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
Q

TB course

A
  • 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
Q

Miliary TB

A
  • 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
Q

Granulomatous lung disease

A
  • TB is classic
  • fungal infections (esp. histoplasmosis in ohio) –> not necrotizing, not a caseous look
  • sarcoidosis
28
Q

Lung cancer facts

A
  • leading cause of cancer deaths
  • risk factors: smoking***** (prevalent for our parents age, asbestos, radon gas, nickel, chromates, pollutants, lung scar)
29
Q

why is lung cancer the leading cause of cancer death?

A

late stage detection

5 year survival for all types is 16%, if its localized then 45% survival rate

30
Q

cancer death rates vs. smoking

A

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
Q

lung cancer clinical

A

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
Q

lung cancer pathology

A

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
Q

pneumoconioses

A

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
Q

pneumoconoses pathology

A

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
Q

silicosis

A

worldwide, most prevalent form of occupational disease

minning etc..

36
Q

abestos bodies

A

inhaled abestos particles covered in iron, found on a radiograph on people with mesothelioma