Lungs Flashcards
Q8. PULMONARY THROMBOEMBOLISM (99% of all PE)
- WHAT IS THE VIRCHOW’S TRIAD?
- MOST COMMON IN WHICH PATIENTS?
- PULMONARY INFARCTION
- COMPLICATIONS, RESOLUTION, PREVENTION
- Blood stasis
- Endothelial injury
- Hypercoagulability
–> immoblized, hospitalized patients, post-surgery & post-op patients, those with mlg tu (e.g. paraneopl sy – thrombophilic state), DVT, DIC, NBTE, CHF etc. – thrombogenic states
- Massive emboli
- Submassive emboli
- Small emboli
- Successive/repeated small emboli
Pulmonary infarction is rare (10%) due to dual circulation, collateral blood supplies.. Occurs with obstruction at small pulmonary arteries at periphery where it’s less supplied by bronchial aa. –> wedge shaped infarction w. tip at obstructed a. and base at surf (pleura).
–> alway hemorrhagic! (+bowel)
Complications = infarcted tissue vulnerable to secondary infections – suppurative infl. –> septic infarction, abscess formation.
Resolution = small emboli may dissolve spontaneously by fibrinolysis
Larger emboli = organization - mature CT, fibrosis.. + remnants - post-embolic bridges
Prevention = movement, be active esp. hospitalized patients.. to prevent blood stasis, risk of thrombosis etc.
(chronic thromboembolism - may sclerosis of PA)
Q9. PULMONARY HYPERTENSION
> 25-30mmHg
causes:
- recurrent PE, lung disorders eg. COPD
- LH failure, mitral stenosis, systemic HTN
- Congenital heart disorders e.g. ASD
- chest disorders e.g. kyphscoliosis
- high altitudes - hypoxia, obesity etc.
primary PH (1%) = unknown, idiopathic secondary PH (99%) = known
e.g. lung disorders –> hypoxia –> pulmonary vasoconstriction (shunt blood away to health lung tissue, problematic if widespread e.g. emphysema) –> PH…
Consequences:
1. High PH (lung edema) –> RV hypertrophy –> Cor Pulmonale (RH failure)
2. Vascular alterations in entire arterial tree:
- large/medium sized vessels –> SM hypertrophy, intima and media thickening - narrows lumen (intimal damage can –> atherosclerosis?, main elastic a - atheroma)
– PA = ‘sclerosis’ - intimal yellowish plaques (arteriosclerosis)
- small arteries/arterioles –> thickening and medial hypertrophy
- in severe case can form plexiform lesions with several lumina in PA = a tuft of capillary formations/network.
– fatigue, dyspnea, chest pain, syncope (specific ones related to underlying causes).
Q10. RESPIRATORY DISTRESS SYNDROME
- ADULT RESPIRATORY SYNDROME (ARDS) - clinical
DAD = DIFFUSE ALVEOLAR DAMAGE - pathological/morphological term
ARDS
- disorder of dyspnea, difficult gas exchange (cyanotic..)
- infiltration of alveolar septa, belongs interstitial group
- damage to capill endoth.- alveol. ep barrier –> diffuse entire lung affected
- uniform effect but many etiologies!
e. g. any shock state ‘shock lung’, trauma, burns, sepsis, DIC, viral infections, aspiration (gastric content, near-drowning), toxic gas inhalation, drugs e.g. heroin, irradiation, diabetic ketoacidosis/coma, air/amniotic/fat embolism, acute pancreatitis etc.
–> increased capillary permeability (dilated, hyperemic) – edema, leakage of protein rich fluid esp. fibrinogen into alveoli +/- necrotic /desquamated alv. ep cells –> infiltration into septa, interstitium –> formation of a fibrinous membrane = ASPHYXIAL/HYALINE membrane lining alveoli - diagnostic of ARDS. Impedes gas exchange.
SUBACUTE = if patient survives - prolif. of type II pneumocytes in attempt to regenerate damaged alveolar ep. - epithelisation.
CHRONIC = hyperemia, dilated capillaries –> fibrotic thickness of alv. septa (membs) covered by type II pneumocytes, lymphocytic infiltration..
contents in alveoli + hylaine membs - organized w. GT –> fibrosis (carnification) - obstruction of alveoli…
- macro = decreased air, heavy, deep red. Chronic - solid, hard and fibrotic.
