PBL #5 Flashcards

1
Q

What are the causes of pulmonary nodules?

A
  • Malignant neoplasms:
    • non-small cell lung cancer, Small cell carcinoma, Solitary metastasis, Primary pulmonary lymphoma, Primary pulmonary carcinoid, Malignant teratoma, Pulmonary blastoma
  • Benign neoplasms:
    • Hamartoma, Chondroma, Hemangioma, Arteriovenous malformation, Fibroma, Neural tumor, Sclerosing hemangioma
  • Infections:
    • Granulomatous infections: T, histoplasmosis, coccidioidomycosis, blastomycosis, cryptococcosis, pulmonary aspergilloma
    • Bacterial infection: nocardiosis, antinomycosis, round pneumonia
  • Measles
  • Septic emboli
  • Abscess
  • Congenital causes: bronchogenic cyst, bronchial atresia w/ mucoid impaction, sequestration
  • Other stuff: amyloid, sarcoidosis, RA, granulomatosis with polyangiitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the prevalence of pulmonary nodules?

A
  • Solitary pulmonary nodule found on up to 0.2% of all chest films
  • Lung nodules found on up to 50% of all lung CT scans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the significance of calcification and cavitation of a pulmonary nodule?

A
  • Calcification:
    • Usually indicates a benign disease.
    • Benign patterns of calcification: central nidus, laminated, diffuse, popcorn.
      • If it has 1 of these 4 patterns and is < 3 cm, it is most likely benign.
  • Cavitation:
    • gas-filled area on the lung in the center of a nodule or area of consolidation (lung tissue filled with water)produced by the expulsion of a necrotic part of a lesion
    • Noninfectious disease associations: Malignancy, granulomatosis with polyangiitis (Wegener’s), pulmonary infarct due to embolism.
    • Infectious associations: Necrotizing pneumonias and lung abscesses, Mycobacterium tuberculosis, Fungal infections, septic emboli.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the organisms responsible for pulmonary infections in HIV+ patients with normal CD4+ counts?

A
  • Strep. Pneumoniae
    • Gm positive, Catalase neg, Alpha Hemolytic, Bile-Esmulin negative, Optochin Susceptible, Quellung positive, IgA Protease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the organisms responsible for pulmonary infections in HIV+ patients with CD4+ counts less than 200?

A
  • Pneumocystis jirovecii pneumonia (PCP)
  • Histoplasmosis (Histoplasma capsulatum)
    • Fungus found in bird/bat fecal material, and soil.
  • Toxoplasmosis (Toxoplasma gondii Encephalitis)
    • Parasite that usually comes from cats (they can only reproduce in cats → shed in cat’s feces )
  • Invasive Aspergillosis (Aspergillus)
    • common mold (a type of fungus) that lives indoors and outdoors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the organisms responsible for pulmonary infections in HIV+ patients with CD4+ counts less than 50?

A
  • Mycobacterium avium infection
  • Interstitial Pneumonia- CMV
    • Cytomegalovirus, HHV-5, dsDNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the agents that can cause TB?

A
  • M. tuberculosis - cause great majority of human disease
  • M. africanum - causes human tuberculosis (TB) in tropical Africa
  • M. bovis - primarily isolated from cattle but causes 1%-2% of TB disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the parameters of a tuberculin test (define PPD)? How are they interpreted?

A
  • PPD test for purified protein derivative
  • 5+ mm is positive in:
    • HIV-positive person
    • Persons with recent contacts with a TB patient
    • Persons with nodular or fibrotic changes on chest X-ray consistent with old healed TB
    • Patients with organ transplants, and other immunosuppressed patients
  • 10+ mm is positive in:
    • Recent arrivals (less than five years) from high-prevalence countries
    • IV drug users
    • Residents and employees of high-risk congregate settings (e.g., prisons, nursing homes, hospitals, homeless shelters, etc.)
    • Mycobacteriology lab personnel
    • Persons with clinical conditions that place them at high risk (e.g., DM, prolonged corticosteroid therapy, leukemia, ESRD, chronic malabsorption syndromes, etc.)
    • Children <4 yoa, or children & adolescents exposed to adults in high-risk categories
  • 15 mm or more is positive in:
    • Persons with no known risk factors for TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you calculate and interpret a positive predictive value?

A
  • Calculate PPV:
    • TP/(TP + FP)
  • IF PPV is high → more likely that the patient actually has the condition he/she has tested positive for
    • ​PPV increases in high prevalence settings
  • IF PPV is low → more likely that your patient has tested FALSELY positive, and does not actually have the condition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the MOA of Isoniazid?

