis

A

-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

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74
Q

What is given for under 3 month babies in meningitis

A

Cefotaxime plus amoxicillin

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75
Q

Why is amoxicillin given in under 3 month babies with suspected meningitis

A

To cover listeria contracted during pregnancy

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76
Q

What Abx is given in addition to the usual in meningitis if there is a risk of pneumococcal infection that is Penecillin resistant

A

Vancomycin

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77
Q

Why might steroids be used in bacterial meningitis

A

To reduce the severity of hearing loss and neurological damage
-dexamethasone 4 times daily for 4 days over 3 months

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78
Q

What do you give for meningitis post exposure prophylaxis

A

Single dose of ciprofloxacin give ASAP

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79
Q

Most common causes of viral meningitis

A

Herpes simplex virus
Varicella zoster virus

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80
Q

How is viral meningitis treated

A

-Supportive tx
-Aciclovir

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81
Q

Complications of meningitis

A

-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

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82
Q

Where is a LP inserted

A

L3-4 invertebral space

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83
Q

What virus causes chickenpox

A

Varicella zoster virus (VSV)

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84
Q

Presentation of chicken pox

A

-widespread red papules progress to vesicles (fluid filled) and crust over
-fever
-itch
-fatigue and malaise

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85
Q

How is chickenpox spread

A

-highly contagious through direct contact with the lesions
-infected droplets from a cough or a sneeze

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86
Q

Complications of chickenpox (6)

A

-bacterial superinfection
-dehydration
-necrotising fasciitis
-conjunctival lesions
-pneumonia
-encephalitis
-shingles
-DIC

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87
Q

What does the reactivation of VSV lead to (2)

A

Shingles
Ramsay hunt syndrome

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88
Q

What is Ramsay hunt syndrome

A

Occurs when there is a shingles outbreaks that affects the facial nerve near one of the ears causing hearing loss and facial paralysis

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89
Q

Mx of chicken pox

A

-usually self limiting

-Aciclovir in immunocompromised patietns/ those at greater risk such as adolescents

-Chlorphenamine for itching

-avoid school

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90
Q

How is chickenpox in a pregnant mother around delivery time managed

A

-varicella zoster immunoglobulins
-Aciclovir

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91
Q

What is a bacterial superinfection

A

A second bacterial infection superimposed by the earlier one typically by another bacterial agent

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92
Q

Symptoms of chickenpox

A

Fever
Malaise
Feeding problems
Vomiting/diarrhoea
Headache
Rash

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93
Q

how to diagnose chickenpox

A

-usually clinical due to presence of fluid filled rash

-viral polymerase chain reaction

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94
Q

What is fetal varicella syndrome and how is it characterised

A

An intrauterine infection 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

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95
Q

What organism is measles caused by

A

Measles morbillivirus

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96
Q

What is the classic presentation of measles

A

-Fever
-coryzal symptoms
-conjunctivitis

Followed by exanthem - widespread rash

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97
Q

Which groups are at increased risk of measles (3)

A

Children less than 1year old
Pregnant
Immunocompromised patients

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98
Q

How is measles spread (2)

A

Person to person contact

Airborne droplets of respiratory secretions

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99
Q

Incubation period of measles

A

6-21 days

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100
Q

What does incubation period mean

A

time from acquisition of the pathogen to development of symptoms

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101
Q

Pathophysiology of measles

A

-virus replicates locally
-then spreads to regional lymph nodes
-spreads to other immune cell sites and around the the body
-leading to symptoms

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102
Q

How long are people infective for when they have measles

A

5 days before rash appearance
4 days after rash appearance

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103
Q

What are the four stages of measles infection

A

Incubation period
Prodromal period
Period of exanthem
Period of recovery

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104
Q

What is the prodromal period of measles

A
  • lasts 2-4 days

Characterised by:

Fever
Malaise
Anorexia
Conjunctivitis
Coryza: runny nose, sore throat, nasal stuffiness
Cough

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105
Q

What are Koplik spots

A

-usually occur 48 hours before exanthem
- white/grey lesions that have a red base
-typically located on buccal mucosa

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106
Q

What is the period of exanthem in measles

A

The development of a widespread erythema to us rash starting on the face then moving down

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107
Q

What type of rash occurs in measles

A

maculopapular, blanching rash that may become non-blanching in the later stages.

