Gastro, Dermatology & Infectious diseases emergencies Flashcards
(85 cards)
1
Q
Can you describe the Rash of Lyme’s disease?
CKS NICE 2018
A
erythema migrans lesion-typically 5cm diameter - annular homogenous with central clearing and a bulls eye lesion
2
Q
How would you make the diagnosis of Lyme’s disease in the presence of erythema migrans lesion vs no lesion ( if there is no rash with the typical lesion )?
CKS NICE 2018
A
Erythema Migrans lesion on examination:
in the presence of the erythema migrans lesion- no diagnositc tests are necessary and will unnecessarily delay commencing treatment.
No Erythema Migrans Lesion on examination:
If Lyme disease is suspected in people without erythema migrans, offer an enzyme-linked immunosorbent assay (ELISA) test for Lyme disease (NICE CKS, 2018)
if the ELISA result is positive- offer immunoblot test
3
Q
What is the 3 serious complications of Lyme’s disease?
A
- Severe neurological symptoms.
* encephalitis
* meningitis
* impaired concentration and memory
* paraesthesia and numbness of the limbs
* Bell’s Palsy - cardiac- myocarditis, arrythmias
- Joints - Lyme Arthritis
- Skin - Acrodermatitis chronica atrophans.
4
Q
What is the first line treatment specific for Lyme’s disease in adults vs children?
A
all children above age 12 and adults- doxycycline 100mg Po BD for 21d ( or amoxicillin 1g po tds for 21d )
all children under the age of 12 years - amoxicillin 30mg/kg po tds for 21d
5
Q
Why is doxycycline contra-indicated in children under age 12 for treatment fo Lyme’s disease?
A
doxycycline can cause yellow tooth discolouration and dental enamel hypoplasia
6
Q
- When can Jarisch-herxheimer reaction occur?
- what is the pathophysiology of the reaction
- what are the symptoms?
A
- A Jarisch-Herxheimer reaction may develop (in up to 15% of people) in the first 24 hours of treatment with any antibiotic for Lyme disease.
- This is a systemic reaction thought to be caused by the release of cytokines when antibiotics kill large numbers of bacteria (NICE CKS, 2018).
- Symptoms include a worsening of fever, chills, muscle pains and headache. It may be mistaken for an allergic reaction and the person may stop their antibiotics (NICE CKS, 2018). The reaction can start between 1-12 hours after antibiotics are started, but can also occur later and can last for a few hours or 1-2 days (NICE CKS, 2018).
7
Q
Name 4 other patholiges that can mimic the changes of pneumonia on chest xray?
A
- pulmonary haemorage
- pulmonary aspiration
- SLE
- carcinoma
- contusion secondary to trauma
- pulmonary infarction
8
Q
If CURB 65 scores > 3, what is the next test that should be requested?
A
pneumococcal urine antigen testing
9
Q
What are the 10 risk factors in red flag sepsis?
A
Brain - GCS only V/P/U AND non-blanching rash
CVS - BP < 90mmhg AND HR > 130bpm
RESP - RR > 24 AND Spo2 < 92% on air
Renal - not passed urine in 18hours or < 0.5ml/kg/hour
Skin - mottled/ashen skin colour/cyanosis/non-blanching rash
OTHER: lactate >2, recent chemotherapy
10
Q
You recognize that a patient has red flag sepsis. What are the components of sepsis 6?
A
- Send blood cultures
- IV fluid resuscitation
- IV antibioitcs
- serial lactate measurements
- monitor urine output hourly
- administer oxygen to maintain spo2 > 94%
11
Q
in treating redflag sespsis - other than sepsis 6, what other 6 management steps need to be followed in the ED &later on the Ward?
A
- sepsis 6 within 60 minutes within 60 minutes
- review by senior st4 + within 60 minutes
- repeat observations half hourly in ED
- repeat lactate within 2 hours
- if septic shock or organ dysfunction - arrange review by critical care team
- arrangement to repeat laboratory bloods in 14 hours
- review y admitting consultant within 14hours
12
Q
What are the 6 management principles of patients recognized to have septic shock , according to the NICE sepsis toolkit 2016?
A
- sepsis 6 As soon as possible and within 60 minutes
- immediate review by senior ST4 + ED doctor
- Immediate referral to critical care outreach team
- ED duty consultant to be informed
- assembled the appropriate staff to initiate invasive monitoring and vasoactive therapy where necessary within 60 minutes of recognition
- where ventilatory support is required- attendance of appropriately skilled staff within 30 minutes of recognition
13
Q
A 26-year old Indian male presented to ED after being unwell for 5 days. He had generalized body weakness, fever and headache. In the last two days he had developed loose bowel motions and non-productive cough with dyspnoea. He had 7 episodes of loose stools and with no blood in the stool. In addition he had chills, rigors and calf pain.
