Revision Sm Gr Flashcards

1
Q

Revision DM Yaws

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T pallidum subsp pertenue. Most cases in children. Major foci W&C Africa and Pacific. Large gaps in understanding of distribution = barrier to eradication. Single dose azithromycin for Rx. Risk of resistance. WHO strategy (Mapping of foci, Treatment of whole community, Likely need several rounds, Then mop up with treatment cases and contacts, Once no more cases switch to serological surveillance). Comment: Use the epidemiological cues

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2
Q

Revision DM HIV-TB

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Priority group for rapid ART initiation (high risk death). After ART: high risk death, unmasking OI, IRIS, failure to fully immune reconstitute, AIDS-related and non-AIDS related comorbidities. At diagnosis, needs screen for 1 TB disease (all patients), 2 Cryptococcal infection (CD4<100, consider <200) If these are negative evaluate for other infections according to clinical presentation and local epidemiology. Check if on ART (and failing)/received prior ART (treatment interruption). Screening TB disease in advanced HIV: A) Screening tools: 4-symptom screen (Current cough, weight loss, fever, night sweats), CRP, CXR, molecular RDT. Choice of tests depends on setting (in patients, outpatients) feasibility and resource. B) This patient has screened positive on 4-symptom screen: Cough and fever. Molecular WHO recommend RDTs recommended as first test for pulmonary TB diagnosis: high sensitivity, specificity, additional drug sensitivity info, urgency of timely diagnosis in this population. CXR may help support diagnosis. Urine LAM may assist diagnosis for the following: (CD4<20 in inpatients, CD4<100 in outpatients, Any CD4 count if symptoms or seriously ill). Comment: CXR reasonable to do, is it the first thing you would do? Possibly? Fever and a cough, but most likely diagnosis is TB (HIV in South Africa). LAM not as useful if you’re not particularly sick, and is usually a screening in an unwell patient. CRP is reasonable but not first test

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3
Q

Revision DM Polio

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Caused by 3 strains of poliovirus. Only humans. Transmission is faeco-oral. Most infected individuals are asymptomatic but about 25% develop a febrile illness usually with GI symptoms. Neurological and paralytic complications are rare (0.5% of the time-typically asymmetrical paralysis of the affected limb (usually the legs) but acute flaccid paralysis (AFP) surveillance remains key to polio efforts. Transmission of wild-type polio is now restricted to Pakistan and Afghanistan. Highly effective vaccines- live oral vaccine (OPV-Sabin) prevents disease and generates sterilising immunity but has risk of vaccine-associated polio disease. OPV used in disease-endemic outbreak affected areas and recently polio-free countries of the world. IPV (Salk) prevents disease but can’t block transmission. IPV used in the rest of the world, where the risk of vaccination-associated paralytic polio is considered greater than the risk of naturally occurring infection. IPV introduced for Polio 2 as wild-type polio 2 no longer circulating. No animal reservoir – should be able to be eradicated. Comment: Pakistan, Afghanistan is wild type Polio (vaccine-derived elsewhere)

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4
Q

Revision DM Viral hepatitis

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Hepatitis A Transmission: faecal oral Incubation: 15-50d. Acute <6yo <1/3 have symptoms, >70% older children and adults have symptoms. Chronic infection – none. Hepatitis B Transmission: at birth, sexual contact, sharing needs. Incubation 60-150d. Acute infection - symptoms <5yo none, >5yo 30-50% symptomatic. Immunocompromised adults, generally none. Chronic infection: 90% birth, 25-50% 1-5y, 5% adults. Hepatitis C Transmission: Sharing needles, anal intercourse. Incubation 14-182d. Acute non-specific symptoms in 10-20%, jaundice in up to 20-30%. Chronic >50%. Hepatitis E Transmission: Faecal oral, contaminated water. Incubation 14-70d. Acute <30% symptomatic. Significant mortality risk in pregnant women. Chronic HEV 3/4 unclear %. Comment: If this question said Egypt – consider hepatitis C. West Africa has lots of hepatitis B with accelerated HCC

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5
Q

Revision DM Buruli ulcer

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Mycobacterium ulcerans. Transmission seems to be linked to water/soil. Can present as an ulcer or a non-ulcer form such as nodule or plaque. Lesions are normally painless and the patient is systematically well. PCR is the test of choice (Swabs from ulcer lesions undermined edge, FNA from non-ulcerative forms). Treatment: Rifampicin and Clarithromycin for 8 weeks, Wound care, May need debridement or skin graft. Comment: Scar, expansive ulcers with contractures. Alternative options Skin snip is for Onchocerciasis. Slit skin smear is for leprosy.