A
  • inhibits the synthesis of mycolic acids (essential component of bacterial cell wall)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the MOA of Rifamycins?

A
  • Inhibits DNA-dependent RNA polymerase.
  • Four R’s:
    • Ramps up P-450
    • Red body fluids
    • Rapid resistance
    • RNA polymerase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the MOA of Pyrazinamide?

A
  • Unknown.
  • Thought to acidify intracellular environment via conversion to pyrazinoic acid.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the MOA of Ethambutol?

A
  • Decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the MOA of Pyridoxine?

A
  • Vitamin B6 supplement
  • Given with Isoniazid to prevent neurotoxicity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the MOA of Streptomycin?

A
  • Protein synthesis inhibitor:
    • binds to the small 16S rRNA of the 30S subunit of the bacterial ribosome
    • causes codon misreading
  • Inhibits both Gram-positive and Gram-negative bacteria (bactericidal)
  • First aminoglycosides discovered.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the MOA of HIV Protease Inhibitors? Examples?

A
  • Example Drugs: Ritonavir, Indinavir, Amprenavir, Saquinavir, Lopinavir, Tipranavir, Atazanavir
    • End in –navir
  • MOA: Blocks HIV Protease → unable to cleave HIV polypeptide into functional groups.
17
Q

What is the MOA of HIV Nucleoside Reverse Transcriptase Inhibitors (NRTIs)? Examples?

A
  • Example Drugs: Zidovudine (AZT), Abacavir, Emtricitabine, Lamivudine
  • MOA: Inhibits Reverse Transcriptase which prevent conversion of HIV RNA → cDNA.
    • require phosphorylation to be active
18
Q

What is the MOA of HIV Nucleotide Reverse Transcriptase Inhibitors (NRTIs)? Examples?

A
  • MOA: competitively inhibit nucleotide binding to reverse transcriptase
    • incorporated into viral DNA chain → causing termination
    • requires phosphorylation to become active
  • Example: Tenofovir
19
Q

What is the MOA of HIV Non-Nucleotide Reverse Transcriptase Inhibitors (NNRTIs)? Examples?

A
  • MOA: bind directly to reverse transcriptase and inhibit enzyme production of viral DNA
  • Examples: Efavirenz, Etravirine
20
Q

What is the MOA of HIV Integrase Inhibitors? Examples?

A
  • MOA: binds to integrase → inhibiting strand transfer and the final step of provirus integration
  • Examples: Raltegravir
21
Q

What is the MOA of HIV CCR5 Antagonists? Examples?

A
  • MOA: Binds CCR5 receptor on surface of T-cells → inhibiting interaction with gp120 on HIV
  • Examples: Maraviroc
22
Q

What is the MOA of HIV Fusion Inhibitors? Examples?

A
  • MOA: Binds gp41 on viral envelope → inhibiting conformational change/viral fusion
  • Examples: Enfuvirtide
23
Q

What does public health surveillance for TB consist of?

A
  • Immigrants moving to the US undergo a health screening, specifically children must meet the following requirements for TB.
  • <2 years old: No tests unless child has signs or symptoms of TB or has been in contact with a person with TB.
  • 2-14 years old: (tuberculin skin test) TST or (interferon-gamma release assay) IGRA* (if positive) → Chest X-ray* (if positive) → sputum smear and cultures (if positive) → DST (drug sensitivity testing) → DOT (daily observed therapy)
  • 15 years old & up: Chest X-ray* (if positive) → sputum smear and cultures (if positive) → DST → DOT
24
Q

What are the Minnesota reporting requirements for latent TB and active TB?

A
  • Latent TB not a reportable condition in MN
  • Active TB (confirmed and suspected cases) reportable condition in MN
    • Confirmed or suspected cases must be reported in <24 hrs
      • Isolation of M. tuberculosis
    • Both pulmonary and extrapulmonary cases reportable
25
Q

What is some of the evolving genetic testing being used as new drugs are developed to target HIV?

A
  • HIV Drug Resistance Testing
    • standard genotypic testing: looking for mutations in reverse transcriptase (RT) and protease (PR) genes
    • genotypic testing of integrase and envelope proteins if this is a concern
  • HIV resistance testing
    • CCR5 Mutation Homozygotes are resistant to ONLY R5 Tropism of HIV
    • CCR5 Mutation Heterozygotes have slower progression of ONLY R5 Tropism
  • HLA-B*5701 testing is recommended for any patients who are going to be put on Abacavir (NRTI used to treat HIV) to avoid Hypersensitivity Reactions.