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HIV & Infections > anti-infectives > Flashcards

anti-infectives Flashcards

1
Q

structure of mycobacterium tuberculosis

A

-weakly gram positive
-strongly acid-fast
-bact can grow&live in presence of oxygen (aerobic bacilli)
-lipid rich cell wall

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2
Q

physiology of mycobacterium tuberculosis

A

resistant to disinfectants, detergents & common antibiotics

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3
Q

what diseases mycobacterium tuberculosis causes

A

-pulmonary infection (primary)
- spread to other sites in the body common in immunocompromised pt or if left untreated

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4
Q

epidemiology of mycobacterium tuberculosis

A

1/3 population infected with organism

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5
Q

treatment, prevention & control

A

-multiple drug regimens + prolonged treatment= prevent resistance
-immunoprophylaxis = BCG injection
-control: monitoring the pt but not giving treatment unless changes in test results, prophylaxis and therapeutic intervention & careful case monitoring

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6
Q

first line anti-mycobacterial drugs

A

-isoniazid (INH)
-rifampicin
-ethambutol
-pyrazinamide

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7
Q

second line anti-mycobacterial drugs

A

-capreomycin
-streptomycin
-cycloserine

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8
Q

what must you always use in treatment of mycobacterial tuberculosis

A

POLYTHERAPY
-isoniazid and rifampicin combination administered for 9 months cures 95-98%
-pyrazinamide added in combination for first 2 months = total duration reduced to 6 months

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9
Q

What happens in latent tuberculosis infection (LTBI)

A

-pt infected with mycobacterium tuberculosis but symptom free
- immune system stimulation because of m.tuberculosis antigens
-pt risk of developing active disease in future

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10
Q

What is treatment of LTBI dependant on

A

age, HIV status and liver function

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11
Q

what is the guidance with prescribing in LTBI

A
  • below 65 = 3 months of isoniazid (with pyridoxine) and rifampicin or 6 months of isoniazid (with pyridoxine)
  • below 35 with liver toxicity concern = 3 months of isoniazid with pyridoxine and rifampicin OR 6 months of isoniazid (pyridoxine) if interactions with rifamycins e.g. HIV
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12
Q

what is the treatment for active TB with no CNS involvement or active peripheral lymph node TB

A

-Isoniazid with pyridoxine, rifampicin, pyrazinamide and ethambutol for 2 months, then isoniazid with pyridoxine and rifampicin for further 4 months

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13
Q

what is the treatment for active CNS TB

A

isoniazid with pyridoxine, rifampicin, pyrazinamide and ethambutol for 2 months, then isoniazid with pyridoxine and rifampicin for 10 months

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14
Q

what is the management for active spinal TB

A

CT/ MRI scan if showing neurolical signs or symptoms. Manage direct spinal cord involvement as CNS TB

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15
Q

management of tb that has spread through the body and bloodstream

A

Test for neurological signs/ symptoms for CNS involvement…. treat as CNS TB

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16
Q

mechanism of Isoniazid

A

-its a prodrug
- activated by bacterial enzymes = inhibitory activity on synthesis of mycolic acids
-bacteriostatic (agent prevents growth of bacteria) at low conc and bactericidal (agent kills bacteria) at high conc

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17
Q

what is isoniazid pk

A

-readily absorbed from GIT…. diffused into body fluids and tissues
-metabolised by acetylation (acetyl group added to compound)
-usually renal excretion

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18
Q

Isoniazid adverse drug reactions

A

-peripheral & optic neuritis
- allergic reaction
-hepatitis (inflammation of liver)
-haemolytic anaemia
-enzyme inhibitor
-CNS toxicity

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19
Q

what is the moa for rifampicin

A

inhibits subunit of bacterial DNA-dependant RNA polymerase= inhibiting transcription
-bactericidal

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20
Q

what is the pk of rifampicin

A

-orally absorbed well
-adequate cerebrospinal fluid
-excreted via liver to bile

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21
Q

rifampicin ADR

A

-harmless red/orange urine, sweat, tears
-rash
-thrombocytopenia (low platelet count in blood)
-nephritis (inflamed kidney tissue )
-cholestatic jaundice & hepatitis
-flu-like syndrome

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22
Q

what are the indications to provide 2nd line treatment

A

-drug resistance
-clinical response failure
-increase risky effects
-pt not tolerating 1st line

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23
Q

what is capreomycin

A

-2nd line in anti-mycobacteria
-injectable agent in treatment of drug resistant tuberculosis
-nephrotoxic & ototoxic (hearing loss)
-not to be given with streptomycin or any ototoxic drugs

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24
Q

how is malaria transmitted

A

female anopheles mosquito between 25-30 degrees and below 16 degrees

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25
Q

give a direct burden of malaria

A

-severe maternal anaemia
-low birthweight

26
Q

name the 7 stages of malaria

A
  1. infected mosquito: parasite transmitted into blood in form of sporozoites
  2. pre-erythrocytic/ hepatic phase: sporozoites mature into schizonts= release merozoites or hypnozoites (remain in liver)
  3. asexual phase: erythrocytes invasion and growth into trophozoites, which develop to schizonts = multiple merozoites infect cells = symptoms
    4-7. sexual phase: differentiation into male/female gametocytes, fuse to form ookinette in gut lumen= stomach wall invasion = sporozoites migration to salivah gland of mosquito
27
Q

what causes malaria

A

plasmodium protozoa, which are unicellular eukaryotic organisms more complex than bacteria

28
Q

when does the asexual phase in malaria happen

A

1-12 weeks after bite

29
Q

symptoms of malaria (malarial paroxysm)

A

-headache & lack of energy
- muscle aches & chills
-fever (up to 40 degrees)
-diarrhoea & vomiting & loss of appetite

30
Q

treatment options for uncomplicated malaria

A

-oral quinine (chloroquine most widely used) + doxycycline or clindamycin in certain circumstances
-Artemisinin combination therapy
-atovaquone + proguanil (malarone)

31
Q

why is mefloquine not recom in malaria treatment

A

side effects + high rate of non-compliance

32
Q

which drugs best for liver with normal function in stage 2 of malaria life cycle

A

-8 aminoquinolines e.g. primaquine, tafenoquine
-atovaquone- proguanil
-proguanil

33
Q

which drug best for liver with affected function in malaria

A

-8 aminoquinolines e.g. primaquine, tafenoquine

34
Q

which drugs used at gametocyte stage in malaria

A

-ACTs
-quinine e.g. chloroquine, mefloquine, amodiaquine
-8 aminoquinolines e.g. primaquine, tafenoquine

35
Q

what drugs used at blood stages in malaria

A

-ACTs
-chloroquine
-mefloquine
-primaquine
-doxycycline
-clindamycin

36
Q

MOA for quinine and related agents (sulfadoxine, sulfone and tetracyclines)

A

-Blood schizonticidal agents (kill schizonts)
-prevent toxicity, as parasites polymerise haem to hemozoin

37
Q

PK for quinine + related agents

A

-good oral bioavai
-half life is 45 days due to binding to tissue
-metabolised vy liver & renal excretion

38
Q

quinine + related agents ADR

A

-chloroquine: nausea, vomiting, diarrhoea, hot flush and rash
-quinine: cinchonism (overdose) , tinnitus, deafness, headaches, nausea, visual effects

39
Q

caution and contraindications of quinine + related agent

A

-reduce dose in liver/ renal disease
-glucose6-phosphate deficiency
-avoid in preg (chloroquine= fetal ototoxicity)
-quinine preferred in pregnancy

40
Q

interactions of quinine and related agents

A

-chloroquine = risk of retinopathy (retina disease) with probencid
-quinine = inhibits renal secretion of digoxin, increases effects of warfarin & prolongs QT= avoid with similar drugs

41
Q

pyrimethamine mechanism of action

A

selective inhibition of dihydrofolate reductase in parasite

42
Q

combinations drug to only admin pyrimethamine with

A

-sulphonamide sulfadoxine

43
Q

PK of pyrimethamine

A

-absorbed from gut and undergoes extensive hepatic metabolism
-half life = 2-6hrs

44
Q

ADR of pyrimethamine

A

-photosensitive
-rashes
-insomnia
-high doses = megaloblastic anaemia (larger size red blood cells) because it inhibits human folate metabolism

45
Q

proguanil MOA

A

-the active metabolite (cycloguanil) inhibits dihydrofolate reductase, which inhibits folate production in pre and erythrocytic parasites

46
Q

PK proguanil

A

-well absorbed from gut
-metabolized by liver = cycloguanil
-half life = 12-24 hrs

47
Q

ADR of proguanil

A

-mouth ulcers
-epigastric discomfort (upper abdomen)
-diarrhoea

48
Q

What is artemisinin

A
  • some of the most potent anti-malaria drugs
    -rapid acting
    -given way to more potent dihydroartemisinin + derivatives e.g. artemether, artemotil & artesunate
49
Q

artemisinin MOA

A

-inhibition of parasite Ca^2+ dependent ATPase
-unstable for chemoprophylaxis and resistance risk due to short half life

50
Q

artemesinin combination therapy examples

A

CoArtem and Lumefantrine

51
Q

decribe CoArtem

A

-artemethere + lumefantrine (riamet)
-highly potent anti-malaria drug
-benefical against resistant strains

52
Q

describe Lumefantrine

A

-an aryl amino acid
-long acting to eliminate residual parasites
-acts against all human malaria parasites
-reduces resistance risk

53
Q

what is the suggested MOA for lumefantrine

A

-suggested MOA = inhibits formation of beta-hematin by forming complex with hemin and inhibits nucleic acid + protein synthesis

54
Q

artemesinin vs dihydroartemisinin

A
  • A has good oral absorption with peak con achieved in 4hrs
    -D more variable oral bioav, dependent on excipients in oral formulation
55
Q

PK of artemesinin combined therapy

A

-well absorbed from gut
-rapid hydrolysed to active metabolite with half life of 2-3hrs

56
Q

ADR of artemesinin combined therapy

A

-abdominal pain
nausea
anorexia
-diarrhoea
-dizziness
-headache
-sleep disturbance
-fatigue

57
Q

what are the principle of malaria prophylaxis (things to do to prevent) (ABCD)

A

-Awareness about risk of malaria….
-avoid mosquito Bites
-Chemoprophylaxia (meds administered to prevent) and compliance
-Diagnosis of febrile illness (illnesses accompanied by fever e.g malaria)

58
Q

chemoprophylaxis in malaria

A

chloroquine + proguanil
-start 2-20 days before travel and uses during stay and 1-4weeks after return
-not recommended in endemic area residents

59
Q

standby treatment in prophylaxis of malaria

A

-mefloquine or quinine
-needs to be treated early, difficult to treat once progresses

60
Q

What are the 2 types of chemoprophylaxis

A

-casual: attacks malaria at the schizont stage in the liver = prevent spread to blood stream
- Suppressive: prevents the
parasite using haemoglobin as an energy source = build-up of superoxide ions to destroy parasites

61
Q

examples of protection against bites

A
  • insect repellent
    -long sleeve clothing if outdoors after sun set
    -mosquito nets
    -insecticides in rooms
    -close doors + windows

HIV & Infections (4 decks)

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