Chapter 4: pulmonary infections

Question 1

what are the factors that predispose the host to develop pneumonia

Answer 1

viral infections damage the cilia and predispose to secondary bacterial infection
smoking damages the ciliary function
alcohol and other drugs depress coughing and epiglottal function
elderly patients have reduced humoral and cell mediated immunity, and may have impaired swallowing
because of stroke
immunosuppressed patient
patients with chronic disease
cold weather dries the mucous membranes and increases person to persons spread of infection

Question 2

what are the symptoms, signs and diagnostic tests that help differentiate viral from bacterial pneumonia

Answer 2

predominance of mononuclearis in sputum cultures is suggestive of mycoplasma
chlamydophila
or virus
predominance of PMNs is suggestive of bacterial infection

Question 3

how useful is sputum gram stain, what are the parameters that are used to assess the adequacy of a sputum sample

Answer 3

adequacy of the sample is assessed by the number of epithelia cells present, more than 10 means extensive contamination with mouth flora
more than 25 PMNs or bronchial epithelial cells per low power field indicated adequate sample

Question 4

how should the clinician interpret the sputum culture, and should sputum cultures be obtained in the absence of sputum gram stain

Answer 4

.

Question 5

how often should chest x-ray be repeated and how long do the radiologic changes associated with acute pneumonia persist

Answer 5

.

Question 6

which antibiotic regimens are recommended for elmiric therapy of community acquired pneumonia and why

Answer 6

.

Question 7

what is nonproductive cough or a cough productive of scanty sputum suggestive of?

Answer 7

atypical pneumonia

Question 8

what is a rusty-colored sputum suggestive off?

Answer 8

S. pneumoniae

Question 9

what’s the pathogenesis of pneumonia, which organisms cause permanent damage and which don’t

Answer 9

pathogens are aspirated or inhaled as small aerosolized droplets
bacterial invasion of the alveoli induces 1) edema fluid that spreads to other alveoli though the pores of Kohn, 2) infiltration by polymorphonuclear leukocytes and red bloods cells, followed by macrophages
infection spreads centrifugally(red hepatization: newer regions in the periphery; grey hepatization: older central regions)
strep pneumonia does NOT cause tissue destruction
staphylococcus aureus(usually happens in ventilator associated pneumonia), Causes permanent damage

Question 10

what is hemoptysis suggestive of

Answer 10

tuberculosis, lung abscess and lung carcinoma

Question 11

what are the things to check for during history taking in pneumonia

Answer 11

• cough: frequency, production of sputum.. color and thicccccness of sputum
• chest pain: pain on deep inspiration, usually sharp, suggest pleural involvement. seen in strep pneumoniae, staph aureus, strep pyogenes. anaerobs like coxsackievirus and chovirus
• shortness of breath: worrisome symptom; may be the result of pleuritic chest pain rather than poor gas exchange.
• epidemiology: travel history, animal exposure, exposure to people with respiratory illnesses, occupational and sexual history

Question 12

whats pleuritic chest pain classically associated with

Answer 12

S. pneumoniae. stabbing sharp pain

associated with friction rub and dull breath sounds during auscultation
since pulmonary parenchyma has no pain sensing nerves, its always associated with pleural inflammation.
diaphragmatic inflammation mimics cholecystitis or appendicitis

Question 13

bad prognostic signs on physical examination

Answer 13

respiratory rate >30/min, blood pressure <90mmhg, temperature <35and>40 and depressed mental status

Question 14

what are the patterns of pneumonia

Answer 14

typical patterns:
lobar pattern: streptococcus pneumoniae. Haemophilus influenzae and legionella
bronchopneumonia pattern: staphylococcus aureus, G- organisms, mycoplasma, chlamydophila and viral
interstitial pattern: influenza, cytomeglovirus, pneumocysitis, miliary tuberculosis
lung abscess: anaerobes, S.aureus
nodular lesion: fungal

P.s. radiographic patterns may be atypical in the immunosuppressed and AIDS patients

Question 15

what are the patterns of pneumonia

Answer 15

typical patterns:
lobar pattern: streptococcus pneumoniae. Haemophilus influenzae and legionella
bronchopneumonia pattern: staphylococcus aureus, G- organisms, mycoplasma, chlamydophila and viral
interstitial pattern: influenza, cytomeglovirus, pneumocysitis, miliary tuberculosis
lung abscess: anaerobes, S.aureus
nodular lesion: fungal

