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Lecture week I > Travel conditions > Flashcards

Travel conditions Flashcards

1
Q

Tests used in HIV diagnosis

A

A) Antibody test: antibodies against HIV

B) Antibody/antigen test: antibodies against HIV and HIV antigen (virus itself)

C) RNA/DNA test: screen for viral RNA -> detects virus directly & DNA -> copies of viral

RNA

• Antibody/antigen test is recommended for screening purposes -> better for identifying

early infection

• The other tests are recommended as confirmatory tests (as follow up after positive result

of antibody/antigen test)

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2
Q

HIV diagnostic workout

A
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3
Q

Aims of HIV management with anti-retroviral therapy

A
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4
Q

What tests are involved in Dx of Malaria?

A
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5
Q

Why it’s important to know % of RBCs infected by parasite? (in malaria)

A

% of RBCs infected by parasites is
important -> patients with >5% parasitemia can have worse outcome

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6
Q

Common lab findings in malaria

A

Common lab findings:

  • thrombocytopenia -> low platelet count
  • elevated lactate levels -> due to hemolysis
  • anaemia: normochromic (normal colour) and normocytic (normal size) BUT anaemia = low RBCs number
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7
Q

Management algorithm in ‘suspected’ malaria case

A
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8
Q

Types of malaria treatment (4)

A
  • Suppressive treatment = Chemoprophylaxis is aimed to kill sporozoites before they infect hepatocytes -> given to travellers that go to endemic malaria countries

• Therapeutic treatment: to eliminate merozoites that are in erythrocytic phase -> given during active infection

  • Gametocidal treatment - to kill gametocytes -> prevent spread of diseases

• Radical treatment - to kill hypnozoites in the liver (P. Vivax and P . Ovale infections)

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9
Q

Name (2) agents used to treat malaria

A

chloroquine, quinine

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10
Q

(2) options for malaria prevention - environmental

A
  • to prevent mosquitoes from biting -> sprays, full body clothing, sleeping in the nets
  • to remove containers with water -> as mosquitoes like to lay their eggs there (to control

mosquitoes population)

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11
Q

What virus family causes Viral Haemorrhagic Fever?

A

Flaviviridae virus family

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12
Q

What is the danger of viral haemorrhagic fever?

A

They can cause fever and bleeding disorders -> possible progression into shock and deaths

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13
Q

Pathogenesis of viral haemorrhagic fever

A
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14
Q

Symptoms of viral haemorrhagic fever

A
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15
Q

What are general blood test findings in a person with viral hemorrhagic fever?

A
  • decrease in total WBC (particularly in the lymphocytes)
  • decrease in platelet count
  • increase in blood serum liver enzymes
  • reduced clotting ability -> measured as increased PT and PTT times
  • hematocrit may be elevated
  • urea and creatinine may be raised (depends on hydration status of the patient)
  • prolonged bleeding time
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16
Q

What is hematocrit?

A

*hematocrit - volume in % of RBCs; normally is around 47% (+/-5%) for men & 42% (+/- 5%) for women)

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17
Q

management of viral hemorrhagic fever

A
  • may require intensive support care
  • antiviral therapy -> IV ribavirin (useful in some cases of VHF)
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18
Q

Why do deaths usually occur in Ebola?

A

death occurs usually from low BP from fluid loss

  • usually 6-16 days after the symptoms appear
  • 50% of infected people die
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19
Q

Simple pathology of Ebola

A
  • Ebola virus enters the immune cells -> infects it -> inflammatory molecules are secreted from an infected cell -> inflammatory process starts; also virus replicated within the cell (as per normal viral mechanism -> hijacking the cell to make new viruses)
  • inflammatory molecules -> damage to vascular integrity -> hemorrhagic fever
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20
Q

Signs and symptoms of Ebola

A

Start usually 2 days - 3 weeks after contracting the virus

A. Early: fever, headache, muscle pain, sore throat (initially remains of a flu-like illness)

B. Later: vomiting, diarrhoea, rash and decreased renal and liver function *

* at later stage -> possible internal and external bleeding

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21
Q

Complications of Ebola

A
  • progression into disseminated intravascular coagulation (DIC) -> presents as low platelet count and elevated D-dimer
  • diffuse /rozproszony/ haemorrhage -> shock
  • multi-organ dysfunction
  • renal and hepatic dysfunction -> elevated creatinie and liver enzymes
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22
Q

How to make a diagnosis of Ebola from the results?

