Lecture 7: Pulmonary Pathology and Pharmacology Flashcards
Which of the following is a group of eight specific tests for electrolyte level, acid-base balance, blood sugar, and kidney status
a) Basic metabolic panel
b) Comprehensive metabolic panel
c) Hepatic function panel
d) Chemistry panel
a
Which of the following is very susceptible to potassium level changes
a) Kidney
b) Heart
c) Liver
d) Intestines
Heart (however, all 4 can be susceptible)
How is the respiratory system is subdivded into what 3 main portions
1) Upper airway
2) Lower airway
3) Terminal alveoli
Whats in the upper airway? (5)
Consistns of:
1) Nasal cavities (humidification)
2) Sinuses
3) Pharynx
4) Tonsils
5) Layrnix
Lower airway consistns of (3)
1) Trachea
2) Bronchi
3) Bronchioles
The ability to move air in and out of the lungs via a pressure gradient
Ventilation (the actual movement, not gas exchange)
The gas exchange supplies oxygen to the blood and body tissues and removes carbon dioxide
Respiration
Between the aveloi/capillaries what is going on, respiration or ventilation
Respiration
this is the gas exchange
What is last to develop in this image below?
The alveolar ducts
This is why in pre matures theres a problem, because w/o these ducts gas exchange cannot take palce
* This is what the steriod is for
Amount of air that is inhales and exhaled during normal resting breathing
Tidal Volume
Volume of air remaining in the lngs following a full or maximal expiration
Residual volume
Volume of air that can be forcefully expelled following a normal expiration
Expiratory reserve volume
Volume of air that can be forecfully breathed in following a normal inspiration
Inspiratory reserve volume
Amount of air that can be forcefully expelled in 1 second following full inspiration
* What is the normal
Forced expiratory volume (FEV1)
75% of FVC should be exhaled within the first second
* If less than you’re proably having trouble getting air out = obstructive
Amount of air under volintional control
Forced vital capavity
this is the amount of air a person can breath out after taking a deep breath
* Note this is different than fev1 because its measuring all the air they can breath out, not just the air in the first 1 second.
vitial capcity
TV+IRV+ERV
Inspiratory capcity
TV+IRV
Total lung capcity
TV+IRV+ERV+RV
sum of residual volume and the forced vital capacity
Functional residual Capacity
ERV + RV
volume of air remaining in the lungs following a normal expiration
What is the most common condition caused by pulmonary disease or injury
Hypoxemia
Deficient oxygenation of arterial blood
hypoxemia
remember, venous blood is already deoxygenated so we don’t care that much about it
s/s vary depending on the level of oxygenation in the blood
Broad term meaning diminished availability of oxygen to the body tissues
Hypoxia
(different than hypoexmia because its much more broad)
What is partial pressure
Refers to the pressure that a single gas in a mixture of gases contributes to the total pressure in.
In a mixture, each gas behaves indepdently, exerting pressure as if it were the only gas present
EX: in the atmosphere, air is a mixture of gases like nitrogen, oxygen, carbon dixoside, and other. Each of these gases has its own partial pressure, and the sum of all the partial pressures equals the total atmospheric pressure
What is PaO2
The partial pressure of oxygen in the arterial blood
* the amount of oxygen in the artial blood
* Measures O2 as a gas exerting itself on blood vessels
It measures the pressure exerted by dissolved oxygen gas molecules in the plasma of the artial blood (GPT)
How do you get a PaO2 reading and why is it hard?
its hard because they have to take it directly from an artery (which is deeper) because it shows how much O2 is actually in that artery (a vein doesnt show us this [doesnt have as much O2)
* arteries are deeper
What is a normal PaO2?
* bad ranges
80=100mmHg
these are s/s of hypoexmia as well because its not enough O2 in the arterial blood
KNOW: PaO2 is not the same thing as oxygen saturation (their norms are similar which is why they get confused)
What is oxygen saturation?
The % of hemoglobin binding sites in the blood that are carrying oxygen (each hb can carry 4)
The amount of O2 bount to hemoglobin gives you the ….
Oxygen saturation
Each hemoglobin carrying 4 = 100%
each carrying 3 = 75%
etc…
NOTE: if the hb molecule is in the carpillaries near the cell feeding it O2 it will decrease the ability of the hb around it to hold O2 and they will all drop their O2
O2 saturation and PaO2 ARE NOT THE SAME THING
This shows us that out O2 satuartation does not = our PaO2
we can have a quick decline in PaO2 but our O2 saturation stays somewhat normal
telling us theres not enough O2 in blood for there to even be binding
Ventilation to perfusion ratio
* We need to have enough air flow coming in and enough BF so that there can actually have gas exchange in the capillaries
* need to have O2 coming in and enough blood to carry that O2
What should v/q be?
v/q = 0.8 = normal
this is
airflow/bloodflow
we need enough airflow and blood flow so that gas exchange is occuring in the capillaries
should be close to 1:1 ideally but 0.8 is the more realistic norm
what 3 things influence the v/q relationship?
airflow / BF
1) Gravity
2) Body position
3) Cardiopulmonary dysfunction
when you have a pumnonary disease it will cause some mismatch in this ratio in either dirction
When sitting / HOB elevated helps this mismatch, but when lying flat this miss match can be more opparent
KNOW: Perfusion is gretest in gravity depdent areas
* lower lobes when sitting
* blood flow is highest in the parts of the body or organs that are positioned lower relative to gravity
* EX: in the lungs, gravity causes more BF to the lower (gravity depdent) regions when a person is standing or sitting. This is because gravity pulls blood downward, increasing the perfusion in these areas compared to the upper parts of the lungs.
