5/1 - Loose Ends

Question 1

Polio is a ________ disease that was prevelant in _______ and mainly affected ______. Describe it.

Answer 1

Neuromuscular disease

1960s

CNS unable to talk to skeletal muscles
-full or limited loss

Question 2

The 2 polio vaccines were ___% effective. Describe the incident with the polio vaccine in the 1955.

Answer 2

During this time was unsure of origin of polio & no way of treating beside iron lung

2 vaccines were created:
1. grew virus in lab –> killed it –> injected dead virus as vaccine
2. Engineered virus that was less potent

They didnt kill a batch of the lab grown virus & as a result:
-40,000 children developed polio
-200 paralyzed & 10 died
Lots ended up in iron lung

Pulled the lab grown/killed virus off the market –> only used engineered less potent vaccine

Question 3

What is our current polio vaccine? What do some people associate this with?

Answer 3

Current: Weakened Engineered virus

They link this to autism

Question 4

Polio was tracked back to _______ and it took them _______ to discover this.

Answer 4

public/school swimming pools

20 years

Question 5

Polio is almost eradicted with the exception of _________ and this is dt ________

Answer 5

3rd world countries

(polio) vaccinations

Question 6

Describe the March of Dimes charity

Answer 6

-started off as a campaign for research to beat polio

-set a dime in an envelope to the charity

-now focuses on other things than polio since it is mainly eradicated

Question 7

The survival rate of childhood cancer is _____%. That is ____ than adult. What are some things used for childhood cancer?

Answer 7

90%

higher
__________________
Drugs
Radiation
Chemo
Bone marrow transplant

Question 8

In Emphysema, there is ______ surface area for gas exchange. Why?

Answer 8

We lose alveoli

Alveoli next to each other –> merger of alveoli –> less recoil/elastic tissue
(this process continues & alveoli will keep merging & getting larger)

Question 9

We have a version of_________, which is a digestive enzyme, in the lung. What is the purpose of it?

Answer 9

Destroys infection & bacteria in the lungs & eliminate fluid problems

(NOTE: Version of Trypsin that we have in the lungs is Neutrophil elastase/protease)

Question 10

How do digestive enzymes constribute to pulmonary edema?

Answer 10

Enzymes destroy bacteria/cells → proteins and fluid leak into the alveoli from damaged capillaries → increased vascular permeability → fluid enters the lungs due to increased permeability → pulmonary edema.

Question 11

________ inhibits trypsin in the lungs specifically. It is made in the ______ & gets to the lungs via the _______. What does this prevent?

Answer 11

Alpha-1 Antitryspin

Liver

Keeps trypsin activity low and prevents trypsin from destroying alveolar walls/springs (made from stretchy proteins)

High trypsin activity breaks down proteins –> Alveoli are destroyed & remaining combine to form larger –> loss of recoil pressure/force & decrease lung function

Question 12

What does inhibition of Alpha-1 Antitrypsin or deficiency cause? What are disorders that cause this? (3) Describe them

Answer 12

1. Inherited (deficiency):
   -Affected 1/3000 ppl
   -Starts from birth
   -Tx: Lung transplant only –> still have deficiency after transplant –> extends life for 30yrs
   -w/o transplant = death by 30 yo
   -good candidated for transplant bc not dt lifestyle
2. Smoke:
   -chemical inhibitor
3. Liver dysfunction:
   -liver impairment –> production impaired
   -dt congenitaal or alcoholism

Question 13

Where is much debris collected at during inspiration? How?

Answer 13

Gets trapped in mucous

Question 14

Why is smoke not able to be filtered?

Answer 14

Lack mass and momentum –> not enough inertia to slam into the walls and to get trapped in mucus

Question 15

Long-term smoking causes _____. Why?

Answer 15

dt having an ongoing chemical inhibitor of alpha-1 antitrypsin in the lungs

Question 16

The liver produces ______ (3) plasma proteins.

