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Pathophys Exam II > Renal Mod 3 > Flashcards

Renal Mod 3 Flashcards

1
Q

how does the body maintain homeostasis if it is constantly producing acids?

A

excrete or metabolize more acids

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2
Q

what are respiratory acids?

A

aka volatile acids
technically carbonic acid is the true resp acid
CO2 is commonly thought of as resp acid bc it produces carbonic acid

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3
Q

CO2 is produced from metabolism of what?

A

carbs and fats

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4
Q

what are metabolic acids

A

aka nonvolatile acids or fixed acids
acids produced by the body: ex. lactic acid & ketoacids
you can also ingest too much acid as well

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5
Q

when is lactic acid produced?

A

anaerobic metabolism

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6
Q

when is ketoacids produced

A

result of fatty acid/protein metabolism in starvation or pathology

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7
Q

mechanisms to maintain acid/base hoemostasis

A
  1. buffering acids - immediate
  2. resp compensation - rapid response (min to hrs)
  3. renal compensation - slower response (up to a few days)
  4. bone plays role in chronic metabolic acidosis (bone density is dependent on acid/base balance)
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8
Q

what are buffering acids

A
  • serve as the first line defense against acid/base variations
  • buffer maintains pH when acids accumulate in the blood
  • buffers can be intracellular/extracellular and occur indifferent locations
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9
Q

give an example of intracellular buffer

A

hemoglobin in RBCs is a major intracellular buffer

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10
Q

how does hemoglobin act as an intracellular buffer

A
  1. as CO2 enters RBC it combines with H2O to form carbonic acid
  2. the carbonic acid further disassociates into H+ and HCO3-
  3. the H+ binds to the hemoglobin
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11
Q

ICF is a major mechanism responsible for buffering what

A

respiratory acids

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12
Q

give an example of extracellular buffer

A

HCO3- in the ECF

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13
Q

bicarb in the ECF is a major mechanism responsible for buffering

A

metabolic acids

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14
Q

respiratory role in acid/base balance

A
  • lungs excrete/eliminate CO2 from the body

- may take a few minutes to a few hours to produce maxiaml influence on acid/base

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15
Q

how does hyperventilation affect acid/base balance

A

increase the body’s pH (more alkaline = getting rid of more CO2)

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16
Q

clinical result of hyperventilation

A
  • creation of resp alkalosis
  • correction of resp acidosis
  • compensation for metabolic acidosis
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17
Q

how does hypoventilation affect acid/base balance

A

decrease body’s pH (more acidic)

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18
Q

clinical result of hypoventilation

A
  • creation of resp acidosis
  • correction of resp alkalosis
  • compensation for a metabolic alkalosis
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19
Q

how do kidneys regulate acid/base balance in arterial blood

A
  1. excrete fixed acids

2. alter bicarb reabsorption/excretion to compensate for acid/base variations

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20
Q

PCT role in acid/base balance

A
  1. production of ammonium - maintain excretion of H+

2. reabsorption of bicarb

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21
Q

how does the PCT reabsorb bicarb

A
  • H+ secreted from PCT into lumen
  • Combines with bicarb to form H2O and CO2
  • H2O and CO2 diffuse back into PCT cell and disassociate into H= and HCO3-
  • HCO3- is reabsorbed into the blood stream
  • H+ is recycled to be secreted into PCT lumen again
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22
Q

result of reabsorption of bicarb in PCT

A

reabsorption of HCO3-

NO excretion of H+ ions

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23
Q

two major actions of DCT in acid/base balance

A
  1. reabsorption of HCO3-

2. excretion of H+ via phosphate and ammonium buffering

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24
Q

how is HCO3- reabsorbed in DCT/collecting duct

A
  • in intercalated cell, H2O and CO2 combine to form H2CO3
  • H2CO3 disassociates into H+ and HCO3-
  • H+ is secreted into late DCT/collecting duct lumen
  • HCO3- is reabsorbed into blood stream
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25
Q

result of reabsorption of HCO3- in DCT/collecting duct

A

reabsorption of HCO3-

excretion of H+ ions in urine

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26
Q

factors that influence HCO3- reabsorption

A
  1. amount filtered at glomerulus
  2. PCO2 of arterial blood
  3. ECF
  4. angiotensin II
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27
Q

