MF1 RESPIROLOGY Flashcards
What are the parts of the sternum
Manubrium, manubriosternal join/sternal angle/angle of Louis, body, xiphoid
Lobes of the lung
Right: upper, horizontal fissure, middle, oblique fissure, lower
Left: upper, oblique fissure, lower
The ribs
Ribs 1-6 are the true ribs
Ribs 7-10 are the false ribs (coming off same costal cartilage)
Ribs 11&12 are the floating ribs
Where do the lungs end in the thorax
6th rib, 8th/10th at midaxillary line
Pleaura ends at the 8th
Pleura
Costal pleura: line the ribs
Diaphragmatic pleura
Mediastinal pleura: on the heart and great vessels
Visceral is touching lung, parietal is touching cavity
Intercostal space
- External intercostals: angled down toward sternum
- Internal intercostals: angled down toward outside of ribs
- Neurovascular bundle: under the rib; vein, artery, nerve
Flail chest
- Par of the ribcage is separated from the rest of the chest wall
- On expiration goes out, on inspiration collapses in
Muscles in the chest to assist breathing (& innervation)
- Scalenes: elevated upper ribs (cranial IX)
- Sternocleidomastoids: elevate sternum (cranial IX)
- External intercostals: elevate rib cage (thoracic spinal nerves)
- Internal intercostals: depress ribcage (thoracic spinal nerves)
- Transversus thoracis: pulls ribs 2-6 inwards
- Diaphragm: stretches flat (phrenic nerve from C3,4,5)
Sinuses
Frontal (forehead)
Ethmoid (bridge of nose)
Maxillary (under eyes, cheeks)
Sphenoid (deep, behind nose)
Narrowest point in kids v adults
Cricoid cartilage: only cartilage that wraps fully around; narrowest in kids
Vestibular fold: narrowest point in adults (glottis)
Angle of right and left mainstem bronchus
Right: 25
Left: 45
Type I v II alveolar cells
Type I: continuous lining of alveolar wall, primary site of gas exchange
Type II: secretes surfactant, reducing surface tension
Normal respiratory rates
<1 year: 30-60 bpm
10 years: 18-30 bpm
Adolescence: 12-18 bpm
Naloxone MOA and effects
- Pure opioid antagonist that competes and displaces opioids at opioid receptor sites
- Administration of naloxone causes the release of catecholamines, which may precipitate acute withdrawal or unmask pain in those who regularly take opioids
- Symptoms of acute withdrawal in opioid-dependent patients may include pain, tachycardia, hypertension, fever, sweating, abdominal cramps, diarrhea, nausea, vomiting, agitation, and irritability.
Croup vs Epiglottitis (path, symptoms, causes, treatment)
— CROUP —
- PATHO: swelling of larynx, trachea, large bronchi due to WBCs
- SYMPTOMS: barking cough, stridor, fever, hoarse voice, noisy breathing
- CAUSES: usually viral
- TREATMENT: corticosteroids (dexamethosone), epinophrine, O2; AVOID beta agonists
— EPIGLOTTITIS —
- PATHO: swelling of epiglottis
- SYMPTOMS: 4Ds (dysphagia, dysphonia, drooling, distress), fever, soar throat, stridor
- CAUSES: usually bacterial (strep pneumonia, A, B, C, staph aureus)
- TREATMENT: O2, IV fluid drip, antibiotics (if bacterial)
Guillain Barre Syndrome
- A disorder characterized by demyelination of peripheral nerves though to be triggered by exposure to an antigen (C. jejuni) resulting in misdirected immune response to similar antigenic determinants on neural tissue or Schwann cells
- Usually history of recent viral or bacterial illness
- Paralysis starts symmetrically in lower extremities and progresses or ascends proximally to the upper extremities and trunk
Shunting v Dead Space
Shunting: shunting blood to other open blood vessels to other alveoli might be better ventilated
Dead space: dead space is the volume of air that is inhaled that does not take part in the gas exchange, because it either remains in
Smoking on the respiratory system
—STRUCTURAL—
- Peribronchial inflammation and fibrosis
- Increased mucosal permeability
- Impaired mucociliary clearance
- Changes in pathogen adherence
- Disruption of resp epithelial cells
—IMMUNOLOGIC—
