infections + A&E Flashcards
contrast the mode of transmission and the main differentiating symptoms of HSV1 vs HSV2
HSV1
- spread in childhood via saliva
- herpes labials, HSV encephalitis
HSV2
- spread via genital contact
- genital herpes (ulcers)
2 main risk factors for HSV
HIV
immunosuppressive medications
describe the symptoms of genital herpes
ulcers
painful
dysuria
pruritus
describe the symptoms of herpes labials
cold sores on/around lips
tingling sensation first, then the lesion develops
describe skin manifestations of HSV
erythema multiform - target lesions
erythema herpeticum - punched out erosions, rapidly progressive painful rash, seen in children with atopic eczema, life threateing –> Tx = IV acyclovir
what type of lymphadenopathy is seen in HSV
Tender Inguinal Lymphadenopathy
list some symptoms for HSV
genital ulcers
cold sores
tender inguinal lymphadenopathy
erythema multiform
eczema herpeticum
severe gingivostomatitis (erythema and painful ulcerations on the perioral skin and oral mucosa)
Ix for HSV
Viral PCR
→ order when lesions are present
Genital Herpes
→ nucleic acid amplification tests (NAAT)
(after obtaining swab of the base of the ulcer)
Viral Culture
Tx for HSV
oral acyclovir
what is the pathological mechanism of HIV
it is a retrovirus, so infects and replicates inside of CD4+ T cells and macrophages
incubation period of HIV
symptoms start 3-12 weeks after infection
signs and symptoms of HIV
fatigue
weight loss
night sweats
lymphadenopathy
shingles
recurrent candidiasis
TB
maculopapular rash
sore throat
oral ulcers
diarrhoea
genital STIs
which appears first, HIV p24 antigen or HIV antibodies?
HIV p24 antigens
what test can be used for staging in HIV
CD4 count
Ix for HIV
Combination Test (standard for diagnosis and screening)
→ HIV p24 Antigen + HIV antibody Test
Serum HIV Enzyme-Linked Immunosorbent Assay (ELISA)
→ positive for HIV antibodies
(however antibodies may not be present in early infection)
CD4 Count
→ indicates immune status and helps in staging process.
medication for HIV? and when should it be started
1st Line
→ antiretroviral therapy (ART) = two NRTIs and one PI/NNRTI
(should be started as soon as HIV diagnosed)
NRTI’s (AToZ)
⇒ zidovudine,
abacavir,
tenofovir
NNRTI’s
⇒ nevirapine,
efavirenz
Protease Inhibitors (all end in -navir)
⇒ indinavir,
nelfinavir,
ritonavir
PrEP vs PeP
HIV Preexposure Prophylaxis (PrEP) for individuals at high risk of contracting HIV
HIV Postexposure Prophylaxis (PEP) which is a short course of ART taken by patients after potential exposure to HIV
when should PEP be started and how long should it be taken for
started 72 hrs after exposure
taken for 4 weeks
what should be given to HIV pt if their CD4 count is <200
co-trimoxazole
prophylaxis against Pneumocystis jiroveci pneumonia
how do you asses for deeper collections or necrotising fasciitis in a surgical site infection
cross sectional imaging
preoperative prevention steps against surgical site infection
Don’t remove body hair routinely
(if you do, use electrical clippers instead of razors)
Antibiotic Prophylaxis
→ if placement of prosthesis or valve
Patient Advice
→ encourage weight loss,
smoking cessation,
optimise nutrition,
ensure good diabetic control
intraoperative prevention steps against surgical site infection
Prepare skin with alcoholic chlorhexidine
Cover surgical site with dressing
risk factors for surgical site infection (pt factors and operative factors)
pt factors
- obesity
- poor glucose control
- age
- smoking
- renal failure
- immunosuppression
operative factors
- preoperative shaving
- length of operation
use of antimicrobial prophylaxis
- skin protection
appropriate gown and sterile equipment
how to manage surgical site infection
remove any sutures and clips and allow pus to drain
empirical abx therapy
incubation period of HSV3 aka VSV
14 days
difference between shingles and herpes
shingles
- caused by VSV (aka HSV3)
only flares up once in lifetime
herpes
- caused by HSV1/2
- can have recurrent flare ups
after primary infection with VSV (chicken pox0, where can it remain latent in body
trigemina ganglia
dorsal root ganglia
in which 2 groups of ppl does VSV often reactivate to produce shingles
HIV
immunocompromised
how can VSV be spread
direct contact with lesions
airborne spread from resp particles
what type of rash is caused by VSV and how does it spread
vesicular rash
appears centrally, then spreads to extremities
describe presentation of shingles
acute, unilateral, painful blistering rash.