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108
Q

Diagnostic tests for measles

A
  • antibody testing:
    IgM - initial response - main diagnostic method
    IgG - long lasting

Viral PCR - samples of blood/ throat

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109
Q

Mx of measles

A

-usually self limiting

Supportive
-rest and fluid
-analgesia
-antipyretic

-avoid work and school

-notify the health protection team as is a notifiable disease

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110
Q

Complications of measles

A

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)

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111
Q

What is the vaccination programme for measles

A

-combines measles mumps and rubella (MMR)
-given at 1 and 3 years

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112
Q

What is encephalitis

A

Inflammation of the brain due to either autoimmune or infective causes

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113
Q

What the most common cause of encephalitis

A

Viral infection via Herpes simplex virus (HSV)

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114
Q

Most common cause of encephalitis in neonates

A

HSV-2 from Genital herpes contracted during birth

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115
Q

What viruses other than HSV can lead to encephalitis

A

-VSV
-CMV
-EBV
-enterovirus
-adenovirus
-influenza
-measles, mumps, rubella
-polio

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116
Q

Presentation of encephalitis in children

A

Fever
Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures

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117
Q

How to diagnose encephalitis

A

-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

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118
Q

Contraindications for a LP (3)

A

GCS below 9
Heamodynamically unstable
Active seizures

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119
Q

Management of encephalitis in children

A

Antivirals:
Aciclovir - treats HSV and VSV

Ganciclovir treats CMV

Repeat LP - to ensure successful treatment

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120
Q

Give 6 Complications of encephalitis (10)

A

Lasting fatigue
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance

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121
Q

What is impetigo

A

A superficial bacterial skin infection usually caused by staph aureus due to a break in the skin allowing them to enter

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122
Q

What are the two classifications of impetigo

A

Bullous or non bullous

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123
Q

What is non bullous impetigo

A

-usually occurs around the mouth and nose
-lesions that release exudate, but do not cause systemic symptoms or make child feel unwell

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124
Q

How to treat impetigo

A

-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

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125
Q

What is bullous impetigo patholophysiology

A
  • 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
Q

What is bullous impetigo

A
  • impetigo that always caused by s.aureus
  • lead to painful itchy areas
  • leads to systemic symtoms like fever, diarrhoea when lesions are widespread
127
Q

What is scalded skin syndrome

A
  • a severe superficial blistering skin disorder which causes outmost skin layer (epidermis), due to exotoxin release from specific strains of staph. Aureus
128
Q

How do you confirm diagnosis of impetigo

A

Swabs of the vesicles

129
Q

Tx of bullous impetigo

A

-Abx - s. Aureus usually with Flucloxacillin either orally/ IV

130
Q

Complications of impetigo

A

Cellulitis - if infection gets deeper

Sepsis

Scarring

Post strep glomerulonephritis - if strep pyogenes

Scalded skin syndrome

Scarlet fever

131
Q

What organism causes whooping cough

A

Bordetella pertussis

132
Q

Presentation of whooping cough

A

Starts with :
-coryzal symptoms
-low grade fever
-mild dry cough

Develops into:
-paroxysmal cough - recurring attacks of coughing
- loud inspiratory whoop

133
Q

Diagnosis of whooping cough (2)

A
  • nasal swab with PCR testing

-antipertussis toxin immunoglobulin G test - tested in oral fluid (5-16) / blood (17+)

134
Q

Management of whooping cough

A
  • supportive care

abx
- macrolides e.g erythromycin within first 21 days
- Vulnerable patients - co- trimoxazole
- vulnerable close contacts given prophylactic antibiotics

135
Q

What is HIV

A

A retrovirus that causes progressive immunodeficiency making the patient increasingly vulnerable to opportunistic infections

136
Q

What is AIDS

A

a state of immunodeficiency that results from infection with HIV

137
Q

What is the CD4 count for someone to have AIDS

A

Less than 200

138
Q

What are the different types of HIV

A

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
Q

How does HIV-1 work

A

-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
Q

Routes of transmission for HIV

A

-sexual transmission
Anal
Vaginal
Oral

-vertical transmission
In utero
Breast feeding

-Contaminated needles
Sharing needles

-Contaminated blood products and organs

141
Q

Three stages of HIV

A

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
Q

Give some examples of some AIDS defining illnesses

A

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
Q

What are the investigations for testing for HIV

A

HIV antibody screen - tests exposure to HIV virus

HIV viral load - tests directly for HIV in the blood

144
Q

When might HIV viral load be undetectable in a patient who has HIV

A

When a patient is on antiretroviral therapy

145
Q

When should babies who have HIV positive parents be tested

A

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
Q

Why might the antibody test be positive for HIV in infants who don’t have HIV

A

This is due to HIV maternal antibodies that have crossed the placenta during pregnancy.

