Random Pulmonary Flashcards
naloxone
- given to treat morphine overdose
atelectasis
- collapse of lung volume
- pulls lung and trachea towards it
pleural effusion
- filling of pleural space with liquid
- pushes trachea in opposite direction
pleurodesis
- a medical procedure in which the pleural space is artificially obliterated.[1] It involves the adhesion of the two pleurae.
thoracentesis
- a procedure to remove fluid from the space between the lungs and the chest wall called the pleural space. It is done with a needle (and sometimes a plastic catheter) inserted through the chest wall.
OSA (obstructive sleep apnea)
x
OHS ( obesity hypoventilation syndrome)
x
cheyne stokes syndrome
x
MUDPILES (Anoin gap)
Methanol Uremia DKA (and other ketoacids, namely EtOH and starvation) Propylene Glycol INH Lactate Ethylene Glycol Salicylates
vocal cord layers
- Epithelium
- Superficial Lamina Propria
- Intermediate Lamina Propria
- Deep Lamina propria
- Vocalis muscle (medial thyroarytenoid)
COPD
COPD is defined by fixed airflow limitation
FEV1/FVC
Blue Bloater
Hypoventilator
Hypoxic
Hypercapnic
Cor pulmonale
Historically
chronic bronchitis
Pink Puffer
Hyperventilator
Less hypoxia /
hypercapnia
Historically
emphysema
Rhonchi
are rattling, continuous and low-pitched breath sounds that are often hear to be like snoring. also called low-pitched wheezes. They are often caused by secretions in larger airways or obstructions.
Acute COPD Exasperation
Increased cough
Sputum volume and purulence
Increased wheezing
Worsening obstruction on PFTs
Unchanged CXR
Precipitated by infection, pollution, PE, unknown factors
Increased work of breathing due to hyperinflation, increased airway resistance
Treated with bronchodilators, steroids, antibiotics
Management of Bronchiectasis
Airway clearance – to promote clearance of secretions
Antibiotics – may be intermittent, chronic, or rotating courses.
Treat reactive airways disease
Bronchodilators, corticosteroids
Bronchiolitis
In kids
Related usually to infection (i.e. RSV)
In adults Related to infection (esp. mycoplasma) less common than in kids Non-infectious causes Toxins, collagen vascular disease (e.g. RA), smoking Lung transplant chronic rejection Hypersensitivity pneumonitis
Cromolyn/nedocromil
• administered by the inhaled route
• • mechanism of action: inhibition of mast cell mediator release
• beneficial effect
preventative therapy for exercise-induced asthma can prevent allergen-induced pulmonary response
Theophylline
• administered by the oral or intravenous route
• mechanism of action: inhibition of phosphodiesterase
• beneficial effect: bronchodilator effect and some anti-inflammatory activity
• adverse effect:
caffeine-like effects such as irritability, gastrointestinal distress.
very narrow therapeutic range and requires blood level monitoring to individualize dose. Significant adverse effects can include seizures and irreversible neurologic damage
Systemic Circulation
High resistance
High Elastance/Low Compliance
High pressure
(CO=5L/min)
Pulmonary Circulation
Low resistance
Low Elastance/High Compliance
Low pressure (CO=5L/min)
Pulmonary edema types
Cardiogenic
- Increased vascular hydrostatic pressure forces liquid out into lung tissue
- Kerley B lines
- use diuretics
- Left PCWP pressure increased
non-cardiogenic
- inflammation
- leaky vascular walls
- can be due to ARDS/pneumonia
- diuretics don’t help
- Left PCWP pressure increased not increased
- Can be due to accident where legs are crushed and inflammation occurs at lung blood vessels and they become more permeable
Pulmonary hypertension
- Mean pulmonary arterial pressure > 25 mmHG (normal is 15-18)
Pre-capillary
- (Pulmonary Arterial Hypertension; PAH)
- PCWP ≤ 15mmHg
- acute PE
- Pneumonia (hypoxic vasoconstriction)
- hypoxia
- thromboembolism
Post-capillary
- (Pulmonary Venous Hypertension; PVH)
- PCWP > 15mmHg
Increased PA Pressure Can be Due to:
- Increased pulmonary vascular resistance
- Increased left atrial pressure
- Increased cardiac output– rarely by itself
Pulmonary embolism
Results in RV strain (“submassive”) / failure (“massive”)
- Increased myocardial O2 demand
- Decreased myocardial O2 delivery
- Cycle leading to death
- can result from DVT also
Chest xray - Hampton’s Hump (Infarcted Lung) - Westermark’s Sign (Hypoperfusion)
- elevated D-dimer
Pulmonary embolism treatment
Stable (submassive) Parenteral Anticoagulation Heparin: Unfractionated or low molecular weight Catheter directed thrombolysis (tPA) Oral Anticoagulation - warfarin
Unstable (hypotensive, RV failure = massive) Heparin Consider thrombolysis (tPA) Consider IVC Filter Consider surgical thrombectomy
Clinical Classification of Pulmonary Hypertension: WHO Groups
- Pulmonary Arterial Hypertension
- PH Due to Left Heart Disease
- PH Due to Lung Diseases and/or Hypoxia
- Thromboembolic Pulmonary Hypertension
- PH With Unclear/Multifactorial Mechanisms
Pulmonary Arterial Hypertension (precapillary)
Mean PAP ≥25 mm Hg plusPCWP/LVEDP ≤15 mm Hg plusPVR > 3 Wood Units
PAH PHYSICAL EXAM
Neck veins: distended
Lung auscultation: normal (no rales)
Cardiac exam; loud P2, murmur of TR
Extremities: edema
Treatment of PVH (pulmonary venous hypertension)
Decrease intravascular filling
Limit fluid intake
Limit sodium intake
Diuresis
Improve LV contractility
Decrease LV aferload (control systemic hypertension)
Correct causes of LV failure
Ischemia
Valvular disease
Do Not Use PAH specific therapy for PVH!!!!