P.s. radiographic patterns may be atypical in the immunosuppressed and AIDS patients

Question 16

blood tests in pneumonia, whats associated with a bad prognosis

Answer 16

blood tests are used for people >50 years of age to assess the severity
a peripheral white blood cell count below 6000/mm3 in S. pneumoniae is a bad prognostic finding
anemia (hematocrit <30%), BUN above 30 mg/dl serum sodium below 130 mEq/L and glucose above 250mg/dl is associated with worse prognosis
arterial blood O2 below 60mmHg and pH below 7.35 worsen prognosis
two blood samples should be drawn before antibiotics are stated

Question 17

what does the predominance of PMNs suggestive of

Answer 17

bacterial infection

Question 18

what does the predominance of mononuclear cells suggestive of

Answer 18

mycoplasma
chlamydophila
or virus

Question 19

treatment of pneumonia, what you shouldn’t do

Answer 19

treatment must start within 4 hours of diagnosis, delays increases mortality
use CRB classification
empiric therapy is different for disease and patient characteristic
1) outpatient with no comorbidity and no previous antibiotics use macrolides (azithromycin or clarithromycin)

2) hospitalized patient: use a third gen cephalosporin (ceftriaxone, ceftaxime)
3) aspiration outpatient: penicillin or clindamycin
4) aspiration inpatient: third gen cephalosporin or respiraor fluroquinolone plus metronidazole

you should NOT use x-ray to monitor improvement, it takes weeks

Question 20

blood tests in pneumonia, what’s associated with a bad prognosis

Answer 20

blood tests are used for people >50 years of age to assess the severity
a peripheral white blood cell count below 6000/mm3 in S. pneumoniae is a bad prognostic finding
anemia (hematocrit <30%), BUN above 30 mg/dl serum sodium below 130 mEq/L and glucose above 250mg/dl is associated with worse prognosis
arterial blood O2 below 60mmHg and pH below 7.35 worsen prognosis
two blood samples should be drawn before antibiotics are stated

Question 21

what increases mortality rate in patients with pneumonia

Answer 21

age >65
liver disease
neoplastic disease
CHF
renal disease
cerebrovascular accident

Question 22

pathogenesis of S. pneumoniae. (Virulent factors)

Answer 22

thickcapsule prevents phagocytosis, thiccccest capsule is type 3
immunoglobulins are important opsonin that help phagocytose it
strep pneumoniae does not produce protease and seldom destroys lung parenchyma
it does not corss anatomic barriers such as lung fissures
disease manifestation are caused primarily by the hosts inflammatory response to the organism

Question 23

pathogenesis of S. pneumoniae

Answer 23

thickcapsule prevents phagocytosis, thiccccest capsule is type 3
immunoglobulins are important opsonin that help phagocytose it
strep pneumoniae does not produce protease and seldom destroys lung parenchyma
it does not corss anatomic barriers such as lung fissures
disease manifestation are caused primarily by the hosts inflammatory response to the organism

Question 24

what increases mortality rate in patients with pneumonia

Answer 24

age >65
infants
liver disease
neoplastic disease
CHF
renal disease
cerebrovascular accident

Question 25

who is specially at risk of S. pneumoniae

Answer 25

patients with opsonins deficiency:
complement deficiency
HIV
hypogammaglobinemia

Question 26

who is specially at risk of S. pneumoniae

Answer 26

patients with opsonins deficiency:
complement deficiency 
HIV
hypogammaglobinemia 
asplenic/ patients with slpeen dysfunction

patients with
cirrhosis 
alcoholism
nephrotic syndrome
CHF
COPD

Question 27

what are the clinical manifestation of S. pneumoniae

Answer 27

3 classic features:
abrupt onset and rigor(abrupt feeling of coldness and raise in temp)
rusty colored sputum
pleuritic chest pain

Question 28

how do you diagnose S. pneumoniae

Answer 28

sputum culture with more than 10 lancet shaped G+ diplococci
blood culture should always be performed
urine pneumococcal antigen test
CXR shows lobar pattern with a little pleural effusion