He denied any vomiting; chest, abdominal or backache.
On examination he was not in any obvious respiratory distress but appeared unwell. His initial vital signs were BP 96/37, HR 119, temp 39.3, RR 26, Spo2 99% in room air and GCS 15/15. He had no jaundice, pallor, his chest was clear and abdominal exam was unremarkable. There was no rash but he had significant calf tenderness. what is the diagnosis?
A
In its mild form, leptospirosis may present as an
influenza-like illness with headache and myalgia.
Severe leptospirosis, characterized by jaundice, renal
dysfunction, and hemorrhagic diathesis, is referred to
as Weil’s syndrome. it isoften associated with viral flu like illness and calf tenderness.
14
Q
In a patient with septic shock - you use noradrenaline infusion - what is the mechanism of action and what dose ?
A
Mechanism of Action: endogenous catecholamine with strong alpha and weak beta adrenoceptor stimulation. dose 0.025mcg/kg/min.
15
Q
In a patient with septic shock - what are the unwanted side effects of noradrenaline?
A
- peripheral vasoconstriction
- reflex bradycardia
- hypertension
- hyperglycaemia
16
Q
In a patient with necrotizing fasciitis - what are the components of the LRINEC score? ( lab results in nec fac)
A
Serum Sodium <135 Glucose >10.0mmol/l Creatinine >140umol/L Haemoglobin <13.5g/dL WCC>15 x 10000/uL CRP >150
SCORE: of > 6 is the cut-off to rule in Nec Fac, but a score < 6 does not necessarily rule it out and 10% cases had nec fac with score < 6 in the study!
LRINEC score was used to distinguish NecFac from severe cellulitis/abscess.
this score was poorly validated in 2017 ( MDCALC resource )
17
Q
Indications for prescribing oral/iv thiamine to dependent alcohol drinkers?
A
- if they are malnourished or at risk of malnourishment or
- if they have decompensated liver disease or
- if they are in acute withdrawal or
- before and during a planned medically assisted alcohol withdrawal.
18
Q
What clinical features would suggest that a patient has alcoholic keto-acidosis?
A
The clinical features that suggest this are:
- History of heavy alcohol abuse, such that this man is malnourished. An alcohol binge, followed by abrupt cessation because of intercurrent illness is characteristic. Patients are invariably dehydrated at presentation.
- A pronounced metabolic acidosis with a normal blood glucose. If his serum chloride was available, then you could work out his anion gap which would be raised. This is rarely clinically useful.
19
Q
What is the role of prescribing a carbohydrate rich diet as part of the management of a patient with alcoholic keto-acidosis?
A
Carbohydrates are required to stimulate endogenous insulin production. This is important to turn off the ketone production.
20
Q
A patient presents witha human bite. you test him for Hepatitis B.
Interpret the following results:
- HBsAG -negative
- Anti-HBs -positive
- Anti-HBc -negative
Resource:
https://www.cdc.gov/hepatitis/hbv/pdfs/serologicchartv8.pdf
A
This patient has immune due to hepatitis B vaccine
- HBsAG
A protein on the surface of hepatitis B virus; it can
be detected in high levels in serum during acute or
chronic hepatitis B virusinfection. The presence of
HBsAg indicates that the person is infectious.
In this case he is not infectious. - Anti-HBs
The presence of anti-HBs is generally interpreted as
indicating recovery and immunity from hepatitis B
virus infection. Anti-HBs also develops in a person
who has been successfully vaccinated against
hepatitis B. - Anti-HBc -
Appears at the onset of symptoms in acute
hepatitis B and persists for life. The presence of
anti-HBc indicates previous or ongoing infection with
hepatitis B virus in an undefined time frame.
if it were positive - then in order to determine wether it is from a recent ( in last 6/12 )infection - send blood for IgM anti-HBc levels - and if the levels are high - it is a recent acute infection
- HBeAG -
if present - it indicates that the virus is replicating and the infected person has high levels of HBV and is highly infectious
21
Q
A 10 year old boy is in ITU. he developed an extensive rash after complaining of coryzal symptoms. the rash likes partial thickness burns to 80% of his body surface area.
What would your differential diagnosis be?
