Pneumonia: Pathology review

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Pneumonia: Pathology review

Pretty much everything about CardioResp

Pretty much everything about CardioResp

Bones and joints of the thoracic wall
Muscles of the thoracic wall
Vessels and nerves of the thoracic wall
Anatomy of the pleura
Anatomy of the lungs and tracheobronchial tree
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Thoracic wall
Anatomy clinical correlates: Pleura and lungs
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Polycystic kidney disease
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Persistent truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Anatomy of the larynx and trachea
Development of the respiratory system
Respiratory system anatomy and physiology
Reading a chest X-ray
Lung volumes and capacities
Anatomic and physiologic dead space
Alveolar surface tension and surfactant
Compliance of lungs and chest wall
Combined pressure-volume curves for the lung and chest wall
Ventilation
Zones of pulmonary blood flow
Regulation of pulmonary blood flow
Pulmonary shunts
Ventilation-perfusion ratios and V/Q mismatch
Breathing cycle
Airflow, pressure, and resistance
Ideal (general) gas law
Boyle's law
Dalton's law
Henry's law
Graham's law
Gas exchange in the lungs, blood and tissues
Diffusion-limited and perfusion-limited gas exchange
Alveolar gas equation
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Breathing control
Pulmonary chemoreceptors and mechanoreceptors
Pulmonary changes at high altitude and altitude sickness
Pulmonary changes during exercise
Choanal atresia
Laryngomalacia
Allergic rhinitis
Nasal polyps
Upper respiratory tract infection
Sinusitis
Laryngitis
Retropharyngeal and peritonsillar abscesses
Bacterial epiglottitis
Nasopharyngeal carcinoma
Tracheoesophageal fistula
Congenital pulmonary airway malformation
Pulmonary hypoplasia
Neonatal respiratory distress syndrome
Transient tachypnea of the newborn
Meconium aspiration syndrome
Apnea of prematurity
Sudden infant death syndrome
Acute respiratory distress syndrome
Decompression sickness
Cyanide poisoning
Methemoglobinemia
Emphysema
Chronic bronchitis
Asthma
Cystic fibrosis
Bronchiectasis
Alpha 1-antitrypsin deficiency
Restrictive lung diseases
Sarcoidosis
Idiopathic pulmonary fibrosis
Pneumonia
Croup
Bacterial tracheitis
Lung cancer
Pancoast tumor
Superior vena cava syndrome
Pneumothorax
Pleural effusion
Mesothelioma
Pulmonary embolism
Pulmonary edema
Pulmonary hypertension
Sleep apnea
Respiratory distress syndrome: Pathology review
Cystic fibrosis: Pathology review
Pneumonia: Pathology review
Tuberculosis: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Obstructive lung diseases: Pathology review
Restrictive lung diseases: Pathology review
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Lung cancer and mesothelioma: Pathology review
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Bronchodilators: Leukotriene antagonists and methylxanthines

Transcript

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Two people came to your clinic one day.

Mariah is a 54-year-old smoker, who came in with with productive cough with yellow sputum and left-sided chest pain.

Physical examination reveals fever, tachycardia, and tachypnea. Her lung sounds are barely audible, but it had crackles at the left base.

Next is Jeremy, a 64-year-old man who was hospitalized for a stroke 2 weeks ago.

He recently developed a cough and right-sided chest pain.

He is tachycardic and has a fever of 38.4°C.

Examination reveals fremitus, decreased breath sounds, and dullness to percussion in the right lower lung field.

Chest x-rays were performed which showed a left lower lobe infiltrate in Mariah’s case, and a right lower lobe infiltrate in Jeremy’s.

Now, both people have pneumonia.

So pneumonia is an infection of the lung tissue.

Some microbes can overcome the innate defenses of the lungs and immune system to colonize the bronchioles or alveoli.

These pathogens then triggers an inflammatory response.

Inflammatory cells, such as white blood cells, dead bacteria, proteins and fluid from the damaged tissue, form a fluid called exudate which can be coughed up and expelled from the body.

However they can also accumulate in the lungs, filling up the alveoli.

We can divide pneumonia into “classic” pneumonia or “atypical pneumonia based on symptoms.

So with classical pneumonia, high yield symptoms might include dyspnea, or shortness of breath, fatigue, and fever.

Individuals might also develop pleuritic chest pain, which is characterized by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling; and productive cough with yellow sputum.

Besides these, High yield signs that might come up on your exam include dullness to percussion, which suggests that there’s a lung consolidation.

This occurs because the air in the alveoli is replaced by pus and fluid so the sound will lose its normal tympanic or drum-like quality.

There’s also tactile fremitus, which is when you can feel increased vibrations when you place your hand on the individual’s chest or back on the area with the consolidation and they say 99.

Similarly, if you auscultate the area with the consolidation, the “99” will sound louder and this is called bronchophony.

This is because sound waves and vibrations travel better through the fluid-filled consolidated tissue than air-filled healthy tissue.

For a similar reason if you put your stethoscope on the area with the consolidation, you can hear bronchial breath sound where the sound of air moving in the bronchi is transmitted clearly through the consolidated area.

This is higher pitched and louder than the normal vesicular breath sound where sound waves pass through more air filled alveoli.

Next is egophony which is increased resonance in the area with consolidation, so when asked to say the “E” it will sound like the letter “A.”

Late inspiratory crackles can also be heard over the affected area.

Crackles are popping lung sounds made when air passes through the fluid in the collapsed alveoli. Finally, people with pneumonia will often have tachypnea and tachycardia.

Now, there are many ways to categorize pneumonia.

One way would be by the causative microbes.

Usually, pneumonia is caused by viruses and bacteria, and rarely fungi as well. In adults, the most common viral cause is influenza.

This type usually has an abrupt onset and tends to develop secondary bacterial pneumonia.

Next is the typical pneumonia, or the classic bacterial pneumonia and its most often caused by either streptococcus pneumoniae, haemophilus influenzae, or staphylococcus aureus.

“Atypical or walking pneumonia” is also caused by bacteria, but the individual won’t develop the classic symptoms.

In atypical pneumonia with mycoplasma pneumoniae, a bacteria without a cell wall, individuals usually present with insidious onset, headache, nonproductive cough, and sometimes, no fever.

If you see these symptoms in a question prompt, it’s safe to assume the answer is atypical pneumonia with mycoplasma pneumoniae.

Another clue is that it tends to occur in areas with many people packed together like in military recruits training camps and prisons.

Also common in these populations, we have chlamydial pneumonia, and it can be caused by Chlamydophila pneumoniae, Chlamydophila psittaci, and Chlamydia trachomatis.

Now, another cause of atypical pneumonia is legionella pneumophila, which causes more severe symptoms like headaches, mild cough, confusion, high fever, and watery diarrhea.

This bacteria can be found in water-systems or water-based cooling systems in hotels, which is why this infection is also common in travelers.

The next high yield concept is that people in certain age groups are more at risk for certain types of microbial infections.

In neonates, or those younger than 4 weeks, the most common cause of pneumonia are Group B streptococci and Escherichia coli.

In those 4 weeks to 18 years, the condition is typically caused by viruses like the Respiratory syncytial virus, but also by bacteria such as Chlamydia trachomatis, which is more common in those younger than 3, and Chlamydophila pneumoniae, which is usually found in school-aged children.

Streptococcus pneumoniae is also a common cause of pneumonia in this age group.

Next, in those 18 to 40 years, the most common causes are Mycoplasma, Chlamydophila and Streptococcus pneumoniae, but also viruses like influenza.

The last age group is individuals over 40, especially the elderly over 65.

The most frequent causes are Streptococcus pneumoniae, anaerobes, and viruses.

Ok besides age, remember that in IV drug users, pneumonia is usually caused by Staphylococcus aureus and Streptococcus pneumoniae.

These also common causes of pneumonia in people with cystic fibrosis, but a very high yield pathogen associated with CF is Pseudomonas aeruginosa.

Another special group is people who are immunocompromised.

The more frequent causes include Staphylococcus aureus, enteric gram negative rods, and viruses.

HIV+ individuals with a CD4+ lymphocyte count under 200 cells per microliter can also suffer from AIDS-related opportunistic pathogens, like the fungus Pneumocystis jirovecii.

This type of pneumonia can cause respiratory failure or pneumothorax if left untreated, and was a common cause of death in AIDS patients.

Moving on, in those who’ve acquired pneumonia after a viral infection, the most common culprit is either Streptococcus pneumoniae, Staphylococcus aureus, or Haemophilus influenzae.

And finally, in post organ transplant patients who are on immunosuppressants, pneumonia with intranuclear and cytoplasmic inclusion bodies histologically points to opportunistic infection by Cytomegalovirus.

Pneumonia can also be categorized by where it’s acquired.

The most common is community-acquired pneumonia, and it’s when a person gets sick outside of a hospital or healthcare setting. It is usually caused by Streptococcus pneumoniae.

Ok, so next is hospital-acquired pneumonia or nosocomial pneumonia, which is when a person gets pneumonia when they are already hospitalized for something else for at least 2 days.

It tends to be more serious because these individuals often have weakened immune systems and the microbes in hospitals are often resistant to the common antibiotics.

Some high yield bacteria to remember are Methicillin-resistant Staphylococcus aureus or MRSA, which is usually carried by asymptomatic hospital staff; Legionella pneumophila, which can be found in water-systems or water-based cooling systems in hospitals is also common.

Another category is ventilator-associated pneumonia, which is a subset of hospital-acquired pneumonia.

It often develops when ill individuals are intubated for more than 48 hours. Oftentimes, bacteria like Pseudomonas aeruginosa and Staph. aureus can form a biofilm on the endotracheal tube.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Fishman's Pulmonary Diseases and Disorders, 2-Volume Set, 5th edition" McGraw-Hill Education / Medical (2015)
  6. "Pneumonia: update on diagnosis and management" BMJ (2006)
  7. "Viral pneumonia" The Lancet (2011)
  8. "Community-acquired pneumonia" The Lancet (2015)