- complication - 50% die in acute phase, 50% in interstitial fibrosis
Q10. RESPIRATORY DISTRESS SYNDROME
- RDS in neonates = ASPHYXIAL/HYALINE MEMBRANE DISEASE
- lack of surfactant so leads to collapsing of alveoli
- esp. in premature babies <1500g
- normally production of alveoli by week 35 (phosphatidylcholine, lecithin)
- causes dyspnea, requires artificial ventilation, if baby dies soon after birth - histological pic of acute DAD - eosinophilic hyaline membs.
- lung consolidated like liver.
- give oxygen but may develop latent lung fibrosis –> bronchopulmonary dysplasia.
causes;
- maternal diabetes –> insulin decreases surfactant production
- caesarian section –> loss of stress-induced labor stimulation that produce steroids - increases synthesis of surfactant.
clinical and complications:
- increased resp effort after birth, tachypnea w use of accessory muscles, grunting
- hypoxemia w cyanosis
- diffuse granularity of lung on x-ray
- hypoxemia increases risk for persistence of patent ductus arteriosus & necrotizing enterocolitis
- supplemental oxygen - increase risk for free radical injury –> blindness, bronchopulmonary dysplasia.
COPD - what diseases?
- Chronic bronchitis
- Emphysema
- -> both associated w. cigarette smoking - Bronchial asthma
- -> allergy
Q12. CHRONIC BRONCHITIS
- chronic obstruction/inflammation of bronchus caused hypersecretion of mucus (mucus plugs) from hyperplasia of gls.
- normally bronchi lined ciliated columnar ep. w gls in submucosa + cartilage underneath (bronchioles don’t)
- e.g. cigarette smoking, foreign pollutants etc. causes hyperplasia of mucus glands measured by Reid’s index
- inflammation – lymphocytic infiltration
clinical
- chronic, productive cough (mucus) for 3 months in 2 consecutive years; morning cough.
- dyspnea, cyanosis –> ‘blue bloaters’ (discoloration)
3 forms:
1. Simple - most patients, coughs up mucus w/o obstruction
2. Mucopurulent - COPD usu. associated w. emphysema in heavy smokers, chronic obstruction
3. Asthmoid/asthmatic - hyper-responsive airways w. intermittent bronchospasms & wheezing.
complications
- increased risk of suppurative secon. infection behind block esp. Staph aureus, Klebsiella pneumoniae
- lung hypoxia –> vasoconstriction - PH - cor pulmonale..
- repeated injury - metaplasia of col.ep to sq. ep –> sq. cell Ca.
- severe bronchiolitis obliterans due to fibrosis
- eventu. mucosa gets thinner, atrophy of gls. - can see underlying cartilage = chronic atrophy bronchitis - can lead to bronchiectasis.
Q13. EMPHYSEMA
causes different forms macro, micro clinical complications
- Hyperinflation of alveoli, difficult expiration +/- chronic obstruction –> may rupture, decrease gas exchange.
- Before it was regarded as passive accumul. of air behind obstruction (mucus plugs).. BUT shown it is also an active mechanism - neutrophils produce proteases to digest intraalev. septa.
Causes:
- Often associated w. chronic bronchitis (COPD), infection behind obstruction/air accumul. behind
- Increased proteases/elastases produced by neutrophils in response e.g.
- infection, inflammation
- smoking!
- -> causes CENTRIACINAR emphysema, more severe in upper lobes - A1AT deficiency (decreased anti-trypsin)
- -> causes PANACINAR emphysema, lower lobes mainly. May also cause liver cirrhosis (misfolded protein still produced by liver, accumul in ER, damages hepatocytes).
- Typical form = VESICULAR emphysema
- More severe form = BULLOUS emphysema - several cms, cyst like dilatation (bubbles); risk of rupture –> pneumothorax.
- INTERSTITIAL emphysema = when septum ruptures, air enters interstitium happens at severe coughing + a complication of artificial ventilation (pressure). Autopsy - bubbles can be seen in pleura, even mediastinum.
- Other types: Irregular, Compensatory etc.
Macro = porous, spongy Micro = destroyed alv. septa, confluent - large air spaces
Clinical
- dyspnea, cough w. min sputum
- ‘pink puffers’
- weight loss, barrel chest
Complications
- alv. rupture, loss of pulmo. cap –> hypoxemia
- hypoxemia – PH –> Cor pulmonale
Q14. BRONCHIAL ASTHMA
NB. initially reversible, later not?
- In recent years also obstructive, obstructive exhalation
- characterized by bronchoconstriction, attacks of dyspnea, paroxysmal history, wheezing and productive cough.
