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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
result of reabsorption of HCO3- in DCT/collecting duct
reabsorption of HCO3- | excretion of H+ ions in urine
26
factors that influence HCO3- reabsorption
1. amount filtered at glomerulus 2. PCO2 of arterial blood 3. ECF 4. angiotensin II
27
how does the amount of HCO3- filtered at glomerulus affect HCO3- reabsortion
GFR determines amount of HCO3 in the filtrate
28
how does the PCO2 of arterial blood influence the HCO3- reabsorption
1. increase in PCO2 will increase HCO3- reabsorption | 2. decrease PCO2 will decrease HCO3- reabsorption
29
how does the ECF influence the HCO3- reabsorption
1. ECF expansion will decrease HCO3- reabsorption | 2. ECF contraction will increase HCO3- reabsorption
30
how does angiontensin II influence the HCO3- reabsorption
stimulates H+/Na+ exchange in PCT which will promote HCO3- reabsorption
31
titratable acid aka
aka phosphate buffering
32
mechanism of titratable acid
1. H+ combines dibasic phosphate (HPO4) to form a monobasic phosphate (H2PO4-) 2. amount of H+ excreted depends on pH in tubular fluid
33
what happens if tubular fluid pH decrease in titratable acid mechanism
--if tubular fluid pH decrease then H+ secretion as H2PO4 will DECREASE
34
what pH range can the tubular fluid NOT overcome to secrete H+ into tubular fluid
--this transport mechanism to secrete H+ into tubular fluid can't overcome a gradient formed by tubular fluid pH of 4.5 or less
35
pH of human urine
4.5-8
36
result of titratable acid buffering
phosphate buffer is most effective at excreting H+ in normal circumstances
37
mechanism of ammonium (ammonia buffering)
1. H+ combines with NH3 (ammonia) to form ammonium (NH4+) | 2. amount of H+ excreted as NH4+ depends on pH in tubular fluid
38
decreases in tubular fluid of pH 4.5 or less will what in ammonia buffering
INCREASE secretion of H+ excreted as NH4+
39
result of ammonia buffering
the ammonium buffer mechanism is the most effective at excreting H+ in acidic conditions
40
factors that influence excretion of H+ from DCT/collecting duct
1. hypokalemia 2. elevated PCO2 3. aldosterone
41
how does hypokalemia influence excretion of H+ from DCT/collecting duct
stimulates NH3 (ammonia) synthesis which will increase H+ excretion
42
how does elevated PCO2 influence excretion of H+ from DCT/collecting duct
(respiratory acidosis) | increases H+ secretion
43
how does aldosterone influence excretion of H+ from DCT/collecting duct
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
4 acid base disorders
1. respiratory acidosis 2. respiratory alkalosis 3. metabolic acidosis 4. metabolic alkalosis
45
which affects K+ concentrations - resp or metabolic acidosis/alkalosis
metabolic acidosis/alkalosis
46
simple acid/base disorders vs mixed acid/base disorders - normal
- 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
if the calculated compensation is EQUAL to the expected normal response then how many disorders are present?