147
Q

Tx for HIV (4)

A

-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
Q

What does antiretroviral therapy consist of
Give an example

A
  • 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
Q

What are the target measurements for viral load and CD4 count in testing

A

-viral load - <50 copies of viral genome/ ml blood

-CD4 count - >350 two readings a year apart

150
Q

What is PrEP

A

Pre exposure prophylaxis usually:
-Tenofovir Disoproxil / emtricitabine

151
Q

Who should PrEP be given to

A

-people who inject drugs
-trans, homosexual men and heterosexual people who have condomless sex especially ANAL

152
Q

What monitoring do patients with PrEP need

A

HIV test - 3 monthly
STI screening - 3 monthly
Renal function - based on age and eGFR

153
Q

How do NRTIs work and Give some examples of NRTIs for HIV (4)

A

Tenofovir disoproxil fumarate
Abacavir
Emtricitabine
Lamivudine

154
Q

Side effects of tenefovir disoproxil fumarate

A

-renal failure
-osteoporosis

155
Q

Lamivudine side effects

A

Pancreatitis

156
Q

Emitricitabine side effects

A

Hyperpigmentation of palms of hand and soles of feet

157
Q

Examples of NNRTIs, and whats the main problem with them

A

Efavirenz
Nevirapine
- resistance to these drugs

158
Q

Examples of integrase inhibitors for HIV
Give some complications of them

A

Dolutegravir
Raltegravir

Can cause weight gain, psychiatric illness, insomnia

159
Q

Protease inhibitor examples and side effects

A

Atazanavir
Darunavir
Lopinavir
-hyperlipidaemia, insulin resistance and hepatotoxicity.

160
Q

Signs and symptoms of rubella

A

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
Q

How to diagnose rubella

A

Serology - rubella IgM

162
Q

Management of rubella

A

Supportive - fluid and rest
Prevention: immunisation with MMR

163
Q

Complications of rubella (4)

A

-arthritis
-myocarditis
-encephalitis
-thrombocytopenia
-deafness if baby gets it from birth

164
Q

What is hand, foot and mouth disease caused by

A

Coxsackie A virus
enterovirus (rarely)

165
Q

Complications of hand foot and mouth disease

A

Dehydration
Bacterial superinfection
Encephalitis

166
Q

Mx of HFM disease

A

Supportive - fluid, analgesia (paracetamol)
Should resolve within 10 days

Avoid sharing towels ad bedding as contagious

167
Q

How can HFM disease be spread (4)

A
  • direct contact with cough or sneeze
  • direct contact of fluid from blisters
  • faeco oral transmission
  • vertical transmission
168
Q

Signs and symptoms of HFM disease (7)

A

Blistering red spots on hand, feet and mouth
Fever
Malaise
Decreased appetite
Cough
Abdo pain
Myalgia

169
Q

What are causes of toxic shock syndrome

A

Toxin-producing staphylococci or streptococci

170
Q

Signs and symptoms of toxic shock syndrome

A
  • high fever
    -Vomiting and diarrhoea
    -shock and hypotension
    -altered conscious level
    -myalgia
    -skin rash - diffuse macular rash
    -desquamation of palms and soles
171
Q

Treatment for toxic shock syndrome (3)

A

IV Antibiotics against staphylococci and streptococci. Clindamycin often added to flucloxacillin

IV immunoglobulin

IV fluids and resuscitation

172
Q

What is toxic shock syndrome

A

Bacterial infection release toxins into the bloodstream that spread to body organs causing multi systemic symptoms

173
Q

What is nikolsky sign

A

Nikolsky sign is where very gentle rubbing of the skin causes it to peel away. This is positive in SSSS.