- Can have severe attacks that last hrs or even days! = ‘ASHTMATIC STATE’ (‘status asthmaticus’)
- It is a type 1 allergic reaction mediated by IgE and mast cells; freq begins as a childhood atopic disease.
- exposure to e.g. food, dust, feathers, pollen etc.
- Can be dues to a combination of
- Early phase –> direct stimulation of subep. vagal receptors + mast cells release mediators e.g. histamines, leukotriens etc. resulting in:
- reflexive bronchoconstriction
- inflammation, edema (increased vasc. permeability)
- mucus secretion - Late phase (4-24hrs)
- release of cytokine –> attracts more leukocytes esp. EOSINOPHILS!
- damages airway ep. (esp major basic protein - toxic)
Complications:
- increase PH –> tendency to chronic cor pulmonale
- ‘acute emphysema’ in autopsy (as bronchi- full of mucus + bronchospasms = obstruction)
- in mucus see ‘CURCHMAN’S SPIRALS’ (detached ep)
- histo - features of chronic bronchitis, eosinophils! –> CHARCOT-LEYDEN crystals (breakdown of eosinophils, granules).
–> bronchodilators/inhalators, corticosteroids etc. + avoid allergen contact.
Q15. BRONCHIECTASIS
- permanent dilation of bronchi & bronchioles –> loss of airway tone resulting in air trapping.
- usu. a secondary disease assoc. w chronic inflammation.
- due to inflammation w. damage to airway walls –> dilation of airways –> mucus stasis –> purulent infection –> more damage… vicious cycle.
pathogenesis –> 1. obstruction 2. chronic persistent infection
causes:
- bronchial obstruction e.g.tumors - bronchial Ca, foreign bodies, mucus.
- can complicate atopic asthma & chronic bronchitis - congenital/hereditary e.g. CF - mucus plugs in bronchi (common cause of death in children - bronchiect. & cor pulmonale)
- immunodeficiency states
- necrotizing/suppurative inflammations e.g. post-pneumonia, TB, aspergillosis etc.
Types:
- Diffuse
- Saccular - in extreme cases, a system of cavities formed ‘honeycomb lung’.
- Spindle
Clinical = cough, dyspnea, foul-smelling sputum, clubbing of fingers... Complications = hypoxemia w. cor pulmonale, secondary amyloidosis AA, brain abscesses (less freq) etc.
Q11. SIDS - SUDDEN INFANT DEATH SYNDROME
NB. ATELECTASIS (know)
- Sudden (unknown, unexpected) death of infant up to 1 yr = ‘cot/crib death’, usu. during sleep.
- highest incidence at 4th month
- rule out any other causes e.g. milk aspiration, congenital disorders etc.
Possible causes:
- prolonged asyphyxia
- maybe arrhythmia, delayed development in cardioresp control, arousal (arcuate nucleus)/disorder
- petechiae is a sign of suffocation
- a theory - common apneic phase in infants but if prolonged & doesn’t resume…
- put face down into pillow
- mothers who smoke dur. pregnancy harm baby’s brain (80% found dur. and post-partum)
morph - slightly obese, enlarged thymus, congested lungs, petechiae…
Q16. PULMONARY INFECTIONS
WHICH ONES?
Can talk about:
- TB
- Pneumonia
- Sarcoidosis
- Legionnaire disease
- Pneumocystic pneumonia (P.carnii)
- Dimorphic fungi - Histoplasmosis, Coccidioidmycosis, Blastomycosis
- Idiopathic interstitial fibrosis - Hamman rich sy
Q17.Q18
LOBAR PNEUMONIA VS. BROCHOPNEUMONIA
(both superficial, other type = interstitial)
Pneumonia = v. common esp in hospitalized patients due to prolonged bed rest, position interferes w. normal lung function.
LOBAR pneumonia
- can appear as primary disease affecting healthy lung.
- strep. pneumoniae (95%) suppurative inflammation + fibrinous exudate (5% Klebsiella)
- diffuse, affecting part/all lobe + sharp demarcation bet. healthy & affected w. fibrinous infl.
- less common
- alveoli full filled w neutrophils, fibrin (due to increased cap perm), bacteria, macrophages
- 4 stages
1. Congestion
2. Red hepatization
3. Gray hepatization
4. Resolution
(infl. edema can spread rapidly throughout whole lobe due to pores of Kohn) - risk groups = chronic disease e.g. COPD, immunological disorders, decreased/absent splenic function.