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6
Q

Revision DM Zika

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Primary vector Aedes aegypti – day biting, breeds in small pools of water (eg containers). Surveillance: Syndromic and case surveillance, Laboratory surveillance, Zika – microcephaly surveillance. Active case finding when outbreaks identified Education: public and HCW (Symptoms and Vector control). Vector control – source reduction (Elimination of containers/fitting lids, Insecticides against aquatic stages, Space spraying (outbreaks), Pupal surveys to target source reduction measures. No vaccination yet Comment: Bed nets not effective as day biting, residual spraying of insecticide not so useful (Aedes aegypti are endophilic- like to bite indoors). Insect repellent useful (throughout the day, not just in the evening).

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7
Q

Revision DM Brucella

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Brucella sp are small aerobic intracellular GNCB. There are four strains medically important to human B melitensis, B abortus, B suis and B canis. Incubation period can be long days to months. Brucellosis is the commonest bacterial zoonosis globally – transmission from animals to humans is usually via uncooked meat, unpasteurised milk/dairy, aerosolization. Clinically non-specific symptoms, with a usually normal examination. Undulating fever, hepatosplenomegaly, arthralgia, elevated liver enzymes, mild moderate thrombocytopaenia may be present. Culture (gold standard) everything you can, ELISA, Rose Bengal and PCR testing is also used diagnostically. Treatment with doxycycline (45d) and gentamicin (7-10d) or streptomycin (15d) is recommended by the WHO. Vaccine is available for animals (B melitensis and B abortus) but not humans. Prevention: BSC3 lab handling – don’t sniff the plates. Appropriate PPE should be used around potentially infected animals and their products. Comment: The alternative diagnosis for 34M Somalia with LN, epididymoorchitis would be TB. Also think of Mongolia and/or slaughterhouse worker for Brucella. Anthrax is also important for slaughterhouse worker.

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8
Q

Revision DM Malaria

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Treatment of malaria relies on classifying if the patient has severe/complicated OR uncomplicated malaria. Signs of complicated malaria: CNS coma/convulsions (cerebral malaria), Lungs ARDS, Kidney AKI, Shock, Hypoglycaemia, Severe anaemia, Respiratory distress or acidosis, Hyperparasitaemia. ACT are first line treatment of uncomplicated malaria caused by all species. For complicated malaria SEQUAMAT and AQUAMAT both showed artesunate to be superior to quinine. Severe/complicated malaria is associated with a high rate of bacteraemia in children – normally due to non-typhoidal Salmonella and therefore treatment with a broad spectrum ab is normally recommended. Comment: Approach to question: Will always favour ACT over quinine. Have they got severe? Probably then Artemether > artemether/lumefantrine. Then decide if giving CRO or not – he is very sick and may have more than just malaria. If fever and positive RDT then would give Artemether/lumefantrine (or whatever ACT) and would not need to give antibiotics. Also, do not generally need to give abx to adults unless very sick. When children are sick, it is generally due to gut leakage/translocation.

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9
Q

Revision DM Rheumatic fever (RHF) and heart disease

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RHF an immunological reaction to GAS (Type 2 hypersensitivity) – classically after pharyngitis. RHF: Duckett-Jones criteria: fever, arthritis, carditis, nodules, chorea. Repeated RHF->RHD. Primary prophylaxis: early treatment streptococcal pharyngitis. Secondary prophylaxis: benzathine penicillin. GAS also associated with glomerulonephritis (Classically after a skin infection, Type 3 hypersensitivity reaction with immune complexes). Comment: Endomyocardial fibrosis is rare, may be associated with chronic eosinophilia and found not in frequently in Mozambique. Undiagnosed congenital heart disease possible, but in a child from Samoa with features of heart failure, it is RHD until proven otherwise.

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10
Q

Revision DM Amoebic dysentery

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Parasitology: non-flagellated protozoan parasite. Transmission via faecal-oral ingestion of mature cysts. Excystation in small bowel and trophozoite esp migrate to large bowel and invade (>ulcers and mucosal loss). Clinically: Subacute onset, over 1-3 weeks, Asymptomatic -> mild diarrhoea -> dysentery (-> fulminant colitis), Fever 50%, Fewer WBCs in stool compared to bacillary dysentery – the ulcers don’t have marked inflammation around them. Geography throughout tropics. Diagnosis: (Hot stool for microscopy for trophozoites – poo to microscope within 20 minutes, or Concentrated stool: microscopy for cysts plus PCR). Misdiagnosis – mistaking amoebic dysentery for inflammatory bowel disease – treating with steroids may precipitate fulminant colitis. Treatment: A Symptomatic intestinal amoebiasis (Metronidazole 5-10d, If severe/fulminant may need Gram negative cover +/- surgery) B Asymptomatic and cyst clearance post A need intraluminal agent (Paromomycin (25-30mg/kg per day orally in three divided doses for 7 days). Iodoquinol may also be considered. Comment: Salmonella enteritis is less common to cause blood in stool. Shigella enteritis – bacillary enteritis is much more abrupt and unpleasant illness – usually faster onset of illness. Clostridium difficile colitis can cause similar presentation, but usually previous antibiotics.