A
Differential diagnosis for partial thicnkness burns:
- Staphylococcus scalded skin syndrome
- Bullous impetigo
- Vasculitis
- Phemphigus and phemphigoid
- Kawasaki’s disease
- Urtricaria
- Burns
- Scarlet fever
- SLE
- Erythroderma/ Exfoliative dermatitis
- Toxic shock syndrome
- Herpetic infection- HSV and varicella - zoster
TABLE ON FRCEMSUCCESS website for causes of a mac-pap-erythematous rash:
measles - morbillivirus
rubella ( german measles ) - rubella virus
scarlet fever -streptococcus pyogenase
Fifths disease /infectiosum - parvovirus
sixth disease / roseola infantum - HHV 6
22
Q
What are the causes of Toxic epidermal necrolysis ( 10-30% skin involvement )
A
CAUSES OF TEN’S:
INFECTION-
Herpes simplex virus, Mycoplasma, TB, Cytomegalovirus, HIV, Adenovirus, Hepatitis, EBV, Histoplasmosis
DRUGS
Antibiotics- Sulphonamide, Penicillin, Chloramphenicol, Macrolides-Erythromycin, Quinolones-Ciprofloxacin
Anticonvulsants :-Barbiturates, Phenytoin, arbamazepine, Valproic acid, Lamotrigine
NSAIDs- Ibuprofen, Indomethacin, Oxicam.
23
Q
What is Nikolsky sign?
A
Nikolosky sign- Lateral pressure with finger on normal skin adjacent to bullous lesions dislodges the epidermis producing denuded dermis.
24
Q
What are the complications of Toxic epidermal necrolysis?
A
Sepsis - staphylococcal and pseudomonal species.
Hypovolaemic shock
Multiorgan failure
Disseminated intravascular coagulopathy
Thrombo-embolism
Respiratory failure- Pneumonia
25
What is erythema multiforme?
This is an acute inflammatory skin condition. The spectrum of skin disorder could range from papular eruption of the skin (EM minor) to a severe multisystem illness Steven Johnson's syndrome (EM major).
Steven johnsons syndrome <10% epidermal detachment.
26
WHat are the possible causes of erythema multiforme?
Causes -
INFECTION:
1. Herpes simplex virus,
2. Mycoplasma
3. TB
4. Cytomegalovirus and
5. HIV
DRUGS
1.Antibiotics- Sulphonamide, Penicillin
2.Anticonvulsants -Barbiturates, phenytoin,
carbamazepine
3.Nsaids
MALIGNANCY
·VACCINATIONS
·Radiation therapy
·Idiopathic.
27
What are the clinical features of erythema multiforme?
1. Malaise, fever, Myalgias, arthralgia and pruritis.
2. Rash features - variable hence the name multiforme. Maculopapular rash and target or iris lesions. Erythematous papules on dorsum of hand and feet, extensor surfaces of extremities. This rash evolves into the classic target lesions.
3. Vesicobullous lesions may appear this is pruritic and painful.
4. Steven Johnson's syndrome -Vesicobullous lesions on the mucosal surfaces, mouth, eyes, vagina, urethra and anus.
5. Ocular involvement in 9% of EM minor
28
What conditions are associated with pyoderma gangrenosum?
1. Crohns
2. Ulcerative colitis
3. Rheumatoid Arthrtitis
4. Haematological malignancy-
* Multiple myeloma ,
* leukaemia
5. Hepatitis
29
What is the differential diagnosis for pemphigus vulgaris?
Note : the incidence of PV = 3 in 100 000
1. Bullous pemphigoid
2. Pemphigus drug induced
3. Pemphigus herpetiformis
4. Herpetic lsions
5. Apthous ulcers
6. Bullous insect bite
7. Bullous impetigo
8. Epidermolysis bullosa
9. Erythema multiforme
10. Urtricaria
11. Dermatitis herpetiformis
12. Lichen planus
30
What is bullous pemphigoid?
http://pemfriends.co.uk/pemphigoid/bullous-pemphigoid/
BP is the most common immunobullous disease in Western Europe with a reported incidence of 43 per million per year in the U.K. It is a blistering skin disease that tends to affect the elderly.
31
What are the symptoms of Bullous Pemphigoid?
http://pemfriends.co.uk/pemphigoid/bullous-pemphigoid/
1. Pruritus is frequent and can occur weeks before rash.
2. Rash- erythematous or urticarial rash
3. Tense blisters or bullae on skin flexures or may be widespread
4. mucosal erosions in upto 25%
5. Intact pruritic fluid filled blisters
Bullous pemphigoid typically starts with a red, ITCHY rash that looks a bit like eczema or hives. This tends to last several weeks or months.
Then, groups of large, itchy blisters usually appear on the red patches, just beneath the surface of the skin. They can be up to 5cm in diameter and full of fluid, with the thick skin of the blisters stretched tightly.
The fluid inside is usually clear, but can turn cloudy or blood stained.
Blisters last a few days before healing without leaving a scar, but a cycle develops in which more form.
The rash and blisters are usually seen on the upper arms and thighs, sometimes spreading to body folds and the abdomen (tummy).
32
Can you describe the mouth and skin lesions of pemphigus vulgaris?
http://pemfriends.co.uk/pemphigus/pemphigus-vulgaris/
the blisters and erosions start first in the mouth, and appear later on the skin. In a few, the skin is affected first.
Other sites affected include the conjunctiva, oesophagus, labia, vagina, cervix, penis, urethra and anus. Most patients get erosions in their mouth at some time; but some never get blisters or erosions on their skin.
