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Integrative Physiology III Flashcards

1
Q

[H+] is very tightly regulated: (4)

A
  • enzymes
  • blood clotting
  • muscle contraction
  • channels
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2
Q

Extreme range
compatible with life
(for a short time):
~ pH

A

6.8 to 8.0

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3
Q

fluid: Arterial Blood (ECF)
[H+]:
pH:

A
  1. 0x10-5

7. 4

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4
Q

fluid: Venous Blood (ECF)
[H+]:
pH:

A
  1. 5x10-5

7. 35

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5
Q

fluid: Interstitial Fluid (ECF)
[H+]:
pH:

A
  1. 5x10-5

7. 35

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6
Q

fluid: ICF
[H+]:
pH:

A

1x10-3 - 4x10-5

6.0-7.4

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7
Q

fluid: Urine
[H+]:
pH:

A

3 x10-2 – 1 x 10-5

4.5-8.0

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8
Q

fluid: Gastric Juice
[H+]:
pH:

A

160

0.8

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9
Q

sources of hydrogen ion gain (4)

A

generation of H from CO2
production of nonvolatile acids from the metabolism of proteins and other organic molecules
gain of H due to loss of HCO3- in diarrhea or other nongastric GI fluids
gain of H due to loss of HCO3- in the urine

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10
Q

sources of hydrogen ion loss (4)

A

utilization of H in the metabolism of various organic anions
loss of H in vomit
loss of H in urine
hyperventilation

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11
Q

Metabolic CO2 production

— mmol/day

A

20,000

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12
Q

Net gain of — mEq H+ daily.

A

40 – 80

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13
Q

Normal ECF [H+] =

A

0.00004 mEq/L.

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14
Q

Fixed” (Non-Volatile) Acid
Production: All Excreted by Kidneys
Adds ≈ — mEq/day

A

80

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15
Q

Protein Catabolism – (2)

A

sulfuric acid and HCl

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16
Q

Phospholipid Catabolism – (1)

A

phosphoric acid

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17
Q

Exercise, hypoxia –

A

lactic acid

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18
Q

Post-absorptive state, diabetes mellitus – (2)

A

acetoacetic, β-hydroxy-butyric acids

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19
Q

Nucleoprotein metabolism – (1)

A

uric acid

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20
Q

Three Primary Systems Regulate the [H+] in Body Fluids

1. Chemical (3)

A

Acid-base buffer systems (body fluids)
 “instantaneous”
Does not add or remove H+ but keeps it “tied up” until balance can
be re-established

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21
Q

Three Primary Systems Regulate the [H+] in Body Fluids

2. Respiratory system (3)

A

 Regulates the removal of CO2 (and acid)
 Change VA
 Seconds to minutes (maximal in hours) “fast.”

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22
Q

Three Primary Systems Regulate the [H+] in Body Fluids

3. Kidneys (3)

A

 Excrete an acidic or alkaline urine
 Hours to days (maximal in days) “slow.”
 Most powerful of the Acid/Base Regulatory Systems

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23
Q

Bicarbonate Buffer System (3)

A

 CO2 + H2O > H2CO3 > H+ HCO3-
 Most Powerful EC Buffer
 CO2 and HCO3- regulated by respiratory and renal systems

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24
Q

Phosphate Buffer System (4)

A

 H2PO4- > H+ + HPO4-2
 Not a significant buffer for ECF
 Concentration significantly lower than Bicarbonate system
 Important for buffering renal tubular fluids and ICF

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25
Q

60-70% of the total chemical buffering of the body fluids is

A

inside

the cells

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26
Q

H+ entry into cells: (3)

A 
 CO2
 Produced: Lactic, 
acetoacetic, β-hydroxyl-
butyric acid
 H+/K+ exchange (contributes 
to hyperkalemia)
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27
Q

Intracellular Buffers (2)

A 
1. Proteins
Ex. Hb/DeoxyHb
2. Organic Phosphates
 ATP, ADP, AMP
 Glucose-1-PO4
 2,3-DPG
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28
Q

Intracellular Buffers (2)

A 
1. Proteins
Ex. Hb/DeoxyHb
2. Organic Phosphates
 ATP, ADP, AMP
 Glucose-1-PO4
 2,3-DPG
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29
Q

CO2 =

A

H+

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30
Q

Resting normal human produces — mL of CO2 per minute.