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11
Q

Revision DM Leprosy

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M leprae. Likely respiratory spread with very long incubation. Clinical presentation depends on immune response. WHO simplified classification: PB 5 or less, MB 6 or more. WHO now recommends 3-drug regimens for all leprosy: Rifampicin 600mg once a month, Clofazimine 300mg once a month and 50mg daily, Dapsone 100mg daily. Duration: PB 6 months, MB 12 months. Many patients experience reactions despite effective treatment (or may present in reaction). Type 1 reaction (Usually painful neuritis with loss of function. Involve existing lesions (thickened nerves become painful). Treated with steroids (as soon as possible)). Type 2 reactions – much more common in Lepromatous Leprosy (Systemic illness with Erythema Nodosum Leprosum, Red shiny painful skin lesions which last a long time, Poorly responsive to steroids, Thalidomide probably the best).

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12
Q

Revision DM IRIS

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Immune reconstitution inflammatory syndrome. Due to inflammation caused by IRIS following ART. Usually within weeks, up to a few months. ‘Paradoxical’ if OI being treated. ‘Unmasking’ if subclinical when started ART. Usually not fatal (except CNS). Treatment usually steroids. Importance of screening for OIs. Patients on antiTBRx given ART -> Paradoxical. Patients not on antiTBRx given ART -> ART-associated TB = Unmasking IRIS (released the pressure on the immune system) – can get with other pathogens. Comment: HIV on SXT = likely very immunosuppressed. Shortly after starting ART. Stopping ART does not solve the problem, give steroids usually, cannot delay ART for too long as they die of other HIV OI. Timing is important – 3 weeks is classic (2-8w is unmasking time). Paradoxical IRIS can occur at any stage in treatment, in people without HIV can happen 4-5 months into treatment.

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13
Q

Revision DM Urethral discharge

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WHO recommends the use of syndromic management of most STIs. Entails treatment of the common causes of a given set of symptoms and signs. Commonest causes of urethral discharge are NT (Rx CRO + azithromycin, CT: Rx with doxycycline or azithromycin). Advantages of syndromic management (Sensitive for symptomatic STIs. No need for lab tests). Disadvantages (Not specific, Results in over-treatment). Ideally offer HIV and syphilis testing also

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14
Q

Revision DM Yellow fever

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Introduction to human in the jungle from mosquitoes that have bitten non-human primates and can then spill over to urban or village. VHF caused by an RNA flavivirus. Incubation 3-6d. Major asymptomatic or mild symptoms. Flu like illness starting about 1 week. Approx 1:7 patients with symptom develop severe infection; high fever, jaundice, bleeding, multi-organ failure. No effective treatment, supportive only, avoid NSAIDS. Infectious for approx. 5d post symptom onset (bed net etc). YF vaccination is safe, effective and provides lifelong immunity – aim for 100% coverage in endemic regions, esp in areas with confirmed epizootic transmission. Comment: Chagas is transmitted by triatomine bugs, Remdesivir is not effective (for almost any virus), Sylvatic cycle is non-human primate jungle cycle.

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15
Q

Revision DM Enteric fever

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S typhi and paratyphi. Faeco-oral transmission. Endemic in south Asia but also across much of the tropics. Best diagnostic test is bone marrow culture although in clinical practice blood culture is the standard. The Widal test though widely used is mostly no good (unless you are in a high prevalence setting and know the background). Is NOT more common in HIV infected people. Increasing resistance to a range of Abx - CRO is now 1st line in S Asia but increasing resistance. Azithromycin an alternative option. XDR strains have emerged independently in Pakistan and Nepal. Fever may take a long time (often a week) to go away even with correct Rx. Complications like bowel perforation and haemorrhage occur in week 3. New conjugate vaccine looks highly effective. Comment: Best diagnostic yield is from BM, but it is probable that 3x BC gives the same yield. Pakistan – think about polio and Nepal. Think about drug resistance

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16
Q

Revision DM PMTCT for HBV

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Risk related to viral load in mother. Once chronic infection is established there is no cure possible. Vaccination needs to be delivered at birth to be effective. Coverage in much of sub-Saharan Africa is <10%. IG at delivery further reduces risk but is rarely available in LMIC. Tenofovir to mother from week 30 reduces the risk. No role for single dose treatment. Comment: TDF from week 30 to week 4 post-partum (probably does reduce transmission but not as critical as vax and immunoglobulin). Slides shown of study of TDF in addition to standard of care – HBVvax and HBIG on first day of life – some benefit, but HBIG seems to be the best.