MOUTH:
* blistering superficial and often appears as erosions
* widespread involvement in the mouth
* painful and slow to heal
* may spread to the larynx causing hoarseness when talking
* may make it difficult to eat or drink
SKIN:
o Skin lesions are flaccid - intact blisters not found ( whereas in bullous pemphigus - tense blisters )
o PAINFUL skin rarely pruritic. ( In BP - it is itchy)
o Nail lesions may be present
o Mucous membrane lesions- painful erosions or
blisters and heal slowly - conjunctiva,
oesophagus or genetalia may be involved
33
How treatment would you prescribe for treating pemphigus vulgaris?
1. Mild oral disease - Topical therapy
2. Majority are treated with systemic steroids - high doses
3. Plasmapheresis to remove antibodies - along with
Cytotoxic drug azathioprine
4. i.v immunoglobulin
34
What are the casues of erythema nodosum?
CAUSES OF ERYTHEMA NODOSUM:
Streptococcal infection, including scarlet fever and rheumatic fever
• Sarcoidosis
• Viruses implicated Epstein-Barr virus, hepatitis B
and hepatitis C and HIV.
* Lymphogranuloma venerum
* Tuberculosis.
* Leprosy
* Sulfonylurea's, gold and oral contraceptives.
* crohn's disease or Ulcerative colitis.
35
How can you differentiate between pemphigus vulgaris and bullous pemphigoid?
Bullous Pemphigoid rash is the commonest autoimmune rash- associated with tense blisters. very itchy
Pemphigus Vulgaris - Flaccid rash- no intact blisters found . ( and the lesions are painful
36
Which drugs are associated with bullous pemphigoid?
1. Antibiotics( penicillamine)
2. captopril,
3. nsaids
4. furosemide
Bullous Pemphigoid is the most common autoimmune blistering disorder. This is characterised by sub epidermal blistering.
Incidence is higher in elderly population age> 65.
37
In Bullous Pemphigoid-
What immediate treatment measures would commence in the ED?
1. High potency topical corticosteroids have been shown to be effective in localised disease and is better tolerated in elderly eg dermovate cream
2. Extensive Disease requires immunosuppression with systemic steroids- prednisolone 30-60mg/day
3. Azathioprine , plasma exchange use - needs further evidence
4. Antibiotics for Secondary bacterial infection.
5. For resistant disease consider Methylprednisolone Cyclophosphamide , cyclosporin, methylpentolate chlorambucil and plasmapheresis
6. Mucosal disease requires difflam and tetracycline mouth washes
38
What are the potential causes of erythroderma?
http://www.pcds.org.uk/clinical-guidance/erythroderma
1. Eczema
2. Psorisasis
3. Lymphoma and leukaemia. Sezary syndrome t-cell
lymphoma associated with Erythroderma.
4. Dermatitis- Atopic, seborrhoeic and contact
5 Drug reaction –
*penicillin,
*phenytoin,
*captopril,
*sulphonamide etc.
6. Idiopathic
39
How do you diagnose scabies?
http://cks.nice.org.uk/scabies#!backgroundsub
1. History and examination. 2/3 burrows appear on
hand and wrists.
2. Borrow ink test
3. Parasitology – scraping of skin and microscopic
examination- sensitivity very low- most diagnosis
is clinically done.
40
What immediate treatment would you consider in your management of scabies?
1. Simultaneously treat all household members and close contacts (sexual) with Permethrin 5% 1st line or Malathion aqueous liquid 0.5%.
2. Treat itch- Topical crotamiton, chlorphenamine(limited evidence)
3. Advice on close contact
4. Inform HPA if outbreak in schools, nursing home or prisons.
41
1. Describe the rash of the scabies?
| 2. What are the complications of scabies?
1. Small burrows underneath the skin &
Skin excoriation- Acrodermatitis
2. Untreated scabies can cause secondary bacterial
infections:
Cellulitis, boils, Folliculitis, Impetigo or lymphangitis
42
1. What is the name of the condition when there is hyperinfestiation with millions of mites in patients with insufficient immune systems?
2. Which specific patient groups are at risk?
3. What causes the intense itch?
1. Norweigian scabies
2. Chronic corticosteroid use, HIV, Malnutrition, Human
T cell lymphocytic virus type 1, Learning difficulty ,
Dementia and Down’s syndrome
3. Symptoms of scabies are from immune reaction
(immediate or delayed) to Saliva, eggs or faeces.
43
1. Who is more likely to get staphylococcal scalded skin syndrome?
2. Which sign is positive on examination?
3. what is the name of the toxin?
