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TUBERCULOSIS Flashcards

1
Q

WHAT WAS TUBERCULOSIS REFERRED TO AS IN THE 1700’S?

A

‘THE WHITE PLAGUE’

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2
Q

THE TUBERCULOSIS BACTERIUM IS ESTIMATED TO BE HOW OLD?

A

70 000

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3
Q

SINCE WHEN IS TUBERCULOSIS KNOWN?

A

THE ANCIENT EGYPTIAN TIMES

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4
Q

TUBERCULOSIS IN HUMANS CAN BE TRACED BACK HOW MANY YEARS (DATA OBTAINED BY SEQUENCING ANCIENT DNA)

A

6 000

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5
Q

WHO ISOLATED THE TUBERCLE BACILLUS AND WHEN?

A

ROBERT KOCH, 1882

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6
Q

INCIDENCE OF TB OVERALL IS INCREASING OR DECREASING?

A

DECREASING

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7
Q

RISK FACTORS FOR TB?

A 
MAIN 5:
- HIV
- MALNUTRITION
- DIABETES
- ALCOHOL USE
- ACTIVE SMOKING
OTHERS:
- CROWDING
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8
Q

WHICH RISK FACTOR IS ATTRIBUTABLE TO MOST TB CASES?

A

UNDERNOURISHMENT

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9
Q

INFECTIOUS DOSE OF TB?

A

3-10 BACILLI (VERY LOW)

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10
Q

HOW IS TB TRANSMITTED?

A
  • THROUGH AEROSOLS CONTAINING M. TUBERCULOSIS

- DOESN’T SPREAD THROUGH CONTACT OR FOOD

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11
Q

STAGES OF TB?

A

EXPOSURE (BEING IN CONTACT WITH SOMEONE WHO HAS TB)
LATENT TB INFECTION (PERSON HAS TB BACTERIA IN THEIR BODY BUT NO SYMPTOMS)
ACTIVE TB DISEASE (PERSON WITH SIGNS AND SYMPTOMS OF AN ACTIVE TB INFECTION)
REACTIVATION (OF LATENT INFECTIONS)

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12
Q

DESCRIBE THE M. TUBERCULOSIS PATHOGEN:

A
  • GRAM POSITIVE
  • LONG RODS
  • WAXY COAT OR ‘OUTER MEMBRANE’
  • HIGHLY AEROBIC
  • INTRACELLULAR PATHOGEN
  • REPLICATES SLOWLY
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13
Q

HOW LONG DOES IT TAKE FOR M. TUBERCULOSIS TO GROW IN THE LABORATORY?

A

3 WEEKS (SLOW REPLICATION)

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14
Q

DESCRIBE THE TB CELL WALL:

A
  • IT RESEMBLES BOTH GRAM POSITIVE AND GRAM NEGATIVE CELL ENVELOPE
  • CONTAINS PEPTIDOGLYCAN AND ARABINOGALACTAN
  • OUTER, WAXY LAYER MADE OUT OF MYCOLIC ACIDS MADE OF LONG CHAIN FATTY ACIDS
  • HYDROPHOBIC MEMBRANE SERVES AS A PERMEABILITY BARRIER (ANTIBIOTIC RESISTANCE!)
  • CELL WALL IS KEY FOR VIRULENCE
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15
Q

WHAT ARE MYCOLIC ACIDS?

A

LONG CHAIN FATTY ACIDS THAT ARE FOUND IN CELL WALLY OF CERTAIN BACTERIA, LIKE M. TUBERCULOSIS

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16
Q

THE HYDROPHOBIC MEMBRANE OF M. TUBERCULOSIS ACTS AS A PERMEABILITY BARRIER AND COMPLICATES TREATMENT AS IT CONTRIBUTES TO:

A

ANTIBIOTIC RESISTANCE

17
Q

WHAT ARE GRANULOMAS?

A

SMALL AREAS OF INFLAMMATION, FREQUENTLY OCCURING IN THE LUNGS

18
Q

TB BACTERIA PRIMARILY REPLICATES AND SURVIVES WITHIN WHICH HOST CELLS?

A

MACROPHAGES

19
Q

APART FROM MACROPHAGES, WHICH OTHER CELLS CAN TB BACTERIA BE FOUND IN?

A

NEUTROPHILS, DENDRITIC CELLS, ALVEOLAR EPITHELIAL CELLS ETC.

20
Q

DESCRIBE M. TUBERCULOSIS PROGRESSION AFTER ENTERING THE HOST:

A
  • MULTIPLICATION IN A UNIQUE NICHE
  • INFECTION OF INDIVIDUAL MACROPHAGES
  • EXPANSION IN INNATE GRANULOMAS
  • GRANULOMA MATURATION
  • GRANULOMA NECROSIS WITH EXTRACELLULAR REPLICATION
  • FURTHER TRANSMISSION
21
Q

WHAT IS ‘MYCOBACTERIUM’?