174
Q

What is Staphylococcal Scalded Skin Syndrome

A

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
Q

Mx of SSSS

A

-IV antibiotics - oxacillin or vancomycin (MRSA)
-fluid and electrolyte balancing
-topical emollient
-dressings

176
Q

Treatment of candid alibicans infection

A

Oral or topical nystatin, fluconazole.

177
Q

Investigations for Candida albicans

A

Skin scrapings for microscopy and culture.

178
Q

Predisposing factors to candida albicans (4)

A

Moist body folds
Treatment with broad spec Abx
Immunosuppression
Diabetes mellitus

179
Q

What is severe combined immunodeficiency (SCID)

A

A severe cause of immunodeficiency due to a combination of different genetic disorders resulting in absent/dysfunctional T and B cells

180
Q

SCID presentation

A

-persistent diarrhoea
-failure to thrive
-opportunistic infections - CMV, chickenpox, pneumocystis jiroveci
-unwell after live vaccinations such as the BCG or MMR
-omen syndrome

181
Q

What is omen syndrome

A

Autosomal recessive syndrome that causes SCID due mutation in RAG1/2 that codes for important T and B cells

182
Q

Management of SCID (4)

A
  • treat underlying infections
  • immunoglobulin therapy
    -patient put in sterile environment
    -heamopoetic stem cell transplantation
183
Q

What is epilepsy

A

A Conditon where there is a tendency to have seizures

184
Q

What are seizures

A

transient episodes of abnormal electrical activity in the brain.

185
Q

What is a generalised tonic clonic seizure

A

Where there is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) movements.

186
Q

What signs are usually accompanied with tonic clonic seizures (4)

A

tongue biting
incontinence
groaning
irregular breathing

187
Q

Mx of tonic clonic seizures

A

1st line - sodium valporate
2nd line - lamotrigine or carbamazepine

188
Q

What happens after a generalised tonic clonic seizure

A

A post ictal period
-confusion
-drowsiness
-patient is irritable

189
Q

What are focal seizures

A

Seizures that start at the temporal lobe, and then can go on to become generalised

190
Q

How can focal seizures present (4)

A

Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot

191
Q

Mx of focal seizures

A

Reverse of tonic clonic

1st line - lamotrigine or carbamazepine
2nd - sodium valproate or Levatiracetam

192
Q

What are abscence seizures

A

A type of seizure that is characterised by the patient becoming blank, staring into space, and have no recollection of the incident

193
Q

Mx of absence seizures

A

First line: ethosuximide
Or sodium valproate

194
Q

What are atonic seizures

A

Seizures where there are Brief lapses in muscle tone usually last no longer than 3 minutes

195
Q

What condition may atonic seizures indicate

A

Lennox gastaut syndrome - a childhood onset epilepsy syndrome

196
Q

Tx for atonic seizures

A

First line: sodium valproate
Second line: lamotrigine

197
Q

What are myoclonic seizures

A

sudden brief muscle contractions where the patient usually remains awake

198
Q

Mx of myoclonic seizures

A

First line: sodium valproate

Other options: lamotrigine, levetiracetam or topiramate

199
Q

What is west syndrome

A

A rare disorder starting at around 6 months characterised by clusters of full body spasms

200
Q

Tx for west syndrome (2)

A

Prednisolone
Vigabatrin - for infantile spasms

201
Q

Investigations for seizures

A

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
Q

When should other pathology be considered for seizures in children e.g tumours (3)

A

-the first seizure is under 2 years
-focal seizures
-no response to 1st line anti epileptic

203
Q

What advice is given to children with seizures

A

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
Q

Sodium valproate side effects (4)

A

Teratogenic- don’t give to girls

Liver damage and hepatitis
Hair loss
Tremor

205
Q

Carbamazepine side effects

A

-Agranulocytosis
-Aplastic anaemia - body fails to make enough RBC
-Induces the P450 system so there are many drug interactions

206
Q

Phenytoin side effects (3)

A

-Folate and vitamin D deficiency

-anaemia (folate deficiency)

-Osteomalacia (vitamin D deficiency)

207
Q

Ethosuximide side effects (2)

A

Night terrors
Rashes

208
Q

Lamotrigine side effects

A

Stevens-Johnson syndrome or DRESS syndrome. These are life threatening skin rashes.
Leukopenia

209
Q

What is the management of when someone is having a seizure

A
  • 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
Q

What is the definition of status epilepticus

A

A seizure that either:
-lasts longer than 5 minutes
Or
-2 or more episodes without regaining consciousness

211
Q

Mx of someone with status epilepticus in hospital

A

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
Q

Medical options for status epilepticus in the community (2)

A

Buccal midazolam
Rectal diazepam

213
Q

What are febrile convulsions

A

type of seizure that occurs in children with a high fever.

214
Q

What are the two type of febrile convulsions

A

Simple
Complex

215
Q

What are simple febrile convulsions

A

Generalised tonic clonic seizures - last less than 15 minutes and only occur ONCE during the illness

216
Q

When can a febrile convulsion be described as a complex febrile convulsions (3)

A
  • when they consist of a partial or focal seizure
    -last more than 15 minutes
    -occur multiple times during the same febrile illness
217
Q

DDX of febrile convulsion

A

-epilepsy
-meningitis, encephalitis
-space occupying lesion in the brain
-syncope episode
-electrolyte abnormality
-trauma NAI

218
Q

Mx of a febrile convulsion

A

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
Q

What do febrile convulsion increase the chance of developing in the future

A

Epilepsy

220
Q

What is global developmental delay

A
  • a child who is displaying slow development in all the domains of development
221
Q

What are the domains of development (5)

A

Gross motor
Fine motor
Cognitive
Speech and language
Social

222
Q

What diagnosis could be indicated in those with global development delay (5)

A

Down’s syndrome
Fragile X syndrome
Fetal alcohol syndrome
Rett syndrome
Metabolic disorders

223
Q

What may gross Motor domain delay indicate (5)

A

-cerebral palsy
-ataxia
-myopathy
-spina bifida
-visual impairment

224
Q

What conditons may fine motor delay indicate (5)

A

-dyspraxia
-Cerberal palsy
-muscular dystrophy
-visual impairment
-congenital ataxia

225
Q

What conditions may a language delay indicate

A

-hearing impairment
-learning disability
-neglect
-autistic
-cerebral palsy
-specific social circumstances - such as multi language household

226
Q

What may a social delay indicate

A

-Emotional and social neglect
-Parenting issues
-Autism

227
Q

Examples of gross motor activities

A

Use of larger muscle groups:
-walking
-pushing
-pulling
-running

228
Q

Examples of fine motor tasks

A

Use of hands to do complex tasks
-eat
-draw
-play
-write

229
Q

What are examples of cognitive skills

A

-learning
-understanding
-problem solving

230
Q

Give 6 features of ADHD

A

-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
Q

What are the frameworks for ADHD diagnosis (2)

A

DSM-V
ICD-11

232
Q

What drugs can you give for ADHD in children (3)

A

1st line - methylphenidate (Ritalin)
2.lisdexafemtamine/ dexamfetamine
3.atomoxetine

233
Q

What is autistic spectrum disorder

A

Refers to a range of people affected by a deficit in social interaction,
communication and
flexible behaviour

234
Q

Risk factors for ADHD

A

-FHx
-low birth weight/pre term
-other neurodevelopement disorders (Autism)
-people with epilepsy
-adults with a mental health condition

235
Q

In which circumstance should you refer to cardiology before starting ADHD meds?

A

-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
Q

What are the three subtypes of ADHD

A

Combined presentation
Predominantly inattentive presentation
Predominantly hyperactive-impulsive presentation

237
Q

What are ADHD hyperactivity and impulsivity symptoms

A

Fidgety
Unable to sit still
Runs about or climbs
Noisy
Talks excessively
Difficulty waiting in line
Interrupts

238
Q

ADHD inattention symptoms

A

-careless mistakes
-difficulty sustaining attention
-difficulty listening
-difficulty organising
-loses things
-easily distracted by own thoughts
-forgetful

239
Q

What is anorexia nervosa

A

-eating disorder characterised by the restriction of energy intake resulting in low body weight and fear of weight gain

240
Q

Most prevalent age for anorexia nervosa

A

13-18 years old

241
Q

Risk factors for anorexia nervosa

A

-female gender
-age- adolescents
-FHx of eating disorders
-previous critics about weight and eating
-low self esteem
-obsessive personality
-history of sexual abuse