Gravity dependent =
something affected or influenced by gravity
V/Q miss match normall happens because of 2 things
1) Dead space
2) Shunt
Ventillation is in excess of perfusion (pulmonary embolus)
Dead space
Perfusion is in excess of ventilation (alveolar collapse from secretion)
Shunt
* situation where blood flows through the lungs without being properly oxygenated
* This happens when areas of the lungs are perfused (recieve BF) but are not ventilated (don’t recieve air), meaning the blood bypasses the gas exchange process
Blood flow to the lungs is greater than the amount of air (ventilation) reaching the alveoli, where gas exchange occurs. This imbalance leads to inefficient oxygenation of the blood
One cause of this mismatch is alveolar callapse due to secretions, which can block or partially obstruct the airways, reducing airflow to certain parts of the lungs. When alveoli collapse, blood still flows to these areas (perfusion), but since theres little to no air exchange, oxygen cannot effectively enter the blood stream, and Co2 cannot leave
S/S of pulmonary disease (6)
1) Cough
2) Dyspnea
3) Chest Pain
4) Cyanosis
5) Clubbing
6) Altered breathing patterns
Cough time frames
3 weeks = acute
3-8 weeks = subacute
8 or more weeks = chronic
Cough w/ clear or white sputum might indicate
irritation
Productive cough w/ yellow/green =
infection
Do you have chest pain quickly w/ pulmonary disease?
* why
* What kind of pain is this
No chest pain until the disease has progressed significantly
Chest pain is usually caused by extension into the pleura space (partial / visceral pleura)
* mass or inflammation doesnt hit for a while (after its expanded)
Pleural irritation is sharp in nature, localized, and aggravated w/ respiration
What does cystic fibrosis do to nails?
Clubbing
rounded
Eupnea is what?
Normal breathing 12-20
Kussmauls
* How many breaths per minute
* What kind of breathing
* What causes it
Deep, rapid breathing >20/min
diabetic ketoacidosis
has to do w/ acid based exchange / pH level
Cheyne-Stokes
* what kind of breathing
* What causes it (3)
Iregular, shallow, periods of apnea
End of life, brain tumors, TBI
Biot’s
* what kind of breathing
* What causes it (2)
Irregular pattern of deep and shallow breaths
caused by stroke or opioid use
Apnea
Stopping in the breathing
tachypnea
fast breathing
Bradypnea
slow breathing
What is most likely to cause a mismatch ventiliation-toperfusion ratio?
a) Pulmonary embolism
b) Decreased pulmonary secretions
c) V/Q ratio of 0.8
d) Gravity
a
pulmonary embolism = increased dead space = change in that ratio (in additional to the normal dead space that we should have un lungs)
gravity will actually cause a match (decrease in miss match)
note having thinner mucus is good = b is incorrect but if its too thin than the alveoli would colapse so it depends on how you read b
* shes assuming its still in a normal range instead of decreased to the point of alveolar collapse
What kind of lung injury ispneumonia considered?
* Wjat causes it 5
Acute lung injury
1) Bacterial
2) Viral
3) Funal
4) Inhalation of toxic chemicals
5) Aspiration (inhaling food) (babbies and older adults)
w/ pneumonia we have bronchole constriction and increased mucus production
* We produce the mucus to catch the baceria then cough it out
KNOW: Pnemonia = 30% bacterial 50% viral
You can clear pnemonia out w/ certain therpuetic tachniques (important to know which lobe of the lung its in to target that area)
Risk factors?
Clinical manifestation:
older adult symptoms?