4. How do you make the diagnosis?
1. children under age 5, and immunocompromised patient
2. Nikolsky sign
3. Epidermolytic toxins A&B
4. diagnosis is made on history, examination, Tsank smear, skin biopsy and bacterial culture
44
WHat complication commonly occurs in pregnant woman exposed to chicken pox?
varicella pneumonitis occurs commonly.
other infections include cellulitis, impetigo, furuncles, NECFAC
also neurological: Reyes syndrome, meningo-encephalitis
RIsk to fetus in the first 28 weeks of pregnancy: Intrau-uterine infections and FVS
45
what is the difference on clinical examination between measles and german measles ( Rubella )
MEASLES:
*more severe disease and in child age 3-5yrs
*3 C's - cough, coryza and conjunctivitis
*1 K - Koplik spots in buccal mucosa (which are tiny
grains of white sand, each surrounded by a red
ring
*Morbili virus
*morbilliform rash usually confluent
RUBELLA:
*milder disease, and in older children & adolescents & adults
* a macular, papular pruritic rash start behind the ears
* examination: lymphadenopathy & FORSCHHEIMER
SPOTS!
* usually no Koplik spots and rash is not confluent
* viurs = rubella virus
46
Name 3 cancers regarded as AIDS defining?
1. Cervical cancer
2. Karposi's sarcoma
3. Burkitt's Lymphoma
47
Can you name any MAJOR AIDS Defining opportunistic infections?
Reference:http://cks.nice.org.uk/hiv-infection-and-aids#!diagnosissub
Major AIDS-defining opportunistic infections
1. Candidiasis of the oesophagus or airways
2. Pneumocystispneumonia
3. Atypical or disseminated tuberculosis
4. cytomegalovirus retinitis
48
What are the common infectious causes of any maculopapular rash?
Common infectious causes of Maculopapular rash
1. Scarlet fever
2. Enterovirus and echovirus infection
3. Fifth disease (erythema infectiosum)
4. Roseola infantum (sixth disease)
5. EBV infection (infectious mononucleosis)
6. Cytomegalovirus infection
7. Scarlet fever
Uncommon causes
1. HIV-seroconversion exanthema
2. Acute hepatitis B virus infection
3. Acute hepatitis C virus infection
4. Rubella (German measles)
5. Rubeola (measles)
6. Meningococcaemia
7. Staphylococcal scalded skin syndrome
8. Toxic shock syndrome (Staphylococcus exotoxin)
9. Rocky Mountain spotted fever or Mediterranean spotted fever
10. Kawasaki disease (mucocutaneous lymph node syndrome)
11. Syphilis (secondary)
49
What are 4 of the clinical symptoms and 4 signs of HIV sero conversion?
SYMPTOMS:
```
Fever
rash
headache
sore throat
diahroea
malaise
arthralgia
```
SIGNS:
Clinical Signs
1. A blotchy maculopapular rash on the trunk, which may
spread to the palms of the hands and soles of the feet.
2. Oro-genital ulceration.
3. Ulcers in the orogenital or perianal areas.
4. Meningism (headache, neck stiffness, and
photophobia) .
5. lymphadenopathy.
6. Oral candidiasis.
7. Shingles.
50
Name 5 travel related infectious diseases?
1. African tick fever
2. Brucellosis
3. Chikungunya fever
4. East African trypanosomiasis (sleeping sickness)
5. Enteric fever (typhoid and paratyphoid fever)
6. Hepatitis
7. HIV seroconversion
8. Leptospirosis -
9. Acute schistosomiasis (katayama fever)
10. Viral haemorrhagic fevers:
11. Dengue
Other viral haemorrhagic fevers, such as yellow fever (Africa, South America), Lassa fever (western Africa), and Crimean-Congo haemorrhagic fever (Eastern Europe, Asia, Africa).
51
What are the clinical features of SEVERE malaria?
https: //cks.nice.org.uk/malaria#!diagnosisSub
http: //cks.nice.org.uk/malaria#!topicsummary
Features of severe or complicated malaria in adults include:
Parasitaemia >10%.
Cerebral malaria — impaired conscious level (Glasgow coma score less than 11) or seizures.
Renal impairment (may present with oliguria).
Acidosis (may present with acidotic breathing).
Hypoglycaemia (<2.2 mmol/l) — common in pregnant women.
Respiratory distress which may be due to pulmonary oedema or acute respiratory distress syndrome (ARDS) — common in pregnant women.
Severe anaemia (may present with pallor).
Spontaneous bleeding/disseminated intravascular coagulation.
Shock (BP < 90/60 mmHg).
Sepsis — more common in pregnant women.
Haemoglobinuria — falciparum can cause severe haemolysis with dark red urine (‘blackwater fever’).
52
WHat are the Complications of Malaria infection?
Plasmodium falciparum Malaria complications:
COMPLICATION OF MALARIA INFECTION:
1. Cerebral malaria (nearly always fatal without
treatment) .
