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Pharma 2 > Lecture 7: Pulmonary Pathology and Pharmacology > Flashcards

Lecture 7: Pulmonary Pathology and Pharmacology Flashcards

1
Q

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

a

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2
Q

Which of the following is very susceptible to potassium level changes

a) Kidney
b) Heart
c) Liver
d) Intestines

A

Heart (however, all 4 can be susceptible)

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3
Q

How is the respiratory system is subdivded into what 3 main portions

A

1) Upper airway
2) Lower airway
3) Terminal alveoli

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4
Q

Whats in the upper airway? (5)

A

Consistns of:
1) Nasal cavities (humidification)
2) Sinuses
3) Pharynx
4) Tonsils
5) Layrnix

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5
Q

Lower airway consistns of (3)

A

1) Trachea
2) Bronchi
3) Bronchioles

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6
Q

The ability to move air in and out of the lungs via a pressure gradient

A

Ventilation (the actual movement, not gas exchange)

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7
Q

The gas exchange supplies oxygen to the blood and body tissues and removes carbon dioxide

A

Respiration

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7
Q

Between the aveloi/capillaries what is going on, respiration or ventilation

A

Respiration

this is the gas exchange

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7
Q

What is last to develop in this image below?

A

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

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8
Q

Amount of air that is inhales and exhaled during normal resting breathing

A

Tidal Volume

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9
Q

Volume of air remaining in the lngs following a full or maximal expiration

A

Residual volume

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10
Q

Volume of air that can be forcefully expelled following a normal expiration

A

Expiratory reserve volume

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11
Q

Volume of air that can be forecfully breathed in following a normal inspiration

A

Inspiratory reserve volume

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12
Q

Amount of air that can be forcefully expelled in 1 second following full inspiration
* What is the normal

A

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

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13
Q

Amount of air under volintional control

A

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.

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14
Q

vitial capcity

A

TV+IRV+ERV

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15
Q

Inspiratory capcity

A

TV+IRV

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16
Q

Total lung capcity

A

TV+IRV+ERV+RV

sum of residual volume and the forced vital capacity

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17
Q

Functional residual Capacity

A

ERV + RV

volume of air remaining in the lungs following a normal expiration

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18
Q

What is the most common condition caused by pulmonary disease or injury

A

Hypoxemia

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19
Q

Deficient oxygenation of arterial blood

A

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

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20
Q

Broad term meaning diminished availability of oxygen to the body tissues

A

Hypoxia

(different than hypoexmia because its much more broad)

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21
Q

What is partial pressure

A

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

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22
Q

What is PaO2

A

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)

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23
Q

How do you get a PaO2 reading and why is it hard?

A

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

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24
Q

What is a normal PaO2?
* bad ranges

A

80=100mmHg

these are s/s of hypoexmia as well because its not enough O2 in the arterial blood

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25
Q

KNOW: PaO2 is not the same thing as oxygen saturation (their norms are similar which is why they get confused)

A
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26
Q

What is oxygen saturation?

A

The % of hemoglobin binding sites in the blood that are carrying oxygen (each hb can carry 4)

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27
Q

The amount of O2 bount to hemoglobin gives you the ….

A

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

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28
Q

O2 saturation and PaO2 ARE NOT THE SAME THING

A
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29
Q

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

A
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30
Q

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

A
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31
Q

What should v/q be?

A

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

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32
Q

what 3 things influence the v/q relationship?

A

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

33
Q

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.

A
34
Q

Gravity dependent =

A

something affected or influenced by gravity

35
Q

V/Q miss match normall happens because of 2 things

A

1) Dead space

2) Shunt

36
Q

Ventillation is in excess of perfusion (pulmonary embolus)

A

Dead space

37
Q

Perfusion is in excess of ventilation (alveolar collapse from secretion)

A

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

38
Q

S/S of pulmonary disease (6)

A

1) Cough
2) Dyspnea
3) Chest Pain
4) Cyanosis
5) Clubbing
6) Altered breathing patterns

39
Q

Cough time frames

A

3 weeks = acute

3-8 weeks = subacute

8 or more weeks = chronic

40
Q

Cough w/ clear or white sputum might indicate

A

irritation

41
Q

Productive cough w/ yellow/green =

A

infection

42
Q

Do you have chest pain quickly w/ pulmonary disease?
* why
* What kind of pain is this

A

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

43
Q

What does cystic fibrosis do to nails?

