resp quizz Flashcards
(235 cards)
1
Q
what is rhinosinusitis?
A
Obstruction of sinus drainage into nasal cavity inflammation and pain over affected area.
2
Q
which site is the most sensitive for epistaxis?
A
Kiesselbach plexus
3
Q
Kiesselbach plexus
A
superior Labial artery, anterior and posterior
Ethmoidal arteries, Greater palatine artery,
Sphenopalatine artery.
4
Q
what is risk factors for head and neck squamous cell carcinoma?
A
tobacco, alcohol, HPV-16, EBV
5
Q
can squamous cell carcinoma occur multiple sites? nasopharyngeal carcinoma?
A
yes, No
6
Q
which head and neck cancer can cause otitis media?
A
nasopharyngeal carcinoma
7
Q
. Benign laryngeal
tumor, commonly affecting areas of stratified squamous epithelium such as the true vocal cords,
especially in children. Associated with HPV-6 and HPV-11.
A
Laryngeal papillomatosis
8
Q
what is DVT
A
Blood clot within a deep vein
9
Q
symtoms of DVT?
A
Swelling – typically in one leg (calf or thigh)
Pain or tenderness – often described as cramping or soreness, especially in the calf
Warmth over the affected area
Redness or discoloration of the skin
Dilated superficial veins – visible veins due to blocked deep flow
10
Q
Virchow triad (SHE):
A
Stasis, hypercoagulability, endothelial injury
11
Q
what we use for DVT diagnosis?
A
D-dimer, doppler ultrasound, venography
12
Q
what is pulmonary emboli
A
obstruction of pulmonary arteries by a thrombus, often with dvt, v/q mismatch.cor pulmonale(right heart failure caused by lung diseases)
13
Q
pulmonary emboli types?
A
fat,air,tumor,amniotic fluid
14
Q
risk factors of PE
A
Primary hypercoagulability, factov V laiden,prothrombin gen e mutation,antiphospolipid antibody
obesity,statis,pregnancy
15
Q
diagnostic studies for PE
A
d dimer for dvt. ct scan angiograma gold standart.
16
Q
treatment of PE
A
(in all cases )anticoagulants,(if massive PE) thrombolytics
17
Q
metaplasia type in chronic bronchitis
A
pseudostratifiedciliated columnar epithelium into stratified squamous epithelium
18
Q
COPD symtoms
A
Chronic cough
Sputum production
Dyspnea (shortness of breath)
Wheezing
Chest tightness
Frequent respiratory infections
Fatigue and reduced exercise tolerance
19
Q
chronic bronchitis symtoms
A
Chronic productive cough
Dyspnea Wheezing and rhonchi
Frequent respiratory infections
Fatigue
Cyanosis
Peripheral edema (in severe disease)
20
Q
in which disease do patients feel better in tripod position
A
acute excerbations of emphysema
21
Q
emhysema types and their differences
A
panaacinar- a1antitrypsin deficiency
centracinar
22
Q
cause of barel chest
A
Loss of elastic recoil → lungs stay expanded during expiration
23
Q
emhysema symtoms
A
Progressive Dyspnea
Pursed-lip Breathing
Prolonged Expiration
Weight Loss
Barrel-Shaped Chest
Pink Puffer” Appearance
Decreased Breath Sounds
Tripod Positioning
24
Q
asthma types
A
Atopic, Nonatopic, druginduced.
25
drug for druginduced asthma
zileuton, montelukast, zafirlukast.
26
COPD treatment
SABA. SAMA, LABA, LAMA
27
Asthma treatment
SABA, ICS, LABA
28
bronchiectasis symtoms
severe cough, hemoptesis, foul-smelling sputum, dyspnea, orthopnea, paroxysmal coughing spell, mucus drainage, clubbing of fingers.
29
diagnostic studies for emhysema
✅ High-Resolution CT (HRCT) scan of the chest – Gold Standard
Sputum culture and sensitivity:🔹 3. Pulmonary function tests (PFTs)
CBC
30
FEV1/FVC ratio changes during obstructive and restrictive lung disease
obstructive - decrease ratio
restrictive - normal or increase ratio
31
bronchiectasis clinical features?
