acid-base physiology Flashcards

1
Q

P02, PCO2, HCO3-, ph - normal ranges

A

PO2: 75-105 mm Hg
PCO2: 33-44 mm Hg
HCO3-: 22-28 mEq/L
pH: 7.35-7.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Metabolic acidosis - HCO3-, PCO2, ph, compensatory response

A

ph –> decreased
PCO2 –> decreased
HCO3- –> decreased
compensatory response –> immediate hyperventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Metabolic alkalosis - HCO3-, PCO2, ph, compensatory response

A

ph –> increased
PCO2 –> increased
HCO3- –> increased
compensatory response –> immediate hypoventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Respiratory acidosis - HCO3-, PCO2, ph, compensatory response

A

ph –> decreased
PCO2 –> increased
HCO3- –> increased
compensatory response –> increased renal HCO3- reabsorption (delayed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Respiratory alkalosis - HCO3-, PCO2, ph, compensatory response

A

ph –> increased
PCO2 –> decreased
HCO3- –> decreased
compensatory response –> decreased renal HCO3- reabsorption (delayed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Henderson-Hasselbalch equation

A

6.1 + log (HCO3-)/0.03PCO2

ph=pk+log(A-/HA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Winters formula is a formula used to evaluate

A

respiratory compensation in a metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Winters formula - equation

A

PCO2=1.5 (HCO3-) + 8 +/- 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Winters formula - explanation

A

If measured PCO2 is bigger than predicted PCO2 –> concominant respiratory acidosis
If measured PCO2 is smaller than predicted –> concomitant respiratory alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diagnosis if acidemia or alkalemia

A

check artrial ph:

a. if more than 7.45 –> alkalemia
b. if less than 7.35 –> acidema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

alkalemia - respiratory or metabolic alkalosis ?

A
  1. if PCO2 less than 36 –> Respiratory alkalosis

2. if HCO3- more than 28 meq/L –> metabolic alkalosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Metabolic alkalosis - DDx

A
  1. loop diuretics
  2. vomiting
  3. antiacids
  4. hyperaldosteronism
  5. thiazide use
  6. Hypokalemia
  7. several renal tubular defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Respiratory alkalosis - DDx

A

Hyperventilation:

  1. Hysteria
  2. Hypoxemia (eg. high altitude)
  3. Pulmoary embolism
  4. Tumor
  5. salicylates (early)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

acidemia - respiratory vs metabolic alkalosis?

A

PCO2 more than 44 mm Hg –> respiratory acidosis

HCO3- less than 20 meg/L –> metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Respiratory acidosis - DDx

A

Hypoventilation:

  1. Airway obstruction
  2. Acute lung disease
  3. Chronic lung disease
  4. Opioids/sedatives
  5. weakening of respiratory muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Metabolic acidosis - next step

A

Check anion gap = Na+ - (CL+HCO3-):
more than 12 –> anion gap metabolic acidosis
8-12 –> normal anion gap metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

anion gap metabolic acidosis - DDx

A
  1. Methanol (formic acid)
  2. Uremia
  3. Diabetic ketoacidosis
  4. Propylene glycol
  5. Iron tablets
  6. ISONIAZIDE
  7. Lactic acidosis
  8. Ethylene glycol (–> oxalic acid)
  9. Salicilates (late)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

normal anion gap metabolic acidosis - DDx

A
  1. Hyperalimentation (artificial supply of nutrients, typically intravenously)
  2. Addison disease
  3. Renal tubular acidosis
  4. Diarrhea
  5. Acetazolamide
  6. Spironolactone
  7. saline infusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Renal tubular acidosis - definition

A

disorder of the renal tubules that leads to normal annion gap (hyperchloremic) metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hyperchloremic acidosis is

A

a form of metabolic acidosis associated with a normal anion gap, a decrease in plasma HCO3- concentration, and an increase in plasma CL- concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Renal tubular acidosis - types

A
  1. Distal tubular acidosis (type 1)
  2. Proximal renal tubular acidosis (type 2)
  3. Combined proximal and distal renal tubular acidosis (type 3)
  4. Hyperkalemic renal tubular acidosis (type 4)
22
Q

Distal tubular acidosis (type 1) - mechanism

A

defect in ability of α intercaleted cells to secrete H+ –> no new HCO3 is generated (CL/HCO3- exchanger in the basolateral membrane) –> metabolic acidosis and urine ph more than 5.5

23
Q

Distal tubular acidosis (type 1) is associated with (an mechanism)

A
  1. hypokalemia (α-cell cannot secrete H+, and cannot reabsorb K+, maybe because H+/K+ pump)
  2. high risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover
24
Q

causes of Distal tubular acidosis (type 1)