Prodromal period with burning pain over affected dermatome for 2-3 days.
Erythematous, macular rash → vesicular rash.
Patients are infectious until vesicles have crusted over
Should avoid pregnant women and immunocompromised whilst infectious.
tx for shingles
Tx = paracetamol and NSAIDs.
Can also give antivirals within 72 hrs.
VSV ix
PCR
VSV tx: supportive care, risk of moderate disease, risk of severe disease
Supportive Care
→ paracetamol
Risk of moderate-severe disease
→ oral antiviral therapy (aciclovir)
Risk of severe disease
→ IV antiviral therapy
Ramsay hunt syndrome cause and presentation
cause is VSV ion the geniculate ganglion of the facial nerve
LMN facial nerve palsy
Auricular pain is first feature, followed by unilateral facial nerve palsy and vesicular rash around the ear (may also get blisters on anterior 2/3 of tongue).
Ramsay hunt syndrome tx
oral acyclovir and prednisolone
cause and presentation of Herpes zoster opthalmicus
reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve.
Causes vesicular rash around the eye and hutchinson’s sign (rash on the tip or side of nose).
Requires urgent opthalmology review
tx of herpes zoster opthalmicus
Requires urgent opthalmology review and oral antivirals for 7-10 days.
common 2 pathogens for surgical site infections
e coli
staph aureus
common 2 pathogens for nosocomial pneumonia
staph aureus
p aeruginosa
common pathogens for VAP (ventilator acquired pneumonia)
gram negative bacilli
- e coli
- klebsiella pneumonia
- p aeruginosa
- acinobacter
gram positive cocci
- stash aureus
most common pathogen for nosocomial UTIs
e coli
most common pathogen for nosocomial bloodstream infections
staph aureus
most common pathogen for nosocomial GI infections
c difficile
the protozoa of which genus causes malaria
plasmodium
which protozoan parasite causes the most deadly malaria
plasmodium falciparum
method of transmission of malaria
bite by an infected female anopheles mosquito or by blood transfusion / organ transplantation
give 2 protective conditions against malaria
sickle cell anaemia
G6PD deficiency
symptoms of malaria
Cyclical Fevers with chills and rigors (shivering)
Haemolytic Anaemia
→ causes jaundice and may turn urine dark
Splenomegaly
Headache
Weakness
Myalgia
Arthralgia
Anorexia
Diarrhoea
give some investigations for malaria
Giemsa-stained thick and thin blood smears
(Thick detects parasites present.
Thin detects species.)
RDTs (rapid diagnostic tests)
detect antigen, quick so useful in health resource-limited areas
FBC
(shows anaemia)
tx for malaria
chloroquine
or
hydroxychloroquine
what news score indicates sepsis
NEWS2 ≥5
when should blood cultures be taken in sepsis
immediately, before antibiotics are started
what is dos serum lactate level in sepsis indicate
determines severity of the sepsis
what does METABOLIC ACIDOSIS WITH RAISED LACTATE indicate
sepsis
how does sepsis affect urine output
decreased urine output
describe the fluid resuscitation used in sepsis
500mL of crystalloid fluid
which 3 drugs can be used for sepsis
Vasopressor + Ionotrope + Corticosteroid
what is the most common causative agent of candidiasis
Candida albicans (a type od dimorphic fungi)
describe the effect of candidiasis on the mouth
Oral Thrush
→ oropharyngeal region affected
White plaque in the oral cavity that can be scraped off, leading to inflamed areas.
Cottony feeling in the mouth.
Fissuring at mouth corners.