how does the amount of HCO3- filtered at glomerulus affect HCO3- reabsortion

A

GFR determines amount of HCO3 in the filtrate

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28
Q

how does the PCO2 of arterial blood influence the HCO3- reabsorption

A
  1. increase in PCO2 will increase HCO3- reabsorption

2. decrease PCO2 will decrease HCO3- reabsorption

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29
Q

how does the ECF influence the HCO3- reabsorption

A
  1. ECF expansion will decrease HCO3- reabsorption

2. ECF contraction will increase HCO3- reabsorption

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30
Q

how does angiontensin II influence the HCO3- reabsorption

A

stimulates H+/Na+ exchange in PCT which will promote HCO3- reabsorption

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31
Q

titratable acid aka

A

aka phosphate buffering

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32
Q

mechanism of titratable acid

A
  1. H+ combines dibasic phosphate (HPO4) to form a monobasic phosphate (H2PO4-)
  2. amount of H+ excreted depends on pH in tubular fluid
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33
Q

what happens if tubular fluid pH decrease in titratable acid mechanism

A

–if tubular fluid pH decrease then H+ secretion as H2PO4 will DECREASE

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34
Q

what pH range can the tubular fluid NOT overcome to secrete H+ into tubular fluid

A

–this transport mechanism to secrete H+ into tubular fluid can’t overcome a gradient formed by tubular fluid pH of 4.5 or less

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35
Q

pH of human urine

A

4.5-8

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36
Q

result of titratable acid buffering

A

phosphate buffer is most effective at excreting H+ in normal circumstances

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37
Q

mechanism of ammonium (ammonia buffering)

A
  1. H+ combines with NH3 (ammonia) to form ammonium (NH4+)

2. amount of H+ excreted as NH4+ depends on pH in tubular fluid

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38
Q

decreases in tubular fluid of pH 4.5 or less will what in ammonia buffering

A

INCREASE secretion of H+ excreted as NH4+

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39
Q

result of ammonia buffering

A

the ammonium buffer mechanism is the most effective at excreting H+ in acidic conditions

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40
Q

factors that influence excretion of H+ from DCT/collecting duct

A
  1. hypokalemia
  2. elevated PCO2
  3. aldosterone
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41
Q

how does hypokalemia influence excretion of H+ from DCT/collecting duct

A

stimulates NH3 (ammonia) synthesis which will increase H+ excretion

42
Q

how does elevated PCO2 influence excretion of H+ from DCT/collecting duct

A

(respiratory acidosis)

increases H+ secretion

43
Q

how does aldosterone influence excretion of H+ from DCT/collecting duct

A

stimulates Na+ reabsorption along with corresponding H+ and K+ secretion from late DCT/collecting duct
–for every H+ secreted there is a corresponding Na+ reabsorbed

44
Q

4 acid base disorders

A
  1. respiratory acidosis
  2. respiratory alkalosis
  3. metabolic acidosis
  4. metabolic alkalosis
45
Q

which affects K+ concentrations - resp or metabolic acidosis/alkalosis

A

metabolic acidosis/alkalosis

46
Q

simple acid/base disorders vs mixed acid/base disorders - normal

A
  • normal compensation responses can be calculated for simple acid/base disorders
    ex. if CO2 increases then there should be a predictable increase of HCO3- that represents normal compensation
47
Q

if the calculated compensation is EQUAL to the expected normal response then how many disorders are present?

48
Q

if calculated compensation IS NOT EQUAL to the expected normal response then how many disorders are present

A

MORE THAN ONE

49
Q

cause of respiratory acidosis

A

limited ventilation

50
Q

primary disturbance in resp acidosis

A

increased PCO2 in arterial blood

51
Q

initial acid/base disruption in resp acidosis

A

increased H+ (decreased pH), normal HCO3-

52
Q

compensation in resp acidosis

A

kidneys increase HCO3- reabsorption and H+ excretion

53
Q

compensated picture of resp acidosis

A

increased PCO2, increased HCO3-, decreased pH with a trend toward normalizing

54
Q

clinical causes of limited ventilation

A
  1. meds reduce resp centers in brainstem - opiates, sedatives, anesthetics
  2. neuromuscular conditions that reduce ventilation - GBS, MS, ALS, polio
  3. pulmonary pathology - obstructive disorders that impair ventilation
55
Q

cause of resp alkalosis

A

increased ventilation

56
Q

primary disturbance of resp alkalosis

A

decreased PCO2 in arterial blood

57
Q

initial acid/base disruption in resp alkalosis

A

decreased H+ (increased pH)