A
  1. amphotericin B toxicity
  2. analgesic nephropathy
  3. congenital anomalies (obstruction of urinary tract)
25
Proximal renal tubular acidosis (type 2) - mechanism
defect in PCT HCO3 reabsorption --> increased excretion HCO3- in urine and subsequent metaboli acidosis. Urine is acidified by α-intercalated cells in collecting tubule (urine ph less than 5.5)
26
causes of Proximal renal tubular acidosis (type 2)
1. Fanconi syndrome | 2. carbonic anhydrase inhibitors
27
Proximal renal tubular acidosis (type 2) is associated with
1. hypokalemia | 2. high risk for hypophosphatemic rickets (low phosphate - maybe from Fanconi)
28
Hyperkalemic renal tubular acidosis - mechanism
Hypoadlosterinism --> hyperkalemia --> low NH3 synthesis in PCT --> low NH4+ excretion --> urine ph less than 5.5
29
causes of Hyperkalemic renal tubular acidosis (generally)
1. low aldosterone production | 2. aldosterone resistance
30
example of low aldosterone production causes
1. diabetic hyporeninism 2. ACE inhibitors 3. angiotensin receptor blockers 4. NSAID 5. heparin 6. cyclosprorine 7. adrenal insufficiency
31
example of aldosterone resistance causes
1. K+ sparing dieuretics 2. nephropahty due to obstruction 3. TMP/SXM
32
Renal tubular acidosis - types/urine ph/potasium/concentration
1. Distal tubular acidosis (type 1) - urine ph more than 5.5 - hypokalemia 2. Proximal renal tubular acidosis (type 2) - urine ph less than 5.5 - hypokalemia 3. Hyperkalemic renal tubular acidosis (type 4) - urine ph less than 5.5 - hyperkalemia
33
Renal tubular defects that cause metabolic alkalosis
1. Syndrome of apparent Mineralocorticoid Excess 2. Liddle syndrome 3. Gitelman syndrome 4. Bartter syndrome
34
Aspirin - pH disturbances
respiratory alkalosis early (hyperventilation) | transition to mixed metabolic acidosis-respiratory alkalosis
35
Why does infusion of normal saline cause metabolic acidosis?
The bicarbonate ions are diluted by the isotonic fluid, and acidosis occurs as a resul
36
Renal tubular acidosis - causes of every type
Distal (type 1) --> a. amphotericin B toxicity b. analgesic nephropathy c. congenital anomalies (obstruction) of urinary tract Proximal (type 2) --> a. Fanconi syndrome b. carbonic anhydrase inhibitors Hyperkalemic (type 4) --> decreased aldosterone production (diabetic hyporeninism, ACE inhibitors, ARB, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance ( K+-sparing diuretics, nephropathy due to pbstruction, TMP/SXM)
37
weak acids - renal diffusion (mechanism and example)
- 2 FORMS: HA + A- - only HA form diffuse - in acidic urine --> HA predominates --> more back diffusion and decreased excretion - in alkaline urine --> A- predominates --> less back diffusion and increased excretion example: the excetion of salicylic acid can be increased in by alkalinizing the urine
38
weak bases - renal diffusion (mechanism and example)
- 2 FORMS: BH+ and B form - only B form diffuse - in acidic urine --> BH+ predominates --> less back diffusion --> increased excretion - in alkaline urine --> B predominates --> more back diffusion --> decreased excretion
39
Types of acid in the body (and which)
1. Volatile --> CO2 | 2. Nonvotalie (fixed) --> sulfuric, phosphoric, ketoacids, lactic acids, salicylic acid
40
Buffers of the body (and pK)
Extracellular --> HCO3 (6.1), phosphate (6.8) | Intracullular --> Organic phosphates, Protein (esp Hb)
41
according to Henderson Hasselbalch equation, when the ph equals the pK --> ....
conentration of HA and A- are equal
42
H+ is renal excreted as
1. H2PO4- (titratable acid) | 2. NH4+
43
renal NH4+ production - regulation
1. acidosis --> adaptive increase in NH3 synthesis | 2. hyperkalemia --> inhibits NH3 synthesis (hyperkalemic renal tubular acidosis)
44
Compensation of chronic metabolic acidosis
adaptive increase in NH3 synthesis (beside hyperventilation)
45
metabolic alkalosis accompanied by ECF (eg. vomiting) | -->
renin - angiotensinin axon --> increased reabsorption of HCO3 increases, worsening the metabolic alkalosis
46
Respiratory alkalosis -symptoms of ...... may occur because
hypocalcemia because H+ and Ca2+ compte for binding sites on plasma proteins --? decreased protein binding causes increased protein binding of Ca2+ and decreased free Ca2+
47
Metabolic acidosis - predicted compensatory response
1 meq/L decrease in HCO3- --> 1.3 mmHg decrease in PCO2
48
Metabolic alkalosis - predicted compensatory response
1 meq/L increase in HCO3- --> 0.7 mmHg increase in PCO2
49
Respiratory acidosis - predicted compensatory response
acute: 1 mmHg increase in PCO2 --> 0.1 meg/L increase in HCO3- chronic: 1 mmHg increase in PCO2 --> 0.4 meq/L increase in HCO3-
50
Respiratory alkalosis - predicted compensatory response
acute: 1 mmHg decrease in PCO2 --> 0.2 meq/L decrease in HCO3- chronic: 1mmHg decrease in PCO2 --> 0.4 meg/L decrease in HCO3-