A
  • IMMOBILE, SLOW-GROWING, ROD-SHAPED, GRAM-POSITIVE BACTERIUM
  • GENUS OF ACTINOBACTERIA, INCLUDES M. TUBERCULOSIS AND M. LEPRAE ETC.
  • DUE TO THEIR SPECIAL STAINING UNDER THE MICROSCOPE, WHICH IS MEDIATED BY MYCOLIC ACID IN THE CELL WALL, THEY ARE CALLED ‘ACID-FAST’
22
Q

DESCRIBE THE M. TUBERCULOSIS AND MACROPHAGE INTERACTIONS:

A
  • MTB ENTERS THROUGH RECEPTOR MEDIATED ENDOCYTOSIS IN A PHAGOSOME (A VESICLE FORMED AROUND A PARTICLE ENGULFED BY A CELL)
  • MTB BLOCKS MATURATION OF THE PHAGOSOME AND PREVENTS IT FROM FUSING WITH A LYSOSOME (THROUGH THE ACTION OF PROTEIN CALLED PtpA)
  • MTB PREVENTS ACIDIFICATION OF THE PHAGOSOMES
  • PRODUCES SEVERAL PROTEINS WHICH INTERFERE IN DIFFERENT ANTIMICROBIAL PATHWAYS (E.G. SapM, KatG)
  • MTB ALSO EVENTUALLY INDUCES CELL DEATH IN MACROPHAGES, WHICH THEN DISSEMINATE AND INFECT OTHER MACROPHAGES
23
Q

EXTRAPULMONARY TB (EPTB):

A
  • HARD TO DIAGNOSE (VAGUE SYMPTOMS) AND TREAT
  • OCCURS OUTSIDE LUNGS
  • CAN AFFECT ALMOST ALL ORGANS, MOST COMMON ORGANS DEPEND ON THE COUNTRY
24
Q

RATES OF EPTB AMONG ALL TB CASES?

A

8-24%

25
Q

RISK FACTORS FOR EPTB?

A
  • HIV INFECTED INDIVIDUALS HAVE THE HIGHEST RISK BECAUSE THEY ARE IMMUNOSUPPRESSED
  • YOUNG CHILDREN ARE TWICE AS LIKELY TO GET EPTB
26
Q

WHICH TYPE OF EPTB IS PARTICULARLY PROMINENT IN CHILDREN?

A

BONE/SPINAL CORD TB

27
Q

SYMPTOMS OF ACTIVE LUNG TUBERCULOSIS INFECTION:

A
  • COUGH WITH SPUTUM AND BLOOD AT ALL TIMES
  • CHEST PAINS
  • WEAKNESS
  • WEIGHT LOSS
  • FEVER AND NIGHT SWEATS
28
Q

HOW CAN TB BE DIAGNOSED + DESCRIPTIONS?

A
  • MANTOUX TEST; SKIN TEST
    (A POSITIVE TB SKIN OR BLOOD TEST ONLY TELLS THAT A PERSON HAS BEEN INFECTED WITH TB BACTERIA)
  • CHEST X RAY (SHOWS ACTIVE DISEASE)
  • BACTERIAL CULTURE FROM SAMPLE OF SPUTUM
  • RAPID MOLECULAR DIAGNOSTIC TESTS
29
Q

WHAT IS XPERT MTB/RIF ULTRA?

A
  • AUTOMATED MOLECULAR TEST THAT HAS IMPROVED THE DETECTION OF TUBERCULOSIS AND RIFAMPICIN RESISTANCE
30
Q

HOW LONG IS TB TREATMENT USUALLY?

A

6-9 MONTHS

31
Q

WHAT ARE THE 1ST LINE ANTI-TB AGENTS USED FOR TREATING PULMONARY TB AND GIVEN TOGETHER?

A
  • ISONIAZID (INH)
  • RIFAMPIN (RIF)
  • ETHAMBUTOL (EMB)
  • PYRAZINAMIDE (PZA)
32
Q

WHAT ARE THE 2 MOST EFFECTIVE ANTI TB DRUGS?

A

ISONIAZID (INH)

RIFAMPIN (RIF)

33
Q

WHAT ARE THE CHALLENGES IN PULMONARY TB TREATMENT?

A
  • SOME DRUGS HAVE SEVERE SIDE EFFECTS
  • ENSURING COMPLETION OF THE TOTAL TREATMENT
  • MULTIDRUG RESISTANCE
34
Q

WHAT IS MDR-TB?

A

Mtb RESISTANT TO 2 OF THE MOST EFFECTIVE ANTI TB DRUGS, ISONIAZID AND RIFAMPIN

35
Q

WHAT IS XDR-TB?

A

EXTREMELY DRUG RESISTANT TB; MDR-TB THAT ARE RESISTANT TO FLUOROQUINOLONE AND ON OTHER INJECTIBLE 2ND LINE DRUGS

36
Q

WHAT ARE THE MAIN CAUSES OF MDR-TB?

A
  • FAILURE TO COMPLETE TREATMENT, INTERRUPTIONS IN TREATMENT
  • LACK OF TB CONTROL PROGRAMMES AND GUIDELINES
  • POOR QUALITY DRUGS
37
Q

LENGTH OF TREATMENT FOR MDR-TB?

A

UP TO 2 YRS

38
Q

TREATMENT OF MDR-TB?

A
  • LONG AND EXPENSIVE
  • LIMITED NUMBER OF DRUGS (NEW EFFECTIVE DRUGS NEEDED)
  • USE OF 2ND LINE DRUGS (E.G. BEDAQUINILINE)
39
Q

BCG - BACILLE CALMETTE GUERIN VACCINE?

A
  • PRIMARILY USED AGAINST TUBERCULOSIS
  • INTERFERES WITH THE SKIN TEST (MANTOUX TEST)
  • NOT VERY EFFECTIVE IN ADULTS WITH PULMONARY TB
  • MORE EFFECTIVE IN CHILDREN, ESP AGAINST TUBERCULOSIS MENEGITIS
  • NEW, ENHANCED VERSION ARE BEING DEVELOPED

INF (40 decks)

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