58
Q

compensation for resp alkalosis

A

kidneys decreased HCO3- reabsorption and H excretion

59
Q

compensated picture of resp alkalosis

A

decreased PCO2, decreased HCO3-, increased pH trend toward normalizing pH

60
Q

clinical causes of increased ventilation

A
  • PE
  • high altitude
  • excessive salicylate ingestion
  • psychogenic hyperventilation (panic/anxiety)
  • anemia
  • pregnancy
  • pulm pathology
61
Q

cause of metabolic acidosis

A

excessive fixed acid formation, ingestion of fixed acid or loss of base

62
Q

primary disturbance of metabolic acidosis

A

decreased HCO3- (either from trying to buffer increased H+ or from actual loss of base)

63
Q

initial acid/base disruption metabolic acidosis

A

increased H+ (decreased pH) due to inadequate HCO3-

64
Q

compensation in metabolic acidosis

A

lungs hyperventilate to reduce PCO2 which in turn will reduce H+

65
Q

compensated picture metabolic acidosis

A

decreased PCO, decreased HCO3-, decreased pH with trend toward normalizing

66
Q

clinical causes of excessive fixed acid formation, ingestion of fixed acid or loss of base - increased anion gap

A
  • ketoacidosis (FFA metabolism in DM)
  • lactic acidosis (hypoxic tissues promote accumulation)
  • salicylate intoxication (aspirin)
  • analgesics (NSAIDs, acetaminophen)
  • methanol (antifreeze, solvent, fuel, formaldehyde)
  • ethylene glycol (antifreeze)
  • carbon monoxide
  • chronic renal failure (can’t excrete H+)
67
Q

clinical causes of excessive fixed acid formation, ingestion of fixed acid or loss of base - normal anion gap

A

aka loss of base

  • diarrhea (GI loss of base)
  • renal tubular acidosis (renal loss of base)
  • diuretics (carbonic anhydrase inhibitors, K+ sparing drugs)
68
Q

cause of metabolic alkalosis

A

loss of fixed acid formation or gain of base

69
Q

primary disturbance in metabolic alkalosis

A

increased HCO3- either from actual gain of base or reduced availability of fixed acids

70
Q

initial acid/base disruption in metabolic alkalosis

A

decreased H+ increased pH

71
Q

compensation in metabolic alkalosis

A

lungs hypoventilated to retain PCO2 which in turn will increase H+

72
Q

compensated picture in metabolic alkalosis

A

increased PCO2, increased HCO3-, increased pH with trend toward normalizing

73
Q

clinical causes of loss of fixed acid formation or gain of base

A
  • vomiting (loss of gastric acid & base if left behind)
  • loop or thiazide diuretics (volume contraction)
  • volume contraction (promotes H+/Na+ exchange)
  • hypokalemia (promotes NH3 synthesis and H+ excretion)
74
Q

what is the serum anion gap

A

anion gap is a comparison of cations (positive charged particles) and anions (negative charged particles) in the blood

75
Q

which cations are measure in the anion gap

76
Q

which cations are not measured in anion gap

A

calcium, mag, potassium, gamma globulin

77
Q

measured anions in anion gap

A

chloride, bicarb

78
Q

which anions are not measured in anion gap

A

proteins (albumin), phosphate, sulfate, lactate

79
Q

how is the anion gap measured

A

Na- (Cl+HCO3) = anion gap

80
Q

normal anion gap

A

12 (range 6-16)

81
Q

in a healthy individual - the gap is due to what

A

unmeasure anions - primarily due to plasma proteins (albumin)

82
Q

human body is always producing acids or bases?