Chronic productive cough
Recurrent respiratory infections
Hemoptysis
Dyspnea and wheezing
Clubbing Fatigue, weight loss
32
diagnosis
✅ High-Resolution CT (HRCT) – Gold standard
Sputum culture
33
what is bronchiectasis
Bronchiectasis is a chronic lung disease characterized by irreversible dilation of the bronchi, caused by chronic or recurrent inflammation and infection, leading to destruction of the bronchial wall.
34
types of restrictive lung disease
Extrapulmonary
Pulmonary
35
what is idiopathic pulmonary fibrosis
restrictive disease, symtomss- dyspnea dry cough, crackels, scarring, fibrosis between alveols.
36
treatment for aspergillus and actinomyces
echinocandins,ampotherici b and AZOLES
37
what can we see in sarcoidosis x ray
hilar and mediastinal adenopathy
38
what causes hypersansitivity pneumonitis
environmental agents, aspergillus actinomyces , bird fancier and farmer
39
sarcoidosis is most common in
black females
40
what happens in sarcoidosis
high ACE levels and CD4/CD8 ratio.immune mediated widespread noncaseating granulomas
41
sarcoidoses is associated with
bells palsy,schaumann and asteroid bodies, rheumatoid arthritis,high calcium,ocular uveitis,interstitial fibrosis,vitamin d activation(high 1 hydroxylasa) skin hanges. SARCOIDS
42
treatment for sarcoidosis
glucocorticoids
43
what kind of cell (bodies) can we see on mesothelioma histology?
psammoma bodies
44
which type of pneumoconiosis hasa high risk of tubercliosis
silicosis
45
pneumoconiosis which effect lower lobe is?
asbestosis
46
which pneumoconiosis has high risk of developing lung cancer and which cancers
asbestosis had high risk of mesothelioma and more commonly bronchogenic carcinoma
47
whats antracosis
associated with coal workers neumoconiosis-macrophages ladenwith carbon.causes black lung
48
golden-brown fusiform rods resemlingg dumbbells on can be found in which type of pneumoconiosis
asbestosis
49
eggshell calcification of hilar lymphnodes
silicosis
50
patient has noncaseasting granulomas,affected upper lobes. has been working at aerospace factory for 10 years now. what might be a cause?
beryliosis
50
pneumoconiosis usually have high risk of what syndrome
caplan syndrome,(rheumatoid pneumoconiosis)
51
patient has been working on a roof for a long time now. disease affacted the lower lobes, we can see ferruginous bodies of prussian blue stain. which pneumoconiosis is it
asbestosis
52
ARDS what happens and symptoms
hypoxemia edema iflamation, dyspnea,tachypnea,cyanosis,alveolar collapse due to loss of surfactant
53
a 45 year old man is admitted to the ICU with severe pancreatitis.three days later he develops sudden onset of dyspnea,hypoxemia.chest xray shows diffuse bilateral infiltrates.pulmonary capilarry wedge pressure is normal.what is the most likely diagnosis
ARDS
54
ARDS CAUSES
sepsis,aspiration pneumonia, pancreatitis,truma,burns,
55
ARDS diagnosis
abnormal chest x ray
respiratory failure within 1 week of alveolar insult
decreasedPAo2
symptomms of respiratory failure are not due to HF/fluid overload
56
how do two types of sleep apnea differ from eachother
Obstructive (airflow blocked despite respiratory effort) vs Central (absent respiratory effort due to CNS dysfunction)
57
What physical exam findings suggest a risk for OSA?
→ Obesity, large neck circumference, crowded oropharynx, retrognathia
58
What condition is commonly associated with central sleep apnea?
→ Congestive heart failure (especially Cheyne-Stokes breathing
59
What is the gold standard for diagnosing sleep apnea?
Polysomnography (sleep study)
60
What is the first-line treatment for moderate to severe OSA?
CPAP
61
Which medication may worsen central sleep apnea?
