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BBS1002 > case 5 > Flashcards

case 5 Flashcards

1
Q

hemoglobin

A

globular heme protein + heme group. binds O2 + CO2. gives red blood cells color and consists of 4 subunits: 2 alfa + 2 beta

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2
Q

subunits hemoglobin

A

each forms a dimer. the four heme groups surround a globin group –> tetrahedral structure.

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3
Q

oxyhemoglobin

A

when hemoglobin binds to O2

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4
Q

reaction hemoglobin O2

A

Hb + O2 HbO2

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5
Q

total amount of O2 in blood

A

O2 dissolved in plasma + bound to hemoglobin

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6
Q

PO2

A

determines how much O2 is unloaded from hemoglobin. when cells increase metabolic activity, PO2 decreases and hemoglobin releases more O2

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7
Q

oxygen binding

A

the 1st binds difficult. the protein shape can change making the others it easier to bind. the 4th also binds a bit difficult.

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8
Q

factors of O2 binding

A
  • PO2 in plasma surrounding RBC

- number of potential Hb binding sites available.

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9
Q

percent saturation of hemoglobin

A

Plamsa PO2 is primary factor determining what % of available Hb binding sites are occupied by O2.

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10
Q

PO2 decrease

A

less O2 is bound to Hb and transported

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11
Q

PO2 established

A
  • composition of inspired air
  • alveolar ventilation rate
  • efficiency of gas echange from alveoli to blood
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12
Q

number of O2 binding sites

A

depends on number of Hb.
estimated by:
- counting RBS and quantifying the amount of Hb per RBS
- determining the blood hemoglobin content.

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13
Q

percent saturation of Hb

A

amount of O2 bound to Hb at any given PO2

(amount of O2 bound/ max that could be bound ) x 100

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14
Q

oxyhemoglobin saturation curves

A

shape reflects properties of Hb and affinity for O2.
normal: 98% saturation.
as long as PO2 stays above 60 mm Hg, Hb is more than 90% saturated

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15
Q

significance shape of curve

A

PO2 40% –> Hb is 75% saturated, only 1/4 of O2 is released. remaining O2 is reservoir when metabolism increases.

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16
Q

Factors that affect the curve

A

Higher temp. + PCO2 decrease affinity and shifts the curve to the right. when they change in opposite direction the affinity increases

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17
Q

bohr effect

A

more CO2 binds to Hb, more O2 is released

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18
Q

Haldane effect

A

if PO2 increases, affinity of Hb for O2 increases and affinity for CO2 decreases.
if PO2 decreases, affinity decreases and affinity for CO2 increases.

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19
Q

2,3-diphosphateglycerate (2,3-DPG)

A

compound made from intermediate of glycolysis pathway, lowers binding affinity of Hb and shifts curve to right

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20
Q

chronic hypoxia

A

triggers increase in 2,3-DPG, lowers binding affinity of Hb and shifts curve to the right

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21
Q

anemia

A

causes an increase in 2,3-DPG. PO2 would be around 40 mm Hg.

22
Q

shape of hemoglobin

A

can alter affinity to O2.

fetal Hb: 2 gamma protein chains instead of beta. these allow to bind O2 in low O2 environment of placenta.

23
Q

CO2

A

7% dissolved in plasma
93% transported by RBS
70% is converted to bicarbonate
23% binds to Hb

24
Q

hypercapnia

A

high CO2 levels. causes pH disturbance, can also depress CNS function

25
Q

acidosis

A

pH disturbance, extreme can denature proteins

26
Q

CO2 + bicarbonate

A

conversion of CO2 to HCO3- has two functions

  • provides additional means of transport
  • HCO3- is a buffer for metabolic acids, helping stabilize pH.
27
Q

conversion CO2

A

to keep the reaction going end products must be removed.