A

Clubbing

rounded

44
Q

Eupnea is what?

A

Normal breathing 12-20

45
Q

Kussmauls
* How many breaths per minute
* What kind of breathing
* What causes it

A

Deep, rapid breathing >20/min

diabetic ketoacidosis

has to do w/ acid based exchange / pH level

46
Q

Cheyne-Stokes
* what kind of breathing
* What causes it (3)

A

Iregular, shallow, periods of apnea

End of life, brain tumors, TBI

47
Q

Biot’s
* what kind of breathing
* What causes it (2)

A

Irregular pattern of deep and shallow breaths

caused by stroke or opioid use

48
Q

Apnea

A

Stopping in the breathing

49
Q

tachypnea

A

fast breathing

50
Q

Bradypnea

A

slow breathing

51
Q
A
52
Q

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

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

53
Q

What kind of lung injury ispneumonia considered?
* Wjat causes it 5

A

Acute lung injury

1) Bacterial
2) Viral
3) Funal
4) Inhalation of toxic chemicals
5) Aspiration (inhaling food) (babbies and older adults)

54
Q

w/ pneumonia we have bronchole constriction and increased mucus production
* We produce the mucus to catch the baceria then cough it out

A
55
Q

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?

A

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

56
Q

KNOW: Pneumonia can be in one lobe or lots

A
57
Q

Pneumocystis Carinii Pneumonia:
* What causes it
* risk factors

A

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

58
Q

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

A
59
Q

Thick wall cavities with purulent exudate; develops beacuse of complications from pneumonia

A

Lung abscess

secretions like mucus get trapped, and become purulent/thick

60
Q

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

A

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

60
Q

Lung abscess:
* Risk factors
* Pathogensis
* Clinical manifestation

A

will present like an infection because it is an inflammatory process (abcess full of puss)

61
Q
A

risk factors = all those things that make it a little bit harder to breathe

62
Q
A
63
Q

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

A
64
Q

KNOW: shes going to use more common medications on questions
* Both names will be included

A
65
Q

What kind of medications supress coughing
* are they for long or short term use?
* they are derivived from what two drugs?

A

Antiussives

Short term use

They are codein and opioid derivatives (why they are for short term use –> addictive)

66
Q

How do decongestants work?

A

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

67
Q

How do Antihistamines work

A

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

68
Q

What do mucolytics do?

A

Decrease the viscosity of respiratory secretions

69
Q

KNOW:

Antiussives + Expectorants often perscribed together

Mucolytics + Expectorants often perscribed together

A
70
Q

What do Expectorants do? (2)

A

Facilitate the production and ejection of mucus

71
Q

These are common antitussives

A
72
Q

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

A
73
Q
A
74
Q

Adverse effects of antitussives
* Most common
* 2 others

A

Primary = sedation (sleepy)

Gastrointestinal upset
Dizziness

NOTE: prone to tolerance increase due to use to the fact that they’re opioid derivivitives

75
Q

Nasal Decongestants

A

all end in ine

76
Q

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

A
77
Q

Adverse effects of decongestions (1)

A

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

78
Q

Antihistamines
* First generation (1)
* Second generation (4)
* difference between these two

A

First = diphenhydramine
* think benedril makes you drwosy

Second: non-drowsy
* Cetirizine (Zyrtec)
* Loratadine (Claritin)
* Desloratadine (Clarinex)
* Fexofenadine (allegra)

79
Q

When are anti histamines used

Moa of anti hishistamines

A

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

80
Q

Adverse effects of antihistamines

A
  • Sedation (first generation)
  • Fatigue
  • Dizziness
  • Blurred vision
  • Incoordiantion
  • GI

Big reaction going on = less sleepy

81
Q

MOA for mucolytic drugs

A

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

Pharma 2 (23 decks)

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