Chapter 4: pulmonary infections Flashcards

(49 cards)

1
Q

what are the factors that predispose the host to develop pneumonia

A

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

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2
Q

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

A

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

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3
Q

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

A

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

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4
Q

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

A

.

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5
Q

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

A

.

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6
Q

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

A

.

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7
Q

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

A

atypical pneumonia

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8
Q

what is a rusty-colored sputum suggestive off?

A

S. pneumoniae

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9
Q

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

A

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

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10
Q

what is hemoptysis suggestive of

A

tuberculosis, lung abscess and lung carcinoma

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11
Q

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

A
  • 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
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12
Q

whats pleuritic chest pain classically associated with

A

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

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13
Q

bad prognostic signs on physical examination

A

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

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14
Q

what are the patterns of pneumonia

A

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

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15
Q

what are the patterns of pneumonia

A

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

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16
Q

blood tests in pneumonia, whats associated with a bad prognosis

A

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

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17
Q

what does the predominance of PMNs suggestive of

A

bacterial infection

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18
Q

what does the predominance of mononuclear cells suggestive of

A

mycoplasma
chlamydophila
or virus

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19
Q

treatment of pneumonia, what you shouldn’t do

A

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

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20
Q

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

A

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

21
Q

what increases mortality rate in patients with pneumonia

A
age >65
liver disease
neoplastic disease
CHF
renal disease
cerebrovascular accident
22
Q

pathogenesis of S. pneumoniae. (Virulent factors)

A

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

23
Q

pathogenesis of S. pneumoniae

A

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

24
Q

what increases mortality rate in patients with pneumonia

A
age >65
infants
liver disease
neoplastic disease
CHF
renal disease
cerebrovascular accident
25
who is specially at risk of S. pneumoniae
patients with opsonins deficiency: complement deficiency HIV hypogammaglobinemia
26
who is specially at risk of S. pneumoniae
``` patients with opsonins deficiency: complement deficiency HIV hypogammaglobinemia asplenic/ patients with slpeen dysfunction ``` ``` patients with cirrhosis alcoholism nephrotic syndrome CHF COPD ```
27
what are the clinical manifestation of S. pneumoniae
3 classic features: abrupt onset and rigor(abrupt feeling of coldness and raise in temp) rusty colored sputum pleuritic chest pain
28
how do you diagnose S. pneumoniae
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
29
treatment of S. pneumoniae
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
30
Haemophilus influenzae pneumonia treatment
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
31
treatment of Staphylococcus aureus pneumonia
``` G+ arobic rare, follows influenza or AIDS patient Destructive bronchopneumonia complicated by lung abscesses pneumothora empyema ```
32
legionella pneumonia, characteristics and clinical presentation
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
33
treatment and diagnosis of legionella pneumonia
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
34
atypical pneumonia: causes, treatment and diagnosis
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
35
atypical pneumonia: causes, treatment and diagnosis
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
36
syndromes associated with aspiration and treament
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
37
actinomycosis
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
38
nosocomial pneumonia risk factors and causative agents
``` endotracheal intubation age >70 depressed mental status underlying disease or malnutrition metabolic acidosis ``` causes are G- bacilli and S. aureus
39
how to differentiate colonization from infection in nosocomial pneumonia
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
40
empyema definition, when do you suspect it, organisms associated and treatment and diagnosis
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
41
how is tuberculosis contracted and how can the disease be prevented
``` 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 ```
42
what is primary tuberculosis
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)
43
what is reactivation tuberculosis
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
44
what are the characteristics pathogenesis of tuberculosis
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
45
what are the typical symptoms and findings in miliary tuberculosis
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 ```
46
how is tuberculosis diagnosed
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
47
why should combination anti tuberculous therapy always be prescribed in active tuberculosis
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
48
what does having a positive PPD or interferon gamma test mean, and how should an individual with a positive test be treated
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)
49
what are the characteristics pathogenesis of tuberculosis
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