- Decreased circulating immunoglobulins
- Depression of Ab response
- Decreased CD4 counts, increased CD8
- Depressed phagocyte activity
***Stongly associated with invasive pneumococcal disease in otherwise healthy adults
Asthma treatment
Intermittent: SABA
Mild: SABA + low dose ICS
Moderate: SABA + medium ICS // LABA + low ICS
Severe: SABA + medium ICS + LABA // SABA + high ICS + LABA // SABA + high ICS + LABA + PO corticosteroids
SABA: B2 receptor binding; albuterol, levalbuterol
Corticosteroids: ICS (inhaled) decrease inflammation by inhibiting steroid release; Fluticasone, Budenoside, Mometasone
LABA: long acting B2 agonist; formoterol, salmeterol
Emphysema
- Alveolar air sacs become damaged/destroyed → become permanently enlarged and loose elasticity, resulting in difficulty exhaling (depending on recoil)
- Elastases, collagenases → break down structural proteins collagen and elastin, which give the tissue their elasticity
- Decreased recoil, increased compliance, decreased DLco
- Centriacinar emphysema: is most common, only damaging the central/proximal (upper lobes) alveoli of the acinus (smoking)
- Panacinar emphysema: where entire acinus uniformly affected; alpha-1 antitrypsin deficiency
- Paraseptal emphysema: where the distal alveoli are the ones most effected, usually near the periphery
Chronic Bronchitis
- Inflammation of bronchiole tubes in the lungs; productive cough for at least three months per year for at least 2 years
- Along with smoking, exposure to air pollutants (S2 and NO2), dust and silica, and genetic factors (family history) are all risk factors
- Exposure to irritants and chemicals can lead to hypertrophy (enlargement) and hyperplasia (increase in number) of bronchial mucinous glands (in main bronchi) and goblet cells (in bronchioles) leading to increased mucus production
Interstitial Lung Disease
- Healthy lung tissue starts getting replaced by collagen fibers (fibrosis) which are stiff and firm and cant stretch as much, meaning they don’t fill with as much air
- Pneumoconiosis (occupational exposures, silicosis, asbestosis)
–>Asbestos if from the rook but affects the lower lobes, silica, coal, and berries (beryllium) are from the ground but affect the upper lobes - Sarcoidosis (systemic disease that can lead to fibrosis if severe; immunologic disorder that leads to lots of small nodules throughout the body)
- Hypersensitivity pneumonitis (reaction to small particles leading to fibrosis)
- Idiopathic pulmonary fibrosis (excess collagen in interstitium of the lung → progressive loss of lung tissue)
ARDS
- Inflammation throughout the lungs leading to pulmonary edema → “non-cardiogenic pulmonary edema”
- Main site of injury is the alveolar-capillary membrane; any damage here increases permeability, causing fluid to move in the alveoli acting as a barrier against normal gas exchange, and dilutes out surfactant molecules making alveoli less able to stay open and compliant, becoming stiff
- CAUSES: aspiration, pneumonia, inhalation injury, embolism, reperfusion, sepsis, trauma, shock, blood transfusion, pancreatitis, drug overdose
- DIAGNOSIS: Abnormal CXR (bilateral lung opacities), Respiratory failure w/in 1wk of alveolar insult, Decreased PaO2/FIo2, Symproms of resp failure not due to fluid overload
Restrictive lung disease
—INTERSTITIAL—
- Hypersensitivity pneumonitis (immune rx to small particles; bird droppings, dust mold)
- Idiopathic pulmonary fibrosis (progressive dyspnea, fatigue, nonproductive cough, crackles, clubbing)
- Sarcoidosis (immune rxn, noncaseating granulomas, accumulate in lymph nodes and lung hylum)
- Pneumoconiosis (occupational exposure)
>Coal workers
>Asbestosis (fibrotic nodule formation)
>Silicosis (lower lobes, pleural paques)
—EXTRA-PULMONARY—
- Pleural effusion
- Chest wall abnormalities
- Neuromuscular
>Guillian-Barre
>Duschenne muscular distrophy
>Myesthenia gravis (autoimmine, prevents diaphragm neurons)
