Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SMP - Renal > PSW 3 and GC 2 - Clinical Acid-Base Disorders > Flashcards

PSW 3 and GC 2 - Clinical Acid-Base Disorders Flashcards

1
Q

Define metabolic acidosis.

A

Abnormal physiologic process characterized by the primary gain of strong acid or
primary loss of bicarbonate from the ECF

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

Define metabolic alkalosis.

A

Abnormal physiologic process characterized by the primary gain of strong base (or loss of strong acid) or the primary gain of bicarbonate by the ECF

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

Define respiratory acidosis.

A

Abnormal physiologic process in which there is a primary reduction in alveolar ventilation relative to the rate of CO2 production

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

Define respiratory alkalosis.

A

Abnormal physiologic process in which there is a primary increase in the rate of alveolar ventilation relative to the rate of CO2 production

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

What are metabolic AB disorders characterized by?

A

Disturbances in plasma [HCO3-]

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

What are respiratory AB disorders characterized by?

A

Disturbances in plasma PCO2

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

How to determine which primary disorders of acid base balance it is? What 2 numbers are needed?

A
  1. Primary disorder: alkalemia or acidemia determines acidosis or alkalosis
    OR if pH is normal but CO2 is not: that means there are 2 primary disorders working in opposite directions
  2. Respiratory derangement? If it does not match the primary disorder than the primary disorder must be metabolic
  3. If primary disorder is respiratory, is it acute or chronic? OR if pH change is higher than 0.8 per 10 mmHg, both respiratory and metabolic disorders happening in same direction?
  4. If chronic, what is the compensatory metabolic disorder (always opposite the primary disorder)?

ONLY pH and PaCO2 needed

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

4 causes of metabolic acidosis?

A
  1. Non-renal: acid ingestion or increased acid production OR base loss
  2. Decreased renal mass
  3. Renal tubular acidosis: proximal or distal
  4. Hypoaldosteronism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

3 causes of metabolic alkalosis?

A
  1. Acid loss
  2. Base excess: ingestion or volume contraction
  3. Excess aldosterone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the anion gap? Normal value and range? Why is it useful for diagnoses?

A

Defined as the difference in the measured major cation (Na+) and measured anions (Cl-+ HCO3-):

Anion gap = Na+ - (Cl- + HCO3-)

Normal = 10-12 mEq/L (range = 8 to 16)

The “unmeasured” anions which account for the normal anion gap include substances normally present in plasma such as phosphate, sulfate, organic acids and proteins, so for diagnosis:

  1. Increase in anion gap means that the acidosis is due to an ACID ISSUE
  2. Normal anion gap means that the acidosis is due to BASE ISSUE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a stridor?

A

High-pitched, wheezing sound caused by disrupted airflow.

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

Normal plasma [HCO3-]?

A

24 mEq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In terms of compensatory respiration for metabolic disease: can you more easily blow off or retain CO2?

A

Easier to blow it off, because as O2 goes down there is a hypoxic response and the brain will force you to breathe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Normal plasma [Cl-]?

A

105 mEq/L

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

4 potential reasons for a high anion gap?

A
  1. Increase in one or more of the anions normally present in the blood (as in renal failure): HPO42-, SO4-, organic acids and proteins, urea (e.g. uremic acidosis)
    Presence in the blood of some other substances not usually present in any quantity:
  2. Lactic acid (in situations where there is anaerobic metabolism due to hypoxia or shock => lactic acidosis)
  3. Ketoacids (in starvation or diabetic acidosis, and alcoholism): beta-hydroxybutyrate, acetoacetate
  4. Exogenously derived substances (e.g. salicylate, paraldehyde, methanol, ethylene glycol, toluene)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is Cl- high when HCO3- is low?

A

Because not enough H+/HCO3- available for Na+ reabsorption, so more Cl- is reabsorbed in the tubule instead of HCO3-

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

Characteristic features of renal failure?

A
  1. Rise in plasma urea nitrogen (BUN)
  2. Rise in plasma creatinine
  3. Decrease in GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What could cause normal anion gap? 2 reasons.

A
  1. GIT: diarrhea, ileostomy, or enteric fistula
  2. KIDNEYS: renal issue with reabsorption:
    - High pH (>5.5): distal renal tubular acidosis
    - Low pH (<5.5): proximal renal tubular acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Normal plasma creatinine?

A

0.7-1.2 mg/dL ~ 1 mg/dL = 1 mg %

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

How to calculate renal function?

A

1/Pcr x 100 %

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

Normal BUN?

A

20 mg%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is azotemia?

A

Build-up of nitrogen products in the blood (urea, creatinine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Normal respiratory rate?

A

12-15 breaths/min

24
Q

Effect of renal failure on ECF volume? BP effect?

A

VOLUME EXPANSION => HYPERTENSION

25
Q

Why might you see high plasma levels of creatinine when there is base loss due to diarrhea?

A

Volume contracted due to dehydration so concentration goes up + GFR is decreased to conserve Na+/H2O

26
Q

When a patient complains of muscle weakness, what should you check?

A

K+ to see if low => hyperpolarization of muscle cells

27
Q

What is renal tubular acidosis? Types? Most common?

A

Issue with renal acid excretion and bicarbonate generation/reabsorption - different types:

  1. Proximal: Na+/H+ exchanger affected: reduced ability to reabsorb HCO3-
  2. ***Distal: H+-ATPase affected: reduced ability to excrete acid (and therefore generate NEW bicarbonate)
28
Q

Urine pH with proximal renal tubular acidosis?