31
Q

Three processes facilitate CO2 transport: (3)

A
  • 10% dissolved in plasma
  • 25% binds to amino groups in Hb (carbaminohemoglobin)
  • Remainder converted to H2CO3 by CA in erythrocytes.
32
Q

— removes CO2

A

Alveolar exchange

33
Q

Disorders of the respiratory system lead to

A

respiratory

acidosis or alkalosis.

34
Q

Changes in — can function to restore pH following

acid/base disturbances

35
Q

Kidneys regulate pH by altering plasma [HCO3-] (2)

A

– Secrete H+

– Reabsorb, produce, or excrete HCO3-

36
Q

For each HCO3- reabsorbed,

a – must be secreted

37
Q

H+ is Secreted by Secondary Active
This pattern of H+
secretion occurs in the (3)

A

proximal tubule, TAL, and

the early distal tubule.

38
Q 
95% of filtered HCO3- 
reabsorbed by this 
process and requires 
--- mEq of H+ to be 
secreted
39
Q

Mechanism does not
establish very high — in
filtrate

40
Q

Rate of tubule H+ secretion =

A

4400 mEq/day

41
Q

Renal Load of HCO3- =

A

4320

mEq/day ([HCO3-]ECF = 24 mEq/L)

42
Q

Excrete – mEq/day of non-
volatile acid produced by
metabolism

43
Q

In Alkalosis,

A

HCO3- load > H+
secretion and excess HCO3- will
be excreted

44
Q

In Acidosis,

A

H+ secretion > HCO3-

load and excess H+ excreted

45
Q

Excess H+ Excretion

Function of (2)

A

late DT and CD

46
Q

Excess H+ Excretion
Responsible for only –% H+ secretion, but enough to
create maximally acidified urine

47
Q

Excess H+ Excretion

Pi and glutamine/NH4+ systems are used for excess

A

H+ excretion (non-volatile acids produced during

metabolism).

48
Q

Excess H+ Excretion

Abnormal H+ production induces

A

renal

compensation

49
Q

Primary Active Secretion of H+ in the —

Cells of Late Distal and Collecting Tubules

A

α-Intercalated

50
Q

Phosphate Buffer System
 When secreted H+ exceeds
filtered load of HCO3-,

 Anytime H+ combines with
a buffer other than HCO3-,
results in

 Most filtered Pi reabsorbed
so

A

H+
can bind to Phosphate
buffer

new HCO3- being
added to the ECF

only small amount of this
buffer available to interact
with H+ in filtrate.

51
Q

Ammonia Buffer System (4)

A

 In PT, TAL and DT, NH4+ is added to filtrate following glutamine
metabolism and represents acid secretion
 In CD, NH3 is secreted into lumen where it combines with H+ to form
NH4+
 Results in new HCO3- being added to the ECF
 Responsible for 50% of the acid excreted and 50% of new HCO3-
added to ECF

52
Q
  1. H+ secretion by tubular epithelium necessary for: (4)
A

 HCO3- reabsorption
 Addition of new HCO3- to ECF
 Acid Excretion
 Rate of secretion must be carefully controlled to maintain acid-base homeostasis

53
Q
  1. Under Normal Conditions: Acid secretion needs to be enough to: (2)
A

 Reabsorb almost all filtered HCO3-

 Rid the body of non-volatile acids produced during metabolism

54
Q
  1. During Alkalosis: Acid secretion decreased (3)
A 
 Not all filtered HCO3- is reabsorbed
 HCO3- is excreted
 No NH4+ or H2PO4-
- No non-volatile acid excreted
- No new HCO3- - added to ECF
55
Q

