Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Micro > chronic necrotizing pneumonia: abscesses, MTB, NTM > Flashcards

chronic necrotizing pneumonia: abscesses, MTB, NTM Flashcards

1
Q

chronic pneumo hallmarks

A

slow, insidious (wks-mod), fever mild-high, night sweats, malaise/fatigue, anorexia (10-20 lb), dyspnea, chronic cough may become prod, hemoptytic, CP (pleur/nonpleur)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

foul smelling sputum is pathognomonic for

A

anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

chronic pneumo CXR

A

consolidation/infiltrates OR cavitary lesions
Apical or subapical consolidation/infiltrates in the upper lobes or superior- posterior segments of the lower lobes +/- caviation (MTB, syst. mycoses), occur over several mos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

lung lesions are NOT

A

NOT visualized by Gs
NOT Cx on blood agar
NOT tx w. PCN, cephs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

tx chronic pneumo empirically?

A

NO; tx too toxic, wait til dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q 
lung abscess (hole):
(cavitary lesions often have air-water interface)
A

local suppurative(pussy) necrotizing collection w/in lung parenchyma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

cavitary lesions caused by

A

90%: anaerobes, facult anaerobes (G+ cocci, G- rods)
via aspiration, wks-2mos
CAN visual by Gs, blood agar if facult., tx w. PCN, cephs

also caused by: prim. SCC of lung (>45yo, 30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

in chronic nec. pneumo, facultative anaerobes are…

A

more virulent w/ shorter onset (2wks)

anaerobic bacteria are less virulent and onset is 4-6 wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

abscess pneumo s/s

A

classic chronic pneumo + foul sputum (50-60%), altered sensorium if progressed
poor dent. hyg., trauma/inj/disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

abscess pneumo CXR

A

solitary cavitary lesion about 4cm in diameter w/ air-fluid level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

abscess pneumo comps

A

empyema formation from bronchopleural fistula
massive hemoptysis
spont. rupture into uninv. lung segments
non-resolution of abscess cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

abscess pneumo tx

A

abx targeting orogingival anaerobes
B-lactamase-inhib/B-lactam OR 2nd/3rd gen. CEPH + clindamycin/metronidazole for 6-8 wks
past: (IV PCN + clindamycin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

if abx unsuccessful for abscess tx

A

resect lung/drain absecs via bronchial airway (if thru chest, non-healing open wound in lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MTB spectrum

A

no illness: LTBI
localized: pulmonary/meningeal TB
massive systemic dissemination: miliary TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MTB staining

A

poorly via Gx

acid-fast : resistant to destain with acid alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MTB cell wall structure

A
  • PTG, G- wall w/ lypophilic substances
  • virulence factors:
    1. mycolic acids (LCFAs (branched), lipids bound to arabinogalactan-PTG polymers) INH target resp. for acid-fastness
    2. trehalose dimycolate (cord factor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MTB deets

A

facult. IC in macrophages, obligate areobe, slow growth (2-3 wks), sp. media, resistant to drying, acids, alkalis, disinf.
sens. to UV light and moist heat (pasteurization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TB transmission only occurs from person with..

A

ACTIVE pulmonary or laryngeal TB via inhalation of 1-10um airborne droplets of 1-3 bacilli (cough) AFB smear neg or pos pts! (need contact for hours) (humans sole host)
also: ingestion of m. bovis milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TB affects what age groups..

A

young imm.COMPETENT (65 as REACTIVATION (pulmonary TB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

most MTB-infected pts control or cure their infection?

A

CONTROL
10% will reactivate (LTBI–>TB) (esp. 0-2 yrs post inf)
90% remain LTBI for life
(some will not control–>TB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

risk factors for ACQUIRING TB

A

foreign born (Africa, Asia, LA)
low-income (homeless, malnutr., crowding)
nursing home, correctional, homeless shelters
HCW or persons employed above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

risk factors for developing TB once infected w. MTB

A

65,
T cell compromise(HIV, maln, chemo, steroids, SOT, old, blood ca)
IVDU, certain diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MTB patho

A

facult. IC of alveolar endothelial/epithelial cells and macrophages
- inh. TB must reach alveolar spaces (periphery), MTB are phago (not killed) by macros and PMNs, multi. IC, disseminate: locally (lungs and LNs) or systemically/lymphohematogenous (any organ)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

MTB replication occurs in orgs/tissues w.

