Respiratory Flashcards
Cartilage and goblet cells extend to where?
bronchi
Pseudostratified ciliated columnar cells extend to where?
beginning of terminal bronchioles
Airway smooth muscle cells extend to where?
end of terminal bronchioles
Prominent secretory cell for mucus after goblet cells end?
club cells
Pathology of trachea of smoker
Replacement of ciliated columnar epithelium with squamous (squamous metaplasia)
Main type of cell in respiratory bronchioles
Cuboidal cells
Main type of cell after respiratory bronchiles up to alveoli
simple squamous cells
Transition of epithelium from nose to alveoli
Ciliated pseudostratified columnar epithelium (“respiratory epithelium”) from nose to terminal bronchioles. Ciliated simple Cuboidal epithelium (respiratory bronchioles) and simple squamous (alveolar ducts and alveoli)
la place law
Collapsing pressure (P)=2 (surface tension)/radius
Surfactant synthesis begins?
Optimal levels?
26
35
Function and location of clara cells?
Function is regeneration of ciliated cells in the bronchioles and are located in terminal portions of bronchioles.
Lobes in right vs left lung
Right-3
Left-2 + lingula
Fissures separating superior/middle lobe on right side and middle/inferior lobe
Transverse and oblique
Fissure separating superior/inferior on left side
Oblique
Relation of pulmonary artery to bronchus at each lung hilum
Right anterior. Left superior (RALS)
Structures perforating diaphragm:
t8: IVC
T10:esophagus, vagus nerve
T12: aorta, azygous vein, thoracic duct
Common bifurcation at
Carotid
Trachea
Abdominal aorta
C4
T4
L4
Intrathoracic spread of lung cancer can do what to cause diaphragmatic paralysis with dyspnea
Irritate the phrenic nerve
What values can’t be measured on spirometry?
RV, FRC, TLC
Typical volume of tidal volume?
500 mL
Volume of gas present in lungs after maximal inspiration
TLC
Physiologic dead space equation
Vd=Vt*PaCO2-PECO2/PaCO2
Largest portion that contributes to alveolar dead space?
Apex of healthy lung
Physiologic dead space vs anatomic dead space?
Physiologic dead space-total volume of lungs that don’t participate in gas exchange. Includes anatomic dead space and alveolar dead space
Anatomic dead space-volume from conducting zone airways
Minute ventilation
Ve=Vt*Respiratory Rate
Alveolar ventilation
Va=(Vt-Vd)*RR
Ventilation is a function of what?
CO2
When is PVR (pulmonary vascular) the lowest and why?
At FRC. This is at end of exhalation which means that you have increased blood in left side of heart so pressure in left atrium is higher that pressure of pulmonary artery. So, looking at the equation PVR=Ppulm artery-Pleft atrium/cardiac output this would make sense.
What prevents lungs to collapse inward and chest wall to spring outward at FRC?
negative IPP
Pressure of airway and alveolar pressure at FRC
0
What is compliance proportional to and give an example why?
FRC
Increased FRC seen in emphysema which has increased compliance because of air trapping. decreased compliance seen in pulmonary fibrosis which has decreased frc
How is compliance related to elastance?
inversely proportional
Explain pathophysiology of poor gas exchange seen in LV failure?
LV failure–>LHF–> pulmonary edema–>decreased compliance–>states of decreased compliance–>negative pressure generated during normal inspiratory not sufficient enough to distent lungs–> poor gas exchange
what acts as a buffer for h+ ions and what is its relation to exercise?
hemoglobin will unload O2 to muscle while binding H+ ions to control the pH, thus acting as a buffer
What is the reason 2,3 BPG does not properly bind HbF
altered presence of serine instead of charged histidine residues
What does 2,3 BPG only bind?
deoxyhemoglobin
Explain pathophysiology of what happens at lower FRC (i.e. fibrosis)?
At lower FRC, less + lung pressure and a more negative chest wall pressure. because of this, collapsed tendency is favored over expansion. This is why you have lower compliance and higher elastic recoil
Explain pathophysiology of what happens at higher FRC?
At higher FRC, increased + lung pressure and more + chest wall pressure. Because of this, expansion favored over collapse. This is why you have higher compliance and lower elastic recoil.
Vitamin that can treat methhemoglobinemia and normal treatment
vitamin C, methylene blue
Cyanide poisoning treatment?
Nitrites followed by thiosulfate
Why left shift with CO poisoning?
Binding of CO to hemoglobin increases affinity of remaining sites for O2 causing left shift.
Why right shift with anemia?
Anemia severe enough can cause lactic acidosis–>increase H+–>lower blood pH and right shift
Would hemoglobin have sigmoid curve if subunits were seperated?
No. no positive cooperativity. would be hyperbolic like myoglobin
Explain pathophysiology behind left or right shift in curves?
Left shift–>for a given P50 (Hb saturation), there is a lower PO2 meaning that less O2 required to maintain 50% of Hb saturation and there is a higher affinity of O2 for Hb
Right shift –>for a given P50 (Hb saturation), there is a higher PO2 meaning that more O2 is required to maintain 50% Hb saturation and there is a lower affinity of O2 for Hb
Equation for O2 content
(O2 binding capacity * % saturation) + dissolved O2
Normal 1 g of Hb can bind ______
Normal Hb amount in blood is ______
Cyanosis results when deoxygenated Hb >________
1.34 mL O2
15 g/dL
5 g/dL
O2 delivery to tissues equation
CO*O2 content of blood
Why is flow same in pulmonary and systemic circulation?