Opioids
62
whats pickwikian syndrome
Pickwickian syndrome, also known as obesity hypoventilation syndrome (OHS), is a disorder seen in severely obese individuals where hypoventilation leads to low oxygen (hypoxemia) and high carbon dioxide levels (hypercapnia) during the day.
63
what is pulmonary hypertension
elevated mean pulmonary artery pressure(>20mm hg) at rest.results in arteriosclerosis,medial hypertrophy,intimal fibrosis of pulmonary arteries,plexiform lessions.
64
what causes pulmonary arterial hypertension(group one)
inactivating mutations in bmpr2 gene. drugs,(amphetamin,cocaine),connective tissue disease,HIV,schistomasomiasis.
65
pulmonary hypertension type 3 lund diseases and hypoxia might be caused by
COPD, interstitial lung disease, sleep apnea
66
pulmonary hypertension types
Group 1: PAH (Pulmonary Arterial Hypertension)
Idiopathic, connective tissue diseases, congenital heart disease
Group 2: PH due to Left Heart Disease
LV dysfunction, mitral/aortic valve disease
Group 3: PH due to Lung Diseases/Hypoxia
COPD, interstitial lung disease, sleep apnea
Group 4: Chronic Thromboembolic PH (CTEPH)
Recurrent pulmonary emboli
Group 5: Miscellaneous/Multifactorial
Sarcoidosis, sickle cell, metabolic disorders
67
causes of atelectasis
obstuctive- old air is resorbed,new air cant get in
compressive-space occuping lesions,effusion,air,tumor
contraction-(cicatrization) scarring(fibrosis)
adhesive-lack of surfactants.NRDS
68
what happens during atelectasis
right upper lobe collapse,alveolar collapse
69
atelectasis treatment
incentive spirometry,(dzlierad ro chaisuntqos), high PEEP(keeps alveoli open during expiration,peventing collapse)
70
what is pleural effusions and treatment for it
excess accumulation of fluid.restricted lung expansion during inspiration.
treatment is thoracocentesis to remove fluid
71
pleural effusion types and causes
exudate-cloudy fluid(cellular)due to infection(pneumonia,tb)malignancy,trauma,.high vascular permiability
transudate-clear fluid(hypercellular). due to high hydrostatic pressure and low oncotic pressure
72
what is pneumothorax and sympthoims(pcd shi rac ewera egenic)
accumulation of air in pleural space. dyspnea,unevan chest expansion.chest pain, decreased tactile fremitus,hyperressonance.trachea shifted toward unaffacted side if tension pneumothorax.
73
types of pneumothorax
73
there was three diffeent kind of pleural effusions.what was that
hemothorax-blood in pleural cavity.
hydrothorax-serous fluid in pleural space
chylothorax-accumulation of chyle(milki fluid containing lymph and fats)
74
primary spontaneous pneumothorax is most common in who and due to whar
due to rupture of apical subpleural bleb or cysts. in tall thin young males.associated with tobacco smoking
74
secondary spontaneous pneumothorax is due to
due to diseased lungs (bullae in emphysema,marfan syndrome, infections)
75
patient comes with a dyspnea, chest pain. she has an accumulation of air in pleural space. her tactile fremitus is decreased and trachea deviates away from affacted lung. what might be the diagnosis
tension pneumothorax
76
whats consolidation and in which disease does it happen
Consolidation = Alveoli filled with fluid, pus, blood, or cells
in lobar pneumonia.
77
patient with the history of recent s aureus came with dyspnea,cough and sputum. he has a multilobar bilateral patchy distribution,which type of pneumonia might he have.
bronchopneumonia
78
what part is affected if aspiration pneumonia happens during standing up
right lower lobe
79
natural history of lobar oneumonia
congestion,red hepatization,gray hepatiation,resolution
80
whats lung abscess and which part will be affected if recumbent laying down
localized collection of pus within parenchyma,rul or rml
81
lung cancer complications
superior vena cava,thoracic outlet syndrome,pancoast tumor,horner syndrome,endocrine paraneoplastic syndrome,recurent laryngeal nerve compression(horseness),effusions.