Risk:
1) older age
2) smoking
3) poor nutrition
4) previous pneumonia
5) COPD
6) asthma
7) reduced function
8) poor oral hygine
9) environmental
10) acid-reducing medications
Manifestation:
1) Upper respiratory injection
2) Pleuritic chest pain
3) Productive cough
4) Dyspnea
5) Tachypnea
6) crackles
7) fatigue
8) fever
9) chills
10) generalized myalgias
Older adults have different sumptoms, often less, and loss of appetitive
KNOW: Pneumonia can be in one lobe or lots
Pneumocystis Carinii Pneumonia:
* What causes it
* risk factors
Caused by funal infection that affects those w/ altered immunity
* graft-versus-host disease
* Immunosuppressants
* Low serum albumin
* HIV
caused by aerosolized particals (droplets that can be a solid or liquid)
fever, alterd respiratory function dyspnea
What happens w/ pulmonary TB:
Virus enters your body
you have an inflamatory response to it and develop a nodule for whatever that pathogen is (will show on chest x-ray)
* can be a carrier if you still have this (can confirm w/ x-ray)
Typically in immunosupressed/older adults
pathogensis: primary infection, latent disease, active disease
* can be a carrier for a long time
clinical manifestation: Productive cough, unexplained weight loss, night sweats, fever, fatigue, chest pain
Thick wall cavities with purulent exudate; develops beacuse of complications from pneumonia
Lung abscess
secretions like mucus get trapped, and become purulent/thick
An inflammation of the trachea and bronchi (tracheobronchial tree) that is of short duration (1-3 weeks) and self-limiting with few pulmonary signs
* Symptoms
* Treatment
* Prognosis
Acute bronchitits
Symptoms = include early symptoms of an upper respiratory infection or a common cold
Treatment is conservative and symptomatic with cough suppressants, rest, humidity, nutrition, and hydration
* need to stay hydrated to break up mucus and break up its viscosity
Prognosis is usually good w/ treatment
white streaks shouldnt be there
Lung abscess:
* Risk factors
* Pathogensis
* Clinical manifestation
will present like an infection because it is an inflammatory process (abcess full of puss)
risk factors = all those things that make it a little bit harder to breathe
KNOW: For the checkpoint questions know what the other things in them do and what would make them right
checkpoint questions are a lot easier than exam questions
exam questions are more for application
KNOW: shes going to use more common medications on questions
* Both names will be included
What kind of medications supress coughing
* are they for long or short term use?
* they are derivived from what two drugs?
Antiussives
Short term use
They are codein and opioid derivatives (why they are for short term use –> addictive)
How do decongestants work?
Alpha 1-adrenergic agonists bind to alpha 1 receptors in the blood vessels and stimulate vasoconstriction
* so basically stops mucus from flowing out
Makes sense adrenergic = some kind of sympathetic drug
* agonist = sitting in the place of that sympathetic drug and causing its effect
* If its in the blood vessels the sympathetic response = vaso consitriction
How do Antihistamines work
block the affects of histamine, mainly H1 receptors located on vascular and respiratory tissue
Histamin is a receptor that allows us to have an immune response. If no immunse response = decreased swelling
What do mucolytics do?
Decrease the viscosity of respiratory secretions
KNOW:
Antiussives + Expectorants often perscribed together
Mucolytics + Expectorants often perscribed together
What do Expectorants do? (2)
Facilitate the production and ejection of mucus
These are common antitussives
Shes going to give us the pathology and we need to know what drug to use
EX: Patient is producing lots of mucus, we should know mucolytis is proably the ideal choice
Adverse effects of antitussives
* Most common
* 2 others
Primary = sedation (sleepy)
Gastrointestinal upset
Dizziness
NOTE: prone to tolerance increase due to use to the fact that they’re opioid derivivitives
Nasal Decongestants
all end in ine
MOA: of decongestants
* bind to alpha 1 adrenergic agonists and cause vasoconstriction (essentailly stoping the flow)
These agents bind to alpha=1 receptors located on the blood vessels of the nasal mucosa and stimulate vasoconstriction, thus effectibely drying up the mucosal vasculature and decreasing local congestion in the nasal passages
Adverse effects of decongestions (1)
Increased sympathetic NS activity and can cause serious cardiovascular and CNS excitation
* Makes since based on their MOA (bind to beta 1 receptors as agonists)
* Mkaes you more awake, palpatations etc. Anything w/ being more exceited
NOTE: Pts should avoid excessive us or abuse. This is common as many of these agents develop tolerance
Antihistamines
* First generation (1)
* Second generation (4)
* difference between these two
First = diphenhydramine
* think benedril makes you drwosy
Second: non-drowsy
* Cetirizine (Zyrtec)
* Loratadine (Claritin)
* Desloratadine (Clarinex)
* Fexofenadine (allegra)
When are anti histamines used
Moa of anti hishistamines
Most common applications of antihistamines are the treatment of respiratory symptoms caused by viral infections such as the common cold and the respiratory allergic response to seasonal allergies
* so cold (because memics allergic rxn) and for allergies
During allergic reactions, respiratory infections, and so forth, the effects of histamine are mediated primarily through the H1 receptors located on vascular, respiratory, and other tissues
* they inhibit histamine, which starts that allergic response / in common colds
Adverse effects of antihistamines
- Sedation (first generation)
- Fatigue
- Dizziness
- Blurred vision
- Incoordiantion
- GI
Big reaction going on = less sleepy
MOA for mucolytic drugs
Remember, these drugs try to decrease the viscosity of respiratory secretions (effectively thining mucus)
Taken w/ Expectorant drugs facilitate the production and ejection of mucus
Acetylcysteine (mucosil, mucomyst)
* Splits the disulfide bonds of respiratory mucoproteinsm thus forming a less viscous secretion
Guaifensin
* not fully understood
* similar to just increasing fluid intake
