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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
give a direct burden of malaria
-severe maternal anaemia -low birthweight
26
name the 7 stages of malaria
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
what causes malaria
plasmodium protozoa, which are unicellular eukaryotic organisms more complex than bacteria
28
when does the asexual phase in malaria happen
1-12 weeks after bite
29
symptoms of malaria (malarial paroxysm)
-headache & lack of energy - muscle aches & chills -fever (up to 40 degrees) -diarrhoea & vomiting & loss of appetite
30
treatment options for uncomplicated malaria
-oral quinine (chloroquine most widely used) + doxycycline or clindamycin in certain circumstances -Artemisinin combination therapy -atovaquone + proguanil (malarone)
31
why is mefloquine not recom in malaria treatment
side effects + high rate of non-compliance
32
which drugs best for liver with normal function in stage 2 of malaria life cycle
-8 aminoquinolines e.g. primaquine, tafenoquine -atovaquone- proguanil -proguanil
33
which drug best for liver with affected function in malaria
-8 aminoquinolines e.g. primaquine, tafenoquine
34
which drugs used at gametocyte stage in malaria
-ACTs -quinine e.g. chloroquine, mefloquine, amodiaquine -8 aminoquinolines e.g. primaquine, tafenoquine
35
what drugs used at blood stages in malaria
-ACTs -chloroquine -mefloquine -primaquine -doxycycline -clindamycin
36
MOA for quinine and related agents (sulfadoxine, sulfone and tetracyclines)
-Blood schizonticidal agents (kill schizonts) -prevent toxicity, as parasites polymerise haem to hemozoin
37
PK for quinine + related agents
-good oral bioavai -half life is 45 days due to binding to tissue -metabolised vy liver & renal excretion
38
quinine + related agents ADR
-chloroquine: nausea, vomiting, diarrhoea, hot flush and rash -quinine: cinchonism (overdose) , tinnitus, deafness, headaches, nausea, visual effects
39
caution and contraindications of quinine + related agent
-reduce dose in liver/ renal disease -glucose6-phosphate deficiency -avoid in preg (chloroquine= fetal ototoxicity) -quinine preferred in pregnancy
40
interactions of quinine and related agents
-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
pyrimethamine mechanism of action
selective inhibition of dihydrofolate reductase in parasite
42
combinations drug to only admin pyrimethamine with
-sulphonamide sulfadoxine
43
PK of pyrimethamine
-absorbed from gut and undergoes extensive hepatic metabolism -half life = 2-6hrs
44
ADR of pyrimethamine
-photosensitive -rashes -insomnia -high doses = megaloblastic anaemia (larger size red blood cells) because it inhibits human folate metabolism
45
proguanil MOA
-the active metabolite (cycloguanil) inhibits dihydrofolate reductase, which inhibits folate production in pre and erythrocytic parasites
46
PK proguanil
-well absorbed from gut -metabolized by liver = cycloguanil -half life = 12-24 hrs
47
ADR of proguanil
-mouth ulcers -epigastric discomfort (upper abdomen) -diarrhoea
48
What is artemisinin
- some of the most potent anti-malaria drugs -rapid acting -given way to more potent dihydroartemisinin + derivatives e.g. artemether, artemotil & artesunate
49
artemisinin MOA
-inhibition of parasite Ca^2+ dependent ATPase -unstable for chemoprophylaxis and resistance risk due to short half life
50
artemesinin combination therapy examples
CoArtem and Lumefantrine
51
decribe CoArtem
-artemethere + lumefantrine (riamet) -highly potent anti-malaria drug -benefical against resistant strains
52
describe Lumefantrine
-an aryl amino acid -long acting to eliminate residual parasites -acts against all human malaria parasites -reduces resistance risk
53
what is the suggested MOA for lumefantrine
-suggested MOA = inhibits formation of beta-hematin by forming complex with hemin and inhibits nucleic acid + protein synthesis
54
artemesinin vs dihydroartemisinin
- A has good oral absorption with peak con achieved in 4hrs -D more variable oral bioav, dependent on excipients in oral formulation
55
PK of artemesinin combined therapy
-well absorbed from gut -rapid hydrolysed to active metabolite with half life of 2-3hrs
56
ADR of artemesinin combined therapy
-abdominal pain nausea anorexia -diarrhoea -dizziness -headache -sleep disturbance -fatigue
57
what are the principle of malaria prophylaxis (things to do to prevent) (ABCD)
-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
chemoprophylaxis in malaria
chloroquine + proguanil -start 2-20 days before travel and uses during stay and 1-4weeks after return -not recommended in endemic area residents
59
standby treatment in prophylaxis of malaria
-mefloquine or quinine -needs to be treated early, difficult to treat once progresses
60
What are the 2 types of chemoprophylaxis
-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
examples of protection against bites
- 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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