ONE
48
if calculated compensation IS NOT EQUAL to the expected normal response then how many disorders are present
MORE THAN ONE
49
cause of respiratory acidosis
limited ventilation
50
primary disturbance in resp acidosis
increased PCO2 in arterial blood
51
initial acid/base disruption in resp acidosis
increased H+ (decreased pH), normal HCO3-
52
compensation in resp acidosis
kidneys increase HCO3- reabsorption and H+ excretion
53
compensated picture of resp acidosis
increased PCO2, increased HCO3-, decreased pH with a trend toward normalizing
54
clinical causes of limited ventilation
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
cause of resp alkalosis
increased ventilation
56
primary disturbance of resp alkalosis
decreased PCO2 in arterial blood
57
initial acid/base disruption in resp alkalosis
decreased H+ (increased pH)
58
compensation for resp alkalosis
kidneys decreased HCO3- reabsorption and H excretion
59
compensated picture of resp alkalosis
decreased PCO2, decreased HCO3-, increased pH trend toward normalizing pH
60
clinical causes of increased ventilation
- PE - high altitude - excessive salicylate ingestion - psychogenic hyperventilation (panic/anxiety) - anemia - pregnancy - pulm pathology
61
cause of metabolic acidosis
excessive fixed acid formation, ingestion of fixed acid or loss of base
62
primary disturbance of metabolic acidosis
decreased HCO3- (either from trying to buffer increased H+ or from actual loss of base)
63
initial acid/base disruption metabolic acidosis
increased H+ (decreased pH) due to inadequate HCO3-
64
compensation in metabolic acidosis
lungs hyperventilate to reduce PCO2 which in turn will reduce H+
65
compensated picture metabolic acidosis
decreased PCO, decreased HCO3-, decreased pH with trend toward normalizing
66
clinical causes of excessive fixed acid formation, ingestion of fixed acid or loss of base - increased anion gap
- 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
clinical causes of excessive fixed acid formation, ingestion of fixed acid or loss of base - normal anion gap
aka loss of base - diarrhea (GI loss of base) - renal tubular acidosis (renal loss of base) - diuretics (carbonic anhydrase inhibitors, K+ sparing drugs)
68
cause of metabolic alkalosis
loss of fixed acid formation or gain of base
69
primary disturbance in metabolic alkalosis
increased HCO3- either from actual gain of base or reduced availability of fixed acids
70
initial acid/base disruption in metabolic alkalosis
decreased H+ increased pH
71
compensation in metabolic alkalosis
lungs hypoventilated to retain PCO2 which in turn will increase H+
72
compensated picture in metabolic alkalosis
increased PCO2, increased HCO3-, increased pH with trend toward normalizing
73
clinical causes of loss of fixed acid formation or gain of base
- 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
what is the serum anion gap
anion gap is a comparison of cations (positive charged particles) and anions (negative charged particles) in the blood
75
which cations are measure in the anion gap
sodium
76
which cations are not measured in anion gap
calcium, mag, potassium, gamma globulin
77
measured anions in anion gap
chloride, bicarb
78
which anions are not measured in anion gap
proteins (albumin), phosphate, sulfate, lactate
79
how is the anion gap measured
Na- (Cl+HCO3) = anion gap
80
normal anion gap
12 (range 6-16)
81
in a healthy individual - the gap is due to what
unmeasure anions - primarily due to plasma proteins (albumin)
82
human body is always producing acids or bases?
acids
83
what does a normal anion gap represent in metabolic acidosis
the concentration of chloride increased (replaced HCO3-) to maintain normal gap
84
what does an increased anion gap indicated in metabolic acidosis
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
in metabolic acidosis - what happens as H+ is getting buffered
anion and HCO3- decreases, therefore another anion must replace decreased HCO3- to maintain electroneutrality in the blood
86
why is determining the anion gap relative?
-to ID the possibility of co-existing metabolic acidosis in other acid/base disorders
87
anion gap represents the presence of what acid/base disorder
metabolic acidosis
88
if metabolic acidosis is the primary disturbance, what does the anion gap tell us?
1. increased anion gap = renal failure, ketoacidosis, toxins, or lactic acidosis 2. normal anion gap: GI or renal loss of base
89
if the anion gap is present in other acid/base disorders, what does this mean?
suggests a mixed acid/base disorder
90
when does the anion gap become a better diagnostic tool
at levels >20
91
5 steps in determining acid/base
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
examples of determining if the compensation is appropriate for the primary disorder
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
normal ABG measurements
``` 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
Step 1: pH 7.4
acidosis 7.4
95
Step 2: primary disturbance respiratory or metabolic acidosis?
respiratory acidosis: increased PCO2 and increased HCO3- | metabolic acidosis: decreased PCO2 and decreased HCO3-
96
Step 2: primary disturbance metabolic or resp alkalosis
resp alkalosis: decrease PCO2 and decreased HCO3- | metabolic alkalosis: increase PCO2 and increased HCO3-
97
Step 3: is compensation appropriate for metabolic acidosis?
PCO2 = [1.5x(HCO3-)]+8 ***within +/- 2*** if not suggestive of secondary resp disorder present
98
Step 3: is compensation appropriate for metabolic alkalosis
increase PCO2 = 0.6 x incr HCO3 (+/-2)**
99
Step 3: is the compensation appropriate for resp acidosis
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
Step 3: is the compensation appropriate? resp alkalosis
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
Step 4: is there a normal or increased anion gap present? if increased then what? if normal then what?
``` if increased (>12) then anion gap metabolic acidosis is present if normal ( ```
102
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
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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