Gastro, Dermatology & Infectious diseases emergencies Flashcards
Can you describe the Rash of Lyme’s disease?
CKS NICE 2018
erythema migrans lesion-typically 5cm diameter - annular homogenous with central clearing and a bulls eye lesion
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
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
What is the 3 serious complications of Lyme’s disease?
- 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.
What is the first line treatment specific for Lyme’s disease in adults vs children?
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
Why is doxycycline contra-indicated in children under age 12 for treatment fo Lyme’s disease?
doxycycline can cause yellow tooth discolouration and dental enamel hypoplasia
- When can Jarisch-herxheimer reaction occur?
- what is the pathophysiology of the reaction
- what are the symptoms?
- 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).
Name 4 other patholiges that can mimic the changes of pneumonia on chest xray?
- pulmonary haemorage
- pulmonary aspiration
- SLE
- carcinoma
- contusion secondary to trauma
- pulmonary infarction
If CURB 65 scores > 3, what is the next test that should be requested?
pneumococcal urine antigen testing
What are the 10 risk factors in red flag sepsis?
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
You recognize that a patient has red flag sepsis. What are the components of sepsis 6?
- Send blood cultures
- IV fluid resuscitation
- IV antibioitcs
- serial lactate measurements
- monitor urine output hourly
- administer oxygen to maintain spo2 > 94%
in treating redflag sespsis - other than sepsis 6, what other 6 management steps need to be followed in the ED &later on the Ward?
- 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
What are the 6 management principles of patients recognized to have septic shock , according to the NICE sepsis toolkit 2016?
- 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
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?
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.
In a patient with septic shock - you use noradrenaline infusion - what is the mechanism of action and what dose ?
Mechanism of Action: endogenous catecholamine with strong alpha and weak beta adrenoceptor stimulation. dose 0.025mcg/kg/min.
In a patient with septic shock - what are the unwanted side effects of noradrenaline?
- peripheral vasoconstriction
- reflex bradycardia
- hypertension
- hyperglycaemia
In a patient with necrotizing fasciitis - what are the components of the LRINEC score? ( lab results in nec fac)
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 )
Indications for prescribing oral/iv thiamine to dependent alcohol drinkers?
- 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.
What clinical features would suggest that a patient has alcoholic keto-acidosis?
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.
What is the role of prescribing a carbohydrate rich diet as part of the management of a patient with alcoholic keto-acidosis?
Carbohydrates are required to stimulate endogenous insulin production. This is important to turn off the ketone production.
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
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
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?
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
What are the causes of Toxic epidermal necrolysis ( 10-30% skin involvement )
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.
What is Nikolsky sign?
Nikolosky sign- Lateral pressure with finger on normal skin adjacent to bullous lesions dislodges the epidermis producing denuded dermis.
What are the complications of Toxic epidermal necrolysis?
Sepsis - staphylococcal and pseudomonal species.
Hypovolaemic shock
Multiorgan failure
Disseminated intravascular coagulopathy
Thrombo-embolism
Respiratory failure- Pneumonia
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.
WHat are the possible causes of erythema multiforme?
Causes -
INFECTION:
- Herpes simplex virus,
- Mycoplasma
- TB
- Cytomegalovirus and
- HIV
DRUGS
1.Antibiotics- Sulphonamide, Penicillin
2.Anticonvulsants -Barbiturates, phenytoin,
carbamazepine
3.Nsaids
MALIGNANCY
·VACCINATIONS
·Radiation therapy
·Idiopathic.
What are the clinical features of erythema multiforme?
- Malaise, fever, Myalgias, arthralgia and pruritis.
- 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.
- Vesicobullous lesions may appear this is pruritic and painful.
- Steven Johnson’s syndrome -Vesicobullous lesions on the mucosal surfaces, mouth, eyes, vagina, urethra and anus.
- Ocular involvement in 9% of EM minor
What conditions are associated with pyoderma gangrenosum?
- Crohns
- Ulcerative colitis
- Rheumatoid Arthrtitis
- Haematological malignancy-
* Multiple myeloma ,
* leukaemia - Hepatitis
What is the differential diagnosis for pemphigus vulgaris?
Note : the incidence of PV = 3 in 100 000
- Bullous pemphigoid
- Pemphigus drug induced
- Pemphigus herpetiformis
- Herpetic lsions
- Apthous ulcers
- Bullous insect bite
- Bullous impetigo
- Epidermolysis bullosa
- Erythema multiforme
- Urtricaria
- Dermatitis herpetiformis
- Lichen planus
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.
What are the symptoms of Bullous Pemphigoid?
http://pemfriends.co.uk/pemphigoid/bullous-pemphigoid/
- Pruritus is frequent and can occur weeks before rash.
- Rash- erythematous or urticarial rash
- Tense blisters or bullae on skin flexures or may be widespread
- mucosal erosions in upto 25%
- 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).
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
How treatment would you prescribe for treating pemphigus vulgaris?
- Mild oral disease - Topical therapy
- Majority are treated with systemic steroids - high doses
- Plasmapheresis to remove antibodies - along with
Cytotoxic drug azathioprine - i.v immunoglobulin
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.