Final Exam - Odds and Ins Flashcards

(23 cards)

1
Q

How are alveoli lost and compliance increased in emphysema?

A

Alvelar tissue is destroyed and can merge

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2
Q

What enzyme in the lungs is digestive and always active?
What does increased activity cause?

A
  • Trypsin, normal activity is low
  • Increased activity destroys normal elastic recoil tissue
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3
Q

What inhibits trypsin in the lungs?

A

⍺1-antitrypsin

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4
Q

What 3 things can cause a ⍺1-antitrypsin deficency?

A
  1. Inherited disorders (1:3,000) - leads to death by 30 w/o transplant
  2. Smoke - chemically inhibts activity, cant be filtered by nose/lungs
  3. Liver problems - causes decreased production of ⍺1-antitrypsin
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5
Q

Why do people who smoke increase how much they smoke when they drink?

A
  • Drinking increases liver activity which increases nicotine metabolism
  • This means they are going through their nicotine levels quickly
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6
Q

What form of iron is normally on Hb?

A

Fe++ - Ferrous

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7
Q

What does oxidative stress do to the iron on Hb?

A

Loss of an electron creating Fe+++ - Ferric
This is bad because it cannot release O2

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8
Q

What percent of Hb is in the Ferric state normally?

A

~1.5%

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9
Q

What enzyme reduces ferric Hb to ferrous Hb?

A

Methemoglobin Reductase - adds an electron

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10
Q

What are two types of sickle cell anemia and their cause?

A

Sickle cell trait = 1 defective β gene
Sickle cell disease = 2 defective β genes

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11
Q

What is the diameter of a capillary?

A

Smaller than size of RBC, meaning RBC change their shape when they move through

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12
Q

What happens to RBC in sickle cell anemia?

A

The RBC becomes sickled in the capillary after the O2 is offloaded leading to ischemia
These abnormal RBC have to be removed from circulation, leading to anemia

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13
Q

Treatments for sickle cell anemia?

A
  • Decrease activity
  • Replace with donor blood
  • Hydroxyurea - increases the amount of HbF (β sububits are replaced by Ɣ subunits)
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14
Q

Why is sickle cell trait still in the gene pool?

A

Causes increased resistance to malaria

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15
Q

What is HbA1C?

A

Adult Hb with looking at 1C position
The more Hb with sugars attached increases likelihood of DM

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16
Q

What is the normal amount of HbCO (carboxy Hb) in our body?
What would be the level if working in an environment where you are exposed?

17
Q

How are the chemoreceptors different in emphysema?
When can this be bad?

A
  • Chronically increased pCO2 and H+ leads to a decreased sensitivity to their changes
  • The respiratory drive changes to looking at pO2 for primary gauge for ventilation
  • A problem when on too much supplemental O2 is that the sensors stop stimulating ventilation - this worsens their acidosis because they are no longer getting blown off
18
Q

How does increased cardiac ouput affect gas exchange?

A
  • Not all of the alveoli/capillaries are being used at rest
  • When CO is increased those capillaries are recruited and increases the SA available for gas exchange
19
Q

How often do we sigh?

20
Q

Why do we sigh?
How does this play into anesthesia?

A
  • In order to sigh, we have a deeper breathe before hand
  • This deeper breathe maintains patency of alveoli and surfactant production
  • Anesthesia machines have a “sigh” setting which causes an increased Vt at regular intervals
21
Q

Why is adding surfactant to a normal ventilator not helpful for lung diseases?

A

Becasue the alveoli that need the surfactant are closed and only adding surfactant is not helpful

22
Q

Why do we yawn?

A

Yawn increases our lung volume before we lay down and decreases our lung volume

23
Q

What can a traumatic brain injury do to the respiratory control centers of the brain?

A

Trauma can cause a physical seperation of the PRG from the medulla leading to apneustic breathing