Electrolyte & Acid Base Disorders +Cases-- Leah** Flashcards
(99 cards)
1
Q
Blood pH is determined by the levels of what two substances in the plasma?
A
- carbonic acid
- bicarbonate
2
Q
What is the normal blood pH
A
7.4 (7.35-7.45)
3
Q
What equation is used to determine blood pH?
A
pH= pKa + log [A-]/[HA]
where A- is bicarbonate and HA is CO2
4
Q
What two organs are responsible for secreting acid in response to the body’s needs?
A
- kidneys (secrete H+/ titratable acid)
- lungs (secrete CO2)
5
Q
Heroin overdose is a classic example of what acid base disorder?
A
respiratory acidosis
-hypoventilation prevents release of CO2
6
Q
Is the metabolic disturbance cause by heroin OD usually compensated for?
A
- No, heroin OD = acute respiratory acidosis, and this cannot be compensated for by the kidneys.
- renal compensation takes 48-72 hours to begin.
7
Q
In what order are the four arterial blood gas findings generally listed and presented in the clinic?
A
pH, CO2, O2, %O2 sat
*He will make this clear on the exam, but in real life/ during rounds, they like you to just read off values in this order.
8
Q
What would you expect the serum bicarb level to be in the case of respiratory acidosis secondary to heroin OD?
A
- normal, because kidneys don’t have time to compensate for the acidosis.
- hypoventilation does not change bicarb values.
9
Q
How do you treat acute respiratory failure? (2)
A
- intubation
- mechanical ventilation
- Before running tests*
10
Q
Three steps for ABG evaluation
Yes, his PPT has 6, Ive just group them nicely.
A
- Use pH and pCO2 to determine primary disorder.
- calculate ion gap, esp important in met. acidosis
- check for compensation/ clues to mixed disorders
11
Q
What is the formula for anion gap?
What is the normal value?
What does a high anion gap most generally mean?
A
Na- (Cl + HCO3) = 4-12 (normal)
- High gap = some extra negatively charged substance in the blood.
- Could be ketones, lactate, ethylene glycol, etc.
12
Q
A patient in sepsis would most likely present with what metabolic derangement?
Would there be compensation?
A
- metabolic acidosis w/ high anion gap, due to lactate build up.
- often see respiratory compensation (LOW CO2, tachypnea)
13
Q
A type 1 diabetic is most at risk for what type of metabolic derangement?
Would you see compensation?
A
- metabolic acidosis with high anion gap due to ketone build up
- may also see metabolic alkalosis due to vomiting and respiratory acidosis due to CNS depression over time (both induced by high ketones in the blood)
*Respiratory compensation may be present, but with time, CNS depression makes this harder to accomplish.
14
Q
What ABG values can best be used to determine the presence of respiratory compensation?
Renal compensation?
A
- respiratory compensatory changes seen by examining pCO2
- renal compensatory changes seen by examining HCO3
*Remember, HCO3 is not directly measured by a blood gas but can be calculated using ABG.
15
Q
We get normal value sheets, but for quick reference/ to be familiar, what are normal pH pCO2 and HCO3 values?
A
- pH: 7.35-7.45
- pCO2: 34-45
- HCO3: 22-28
16
Q
Treatment of DKA:
A
-IV bolus insulin + fluids
17
Q
CO2 is a product of _______.
Titratable acid is a product of _____.
How are these two substances removed?
A
- CO2: cellular metabolism, removed by lungs
- titratable acid: protein catabolism, removed by kidneys
18
Q
In what part of the nephron is H+ secreted?
A
-H+ is secreted in the collecting duct, especially in the presence of aldosterone.
*Remember H+ and K+ follow each other!
If H leaves the duct, K leaves too.
This is why aldo antagonists are K+sparing diuretics
19
Q
Which diuretic causes hyponatremia?
hypocalcemia? hyperuricemia?
A
- thiazides cause hyponatremia and hyperuricemia
- loops cause hypocalcemia
20
Q
Acetalozamide: mechanism of action and classic use
A
carbonic anhydrase inhibitor, classically treats mountain sickness by inducing ^Cl metabolic acidosis –> stimulates compensatory respiratory drive!!
21
Q
How effective is renal compensation?
A
- slow, takes up to 72 hours
- cannot handle large acid loads
22
Q
How effective is pulmonary compensation?
A
- rapid, takes place nearly instantly via chemoreceptor stimulation of respiratory drive
- can handle much larger acid load than the kidneys
23
Q
Function of compensation?
A
- corrects pH
- ASSUME THAT IT NEVER OVERCORRECTS!!!!!!
- If you are suspecting “over correction”, you should really be thinking of a second disorder.
24
Q
What is an example of “false overcompensation”
A
- respiratory alkalosis in sepsis.
- we know lactate = metabolic acidosis sepsis + respiratory compensation.
- HOWEVER, if alkalosis is present, you should assume that there is a SECOND DERAGEMENT caused by the sepsis, NOT overcompensation by the lungs.
Summary: diagnose the patient with metabolic acidosis + respiratory alkalosis, NOT over compensation.
25
#1 Cause of lactoacidosis
-failure to perfuse organs
26
#1 Causes of ketoacidosis (3)
- DKA
- starvation
- alcohol intox
27
Cause of metabolic acidosis that are NOT related to lactate or ketones (2)
- loss of bicarb: renal failure or diarrhea
| - toxic ingestion: ethylene glycol, methanol, salicylates
28
What metabolic acidoses have HIGH anion gaps?
-lactoacidosis, ketoacidosis, ingestion of some toxins (i.e. ethylene glycol)
29
What metabolic acidosis have NORMAL anion gaps?
-loss of bicarb: diarrhea or renal failure
30
The degree of anion gap should correlate to?
-the degree of bicarb decrease
31
Four causes of metabolic alkalosis
- diuretics **RX QUESTION**
- alkaline ingestions
- vomiting (HCL loss)
- primary and secondary hyperaldosteronism
32
How do diuretics induce metabolic alkalosis
-Cl wasting diuretics cause increased bicarb reabsorption
33
Three causes of respiratory acidosis
- CNS depression
- OBSTRUCTIVE DISEASE exacerbation
* *EXCEPT NOT ASTHMA, ASTHMA = alkalosis**
- neuromuscular disorders
34
Five causes of respiraory alkalosis
- PE, asthma
- salicylates
- sepsis
- hypoxia
- hyperventilation
35
Two examples of combined metabolic derangement
- sepsis: metabolic acidosis + respiratory alkalosis +also occasionally met. alkalosis (vomiting)
- DKA: metabolic acidosis + metabolic alkalosis + respiratory alkalosis (eventual acidosis w resp depression)
36
Normal levels of compensation BY THE LUNGS in metabolic acidosis and alkalosis
- metabolic acidosis: CO2 down by 1.25 mmHg for every 1 meq/L HCO3-
(acidosis: 1.25:1)
- metabolic alkalosis: CO2 up by 0.75 "..."
(alkalosis: 0.75:1)
37
When might compensation fail to appropriately occur?
- neuro diseases
- drug intoxication
*This is different than the body just not being able to compensate for an extreme amount of acid.
38
Normal levels of compensation by the kidneys in acute or chronic respiratory derangement:
acidosis:
- acute bicarb ^ 1 for every 10 CO2 ^
- chronic bicarb ^ 4 for every 10 CO2 ^
(1: 10, 4:10 in acidosis)
alkalosis:
- acute bicarb DOWN 2 for every 10 CO2 decrease
- chronic bicarb DOWN 4 for every 10 CO2 decrease
(2: 10, 4:10 in alkalosis)
39
In the event of metabolic acidosis AND alkalosis, what findings would be seen on arterial blood gas?
When might this actually happen?
- anion gap change would NOT be proprtional to the change in bicarb
- NORMAL bicarb w/ very HIGH anion gap
-this happens when a patient is in DKA OR septic w/puking
40
7.30/ 50/ 60/ O2 sat not listed
Bicarb: 27
This is an example of?
- low pH= acidosis
- high CO2, normal bicarb
- RESPIRATORY acidosis, uncompensated.
41
7.47/ 30/ 80/ O2 sat not listed
Bicarb: 19
This is an example of?
