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Optional Modules > Tropical Medicine and Beyond > Flashcards

Tropical Medicine and Beyond Flashcards

1
Q

What is a nematode?

A

Microscopic roundworm

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2
Q

What are the 3 classifications of tissue nematodes?

A

Lymphatic, subcutaneous, conjunctiva

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3
Q

What is filariasis?

A

Tissue infection with nematodes belonging to Filaroidea (known as elephantitis)

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4
Q

What is the most prevalent type of filariasis?

A

Lymphatic

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5
Q

What are the causative agents of filariasis?

A

Wucheria bancrofti
Brugia malayi
Brugia timori

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6
Q

What is the most common filariasis cause in Malaysia?

A

Brugia malayi

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7
Q

What is sub-periodic periodicity zoonotic infection

A

Irregular periodicity infection that is transmitted between animals and humans

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8
Q

Describe the periodicity of W bancrofti and B malayi infection

A

Nocturnal and sub-periodic

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9
Q

Describe the pathogenesis of lymphatic filariasis

A

Larvae transmitted by mosquito
Larvae invade lymphatics and lymph nodes where they mature
Mate and release microfilariae into lymphatics and bloodstream
Mosquito takes a meal and invests microfilariae

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10
Q

Describe filarial oedema

A

Adult worms in lymph vessels die but bacterial colonisation of tissues causes inflammatory process - proliferation of connective tissues leading to fibrosis which obstructs lymph drainage leading to oedema

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11
Q

Describe the clinical manifestations of filariasis

A

Most are asymptomatic

Lymphoedema occurs years after infection

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12
Q

What is tropical pulmonary eosinophilia in filariasis?

A

Lung disease presenting with a nocturnal cough, wheezing and fever resulting from immune hyperesponsiveness to microfilariae in pulmonary capillaries

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13
Q

Describe the renal pathology of filariasis

A

Microfilaria lead to dilation of renal lymphatic system, rupture and lymph fluid passed into renal pelvis. Causes chyluria (lymph in urine) which leads to a milky urine appearance.

Potential haematuria and proteinuria also

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14
Q

What is the difference between acute and chronic filariasis

A

Acute - lymphoedema of extremities

Chronic - elephantitis due to recurrent bacterial infection

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15
Q

How would you diagnose lymphatic filariasis?

A

Ultrasound to detect worms in lymphatic vessels

Blood for thin and thick film, collected at night (due to nocturnal periodicity of microfilaria)

Antigen detection (serology)

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16
Q

What drug is used to treat filariasis?

A

Diethylcarbamazine (DEC) which kills microfilaria and adult worms

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17
Q

What mosquito transmits dengue fever?

A

Aedes aegypti

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18
Q

How many serotypes of dengue fever are there?

A

4 (DEN1, DEN2, DEN3, DEN4)

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19
Q

Describe the dengue virus genome and structure

A

Single strand of positive sense RNA (translated directly to single long polypeptide which is cut into ten proteins)

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20
Q

Describe the pathophysiology of dengue fever

A

Skin inoculation by insect
Infection of dendritic cells
Infection of lymph node
Viremia

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21
Q

Why is second infection with different dengue fever serotype worse?

A

Larger inflammatory response leading to worse symptoms including dengue haemorrhagic fever

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22
Q

What are the risk factors for severe dengue?

A

Pre-existing dengue antibody (previous infection or maternal antibody)

Location with 2 or more serotypes in circulation at high levels

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23
Q

What are the 2 main methods of laboratory diagnosis of dengue fever?

A

Detection of dengue virus

Detection of anti dengue antibodies

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24
Q

What is the difference in serotype between primary and secondary dengue fever

A

In secondary, IgG antibodies are present immediately however in primary, only IgM are present until about day 7, when IgG can be found

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25
Q

What is the treatment for dengue?

A

Rehydration, bed rest, pain relief

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26
Q

Who should be vaccinated against dengue? How often are they vaccinated?

A

People with a previous dengue infection. Vaccination dose every 6 months

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27
Q

What is the vector for Chikungunya?

A

Aedes mosquito

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28
Q

What is the main symptomatic difference between dengue and Chikungunya?

A

Severe joint pain

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29
Q

How would you diagnose Chikungunya?

A

Clinical - high fever, joint pain
Epidemiology - traveled to endemic area in last 12 days
Laboratory - decreased lymphocytes, serological diagnosis

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30
Q

What is the incubation period for dengue?

A

12 days

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31
Q

What is the time frame for antigen and antibody detection of Chikungunya?

A

IgM at day 4-7

IgG at day 15

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32
Q

What is the difference between pharmacokinetic and pharmacodynamic durg interactions?

A 
pharmacokinetic = one drug affects the absorption, distribution, mtabolism, excretion of another drug
pharmacodynamic = drugs influence each other's effects directly
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33
Q

Describe drug interactions at the absorption level

A

Formation of complexes can considerably reduce bioavailability of drugs

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34
Q

Describe drug interactions at the distribution level

A

A second drug can displace a drug from a plasma protein and increase levels of the unbound active drug available to cause effect

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35
Q

Describe drug interactions at the excretion level

A

Drug-induced reduction in GFR can lead to reduced clearance and higher plasma conc. of drugs. Competition for tubular transporters

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36
Q

Describe drug interactions at the metabolic level (cytochrome P450)

A

Inhibition/competition for cytochrome P450 can result in higher drug levels in body

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37
Q

What are the common interactions with St. John’s Wort?

A

Reduced efficacy of oral pill - unwanted pregnancy

Reduced plasma conc. of antiretroviral and anticancer drugs

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38
Q

What are the interaction problems caused by grapefruit juice?

A

Inhibits CYP3A4 which leads to increased drug conc.

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39
Q

What are the factors associated with Salmonella food poisoning?

A

Consumption of inadequately cooked meat/poultry
Cross contamination of food from infected handlers
Presence of flies, cockroaches, rats in food environment

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40
Q

What is the causative agent for typhoid?

A

Salmonella typhi

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41
Q

What are the risk factors for typhoid?

A

Poor sanitation, overcrowding

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42
Q

What is the incubation period for typhoid?

A

2 weeks (may vary between 3-28 days)

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43
Q

What are the symptoms and complications of typhoid?

A

Fever, headache, constipation, bradycardia.
Can lead to intestinal perforation and becoming a chronic carrier (persistent positive stool culture for salmonella a year after onset)

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44
Q

What organism causes cholera? How does it have its effect?

A

Vibrio cholera. Multiply in small intestine to produce potent enterotoxin = pouring out of isotonic fluid by gut mucosal cells

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45
Q

What are the signs and syptoms of cholera?

A

Rice-watery stool, dehydration, vomiting, muscle cramps, hypovolemic shock, scanty urine

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46
Q

How is chloera managed?

A

Rehydration, monitor, antibiotic (severe cases), vaccination

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47
Q

What is dysentery?

A

Bloody diarrhoea caused by a variety of organisms including shigella spp

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48
Q

What is shigellosis?

A

Frequent passage of sacnty amounts of stools mixed with blood and mucus. Fever, abdominal cramp and tenesmus (pain around anus during defacation)

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49
Q

What are the complications associated with E.coli O157

A

Bloody diarrhoea, colitis, sub-mucosal edema. Hemolytic Uremic Syndrome (HUS) can lead to death

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50
Q

What kind of bacteria is staphylococcus aureus?

A

Non-spore forming gram positive coccids. Heat stable and pH stable (resistsant to most proteolytic enzymes

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51
Q

What is the incubation period for staphylococcus aureus?

A

1-6 hours

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52
Q

What are the problems associated with listeria monocytogenes?

A

Abortion in pregnant women due to trans-placental spread and meningitis in immunocompromised

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53
Q

What kind of bacteria is Clostridium botulinum?

A

Obligate, gram-positive, spore-forming anaerobe. Heat labile and unstable at alkaline pH (resistant to acidic stomach)

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54
Q

What is the incubation period for Clostridium botulinum?

A

12-72hrs

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55
Q

What is the incubation period of hepatitis A?

A

30 days average

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56
Q

What is pharmacogenomics?

A

The science that allows us to predict a response to drugs based on an individuals genetic makeup

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57
Q

What is Steven Johnson Syndrome and toxic epidermal necrolysis?

A

Severe erythema multiforme characterized by erosive lesions of skin, mucous membranes and conjunctivitis.

58
Q

What is the cause of Steven Johnson Syndrome and toxic epidermal necrolysis?

A

Caused by infectious illness or adverse drug reaction

59
Q

What 2 drugs most commonly cause teven Johnson Syndrome and toxic epidermal necrolysis?

A

Allopurinol and carbamazepine

60
Q

What is the anthropogenic factor that contributes to Malaysian Haze?

A

Clearance of tropical peatlands for agriculture and urbanization releases carbon store

61
Q

What is the El Nino effect and how does it lead to haze?

A

Severe warm weather leading to draught that triggers natural forest fires

62
Q

How is air quality assessed in Malaysia?

A

Air Pollution Index (API) reflects the effect of air quality on human health (>100 = haze)

63
Q

What is haze induced airway inflammation?

A

Small particulate matter sizes deposit onto lower respiratory tract and result in an inflammatory response due to unique chemical composition.

64
Q

What does mast cell degranulation lead to in response to haze ?

A 
Mucus production (rhinitis, runny nose)
Bronchoconstriction (asthma, wheezing)
Increase vascular permeability (fluid in tissues, oedema)
65
Q

List the medical interventions used during haze episodes

A

Surgical mask/N95 respirator - prevent inhalation of particles
0.9% NaCl eye drops and nasal rinse - irrigation to remove pollutants
Antihistamines - combat allergic reactions
Analgesics - fever, aches and pain
Antibiotics - conjunctivitis, pneumonia
Bronchodilators - wheezing/SoB
Corticosteroids - skin irritation and dermatitis. Inflammation

66
Q

What are the 3 therapies employed by a ‘bomoh’ (traditional Malay healer)?

A

Supernatural rituals
Natural resources from plants, animals and minerals
Cupping, bone setting, massage…

67
Q

What gives Hempedu bumi its bitter taste?

A

Diterpene lactones, particularly andrographolide (strong anti-cancer and anti-HIV properties)

68
Q

What are the medicinal effects of the Tongkat Ali root? What is the main bioactive component?

A

Aphrodisiac effects to improve sexual health. The quassinoids are the main component

69
Q

What component of Tongkat Ali gives it its anticancer properties?

A

Eurycomanone - lung carcinoma and breast cancer

70
Q

What are the medicinal uses of Dukung Anak?

A

Treats kidney stones, gallstones, jaundice. Alleviates liver injury

71
Q

What are the medicinal properties of Misai Kucing?

A

Diuretic effects for rheumatoid disease, hypertension, diabetes…

72
Q

What mosquito transmits malaria?

A

Anopheles

73
Q

What are the 5 types of malaria parasite?

A

Plasmodium falciparum, P. vivax, P. ovale, P. malariae and P. knowlesi

74
Q

Describe the life cycle of the malaria parasite

A

Anopheles mosquito injects parasite into host in form of sporozoites into subcutaneous tissue and bloodstream.
Parasites enter liver, mature into schizonts and rupture to release merozoites.
Merozoites released and begin red blood cell invasion

75
Q

Describe the clinical presentation for the different malaria parasites.

A

P. falciparum - fever may occur every 48hrs
P. vivax and P. ovale - schizonts mature every 48hrs so periodicity is tertian
P. malariae - fever every 72hrs
P. knowlesi - 24hr cycle manifests fever every day

76
Q

What is the most common species of malaria infection in Malaysia?

A

P. vivax. Causes relapse via hypnozoites (hard to eradicate)

77
Q

How do quinolines work as anti-malarial drugs?

A

Inhibit parasite haem detoxification in the food vacuole

78
Q

How do antifolates work as anti-malarial drugs?

A

Inhibits dihydrofolate reductase during folate synthesis, key for parasite survival

79
Q

How does artemisinin work as an anti-malarial drug?

A

Produces hydroperoxide - free radicals

80
Q

How do antibiotics work as anti-malarial drugs?

A

Inhibits protein synthesis at low molar range

81
Q

How would you treat P. falciparum malaria?

A

IV artesunate

82
Q

How would you treat P. vivax and P. ovale malaria?

A

Step 1 - cure acute blood stage infection: chloroquine, artemisinin derivatives
Step 2 - clear hypnozoites from liver to prevent relapse: primaquine therapy

83
Q

How would you treat P. malariae and P. knowlesi?

A

Chloroquine (artemisinin combination therapy for complicated P. knowlesi)

84
Q

What are fungal immunomodulatory proteins (FIP)?

A

Family of proteins that exhibit homolgy to the family of immunoglobulins and phytohaemagglutinin. Demonstrate some antitumor activities.

85
Q

What is ergothioneine (ERGO)?

A

Antioxidant found in mushrooms with chemoprotective benefits for ageing-related diseases

86
Q

What is ganoderma lucidum?

A

Mushroom with longest record of medicinal use in China, Japan and tropical Asia. Used as a health tonic, anti-fatigue, anti-aging…

87
Q

What is cordyceps spp?

A

Most famous tonic and health supplement in TCM

88
Q

What is lignosus rhinocerotis?

A

Tiger’s milk mushroom with bronchodilator effect and relaxation effect on other smooth muscle including blood vessels and bladder

89
Q

What are the main risk factors for lung cancer?

A

Tobacco, air pollution and occupational exposure

90
Q

What are the main causes of liver cancer?

A

Heavy alcohol intake, hepatitis B and C, aflatoxin-contaminated foodstuffs, obesity, smoking, type 2 diabetes

91
Q

What is the most prevalent cancer in India and why?

A

Lip and oral cavity due to chewing and smoking tobacco

92
Q

What are the WHO recommendations for managing cervical cancer?

A

HPV vaccine of girls aged 9-13

Screening of women aged 30-49

93
Q

What is the difference between venomous and poisonous?

A

Venomous - organisms that bite/sting to inject toxins

Poisonous - toxins are synthesized as metabolites that are unloaded if eaten

94
Q

What is the effect of snake venom on blood coagulation?

A

Procoagulant activity - widespread clot formation/defibrinogenation

95
Q

How do we determine venom dose lethality?

A

Dose of venom which kills 50% of mice over a 24/48hr period

96
Q

What is the difference between presynaptic and postsynaptic venom neurotoxins?

A

Postsynaptic - responds to anticholinesterases and antivenom

Presynaptic -only responds to antivenom if given early

97
Q

What bacteria causes tuberculosis?

A

Mycobacterium tuberculosis (bacillus)

98
Q

What is multi-drug resistant TB?

A

Form of TB caused by bacteria that does not respond to two of the most powerful drugs (treatment is limited and expensive)

99
Q

What is the biology of the mycobactrium tuberculosis cell wall?

A

Rich in mycolic acid - waxy coast. Slow growth

Affects acquisition of nutrients and impedes uptake of antibiotics

100
Q

How is tuberculosis identified?

A

Ziehl-Neelsen stain (acid fast stain)
Growth on selective culture media
PCR

101
Q

What is TB cord factor?

A

Glycolipid which causes cells to grow in serpentine cords and toxic to mammalian cells with inhibition of neutrophil migration

102
Q

What is TB antigen 85 complex?

A

Binds host ECM and involved in tubercle formation

103
Q

Describe the pathogenicity of primary TB

A

Inhaled micro-droplets containing TB taken up by alveolar macrophages (not activated initially)
Bacteria replicate inside macrophage and T-cells finally induce response.
Small foci of inflammation forms a granuloma (walls off bacteria)

104
Q

What are the different types of TB?

A

Primary TB - Often clinically silent, possible formation of
granuloma of Ghon focus (latent)
Post primary TB - Reactivation. Pulmonary infectious TB
Miliary TB - Disseminated TB with spread to blood and other tissues

105
Q

What is the aetiology of post-primary TB?

A

Expanding granulomata that release numerous mycobacteria and establish more lesions. Little spontaneous healing = cavities and extensive damage to tissues including airways and vessels. Patients are infectious

106
Q

What are some examples of extra-pulmonary TB?

A

Tuberculous meningitis
Renal tuberculosis
Tuberculosis of bones and joints

107
Q

How does the tuberculin skin test work?

A

Inject mycobacterium-derived protein under skin and assess size of induration after 3 days

108
Q

Describe yin and yang in relation to TCM

A

Upper part of body and back are yang, lower part is yin. Related to cold and heat symptoms

109
Q

What is yin and yang vacuity?

A

Yin vacuity - heat sensations, sweats, insomnia, dryness, rapid pulse
Yang vacuity - cold, pale complexion, clear urine, diarrhoea, weak pulse

110
Q

What are the 5 elements of TCM?

A

Wood, fire, earth, metal and water (zang-fu concept)

111
Q

What is channel theory?

A

Pathways in which qi and blood circulate. Connect exterior and interior of the body

112
Q

Describe the TCM model of the body

A

Vital energy (qi/chi) circulates through channels (meridians). Focus on body function

113
Q

What is zang-fu?

A

Zang refers to the 5 entities considered to be yin in nature: heart, liver, spleen, lung, kidney.
Fu refers to the 6 organs considered to be yang in nature: small intestine, large intestine, gallbladder, urinary bladder, stomach and sanjiao

114
Q

What are meridians?

A

Channels running from zang-fu in interior to limbs and joints, transporting qi and xue (blood)

115
Q

Describe the concept of disease in TCM

A

Disease = imbalance/disharmony in interactions of yin, yang, qi, xue, zang-fu, meridians etc. Pattern discrimination is important step of diagnosis

116
Q

What is zheng (syndrome)?

A

Summarization of the pathological changes of a disease at a certain stage in its course

117
Q

What is the foundation text of TCM?

A

Huang Di Nei Jing (Yellow Emperor’s Inner Classic)

118
Q

Describe the use of herbs to treat in TCM

A

Thermal property used. i.e. cold/cool herbs used to treat diseases with heat signs and symptoms (vica versa)

119
Q

Describe the directional affinity of herbs

A

4 directions (ascending, descending, floating/outwards, sinking/inwards). Used to guide therapeutic effect of other herbs to a particular area of the body

120
Q

What is the TCM theory behind acupuncture?

A

Illness occurs when something blocks/unbalances chi. Acupuncture is a way to unblock and restore balance. Stimulates various meridians

121
Q

How many meridians are there?

A

12 main and 8 secondary

122
Q

What is gua sha?

A

Used to relieve muscle and joint pain, and help immune system. Creates microtrauma (bursts capillaries on surface) that create response in body to break up scar tissue and fibrosis

123
Q

What bacteria causes leprosy?

A

Mycobacterium leprae

124
Q

What are the 2 major forms of leprocy?

A

Lepromatous - TH2 response

Tuberculoid - TH1 response

125
Q

How do you identify leprocy?

A

Skin lesions - hypoaesthetic and hypopigmented

Signs of neural damage - peripheral nerve disease

126
Q

What investigations can be carried out to confirm leprocy?

A

Slit skin smear (SSS)
Skin biopsy
PCR

127
Q

What is a skin slit smear test?

A

Slit the skin at 6 sites and smear the blood (both ears and 4 other active lesion sites). Bacteriology index (BI) shows the concentration of the acid fast bacilli, morphology index (MI) shows the percentage of live bacteria (severity of infection)

128
Q

How does a skin biopsy work in leprosy diagnosis?

A

Used in suspected cases with negative SSS/evidence of relapse/no improvement after treatment. Skin biopsy injected into mouse foot for antibiotic sensitivity testing

129
Q

Describe the different types of leprocy disease complications

A 
Type 1 (reversal reaction) - type IV cell mediated hypersensitivity in patients immunologically unstable . Manifests with erythemea, inflammation, neuralgia, oedema
Type 2 (erythema nodosum leprosum) - type 111 humoral hypersensitivity reaction in patients with high bacteria load. Systemic involvement
130
Q

What are the three drugs used to treat leprocy? What is the aim of treatment?

A

Rifampicin, Clofazimine, Dapsone. Aim is to reduce inflammation and pain while also reducing neuronal damage.

131
Q

What are the complications of leprocy drug treatment?

A

Dermatitis, steven johnson’s syndrome, GI symptoms… Hand, foot and eye care important to prevent complications.

132
Q

Describe prophylaxis of leprocy

A

Single dose Rifampicin therapy and BCG given at birth

133
Q

What is TB chancre?

A

Direct inoculation. Chancre appears 2-4 weeks after inoculation on face, oral cavity, hands, lower extremities. Slowly progressive

134
Q

What is TB verrucosa cutis?

A

Paucibacillary disorder on hands and lower extremities. Small asymptomatic papule. Slow progression may last for many years

135
Q

What is Lupus vulgaris?

A

Chronic infection in individuals with moderate immunity and high degree of tuberculin sensitivity. More frequent in females. New lesions may appear within old scars. Complete healing unlikely without therapy. 90% head and neck involved, usually starting on nose, cheek, earlobe or scalp and extending out.

136
Q

How would you diagnose lupus vulgaris?

A

Positive PCR results for M. tuberculosis, tuberculin skin test positive.

137
Q

What are the complications of lupus vulgaris?

A

Involvement of nasal/auricular cartilage leading to disfigurement and destruction. Long lasting can lead to squamous cell carcinoma

138
Q

What is scrofuloderma?

A

Cold abscess formation and secondary breakdown of skin, prevalent in elderly and adolescents. Most common in parotid, submandibular and supraclavicular regions, may be bilateral. Firm nodule, well defined and freely movable. Spontaneous healing but very protracted. LV may develop at site of scar

139
Q

What is orificial TB?

A

Rare TB in mucous membranes/orifices. Autoinoculation from progressive TB of internal organs

140
Q

What is metastatic tuberculous abscess (tuberculous gumma)

A

Cold abscess devlops at extremities or trunk of patients with no involvement of underlying tissue due to metastatic hematogenous spread of mycobacteria that remain latent until the infection manifests itself

141
Q

What is acute miliary TB?

A

In advanced pulmonary, meningeal or disseminated TB common in measles and HIV where cell mediated immunity is depressed. Acute eruption of discrete pinhead blue-red papules

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