A

high O2 levels: apical-post. areas of lung, LN

also: kidney, brain, bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
MTB immunity
CMI (both CD4+ and CD8+) exposure-->MTB-sp. CD4+ cells proc. IFN-y-->activate macros-->prod. ROIs that kill MTB cells phagocyt. by act. macros MTB-sp. CD8+ cells kill MTB-inf. NON-ACT. macros-->rel. MTB cells, killed by act. macros **CMI resp. for most tissue damage and symptoms of disease, MTB does NOT produce toxins**
26
host attempts to contain MTB infections-->inflammatory response-->adaptive response-->
GRANULOMA (caseation-seen in histo biopsy not CXR/CT/MRI) made of macrophage-derived epithelioid cells, lymphocytes viable MTB @ center (w. CMI: arrested, but viable for years) if inadequate CMI: LTBI-->TB
27
CMI response converts granuloma-->organized granulomas: tubercles
dynamic, continuous process core: dormant MTB, lymphos, epithel. histocytes, multinuc. Langerhans giant cells periphery: fibroblasts, monocytes (blood), lymphos, zone cells alive, must be replenished
28
over time tubercles can heal
>1 yr | fibrosis-->scarring-->calcification (can now see on XR)
29
primary pulm. TB
happens when IR fails to form granuloma (inade. CMI) old, T cell compromised, immunocompetent kiddos (less common in US)
30
*reactivation pulmonary TB* due to
systemic immunosuppression: advanced HIV/AIDS, Ca, old, chronic ill health immunosupp-->brkdwn of granulomas w. LTBI-->reactivation *most common TB in US*
31
miliary TB
massive disseminated inf. involving multiple organs (foci-size of millet seed) other: extrapulmonary refers to other organ system
32
if infection progresses in pulmonary TB...
consolidation happens-->cavitary lesions-->bronchiectasis
33
in reactivation TB, the caseous center continues to enlarge as MTB multiply-->liquifies tissues-->
- formation of air-liquid filled cavities: huge inc. in MTB #s-->abx resistance, spread - rupture into airways-->hemoptysis, release of caesium (spread) - inhal. of MTB to other parts of lung (tuberculous bronchopneumonia) - erosion of vein wall and leak of caesium into blood-->hemoptysis, miliary TB
34
LTBI clinical manifestations
absence of s/s CXR norm or shows evidence of past TB neg. stain/sputum Cx
35
*LTBI proven only by*
positive PPD positive Quantiferon test (CANNOT distinguish btw LTBI and active TB disease) i.e. disease may or may not be present
36
TB disease (active) dx by
s/s, AFB in sputum, Cx
37
TB disease (active) s/s (only after inf. has progressed)
slow, insidious, fever (of "unknown origin": FUO), night sweats, malaise, fatigue, anorexia + weight loss chronic persistant cough, pleuritic pain, pleural effusions (MTB inf or IR), dyspnea
38
TB in late stage of HIV/AIDS
mostly pulm. TB, but coin-like or cavitary lesions uncommon *diffuse pulmonary infiltrates happen due to poor CMI* (disseminated TB 1/3 cases, inc. mortality)
39
PPD
not 100% sp/sn, injected intradermally (into not under skin) | 1st detected 3-8 wks post-primary infection
40
positive PPD
induration (50% monos/macros, 50% MTB-sp Th1 cells) 48 hrs post-inf > 15 mm for all pops not specified > 10 mm for foreign born (see above), IVDU, med-underserved, low income, HCW etc (see above), residents of (see above), certain conditions, kiddos >5 mm for HIV+, close TB contacts, abnorm. CXR (upper lobe fibrosis), immunsuppr. w. at leat 15 mg prednisone/day last 1 mo
41
QuantiFERON-TB Gold test
in vitro, measure amount of INF-y prod. by cells in whole blood that have been stim. by MTB peptides - mimics ESAT-6 and CFP-10 proteins, present in MTB but not BCG and NTM - dx for MTB, NOT dx for LTBI vs active TB - no boosting effect
42
new IGRAs (IFN-y release assay)
dx both LTBI and active TB (MTB) | -QFT-GIT and T-SPOT TB test
43
detection of DISEASE (active)
med hx, s/s CXR | report to HD
44
active TB CXR
-consolidation/infiltrates in apical/subapical in upper lobes or sup-post segments of lower lobes +/- cavitation (or nodular/cavitary lesion w. no surrounding infiltrates) -immunocompetent: solitary pulm. nodule 1 cm in diam. surrounded by lung parenchyma, no other abnorm., opaque due to calcification (granuloma form. evident in biopsy specimen)
45
ddx active MTB (based on CXR)