82
lung cancers located centrally
small cell carcinoms,sqamous cell carcinoma
82
patient has a bloody cough,wheezing and bronchial obstructions. u can see pneumonic "coin" lesions on CXR.patient has been smoking for last 40 years.
lung cancer
83
65 years old jemaliko came with bloody cough, wheezing. his cxr shows coin lesions.his test results hows positive chromogranin A,synaptophysin and neuron specific enolase. what type of cells neoplasm causes this kind of diseiases
small cell carcinoma, neoplasm of neuroendocrin kulchitsky cells.
84
patient has been tobaco smoking for 50 years now. he has peripheral tumor. and enlarged breats due to excessive production of HGG.what type of lung cancer is it
large cell carcinoma
85
patient has peripheral tumor. has never smoked before. she has clubbing and cxr shows hazy infiltrates similar to pneumonia.has mutations in KRAS,EGFR,ALK genes. often stains mucin positively.what type of cancer is it
adenocarcinoma
86
patient test shows keratin pearls and desmosome intercellular bridges.has been smoking for 30 years.she has cavitation, excessive PTHrpits located centrally.what type of disease is it
squamos cell carcinoma
87
patient has carcinoid syndrome,flushing,diarrhea and wheezing. his results show positive chromogranin and nest of neuroendocrine cells.its located peripherally and centrally.which disease can it be
bronchial carcinoid tumor
88
patient has a lung cancer . she also feels swelling of the face. her face is swelled and blue.she has facial plethora,note blanching after fingertip pressure.she has jugular venous distention and feels dizziness and headaches.patient has one of those lung cancers complications which is?
superior vena cava syndrome
89
What is the average tidal volume (TV) in a healthy adult?
~500 mL or 6–8 mL/kg.
90
Which volume is the extra air you can inhale after a normal inspiration?
Inspiratory Reserve Volume (IRV).
91
What is the volume of air that remains in the lungs after a maximal exhalation?
Residual Volume (RV).
92
Which lung volume cannot be measured by spirometry?
Residual Volume (RV).
93
What is the extra air you can exhale after a normal expiration?
Expiratory Reserve Volume (ERV).
94
Which capacity is the sum of TV and IRV?
Inspiratory Capacity (IC).
95
What is the Functional Residual Capacity (FRC)?
ERV + RV; the volume left in the lungs after normal expiration.
96
Which lung capacity represents the total amount of air the lungs can hold?
Total Lung Capacity (TLC).
97
Which capacity is the maximum air you can exhale after a full inspiration?
Vital Capacity (VC).
98
Which capacities include Residual Volume (RV) and thus cannot be measured by spirometry?
FRC, TLC.
99
What does the work of breathing refer to
The energy or oxygen consumed by respiratory muscles to produce ventilation that meets the body’s metabolic demands.
100
What are the two main components the respiratory muscles must overcome during breathing?
Elastic recoil and airway resistance.
101
What is the formula for mechanical work in breathing?
Work = Force × Distance = Pressure × Volume.
102
How is the work of breathing minimized?
By optimizing respiratory rate (RR) and tidal volume (VT).
103
In restrictive lung diseases, which aspect of breathing is most affected and how is work optimized?
Increased work to overcome elastic recoil; achieved with increased RR and decreased VT.
104
In obstructive lung diseases, which aspect of breathing is most affected and how is work optimized?
Increased work to overcome airway resistance; achieved with decreased RR and increased VT.
105
80 years old patient has been smokig for last 60 years now. he has been coughing nonstop for three months for 2 years now.patient has bluish color on her face. he has resonant percussion but you hear wheezing and crackles sound.patient has high RV,FRC AND TLC. what kind of disease does he have.
tralalelo tralala chronichito bronchitico
106
patient has an alveolar collapse,trachea deviation toward the side of collapse,dullness, dyspnea,tachypnea. high PEEP, low RV,TLC AND VC.which disease do u suspect bitcheessss
atelectasis
106
whats work of breathing
It's the effort your body uses to breathe — to move air in and out.