Question 29

treatment of S. pneumoniae

Answer 29

for penicillin sensitive strains use ampicillin and ampicillin

cephalosporins and high dose parenteral penicillin for intermediately sensitive ​strains

for highly sensitive strains use respiratory fluoroquinolone [gentiflloxacin, moxifloxacin] (except in those with meningitis, for that use vancomycin)

vaccinate those older than 65

Question 30

Haemophilus influenzae pneumonia treatment

Answer 30

G- pleomorphic(it occurs in more than one distinct form) cobacilii

treat with parenteral ceftriaxone or cefotaxime in hospitalized patients.
in outpatient: multiple oral amoxicillin-clavulanate/macrolides/fluoroquinolones are useful

Question 31

treatment of Staphylococcus aureus pneumonia

Answer 31

G+ arobic
rare, follows influenza or AIDS patient
Destructive bronchopneumonia complicated by 
lung abscesses
pneumothora
empyema

Question 32

legionella pneumonia, characteristics and clinical presentation

Answer 32

G-, found in soil (but dont form spores)

elderly, smokers and immunocompromised are at increased risk

clinical presentation
minimal presentation
confusion and headache
GI symptoms and hyponatremia

Question 33

treatment and diagnosis of legionella pneumonia

Answer 33

diagnosis
culture on buffered charcoal yeast extract agar
direct fluoresscent antibody stain (low sensetivity)
polymerase chain reaction
urinaryantigen to serotype I which is sensetive and specific

treatment of choice with azithromycin and fluroquinolone

Question 34

atypical pneumonia: causes, treatment and diagnosis

Answer 34

physical findings nonproductive cough
CXR findings are worse than physical

causes are:
mycoplasma
chlamydophila
respiratory viruses:influenza, adenovirus, RSV
treatment with macrolide or tetracycline
if influenza is diagnosed, treat with amantadine within 48h of illness

Question 35

atypical pneumonia: causes, treatment and diagnosis

Answer 35

physical findings nonproductive cough
CXR findings are worse than physical

causes are:
mycoplasma
chlamydophila
respiratory viruses:influenza, adenovirus, RSV
treatment with macrolide or tetracycline
if influenza is diagnosed, treat with amantadine within 48h of illness

Question 36

syndromes associated with aspiration and treament

Answer 36

chemical burn pneumonitis: aspiration of acidic contents, acid damage causes pulmonary capillaries to leak fluid and release cytokines and permit infiltration by PMNs, eventually cause ARDS

Bronchial obstruction resulting from aspiration of food particles

Pneumonia resulting from a mixture of anaerobic and aerobic mouth flora, especially in patients with gingivitis which have higher bacteria colony counts

treatment: penicillin for community acquired infection
third generation cephalosporin for hospital acquired infection
bronchoscopy for obstructing foreign bodies

Question 37

actinomycosis

Answer 37

G+, slow growing modified acid fast negative, microaerophillic or anaerobic
infection associated with poor oral hygene
slowly progressive infection, breaks though fascial planes, causes pleural effusions and fistula tracks, forms sulfure granules
alert clinical microbiology to hold anaerobic cultures
treatment must be prolonged high dose IV penicillin for 2-6 weeks followed by 6-12mont of oral penicillin

Question 38

nosocomial pneumonia risk factors and causative agents

Answer 38

endotracheal intubation
age >70
depressed mental status
underlying disease or malnutrition
metabolic acidosis

causes are G- bacilli and S. aureus

Question 39

how to differentiate colonization from infection in nosocomial pneumonia

Answer 39

worsening fever and leukocytosis with left shift
sputum gram stain with increased PMNs predominance of one organism
decreasing PaO2, indicative of pulmonary shunting(perfusion is fine but ventilation is fucked)
expanding infiltrate on chest radiographs

treat with broad spectrum antibiotics after blood samples are obtained

Question 40

empyema definition, when do you suspect it, organisms associated and treatment and diagnosis

Answer 40

purulent pleuritis.
suspect if fever persists after pneumonia treatment
common organisms, s pneumoniae, s. aureus, s. pyogenes and mouth anaerobes

diagnose with chest radiograph in decubitus (lying on the side) then thoracentesis
when pH is <7.2, glucose <40mg/dl, lactate dehydrogenase exceeds 1000IU/L, empyema is strongly suggested
early diagnosis and drainage prevent lung and pleural compromise
mortality is high in young patient and elderly ones