Factors that affect ventilation (VA)
Obstructive disease (e.g., COPD)
Compliance problems
Generally, total ventilation is affected only by severe disease conditions.
Exercise (ventilation can increase up to 10-fold)
Gravity (introduces regional variations in ventilation)
High altitude
Bohr effect
CO2 binding reduces O2 affinity for Hb
Haldane effect
O2 binding reduces CO2 affinity for Hb
Hypoxia
Low O2 in tissue
due to low Q or low arterial o2 saturation with hypoxemia
Hypoxemia
low arterial blood O2 saturation
Intracellular buffer
Organic Phosphates
Proteins
Hemoglobin
Extracellular buffers
Proteins
Albumin
Phosphate
Bicarbonate
Normal pH
7.38-7.43 (bit higher in Denver)
Normal venous pH
range 7.34-7.37
Hemoglobin Buffering
Deoxyhemoglobin is such a good buffer that venous pH is only slightly lower and venous pCO2 is only slightly higher (~45 Torr) than arterial blood despite amount of CO2 being carried
Two categories of metabolic acidosis:
Anion Gap
Non-Anion Gap
Non-Anion gap is caused by loss of bicarbonate
GI losses (severe gonnorhea) Renal losses
metabolic alkalosis causes
Vomiting or NG tube suction (loss of gastric acid)
Ingestion NaHCO3
Ingestion of other alkali (milk-alkali syndrome)
Hypovolemia, so-called contraction alkalosis
Diuretics
Peripheral chemoreceptors
Located in carotid bodies
Mediate increases in ventilation in response to:
- Low arterial O2 (relatively insensitive until PaO2
Properties of central chemoreceptors
Located on ventral surface of medulla (in the brain!)
Bind protons in CSF but sense arterial CO2
Response is slow (minutes)
Mediate 80% of ventilatory response to high PaCO2 under long-term conditions
Most important day-to-day regulator of ventilation
Motor neurons that control respiratory muscles
Tidal Volume
Breathing Rate
Crackles and rales
discontinuous and typically during inspiration; Specific cause is not clear; “Velcro sound” ;
Associated with:
Pulmonary edema
Pneumonia
Interstitial lung disease/fibrosis
5 causes of hypoxemia
Normal A-a O2 gradient
Altitude Hypoventilation -OHV (obesity hypoventilation) -central apnea aka Ondine’s curse -neuromuscular dz (Lou Gerhigs, myasthenial gravis) -Drugs (opiates, benzo)
Low V/Q causes
Hypoventilation Asthma Chronic Bronchitis Emphysema (late) ILD (interstitial – fibrosis)
Shunt causes
Pulmonary Edema ARDS Pneumonia Intracardiac/Congenital Heart Dz Pulmonary AVM arteriolevenous malformation Atelectasis
sildenafil
treatment for PAH. vasodilator
Acute restrictive diseases
Pulmonary edema
ARDS/DAD
Pneumonia
Pleural effusion
Chronic restrictive diseases
ILD - interstitial lung diseases
Pleural fibrosis / plaques
Pleural effusion
ALS is often called Lou Gehrig’s disease
A nervous system disease that weakens muscles and impacts physical function.
