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Pulmonary Block > Micro TB/URTI > Flashcards

Micro TB/URTI Flashcards

1
Q

Pathogen that causes the most death worldwide

A

MTB

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2
Q

Reservoir and transmission of MTB

A

humans are the natural reservoir and spread is person-to-person via aerosols from coughing; 90% of people who are infected do not develop the disease

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3
Q

MTB staining properties

A

does not gram stain, stains with Acid-fast because of mycolic acid within cell wall

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4
Q

MTB cell wall

A

contains many waxy-like substances that make the cell wall impermeable to many host defense systems including: mycolic acid, glycolipids, arabinogalactans, free lipids

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5
Q

Risk factors for TB

A

prison (crowded conditions), immigration from high burden country, malnourished, alcoholism, poverty, debilitating illness, AIDS, elderly, DM, Hodgkin lymphoma, CKD, malnutrition, immunosuppression; RA on TNF alpha antagonists

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6
Q

Primary TB

A

usually asymptomatic; only evidence may be a calcified lung nodule at site of initial infection; the organisms remain dormant until immune defenses are lowered

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7
Q

Secondary infection TB

A

usually involves apices of lungs due to high oxygen content; cavitation frequently occurs; erosion of cavities into airway is source of infection - person is expectorating organisms

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8
Q

MTB steps of initial pathogenesis

A

enters macrophages by phagocytosis, inhibits the formation of phagolysosome, allowing the bacteria to replicate, IL-12 is produced stimulating a T-helper response, IFNgamma is then produced by TH-1 cells and enables macrophages to contain infection

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9
Q

MTB and Macrophages

A

MTB can grow within macrophages, allowing it to avoid antibodies and complement; once phagocytksed it can inhibit phagosome-lysosome fusion via PknG protein

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10
Q

IFN gamma and TB

A

critical mediator allowing macrophages to contain the infection

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11
Q

TH1 and TB

A

Th1 response leads to granuloma formation and caseous necrosis

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12
Q

Activated macrophages and TB

A

macrophages secrete TNF and cytokines which recruit more monocytes (TNF alpha is extremely important)

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13
Q

Erythema Nodosum

A

painful rash on legs in a TB patient that indicate the body is fighting the infection

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14
Q

Diagnostic methods for TB

A

acid fast stain of sputum, nucleic acid amplification test on sputum, culture on Lowenstein-Jensen solid agar, culture in liquid media

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15
Q

Initial treatment of TB

A

Isoniazid, Rifampin, Ethambutol. Pyrazinamide

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16
Q

MDR TB

A

resistance to INH and RIF is most common; seen in AIDS patients

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17
Q

XDR TB

A

resistance to INH, RIF, fluoroquinolone and one more drug.

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18
Q

Risk factors for development of resistance in TB

A

noncompliance - use directly observed therapy to combat

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19
Q

Why is the TB therapy so long?

A

slow growth of the organism, caseous material blocks penetration by drugs, organisms is intracellular, metabolically inactive organisms in the lesion

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20
Q

Progressive primary TB

A

initially looks like acute bacterial pneumonia with lobar consolidation, infiltrates, adenopathy; the tubercle can erode into a bronchus, spill its content and the infection will disseminate

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21
Q

Miliary TB

A

caused by dissemination of infection; meningitis, Pott’s dsisease/vertebral osteomyelitis, GI involvement, urinary tract involvement with sterile pyuria, lymphadenitis most common manifestation of extra pulmonary TB

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22
Q

Typical treatment length for disseminated TB

A

9-12 months using all 4 drugs

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23
Q

TB and HIV

A

low CD4 count is an important risk factor; the pulmonary manifestations are variable with false negative common and absence of granulomas; no bronchial damage and few AFB in sputum

24
Q

Difference in purified protein derivative test and the interferon gamma release assay when testing for TB?

A

the PPD can be false positive if the patient has been exposed to other Mycobacterial species; the IGRA is specific only to MTB

25
Q

Typical treatment following a positive TB test

A

INH for 6-9months or INH and Rifapentine for 3 months

26
Q

The Bacillus Calmette Guerin vaccine

A

TB vaccine used in high incidence areas, contains live attenuated mycobacterium bovid; used in US for young children with close contact to someone with TB and military personnel; contra in immunocompromised

27
Q

What is a positive PPD

A

If no risk factors: >15mm
If homeless, IVDU, nursing home resident, recent immigrant, children under 4yo: 10-15mm
If HIV, recent contact with TB, fibrotic change oN CXR consistent with prior TB, organ transplants, immunosuppressed: 5-10 mm

28
Q

TB prevention

A

prompt identification and treatment; use masks and respiratory isolation; treat latent converters; screen those at high risk