A

A. History, S&S
B. Decreased WBC -> then elevated WBC
C. D-Dimer -> elevated
D. platelet count decreased (DIC)
E. Prolonged PT and PTT (due DIC)
F. Liver enzymes -> elevated (hepatic dysfunction)
G. Urea and creatinine -> elevated (renal dysfunction)
E.ELISA (antigen recognition test) and PCR

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23
Q

IgM and IgG detection in Ebola (timeframes)

A
  • IgM detected 2 days after symptom onset
  • IgG antibodies 6- 18 days after symptom onset
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24
Q

Management of a patient with Ebola

A

* prevention measures (washes,disinfection, contact tracing, isolation, protective equipment, safe disposal, safe burial etc.)

  • Supportive care as no specific treatments are available
  • No licensed vaccine or anti-Ebola products developed

Supportive:

  • Rehydration via oral or IV route
  • analgesia
  • nausea, fever and anxiety treatments
  • blood products (fresh frozen plasma, RBCs, platelets)
  • Heparin -> in effort to prevent DIC
  • Clotting factors -> to decrease haemorrhage

Intensive care in developed worlds: maintaining blood volume and electrolytes (salt) balance, treating any bacterial infections that may develop

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25
Q

What meds and why to avoid in Ebola

A

*avoid ibuprofen or aspirin -> as risk of bleeding

26
Q

How to distinguish Dengue from Ebola?

A

They are both types of viral haemorrhagic fever

distinction from Ebola: no renal/hepatic failure, no DIC

27
Q

WHat virus causes Dengue?

A

mosquito-borne, tropical disease -> caused by dengue virus (enveloped, single stranded, positive sense, RNA virus)

28
Q

Symptoms of Dengue infection

A

*start 3 - 14 days after infection

High fever, headache, vomiting, muscle and joint pain, characteristic skin rash

29
Q

What’s prognosis in Dengue?

A
  • Recovery usually takes <2 - 7 days
  • Complication (in small proportion of cases), potentially fatal:

A. Dengue hemorrhagic fever -> bleeding, low platelet count, blood plasma leakage

B. Dengue shock -> extremely low BP

30
Q

Diagnosis of Dengue

A

Diagnosis made on basis of S&S and physical examination -> however early manifestationsare difficult to be differentiated from other viral diseases/infections

Number of different tests available for diagnosis:

  • detection of antibodies to the virus
  • detection of viral RNA
31
Q

Management of Dengue

A

No specific anti-viral drug is available

Rx depends on a status of a person:

  • those whose hydration status is OK (drinking and passing urine) and are otherwise healthy (no warning signs) -> can be managed at home with daily follow-up and oral rehydration therapy
  • patients with hydration and other health problems -> need to be hospitalised for a regular follow up

A. Preventative: vaccine available, reduction mosquito habitat, limitation of exposure to bites

B. Acute dengue fever -> supportive treatment:

  • fluids (oral or IV) - mild to moderate disease
  • blood transfusion - for severe forms of disease (if haematocrit is decreasing and vital signs are unstable)
32
Q

What to avoid in pt with Dengue?

A

To avoid:

  • invasive medical procedures e.g. NG tube, IM injections etc -> as risk of bleeding
  • Do not use NSAIDs as they may increase risk of bleeding

*use Paracetamol (acetaminophren) instead (for fever and pain relief)

33
Q

What’s atypical pneumonia?