May be caused by ICS (beclamethasone) use in asthmatics
what manifestation of candidiasis is considered an AIDS defining illness
oesophageal candidiasis
- causes odynophagia (retrosternal pain on swallowing)
‘Cottage cheese’, non-offensive discharge from vagina
diagnosis
vulvovaginitis (vaginal yeast infection)
what is vulvitis and what are the main symptoms
yeast infection if the outer part (vulva)
dysuria, dyspareunia
vulvitis vs vaginitis vs vulvovaginitis
vulvitis = affect outer part (vulva)
vaginitis = affects inner part (vagina)
vulvovaginitis = affects both
candidiasis investigation
Superficial Smear of Lesion for Microscopy
tx for vaginl candidiasis
oral fluconazole
list some topical antifungals
clotrimazole,
miconazole,
nystatin
which antifungal can be used for systemic antifungal testament in severe candidiasis disease
fluconazole
which 2 causative agents of dysentry have a short incubation period of 1-6 hrs
s aureus
bacillus cereus
which 2 causative agents of dysentry have a long incubation period of 7 days
giardiasis
amoebiasis
which causative agent of dysentry is common amongst travellers
e coli
which causative agent of dysentry can cause steatorrhea, and lactose intolerance afterwards
giardiasis
which causative agent of dysentry can cause GBS
campylobacter
which causative agent of dysentry can cause profuse watery diarrhoea, severe dehydration and weight loss
cholera
which causative agent of dysentry can cause HUS
haemolytic e coli
which causative agents of dysentry can cause severe/projectile vomiting
s aureus - severe vomiting
bacillus cereus - vomiting within 6 hrs, diarrhoea after 6 hrs
norovirus - projectile vomiting
which antibiotic can be used for severe campylobacter
clarithromycin
which anabiotics can be used for moderate vs severe c diff
moderate - oral vanconycin
severe - IV metronidazole
is HIV a notifiable disease
no
process of reporting notifiable diseases
medical practitioner –> proper office at local health protection team –> health protection agency
report immediately, dont wait for lab confirmation
report within 3 days via form, or if urgent verbally within 24 hrs
which antivirals can be used for hep c, and also for chronic hep b
interferon alpha
rivibarin
what ix can be done to asses degree of cirrhosis in chronic hep c
liver biopsy
which heps are RNA and which are DNA
RNA virus
- A, C, D, E
DNA virus
- B
what type of virus is hep A
picarnovirus
what type of virus is hep E
calcivirus
what type of virus is hep B
hepadnovirus
common cause of a chronic hep B pt having a super flare up
hep D infection
which pts can hep D infect and why
is coated with HBsAg
so can only co-infect with hep B, or infect someone who already has hep B
what does anti HBsAg antibodies indicate
immunisation either from
- recovery of infection –> if with IgG anti HBcAg
- vaccination —> if just alone, no HBcAg (only comes with an actual infection)
which hep b antigen indicates high infectivity if present
HBeAg
3 types of Hep b antigens
HBsAg –> surface (always present, antibodies don’t form against it until immunisation is reached either from recovery or vaccination)
HBcAg –> core (always present, antibodies form against it from start of infection, IgM indicates acute, IgG indicates chronic)
HBeAg –> envelope (not always present, but indicates high infectivity)
which of IgG and IgM indicate chronic vs acute infections
IgM - acute
IgG - chronic
most common cause of hepatocellular carcinoma worldwide vs UK
worldwide = chronic hep b
UK = chronic hep c
main risk factors for hepatocellular carcinoma
liver cirrhosis secondary to hep B and C
alcohol
NAFLD
α-1-antitrypsin deficiency
Haemachromatosis
raised ‘X’ is a useful diagnostic marker for hepatocellular carcinoma
AFP
what 2 things are used for screening for hepatocellular carcinoma in ppl with hep b/c, haemochromatosis, alcohol abuse etc
USS
AFP levels
which hep is particularly associated with travellers
hep A
which hep is particularly associated with pregnancy
hep E
incubation period of hep b / d
3 - 6 months
incubation period of hep a / e
3 - 6 weeks
which heps have vaccinations
hep A
hep B
symptoms of acute vs chronic hep c
acute
- asymptomatic
chronic
- arthritis,
arthralgia,
eye problems (sjogren’s syndrome),
cirrhosis,
hepatocellular cancer,
cryglobulinaemia (vasculitis)
membranoproliferative glomerulonephritis (leading to renal dysfunction)
what type of hypersensitivity is anaphylaxis
type 1 hypersensitivity reaction due to IgE-mediated mast cell activation
