Pulmonary Path 2 Flashcards

1
Q

Pulmonary infections

A

pneumonia, acute resp distress syndrome, pulmonary abscess and TB

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2
Q

Pneumonia

A

one of the leading causes of death, often complicates other chronic debilitating diseases
-any organism can cause pneumonia (bac common, viral, fungal (immunocomp pts.), parasites)

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3
Q

bacterial pneumonia predisposing factors

A

loss of cough reflex, injury to cilia and decreased phagocytosis (all 3 above from smoking) pulmonary edema, immunocomp condition (ex. pregnancy complication)

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4
Q

clinical presentation

A

cough, dyspena, fever, chills, sputum production (blue/green from myloperoxase and neutrophils but also bloody from destruction)

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5
Q

bronchopneumonia

A

patchy, begins around the small bronchi

-common in the very young and very old

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6
Q

lobar pneumonia

A

involves the entire lobe

  • happens in healthy adults
  • strep pneumonia is the cause in 90% of cases
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7
Q

2 forms of bacterial pneumonia

A

bronchopneumonia and lobar pneumonia

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8
Q

2 stages of the infammatory process in LOBAR pneumonia

A
  1. congestion - increased red blood cells with (WBC) neutrophils that start to fill the air spaces
  2. red hepatization - purulent exudate with many RBC (looks like the liver)
  3. gray hepatization - rbc lyse and get taken out and replaced with exudate with fibrin and macrophages
  4. resolution - doesn’t completely repair - the air spaces will open and the scaring will be in the interstitium
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9
Q

complicaitons of pneumonia

A

abcess, pleuritis, pericarditits (lung wrapped around teh heart) and bacteremia (because there is so much vascularization

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10
Q

interstitial/atypical/walking pneumonia

A

seen with mycoplasma pneumonia and viruses

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11
Q

clinical interstitial pneumonia

A

highly variable - fever, DRY cough (b/c no PMNs), myalgia (mm. cramps) to life threatening

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12
Q

pathologay of interstitial pneumonia

A
intersitital inflammation (in the walls), mononuclear cells (macrophages), congestion and hyaline membrane (diffuse alveolar damage)
-pneumocytes (type 1 ) can be injured by macros and neutrophils and cause hyaline membrane formation
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13
Q

Acute Respiratory Distress Syndrome (ARDS)

A

rapidly developing serious condition with same histologic features as interstitial pneumonia

  • serious complication of that has many triggers
  • *can cause death in a few days
  • 30% mortality
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14
Q

what causes ARDS?

A

many triggers

shock (ex. prego complications), infections, trauma (ex. vehicle accident), drug overdoses, irritants etc..

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15
Q

pathology ARDS

A

injury to endothelium and alveolar epithelium and increased endothelial permeability

  • cytokines activate “ases” and macrophages so shit is ripped up like bronchial epithelium and hyaline membranes form
  • alveolar spaces are there, but all the type 1 pneumocytes are damaged and the type 2 are trying to regenerate and fill in the spaces
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16
Q

clinical pulm abscess

A

cough, fever, purulent sputum (PMN, possibly blood)

** pulm abcess have air-fluid lines on a radiograph dileniating where the pus is vs. air

17
Q

predisposing factors pulm abcess

A

bronchiectasis, aspiration, septic emboli, airway ob, dental sepsis (aspiration form procedures)
**harder to cause an abcess in the lung than in the mouth from say an extraction

18
Q

course of a pulm abcess

A

scar, cavitate, progressively enlarge

-cavities will only heal through scarring, tissue not coming back

19
Q

TB frequency

A

myobacterium tuberculosis

  • 1/3 of the world infected - most infectious cause of death in the world (3 million deaths/yr)
  • in 80s (with HIV) the US cases rose, but since 1992, have been declining
20
Q

exceptions to TB decline in frequency in the US

A

HIV infections (immunocomp), overcrowding, poor living conditions, patches of immigrant populations

21
Q

myobacterium tuberculosis

A

acid fast bacillus (rod), aerobe, non-motile, slow groeht

  • waxy coat that is resistant to acid destaining (but we have a special stain to find it in the tissues
  • caseating (cheesy) granulomatous inflammation - tissue reaction
22
Q

pathology TB

A

casseating granuloma (multinuc giant cells)

23
Q

TB pathogenesis

A
  • almost always airborne (inhalation) b/c bacillus 3-4 micros in size
  • Ghon lesion (site of early infec) - inflammation trying to wall off the infection in the lung
  • Ghon complex (lung lesion + hilar lymph nodes) - nodes are the secondary area of infection from spread of bacteria
24
Q

cavitary TB

A
  • apex of the lung
  • when destruction out weighs the isolation of the granulmoa
  • significant scarring (can only heal through scarring, will not regen)
  • this much destruction may seed the large airways, lymph nodes or blood (bacteremia)
  • -> sputum from the airways may lead to TB infection in the mouth
  • direct extension to the pleura (thickening) - effusion
25
TB course
- may become inactive or progress (90-95% of primary cases (single foci) resolve) - may reactivate if immunity wanes - -> reactivation leads to type IV hypersens and tissue necrosis (cavities may form) - -> may widely disseminate (Mililary TB has multi organ involvement)
26
Miliary TB
- from spread via the lymphatics or blood (lymphohematogenous) - "millet seeds" are like small granulomas that take over the organ - other lung, CNS, kidney, adrenals, bones, bone marrow, liver and spleen
27
Granulomatous lung disease
- TB is classic - fungal infections (esp. histoplasmosis in ohio) --> not necrotizing, not a caseous look - sarcoidosis
28
Lung cancer facts
- leading cause of cancer deaths - risk factors: smoking***** (prevalent for our parents age, asbestos, radon gas, nickel, chromates, pollutants, lung scar)
29
why is lung cancer the leading cause of cancer death?
late stage detection | 5 year survival for all types is 16%, if its localized then 45% survival rate
30
cancer death rates vs. smoking
1990 - peak for men, 2000 - peak for women in deaths, which correlates with smoking "fad" and decline ** women later because of the thought, "if men can do it, we can do it"
31
lung cancer clinical
cough, weight loss, chest pain, hemoptysis, dyspnea - tumors can produce hormones (or hormone-like susbtances) --> paraneoplastic syndrome, ADH, ACTH, PTH and others ex. PTH will produce hypercalcemia to lead to seizures or bone resorption
32
lung cancer pathology
squamous cell carcinoma and adenocarcinoma (make up half of lung cancers) are the leading causes, but also small cell and large cell and mesothelioma pleural malignancy (abestos assoc)
33
pneumoconioses
group of lung disorders caused by inhalation of dusts/particles -size, shape and concentration of the particles is important (1-5 micron diameter are the most dangerous, smoke particles are this size) -induce fibrosis, esp if particles inhaled in large amount and macrophages can't keep up (scarring)
34
pneumoconoses pathology
usually from occupational and environmental causes - coal workers pneumoconiosis --> nodular or diffuse fibrosis with coal macules, progressive massive fibrosis - abestos and some drugs (drugs are not inhaled, but the fibrosis is the same)
35
silicosis
worldwide, most prevalent form of occupational disease | minning etc..
36
abestos bodies
inhaled abestos particles covered in iron, found on a radiograph on people with mesothelioma