A

Atypical pneumonia aka walking pneumonia

  • pneumonia that is not caused by one of commonly pneumonia causing organisms
  • different clinical presentation to that of a typical pneumonia
34
Q

Difference between typical vs atypical pneumonia

  • antibiotics used to Rx
  • appearance on X ray
A
35
Q

Difference between typical vs atypical pneumonia

  • clinical presentation
A
36
Q

Cause of Ameobic Abscess

A
  • liver abscess caused by amebiasis -> as liver tissue is involved in the infection by thropozoites of Entamoeb histolytica -> abscess due to necrosis
37
Q

Symptoms and signs of amoebic abscess

A

Symptoms:

  • pain in R hypochondriac area (referred to R shoulder)
  • pyrexia
  • sweating and rigors
  • loss of weight
  • earthy complexion - patchy pigmentation of the face

Signs:

  • pallor
  • tenderness in R hypochondriac area
  • palpable liver
  • intercostal tenderness
  • basal lung signs
38
Q

Management of amoebic abscess

A

A.Abscess aspiration

B.Repeated liver imaging

C.Metronidazole - antibiotic and antiprotozoal medication

39
Q

What is the cause of Leptospirosis?

  • how is it spread
  • who is at risk
A

Caused by a bacteria called Leptospira

  • spread by wild and domestic animals (rodents e.g. rats, mice, hamsters, squirrels)

*in developing world - farmers and low-income people living in the cities and slums
* in the developed world - outdoor activities in warm and wet areas

40
Q

Signs and symptoms of leptospirosis

A

S&S may range from:

A) none to mild: headaches, muscle pains, fevers

B) severe: bleeding from the lungs or meningitis

41
Q

(2) serious complications of Leptospirosis

A
  • Weil’s disease -> when a person infected with leptospira turns yellow, have kidney failure and bleeding (death rate >10%)
  • Severe pulmonary haemorrhage syndrome -> bleeding into the lungs (death rate >50%)
42
Q

Diagnosis/Ix of Leptospirosis

A

Early diagnosis - test blood and urine:

  • blood and CSF -> infection can be found within first 10 days
  • after 10 days -> infection moves to kidney -> can be found in fresh urine
  • U&Es and LFTs, creatinine and nitrogen
  • enzyme- linked immunosorbent assay (ELISA) and PCR -> confirm diagnosis
  • MAT (microscopic agglutination test) -> gold standard in diagnosis of leptospirosis
43
Q

Occupations at risk of Leptospirosis

A

Occupations at risk: vets, slaughterhouse workers, farmers, sailors, waste disposal

workers

Adventure tourism: kayakers, rowers, canoeists

44
Q

Treatment of Leptospirosis

A

A. Usually effective antibiotics - Penicillin G, ampicillin, amoxicillin, deoxycline
B. More severe cases: cefotaxime or ceftriaxone
C. Glucose and salt infusions
D. Dialysis - if kidney affected severly
E. Measure potassium (as elevation is common)

45
Q

Cause of Schistosomiasis

A

Schistosomiasis aka ‘snail fever’

  • disease caused by parasitc flatworms (schistosomes)
  • Parasites infect fresh water snails
46
Q

Schistosomiasis

  • site of infection
  • long- term complications
A
  • Sites of infection: urinary tract or intestine
  • long time infection may result in: liver damage, kidney failure, bladder cancer, infertility
47
Q

Risk groups of schistosomiasis

A
  • Disease is particularly common among children in developing countries -> as they play a lot in fresh water (water is contaminated with shistosomes)
  • farmers, fishermen, people using unclean water
48
Q

Symptoms of schistosomiasis

A

Symptoms: abdominal pain, diarrhoea, bloody stool, blood in the urine

Children: poor growth and learning difficulties

49
Q

Dx / Ix of schistosomiasis

A
  • finding eggs of the parasite in a person’s urine or stool
  • finding antibodies against the disease in the blood
50
Q