-high pH = alkalosis
-CO2 low, bicarb low
respiratory alkalosis with metabolic compensation
(likely chronic because bicarb is significantly low.)
42
7.37/ 28/ 70/ O2 sat not listed
Bicarb: 15
This is an example of?
-pH on the low end of normal
-CO2 is low
-bicarb is low
metabolic acidosis with respiratory compensation
43
7.45/ 47/ 70/ O2 sat not listed
Bicarb: 32
This is an example of?
- pH on the high end of normal
- CO2 is high, bicarb is high
- metabolic alkalosis with respiratory compensation
44
If the PCO2 and the bicarb change in the same direction the disorder is usually?
If hey change in opposite directions?
same direction: metabolic
| opposite direction: respiratory
45
Major intracellular and extracellular cations?
- Just remember, its like there's a banana floating around in the salty sea.
- Na extracellular fluid, K intracellular
46
Abnormalities in sodium CONCENTRATION reflect?
-problems with free water handling, not sodium handling.
47
Definition of hyper and hyponatremia
hyper: >>145, too much water
48
Most common cause of hypernatremia
not drinking enough, esp in the elderly/ chronically ill who cannot drink on their own
49
PE findings assc with hypernatremia (4)
- volume depletion = tachycardia and low BP
- dry mucous membranes
- thirsty and lethargic
- poor skin turgor
50
Describe the TYPICAL urine findings assc with hypernatremia
-high osmolality because patient is trying to retain fluid
51
When might a patient have hypernatremia and DILUTE urine?
-diabetes insipidus, due to LOSS of ADH
52
Treatment of symptomatic hypernatremia: (2)
IV fluids, hypotonic solutions
| goal = stabilize the hypotension
53
Hyponatremia is usually ______ ________, in comparison to hypernatremia.
physiologically complex, whereas HYPERnatremia often just involved poor fluid intake!!
54
PE findings assc with hyponatremia (2)
- usually asx unless severe
| - nausea, H/A and neurodeficits may occur at very low levels
55
Three types of hyponatremia
- hypovolemic
- hypervolemic
- euvolemic
56
Urine osmolality is a surrogate for what?
| Urine Na is a surrogate for what?
- osmolality ~ ADH activity
| - Na ~ volume status
57
Three causes of HYPERvolemic hyponatremia
-CHF, cirrhosis, nephrotic syndrome
58
One cause of euvolemic hyponatremia
-SiADH, i.e. small cell lung cancer
59
What would be the OPPOSITE of SiADH?
-Diabetes insipidus, pituitary condition
60
Cause of HYPOvolemic hyponatremia
-Thiazide diuretics
61
Treatment for SiADH
-fluid restriction
62
How is symptomatic HYPOnatremia treated?
- slow replacement with HYPERtonic saline
| - must do this SLOWLY to prevent pontine demyelination (locked in syndrome)
63
When might K+ shift across cellular membranes? (3)
- When there are changes in pH
- acidosis = HYPERkalemia
- alkalosis= HYPOkalemia
64
Causes of hyperkalemia? Which is most common? (6)
* #1: renal failure*
- excess intake
- acidosis
- lack of aldosterone
- severe volume depletion
- drugs
65
What causes pseudohyperkalemia?
-lysed RBCs spill K+ in blood sample tube
66
HYPERkalemia EKG changes?
| HYPOkalemia EKG changes?
- hyper: tall, peaked T wave
| - hypo: prolonged QT interval, risk of torsades
67
Treatment of HYPERkalemia in the presence of EKG changes: (3)
- calcium gluconate (only for weird EKG)
- insulin and albuterol to shift K+ into cells
- resin to increase K+ excretion
*or dialysis if cause is acute renal failure
68
Four causes HYPOkalemia
- diuretics
- diarrhea
- alkalosis
- Mg deficiency
DDAM GIRL, YOU HYPOKALEMIC.
69
Symptoms of severe HYPOkalemia (2)
-arrythmia and muscle twitches
70
Test that is not useful for K+ levels
urine concentrations
71
Treatment of HYPOkalemia; what do we avoid?
- Gradually give ORAL K+
| - AVOID IV KCl: causes sclerosis
72
Mg is a cofactor for?
-ATPases
73
Causes of Mg deficiency (3)?
- CKD
- Diuretics
- alcoholism
74
Low Mg can cause low _____.
K+
75
Avoid Mg loading in ______.
renal disease
76
What are the three types of RTAs?
Type I- distal
Type II- proximal
Type IV- hyperkalemic
77
What is the defect in type I RTA? What is the urine pH? K+ levels?
distal a-intercalated cells cannot secrete H+; urine is basic (5+); K+ is LOW
78
What is the defect in type II RTA? What is the urine pH? K+ levels?
proximal tubule cannot reabsorb bicarb; urine is normal (acidic) because distal tubule compensates for the defect. K+ is still low.
79
What is the defect in type IV RTA? What is the urine pH? K+ levels?
Lack of Aldo or resistance to Aldo; predominately seen in diabetes; urine is acidic (normal pH) but LOW IN AMMONIA! type (4) is low in NH(4); K+ is HIGH due to low aldosterone
(similar to giving a K+ sparing diuretic!)
80
What RTA can cause calcium stones?
| What RTA can cause rickets/osteomalacia?
Type I- causes stones
| Type II- causes hypophosphatemic rickets
81
What are some causes of type I RTA?
```
Autoimmune disease (i.e. Sjorgens)
Chemotherapy, Amphotericin, Analgesics
Obstruction
```
82
Type II RTA causes (2)
- carbonic anyhdrase inhibitors
| - Fanconis Symdrome
83
Most common/important cause of type IV RTA?
DM
84
Describe total body weight compartments (water, non-water mass, ECF/ICF/plasma)
Total Body Water --> 60% body weight
Of the water --> 2/3 ICF; 1/3 ECF
Of th ECF --> 1/4 is plasma
(60, 40, 20 rule--> 60% body weight = H20, 40% = intracellular, 20%= Extracellular)
85
Diuretics most likely to cause hyponatremia?
Thiazides
86
Findings assc with diabetes insipidus:
Hypernatremia; dilute urine
87
Over what period of time should you correct hyponatremia?
| When is this most important?
48 hours --> slow to prevent pontine myelinolysis
| *esp in pre menopausal females*
88
HIV drug assc with kidney stones
Indinavir
89
Hallmark presentation of kidney stones
Flank pain and blood in the urine
90
What is the urinary ion gap?
When is it useful?
What is it essentially a surrogate for?
[(Na+K) -Cl]
Used in non ion gap metabolic acidosis (i.e. Diarrhea)
Essentially a surrogate for ammonia
91
If someone is HYPERnatremic, what should their urine look like (assuming they are healthy?)
Concentrated, HYPERnatremia suggests a lack of free water-- the body should be trying to RETAIN Fluid (via ADH).
One example of this failing is Diabetes insipidus
92
Which is a bigger problem: hypotension or hypernatrmia?
Hypotension! If you have both in a patient, correct the hypotension first.
(Although I'm a little confused because I think you give fluids to both hypotensive and hypernatremic patients........)
93
What two things can all diuretics cause?
volume depletion, pre-renal azotemia
94
What are the primary uses of:
- thiazides
- Loops
- K+ sparing
- Mannitol
- CAi
- thiazides: HTN
- Loops: edema
- K+ sparing: hyperalo, weak-antiHTN, reduce renal/CHF mortality
- Mannitol- increased ICP, trauma, renal failure
- CAi- mountain sickness, glaucoma
95
What is the mechanism of action for:
- Thiaizdes
- Loops
- Triameterene
- Spiro
- Thiaizdes: block NaCl transport at DCT, CD
- Loops: block Na/K/2Cl transport at LOH
- Triameterene: block Na/K transport at CD
- Spiro: Blocks aldosterone
96
What acid base carbonic anhydrase inhibitors cause?
Metabolic acidosis
97
Diuretic than can prevent kidney stone?
Thiaizdes, because decreased amount of Ca in urine
98
Loop used in patients allergic to sulfa drugs
Ethacrynic acid
99
Metabolic changes assc with thiazides
- low Na, K
| - high Ca, Uric acid, glucose