2. Severe anaemia.
3. Renal failure.
4. Pulmonary oedema.
5. Hypoglycaemia.
6. Hypovolaemia.
7. Disseminated intravascular coagulation.
8. Metabolic acidosis.
9. Complications during pregnancy.
10. Plasmodium falciparum Malaria complications:
53
A patients blood test confirms malaria. How would you treat this patient in the ED?
1. If the person is shocked: cefotaxime should be given intravenously as the patients may have secondary bacterial infection.
2. Treatment for confirmed non-falciparum malaria will usually be advised by a specialist and includes:
Chloroquine.
3. For people with malaria due to Plasmodium vivax or Plasmodium ovale:
Primaquine
4. Paracetamol or ibuprofen for fever.
5. All cases of malaria should be notified to the public health authorities.
54
What are the indications to admit patients with Malaria?
Malaria is a medical emergency and immediate admission should be arranged for:
1. People with suspected severe or complicated malaria.
2. People with suspected falciparum malaria.
3. Pregnant women.
4. Children.
5. People who are older than 65 years of age.
55
What specific drugs would you consider prescribing in patients with confirmed malaria?
https://cks.nice.org.uk/malaria#!scenario
Antimalarial drugs recommended in the UK malaria treatment guidelines 2016 [Lalloo et al, 2016] include:
1. ARTESUNATE:
Parenteral artesunate is used treat severe or complicated malaria. Intravenous artesunate can cause haemolysis and follow-up blood tests are required.
2.QUININE:
Quinine may be used initially to treat severe or complicated malaria if artesunate is unavailable.
3. ARTEMISININ combination therapy (ACT):
ACT may be used to treat uncomplicated malaria and is the preferred treatment for mixed infection.
4. if ACT is unavailable:
Atovaquone-proguanil, OR
Quinine plus doxycycline
5. CHLOROQUINE
Chloroquine may be used to treat uncomplicated P. malariae, P. ovale and P. knowlesi and most cases of P. vivax malaria but use depends upon patterns of resistance and tolerance.
6. PRIMAQUINE
Primaquine is the only currently effective drug for the eradication of hypnozoites (dormant parasites which persist in the liver after treatment of P. vivax and P. ovale).
56
What 4 pathogens can cause necrotising fasciitis?
1. monomicrobial pathogens including:
(i) streptococci especially Streptococcus pyogenes (approximately 10% are caused by group A streptococcus alone)
(ii) Clostridium perfringens (gas gangrene) and other clostridial species,
(iii) Staphylococcus aureus,
(iv) Vibrio vulnificus and other Vibrio species,
(v) Aeromonas hydrophila
2. polymicrobial synergistic gangrene involves:
(i) mixed aerobe-anaerobe bacterial flora (eg Escherichia coli, Bacteroides fragilis, streptococci and staphylococci)
57
A 34 year old presents to ED he has recently arrived from Saudia Arabia pursuing his graduate studies. He has fevers and myalgia.
1. What is the organism implicated in MERS- Middle east respiratory syndrome.
2. what complication can occur?
1. Coronavirus
| 2. ARDS
58
What are the estimated percutaneous seroconversion risks for HIV infected blood and Non immune individual to HBeAg positive source. Please answer in Percentage
http://www.nhsemployers.org/~/media/Employers/
Documents/Retain%20and%20improve/Needlestick20injury.pdf
0.3% for HIV infected blood
30% for percutaneous exposure of Non –immune individual to HBeAg +ve source.
59
A 84 year old lady presents with a history of left loin and groin pain. She has a wound in the left loin area following a fall at nursing home 1 week back .
You suspect Necrotising fasciitis List any 2 risk factors for developing this condition.
1. Skin injury including insect bite, trauma and surgical wounds.
2. alcohol abuse,
3. intravenous drug abuse,
4. chronic liver or renal disease,
5. diabetes,
6. malignancy,
7. immunosuppression and possibly, tuberculosis
60
A patient with alcoholic ketoacidosis presents with metabolic alkalosis. explain the change in the blood gas state?
Prolonged Vomiting, Volume depletion and Hyperventilation (delirium tremens)
61
What is the pathophysiology of diabetic keto-acidosis?
the poor oral intake results in decreased glycogen stores, a decrease in insulin levels and an increase in glucagon levels
Insulin deficiency results in increased mobilisation of free fatty acids from adipose tissue.
ActeylcoA is produced in excess and this forms Acetoacetate and Ketoacid.
62
Other than Diabetic ketoacidosis and Alcohol ketoacidosis. Give an important differential for ketoacidosis.
Starvation keto-acidosis
63
What is the Initial fluid of choice in the treatment of Alcohol Ketoacidosis? explain
5% Dextrose as Saline may paradoxically worsen acidosis in initial stages of treatment.
64
A young female presents with Crohns disease.
1. what gynaecological features may she have ?
