TBC (pathoma ir UW) 12/12 Flashcards
4 drugs for TBC treatment?
RIPE:
Rifampin
Isoniazid
Pyrazinamide
Ethambutol
Rifampin mechanism?
Inhibition of bacterial DNA-dependent RNA polimerase -> halts bacterial proteins synthesis
Inhibition of bacterial DNA-dependent RNA polimerase.
Drug?
Rifampin
Rifampin. 4 side effects?
GI, rash, red-orange body fliuds, cytopenias
GI side effect?
Rifampin.
Rash side effect?
Rifampin.
red-orange body fliuds?
Rifampin.
Cytopenias?
Rifampin.
Isoniazid mechanism?
Inhibition of mycolic acid synthesis
Inhibition of mycolic acid synthesis?
Isoniazid
Isoniazid side effect?
Neurotoxicity (give vitB6/pyridoxine) -> peripheral neuropathy, therefore with drug give simultaneously pyridoxine
hepatotoxicity -> during first 4-6 months of treatment
Neurotoxicity (give vitB6/pyridoxine)?
Isoniazid
Hepatotoxicity (2)?
Isoniazid, Pyrazinamide
Pyrazinamide mechanism?
Unclear
Pyrazinamide side effects?
Hepatotoxicity, hyperuricemia
hyperuricemia?
Pyrazinamide
Ethambutol mechanism?
Inhibition of arabinosyl transferase
Inhibition of arabinosyl transferase?
Ethambutol
Ethambutol side effect?
optic neuropathy
optic neuropathy?
Ethambutol
Resistance (2)?
- Mutations in genes that responsible for mycolic acid synthesis (isoniazid)
- Mutations in genes responsible for mycobacterial RNA polymerase (rifampin)
What are virulence factors? (3 were mentioned)
sulfatides, wax D, CORD FACTOR
Severity of hepatotoxicity due to isoniazid?
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.
M. Tuberculosis on microscopy?
arranged in long, slender, serpentine cords dur to cord factor.
Cord factor - composition?
two mycolid acids bound to the disssacharide trehalose.
Cord factor where is present?
its hydrophobic surface glycolipid
Cord factor effect?
forms cylindrical micelles, that surround the organism and prevent macrophage -mediated destruction within phalolysosome.
Cord factor other effect?
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
pathoma. Primary TB arises with ….
initial exposure
pathoma. primary tuberculosis composed of?
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
pathoma. Primary TB - symptoms?
asymptomatic or mild flu like symptoms
Positive PPD
pathoma. secondary arises due to….
reactivation of bacteria in immunocompromised patients (AIDS, elderly)
pathoma. secondary occcurs where?
upper lobes (due to relatively poor lymphatic drainage and high oxygen tension)
pathoma. what happens in secondary?
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.
pathoma. miliary. meninges?
meningitis
pathoma. miliary. cervical lymph nodes?
lymphadenitis in neck (scrofula)
pathoma. miliary. kidneys?
sterile pyuria
pathoma. miliary. lumbar vertebrae?
Pott disease
pathoma. miliary. liver?
hepatitis
pathoma. miliary. adrenal glands?
addison disease
pathoma. biopsy?
caseating granulomas
pathoma.AFB stain?
acid-fast balili
pathoma. symptoms?
fever, night sweats, hemoptysis, weight loss
What immunity?
Cell mediated.
mechanism of cells/cytokines?
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.
