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Medicine Year 2 > Scenario 15 > Flashcards

Scenario 15 Flashcards

1
Q

What are the 3 classes of microorganisms?

A

Viruses, prokaryotes (bacteria/ mollicutes), eukaryotes (fungi, protozoa, nematodes, ectoparasites)

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2
Q

What is the difference between a parasite and commensal?

A

Both live in/ on another organism but commensal does not injure the organism

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3
Q

What colour is gram positive?

A

Purple/blue

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4
Q

What colour is gram negative?

A

Red

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5
Q

What classification are mycobacteria?

A

Gram positive but dont take up aq gram stain- walls made up of waxy my colic acid (use ziehl nelson stain)

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6
Q

What are the properties of gram positive bacteria?

A

survive well on drying some produce spores/ toxins and have teichoic acids in their cell wall

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7
Q

What are the properties of gram negative bacteria?

A

dont survive drying, no spores, have endotoxin in their cell wall (LPS)

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8
Q

Is staph aureus gram negative or positive?

A

Gram positive coccus which forms clusters

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9
Q

What are some distinguishing factors of staph aureus?

A

Grow readily on blood agar, golden colonies after 48 hours, coagulase and DNAase production

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10
Q

What are the virulence factors of staph aureus?

A

Protein A- anti-phagocytic and secretes coagulase and exotoxins

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11
Q

Where is it found/ transmitted?

A

Normal human flora, transmission from some carriers and close contact

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12
Q

What infections does staph aureus cause?

A

Skin and soft tissue, ENT, pneumonia, bone and joint, sepsis, infective endocarditis, implanted prosthetics

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13
Q

What toxin mediated problems does it cause?

A

Staphylococcal toxic shock and food poisoning

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14
Q

What do you use to treat s aureus?

A

NOT penicillin- 90% resistant sue to beta lactamase, can use fluoxacillin or co-amoxiclav or macrolides (erythromycin) for MRSA use vancomycin

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15
Q

How do you classify streptococcus pyogenes?

A

gram positive cocci in chains, grows readily on blood agar

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16
Q

What are the virulence factors of s.pyogenes?

A

M protein in cell wall and endotoxins

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17
Q

Where is it found and how is it transmittes?

A

In nose and throat of 1-5% of population and transmitted by close contact

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18
Q

What infections does s.pyogenes cause?

A

pus forming, ENT and RT, skin and soft tissue (impetigo), puerpal fever, blood stream, streptococcal toxic shock

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19
Q

What are some post infecitve manifestations of s.pyogenes?

A

non suppurative sequalae, acute rheumatic fever, acute glomerulonephritis

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20
Q

How do you treat s.pyogene?

A

PENICILLIN OR AMOXICILLIN erythromycin, vancomycin if allergy

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21
Q

How do you distinguish streptococcus pneumonia?

A

Gram positive cocci in pairs/short chains up to 4 cells long, produced pheumolysin in alpha haemolysis on blood agar

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22
Q

What are the virulence factors of s. pneumo

A

pneumococcal teichoic acid c-polysaccharide and polysaccharide capsule which is anti-phagocytic

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23
Q

Where is it found?

A

Commensal URT flora in humans, transmission by resp secretions

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24
Q

What infections does s.pneumo cause?

A

URTIs, LRTIs, CNS (meningitis), sepsis, peritonitis, endocarditis

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25
Q

What is the treatment for s.pneumo?

A

2 vaccines in UK, penicillin (90%), erythromycin (not in meningitis), ceftriaxone in meningitis

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26
Q

What are some other gram positive bacteria?

A

Coagulase-negative staphylococci (normal skin flora, implanted prosthetics), Clostridium (spore forming rods, commensals in GIT produce endotoxins, difficile, tetani, botulinum, perfringens) Bacillus (rods, anthrax and cereus), cornyebacterium species (non spore forming rods, skin commensals)

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27
Q

What are the distinguishing factors of E coli?

A

gram negative bacilli, grow on blood agar, fements lactose, cell wall contains LPS, proteins and porins, motile (flagellae, fimbiae)

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28
Q

What are the virulence factors of E coli?

A

LPS, iron binding proteins, small polysaccharide capsule, fimbiae or pili, endotoxin priduction

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29
Q

Where is it found and how is it transmitted?

A

normal colonic flora, contaminated food/water, ascending infection

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30
Q

What infections does e coli cause?

A

UTI, diarrhoeal illness, intraabdominal infection, sepsis, pneumonia, meningitis

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31
Q

How do you treat e coli?

A

Amoxicillin

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32
Q

How do you distinguish pseudomonas aerginosa

A

Gram negative non sporing bacillus, non lactose fermenting, outer membrane with LPS, porins and proteins, large genome

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33
Q

What are the virulence factors of pseudomonas aerginosa

A

Endotoxins, exotoxins, iron binding proteins

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34
Q

Where is it found and how is it transmitted?

A

Soil and water, colonises UT, transmitted on medical equipment, water, spas and whirlpools

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35
Q

How do you treat p. aeruginosa?

A

Resistant to co-amoxiclav, trimethoprim, nitrofurantoin use piperacillin-tazobactam and gentamycin

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36
Q

How do you distinguish Haemophilus influenzae?

A

Gram negative rod (sometimes coccobacillus) needs media with growth factors and cell membrane with LPS, proteins and porins

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37
Q

What virulence factors are present in haemophilus influenza?

A

Endotoxin, large polysaccharide capsule, IgAse, adhesins in cell wall

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38
Q

Where is h.influenzae found?

A

Mucosal surfaces transmitted with close contact and droplets

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39
Q

What infections does it cause?

A

Bloodstream infection in young children (capsulate) and ottis media, sinusitis, conjunctivitis all ages (not capsulate)

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40
Q

How do we treat H.i?

A

Vaccine in childhood, amoxicillin (15% resistance) chemoprophylaxis, IV ceftriaxone for invasive infections

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41
Q

What other gram negative bacteria are there?

A

Bacteroides (rod- colonise the mouth), neisseria (cocci in pairs, mucous membranes, inside neutrophils- meningococcus, gonococcus), legionella (rod, pneumonia), heliobacter pylori (rod, stomach)

42
Q

What is the basic structure of a virus?

A

DNA or RNA core with protein coat, some have an envelope studded with glycoproteins

43
Q

Where do non-enveloped viruses survive best?

A

Outside of cells and bile resistant

44
Q

Where do enveloped viruses survive best?

A

In cells- only spread by close contact eg. Hep B HIV

45
Q

Which viruses are RNA?

A

Retrovirus, coronvirus, picornavirus

46
Q

Which viruses are DNA?

A

Adenovirus, herpesvirus, poxvirus

47
Q

What are the steps in viral replication?

A

Attachment, penetration, uncoating, transcription, translation, replication, assembly, release

48
Q

How do DNA viruses replicate?

A

Large replicate on their own, small encode only a few genes and use host cell DNA polymerase etc

49
Q

How do RNA viruses replicate?

A

Most RNA viruses encode their own RNA-dependent RNA polymerase using complementary RNA as template

  • Positive strand RNA- equivalent to mRNA can often be immediately translated into proteins then synthesise a -ve copy copied back into -ve mRNA messages to produce structural proteins to package progeny +ve RNA into visions
  • Negative strand RNA- first converted into +ve RNA (.RNA) by RNA dependent RNA polmerase then same as abover
50
Q

Why do RNA viruses replicate more quickly?

A

RDRP lacks proofreading ability and makes more mistakes

51
Q

How do retroviruses replicate?

A

encode reverse transcriptase which makes dsDNA from RNA

52
Q

What is a latent infection?

A

Viral DNA persists but doesnt replicate to produce new infectious virus e.g. herpes, varicella zoster

53
Q

What is pathogenesis?

A

Process where infecion leads to disease

54
Q

What are the virus properties that allow it to inhabit cells?

A

Concealment (prevent antigen presentation, latency, integration into genome- retrovirus), intefere with cytokine network (mimic receptors and inhibitory cytokines and interfeon), antigenic variation (mutation and antigenic shift), modulation of lymphocyte function (immuno suppression)

55
Q

What is the eclipse phase?

A

Virus entry until new infectious virions released

56
Q

What is the classification of family herpesviridae?

A

Large dsDNA icosahedral capsid and lipid envelope

57
Q

What subfamiliy does varicella zoster belong to?

A

Alphaherpesviridae

58
Q

Where is chicken pox latent?

A

Dorsal root or cranial nerve ganglion- reactivation= chicken pox

59
Q

What is the incubation period for varicella?

A

10-21 days- prodrome (fever, pharyngitis, malaise)

60
Q

What are the complications of varicella?

A

Sever haemorrhagic, pneumonia, acute cerebellar ataxia, encephalitis

61
Q

What memory immunity is stored in varicella?

A

VZV specific IgA and IgG antibodies and CD8/4 T cells (needed to prevent reactivation)

62
Q

What is zoster?

A

Reactivation of latent VZV painful vesicles (1-2 vesicles) most commonly thoracic

63
Q

How is zoster transmitted?

A

Spread by resp and skin lesions and congenital infection of fetus in first 20 weeks

64
Q

When should post exposure prophylaxis be given?

A

Pregnant, immunocompromised or neonate of seronegative mother

65
Q

What treatment should be used in zoster?

A

First line antiviral agents- aciclovir, valaciclovir and famciclovir

66
Q

How are virus’ detected?

A

Electron microscopy , cytopathic effect, cmv, protein antigen, nucleic acid (PCR, ELISA)
Specific antigen response- serology, seroconversion

67
Q

What is therapeutic index?

A

Minimum cell toxic dose/ minimum virus inhibitory dose= at least 10

68
Q

What are examples of nucleoside analogues?

A

Aciclovir, ganciclovir

69
Q

What are examples of nucleotide analogues?

A

Cidofovir

70
Q

How does aciclovir work?

A

Nucleoside analogue, competitive substrate for viral DNA polymerase inhibiting viral DNA polymerase and terminating the chain

71
Q

How is aciclovir selective to infected DNA?

A

Preferential monophosphorylation- infected has 40-50x more phosphorylation, cellular DNA less susceptible (no viral DNA polymerase), effective chain termination due to lack of OH group

72
Q

What are the issues with aciclovir?

A

poor oral absorptuon, short half life (need 5 a day) 85% excreted in urine
Use valaciclovir- 80% taken up

73
Q

Why are some cells resistant?

A

Virus thymidine kinase absent or viral DNA polymerase altered

74
Q

How does ganciclovir work?

A

Requires tri phosphorylation to active form. Works by inhibiton of CMV polymerase, not a chain terminator- need to add valine to be absorbed

75
Q

Why is resistance to anti-retroviral therapy so high?

A

Error rate high so lots of mutations, selective pressure exerted if treatment stopped then resistant strain becomes latent

76
Q

What are the targets for RNA anti-virals?

A

Viral proteases, viral surface proteins, immune modulation

77
Q

What is advised after a splenectomy?

A

Prophylaxis and immunisation

78
Q

What is defects in humoral immunity?

A

Immunoglobulin deficiency, congential B cell deficiencies
Frequent ear and sinus infection, infants fail to grow, pneumonias, obsesses, chronic enterovirus meninenephalitis, increased incidence of autoimmun and CT disorders

79
Q

How do we prevent infection in defect in humoral immunity?

A

Ig replacement therapies

80
Q

What infections are likely in people with congenital complement abnormalities?

A

Resembles hypospeism- streptoccocus pneumoniae, haemophilus influenzare, nisseria meningitidis)

81
Q

What is defect in neutrophil number defined as?

A

less than 1x10^9 /l
May occur after haemopoetic stem cell transplantation, chemo, immunosuppresion, haematological malignancy, prolonged placement of catheters

82
Q

What are the risks after solid organ transplantation?

A

Immediately after upper/lower RTIs but long term need lifelong immunosuppression, risk of transmitting infection i the organ and some inevitable CMV, toxoplasma- need prophylaxis

83
Q

What is cytomegalovirus?

A

Transmitted by intimate contact 50% of adults, majority asymptomatic
If donor positive and recipient negative- primary infection
If donor negative recipient positive- reactivation
If both positive- recurrent infection

84
Q

What is CD4?

A

A cell surface molecule which is on T helper cells and expressed on dendritic cells and macrophages. Stabilises a T helper 1 cells interaction with MHC class II and recruits signalling molecule, T helper 2 cells stimulate b cells for antibody production and aids CD8 T cells.

85
Q

How are the number of CD4 cells depleted?

A

Direct cytopathicity of the virus, killing by specific cytotoxic T cells, memory pool particularly depleted

86
Q

What is the host response in HIV infection?

A

CD4 count fails early and functional impairment of CTL response, cytotoxic T cells can kill HIV infected cells and HIV specific neutralising antibody response- antigenic diversity of HIV is a challenge

87
Q

What is a primary immunodeficiency?

A

Innate defect at a genetic/ developmental level- failure to produce a class of antibody/ complement./ enzymes

88
Q

What is a secondary immunodeficiency?

A

Factors not innate to the patient, nutrition, malignancies, aging, drugs, stress, splectomy

89
Q

What are the steps of the formation of a HIV provirus?

A

Reverse transcriptase copies an RNA template onto dsDNA copy then covalent insertion of viral DNA into the genome of the infected cell (cant be cured)

90
Q

What is the genetic organisation of a retrovirus?

A

9 genes synthesising 3 polyproteins
Gag- group specific antigen- viral core proteins, matrix, capsid
Pol- polymerase- enzymes, protease, reverse transcriptase, integrase
Env- envelope glycoprotein

91
Q

What is the structure of a mature HIV-1 particle?

A

Outer envelope consists of a lipid bilayer and inside a shell of gag proteins, core contains two genomic RNA strands tRNA^lys and 50 copies of each viral enzyme

92
Q

What are the basic steps of retroviral replication?

A

Attachment and receptor binding, membrane fusion and entry (requires CD4 and a chemokine receptor CDR5/CXCR4), uncoating and reverse transcription, nuclear import, intergration (RT makes a full length dsDNA which is cut in a stagerred cut at 3’ end short replication of target sequence and gap repair), transcription, RNA processing, nuclear export, translation, assembly, budding (24hours)

93
Q

What are the regulatory/accesory proteins

A

Adaptors that facilitate molecular interactions, good models for study, evasion of host mechanism, therapeutic targets

94
Q

When should HAART be started?

A

When CD4 count reaches 300 (central to adaptive immunity)

95
Q

What correlates with the recovery from acute infection and the suppression of the virus burden?

A

CD8 T cell response

96
Q

What correlates with the disease stage?

A

CD4 T cells

97
Q

What correlates with the tempo of the disease?

A

Viral set point

98
Q

What are the current targets of HAART?

A

Protease inhibitors and RT inhibitors

99
Q

What is the pathology of TB?

A

granulomatous inflammation with caseous necrosis in the centre (filled with pus) perhaps with visible acid fast bacili

100
Q

What does it show on a CT scan?

A

Extensive consolidation with a cavity- cavitating pneumonia

101
Q

How can you test for latent TB?

A

Mantoux test, interferon gamma release assay (more specific)

102
Q

What is the treatment for TB?

A

Chemo- 4 drugs for 2 months then 2 drugs for another 2 months

Medicine Year 2 (19 decks)

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