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17
Q

Revision DM Cervical Cancer

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High prevalence of CxCa across SSA. Strongly associated with HPV 16 18. Increased risk for people living with HIV = synergy for CaCx esp in Africa. Screening for HPV is the most sensitive test. HPV vaccination is highly effective in prevention of cervical cancer and probably in preventing other HPV-associated cancers. Evidence increasingly supports need for only 1-2 doses of HPV vaccination. Comment: Smoking is a risk factor, but not the most important risk. Individuals living with HIV are at an increased risk of CaCx. Genital Schistosomiasis may mimic CaCx, but is less common than HPV-associated CaCx.

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18
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Revision DM Scabies

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Sarcoptes scabiei. Ectoparasite. Spreads person to person by prolonged skin to skin. Treatment: Ivermectin oral – 2 doses, 7 days apart (Contraindicated if pregnant, BG <15kg or less than 5yo. Topical therapy: Benzylbenzoate or Permethrin (probably the best)

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19
Q

Revision DM Rapid ART

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When is rapid ART NOT recommended: Crypto meningitis (Increased mortality with immediate ART. Defer until 4-6W after CM treatment start) and TB meningitis (Delay ART for at least 4W but start within 8W of anti-TB treatment. Consider adjuvant steroids). Important considerations in treatment of HIV-TB coinfection (1 Interactions with ART, if on or due to start ART, 2 When to start ART if not on ART, 3 TB-IRIS). ART should be started in all TB patients living with HIV regardless of their CD4 count. TB treatment should be initiated first, followed by ART as soon as possible within the first 8 weeks of treatment (Strong recommendation). HIV-positive patients with profound immunosuppression (CD4<50) should receive ART within the first 2 weeks of initiating. Comment: exclude TB is right, but ‘check no clinical evidence of meningitis’ is better. CD4 is useful to assess risk of OIs, but not essential prior to initiation of ART. All patients living with HIV eligible for ART. Need to start investigations for active TB (weight loss = screen positive), however, providing no evidence of meningitis you don’t need to wait for results before starting ART. All HIV patient should be screened for STI but this should not delay starting ART. Adherence support is important

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20
Q

Revision DM Visceral leishmaniasis

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VL caused by L donovani and L infantum. Major foci India/Bangladesh, Horn of Africa, S America. Clinical syndrome: fever, pancytopaenia, massive splenomegaly. Human -> Phlebotamine Sandfly ->Human – animal reservoirs also important esp in S America. Diagnosis (DAT (direct agglutination test), Rk39, Splenic aspirate, Bone marrow). Treatment options (Sodium stibogluconate, Amphotericin B & Miltefosine- do not need to know doses). HIV and Leishmaniasis = bad – almost impossible to get rid of leishmania even with immune reconstitution – likely to need secondary prophylaxis for the long-term. (Less good cure of VL and Less good immune recovery of HIV). Comment: Chronic malaria could cause this with thrombocytopaenia – very rare. Simulium black fly is vector of Onchocerca volvulus. Cows milk in some parts of the world is still a risk for Myobacterium bovis, and Goats milk unpasteurised is a risk for Brucella melitensis.

21
Q

Revision DM Lassa

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Arenavirus. Reservoir in multimammate rodent. More contact with humans after harvest may account for seasonality. Most individuals have a mild self-limiting illness. Spread rodent to human via excreta. Human to human nosocomial spread. Two foci in West Africa – Guinea/Sierra/Leone, and Nigeria. Currently no vaccine. Comment: Lassa is an endemic disease, ring vaccination is used for Ebola not Lassa. Some (weak) evidence that ribavirin is an effective drug (this has been questioned though ribavirin still used)

22
Q

Revision CW Dengue

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Severe dengue: severe plasma leakage, severe haemorrhage, severe organ impairment. Warning signs: Abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation, mucosal bleed, lethargy/restlessness, liver enlargement >2cm, increase HCT with concurrent rapid decrease in Plt. Probable dengue: live in/travel to dengue endemic/hotspot/outbreak area. Fever and two of the following criteria: nausea, vomiting, rash, aches and pains, leucopaenia, any warning sign. Laboratory-confirmed dengue (important when no sign of plasma leakage)

23
Q

Revision CW Mosquito vectors

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Aedes: DEN, CHIK, LF, Rift Valley fever, YF. Anopheles: Malaria, LF. Culex: JEV, LF, WNV

24
Q

Revision CW Epidemic curves

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Point source (straight up and down, one exposure, those exposed had the infection or not, and there were no further events eg food source). Propagated source (waves increasing, eg respiratory viruses). Extended common source (increases then dips up and down a little before plateauing - common source ie contaminated water, eg Cholera) and Intermittent source (intermittent short bursts, interspersed with no cases eg> Listeria in smoked salmon - opened at different times) - a question could be which disease causes this, or could be choose the source