Difficulty walking, tripping or difficulty doing your normal daily activities
Weakness in your leg, feet or ankles
Hand weakness or clumsiness
Slurring of speech or trouble swallowing
Muscle cramps and twitching in your arms, shoulders and tongue
Difficulty holding your head up or keeping a good posture
Respiratory muscle weakness
Inadequate ventilation (CO2 rises)
Nocturnal hypoventilation (worse than normal people where brain is asleep and breathing decreases a bit at night)
Weak cough
Major: Dysphagia –> lots of recurring pneumonia from aspiration
TREATMENT
Noninvasive positive pressure ventilation to help breathe)
Aspiration precautions
Cough assistance
guillain-barré syndrome
A condition in which the immune system attacks the nerves.
Prickling, “pins and needles” sensations in your fingers, toes, ankles or wrists
Weakness in your legs that spreads to your upper body
Unsteady walking or inability to walk or climb stairs
Difficulty with eye or facial movements, including speaking, chewing or swallowing
Severe pain that may feel achy or cramp-like and may be worse at night
Difficulty with bladder control or bowel function
Rapid heart rate
Low or high blood pressure
Difficulty breathing
Rheumatoid arthritis
Pleuritis
Pleural Effusion
Pleural Thickening
Pneumothorax
Upper airway obstruction (cricoarytenoid arthritis)
Small airway obstruction (bronchiolitis,bronchiectasis)
Interstitial Lung Disease (UIP > NSIP)
Organizing pneumonia
Nodules
Pulmonary Hypertension
Vasculitis
Drug reactions (esp methotrexate, sulfasalazine)
Pulmonary infections due to immunosuppression
IPF meds
- nintedanib, pirfenidone
- Does not respond to anti-inflammatory meds
Idiopathic Pulmonary Fibrosis
IPF is a scarring lung disease with a pattern of injury of
usual interstitial pneumonia (UIP).
Etiology is idiopathic.
(There are known causes for the same UIP pattern of injury).
Disease of older patients ( > 6th decade)
Associated with tobacco use
Cough, DOE, fatigue
Physical exam: Basilar predominant “velcro-crackles.” Digital clubbing in advanced cases.
Median survival from diagnosis is 2-3 years.
Smoking
- Chronic bronchitis
- pneumonia
- IPF
- COPD
- Emphysema
- respiratory bronchiolitis
- desquamative interstitial pneumonia
- Pulmonary Langerhans Cell Histiocytosis
Pulmonary Langerhans Cell Histiocytosis
Young smokers Imaging: cysts and nodules Upper lobe predominant Mixed PFTs PTX common 15% extrapulm dz—including bone lesions, pituitary involvement Treatment is smoking cessation
Systemic diseases associated with diffuse alveolar hemorrhage and renal disease
Granulomatosis with polyangiitis (formerly Wegener’s) Microscopic polyangiitis Churg-Strauss Syndrome Goodpasture’s Syndrome (Anti-GBM disease) Systemic Lupus Erythematosus Systemic Sclerosis (Scleroderma) Henoch-Schonlein Purpura Cryoglobulinemia
Goodpasture’s Syndrome (Anti-GBM disease)
Goodpasture’s syndrome is an idiopathic disease that manifests as diffuse alveolar hemorrhage and rapidly progressive glomerulonephritis.
Mediated by antibodies directed against glomerular basement membrane
Occurs almost exclusively in smokers
Pulmonary Manifestations of Sickle Cell Disease
Infection
Embolic phenomena due to bone marrow infarction and fat emboli
Infarction caused by in-situ thrombosis
Hypoventilation due to rib and sternal infarctions
Pulmonary Edema due to excessive hydration
Pulmonary hypertension
Chronic lung disease
Histiocytes and macrophages
As nouns the difference between macrophage and histiocyte is that macrophage is (immunology|cytology) a white blood cell that phagocytizes necrotic cell debris and foreign material, including viruses, bacteria, and tattoo ink it presents foreign antigens on mhc ii to lymphocytes part of the innate immune system while histiocyte is a macrophage, derived from bone marrow, found in connective tissue
TGV (Thoracic Gas Volume)
represents the point when the inward recoil of the lung is exactly balanced by the outward recoil of the chest wall. This is measured at the end of a normal tidal volume. Anything that makes the lung stiffer (such as interstitial lung disease or loss of surfactant) without changing the chest wall compliance will decrease the TGV. Conversely anything that increases lung compliance (such as emphysema) will increase the TGV. Note that TGV and FRC both indicate the same thing but are measured differently. They should be the same in normal people, but can vary in disease.
diet pills
pulmonary hypertension
scleroderma
Chronic hardening and tightening of the skin and connective tissues. related to joint pain
smoking and birth control pills
chronic thromboembolic disease
cor pulmonale
(right heart failure due to
pulmonary hypertension).
Pulmonary Hypertension facts
WHO Group 1 and WHO Group 4 disease will have
normal lung volumes and spirometry, and a decreased DLCO due to a decrease in
the vascular surface area.
Loud P2
Pulmonary Hypertension