Question 41

how is tuberculosis contracted and how can the disease be prevented

Answer 41

humans are the onl reservoir of this disease.
spread by person to person aerosolized droplets
laryngeal tuberculosis is highly infectious
those people are at high risk:
immigrants
alcoholic
urban poor
single men
intravenous drug abusers
migrant farm workers
prison inmates
HIV
elderly

Question 42

what is primary tuberculosis

Answer 42

first eposure to inhaled infectious particles
flu like illness
spread is controlled over 4-8 weeks with cell mediated immunity
Ghon foci are calcified lung lesions at the site of primary infection
bacteremia develops and seeds the kidneys, epiphyses of long bones and vertebral bodies (areas with high oxygen content)

Question 43

what is reactivation tuberculosis

Answer 43

occurs in 10% of patients
most common in men 30-50
apical infection is most common (high O2)
symptoms progress slowly over months, worsening cough, sputum production, low grade fever, night sweats, fatigue and weight loss
hemoptysis or pleuritic pain indicates severe disease
CXR shows apical cavities without fluids
cavitary disease is highly infectious, isolate all patients. in HIV infection, chest doesn’t show cavities. all patients with AIDS are considered to have tuberculosis until proven otherwise

Question 44

what are the characteristics pathogenesis of tuberculosis

Answer 44

not gram stainable because of the lipid mycolic acid. acid fast bacteria because it takes red dye fuchsin

lipid wall lets the M. tuberculosis survive disinfectant and macrophages thus they are trasported wtihin the macrophages to lymph nodes where a cell mediated immune response is generated

caseating granulomas forms as a consequence of cell mediated immunity and the accumulation of lipid rich bacteria
increase in IL1 causes fever and weight loss

Question 45

what are the typical symptoms and findings in miliary tuberculosis

Answer 45

develops in very young, very old HIV patients
associated with alcoholism, malignancy, connective tissue disease, renal failure, and pregnancy

in children it presents with high fever, night sweats and weight loss, hepatosplenomegaly, and lymphadenopathy

adults show moderate to low grade fever, night sweats, malaise, anorexia, weakness, and weight loss

look for choroid tubercles (patches in the eye during fundoscopy)
micronodular interstitial pattern on chest radiographs, maybe be NEGATIVE IN HIV AND THE ELDERLY
blood samples, transbronchial biopsy, bone marrow samples and liver biopsy may all yield positive cultures

treatment for all suspected cases using 
isoniazid
rifampin
ethambutol
pyrazinamide

Question 46

how is tuberculosis diagnosed

Answer 46

ziehl-Neelsen acid-fast stain can detect 10 to the power of 4 organisms per milliliter with 60% sensitivity
release of acid-fast bacilli from cavity lesions is intermittent. to ensure low infectivity, three negative smears are needed.
culture remains the most sensitive, it grows slowly (1/20th speed of normal bacteria), automated techniques detects within 9-16days
PCR should be performed

Question 47

why should combination anti tuberculous therapy always be prescribed in active tuberculosis

Answer 47

reduce the selection into resistant strain (reduce resistance).
to reduce secondary resistance (resistance in someone who already received treatment before DOT is recommended [Directly observed therapy])
treatment for all suspected cases using
isoniazid
rifampin
ethambutol
pyrazinamide

Question 48

what does having a positive PPD or interferon gamma test mean, and how should an individual with a positive test be treated

Answer 48

PPD (purified protein derivative) test[a test that says you’re positive for M. tuberculosis only if] the followig is met:

• positive test at more than 5mm in HIV or immunocompromised patients
• more than 10mm in people at over all risk of exposure
• more than 15 in people with no risk factors

Interferon gama test has similar sensetivity (watch a youtube about this whole card, im confused)

Question 49

what are the characteristics pathogenesis of tuberculosis

Answer 49

no gram stainable because of the lipid mycolic acid. acid fast bacteria because it takes red dye fuchsine

lipid wall lets the M. tuberculosis survive disinfectant and macrophages thus they are transported within the macrophages to lymph nodes where a cell mediated immune response is generated

caseating granulomas forms as a consequence of cell mediated immunity and the accumulation of lipid rich bacteria
increase in IL1 causes fever and weight loss