infectious: nocardia, actinomyces israelii, systemic mycosis (fungi) - infection, not disease lung cancer hamartoma/adenochondroma
46
in HIV/AIDS pts, no cavitations but
diffuse infiltrate is common
47
lab dx MTB
``` AFB in sputum (consid. infectious, quantified) positive Cx (confirms dx)-->drug susc/abx sens test, monitor tx response ```
48
if extrapulm. TB suspected
blood cx to see if disseminating
49
nucleic acid amplification (NAA) testing
detects MTB 1+ wks earlier than Cx, cannot dist. btw live/dead
50
MTB-sp. CD4+ T cells expressed immune markers
CD38, HLA-DR, Ki-67+
51
MTB tx for who?
LTBI and active TB -confirmed! not close contacts | tx too toxic
52
MTB tx: 1st line drugs
Isoniazid: interferes w. mycolic acid syn Rifampin: inhib. RNA syn Pyrazinamide: bactericidal for repl. orgs Ethambutol: inhib. cell wall sun and is bacteriostatic
53
MDR-TB
resistance to Rifampin and INH
54
XDR-TB
resistant to Rifampin and INH and any FQ and at least 1/3 inj. 2nd line drugs (amikacin, kanamycin, capreomycin)
55
LTBI/MTB infection (not active) 2 tx regimens | HIV or non-HIV
1. INH for 6-9* mos | 2. Rifampin for 4 mos for LBTI + close contacts w. INH-res. TB/cannot tolerate INH/pyrazinamide
56
TB disease (active) tx: drug-sens
1. INH alone 18 mod 2. INH and Rifampin for 9 mos 3. 4 1st LD for 3 mos, 2 1st LD for 4 mos
57
TB disease (active) tx: DR
combined chemo to prev. MDR-TB 3 drugs 6-9 mos (e.g., rifampin, pyrazinamide, INH for 2 months then rifampin and INH for 4 mos -still OK)
58
TB disease (active) tx: MRD
4-5 drugs for 18-24 mos (2 yrs!)
59
Tb disease tx monitored via
``` sputum Cx (3 wks post tx) considered inf. as long as orgs cx, cured when 3 successive neg cx CANNOT monitor with PPD, Quantiferon test ```
60
MDR-TB..
due to chromosomal mutations | high mortality rate
61
extensive tx for XDR-TB
lung resection and antimicrobial tx
62
DOTS
HCW observe swallowing, monitor progress, short-course (6-9 mos)
63
BCG vaccine
M. bovis, cannot cause dis. in immcompetent person life-long, latent infection, can reactivate latent inf-->active in immunocompromised pts used to tx bladder Ca (IR delays Ca recurrence)
64
NTM etiology
environment AND human NF (MTB just NF)
65
NTM spp.
M. kansasii M. fortuitum M. avium complex (MAC): M. intracellulare and M. avium
66
NTM deets
``` rapid growers: 7 days slow growers >7d-6weeks some AF, cross-reac. Ags to MTB Ag most MDR (esp. MAC) incidence inc. due to HIV/immsuppr pop affects oldies, immsuppr, underlying dis. ```
67
NTM transmission
NOT person-person, NO reactivation of latent inf. | resevoir is environ. (all contrast MTB)
68
NTM patho
may cause slight + PPD, less virulent *rarely causes dis. in immunocompetent person, diff to elim. due to MDR
69
NTM slow growers: Group 1: photochromogens, Runyon group I (7d-6wks)
M. kansasii: water supplies, MW US, pulm dis., min. contagious (unlike MTB) M. marinum: skin inf. M. haemophilum: skin, jt, bone, pulm. inf. in immunocompromised persons and lymphaden. in kiddos
70
NTM slow growers: Group 2 : scotochromogens (pigment in dark), Runyon group II
M. gordonae | M. scrofulaceum: cervical adenitis
71
NTM slow growers: Group 3: noncrhomogenic, Runyon group III
MAC: M. avium complex: ubiquitous environ. org | SE US, inhal. and ingestion-->across mucosa-->infects macros of LP-->submucosa-->LN
72
DMAC
disseminated MAC in HIV/AIDS pts. (20-40% of pts w. CD4 count
73
DMAC manifests in AIDS pt
fever, night sweats, weight loss-wasting, swollen abd. LNs (unilat), diarrhea, hepsplnmeg, anemia, elev. PB liver enzymes, localized disease LESS common, but rarely in (LRT, pericarditis, GIT, CNS, skin, joints)
74
Cx for slow growers req.
2-6 wks, alert lab! | nucleic acid testing quicker
75
NTM rapid growers: (2-7 days) Runyon group IV
M. fortuitum, M. abscessus, M. chelonae, M. massiliense, M. bolletii (fortuitum complex) contaminant in clinical specimens sig. opportunistic pathogen of (skin, ST, bone, LRT (chronic), site of wound trauma, surgical prosthetic implants) -resis to alk. glutaradehyde, low susc. to high lev. disinfect.
76
NTM dx
Cx must be done, need repeated isolation of org for dx, ID to species level!
77
NTM tx
depends on ID of species, sensitivity testing must be done on Cx+ isolates

Micro (61 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions