TBC (pathoma ir UW) 12/12 Flashcards

1
Q

4 drugs for TBC treatment?

A

RIPE:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol

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2
Q

Rifampin mechanism?

A

Inhibition of bacterial DNA-dependent RNA polimerase -> halts bacterial proteins synthesis

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3
Q

Inhibition of bacterial DNA-dependent RNA polimerase.
Drug?

A

Rifampin

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4
Q

Rifampin. 4 side effects?

A

GI, rash, red-orange body fliuds, cytopenias

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5
Q

GI side effect?

A

Rifampin.

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6
Q

Rash side effect?

A

Rifampin.

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7
Q

red-orange body fliuds?

A

Rifampin.

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8
Q

Cytopenias?

A

Rifampin.

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9
Q

Isoniazid mechanism?

A

Inhibition of mycolic acid synthesis

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10
Q

Inhibition of mycolic acid synthesis?

A

Isoniazid

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11
Q

Isoniazid side effect?

A

Neurotoxicity (give vitB6/pyridoxine) -> peripheral neuropathy, therefore with drug give simultaneously pyridoxine

hepatotoxicity -> during first 4-6 months of treatment

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12
Q

Neurotoxicity (give vitB6/pyridoxine)?

A

Isoniazid

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13
Q

Hepatotoxicity (2)?

A

Isoniazid, Pyrazinamide

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14
Q

Pyrazinamide mechanism?

A

Unclear

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15
Q

Pyrazinamide side effects?

A

Hepatotoxicity, hyperuricemia

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16
Q

hyperuricemia?

A

Pyrazinamide

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17
Q

Ethambutol mechanism?

A

Inhibition of arabinosyl transferase

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18
Q

Inhibition of arabinosyl transferase?

A

Ethambutol

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19
Q

Ethambutol side effect?

A

optic neuropathy

20
Q

optic neuropathy?

A

Ethambutol

21
Q

Resistance (2)?

A
  1. Mutations in genes that responsible for mycolic acid synthesis (isoniazid)
  2. Mutations in genes responsible for mycobacterial RNA polymerase (rifampin)
22
Q

What are virulence factors? (3 were mentioned)

A

sulfatides, wax D, CORD FACTOR

23
Q

Severity of hepatotoxicity due to isoniazid?

A

Mild - elevated ALT/AST, tend to return to baseline.
Rare cases: frank hepatitis (resembles viral hepatitis, with fever, anorexia, nausea, jaudince) –> can progress to severe form with progressive liver dysfunction and death.

24
Q

M. Tuberculosis on microscopy?

A

arranged in long, slender, serpentine cords dur to cord factor.

25
Q

Cord factor - composition?

A

two mycolid acids bound to the disssacharide trehalose.

26
Q

Cord factor where is present?

A

its hydrophobic surface glycolipid

27
Q

Cord factor effect?

A

forms cylindrical micelles, that surround the organism and prevent macrophage -mediated destruction within phalolysosome.

28
Q

Cord factor other effect?

A

fors highly toxic crystaline monolayer hydrophobic surfaces (oir-water/air-water interface (eg edge of cavitation), that helps to drive the formation of caseating granulomas

29
Q

pathoma. Primary TB arises with ….

A

initial exposure

30
Q

pathoma. primary tuberculosis composed of?

A

Focal caseating necrosis in lower lung lober (subpleural) (GHON FOCUS) + caseosis of HILLAR LYMPH NODES –> BOTH TOGETHER CALLED GHON COMPLEX.

When complex undergo fibrosis and CALCIFICATION, its called RANKE complex

31
Q

pathoma. Primary TB - symptoms?

A

asymptomatic or mild flu like symptoms
Positive PPD

32
Q

pathoma. secondary arises due to….

A

reactivation of bacteria in immunocompromised patients (AIDS, elderly)

33
Q

pathoma. secondary occcurs where?

A

upper lobes (due to relatively poor lymphatic drainage and high oxygen tension)

34
Q

pathoma. what happens in secondary?

A

forms CAVITARY foci of caseous necrosis. It spreds disseminates in the lungs (man atrodo per lyphatics) –> cause tuberous bronchopneumonia
or disseminates to vassular -> miliary TB.

35
Q

pathoma. miliary. meninges?

A

meningitis

36
Q

pathoma. miliary. cervical lymph nodes?

A

lymphadenitis in neck (scrofula)

37
Q

pathoma. miliary. kidneys?

A

sterile pyuria

38
Q

pathoma. miliary. lumbar vertebrae?

A

Pott disease

39
Q

pathoma. miliary. liver?

A

hepatitis

40
Q

pathoma. miliary. adrenal glands?

A

addison disease

41
Q

pathoma. biopsy?

A

caseating granulomas

42
Q

pathoma.AFB stain?

A

acid-fast balili

43
Q

pathoma. symptoms?

A

fever, night sweats, hemoptysis, weight loss

44
Q

What immunity?

A

Cell mediated.

45
Q

mechanism of cells/cytokines?

A

alveolar macrophage that contains bacteria within phagosome goes to lymph nodes, there presents (as APC) to naive T cell and release IL-12 -> naive converts to Th1 CD4 -> release IFN-gamma -> further activates macrophages -> become epithelioid cells and merge forming langhans giant cells.