107
What is the formula for calculating physiologic dead space (VD)?
VD = VT × (PaCO₂ – PECO₂) / PaCO₂
108
What does VD represent in the dead space equation?
What does VD represent in the dead space equation?
109
What does VT represent in the dead space equation?
Tidal volume (the total volume of air inhaled in a breath).
110
What does PaCO₂ represent in the equation?
Arterial partial pressure of CO₂.
111
What does PECO₂ represent in the equation?
Partial pressure of CO₂ in expired air.
112
What contributes to physiologic dead space?
Anatomic dead space (conducting airways) plus alveolar dead space.
113
In healthy lungs, physiologic dead space is approximately equal to what?
Anatomic dead space.
114
Which part of the healthy lung contributes most to alveolar dead space?
The apex of the lung (due to poor perfusion).
115
When is physiologic dead space greater than anatomic dead space?
In diseases with ventilation/perfusion (V/Q) mismatch.
116
What is the formula for minute ventilation (VE)?
VE = VT × RR
117
What does VE (minute ventilation) represent?
The total volume of gas entering the lungs per minute.
118
What is the normal respiratory rate (RR) in adults?
12–20 breaths per minute.
119
What is the normal tidal volume (VT) per breath?
500 mL.
120
What is the approximate anatomic dead space (VD) per breath?
150mL
121
What is the formula for alveolar ventilation (VA)?
VA = (VT − VD) × RR
122
What does VA (alveolar ventilation) represent?
The volume of gas that reaches the alveoli per minute
123
Why is alveolar ventilation (VA) less than minute ventilation (VE)?
Because dead space (VD) air does not participate in gas exchange.
124
In what unit are pulmonary pressures usually expressed?
cm H₂O (centimeters of water).
125
What is elastic recoil in the respiratory system?
The tendency of the lungs to collapse inward and the chest wall to spring outward.
126
Define lung compliance and its formula.
Compliance = ΔV/ΔP (change in volume per change in pressure); it reflects how easily the lungs can expand.
127
What happens to lung compliance in emphysema or aging?
Increased compliance – lungs are easier to fill due to loss of elastic tissue.
128
What happens to compliance in conditions like pulmonary fibrosis, ARDS, or pneumonia?
Decreased compliance – lungs are stiffer and more difficult to fill.
129
What is hysteresis in lung physiology?
hysterisis in oxygen-hemoglobin dissociation curve=the lag/difference between loading and unloading of oxigen from hemoglobin.how o2 is loaded vs unloaded from hb.it gives curve its Sigmoidal shape.
130
What is the pressure in the alveoli and airways at FRC (functional residual capacity)?
Zero (equal to atmospheric pressure).
131
What is the intrapleural pressure at FRC?
Negative, to prevent alveolar collapse (atelectasis).
132
At FRC, what is the relationship between lung and chest wall forces?
Inward recoil of the lungs is balanced by the outward recoil of the chest wall.
133
When is pulmonary vascular resistance (PVR) at its minimum?
At FRC.
134
how is v/q aquation in 1 zone of the lung
V/Q IS HIGH. blood cant get to the first zone due to gravity.ventilation is higher than blood flow
134
how can we determine the physiological dead space
vd=VT x (PaCO2-PECO2)/Paco2
135
what happens if V/Q is 0
airway obstruction.shunt
136
what happens if V/Q IS ∞
physiological dead space blood flow is obstructed.
137
how can we measure alveolar gas equation. how much oxygen is inside your alveoli,where gas exchange happens
PAo2=PIo2- Paco2/RQ
1.oxygen pressure i the alveoli
2. oxygen in the air you Inhale
3.co2 pressure in arterial blood
4.CO2 made/o2 used
137
three ways co2 moves in the blood
bicarbonat(HCOE),carbaminohemoglobin(binds to globin part of hb).free disolved co2.
138
what do we need to balance hco3 in the blood
CL and hco3 exchange to keep things electrically balanced. chloride shift.
