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pathology Flashcards

1
Q

What are neglected tropical diseases?

A

Diseases occurring in hot humid low-income places where little attention or research is put into them and there is poor sanitation, a lack of clean water and insufficient healthcare

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2
Q

4 types of neglected tropical diseases?

A

Bacteria, protozoa, virus, helminths (parasitic worms)

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3
Q

What is leprosy?

A

A chronic bacterial infection by Mycobacterium leprae caused by aerosol transmission and eating armadillos

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4
Q

Pathogenesis of leprosy?

A

M. leprae multiplies slowly and causes skin sores, nerve damage and muscle weakness leading to permanent damage to skin, nerves, limbs and eyes

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5
Q

How is leprosy detected?

A

Slit skin smear = small incision in the skin, stained for bacteria (will be pink and rod shaped)

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6
Q

What are the two types of leprosy?

A
  1. Tuberculoid leprosy
  2. Lepromatous leprosy
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7
Q

What is tuberculoid leprosy?

A

Leprosy fought with strong cell-mediated immunity to contain the infection, appears as dry hypo/hyperpigmented patches on skin, loss of sensation

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8
Q

What is lepromatous leprosy?

A

Leprosy not fought due to weak cell-mediated immunity, bacteria multiply freely (high bacterial load), appears as poorly defined shiny nodules or plaques, does not always cause a loss of sensation

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9
Q

How does the histology of tuberculoid vs lepromatous differ?

A

Tuberculoid = granulomas with many lymphocytes (local inflammation), few bacilli

Lepromatous = foamy macrophages packed with bacilli (more contagious), few lymphocytes, thickening of peripheral nerves

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10
Q

What are the possible mechanisms of nerve damage in leprosy?

A

Ischaemia, apoptosis, demyelination

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11
Q

What is leprosy sequelae?

A

Irreversible disability and disfigurement due to leprosy (e.g. loss of fingers and toes, blindness)

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12
Q

What is the treatment of leprosy?

A

Multi-drug therapy using:

  1. Dapsone to inhibit bacterial synthesis of dihydrofolic acid used to synthesise dna bases
  2. Clofazimine that binds guanine bases of bacterial dna = no replication can occur
  3. Rifampicin that inhibits bacterial rna polymerase to prevent rna synthesis
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13
Q

How does treatment vary between tuberculoid and lepromatous leprosy?

A

Tuberculoid needs 6 months of multi-drug therapy, lepromatous needs 12

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14
Q

What is rabies?

A

Viral disease caused by lyssavirus that is transmitted through the saliva of animals

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15
Q

7 steps of rabies pathogenesis?

A
  1. Virus inoculated
  2. Viral replication in muscle for 1-3 months
  3. Virus binds to nicotinic acetylcholine receptors at neuromuscular junctions
  4. Virus travels in axons of peripheral neurons via retrograde fast axonal transport
  5. Replication in motor neurons of the spinal cord and local dorsal root ganglia and rapid ascent to brain
  6. Infection of brain neurons with neuronal dysfunction
  7. Centrifugal spread along nerves to salivary glands, skin, cornea and other organs
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16
Q

Common sign of rabies in neurons in brain, salivary glands and tongue?

A

Inclusion bodies called Negri bodies (where viral transcription and replication occurs)

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17
Q

2 types of rabies?

A
  1. Furious rabies (most cases)
  2. Paralytic rabies
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18
Q

How is furious rabies present?

A

Hyperactivity and hydrophobia, death after a few days, function of anterior horn of spinal cord are disrupted

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19
Q

How does paralytic rabies present?

A

Gradual muscle paralysis, slow coma development, death, peripheral nerves are demyelinated (muscle weakness)

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20
Q

Why does rabies cause different presentations?

A

Unknown but could be due to type of animal vector, site of wound, incubation period or history of rabies vaccine

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21
Q

Treatment of rabies?

A

Active immunisation of humans and dogs

Passive immunisation = immunoglobulins against lyssavirus used as an antidote

22
Q

What is chagas disease?

A

Parasitic protozoan trypansoma cruzi transmittd through triatomine bugs, blood transfusion, oral, congenital

23
Q

Steps of chagas disease in humans?

A
  1. Triatomine bug takes blood meals and passes parasite in faeces which either enters wound through rubbing or is rubbed into eyes
  2. Metacyclic trypomastigotes penetrate various cells at bite wound site and transform into amastigotes
  3. Amastigotes multiply by binary fission in cells of infected tissues
  4. Intracellular amastigotes transform into trypomastigotes that burst cell and enter bloodstream
24
Q

2 phases of chagas disease?

A
  1. Acute phase = localised swelling at wound site
  2. Chronic phase = infection of other areas of the body like essential organs
25
Phases of chagas disease in bug?
1. Triatomine bug takes blood meal and ingests parasite 2. Epimastigoles in midgut 3. Multiply in midgut 4. Metacyclic trypomastigotes in hindgut
26
How is acute phase of chagas disease identified?
Early weeks/months, mild symptoms like fever, vomiting, rash, romana's sign (swollen eye), myocarditis or meningoencephalitis, heart and brain inflammation, most cases end here but some enter chronic phase
27
How is chronic phase of chagas disease specified?
Life threatening heart, nervous and digestive systems dilations, cell death, inflammation, cellular lesions, fibrosis, cardiomyoopathy, megaoesophagus, megacolon
28
Treatment of chagas disease?
Prevention through insecticides and bed nets Early infections treated with anti-parasitic medication
29
What is lymphatic filiasis?
Nematode worms (wuchereria bancrofti, brugia malayi, brugia timori) enter body via mosquitos and lodge in the lymphatic system to cause lymph flow blockages = lymphoedema (build up of interstitial fluid)
30
How are filiarial worms identified?
Haematoxylin and eosin staining
31
What can lymphatic filariasis present as?
Asymptomatic all the way to hugely swollen legs or genitals, also causes skin thickening due to increased risk of bacterial infection
32
Treatment of lymphatic filariasis?
Prevention via mosquito nets and insecticide Antimalarial drugs Mass drug administration
33
What is COVID-19?
SARS-CoV-2 virus that is transmitted through airborne droplets, bodily fluids and on surfaces Children are most prominent contractors and asymptomatic individuals transmit it the least
34
What is SARS-CoV-2 like?
Covered in spike glycoproteins (S1 and S2) mediate attachment to host cells (ACE2 receptor)
35
Where does coronavirus attach?
S1 glycoprotein binds to angiotensin-converting enzyme 2 (ACE2) receptor on host cell, then a protease binds the S2 side leading to activation of S2 domain and fusion of membranes so viral DNA enters host cell
36
How does SARS-CoV-2 effect cell?
Downregulates ACE2 and distrubs physiological balance of renin angiotensin aldosterone system (RAAS) = increased angiotensin ii = overactivation of RAAS = vasoconstriction, fluid retention, inflammation, cardiac stress, hypertension
37
What does the pathogenesis of COVID-19 look like?
Dependent on where SARS-CoV-2 lands --- if it goes to the lungs it cause immune cell overcrowding in alveoli which causes laboured breathing --- increased angiotensin ii is bad for heart as it is cardiotoxic --- brain can be affected = strokes and confusion --- causes issues with eyes, nose, liver, kidneys and intestines
38
Treatment of COVID-19?
Anti-viral drugs, painkillers, neutralising monoclonal antibody, corticosteroids, vaccines
39
What is ebola?
A filamentous virus that is transmitted via fruit bats or human-human bodily fluid transfer
40
What does ebola cause?
Fever, fatigue, muscle pain, headache, sore throat THEN vomiting, diarrhoea, impaired liver and kidney function, brain damage, internal bleeding, death
41
What is the ebola virus like?
Long filamentous shape, ss negative sense RNA, glycoprotein spikes allow binding and infection of target cells
42
What does the systemic spread (into the bloodstream) of ebola cause?
Enters body and infects macrophages at site ---> infected immune cells travel to lymph nodes then bloodstream (viremia) ---> spreads to major organs and triggers massive cell death This then causes dysregulated host immune response, coagulation abnormalities, impairment of vascular system, hypotension
43
Treatment of ebola?
2 treatments and there are some vaccines for some strains
44
What is zika?
A flavivirus from aedes mosquitoes, sexual transmission, mother-to-child or blood transfusion
45
What is the pathogenesis of zika?
Mild symptoms for 2-7 days but infection during pregnancy can cause microcephaly
46
What is the zika virus like?
Enclosed in capsid membrane, ss positive sense RNA, envelope glycoprotein allows attachment of viral particle to host cell receptor
47
What is antibody-dependent enhancement and how does it link to zika?
When non-neutralising antibodies from a dengue infection bind zika as they are very similar, it helps it infect immune cells and cause a more severe case (can increase risk of microcephaly)
48
What is microcephaly?
Small head of baby, dwarfism, sloping forehead, seizures, delays in speech and movement
49
How does zika virus cause cell death?
Massive vacuole formation in cells = implosive cell death
50
What is a direct target of zika virus?
Human neural progenitor cells --- disturbs proliferation, increases apoptosis and impacts human brain development (causing microcephaly)
51
Treatment of zika?
No treatment so you can only prevent it via insect repellent and nets etc

Biomed (11 decks)

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