83
Q

what does a normal anion gap represent in metabolic acidosis

A

the concentration of chloride increased (replaced HCO3-) to maintain normal gap

84
Q

what does an increased anion gap indicated in metabolic acidosis

A

non-measured anions increased (lactate, b-hydroxybutyrate) to maintain normal gap BUT they are not measured clinically so they show as an anion gap

85
Q

in metabolic acidosis - what happens as H+ is getting buffered

A

anion and HCO3- decreases, therefore another anion must replace decreased HCO3- to maintain electroneutrality in the blood

86
Q

why is determining the anion gap relative?

A

-to ID the possibility of co-existing metabolic acidosis in other acid/base disorders

87
Q

anion gap represents the presence of what acid/base disorder

A

metabolic acidosis

88
Q

if metabolic acidosis is the primary disturbance, what does the anion gap tell us?

A
  1. increased anion gap = renal failure, ketoacidosis, toxins, or lactic acidosis
  2. normal anion gap: GI or renal loss of base
89
Q

if the anion gap is present in other acid/base disorders, what does this mean?

A

suggests a mixed acid/base disorder

90
Q

when does the anion gap become a better diagnostic tool

A

at levels >20

91
Q

5 steps in determining acid/base

A
  1. determine acidemia or alkalemia
  2. determine primary disturbance: resp or metabolic
  3. is the compensation appropriate for primary disorder?
  4. is there a normal or increased anion gap?
  5. if metabolic acidosis, then determine if additional metabolic disorder is occuring
92
Q

examples of determining if the compensation is appropriate for the primary disorder

A
  1. if metabolic acidosis, is resp compensation appropriate? or is there a secondary resp acidosis/alkalosis present?
  2. if metabolic alkalosis, is resp compensation appropriate? more difficult to determine which means more difficult to estimate if secondary disorder is present
  3. if resp acidosis/alkalosis, is reanl compensation appropraite for an acute or chronic? if not, suggestive of combined “acute on chronic” resp disorder
93
Q

normal ABG measurements

A 
pH: 7.4
PCO2: 40 mmHg
HCO3-: 24 mEq/L
normal anion gap: 12
--need to know Na+, HCO3-, and Cl- levels to calculate
94
Q

Step 1: pH 7.4

A

acidosis 7.4

95
Q

Step 2: primary disturbance respiratory or metabolic acidosis?

A

respiratory acidosis: increased PCO2 and increased HCO3-

metabolic acidosis: decreased PCO2 and decreased HCO3-

96
Q

Step 2: primary disturbance metabolic or resp alkalosis

A

resp alkalosis: decrease PCO2 and decreased HCO3-

metabolic alkalosis: increase PCO2 and increased HCO3-

97
Q

Step 3: is compensation appropriate for metabolic acidosis?

A

PCO2 = [1.5x(HCO3-)]+8

within +/- 2

if not suggestive of secondary resp disorder present

98
Q

Step 3: is compensation appropriate for metabolic alkalosis

A

increase PCO2 = 0.6 x incr HCO3 (+/-2)**

99
Q

Step 3: is the compensation appropriate for resp acidosis

A

for every incr PCO2 by 10mmHg then there is an incr of HCO3 should be 1 if acute resp, or 4 if chronic resp

**because kidneys take longer to compensate

100
Q

Step 3: is the compensation appropriate? resp alkalosis

A

for every decr PCO2 by 10 mmHg, then decr of HCO3 should be 2 if “acute” resp or 5 if “chronic” resp
–if renal compensation is not appropriate for an acute or chornic then suggestive of combined “acute on chronic” resp disorder

101
Q

Step 4: is there a normal or increased anion gap present?
if increased then what?
if normal then what?

A 
if increased (>12) then anion gap metabolic acidosis is present
if normal (
102
Q

acid base analysis example: a 21 year old student presents with excessive vomiting after binge drinking
ABG: 7.5, pCO2: 44, pO2: 100
Na: 138 Cl: 100 HCO3: 30
1. acidosis or alkalosis?
2. resp or metabolic?
3. is compensation appropriate
4. is there normal or increased anion gap

A
  1. alkalosis
  2. metabolic: doesn’t make sense to have incr CO2, but pH is incr so look at HCO3-
  3. metabolic alkalosis
  4. normal gap

Pathophys Exam II (5 decks)

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