Answer 16

-coagulation factors
-albumin
-alpha-1 antitrypsin

Question 17

Describe drinking & chain smoking

Answer 17

Smoking/drinking at same time

Drinking activate liver –> metabolize/cleared nicotine faster –> causes you to smoke more/faster –> more lung damage faster dt A1AT being inactivated

Liver activation accelerate smoking

Notes:
-Faster level of chemical inhibitor of alpha-1 antitrypsin –> lungs probably go bad alot faster.

Question 18

A1AT =

Answer 18

Alpha-1 Antitrypsin

Question 19

A1AT deficiency involves _____ molecule(s)

Answer 19

one

Question 20

Cystic fibrosis is a __________ disorder that can be potentially cured by _______ therapy

Answer 20

Genetic lung

gene

Question 21

The hemoglobin molecule has _____. Describe the 2 different kinds.

Answer 21

Ferrous – Fe²⁺
-capable of binding/releasing O2
-“Good iron”
-97.4% hb saturation

Ferric – Fe³⁺
-O2 permanently binds –> cant release O2 where needed
-“Bad iron”
-1.5% hb saturation

Question 22

Adding a positive charge to an element is the same as ______

Answer 22

removing an electron

Question 23

Taking away a positive charge to an element is the same as _______

Answer 23

Adding an electron

Question 24

Ferric is made via _______ of ferrous. What is happening?

Answer 24

Oxidation –> removing an electron = adding 1 + charge

Question 25

________ is an enzyme that reduces Ferric iron into _____ via a ________ reaction. What does it do?

Answer 25

Methemoglobin reductase Ferrous iron Reduction --------------------- Reduction reaction --> adds an electron = takes away 1 positive charge

Question 26

Another name for Ferric iron is ________

Answer 26

Methemoglobin

Question 27

The reaction that iron does thru in the body is called _____

Answer 27

REDOX!!!!!!!! it is a combo of both!!! Its not just 1!!!!! The body does both.

Question 28

Hb can carry _____ O2 molecules. Differentiate between HbA & HbF.

Answer 28

4 ----------------- HbA: -lower affinity for O2 compared to HbF -2 alpha & 2 beta chains HbF: -higher affinity for O2 -2 alpha & 2 gamma chains

Question 29

Sickle cell anemia _____ & is a result of ___ defective _____ chain(s) in Hb, while sickle cell trait is a result of ____.

Answer 29

Genetic 2 Beta 1

Question 30

Sickle cell anemia/trait is an issue with _______ & we are losing ______ via _______. Describe the pathology.

Answer 30

Hemoglobin structure RBC Hemolytic anemia ------------------- Notes: RBC decrease dt structure bc now they rupture easily (hemolytic anemia) & decreased lifespan bc they get stuck in capillaries --> **O2 carrying capacity reduced**

Question 31

Explain how healthy RBC get thru capillaries vs sickled RBC

Answer 31

Internal diameter for capillaries are smaller than diameter for RBC --> RBCs have to be flexible to get thru RBC rubbing directly on walls of capillaries w/ minimal fluid in between = good for O2 exchange -------------- Sickled RBCs: Deoxygenation of RBCs (O2 unloading) = sickling & rigidity --> **Not flexible**--> Cant pass thru & gets **stuck in capillaries** --> Causes **pain & ischemia** to the area (unless there's collateral circulation) --> **capillary destroyed** dt blockage/damage from sickled RBCs

Question 32

What are Tx for sickle cell anemia disease? (2) Describe them

Answer 32

Blood transfusion: Replace all blood volume (massive transfusion) -may be used in severe crisis -Risks: infection; rejection Drug: **Hydroxyurea** -Turns on fetal genes **-Body will produce HbF instead of HbA** -HbF: 2 alpha & 2 GAMMA chains instead --> less defective beta chains dt less HbA --> less sickling episodes

Question 33

Sickle cell disease anemia can cause ________ metabolism dt _______ offloading of O2 to the tissues. This generates __________ which will _______ our CO2 production.

Answer 33

anaerobic decreased nonvolatile acids decrease -------------------- Note: CO2 is a byproduct of aerobic metabolism

Question 34

Decreasing activity = ________ metabolism --> _____ sickling in sickle cell anemia/trait

Answer 34

decreased decreased

Question 35

What does an increased O2 consumption indicate in sickle cell anemia/trait? How does oxygenatuion affect this?