2. what are the diagnostic features on colonoscopy?
```
1. Gynae featuers of crohns disease:
amenorhea
menorhoegia
dysmenorhoea
pyoderma gangrenosum of the vulva
```
```
2. colonoscopy features of Crohns:
skip lesions
rectal sparing
cobblestone appearance
foecal ulceration
strictures
```
65
What is Reynolds pentad?
Charcot’s triad (fever, jaundice and right upper quadrant pain)
with
hypotension and altered mental status.
66
1. How is leptospirosis spread?
2. what are the clinical features?
https: //www.cdc.gov/leptospirosis/infection/index.html
1. The bacteria that cause leptospirosis are spread through the urine of infected animals i.e. rats, cattle,
```
2. High fever
Headache
Chills
Muscle aches
Vomiting
Jaundice (yellow skin and eyes)
Red eyes
Abdominal pain
Diarrhea
Rash
```
67
What are the complications of Weil's disease?
1. haemorage
2. jaundice
3. renal failure
68
WHat are the 4 clinical stages of hepatic encephalopathy?
Hepatic Encephalopathy Clinical staging.
Stage I drowsy but coherent not confused: mood
change
Stage II drowsiness, confused, asterixis
Stage III Stupor with hyperreflexia, extensor plantar reflexes,restless, screaming
stage IV Coma
69
What is the name of the scoring criteria for non-gallstone pancreatitis?
Reference:http://bestpractice.bmj.com/best-practice/monograph/66/diagnosis/tests.html
Ranson criteria (non-gallstone pancreatitis)
Used for prediction of severe acute pancreatitis - not diagnosis.
Criteria on admission:
1. age >55 years
2. glucose >11.1 mmols/L (200 mg/dL)
3. WBC count >16 x 10^9/L (16 x 10^3/microlitre)
4. serum AST (SGOT) >250 units/L
5. serum LDH >350 units/L.
Number of criteria and approximate mortality (%):
0 to 2 = 0%
3 to 4 = 15%
5 to 6 = 50%
>6 = 100%.
70
In a patient with acute pancreatitis - what does the bruising in the flanks signify?
Grey Turner's sign - bruising in the flanksis an uncommon and late finding in pancreatitis.It indicates retroperitoneal and intra-abdominal haemorrhage seen in severe necrotizing pancreatitis.
71
in a patient with upper GI bleeding. name the components of the Rockall score?
Rockall score components:
Age > 60
shock ( HR > 100 )
co-morbidities
72
What treatment options would you consider for a patient with upper GI bleeding due to variceal bleed?
http://www.nice.org.uk/guidance/cg141/chapter/1-recommendations
1. Use band ligation in patients with upper gastrointestinal bleeding from oesophageal varices.
2. Consider transjugular intrahepatic portosystemic shunts (TIPS) if bleeding from oesophageal varices is not controlled by band ligation
3. baloon tamponade with sengstaken blakemore tube
73
A 51 year old man presents with severe haematemesis. He has history of peptic ulcer disease and drinks up to 80 units of alcohol in a week. His observations are as follows.
HR 110/min, BP 110/60 mmHg, RR18, SaO2 98% on air
Your patient has had a further episode of Haemetemesis in resus, he has 2 wide bore intravenous access and iv fluids running. What 4 other immediate treatment steps would you institute?
Management of Variceal bleeding
1. Transfuse with Blood, Platelets and clotting factors 2. Activate massive transfusion protocol if available.
2. Terlipressin
3. Prophylactic antibiotics
74
How do you described the rash fo shingles?
a erythematous macular papular vesicular rash confined to a single dermatone that does not cross the midline.
75
describe the rash of erythema multiforme
Dusky dark red centre with a blister , a pale pink raised middle ring and an outer bright red ring- most common cause is herpes simplex virus
76
What is the clinical presentation of scarlet fever?
Age 2-10 year olds developed:
Face: facial flushing ,
Peri-oral: Forscheimers spots on hard and soft pallate
Pharynx: exudative pharyngotonsillitus
Neck: cervical lymphadenopathy
CHest: sandpaper rash starting on trunk spread to
extremities
FLUSH THE FACE WITH FORSCHEIMERS
FEEL FOR NECK LYMPH NODES AND WIPE THE TRUNK WITH SANDPAPER!
77
A 19 year old traveller presents with bloody diahroea.
1. What is the most common causative organism of travellers diahroea?
frcemexamprep
Commonest causative organism of travellers diahroea:
Enterotoxigenic escherichia coli. it can also cause bloody diahroea.
travellers diahroea is defined as 3 or more unformed stool passed by a traveller in 24 hours.
78
List the infective vs non-infective causes of bloody diahroea?