describe the steps that lead up to an anaphylactic shock
Degranulation of Mast Cells
→ Massive Histamine Release
→ Systemic Vasodilation
→ Increased Capillary Leakage
→ Anaphylactic Shock
list symptoms of anaphylaxis
Airway Swelling (Angio-Oedema)
Stridor,
Dyspnoea,
Wheezing,
Respiratory Arrest
Pale,
Clammy skin,
Hypotension,
Tachycardia,
Confusion
Urticaria,
Erythema,
Pruritus
what can we look for in blood the indicates an anaphylactic shock
Mast-Cell Tryptase
→ may remain elevated for up to 12hrs after acute episode
steps in managing anaphylactic shock
- remove trigger and call for help
- IM adrenaline + ABCDE + High flow oxygen (15L/min non-rebreathe mask)
- IV chlorphenamine 10mg + IV hydrocortisone 200mg
ALWAYS GIVE ADRENALINE IM EVEN IF PT HAS IV ACCESS (unless have refractory anaphylaxis)
what are the adrenaline doses for different ages
< 6months = 100-150 mcg
6m - 6yrs = 150 mcg
6 - 12 yrs = 300 mcg
12yrs + = 500 mcg
what is refractory Anaphylaxis and how is it treated
Refractory Anaphylaxis
⇒ persists despite 2 doses of IM adrenaline
(Tx with IV adrenaline and IV fluid bolus)
what type of bleed is extradural, from which vessel and where on skull
arterial bleed
from middle meningel artery
pterion (thinnest part of skull)
between which 2 layers is an extradural haemorrhage
dura
skull
which layer is subdural haemorrhage in
outermost meningeal layer
which lobes do subdural haemorrhages most commonly occur around
frontal
parietal
2 main risk factors for subdural haemorrhage
old age
alcoholism
onset of symptoms in subdural vs extradural haemorrhage
slower onset in subdural
causes of subarachnoid haemorrhage
spontaneous due to cerebral aneurysm rupture
vs
traumatic brain injury
classical presentation of extradural haemorrhage in terms of consciousness, neurological deficits and eyes
1) initial loss of consciousness following head injury
2) temporary recovery of consciousness with return to normal neurological function (lucid interval)
3) neurological status declines again due to haematoma expansion
contralateral focal neurological deficits
Signs of raised ICP
Compression of Occulomotor Nerve (CN3)
→ Fixed, dilated pupil
which imaging is used for extradural haemorrhage and what does it show
Non-Contrast CT Scan
- biconvex lesion,
- hyperdense in appearance (brighter),
- limited by suture lines
- midline shift
eXtradural is conveX
how can extradural haemorrhage lead to death
haematoma expansion
–> raised ICP
–> coning
–> death
management of extradural haemorrhage
craniotomy and haematoma evacuation
ICP management
anticoagulants reversal
what is resp arrest definition
cessation of breathing
pt has pulse
extrapulmonary causes of resp arrest
CNS depression (opioid intoxication),
respiratory muscle weakness (myasthenia gravis, ALS),
airway obstruction (aspiration),
drowning,
Trauma
pulmonary causes of resp arrest
airway obstruction (bronchospasm in asthma/COPD patients),
impaired alveolar diffusion(pulmonary oedema, pneumonia)
resp arrets main symptoms
cyanosis
tachycardia
diaphoresis
altered mental state
2 main ix for resp arrest
ABG
→ reduced oxygen,
increased carbon dioxide
Pulse Oximetry
management of resp arrest
Intubation
Mechanical Ventilation
define unstable angina
Myocardial ischaemia at rest or on minimal exertion in the absence of acute cardiomyocyte injury/necrosis
sx of unstable angina
chest pain
dyspnoea
sweating
syncope
ECG and troponin in unstable angina
ECG = normal
troponin = not elevated
1st line for unstable angina
300 mg aspirin
describe the steps from infection to MODS
SIRS + infection –> sepsis –> severe sepsis –> MODS
what is MODS defined as
development of progressive and potentially reversible physiologic dysfunction of 2 or more organs or organ systems that is induced by a variety of insults, including sepsis
stage 1 of MODS
- increased volume and insulin requirements,
mild respiratory alkalosis,
oliguria,
hyperglycaemia,
stage 2 of MODS
- tachypnoea,
hypocapnia,
hypoxaemia,
moderate liver dysfunction
haematologic abnormalities
stage 3 of MODS
- shock,
azotaemia (high nitrogenous waste/creatinine/waste products in the blood),
acid-base disturbance,
significant coagulation abnormalities
stage 4 of MODS
- vasopressor dependent,
oliguria or anuria,
development of ischaemic colitis and lactic acidosis
Mx of MODS
IV fluids
abx
vasopressor meds
blood transfusions
O2 therapy
technical ventilation
dialysis
ECMO
(+ surgeries needed etc)
how to vasopressors affect bp
used to increase bp