- complications:
1. supprative/fibrinous pleuritis –> empyema/pyothorax
2. abscesses
3. carnification
BRONCHOpneumonia
- often a secondary disease, a complication esp. those immunocompromised, prolonged bed rest etc.
- gram +/- ve bacteria e.g. strep, klebsiella, pseudomonas, H.influenzae etc
- starts w. supprative infl. of bronchi/bronchioles w neutrophils in lumen (pus), then infiltrates into parechyma
- patchy/nodular infiltrate generally involving more than one lobe; no sharp demarcation
- more common
- gross = empty alveoli (concentric spread outwards)
- less neutrophils, fibrin (alv. memb less permeable)
- types: noscomial pneumonia, aspiration (common w. alcholics), terminal, hypostatic (poorly dilating parts exposed e.g lower lobes, dorsal), dystelectatic, bronchostenotic (e.g. tu, infection behind stenosis)
- -> so e.g. death at flu! influenza injuring bronchi - bronchopneumonia..
- less common pleuritis, pyo/pneumothorax but may have abscesses and carnification
WHAT IS INTERSTITIAL/ATYPICAL/COMMUNITY-ACQUIRED PNEUMONIA?
- Interstitial pneumonia restricted to septa/interstitium.
- ‘round infiltrate’
- causative agents e.g. Mycoplasma pneumonia, viruses (non-bacterial - more common), Chlamydia pneumoniae, Coxiella burnetti, Pneumocystic carnii.
- less common that superficial
- diffuse and bilateral
- alveolar free of exudate
- red-blue congested, can vary from chest cold, sever URT infection to fulminant life threatening.
NB. ARDS in an interstitial pneumonia
Q19. Tuberculosis
Final notes
PRIMARY - usu childhood
bacteria in –> macrophages, multiply –> cell-mediated immunity - granulomas w. central casseous necrosis –> Ghon focus –> hilar LN - casseating + lymphadenopathy = gohn complexes (usu. subpleural, lower lobes) –> undergoes fibrosis and carnification –> Ranke complexes
So usu. viable bacteria usu. walled off, latent
SECONDARY
- e.g. immunocompromised –> reactivation - spreads to upper lobes/spice w. high O2 (aerobic) –> further granulomas, necrosis –> cavitation + liquefaction of necrotic material –> predispose to spreading –> can e.g. open into bronchus = bronchopneumonia, or to e.g. cerviial LNs, enlarge = ‘scrofula’, mycob. cervical lymphadenitis.
local - miliarty pulmon diseas, pleuritis etc.
can further –> pulmo. a (blood) - single organ/system (if small amount) or even systemic - granulomas everywhere = systemic miliary TB.
others e,g, meningitis, Pott’s disease, streile pyuria, TB nephritis, adrenalitis - Addison’s, ulcerative bowel etc.
Cavernous TB - draining of TB leaves an empty cavern behind.
Q20. SARCOIDOSIS
Final notes
(PRACTICAL histo - 2 peaks –> young adults 20-30yrs both M&F, older women >50yrs; granulomas mainly perivascular/peribronchial; more epithelioid cells, few Langhan cells opp to TB)
Q21. PLEURAL LESIONS - REVIEW
Secondary complication to a pulmonary disease
- secondary infections, pleural adhesions
- Pleural effusion
- tranusdate (hydrothorax) e.g. from CHF
- exudate (protein>2.9g/dL + inflammatory cells) suggest pleuritis e.g. infection, cancer, viral hep, SLE, RA, uremia, thoracic surgery etc.
- transudates and serous exudates usu. reabsorbed w/o residual effects
- fibrinous, hemorrhagic, suppurative exudates may lead to fibrous organization –> adhesions, fibrous, pleural thickening and potentially calcifications. - Pneumothorax - air or gas in pleural cavity
1) Open pneumorthorax
- simple e.g. COPD, TB, emphysema etc.
- spontaneous (most of time smoking forms subpleural blebs - rupture..)
2) Closed pneumothorax (seals off)
3) Tension pneumothorax - from trauma e.g. a stab wound or blunt - car accident –> medical emergency, surgery (drain air).
In hospitals from positive pressure ventilation can puncture lung. - Hemothorax - blood in pleural cavity
e.g. from complication of intrathoracic aortic aneurysm
blood can clot within pl. cavity. - Chylothorax - milky lymphatic fluid cont. lipid microglobules - obstruction of a major lymph duct (cancer).