INFECTIVE CAUSES:
* shigella
* salmonella (salmonella typhi¶typhi =enteric fevers)
* Shistosomiasis
* Clostridium dificile
* enteroinvasive Escherichia Coli
NON-INFECTIVE CAUSES:
* inflammatory bowel disease
* colonic carcinoma
79
WHat are the pathognomonic clinical features of enteric/typhoid fever?
GIve the name of the drug you would prescribe to treat this infection?
frcemexamprep
CLINICAL features:
1st week - feel weak and lethargic , cough, fever, headache, abdominal pain,initially constipation then diahroea, epsitaxis
2nd week- so tired cant stand up ( prostration ) , prominent diahroea, confusion, abdominal distension, mild tenderness, splenomegaly.
3rd week- complications occur- intestinal haemorage, perforation, secondary pneumonia, myocarditis, encephalitis, septic shock
pathognomonic features:
1. ROse spots( crops of red macules) on the upper third
of the chest
2. Fagets sign - typhoid fever occurs with a relative
bradycardia
TREATMENT: azithromycin or flouroquinolones
80
A 42 year old humanitarian aid worker returns from liberia. he developed flu like symptoms a few days earlier. but now has marked muscle pain, abdmonial pain, haematemesis AND epistaxis. on examination his temperature is 38.9 degrees and you see extensive purpura on abdomen and limbs.
1. what is the likely diagnosis?
2. what immediate steps/measures should you take in the ED?
1. Ebola virus - viral haemorragic fever from West Africa, natural reservoir is in the fruit bat. spread is via contact with bodily fluids & SExual intercourse. incubation period between4-10 days but also up to 3 weeks.
2. IMMEDIATE STEPS IN THE ED:
* immediately isolate the patient
* Inform consultant in charge of the department
* inform local infectious deisease expert
* contact health protection team
* wera appropriate PPE
* organise immediate transport of patient to a HLIU ( High -Level Isolation Unit
81
What advice would we give to a mother who's child has been diagnosed with Measles?
1. That measles is usually a self-limiting condition
2. s likely to cause unpleasant symptoms
3. Symptoms usually resolve over the course of a week.
4. Rest, drink adequate fluids, and take paracetamol or ibuprofen for symptomatic relief
5. To stay away from school or work for at least 4 days after the initial development of the rash (ideally until full recovery to reduce the risk of infective complications).
6. To avoid contact with susceptible people (that is, people who are not fully immunized through vaccination or natural exposure, infants, pregnant women, or immunosuppressed people).
7. To seek urgent medical advice if they develop signs of a complication of measles
82
What is the recommended protocol or checklist for patients with needle stick injury?
A protocol or checklist is recommended. The initial care should include:
o A risk assessment for the transmission of blood borne viruses and discussion
with the patient of those risks.
o Taking blood for baseline hepatitis B, C and HIV status with consent.
o Provision of the first dose of hepatitis B vaccine, if required.
o Provision of the first doses of post exposure prophylaxis for HIV in the form
of triple therapy antiretrovirals, if required.
o Availability of microbiology advice to support decision making.
83
A colleague sustained a needle-stick injury.
what is the PEP regime that you prescribe, and what 4 pieces of advice do you give them ?
resource:
https://patient.info/doctor/needlestick-injury-pro#nav-0
Truvada®one tablet twice a day, plus
Kaletra® two tablets twice daily.
course of 28 days
advise:
If they choose to have sex, to practise safe sex and to ensure that they follow such advice for a period of three months.
Not to donate blood until all necessary screening tests are clear.
To see their GP if they develop a fever.
84
Which features of percutaneous needle stick injury carry a particularly high risk?
resource:
https://patient.info/doctor/needlestick-injury-pro#nav-0
1. A deep injury.
2. Terminal HIV-related illness in the source patient.
3. Visible blood on the device which caused the injury.
4. Injury with a needle which had been placed in a source patient's artery or vein.
85
What are the 3 clinical stages of Lyme's Disease?
RCEM Learning SAQ
CKS NICE 2018
Stage 1 - localised infection
*fever, EM target lesions at site of bite the &
lymphadenopathy
Stage 2 - Early disseminated infection ( weeks to months after initial infection )
* Erythema migrans - multiple spreading lesions
* Secondary (disseminated) erythema migrans
* Lymphadenopathy
* Neuroborreliosis (acute neurological problems) occurs in 10-15% of untreated individuals and includes CN palsy, bell's palsy, meningitis and encephalitis
* Borrelial lymphocytoma -a purplish lump that may develop on the ear lobe, nipple or scrotum
* Irregular pulse/tachycardia
*Radiculopathy – radicular pain, weakness, numbness, or difficulty controlling specific muscles
Stage 3- Late Disseminated Infection- years later:
Joint involvement – oligoarthritis (also known as Lyme arthritis)
Skin involvement – acrodermatitis chronica atrophicans (figure 4)
Peripheral and central nervous system involvement (NICE CKS, 2018).