25
Q

Revision CW Malaria 12 signs of severity

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One or more of the following, occurring in the absence of an identified alternative cause and in the presence of P falciparum asexual parasitaemia: Impaired consciousness, prostration, multiple convulsions, acidosis, hypoglycaemia, severe malaria anaemia, renal impairment, jaundice, pulmonary oedema, significant bleeding, shock, hyperparasitaemia (>10% endemic, >2% non-endemic)

26
Q

Revision CW Scorpion Envenoming

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Excruciating local pain! Rx local anaesthetic. Most scorpion stings produce immediate agonising burning local pain with minimal swelling. 1.2M stings, 3250 deaths a year. Highest in Brazil. Children worse affected by envenomation. Na, K, Ca ion channel disruption by venom. Treatment: infiltration/digital block 1% lignocaine for severe envenoming with systemic features give supportive care and antivenom. Severe envenoming: 1 Autonomic storm: Parasympathetic (vomiting, sweating, hypersecretion, pancreatitis, priapism). Sympathetic (goose bumps, tachycardia, cardiovascular disturbances, myocarditis, pulmonary oedema, hyperglycaemia). 2 Neurotoxicity. Prevention: wear gloves, solid foot wear, long clothing. Shake out clothing before putting on. Check campsite with UV light (fluorescent exoskeleton), Minimise leaf litter rubbish - places to be hidden. Comment: Snake envenoming (pressure immobilisation). Scorpion antivenom (if there are systemic features). Marine envenoming (immerse in hot water - toxins inactivated in hot water - stinging fish, jelly fish etc). Never advise to suck venom out with a suction device - manipulation may more venom into a space it was not in previously and increases the risk of infection

27
Q

Revision CW Cholera

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Vibrio cholerae. Comma shaped Gram negative anaerobe. Abrupt onset, watery stools, rice water, >10-20L per day, dehydration, <5% fever. Cholera toxin binds to specific receptor on mucosa of intestine (ganglioside), activates the adenylate cyclase enzyme, inhibits NaCl absorption and increase Cl excretion -> loss of Na, Cl, HCO3, K and water. Treatment: supportive, ORS or IV fluids, Zinc (<5yo), antibiotics shorten duration: macrolides, quinolones, tetracyclines.

28
Q

Revision CW TB drug symptoms

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N&V (prothionamide, paraaminosalicylate, pyrazinamide), Gastritis/reflux (paraaminosalicylate, prothionamide), Diarrhoea (paraaminosalicylate), low potassium (capreomycin, kanamycin), Psychosis (cycloserine, isoniazid, fluoroquinolones, ethionamide, prothionamide). Depression (cycloserine, fluoroquinolones, isoniazid, prothionamide), Hypothyroidism (paraaminosalicylate, prothionamide), Peripheral neuropathy (cycloserine, prothionamide), ototoxicity (injectable agents streptomycin, kanamycin, capreomycin), Optic neuritis (ethambutol), rash (all TB drugs), Renal toxicity (injectable agents streptomycin, kanamycin, capreomycin), Seizures (cycloserine, kanamycin, capreomycin), arthralgias (pyrazinamide, fluoroquinolones), hepatitis (pyrazinamide, rifampicin, prothionamide, paraaminosalicylate)

29
Q

Revision CW TB drug AE

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Isoniazid (rash, hepatitis), Rifampicin (abdominal pain, nausea, vomiting, hepatitis, thrombocytopaenic purpura), Pyrazinamide (arthralgia, hepatitis), Ethambutol (retrobulbar neuritis, ocular side effects), Paraaminosalicyclic acid (anorexia, N&V, hypersensitivity reactions), Cycloserine (dizziness, headache, depression, psychosis), Ethionamide (diarrhoea, abdominal pain, hepatotoxicity), Bedaquline (QT prolongation)

30
Q

Revision CW Phase of malnutrition management

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1 Hypoglycaemia 2 Hypothermia 3 Dehydration 4 Correct electrolyte imbalance 5 Treat infection 6 Correct micronutrient deficiencies 7 Cautious feeding 8 Increase feeding to recover lost weight ‘catch up growth’ 9 Stimulate emotional and sensorial development. 10 Prepare for discharge. Early 1-3 5 & 7, Throughout 4, 6, 9, Late 8, 10. Additionally do not give antihelminth albendazole at the beginning - give it a few weeks into treatment - ABZ causes anorexia and nausea which may make it even harder to get them to start eating. Wait for them to be sustained on a reasonable diet before starting deworming.