A
  1. Initial phase: alkaline because HCO3- excreted

2. Steady-state phase: load in tubule is decreased so pH is acidic (no HCO3- excreted), but NOT as acid as it should be

29
Q

What can cause renal tubular acidosis?

A

Drugs for anxiety and depression

30
Q

How is [K+] affected by distal renal tubular acidosis? What can this lead to? Treatment?

A

Depleted because less H+ being secreted by H+-ATPase, so less K+ being reabsorbed (preferential loss of K+) to compensate for Na+ reabsorption

Major muscle weakness in which the intercostal muscles are not working as well and patient can no longer hyperventilate to compensate for the acidosis => COMA => intubate to decrease PCO2 to drop pH and THEN adjust HCO3- and K+ levels

31
Q

What does it mean to have high salicylate levels?

A

Aspirin intoxication

32
Q

If the body needs to choose between AB status or K+ balance, what does it pick?

A

AB status

33
Q

Urine in people who drink ethylene glycol?

A

Calcium oxalate crystals

34
Q

How to calculate ECF volume?

A

1/3rd of TBW (=42 L) = 14 L

35
Q

Once excess acid load is stopped, does ammoniagenesis stop?

A

Takes 1-2 days (less time than to ramp up)

36
Q

During metabolic acidosis, why don’t we just hyperventilate until the pH is completely back to normal?

A

Because the drive stops once we have entered the normal pH RANGE, not value

37
Q

What 2 ions are lost during diarrhea in the GIT? Which is a more important loss?

A
  1. ***HCO3-

2. K+

38
Q

Why does diarrhea cause K+ depletion?

A
  1. K+ lost in feces due to increased motility => decreased reabsorption
  2. Volume contraction => aldosterone stimulated => K+ secretion in kidneys stimulated
39
Q

Why can low CO2 levels (respiratory acidosis) cause light-headedness?

A

Because cerebral vessels constrict in response to low CO2

40
Q

What is Kussmaul breathing?

A

Deep breathing, usually to compensate metabolic acidosis

41
Q

Normal postprandial glucose (2h after meal)?

A

140 mg %

42
Q

Why would plasma [Na+] be low in diabetic ketoacidosis?

A

Very high blood glucose => increase in ECF volume to maintain normal osmolarity => low plasma [Na+]

43
Q

What are a good amount of diabetic ketoacidoses due to?

A

Infections

44
Q

How to treat diabetic ketoacidosis?

A
  1. Give insulin to reduce the blood glucose: this will stop the osmotic diuresis and will reduces the ketoacid production
  2. Exogenous K+: insulin “chases” K+ into cells (stimulates the Na+/K+ ATPase) making severe hypokalemia a possibility, so administering extra K+ is very important!
  3. Infuse saline to fix the volume loss
45
Q

How to calculate the increase in osmolarity that is due to excess glucose?

A
  1. Normal blood glucose contribution to osmolarity = 90 mg%/18 = 5mM
  2. High glucose mg%/18 = x mM

=> look at difference between the 2

46
Q

Is most of the H+ secreted by the tubule excreted as NH4+ or consumed in the reabsorption of filtered bicarbonate?

A

Consumed in the reabsorption of filtered bicarbonate!!

47
Q

Which nephron segment is the primary site of organic acid secretion?

A

PCT

48
Q

Would Cl- contribute to an increased anion gap?

A

NOPE

49
Q

When given the excretion rate of a titratable buffer, the A:B ratio in blood, and the urine pH, how can you calculate the H+ secreted as buffered by this buffer?

A
  1. Calculate A:B ratio in urine with the HH equation

2. Calculate how much was secreted for that ratio to be obtained compare the blood ratio

50
Q

How do you know when a compensation is full or partial?

A

If pH is outside the normal range it is partial

51
Q

What kind of electrolytes are lost in the vomit?

A

HCl mainly and K+ in vomit

52
Q

Describe the impact of vomiting on the AB balance.

A

Loss of gastric HCl, leads to:

  1. Loss of fixed H+ => metabolic alkalosis
  2. ECF volume contraction =>
    - Increase Ang II => increase Na+/H+ exchange => increase HCO3- reabsorption
    - Increase aldosterone => increase K+ secretion + increase H+ secretion and HCO3- generation
    => metabolic alkalosis + hypokalemia
53
Q

Urine pH in chronic vomiting?

A

You would think it would be alkaline due to the metabolic alkalosis, but because the HCO3- reabsorption is so high, it is actually acidic

54
Q

Why do patients with chronic vomiting have high BUN and creatinine?

A

Because of volume depletion

55
Q

Treatment for patients with chronic vomiting? Explain the rationale.

A

IV saline to expand ECF:

  1. Increase in urinary HCO3- due to decrease proximal tubular reabsorption
  2. Provide more Cl- to the collecting tubule to increase HCO3- secretion by the beta-intercalated cells
  3. Reduce H+ secretion by the alpha-intercalated cells (no longer stimulated by RAA system)
  4. Reduce generation of new HCO3- in the collecting tubule (same as #3)
56
Q

Does NH4+Cl- affect the anion gap?

A

NOPE because HCO3- is replaced by Cl- which is the anion

SMP - Renal (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions