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Medical Flashcards

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1
Q

Antimicrobial resistance mechanisms

A

Efflux (antibiotics pumped out of cell)
Modification of antibiotic targets
Immunity bypass (Stop antibiotics accessing target )
Enzymes that stop antibiotics functioning

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2
Q

What class virus is HIV, and why?

A

It is a Class 6 virus, because it is a retrovirus

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3
Q

What Class virus is Influenza, and why?

A

Class 5 because it is a single, negative strand RNA virus.

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4
Q

What are the 4 types that make a virus a virus?

A
  1. Obligate intracellular
  2. All viruses encode capsomeres
  3. All viruses replicate
  4. They all have the capacity to evolve
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5
Q

What are the types of mechanisms viruses use to penetrate a cell?

A

Receptor mediated endocytosis, using either a clathrin protein or caveolin protein.
Phagocytosis, where the membrane engulfs the virus, the exposure to the phagolysosome triggers uncoating.
Membrane fusion, catalysed by SNARE proteins

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6
Q

What directions do kinesin and dynein’s work in?

A

Kinesin - carry out of cell (towards plus end)

Dynein - carry into cell (towards minus end)

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7
Q

What’s the difference between T cell receptors and B cell receptors?

A

TCR’s can recognise short peptides from pathogenic proteins, whereas BCR’s can recognise whole pathogen structures.

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8
Q

How are lymphocyte receptors (TCR’s and BCR’s) made?

A

Use somatic genetic recombination to create sequence diversity (VDJ)

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9
Q

What does the immune system respond to in GOUT?

A

Urate crystals

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10
Q

Difference between antigenic drift and antigenic shift?

A

Antigenic drift is caused by a point mutation in key proteins that causes the seasonal changes in flu.
Antigenic shift is a significant alteration in the sequence, which causes the immune system to not recognise a new antigen, as it has no time to adapt, it is a sudden change.

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11
Q

How do beta lactam antibiotics work?

A

Inhibit bacterial wall synthesis by binding to penicillin binding protein. (PBP.) And prevent synthesis of peptidoglycan

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12
Q

What is the characteristics for M. tuberculosis? And its virulence mechanism?

A

Gram negative, long rod bacterium has a waxy outer membrane that contributes to its virulence. It is highly aerobic, intracellular, and is slow at replicating. Its waxy coat makes it hydrophobic, which prevents antibiotics from penetrating it.

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13
Q

How does TB infect us?

A

It enters the body via aerosols, and attaches to lung surfaces (alveoli) The bacteria triggers macrophage recruitment, which then engulf he bacteria. This causes more lymphocytes ect to migrate to the site, causing ‘granulosa maturation’ The granulosa then undergoes necrosis and the bacteria begin to replicate

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14
Q

How does TB survive in a host?

A

In phagosomes, they prevent phagolysosome formation through PTpA, prevent acidification of phagosomes.

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15
Q

What are the wo types of gram-negative

infections and their characteristics?

A

Aerobic bacilli- Non spore forming bacteria that have a wide range of habitats. They all have LPS, and do not ferment carbohydrates.
Enteric pathogens – Usually exist in intestines of animals and humans. Most frequent cause on diarrhoea through enterotoxins

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16
Q

What are the WHO priority diseases?

A

COVID, Congo haemorrhagic fever, Ebola, Lassa fever, MERS, SARS, zika virus, Rift valley. And Nipah and henipaviral diseases.

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17
Q

What’s the difference between gram negative and harm positive bacteria?

A

Gram positive stain purple, that have a thick peptidoglycan layer, no outer membrane. Whereas gram negative have a thin peptidoglycan layer in the the periplasmic space, they also have LPS.

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18
Q

How many segments is their in an influenzas genome? And how many proteins do they code for?

A
  1. 13
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19
Q

How does influenza infect us? (virulence mechanisms)

A

It has 2 main spike proteins (surface antigens) Haemagglutinin, and neuraminidase. These bind to the glycocalyx on the respiratory tissues. (Sialic acid)
It steals caps from host derived mrna, and makes poly A tails via stuttering.

The head domain is involved in attachment, and tail domain is involved in fusion

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20
Q

Which types on influenza do we have circulating in the human body?

A

H1N1, H3N2

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21
Q

What caused the Spanish flu?

A

Influenza H1N1 transferred from pigs to humans

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22
Q

How may deaths does Influenza cause each year?

A

200-000 - 600,000

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23
Q

Which part of the influenza protein HA is less variable?

A

The stem domain, and the internal proteins: Nucleocapsid (NP), and matrix protein (M1)

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24
Q

What is the efficacy rate of the influenza vaccine?

A

33%

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25
What type of virus is COVID 19?
A positive single stranded virus
26
How does COVID infect us?
Spike proteins attach to ACE -2 receptor. A co receptor called TRPSS R2 cleaves the spike protein, which triggers endocytosis, and fusion.
27
How many different types of bacteria species are there estimated to be?
500 - 1000
28
How can you describe bacteria?
shape, size, colony morphology, and smell
29
Which type of bacteria use carbon as their main source of energy?
Autotrophs
30
How do bacteria replicate? Where does it start and what enzyme drives it?
Asexual reproduction - binary fission: DNA replication starts at the origin of replication, it is driven by protein FTSZ
31
In which phase do the bacteria undergo binary fission?
Log phase
32
What are the types of bacterial DNA transfer:
Conjugation - Direct contact, i e pili Transduction - HGT, viral infection (bacteriophages) Transformation - HGT, naked DNA is taken up Transposition - DNA moves location, and integrates back into DNA.
33
What is an operon?
A region of the chromosome where structural proteins with related functions are usually encode, that are transcribed together under the control of a single promoter.
34
What is a regulon?
A group of genes that are turned on or off in response to the same regulatory protein.
35
What are Kochs 4 postulates
1. Must be in diseased individuals 2. Must be cultured from the individual 3. Inoculation of the same microorganism to a healthy person must causes same disease 4. Th same microorganism must be re - isolated from inoculated individual
36
What is the role of EPS?
Promotes close contact with the host cell, creating hydrophobic structures. It also protects the bacteria from the hosts immune cell by preventing the antibiotics from penetrating them
37
What is the Zipper mechanism in bacterial virulence?
Bacteria express proteins that bind with high affinity to host cell adhesion receptors. This triggers host cells to form cell junctions and engulf the bacterium.
38
What is the trigger mechanism in bacterial virulence?
Bacteria express proteins known as effectors. These activate signalling pathways leading to cytoskeleton rearrangements, and forms membrane ruffles that extend and fuse around the bacterium, engulfing them.
39
How do bacteria avoid immune system?
Some leave their vesicles Hide from autophagy- Mask bacterial surface with proteins Avoid lysosomal killing - interfering with endosome maturation pathway.
40
What is an Exotoxin and how do they work?
Exotoxins are secreted proteins. Subunit A is responsible for enzymatic activity. Subunit B is responsible for binding to receptors. (Pore forming, superantigens)
41
What are endotoxins and how do they work?
They refer to LPS, only found in gram negative pathogens. Made of o antigen, core part and lipid A.
42
What is the incubation period?
The time between a person being infected and when they start to show symptoms
43
What is the latent period?
The time between a person being infected and when they start being infectious to others
44
What is the epidemiology of meningitis?
Time - seasonal, winter Place - meningitis belt (spans widest part of Africa) Person - overcrowding, smoking having flu
45
When do you have your meningitis jabs?
Men B - - 12months | Men C - +14years
46
What is the incubation period for meningitis?
3-5 days
47
How can you describe N. meningitidis
Gram negative, aerobic, diplococcal
48
What is the incubation period for chlamydia?
1-3 weeks
49
How would you describe chlamydia trachomatis?
Gram negative, obligate, intercellular
50
What is the incubation period for legionella pneumophila?
2 - 10 days
51
How would you describe legionella pnuemophila?
Gram negative, rod shaped, facultive intracellular.
52
What temperature range does legionella bacteria prefer?
25 - 42 c
53
What is the public health management of legionella?
ESQ's (enhanced surveillance questionnaires) | Control measures taken when needed, E.G shock dosing)
54
What is the incubation period for STEC?
2- 4 days
55
What are the complications of STEC?
HUS (haemolytic uraemic syndrome) Anaemia
56
How do you describe Clostriodides difficile?
Gram positive, anaerobic, rod shaped, that forms spores
57
What is the transmission of Clostridiodes difficile?
Faecal oral route
58
What is the complication of Clostridiodes Difficle?
Pseudomembranous colitis (inflammation of the large intestine) in severe cases.
59
What are the prevention stragies for C. Difficile?
``` Use antibiotics correctly SIGHT Suspect Isolate Gloves Hand washing Test sool ```
60
How can you describe S. aureus?
Gram positive, facultvie intracellular, occurs in 30% of healthy people.
61
What are the virulence mechanism of S aureus?
Adhesions on surface, hey can invade deep into skin, and they form biofilms.
62
How would you describe A . baumanni?
Gram negative, rod shaped, aerobic.
63
Wat are A. bumanni virulence mechanisms?
Resistant to disinfectants< has secretion systems and forms biofilms
64
Cercaria swim towards human hosts via what mechanisms? (schistomiasis)
Phototropism, and chemoattractants
65
What is the lifecycle of Schistosomiasis?
Humans infected in contaminated water, via parasitic worms, they lay 200-300m eggs per day in the blood, eggs make their way to the gut lumen, and are excreted via faeces. When they reach fresh water, eggs hatch. They find snail species, then find new host and penetrate skin.
66
What is Kataymaya syndrome?
Nocturnal fever, cough, myalgia (muscle aches), headache and abdominal tenderness. (Acute phase of schistosomiasis)
67
What are the chronic symptoms of schistosomiasis?
Weakness, granuloma formation, fibrosis and lesions of organs containing eggs. Kidney dysfunction, blood in urine, make and female fertility defects
68
What is the life cycle of Dracunculiasis?
People become infected when they drink contaminated water (water fleas) They are then killed by digestive enzymes, releasing parasite where they penetrate intestine wall Males die, females mature for 10- 14 months, slowly ,migrating to surface of skin. Blister then forms where worm emerges
69
What are risk factors for Dracunculiasis
14 - 45 year olds, farmers, those fetching water, having it the year before
70
What are the short and long term affect from Dracunculiasis?
Short - fever, rash, nausea, vomiting Long - (if a wound gets infected) Sepsis, tetanus, abscesses, cellulitis, but rarely lethal
71
What are the disease stages of African sleeping sickness?
1. Inflammation ( trypanosome chancre) 2. Haemolytic stage, parasites enter blood, lymphatic system and tissue, causing fever 3. Late stage, enters the blood brain barrier, causes loss of consciousness, abnormal behaviour.
72
Describe the Slender trypanosomes
Longer, slender, proliferative, specialised glucose metabolism, differentiates into stumpy form in response to secreted quorum sensing factors, non transmissible (killed by proteases in insect midgut)
73
Describe the stumpy trypanosomes
Short, stumpy, non proliferative, preadapted to survive in insect midgut, metabolic, rapidly differentiates into insect procyclic from in midgut, expresses sensory proteins.
74
Trypanosome lifecycle in the insect
75
Describe a trypanosome lifecycle
1. Slender forms in a host, proliferate due to quorum sensing into stumpy forms 2. Stumpy forms are adapted to survive in teste fly midgut 3. Differentiate into procyclic forms in midgut 4. Differentiate into metacyclic forms in the salivary gland, these inoculate a new host
76
Where does the trypanosomes inhabit in the host?
Blood, skin, adipose fat, central nervous system (in late stage of disease)
77
How do trypanosomes avoid hosts immune systems? (3)
VSG - These are variant surface glycoproteins that act as a physical barrier. It prevents antibodies from recognising them as foreign, and from being punctured. Hydrodynamic flow- This is where an antibody complex is engulfed by the parasite, and swept to the flagella pocket at the posterior end, where it is internalised by endocytosis. Antigenic variability - Trypanosomes have 20 different VSG loci, and thy are able to switch to different sites. They also have 1000+ genes elsewhere, which can be swapped via homologous recombination.
78
When is hydrodynamic flow less affective, and why?
At high antibody titres, because VSG is highly immunogenic, attracting lots of antibodies, which overwhelms and kills the parasite.
79
What are the three types of traypanasomatid human parasites?
Trypanasoma brucei - HAT, nagana, transmitted by tsetse fly Trypanasoma cruzi - Causes Chagas disease, transmitted by bugs Leshmani spp - Causes leishmaniasis, transmitted by sand flies
80
Why is leishmania burden likely to increase?
Population mobility - associated with migration. Environmental changes - urbanisation Climate change - change in temp, rainfall, humidity ect can impact vectors and resivour hosts by altering their distribution and influencing their survival and population sizes
81
Where is mitochondrial DNA kept in a promastigote?
Kinetoplast
82
What characteristics does the promastigote have that helps its motility?
Inner and outer dynein arms, provide mechanico - chemical energy that allows flagella to beat. Radial spokes help coordinate them PER (paraflagellar rod) essential for beating but unknown why
83
Describe the leshmania life cycle (In the host)
Female fly regurgitates promastigote forms into host (Biting) Immune cells are recruited to bite site Macrophages phagocytoses parasites, creating a PV (Parasitophosphorus vacuole) In the PV, it turns into an amastgote, stimulated by lysosomes fusing with PV Amastigotes escape PV +enter blood stream
84
How does the PV subvert phagocytosis?
Nutrients are fed to the parasites, damaging factors are less able to fuse with PV membrane, macrophage is prevents from activating other immune cells
85
Describe the leishmania lifecycle (In the sandfly)
Amastigotes are taken into the midgut They transform into promastigotes They bind to the midgut epithelium, and some get taken out with blood meal. The others migrate to the stomodaeal valve, and secrete PSG. They then differentiate into metacyclic forms
86
How do parasites in sandflies overcome defence mechanisms?
They create chitinase which helps them break free from the peritrophic matrix. They secrete protease inhibitors, and downregulate protease genes in sandlfies They downregulate genetic pathways that make AMP's They prevent themselves from being expelled by binding to specific receptors, and preventing peristaltic movement
87
How do leishmania parasites encourage regurgitation?
They secrete PSG which forms a plug.
88
How does sand-fly saliva promote leishmania infection?
Sand-fly saliva keeps blood liquid, promoting blood flow, it contains anticoagulants, vasodilators, attractants (that attract macrophages), and activators (that activate macrophages)
89
What are some of the symptoms of secondary stage syphilis? | And when do they occur?
2- 8 weeks after infection | Rash over body, sores, warts, fever, weight loss, hair loss
90
Whats the 2nd most common STI?
Genital warts
91
What is the most common cause of gastroenteritis
Campylobacter
92
What causes genital warts?
HPV (human papilloma virus)
93
What are the 6 F's for faecal oral transmission
Food, fingers, fluid, faeces, flies, fomites
94
How would you describe enteric fever?
Caused by typhoid, and paratyphoid. Can be life threatening, usually acquired abroad, is highly contagious.
95
Which 2 GI infections can be localised to public water sources?
Cryptosporidiosis, Giardiasis
96
What are the symptoms of Giardiasis?
Flatulence, greasy stools, losing weight
97
What are the symptoms of hepatitis A
Jaundice, fever, loss of appetite, dark urine, pale stools
98
What type of plasmodium causes most malaria?
Plasmodium falciparum
99
What are the 6 countries that malaria is prevalent in?
Nigeria, DRC, uganda, cote d ivore, and niger.
100
What are the symptoms of malaria?
Every other day fever, anaemia
101
How does complicated (severe malaria) occur? (sequestration)
Infected red blood cells change shape and develops knobs, that contain ofEMP1 These red blood cells become sticky, binding to healthy red blood cells causing rosettes, and epithelial cells. This blocks vasculature (sequestration) If this occurs in the brain, it can cause swelling, haemorrhage, coma and death.
102
Describe the plasmodium lifecycle in a host (malaria)
The sporozoites reach liver within first hour of infection. They then begin to replicate in a PV, creating thousands of merozoites They PV then ruptures, and they go on to infect RBC's They then must differentiate into gametocytes in order to infect mosquitos.
103
Describe the plasmodium lifecycle in a mosquito
Gametocytes are taken up into the mosquitos midgut. Male gametes fertilise female gametes, forming a zygote. These cells then migrate to the basal lamina of the midgut Sporozoites are released into the blood, and they go to the salivary glands They go to the salivary duct, where they will inncoluate a new host
104
What are the mechanisms of malaria protection of sickle celled individuals?
1. Enhanced removal of parasitized RBC's 2. Parasites are less able to grow in sickled RBC;s 3. Reduced sequestration (produced less pfEMP1) 4. Decreased rosette formation
105
What is balanced polymorphism? (in terms of malaria)
The sickle cell allele is maintained in areas with high malaria because heterozygotes are protected against malaria.
106
How does chloroquine work against malaria?
Chloroquine prevents heme breakdown, causing accumulation of heme which is toxic to the parasite.
107
How do cells become resistant to chloroquine?
Mutations of pfcrt protein, which is a transporter of chloroquine. This mutation allows it to export chloroquine out of food vacuole
108
What is point prevel
108
What is point prevel

Infection (2 decks)

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