242
Q

symptoms of anorexia nervosa

A

-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
Q

What are some clinical features of anorexia nervosa

A

-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
Q

Investigations for anorexia nervosa

A

-ECG - for arrhythmia, prolonged QT

-blood sugar - hypoglycaemia

-blood tests - FBC, LFT, renal function, thyroid function to check for aneamia and thyroid dysfunction

245
Q

Management of anorexia nervosa

A

mostly managed in the community
- talking therapy
- supervised weight gain

If more servers then in urgent care/hospital
-nasogastric tubes feeding
-fluid intake
-daily ECG
-sedation if resisting feed

246
Q

What is re feeding syndrome

A

Fatal complication when malnourished patients receive sudden intake in calorific intake resulting in electrolyte imbalance and fluid retention

247
Q

What is the scoff questionaire

A

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
Q

What are some examinations done on people with anorexia

A

Vital signs - bradycardia, hypothermia and postural hypotension

Sit up, squat- stand test - assess difficulty lower the score worse it is

249
Q

What is bulimia Nervosa

A

A cycle of recurrent episodes of binge eating followed by inappropriate compensatory behaviours to avoid weight gain.

250
Q

What is a binge

A

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
Q

In bulimia Nervosa what are some inappropriate compensatory behaviours they use to prevent weight gain (4)

A

Behaviours known as PURGING
-self induced vomiting
-misuse laxatives
-exercise excessively
-fast

252
Q

Management of bulimia nervosa in children

A
  • 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
Q

Management of autism

A

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
Q

What are the three types of autistic features seen in people with autism
Give some examples of each

A

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
Q

Is rubella a notifiable disease

A

YES

256
Q

Scarlet fever cause

A

Group A strep e.g pyogenes

257
Q

Complications of scarlet fever (4)

A

Otitis media
Post strep glomerulonephritis
Acute rheumatic fever
Sepsis

258
Q

Complications of scarlet fever (3)

A

Otitis media
Post strep glomerulonephritis
Acute rheumatic fever

259
Q

Is scarlet fever a notifiable disease

A

Yes

260
Q

Features of scarlet fever

A

-Red, blotchy, macular rash
-sandpaper rash - on trunk first
- strawberry tongue
-sore throat
-fever
-lethargy
-cervical lymphadenopathy
-Flushed face

261
Q

Tx of scarlet fever

A

Penicillin V for 10 days
Kept off school for 24 hours

262
Q

Why do you want to avoid NSAIDs for patietns with chickenpox

A

Can cause bacterial superinfection

263
Q

What is a common asscoatied risk for toxic shock syndrome in women

A

Leaving a tampon or menstrual cup in for too long

264
Q

What organism causes slapped cheek syndrome/ fifth disease

A

-Parvovirus B19

265
Q

Symptoms of slapped cheek syndrome

A

-Bright red rash on both cheeks
-fever
-headache
-cough
-sore throat
-joint pain

266
Q

When are people with parvovirus B19 most infectious

A

They only are infectious 7 – 10 days before the rash appears

267
Q

Complications of parvovirus B19 during pregnancy (4)

A

Miscarriage or fetal death

fetal anaemia

Hydrops fetalis (fetal heart failure)

Maternal pre-eclampsia-like syndrome

268
Q

Investigations for parvovirus B19

A

-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)

269
Q

How does parvovirus cause fetal anemia & hydrops fetalis

A

-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)

270
Q

How does parvovirus cause fetal anemia

A

-Parvovirus B19 infects erythroid progenitor cells in the fetal bone marrow and liver which produce RBC that are faulty and have shorter life span

271
Q

What is maternal pre eclampsia syndrome

A

-complication of severe fetal heart failure (hydrops fetalis).
It involves a triad
-hydrops fetalis,
-placental oedema
-oedema in the mother

272
Q

Tx of parvovirus B19

A

Supportive treatment

-Intrauterine blood transfusion

273
Q

What is the complications of listeriosis is pregnant women

A

High rate of miscarriage
Fetal death
Neonatal infection

274
Q

What is the complications of listeriosis is pregnant women

A

High rate of miscarriage
Fetal death
Neonatal infection

275
Q

How is listeria transmitted (2)

A

Eating unpasteurised dairy products
Eating contained processed meats

276
Q

Mx of listeriosis

A

Amoxicillin
If listeria meningitis - IV amoxicillin

Pregnant woman - avoid high risk food such as blue cheese

277
Q

Ix for suspected listeria

A

Blood cultures - tumbling motility on wet mount (random reorientation of the bacteria during moving(

