Physiology Test 3

Front 1

What happens to all the HCO3 filtered from the glomerular cappilaries?

Back 1

Reabsorbed back into blood.

Front 2

Bicarbonate concentraion is regulated by the kidneys via?

Back 2

Tubular secretion of H+.

Front 3

In alkalemia kidneys compensate by?

Back 3

1) failing to reabsorb all the filtered bicarbonate therefore HCO3 ions are secreted.

Front 4

Loosing a base has the same effect on blood as?

Back 4

Gaining an acid (by loosing a base blood is more acid)

Front 5

When kidneys conpensate by adding all filtered bicarbonate ions and new HCO3- to blood. What is wrong?

Back 5

Acidemia

Front 6

NH3+ is what in acidosis?

Back 6

Primary urinary buffer

Front 7

What is the difference between NH3 and NH4?

Back 7

NH3 (ammonia) is lipid soluble and diffuses from the renal cells into the tubbules.
NH4 (ammonium) is NH3 combined with H+ and is lipid insoluble so it stays in tubules and is excreted in urine.

Front 8

When you pee out HCO3 you have?

Back 8

Alkalemia

Front 9

Urea is permeable in the collecting duct when _________ is present.

Back 9

ADH

Front 10

Addisons disease?

Back 10

Acidemia

Front 11

Elastin Fibers

Back 11

Found in walls of alveoli and bronchioles.(stretch to double their size by unfolding/ rearranging their fibers. Recoil to original shape)

Front 12

Atelectasis

Back 12

Collapsed Alveolis

Front 13

Intramolecular attraction

Back 13

No Surfactant and surface molecules are attracted to one another therefore they exert a pull on one another. (The greater the ST the greater the force)

Front 14

Small Alveolus

Back 14

No Surfactant; Molecules are closer together therefore greater attraction force. *smallest during expiration so most likely to collapse during expiration.

Front 15

Large Alveolus

Back 15

Decrease Surface Tension (ST)

Front 16

Law of La Place

Back 16

P= 4 x T
_____
r
(P=pressure to keep alveolus open, T=ST, r = size)

Front 17

Atelectasis

Back 17

Collapsed Alveolis

Front 18

Intramolecular attraction

Back 18

No Surfactant and surface molecules are attracted to one another therefore they exert a pull on one another. (The greater the ST the greater the force)

Front 19

Small Alveolus

Back 19

No Surfactant; Molecules are closer together therefore greater attraction force. *smallest during expiration so most likely to collapse during expiration.

Front 20

Large Alveolus

Back 20

Decrease Surface Tension (ST)

Front 21

Law of La Place

Back 21

P= 4 x T
_____
r
(P=pressure to keep alveolus open, T=ST, r = size)

Front 22

Alvoles would collapse with out
___________?

Back 22

Surfactant

Front 23

Surfactant

Back 23

1. Lowers normal ST forces.
2. Surfactant molecules repel each other.
3. Prevents atelectosis. (esp. during expiration)

Front 24

ST inversely proportionally to _____ and proportional to ___________.

Back 24

surfactant, pressure

Front 25

Lack of surfactant at birth?

Back 25

Hyaline Membrane Disease
(Increase glucocorticoids in the 9th month responsible for maturation of surfactant)

Front 26

Causes of Surfactant decrease

Back 26

1. smoking
2. obstruction of pulmonary circulation
3. obstruction of bronchi
4. long term use of 100% oxygen/HBO

Front 27

Normal ST Pull _______
Pulmonary Interstitial Pressure _____
Which does the net pressure gradient favor?

Back 27

ST -3mmHg
PI -9mmHg
Interstitium bc it tends to absorb fluid from the alveolus therefore keeping them dry.

Front 28

Decrease ST =

Back 28

Increase Surfactant
*Prevents transudation of fluids

Front 29

Increase ST =

Back 29

Decrease Surfactant
*Tends to pull fluid into alveoli from alveolar wall cap. and intersitium causing alveolar edema.

Front 30

Compliance

Back 30

-distensibility x volume or C= V/P
-measures the ease lungs can be inflated

Front 31

Decreased Compliance

Back 31

-increase pressure for a given volume to inflate lungs
-lungs are more stiff so WOB increases
ex. scar tissue, atelectasis, decreased surfactant-increase ST, pulmonary edema (pneumonia)

Front 32

Increased Compliance

Back 32

- less P for a given vol. to inflate lungs
-age or emphysema

Front 33

what does higher saturation mean?

Back 33

increased affinity between hgb and o2

Front 34

HBO

Back 34

Hyperbaric oxygenation
-drives O2 into solution
-O2 is administered under great pressure (2-3x atmp)

Front 35

Ischemia

Back 35

Decrease oxygen

Front 36

saturation

Back 36

amount of O2 bound to Hgb compared to Hgb's maximal capability for binding O2

Front 37

Decreased PH (1)
Increased PH (2)

Back 37

(1) more acid
(2) more alkalemia

Front 38

Shift to the right

Back 38

At any given PO2 there is less saturation (less affinity b/w hmg and O2) therefore less loading
-decreased ph
-increased pco2
-increased temp
-organic phosphate in RBC bind w/hmg

Front 39

Incrase Affinity

Back 39

Favors loading but inhibits unloading

Front 40

S-shaped curve

Back 40

Lrg change in PO2 results in small change in SO2

Front 41

PO2 increase and decrease

Back 41

Increase - drives loading (lung level) O2
Decrease - promotes unloading (tissue)

Front 42

Shift to the Left

Back 42

-increase saturation
-increase ph
-decrease temp
-decreased organic phosphate
*usually CO poisoning ***worse than shift to right

Front 43

AVO2D

Back 43

arterial-venous oxygen difference
*reflects amt of O2 in tissues (increase when tissues are starving)PaO2-PVO2

Front 44

CO2 transport in Blood

Back 44

1. dissolved in plasma 7-10%
2. combined w/amino groups on Hgb (carbaminohemoglobin) 20-23%
3. carbonic acid and bicarbonate (in plasma) 70%

Front 45

Hyperventilation

Back 45

Increase RR and depth (alkalosis)
*decrease co2
*asthma, pneumonia, panic brain injury
*compensation for resp. acidosis

Front 46

Hypoventilation

Back 46

decrease RR and depth
*increase co2 and increase H+
*narcotic overdose. chronically retain o2, compensation for metabolicalkalosis

Front 47

Physiological dead space

Back 47

Vd/Vt
volume of air that does not excahnge with pulmonary blood.

Front 48

alveolar ventilation

Back 48

Va= (Vt-Vd) X (RR)