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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
60-70% of the total chemical buffering of the body fluids is
inside | the cells
26
H+ entry into cells: (3)
```  CO2  Produced: Lactic, acetoacetic, β-hydroxyl- butyric acid  H+/K+ exchange (contributes to hyperkalemia) ```
27
Intracellular Buffers (2)
``` 1. Proteins Ex. Hb/DeoxyHb 2. Organic Phosphates  ATP, ADP, AMP  Glucose-1-PO4  2,3-DPG ```
28
Intracellular Buffers (2)
``` 1. Proteins Ex. Hb/DeoxyHb 2. Organic Phosphates  ATP, ADP, AMP  Glucose-1-PO4  2,3-DPG ```
29
CO2 =
H+
30
Resting normal human produces --- mL of CO2 per minute.
200
31
Three processes facilitate CO2 transport: (3)
- 10% dissolved in plasma - 25% binds to amino groups in Hb (carbaminohemoglobin) - Remainder converted to H2CO3 by CA in erythrocytes.
32
--- removes CO2
Alveolar exchange
33
Disorders of the respiratory system lead to
respiratory | acidosis or alkalosis.
34
Changes in --- can function to restore pH following | acid/base disturbances
VA
35
Kidneys regulate pH by altering plasma [HCO3-] (2)
– Secrete H+ | – Reabsorb, produce, or excrete HCO3-
36
For each HCO3- reabsorbed, | a -- must be secreted
H+
37
H+ is Secreted by Secondary Active This pattern of H+ secretion occurs in the (3)
proximal tubule, TAL, and | the early distal tubule.
38
``` 95% of filtered HCO3- reabsorbed by this process and requires --- mEq of H+ to be secreted ```
4000
39
Mechanism does not establish very high --- in filtrate
[H+]
40
Rate of tubule H+ secretion =
4400 mEq/day
41
Renal Load of HCO3- =
4320 | mEq/day ([HCO3-]ECF = 24 mEq/L)
42
Excrete -- mEq/day of non- volatile acid produced by metabolism
80
43
In Alkalosis,
HCO3- load > H+ secretion and excess HCO3- will be excreted
44
In Acidosis,
H+ secretion > HCO3- | load and excess H+ excreted
45
Excess H+ Excretion | Function of (2)
late DT and CD
46
Excess H+ Excretion Responsible for only --% H+ secretion, but enough to create maximally acidified urine
5
47
Excess H+ Excretion | Pi and glutamine/NH4+ systems are used for excess
H+ excretion (non-volatile acids produced during | metabolism).
48
Excess H+ Excretion | Abnormal H+ production induces
renal | compensation
49
Primary Active Secretion of H+ in the --- | Cells of Late Distal and Collecting Tubules
α-Intercalated
50
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
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
Ammonia Buffer System (4)
 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
1. H+ secretion by tubular epithelium necessary for: (4)
 HCO3- reabsorption  Addition of new HCO3- to ECF  Acid Excretion  Rate of secretion must be carefully controlled to maintain acid-base homeostasis
53
2. Under Normal Conditions: Acid secretion needs to be enough to: (2)
 Reabsorb almost all filtered HCO3- |  Rid the body of non-volatile acids produced during metabolism
54
3. During Alkalosis: Acid secretion decreased (3)
```  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
During Acidosis: Acid secretion is increased (2)
 Almost all filtered HCO3- is reabsorbed  NH4+ and H2PO4- generated - Acid excreted - New HCO3- added to ECF
56
Two Most Important Stimuli that increase H+ secretion by tubules:
1. Increase in PCO2 of ECF | 2. Increase [H+]ECF
57
increase H+ Secretion and HCO3- Reabsorption (5)
``` increase PCO2 increase H+, decrease HCO3- increase Ang2 increase aldosterone hypokalemia ```
58
decrease H+ Secretion and HCO3- Reabsorption (5)
``` decrease PCO2 decrease H+, increase HCO3- decrease Ang2 decrease aldosterone hyperkalemia ```
59
Respiratory Acidosis (2)
 Problems with ventilation or gas exchange Ex. Hypoventilation, Pulmonary Edema, COPD, Damage to respiratory centers in brain stem  Increased PCO2
60
Respiratory Acidosis | Compensation (2)
1. Buffer of Body | 2. Renal Compensation
61
2. Renal Compensation (2)
reabsorb all filtered HCO3- | secrete excess H+ and add new HCO3- to ECF (increased glutamine metabolism and NH4+ excretion)
62
Metabolic Acidosis
 All changes in pH not associated with an increase in CO2 levels
63
Metabolic Acidosis |  All changes in pH not associated with an increase in CO2 levels (4)
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
Metabolic Acidosis | compensation (3)
buffer of body renal compensation (assuming this is not the problem) respiratory compensation
65
renal compensation (assuming this is not the problem) (2)
reabsorb all filter HCO3- | secrete excess H+ and add new HCO3- to EXF (increased glutamine metabolism and NH4+ excretion)
66
respiratory compensation (1)
compensatory increase in VA in response to metabolic acid
67
Respiratory Alkalosis (3)
 Rare  Excessive ventilation Ex. Hyperventilation  Leads to Decreased PCO2
68
Respiratory Alkalosis | Compensation (2)
buffer of body | renal compensation
69
renal compensation (2)
increased HCO3- excretion | decreased H+ excretion (decreased glutamine metabolism and NH4+ excertion)
70
Metabolic Alkalosis
 All changes in pH not associated with a decrease in CO2 levels
71
Metabolic Alkalosis |  All changes in pH not associated with a decrease in CO2 levels (4)
1. Diuretics 2. Excess Aldosterone 3. Excessive vomiting 4. Ingestion of Alkaline drugs (ex. NaHCO3-)
72
Metabolic Alkalosis | Compensation (3)
buffer of body renal compensation respiratory compensation
73
skipped | Oral Complications of Renal Disease (7)
 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
skipped | Treatment considerations for: (3)
 Stages of Renal Disease  Dialysis  Renal transplants

Physiology (53 decks)

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