CSF - raised protein
- reduced glucose
- pleocytosis - increased cell count

278
Q

In which group of people f is listeria a lot more likely to occur

A

Pregnant women

279
Q

In which group of people f is listeria a lot more likely to occur

A

Pregnant women

280
Q

How do neonates get group B strep infection

A

-it may be present in the mothers bowel flora
-infants may be exposed to this during labour and therefore develop infection

281
Q

Risk factors for group B strep infection (4)

A

-prematurity
-prolonged rupture of the membrane
-previous siblings having Group B strep infection
-maternal fever due to infection

282
Q

Mx of group B strep in pregnant woman

A

Swabs at 35-37 weeks gestation

Intrapartum ABX prophylaxis - benzylpenecillin

283
Q

When should a woman be given Intrapartum antibiotic prophylaxis for group B strep (4)

A

-detected GBS in a previous pregnancy
-previous baby with GBS diseases
-preterm labour
-pyrexia above 38 degrees

284
Q

Risk factors for necrotising enterocolitis (6)

A

-low birth weight
-premature
-are on formula feeds
-respiratory distress/ assisted ventilation
-sepsis
-Patent ductus arteriosus

285
Q

Presentation of baby with necrotising eneterocolitis

A

-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

286
Q

How is poliovirus transmitted (2)

A

Faecal-oral transmission
aerosol droplets

287
Q

How does polio virus spread when in the body

A

-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

288
Q

Sx of poliovirus

A

high fevers
Vomiting
intense muscle pain
spasms and weakness,
loss of muscle reflexes
paralysis - affects upper legs and arms first

289
Q

Dx of poliovirus (3)

A

-Stool sample
Throat sample

-CSF sample + PCR

290
Q

Tx of polio

A

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

291
Q

Risk of giving live attenuated polio virus

A

Can revert to paralytic polio

292
Q

What is bulbar polio

A

When polio virus affects the motor nerves involved with speaking and swallowing

Leading to impaired breathing if motor nerves to the diaphragm get damaged

293
Q

What is post polio syndrome

A

Decades after infection causes aging of neurones and they die
Causes extensive loss of muscle function due to collateral nerves also being affected

294
Q

What is post polio syndrome

A

Decades after infection causes aging of neurones and they die
Causes extensive loss of muscle function due to collateral nerves also being affected

295
Q

What stain is used to detect mycobacterium tuberculosis

A

Ziehl Nielsen stain - goes bright red as it is ACID. Fast bacteria

296
Q

Mode of Transmission for TB

A

Inhalation

297
Q

What happens when TB first enters the lung and how does it progress

A

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

298
Q

What is systemic miliary TB?

A

Where TB spreads into the vascular system and can infect other organs e.g KIDNEYS, MENINGES, ADRENAL GLANDS

299
Q

How to test for TB

A

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

300
Q

Tx for TB

A

Active TB:
Rifampicin 6 months
Isoniazid 6 months
Pyrazinamide 2 months
Ethambutol 2 months

Latent TB:
Isoniazid and Rifampicin 3 months

301
Q

How many samples have to be collected for TB sputum culture

A

3 separate samples

302
Q

What occurs in reactivated TB

A

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

303
Q

Presentation of TB

A

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)

304
Q

Complications of eating disorders

A

Hypoglycaemia
Re feeding syndrome
Rhabdomyolysis
Osteoporosis
Arrhythmias
Seizures

305
Q

What is henoch schonlein purpura (HSP)

A

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.

306
Q

What organs are affected in HSP

A

skin
kidneys
gastro-intestinal tract

307
Q

4 classic features of HSP

A

Purpura (100%),
Joint pain (75%),
Abdominal pain (50%)
Renal involvement (50%) IgA nephritis

308
Q

Investigations for HSP

A

Exclude other pathology

FBC
Renal profile
Serum albumin
CRP
Blood cultures
Urine dipstick
BP

309
Q

Mx of HSP

A

Supportive - analgesia, fluid and rest

Repeated BP and urine dip for renal complications an HTN

310
Q

What is given to all HIV patietns with CD4 count less than 200/mm3

A

Co-trimoxazole to protect against pneumocystis jiroveci pneumonia

Phase 3a - Arun&Erin (15 decks)

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