During Acidosis: Acid secretion is increased (2)

A

 Almost all filtered HCO3- is reabsorbed
 NH4+ and H2PO4- generated
- Acid excreted
- New HCO3- added to ECF

56
Q

Two Most Important Stimuli that increase H+ secretion by tubules:

A
  1. Increase in PCO2 of ECF

2. Increase [H+]ECF

57
Q

increase H+ Secretion and HCO3- Reabsorption (5)

A 
increase PCO2
increase H+, decrease HCO3-
increase Ang2
increase aldosterone 
hypokalemia
58
Q

decrease H+ Secretion and HCO3- Reabsorption (5)

A 
decrease PCO2
decrease H+, increase HCO3-
decrease Ang2
decrease aldosterone
hyperkalemia
59
Q

Respiratory Acidosis (2)

A

 Problems with ventilation or gas exchange
Ex. Hypoventilation, Pulmonary Edema, COPD, Damage to
respiratory centers in brain stem
 Increased PCO2

60
Q

Respiratory Acidosis

Compensation (2)

A
  1. Buffer of Body

2. Renal Compensation

61
Q
  1. Renal Compensation (2)
A

reabsorb all filtered HCO3-

secrete excess H+ and add new HCO3- to ECF (increased glutamine metabolism and NH4+ excretion)

62
Q

Metabolic Acidosis

A

 All changes in pH not associated with an increase in CO2 levels

63
Q

Metabolic Acidosis

 All changes in pH not associated with an increase in CO2 levels (4)

A
  1. Failure of kidney to excrete metabolic acids (Renal Failure, Addison’s Disease)
  2. Formation of excess quantities of metabolic acid (ketoacidosis)
  3. Increased input of of metabolic acids (aspirin and methyl alcohol)
  4. Loss of base from body (Diarrhea)
64
Q

Metabolic Acidosis

compensation (3)

A

buffer of body
renal compensation (assuming this is not the problem)
respiratory compensation

65
Q

renal compensation (assuming this is not the problem) (2)

A

reabsorb all filter HCO3-

secrete excess H+ and add new HCO3- to EXF (increased glutamine metabolism and NH4+ excretion)

66
Q

respiratory compensation (1)

A

compensatory increase in VA in response to metabolic acid

67
Q

Respiratory Alkalosis (3)

A

 Rare
 Excessive ventilation
Ex. Hyperventilation
 Leads to Decreased PCO2

68
Q

Respiratory Alkalosis

Compensation (2)

A

buffer of body

renal compensation

69
Q

renal compensation (2)

A

increased HCO3- excretion

decreased H+ excretion (decreased glutamine metabolism and NH4+ excertion)

70
Q

Metabolic Alkalosis

A

 All changes in pH not associated with a decrease in CO2 levels

71
Q

Metabolic Alkalosis

 All changes in pH not associated with a decrease in CO2 levels (4)

A
  1. Diuretics
  2. Excess Aldosterone
  3. Excessive vomiting
  4. Ingestion of Alkaline drugs (ex. NaHCO3-)
72
Q

Metabolic Alkalosis

Compensation (3)

A

buffer of body
renal compensation
respiratory compensation

73
Q

skipped

Oral Complications of Renal Disease (7)

A

 Increased levels of urea leads to halitosis and an unpleasant metallic taste
 Altered saliva pH and volume
 Altered taste sensations – especially, sweet and acid flavors
 A burning sensation in the lips and tongue of a neuropathic origin, or a sensation
of an enlarged tongue
 Uremic stomatitis is an oral complication of unknown etiology and it is relatively
uncommon, usually seen in patients with an end stage or untreated renal disease
 Bleeding tendency
 Oral lichen planus may arise, associated with antihypertensive medication
(diuretics, beta- blockers).

74
Q

skipped

Treatment considerations for: (3)

A

 Stages of Renal Disease
 Dialysis
 Renal transplants

Physiology (53 decks)

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