138
whats halden effect
mechanism where oxygenated hemoglobin helps CO2 leave the rbcs in the lungs. anu jangbadi umagrdeba hemeze da globinidan shordeba co2.
139
myoglobins curve will be sygmoidal or hyperbolic,is affinity higher or lower than hb and why
hyperbolic (steady) because it only binds to one oxygen, unlike hemoglobin sygmoidal curve, in myoglobin there is no positive cooperativity. it will have higher affinity
140
how do we measure total o2 delivery
cardiac output* o2 content.
140
during polycytemia there will be high total o2 content due to
high levels of red blood cells and hemoglobin.
141
during co poisoning Sao2 and total o2 content will be? magali tu daballi da rato
sao2 will be low because co competes with o2. total o2 content will also be low.
141
what happens during methemoglobinemia and how does it effect sao2 and total o2 content
fe2 of hemoglobin becomes fe3 which has poor binding of o2. total o2 cotant will be low do to poor binding.
142
hb has low affinity for o2 and realises o2 easily in tissue. shift will be on which side
right shift realises o2 easily to tissues
143
if curve is shifted to the left. oxygen and co2 levels will be
oxygen will be high, less to tissue, low affinity. co2 will be low.
144
high altitude response.co2 and oxygens level will be? what happens to hco3
paco2,pao2 will be low. respiratory alkalosis, renal hco3 excretaion
145
methemoglobinemia curve and treatment
shifted to left, because fe3 has low affinity of o2. ad treatment is vitamin c and methylene blue
145
during exercise curve what happens and curve will be to which side
right, high level of o2 is released in tissues..pumonary blood flow and rr is high. but body keeps arterial gases normal,venous blood shows the real changes .
146
during high altitude response curve will be shifted
right due to low o2 and high 2,3 bpg,mitochondria and erythropoetin.
147
what happens during cyanide poisoning
blood has enough oxygen, cells have enough oxygen but hant use it because cyanide blocks the electron transport change(complex iv) no atp=death.
147
cyanide poisoning lab results shows metabolic acidosis,there is high level of what
lactate. cells start anaerobic lactate metabolism.lactate build up in the blood
148
pa o2 and sao2 in cyanide poisoning will be high low or normal
normal becuase there is enough oxygen the problem is in cells.
149
pao2 and sao2 in carbon monoxide will be high low or normal and why.
pao2 will be normal because oxygen dissolved in plasma. co doesnt affect how much oxygen is dissolved in the liquid part of blood.sao2 will be falsely high on the pulse oximeter(it cant tell the difference between hemoglobin and co in the hb).so less o2 is carried but oximeters show high because co binds to the same spot as o2.
150
during cyanide poisoning curve will be
normal. oxygen sisxlshi gvaq cellebshia problema
151
during carbon monoxide poisoning curve will be
left. high affinity of o2. hb binds o2 tightly and wont let go in the tussue=hypoxia
151
five mechanism of hypoxemia
1. inspired oxygen tension is low(pio2)
2. hypoventilation (due to high paco2)
3.diffusion limitation(fibrosis)
4. V/Q mismatch
5. right to left shunt
151
lung development stages.how long is embrionic stage.lastly in this stage will develop what. and errors at this stage will cause what disease.
embrionic(4-7)
pseudoglandular(5-17)
canalicular(16-25)
saccular(24-bieht)
alveolar (36-8 years)
weeks 4-7.lung bud-trachea-bronchial buds-mainstem bronchi-secondary -tertiary. error at this stage can lead to trancheoesophageal fistula.
152
pneumocytes develops at which week
week 20. uring canalicular
152
respiration is capable at which stage and week.
week 24. canalicular(16-25) and saccular(24-birth).because in canalicular fetus develops respiratory bronchioles.
152
in uterus babys pulmonary vascular resistence is
high due to fluid in lung. baby doesnt really breath so no expansion happens. after birth baby takes air into the lungs so it expands. pvr will drop low.