Answer 35

increased metabolism --> increased O2 being offloaded from Hb --> increased sickling ------------------- **Give 100% O2** Supplemental oxygen reduces risk of sickling by saturating Hb w/ O2 Not very effective because O2 is not soluble in blood so only so limited to absorption in blood -- Wont raise O2 content alot but helps

Question 36

Sickle cell trait _______ resistance to malaria

Answer 36

increases

Question 37

_________ uses iron to pull oxygen into skeletal muscles

Answer 37

myoglobin

Question 38

Describe HbA1C

Answer 38

Glycated Hb: extra sugar stuck to Hb at the **1c** location Caused by hyperglycemia

Question 39

___% of HbCO is normal & above ___% is abnormal. When would this be elevated?

Answer 39

1% 4% ----------------------- When moving or working a drive thru

Question 40

T/F: Your body should not have any HbCO in it

Answer 40

F

Question 41

What is a normal HbA1c?

Answer 41

5% or less

Question 42

______ ⇋ H2CO2 ⇋ H+ + _______

Answer 42

CO2 HCO3-

Question 43

Arterial CO2 content:

Answer 43

48 ml CO2/dL of blood

Question 44

Venous CO2 content:

Answer 44

52.5 ml CO2/dL of blood

Question 45

With obstructive lung diseases such as _________(2) depends on ________ sensors for their primary gauge to change ventilation. Why?

Answer 45

Emphysema, COPD O2/hypoxic ---------------------- Pts have **chronically high CO2 & protons** dt not being able to exhale properly (Less ER) --> system adjusts to looking at O2 levels to increase/decrease ventilation.

Question 46

What happens if you give an obstructive lung disease pt 100% O2? Why?

Answer 46

They will stop breathing --------------------- They've lost the drive they use to breath These pts rely on O2/hypoxic sensors (specifically peripheral chemoreceptors) for ventilation. Slightly lower PO2 drives their ventilation. ------------------------- 100% O2 --> remove hypoxic drive -- > signals chemoreceptors that O2 is sufficient --> **decrease ventilation** --> **FURTHER CO2/PROTON BUILD UP --> ACIDOSIS --> RESPIRATORY FAILURE**

Question 47

Increasing CO = ______ PVR = ________ capillary surface area = ________ gas exchange. Describe this process. Why is this important?

Answer 47

Decreased Increased Increased ----------------------- Recruitment & distention increasing contribute to the increased surface area & # of capillaries involved --> increased gas exchange ----------------------- Important bc O2 is not very soluble in solution Increased surface area = increased opportunity for O2 absorption

Question 48

T/F: we don't use all of our alveoli all the time. Why?

Answer 48

T ----------------- Caps not being used = alveoli not being used This is a safety factor -limits exposure to toxins by not exposuring unused alveoli

Question 49

We sigh _____x per _____. Describe this. What is it used for?

Answer 49

12-15x hour ------------------ Unconscious thing that we do -not always related to emotion -**slightly deeper breath in** ------------------ Maintaining patency of alveoli (unused/collapsed)

Question 50

Sighing helps produce ______ and is similar to a ______

Answer 50

Surfactant Yawn

Question 51

T/F: there is a sigh & yawn button on the ventilator

Answer 51

F There may be a sigh button -there is not a yawn button -most ventilators have "sigh" built-in so still no button

Question 52

What is yawning comparable to? How is it beneficial?

Answer 52

Comparible to sigh -- deeper breath than a sigh ------------------ Beneficial before someone who is about to lay down or go to sleep -Decreases FRC --> Helps prepare lungs for low lung volumes

Question 53

T/F: PRG is considered a higher order center for ventilation

Answer 53

T

Question 54

What can a physical head injury cause? Is this recoverable?

Answer 54

Injury to brainstem --> physical separation at the junction of the pons & medulla --> cuts off communication between the PRG & DRG --> apneustic breathing ---------------------- Could be depending on what caused it Massive trauma = no.