31
Q

Revision CW Rabies exposure

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Cat1 Touching or feeding animals. Licks intact skin (Drinking milk from a rabid cow). Cat2 Nibbling of uncovered skin. Minor scratches or abrasions without bleeding. (Stop Rx if animal remains well throughout 10d observation period or is proven to be negative. Treat as Cat3 if bat exposure involved or bites on head. neck, face, hands, genitals - due to innervation in these areas). Cat 3 Single or multiple transdermal bites or scratches. Contamination of mucus membranes or broken skin with saliva from licks. Exposure due to direct contact with bats (Exposure to raw meat of rabid animals. Stop Rx if animal remains well throughout 10d observation period or proven to be negative)

32
Q

Revision CW Rickettsia

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O tsutsugamushi in triangle, associated with painless eschar (look hard!) Gram negative intracellular bacteria. Diagnosis: Clinica, Serum ELISA IgM/IgG, PCR Eschar/blood. Treatment: Doxycycline. Comment: Typhus group R typhi and R prowazekii will not have eschar as associated with vector poo (R typhi flea faeces rubbed into mucus membranes -> inoculation with endemic/murine typhus; R prowazekii louse faeces, outbreak based, high density poor sanitation concentration camps, displaced people). R africae (Africa & Caribbean), R conorii can have an eschar. Comment: Classic cause of ‘doxycycline deficiency’

33
Q

Revision CW Rickettsia

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Spotted group Rr Rafricae Rc Rakari - all tick borne except Rakari (mite). Typhus group Rt flea (mouse) Rp louse (epidemic, can recur). Scrub typhus Otsutsugamushi Trombiculid mite

34
Q

Revision CW Paracoccidiodomycosis

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Dimorphic fungal infection found in South America. Two clinical forms 1 Juvenile (rare associated with eosinophilia, acute, subacute, reticuloendeothelial spread) 2 Chronic (90% of cases, mainly in men 30-60yo - reactivation, 90% lung involvement, mucosal ulcers, lung fibrosis, men in agriculture). Diagnosis: culture/biopsy. Treatment: mild to moderate cases 6-12m itraconazole/SXT, severe cases amphotericin. Comment: this is usually painful (DDx leish which is painless). General rule of thumb for dimorphic fungi if severe infection treat with amphotericin initially then itraconazole. If mild to moderate just use itraconazole. Histoplasma (yeast with narrow neck budding, no capsule - cave, starling birds). Blastomycosis (broad based budding yeast - look like bowling skittle with chunky neck, often Canada, N America - decomposing areas). Sporotrichosis (cigar shaped yeast, rose gardener who has inoculated whilst trimming roses - only disseminates in highly immunocompromised).

35
Q

Revision CW HTLV-1

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RNA retrovirus, spread by cell-to-cell contact. Parenteral (transfusion cells, solid organ, high risk for HAM, screening in blood banks/donors), MTC (breastfeeding-related with duration >3m, rare before and during childbirth, screen/no breast feeding if secure alternatives in place), Sexual. 5-10 million carriers globally. Geographic foci: Japan, Latin America, Caribbean, Africa, Central Australia. Transmission: vertical, horizontal, blood products. 95% of carriers remain asymptomatic lifelong. HTLV1-associated myelopathy (HAM) or tropical spastic paraparesis. (May be rapid or slow progression. Usually symmetrical, bladder disorders common and lumbar pain. Chronic inflammation of white and grey matter of lower thoracic spinal cord (infiltration of T-cells - bystander effect/autoantibodies followed by atrophy). Highly oncogenic virus-causing adult T-cell lymphoma/leukaemia (ATL) (Broad clinical spectrum of presentation). Systemic complications: infective dermatitis (3-15yo, generalised papular rash, exudates and crusting on different areas, lymphadenopathy, failure to thrive), strongyloides hyperinfection infection (mortality 15-87% - > look for this PRIOR to steroids in HTLV-1 pt), autoimmune infections. Diagnosis: serology EIA/Western blot, Proviral PCR. Prevention: No vaccine, avoid infected bodily fluid transmission. Treatment: no proven antiviral treatment. Comment: Konzo occurs with inadequately prepared casava -> cyanide toxins building up, often happens in times of famine. Big populations getting this at the same time - not multigeneration. Also only found in Africa.

36
Q

Revision CW HIV

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Routine VL monitoring for early detection of treatment failure: by 6m and then 12m after ART initiation, yearly thereafter. <50 - maintain ART. VL >50 - enhanced adherence counselling and repeat VL testing after 3m (exception is >1000 on NNRTI -> switch. On repeat <50 maintain ART >50-<1000 maintain ART continue enhanced adherence counselling, repeat VL in 3M, if >1000 -> switch. ART failure common, especially in hospitalised patients. Adherence, transmitted or acquired drug resistance. Dolutegravir based therapy should make less common. Poor access to HIV resistance genotype testing. Most guidelines suggest adherence support and recheck in ~3m. Second-line treatment problematic, so good to avoid if possible. May delay switching if developed resistance.

