Diff from spontaneous pneumothorax. MC due to knife injuries into the lung. There’s tear of pleura (flap), sp when you breathe in the flap goes up and on expiration it closes. So, the air stays in the pleural cavity. So, every time you breathe, the flap goes up, air stays in, and on expiration it closes. So, for every breath you take, it keeps increasing and the pressure in the lung. The lung hasn’t collapsed yet. The increase in pressure starts pushing the lung and the mediastinum to the opposite side. When it pushes it, it compresses the lung and it leads to compression atelectasis (it is not deflated b/c of a hole – there isn’t a hole – it’s a tear that when the air went in it went up and it shut on expiration, and that pos pleural pressure is pushing everything over to the opposite side). This compression will push on the SVC, right vent, and left atrium on the opposite side. This will compromise blood return and breathing, leading to a medical emergency. So, it’s like filling tire up with air, but cannot get out. Air is filling pleural cavity and cannot get out. It keeps building up and starts pushing everything to the opp side. With a pos intrathoracic pressure, the diaphragm will go down (goes up in spontaneous pneumothorax).
V. Pulmonary Infection A. Pneumonia
1. 2 kinds – Typical and Atypical
Typical – wake feeling normal, then suddenly develop a fever, productive cough Atypical – slow, insidious onset (feel bad over few days)
2. Community vs. Nosocomial (hospital acquired)
If you get pneumonia in the community and it’s typical, it is Strep pneumoniae. If you get pneumonia in the community and it is atypical, it’s mycoplasma pneumoniae.
Organisms in the hospital (nosocomial) = E coli, Pseudomonas, Staph aureus (will not get strep pneumoniae in the hospital).
3. Productive cough in Typical pneumonia
Reason for productive cough in typical pneumonia: have exudate (pus) and signs of consolidation in the lung – Slide: yellow areas with microabcesses which are consolidation in the lung. Ie lobar pneumonia = see consolidation in lung, within alveoli, causing consolidation. Therefore, with typical, see consolidation and pus in the lung. Physical dx’tic tools of lung consolidation: decreased percussion, increased TVF (when the person talks, feel vibrations in chest – if have consolidation in ie the upper left lobe, will have increased TVF b/c it is a consolidation, compared to the other side – so,
increased TVF indicates consolidation), having an “E to A” (egophony) sign (pt says E and you hear A), whispered pectoriloquy (pt whispers “1, 2, 3” and I will hear it very loud with the stethoscope). Therefore, decreased percussion, increased TVF, egophony, and pectoriloquy = consolidation.
What if there is a pleural effusion overlying the lung? Only thing you would have is decreased percussion (this separates pleural effusion from pneumonia).
4. Atypical pneumonias
They do not have a high temp and do not have productive cough b/c they are interstitial pneumonias. They have inflammation of the interstitium – there is no exudate in the alveoli – which is why you are not coughing up a lot, and therefore do not have signs of consolidation. So, will not have increase TVF, “E to A”, with an atypical. Atypical pneumonia has an insidious onset, relatively nonproductive cough, no signs of consolidation.
MCC typical pneumonia = strep pneumoniae (know the pic) – gram “+” diplococcus (aka diplococcus) – Rx = PCN G
MCC atypical pneumonia = mycoplasma pneumoniae; 2nd MCC = Chlamydia
pneumoniae; which are all interstitial pneumonias.
Bronchopneumonia: MC due to strep pneumonia, and community acquired. Lobar pneumonia. Slide: lobar consolidation on chest x-ray – strep. Pneumonia.
a) Viral pneumonias
1) Rhinovirus = MCC common cold; they are acid labile – meaning that it won’t lead to gastroenteritis in the stomach b/c is destroyed by the acid in the stomach. Never will have a vaccine b/c 100 serotype.
2) RSV – MCC bronchiolitis – whenever you inflame small airways, its leads to wheezing. This is a small airway dz and bronchiolitis is MC due to RSV and pneumonia. So, pneumonia and bronchiolitis is MC due to RSV in children.
3) Influenza – drift and shift – have hemagglutinins, which help attach the virus to the mucosa. Have neuraminidase bore a hole through the mucosa. Antigenic
drift = minor change/mut’n in either hemagglutinins or neuraminidase; do not need a new vaccine; antigenic shift= major change/mut’n in either hemagglutinins or neuraminidase need a vaccine. The vaccine is against A Ag.
b) Bacterial pneumonias
1) Chlamydia psittacosis – from birds (ie parrots, turkeys).
2) Chlamydia trachomatis – a little kid was born and a week later he was wheezing (big time), pneumonia, increased AP diameter, tympanic percussion sounds, no fever, eyes are crusty (both sides), weird cough – staccato cough (short coughs). He got it from his mom’s infected cervix. (MCC conjunctivitis in 2nd week = Chlamydia trachomatis). (MC overall of
conjunctivitis is inflammation of erythromycin drops). c) Hospital-acquired gram-negative pneumonias
1) Pseudomonas – water loving bacteria, therefore see in pt in ICU when on a RESPIRATOR. pt water unit with green productive cough with.
2) Klebsiella – famous in the alcoholic; however, alcoholic can also get strep pneumonia. So, how will you know strep vs. Klebsiella? Alcoholic with high spiking fevers, productive cough of MUCOID appearing sputum – the capsule of Klebsiella is very thick. Lives in the upper lobes and can cavitate, therefore can confuse with TB.
3) Legionella – atypical cough, nonproductive cough, very sick can kill you, from water coolers (water loving bacteria), seen in mists in groceries or at restaurants. Example: classic atypical pneumonia, then pt had hyponatremia – this is
Legionella. Legionella just doesn’t affect the lungs, also affects the other organs such as liver dz, interstial nephritis and knocks off the juxtaglomerlur cells, and kills the renin levels, low aldosterone and therefore lose salt in the urine, leads to hyponatremia (low renin levels with low aldosterone). Rx = erythromycin