153
what is choanal atresia
Choanal atresia is a congenital condition (present at birth) where the back of the nasal passage (choana) is blocked — either by bone, soft tissue, or both.
153
CHARGE Syndrome
Coloboma of eye
Heart defects
Atresia of choanae
Restricted growth and development
Genitourinary defects
Ear defects
154
which malformations is associated with potter sequence and what is it?
Pulmonary hypoplasia and renal agenesis
155
what is pulmonary hypoplasia
Pulmonary hypoplasia is a congenital condition where the lungs are underdeveloped — meaning:
Fewer and smaller alveoli
Reduced lung tissue and airways
Impaired gas exchange
Poorly developed bronchial tree with abnormal histology. Associated with congenital diaphragmatic
hernia (usually left-sided), bilateral renal agenesis (Potter sequence).
156
what is bronchial cyst?
A bronchogenic cyst is a benign, congenital, fluid-filled cyst near the trachea or bronchi, formed from abnormal airway development. It can cause breathing issues or infections and is typically removed surgically.
157
what is neonatal distress syndrome
Surfactant deficiency -> surface tension ->
alveolar collapse
158
what is the treatment for neonatal distress syndrome
treatment: maternal glucocorticoids before birth; exogenous surfactant for newborns
159
What type of cells are Type I pneumocytes?
Squamous epithelial cells that cover 97% of the alveolar surface for optimal gas exchange.
160
What is the main function of Type I pneumocytes?
Form the thin barrier necessary for efficient gas exchange.
161
What are Pores of Kohn?
Connections between alveoli that allow air, fluid, macrophages, and bacteria to pass between them.
162
What type of cells are Type II pneumocytes?
Cuboidal and clustered cells that make up about 3% of alveolar surface.
163
Name the two main functions of Type II pneumocytes.
Act as stem cells for both Type I and Type II pneumocytes.
Secrete surfactant from lamellar bodies.
164
What is the main component of pulmonary surfactant?
Dipalmitoylphosphatidylcholine (DPPC).
165
What does surfactant do to lung mechanics?
↓ Surface tension
↓ Alveolar collapse
↓ Lung recoil
↑ Compliance
166
When does surfactant synthesis begin and mature in gestation?
Begins ~20 weeks; matures by ~35 weeks.
167
What hormone promotes fetal surfactant synthesis?
Glucocorticoids.
168
What is the formula for collapsing pressure in alveoli (Law of Laplace)?
P = 2 × surface tension / radius
169
What are the functions of alveolar macrophages?
Phagocytose foreign materials
Release cytokines and proteases
170
When are hemosiderin-laden macrophages seen in the alveoli?
In conditions like pulmonary edema or alveolar hemorrhage.
171
what is conducting zone and where does it stop?
conducting Zone – Summary:
Function: Air passage only (no gas exchange)
Includes: Nose → nasopharynx → larynx → trachea → bronchi → bronchioles → terminal bronchioles
Ends at: Terminal bronchioles
Main roles: Warm, humidify, filter air; mucociliary clearance; vocalization
172
what is respiratory zone and its function
Lung parenchyma; consists of respiratory bronchioles, alveolar ducts, and alveoli. Participates in gas
exchange. main function is gas exchange
173
olfactory area their function and where it is lovated
thick pseudrostratified columnar epithelium and its function is olfaction
174
respiratory epithelium and those location
ciliated, pseudostriatified columnar epithelium, most areas of nasal cavity, nasopharynx and posteriororopharynx, larynx
175
upper respiratory tract and lower repiratory tract parts
176
superior mediastinum
thymus, great vessels , xnerves, trachea, esophagus, thoracic duct
177
inferior mediastinum
anterior- between sternum and pericardium
middle- central portion
posterior - behind the mediasternum
178
What structures are included in the upper respiratory tract?
Nose, nasal cavity, pharynx, and larynx.
179
What structures are included in the lower respiratory tract?
Trachea, bronchi, bronchioles, and lungs
180
What is the function of the nasal conchae?
To increase surface area for warming, humidifying, and filtering air.
181
Which structure prevents food from entering the trachea during swallowing?