37
Q

Revision CW Histoplasma capsulatum

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Thermally dimorphic fungi. Global coastal distribution, acquisition by inhalation. Clinical spectrum: Immunocompetent (asymptomatic primary, acute symptomatic pulmonary histoplasmosis), Underlying chronic lung disease (Chronic pulmonary histoplasmosis), Cutaneous/mucous histoplasmosis. HIV patients (and other immunocompromised -> disseminated). Diagnosis: microscopy budding yeast does not have capsule, Culture. BDG, Histoplasmosis urinary Ag. Treament: most infections self limited, severe: Amphotericin followed by itraconazole. Comment: Yersinia pestis question would use plague endemic area (Madagascar) and frame the question around common outbreaks. B pseudomallei is not cave related. Paragonimus westermani possible from eating raw crayfish, but has incubation of 5-6w

38
Q

Revision CW Paragonimus westermani

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Egg 80-90um with operculum (escape hatch) which releases miracidia in fresh water, these infect snail, develops to cercariae which infect freshwater crab or crayfish and become metacercariae, and infect human on ingestion of undercooked crab. Flukes copulate in lungs and cause chronic respiratory symptoms such as pleurisy and haemoptysis. Time from ingestion to lung infection. 5-6w

39
Q

Revision CW Strongyloides hyperinfection

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Risk groups: Steroids, HTLV-1, transplant. Recurrent Gram negative sepsis, associated with normal eosinophils. Diagnosis: direct examination, serology. Treatment: Ivermectin. Complications: larva currens, nephrotic syndrome, ARDS, recurrent GNB, chronic diarrhoea, small bowel obstruction. Comment: Ivermectin vet preparation if patients critically unwell. Pt can get meningoencephalitis. Lifetime travel history is important in this diagnosis. Note: cutaneous larva migrans is serpiginous

40
Q

Revision CW Melioid

A

Burkholderia pseudomallei. Gram-negative bipolar staining intracellular rod, Paddy fields, rainy season. Acquisition: percutaneous inoculation, ingestion, inhalation. Clinical: Asymptomatic. Local ulcer, GI tract mucosal ulceration or lymphadenopathy, Skin lesions in disseminated disease, Pneumonia, Severe sepsis or latent disease, any organ can be affected. RF: Diabetes, EtOH, CKD, cancer. Parenteral Rx: Ceftazidime 2-8w, oral eradication SXT 12-20w. Other bipolar staining organisms: Yersinia, Pasteurella, Tularaemia.

41
Q

Revision CW Eosinophilic meningitis

A

Angiostrongylus cantonensis, Baylisascaris procyonsis, Gnathostoma spinigerum. Other possible causes: coccidioidal meningitis less commonly cryptococcosis. Toxocariosis, neurocysticercosis, strongyloidiasis, trichinellosis, fascioliasis, Paragonimus westermani, echinococcosis, schistosomiasis, myiasis. Non ID: CNS lymphoma, hypereosinophilic syndromes, adverse drug reactions, presence of VP shunt.

42
Q

Revision CW Angiostrongylus cantonensis

A

Rat lung worm. Migrating larvae inherently neurotropic. SE Asia, Pacific Islands. Humans acquire by eating raw or undercooked snails or slugs, infected animals (crab, shrimp, centipedes, contaminated ground veggies. Treatment: Supportive, advise against antihelminthic agents which may elicit inflammatory responses to dying organisms. Most common parasitic cause of eosinophilic meningitis

43
Q

Revision CW Baylisascaris procyonsis

A

Migrating larvae inherently neurotropic. Prevalent in US raccoons. Humans acquire by ingesting infective eggs from environment. Often described with young children playing in dirt or sandbox (aka raccoon latrine) or person eating out of contaminated area. Can migrate to variety of tissues (larva migrans) eosinophilic meningitis more rare. Treatment: Supportive, unclear utility of antihelminthic agents. Summary: acute severe headache, no migratory swelling, pain with focal numbness. CSF appears like coconut juice, CTB no pathognomonic sign, history of uncooked snails or slugs.

44
Q

Revision CW Gnathostoma spinigerum

A

Migrating larvae in visceral, cutaneous, and/or neural tissues. Endemic in SE Asia, China, Japan but occurs broadly. Humans acquire by ingesting intermediate hosts (eg fish, frog snake) containing larvae or by drinking contaminated water. Possible triad: eosinophilia, migratory cutaneous swelling/nodules, raw fish consumption. Larval penetration into brain usually related to migration along nerve tract, so might have sudden onset radicular pain or headache. Treatment: Supportive. Unclear utility of antihelminthic agents with CNS disease. Cutaneous disease can be treated with albendazole or ivermectin as well as surgical excision of worms. Summary: motor weakness, migratory swelling, pain along nerve root. CSF non-traumatic bloody, CTB SAH, Associated with uncooked poultry, fish.