29
Q

Viruses that cause common cold

A

Coronavirus and Rhinovirus

30
Q

Rhinovirus structure

A

Picornavirus family; icosohedral, non-enveloped, positive sense single stranded linear RNA

31
Q

Coronavirus structure

A

Helical, enveloped, positive sense single-stranded linear RNA

32
Q

Rhinovirus and Coronavirus role in LRTI

A

they do not cause LRTI except for 2 coronaviruses (SARS and MERS)

33
Q

GI issues and Rhinovirus and Coronavirus

A

Rhinovirus is acid-labile so it will be killed by gastric acid rather than cause gastroenteritis; coronavirus can cause GI illness

34
Q

Most effective prevention of Rhinovirus

A

handwashing; no vaccine and no treatment due to limited course of infection and number of antigenic types; spread by direct contact and aerosols

35
Q

Rhinovirus facts

A

2-3 day incubation period, resolves in 1 week; causes minimal pathology to respiratory epithelium; pathogenesis associated with chemical mediators of inflammation that cause vasodilation, mucous secretion, stimulation of sneeze and cough reflexes

36
Q

Common complication of viral URTI

A

acute bacterial sinusitis

37
Q

Organisms that cause otitis media

A

H. influenza, S. pneumonia, M. catarrhalis

38
Q

Primary therapy for otitis media

A

Amoxicillin; if purulent conjunctivitis (H. flu) give Augmentin due to beta lactam resistance

39
Q

Diphtheria pathogenesis

A

A-B toxin blocks protein synthesis by inactivating EF-2 by ADP ribosylation, resulting in decreased protein synthesis

40
Q

Pertussis pathogenesis

A

A-B toxin stimulates adenylate cyclase by catalyzing the addition of ADP ribosylation to the inhibitory subunit of the G protein complex (inhibiting it), resulting in overactive cAMP-dependent protein kinase activity; causes decreased cilia activity

41
Q

H. flu pathogenesis

A

Produces IgA protease facilitating attachment to the mucosa; also is encapsulated and evades phagocytosis

42
Q

Rhinovirus pathogenesis

A

binds to intercellular adhesion molecule 1 (ICAM-1)

43
Q

Pseudomembrane

A

graying membrane in the throat of someone infected with diphtheria; composed of fibrinous exudate and necrotic cells; serves as platform for bacterial growth and toxin production; can extend and cause mechanical obstruction

44
Q

3 complications of diphtheria

A

mechanical obstruction, myocarditis accompanied by arrhythmias and circulatory collapse, and nerve weakness or paralysis, esp of cranial nerves

45
Q

Micro characteristics of diphtheria

A

gram positive bacillus, pleomorphic, club shaped, arranged in palisades, beaded appearance

46
Q

Diagnosis of Diphtheria

A

throat swab cultures on Loeffler’s medium, tellurite plate and blood agar; then check for toxin with antibody inoculation, antibody-based gel diffusion precipitin test, or PCR; smears of throat swab should be stained with gram stain and methylene blue (reveals typical metachromatic granules)

47
Q

Treatment for Diphtheria

A

Antitoxin administration and either penicillin or erythromycin

48
Q

Diphtheria prevention

A

vaccine (inactivated toxin) at 2,4,6 15-18 months and 4-6 years with booster at 11 and 20

49
Q

Pertussis symptoms

A

“Whooping cough,” severe cough, runny nose, malaise, hacking cough with mucus production; coughing can lead to vomiting; contagious; CBC will have lyphocytosis

50
Q

Treatment for Pertussis

A

Azithromycin can help very early in the illness to shorten duration of damage and decrease risk of transmission, but toxins damage respiratory mucosa very early

51
Q

Stages of Pertussis infection

A

Cararrhal: 2 weeks of mild URT symptoms; Paroxysmal (2-3 months): cough stage; Convalescent phase: reduction in coughing (1-2 weeks)

52
Q

Pertussis diagnosis

A

NP swab: DFA or PCR

53
Q

Pertussis toxin effects

A

causes striking lymphocytosis; inhibits signal transduction by chemokine receptors, resulting in failure of lymphocytes to enter lymphoid tissue such as spleen and lymph nodes

54
Q

Epiglottitis

A

acute inflammation in the supraglottic region of the oropharynx with inflammation of epiglottis, valleculam and arytenoids

55
Q

Causes of epiglottitis

A

H. flu usually; also H. parainfluenza, S. pneumonia, and GAS

56
Q

Typical presentation of epiglottitis

A

urban 40yo male with sore throat, odynophagia/dysphagia, muffled voice all with rapid onset

Pulmonary Block (8 decks)

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