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Respiratory Pharmacology > L13 - Lung of immunocompromised patient > Flashcards

L13 - Lung of immunocompromised patient Flashcards

1
Q

Innate defences

A

mucociliary, neutrophils and macrophages

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2
Q

adaptive defences

A

B cells, T cells

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3
Q

Cystic fibrosis

A

autosomal recessive disease causes mutations
defective exchange of chloride leads to extracellular dehydration with excessive thick sputum, infection and severe bronchiectasis

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4
Q

CF type I

A

no protein produced

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5
Q

CF type 2

A

protein produced but not transported to the cell membrane

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6
Q

CF type 3

A

protein transported to cell membrane but does not work properly

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7
Q

CF type 4

A

gets to cell membrane and functions, but is less effective than the WT

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8
Q

CF type 5

A

less proteins produced that make it to the cell membrane

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9
Q

CF type 6

A

less stable proems produced so many don’t make it to the cell membrane

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10
Q

Ivacaftor

A

potentiates channel open probability, improvements in lung function, nutrition and CFTR function

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11
Q

HIV

A

lenti/retrovirus that infects cells via CD4 receptors and co-receptors on T helper cells, macrophages and dendritic cells

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12
Q

AIDS

A

Occurs when viral replication kills the infected cells

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13
Q

HIV drug resistance

A

replication is error prone therefore mutations arise that induce resistance

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14
Q

HIV mechanism

A

glycoproteins on HIV allow it to dock and fuse to CD4 and CCR5 receptors
viral capsid enters the cell, enzymes and nucleic acids are released
Using reverse transcriptase ssRNA is converted to dsRNA
Viral DNA is then integrated into the cells own DNA by integrase enzyme
When infected cell divides, viral DNA is read and viral proteins are made
innate virus leaves the cell, taking the cell membrane with it
undergoes maturation

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15
Q

HIV maturation protein chains

A

in the new viral particle are cut by the protease enzyme into individual proteins that combine to form a working virus

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16
Q

ARVs

A

work by interfering with virus replication by preventing HIV docking and interfering with action of the major HIV enzymes

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17
Q

major HIV enzymes

A

reverse transcriptase, integrase and protease

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18
Q

Fusion inhibitor drugs

A

Enfurvitode, T-20

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19
Q

Miraviroc

A

CCR5 receptor blocker

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20
Q

NNRTI

A

non-nucleotide reverse transcriptase inhibitor

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21
Q

Efavirennz

A

NNRTI

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22
Q

Nervirapine

A

NNRTI

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23
Q

Rilpivirine

A

NNRTI

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24
Q

NRTI

A

Nulceotide reverse transcriptase inhibitor

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25
Q

3TC Lamivudine

A

NRTI

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26
Q

FTC Emtricitatine

A

NRTI

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27
Q

AZT Zidovurine

A

NRTI

28
Q

TDF Tenofovir

A

NRTI

29
Q

ABC Abacavir

A

NRTI

30
Q

Dolutegravir

A

integrase inhibitor

31
Q

Raltegravir

A

integrase inhibitor

32
Q

Elvitegravir

A

integrase inhibitor

33
Q

Dorunavir

A

protease inhibitor

34
Q

Atazanavir

A

protease inhibitor

35
Q

Lopinavir

A

protease inhibitor

36
Q

HAART

A

HIV treatment. comprises of combinations of 3 different ARVs, using two NRTIs plus either another NNRTI, protease inhibitor or integrase inhibitor

37
Q

HAART benefits

A

recommended for all patients as it reduces transmission and increases life expectancy

38
Q

HAART problems

A

many tablets for life, complex for patients, missed doses encourage treatment failure and resistance, many side effects

39
Q

B cell defects and antibody deficiency

A

particularly associated with CVID and anti-CD20 monoclonal antibody therapy and other immunosuppression
increased risk of encapsulated bacteria and oto-sino-pulmonary infection

40
Q

Primary antibody deficiency

A

immunoglobulin replacement has dramatically increased survival, reduces infections including pneumonia

41
Q

secondary antibody deficiency

A

immunoglobulin replacement indications are less clear, only might be used

42
Q

Immunoglobulin replacement

A

prepared from pooled plasma from healthy donors, can be administered by intravenous and subcutaneous lifelong

43
Q

Infection prophylaxis

A

prophylactic agents need to be taken continuously

44
Q

decision to institute prophylaxis depends on many factors…

A

nature and severity of underlying condition, risk of infection, previous infection history, evidence it will benefit situation, availability of agents, route, frequency and side effects, treatment burden, antimicrobial stewardship

45
Q

Antibiotic prophylaxis

A

used in myelotoxic chemotherapy with neutropenia, can be predicted in both time and severity

46
Q

Antibiotic and anti fungal prophylaxis

A

in chronically neutropenic patients, e.g. bone marrow transplant or those with inherited defects

47
Q

Pneumocystic pneumonia prophylaxis

A

used in HIV and immunosuppression

48
Q

Pneumocystic pneumonia

A

life-threatening opportunistic lung infection of immunocompromised individuals

49
Q

Pneumocystic pneumonia cause

A

by pneumocystis jinvecii, a fungus with some protozoal features

50
Q

Pneumocystic pneumonia occurs in..

A

patients with reduced Th cell number of function, e.g. HIV, chronic high dose steroids, solid organ or bone marrow transplantation

51
Q

Co-trimoxazide

A

Oral
inhibit folate biosynthesis
rashes, bone marrow suppression and GI problems,
extremely effective

52
Q

Nebulised pentamidine

A

Nebulised monthly
uncertain mode of action, anti-parasitic,
cough, bronchospasm and need to protect staff
effective but some failures

53
Q

pulmonary infection presentation in immunocompromised patients

A

may be non-specific
chest X-ray or CT, blood tests
investigation of sputum samples

54
Q

PCP

A

fungus with some protozoan features, usually killed by alveolar macrophages, requiring CD4+ activated Th cells
progressive breathlessness and dry cough with ground glass opacity on CTs

55
Q

PCP treatment

A

high dose co-trimoxazole
toxicity: fluid load, rash, renal/liver toxicity, low blood K+, neutropenia and low blood glucose
Adjunctive corticosteroid therapy for moderate to severe PCP enhances survival in HIV - reduces inflammation to dying organisms

56
Q

Invasive aspergillosis

A

environmental fungus affecting neutropenic or immunocompromised patients
can be progressive and fatal
pulmonary nodules or infiltrates on CT

57
Q

Echinocandins

A

inhibit synthesis of B glycans

58
Q

Trizoles

A

inhibit lanosteol-14a-demethylase, which converts lanasterol into ergosterol

59
Q

Polyenes

A

bind ergosterol to weather the membrane and make i t’leaky’

60
Q

Invasic aspergillosis treatments

A

echinocandins, amphatericin B and nephrotoxic

61
Q

Echinocandins side effects

A

well tolerated but there is GI disturbance, hepatotoxicity, allergic reactions, not very effective alone

62
Q

Amphotericin B

A

IV only but lipsomal formulation to reduce toxicity

63
Q

Neprhotoxic

A

hypokalaemia, chills and allergic reactions

64
Q

Voricanazole

A

fist line invasive aspergillosis treatment
reduces immunosuppression
oral or intravenous

65
Q

Voricanazole side effects

A

visual disturbance, cardiac rhythm disturbance, hepatotoxic rash, convulsions

66
Q

Voricanazole response rates

A

50-90% as fungal resistance is emerging

Respiratory Pharmacology (17 decks)

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