45
Q

Revision CW Hypertension

A

Aim is to reduce risk of morbidity/mortality from complications. Good evidence this achieved through lowering BP and control of other CVS risk factors. Decision to treat depends on grade of hypertension and overall CVS risk. Non-pharmacological treatments (NPT) (weight reduction, salt reduction, smoking cessation, increased physical activity, improved diet/fruit and veg consumption can be effective). Initiation of pharmacological treatment is recommended for high risk patients, and should be considered for medium risk patients if a trial of NTP is unsuccessful. Choice of drug will depend heavily on availability and cost: monotherapy with betablockers and ACE/ARBs are relatively ineffective in people of African origin. Calcium antagonists or thiazides would be first line. Other possibilities include methyldopa, hydralazine and low dose reserpine. Comment: NCD questions are testing general medicine knowledge - they will try to make it situationally different - the idea is you have a patient who has wasted a massive amount of time waiting to be seen, do not have time to follow them up nor the resources to do further testing. WHO guidance for hypertension in Africa firstline is Ca channel blockers.

46
Q

Revision CW Chagas treatment

A

Recent chronic infection: Benznidazole <40kg 7.5mg/kg/d >40kg 5mg/kg/d in 2-3 doses per day for sixty days

47
Q

Revision CW Lymphatic filariasis

A

Filaria with a sheath (Wb Bm Ll) are seen in blood (need a wetsuit) and Rx with DEC. Filaria without a sheath are in tissue (no need for wetsuit). Comment: Skin snips - O volvulus near bony prominences, Lymphoscintigram expensive, technically difficult, identifies obstruction but not cause. Day blood film - Loa loa comes out at lunch. Loa loa does not have Wolbachia so Doxy ineffective. O volvulus (Simulium fly) Rx Ivermectin & Doxy. LF (mosquitoes) DEC & Doxy. Loa loa (high infection) can have a fatal encephalitis if given ivermectin - need to check level of microfilaria. Treatment is so controversial it will not be examined - all the guidelines have different cut offs for where you use different drugs. But may be asked about Ivermectin use and complications

48
Q

Revision CW Schistosomiasis

A

Cercariae in fresh water penetrate human skin, lose tail and migrate through skin as schistosomulae, migrate through blood stream to liver, adult worms migrate to target mesenteric or vesical plexus where they mate (this takes 3 months), and then produce huge numbers of eggs, that penetrate the tissue on their way out into urine or faeces. Water sources become contaminated with eggs from human urine or faeces, miracidia hatch on water contact, penetrate the foot pad of the host snail (Bulinus Sh, Biomphalaria Sm) mature, and then released in water as cercariae ready to infect human (cercariae live ~48h from release). Summary: Sm bowel, lateral spine, stool microscopy, BioMphalaria snails. Sh bladder, terminal spine, terminal urine, BUlinus snail. Comment: Praziquantel only kills adults, need 3m for adults to arise. Schisto can be acquired from piped water into showers/sinks etc with cercariae. Praziquantel is the only treatment. Sh is a classified carcinogen - eggs laid around the bladder wall, migrate through bladder wall to get into urine. Not all make the migration through the wall, some get stuck and cause inflammation which can cause calcification or malignant transformation surrounding tissue, leading to bladder cancer - usually heavy infection. On cystoscopy see sandy patches on inner bladder wall.

49
Q

Revision CW Onchocerciasis

A

Sub-Saharan Africa, Mexico, Brazil. Clinical: Chronic inflammation, generalised itching, inflammatory papules/plaques, skin atrophy, more common in forested areas. Nodules (Onchocercomas - 0.5-3cm, 1-2 male and 2-3 female worms, most are not palpable, usually at bony prominences). Depigmented leopard skin, hanging groin, more common in Savannah regions. See on slit lamp examination -> punctate keratitis -> sclerosing keratitis. Diagnosis: Skin snip (iliac crest, scapula, lower extremities - six snips provide the most diagnostic sensitivity). Slit lamp examination. Treatment: Single dose Ivermectin eliminates 80% Mf from skin, retreat every 6-12 months. Less AE than DEC. Moxidectin (recent FDA approval, longer half live than iVM potential for fewer rounds of Rx), Doxycycline 200mg/d 4 weeks with ivermectin on d1 and at 3 months. Lifecycle: Simulium takes a blood meal, L3 larvae enter the bite wound - migrate through subcutaneous tissues, adults develop in subcutaneous nodules, mate and produce large number of unsheathed microfilariae per day, typically found in skin and lymphatics. Simulium fly takes a blood meal and ingests microfilariae. Mf penetrate midgut and migrate to thoracic muscle, mature from L1 to L3 larvae, migrate to head and proboscis ready for transmission at blood meal. Comment: Oncho causes itch and affects integrity of skin - collagen is lost in groin and bits start falling out, change in pigmentation from scratching. To look for eye changes, as the patient to put their head upside down for a few minutes to resuspend Mf in their chambers and look in the eye they will be floating around.