Because pulmonary pressure and resistances are proportionately lower than systemic pressures and resistance
Equation for PVR
PVR=Ppulm artery-Pleft atrium/Cardiac output
Why increased PVR with decreased blood O2 content?
Decrease blood o2 content–>pulmonary vessel vasoconstriction so blood shunted to well ventilated areas–>increase pulmonary artery pressure–>increase PVR
Alveolar gas equation PAO2=
150 mmHg-PaCo2/0.8
Normal A-a gradient
10-15 mm Hg
State in which V/Q ratio approaches 1
Exercise
Why do blood in the left atrium have lower Po2 than blood in pulmonary capillaries?
Mixing with deoxygenated blood from the bronchial veins returning blood from lungs to right heard with the pulmonary veins
3 forms CO2 transported from tissues to lungs
1) HCO3-
2) Carbaminohemoglobin or HbCO2 (CO2 bound to Hb at N-terminus of globin)
3) Dissolved CO2
How is CO2 released from RBC?
How is H+ loaded onto RBC?
- Oxygenation of Hb in lungs shifts H+ dissociation from Hb. This shifts equilibrium toward CO2 formation via carbonic anhydrase and therefore CO2 released from RBC. (haldane effect)
- In tissue, high concentration of H+ causes cure to shift to right, unloading O2 (bohr effect)
What is majority of blood CO2 carried as in plasma?
HCO3-
Describe pathophys of high altitude with regards to PaO2 and PaCO2
High altitude–>decrease in PO2 of inspired air–>decrease in PAO2–>decrease in PaO2–>increase in ventilation–>decrease in PaCO2 (chronic increase in ventilation should augment with acetazolamide to get rid of increased HCO3- concentration)
Describe why you would get RVH in chronic high altitude
High altitude–>decrease PaO2–>pulmonary vasculature vasoconstriction–>increase pressure of pulmonary artery–>RVH–>right heart failure
pH equation
HCO3-/pCO2
What happens to oxygen and co2 content in arterial and venous side during exercise?
What happens to pH?
no change in PaCO2 or PaO2+ no change in pH, but increase in venous CO2 and decrease in venous O2 (greater extraction) so decreased pH
Sinus involved in adults/children for rhinosinusitis
children-ethmoid
adults-maxillary
3 Superimposed bacterial infections to cause rhinosinusitis
S. pneumoniae, h influenza, m catarrhalis
Most likely location for orbit fractures involving what sinuses and why?
Maxillary and ethmoid sinuses. Superior and lateral parts of orbit are very strong but inferior and medial are thin. Can affect maxillary and ethmoid sinus this way
Epistaxis 2 locations involving anterior segment vs posterior segment
Anterior segment-kisselbach plexus (nose bleed)
Posterior segment-Sphenopalatine artery (branch of maxillary artery)
Drug of choice for prevention of venous thrombosis in non-ambulating patients or patients undergoing elective hip/knee surgery
Heparin
What should be considrered in patients younger than 50 who present with thrombosis and no obvious explanation for acquired prothrombotic state?
Inherited hypercoagulability (eg factor v leiden mutation)
Metabolic abnormality in pulmonary embolus and explain why?
V/Q mismatch–>hypoxemia–>hyperventilation–>respiratory alkalosis
How do you know if embolus is formed before or after death?
Lines of zahn present which are interdigitating areas of pink (platelets, fibrin) and red (RBC) found only in thrombi fomred before death
Where do large/small emboli end up?
Large–>pulmonary artery bifurcation (“saddle emboli”)
Small–>distal pulmonary artery branches (hemorrhagic infarcts that are wedge shaped
Gold standard test for PE
CT pulmonary angiography
Pressure in Zone 1, Zone 2, Zone 3
Zone 1: PA>Pa>Pv
Zone 2: Pa>PA>Pv
Zone 3: Pa>Pv>PA
Triad of fat emboli
hypoxemia, neurologic abnormalities, petechial rash
Pathophys of why amniotic fluid emboli can lead to DIC?
Amniotic fluid have tissue thromboplastic and can activate coagulation cascade–> DIC
4 drugs that can cause pulmonary fibrosis
Bleomycin, busulfan, amiodarone, methotrexate
Bugs involved in lobar pneumoniae
S pneumoniae, Legionell, Klebsiella
Bugs involved in bronchopneumoniae
S pneumoniae, S aureus (secondary to upper viral respiratory infection), H influenzae, Klebsiella
Bugs involved in Interstitial (atypical pneumoniae)
Viruses (influenza, CMV, RSV, adenoviruses), Mycoplasma, legionella, chlamydia
Lung abscess treatment
Clindamycin
Common causes of lung abscess
Anaerobes (bacteriodes, fusobacterium, peptostreptococcus), S auresu, klebsiella pneumoniae
Most common site of metastasis from lungs?
Adrenals
Bronchial hamartoma contains?
Lung tissue and cartilage often calcified on imaging