28
Q

mechanisms for removing H+ and HCO3-

A
  • bicarbonate leaves on an antiport protein. chloride shift, exchanges HCO3- for CL-. maintains elecriticy. makes the buffer available
  • removes free H+. Hb acts as buffer and binds H+. prevents changes in pH.
29
Q

respiratory acidosis

A

is PCO2 is elevated, buffer doesn’t work H+ accumulates in plasma
metabolic system will help
- alkalosis: high breath rate
- acidosis: low breath rate

30
Q

metabolic acidosis/alkalosis

A

respiratory will help maintain homeostasis

  • alkalosis: vomiting
  • acidosis: renal system doesn’t remove acid
31
Q

hemoglobin + CO2

A

when O2 leaves the binding site, CO2 binds to Hb at exposed amino groups
forming: carbaminohemoglobin

32
Q

CO2 removal

A

PCO2 of alveoli is lower than venous blood in pulmonary capillaries, CO2 diffuses. plasma PCO2 falls. CO2 diffuses out of RBC.

33
Q

more altitude

A

thinner air –> less O2

34
Q

Altitude general

A

PO2 drops –> altitude acclimatization

lower saturation of O2, increase in breathing depth + rate (hyperpnea). also causes adverse effect of alkalosis.

35
Q

altitude general 2

A

heart beats faster, stroke volume is decreased, and non-essential bodily functions are suppressed. decline in food digestion

36
Q

acclimatization altitude

A

renal excreation of bicarbonate. body undergoes physical changes –> lower lactate, decreased plasma volume, increased hematocrit, increased RBC mass, higher concentration of capillaries in skeletal muscle, increases aerobic enzyme concentration, increase in 2,3-DPG

37
Q

acclimatization leads to:

A
  1. increased pulmonary ventilation
  2. increase RBC
  3. increased diffusing capacity
  4. increased tissue capillarity
  5. cellular acclimatization
38
Q

full adaptation

A

increase of RBC reaches a plateau and stops

39
Q

EPO

A

secreted by kidney in response to hypoxia, stimulates RBC production in bone marrow

40
Q

nucleus tractus solitarius (NTS)

A

contains dorsal respiratory group (DRG), control mostly muscles of inspiration. output goes via phrenic nerves to diaphragm and via intercostal nerves to intercostal muscles.
also receives info from chemo + mechanoreceptors.

41
Q

respiratory neurons in pons

A

receive sensory info from DRG and influence initiation and termination of inspiration

42
Q

ventral respiratory group (VRG)

A

multiple regions.

  • pre-Botzinger complex: spontaneously firing neurons–> act as pacemakers for rhythm. has influence on starting respiration.
  • pontine respiratory group: receive input from higher brain centers + transmit impulses to VRG of medulla –> coordinates smooth respiratory
43
Q

medullary inspiratory center

A

generates rhythmic action potentials

44
Q

pneumotaxic area

A

stop the lungs from inflating

45
Q

apneustic area

A

prolonging contractions (slow breathing)

46
Q

neurons of VRG

A

mainly active during forced respiration

- active expiration –> neurons activate the internal intercostal and abdominal muscles

47
Q

chemoreceptors

A

input from central + peripheral receptors modifies rhythm and help maintain blodo gas homeostasis
CO2 is primary stimulus.
arterial circulation –> O2 and CO2

48
Q

peripheral

A

located in carotid + aortic arteries, sense change in PO2, PCO2 + pH.
when specialized in glomus cells, they trigger a reflex increase in ventilation

49
Q

central chemoreceptors

A

respond to changes in CO2 in cerebrospinal fluid. effect on voluntary respiration. set the pace.
receptors signal to increase rate and depth of ventilation –> enhancing alveolar ventilation and removing CO2.
respond on pH. CO2 is converted into carbonate ions + H+.

50
Q

inflation reflex

A

Hering-Breuer inflation reflex
triggered to prevent over-inflation of lungs.
pulmonary strech receptors respond to excessive stretching of lung during large inspiration.
signal to medulla and apneustic center of pons.
inspiratory area is inhibited directly and apneustic center is inhibited from activating the inspiratory area.

BBS1002 (10 decks)

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