Prevention of Schistosomiasis

A
  • improving access to clean water
  • reduction of water snail population
  • meds Praziquantel (drug against some parasites) given once yearly to the populations at risk
51
Q

Treatment of Schistosomiasis

A

All cases of schistosomiasis should be treated regardless of presentation -> as parasite can live in host for years

Preferably use Praziquantel (drug against some parasites) and combination of other

drugs (mostly these used to treat malaria as anti-parasitic activity)

52
Q

Exotoxin mechanism of diarrhoea + bacteria causing it

A
  • exotoxins -> effect on the stomach, small bowel -> mucosal inflammation symptoms of food poisoning (Bacillus Cereus and Staphylococus Aureus)
53
Q

Enterotoxin mechanism of diarrhoea + bacteria causing it

A

enterotoxins -> watery diarrhoea without fever (E. Coli) - usually no blood or mucous

54
Q

Enteroinvasive mechanism of diarrhoea + bacteria causing it

A

enteroinvasive -> invade intestinal mucosa (Enteroinvasive E. Coli, Shigella and Campylobacter) -> fewer, lower abdominal pain, bleeding diarrhoea + fever (dysentery)

55
Q

Possible complications of diarrhoea

A

electrolyte imbalances, renal impairment, dehydration, defective immune responses, inefficiency of administrated drug -> as medication travels too quickly through digestive tract

56
Q

Medical management of diarrhoea

A
  • Oral rehydration therapy -> slightly sweetened and salty water -> used to prevent dehydration; it can be given via NG tube; usually include zinc

supplementation

  • Medication: antibiotics used only in certain cases of diarrhoea (bacterial) - > beneficial in resource poor countries; antibiotics may contribute to diarrhoea

Other medications (used only if the bloody diarrhoea is not present):

  • Bismuth compounds (Pepto-Bismol) -> decreases number of bowel movements in traveler’s diarrhoea but do not decrease length of illness
  • Loperamide -> anti motility agent -> to reduce number of stools but again, not the illness duration
  • Bile acid sequestrants (bile reabsorption prevented from the gut) -> for those with chronic diarrhoea due to bile acid malabsorption
  • Zinc supplementation -> beneficial for children over 6 months old
  • Probiotics -> reduce duration of symptoms by one day + reduce chance of symptoms lasting longer than 4 days (by 60%)
57
Q

Diet recommendation in diarrhoea

A
  • Fluid and food: Replacing lost fluids (usually by oral rehydration therapy), in severe cases IV
  • diet restrictions are not recommended (even for babies and children; including those breast fed) -> as nutrient is usually still absorbed and support children with growth and also eating as usual has an effect on speed up of recovery as support normal intestinal functioning; limitation of food has no effect on duration of diarrhoea
58
Q

Antibiotic-associated diarrhoea

  • common bacteria
  • severe form (names )
  • age groups at risk
  • when develops
A
  • bacterial overgrowth with C. Difficile
  • severe -> can lead to acute colitis/ pseudomembranous colitis
  • common in young and elderly
  • diarrhoea develops 2 days - 4 weeks after taking antibiotics
59
Q

Risk factors for C Diff infection

A

Risk factors: Prolonged hospital stay, multiple or prolonged antibiotic therapy, GI surgery, proton pump inhibitor use

60
Q

Ix and what can be seen in C Diff

A
  • detection of C.Diff toxins (in stool by enzyme-linked immunosorbent assay ELISA)
  • stool culture -> C diff isolation (in 30%)
  • sigmoidoscopy -> ulceration and a white pseudomembrane
61
Q

Management of C Diff infection

A
  • antibiotics should be stopped
  • to treat dehydration (oral, IV fluids)
  • infection control measures) -> barrier nursing and hand washing
  • antibiotics against C.Diff (metronizadole or oral vancomycin) should be started following a diagnosis
  • more severe in the elderly -> colectomy may be required for toxic megacolon

Lecture week I (6 decks)

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