The epiglottis.
182
What is the name of the cartilage that forms the Adam’s apple?
Thyroid cartilage.
183
At which vertebral level does the trachea bifurcate?
Around the level of T4-T5 (the sternal angle).
184
What are the three parts of the pharynx?
Nasopharynx, oropharynx, and laryngopharynx.
185
What is the name of the smallest airways that lack cartilage and glands?
Terminal bronchioles.
186
What are the three single cartilages of the larynx?
Thyroid, cricoid, and epiglottis.
187
What are the three paired cartilages of the larynx?
Arytenoid, corniculate, and cuneiform cartilages.
188
Which cartilage is the only complete ring in the airway?
Cricoid cartilage.
189
What is the function of the vocal folds (true vocal cords)?
Sound production and regulation of airflow into the lungs.
190
What is the name of the space between the vocal cords?
The rima glottidis.
191
What is the pathway of airflow from the trachea to the alveoli?
Trachea → primary bronchi → secondary bronchi → tertiary bronchi → bronchioles → terminal bronchioles → respiratory bronchioles → alveolar ducts → alveolar sacs → alveoli.
192
Which lung has three lobes and two fissures?
Right lung.
193
Which lung has two lobes and one fissure?
Left lung.
194
What is the tongue-shaped projection of the left lung called?
The lingula.
195
What are the pleural layers covering the lungs?
Visceral pleura (on the lung surface) and parietal pleura (lining the thoracic wall).
196
What is the function of the pleural cavity?
To reduce friction during breathing and provide surface tension for lung expansion.
197
Which bronchus is more vertical, shorter, and wider—making it more likely to receive aspirated objects?
The right main bronchus.
198
Which paired cartilages are involved in vocal cord movement by attaching to the vocal ligaments?
Arytenoid cartilages.
199
What is the function of the corniculate and cuneiform cartilages?
To support and stiffen the vocal folds and lateral aspects of the epiglottis.
200
What muscle tenses the vocal cords and raises pitch?
Cricothyroid muscle.
201
What muscle is the only one that abducts (opens) the vocal cords?
Posterior cricoarytenoid muscle
202
Which muscles adduct (close) the vocal cords?
Lateral cricoarytenoid and transverse arytenoid muscles.
203
Which muscle relaxes the vocal cords to lower pitch?
Thyroarytenoid muscle (including the vocalis portion).
204
What is the function of the aryepiglottic muscle?
It pulls the epiglottis down to cover the laryngeal inlet during swallowing.
205
what is Which intrinsic laryngeal muscle is located within the vocal fold and fine-tunes tension?
Vocalis muscle.
206
What nerve innervates the cricothyroid muscle?
External branch of the superior laryngeal nerve (from CN X).
207
What is the clinical significance of the recurrent laryngeal nerve?
Damage to it can cause hoarseness or loss of voice due to paralysis of most laryngeal muscles
208
What membrane is pierced during emergency cricothyrotomy?
Cricothyroid membrane.
209
Oligohydramnios
Oligohydramnios refers to a condition in pregnancy characterized by too little amniotic fluid — the protective liquid that surrounds the fetus in the uterus. It’s typically diagnosed when the amniotic fluid index (AFI) is less than 5 cm or the single deepest pocket of fluid is less than 2 cm on ultrasound.
210
terminalbronchiol cell types
simple cuboidal and ciliated simple columnar
211
treatment for influenza B
Amantadine, rimantadin
212
amantadine side effects
livedo reticularis
213
what is livedo reticularis
214
how amantadine acts
enhencing release of dopamine
214
treatment for influenza A &B
oseltamivir and zanamivir
214
antiherpes drugs
inhibit viral dna polymerase -> blocks dna synthesis
215
antiherpes drugs
Acyclovir - mimics normal compounds not affective cmv
216
herpes types
HSV-1 ORAL HERPES
HSV-2 GENITAL HERPES
HSV-3VARITSELLA ZOSTER VIRUS
HSV-4 ABV
HSV-5CYTOMEGALOVIRUS
