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Physiology Exam 1(Lauren) > Classification Of A/B Status And Clinical Disroders > Flashcards

Classification Of A/B Status And Clinical Disroders Flashcards

1
Q

What will the anion gap be like in Type IV RTA?

A

NORMAL

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2
Q

Are buffers fast or slow?

A

Fast

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3
Q

What effect will aldosterone have on K+?

A

It will cause HYPOkalemia

Due to it increaseing K+ secretion from principal cells

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4
Q

Well shit your patient has been vomiting and using diuretics and now they are in metabolic alkalosis AND their kidneys are maintaining it due to the ECF volume contraction! How do you treat it?

A

Administer SALINE

Restores their plasma volume and suppresses RAS.
Will result in excretion of bicarb

This will correct the saline-responsive forms of metabolic alkalosis (like this one.)

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5
Q

Will the anion gap increase if you lose HCO3-?

Anion gap= Na- Cl - HCO3-

A

No, because Cl- will increase to meet the drop in HCO3- and this will maintain the anion balance

(Ex: acidosis caused by diarrhea or Renatl tubular acidoses)

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6
Q

True or false:

Angiotensin II will stimulate Na-H antiporter and HCO3- reabsorption

A

True

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7
Q

Will Type I renal tubular acidosis have a normal anion gap?

A

YES

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8
Q

What is pretty much the only cause of respiratory alkalosis?

A

Hyperventilating

High altitude, stress, hypoxemia, etc

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9
Q

What is the difference between mild and severe Type II RTA?

A

Mild= mild acidosis

Severe= hypokalemia too

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10
Q

Which types of renal tubular acidosis are associated with hyperkalemia?

A

Type IV

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11
Q

What causes respiratory acidosis?

A

Not breathing enough

Drug overdose that impairs respiratory center, chest wall dysfunction, impaired gas exchange, etc

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12
Q

What is Conn syndrome?

A

Hyperaldosteronism

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13
Q

What are the 3 types of renal tubular acidosis

A
  1. Type I (distal)
  2. Type II (proximal)
  3. Type IV

Yeah there’s no type III idk 🙄

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14
Q

What is a normal anion gap?

A

8-16 mM

***must know

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15
Q

Why won’t saline help fix your metabolic alkalosis if it’s due to an Aldosterone-secreting tumor?

A

Because the patient is already volume EXPANDED!

It’s not going to turn off the renin-angiotensin-aldosterone system like it did for the patient who was vomiting and using diuretics.

This patient’s RAS system is not on due to a volume contraction, they’re secreting aldosterone because of a tumor

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16
Q

What kinds of metabolic acidoses will increase the anion gap?

A

Any kind that is caused by fixed acids:

lactic acidosis

Ketoacidosis

Renal failure: accumulation of phosphoric and sulphuric acids

Salicylate poisoning (aspirin)

Ethylene glycol poisoning- converted to glycolic and oxalic acids

Methanol poisoning- converted to Formic acid

(Remember that HCO3- will combine with these to neutralize them, thus decreasing HCO3 levels with no increase in Cl- levels. Hence you get an increased anion gap)

17
Q

In all types of Renal tubular acidoses, the anion gap is ___________

A

Normal

18
Q

What is going on with the Type II (proximal) renal tubular acidosis?

A

The Na-H+ exchanger in the proximal convoluted tubule is defective

Leads to an impairment of H+ secretion
AND bicarbonate recovery, since there is less H+ in the lumen

19
Q

How do you calculate anion gap?

A

Anion gap= Na - Cl - HCO3-

Basically, Cations - Anions

20
Q

Will Type I renal tubular acidosis include a hypokalemia?

A

YES

******

21
Q

Disorders that increase the anion gap generate ___________ which reduce HCO3- concentrations

A

Non-volatile (fixed) acids

Ex: lactic acid, oxalic acid

Anions associated with these acids (lactate, oxalate) take the place of HCO3- so Cl- levels will NOT change. The anion gap increases!

Anion gap= Na- Cl- HCO3

22
Q

WHYYY is there an associated HYPOkalemia with a severe Type II RTA?

A

Your Na-H exchange pump in the PCT is not working, so you’re losing a lot of Na+ in the urine

This leads to a lot of fluid loss

= activation of RAAS

=increased K+ secretion- BOOM hypokalemia

23
Q

Is respiratory compensation fast or slow?

A

Very fast, but usually incomplete

Always active when the primary problem is metabolic

24
Q

High aldosterone levels cause H+ (loss/gain)

A

Loss

25
Q

When the kidneys maintain a metabolic alkalosis, what is the critical factor?

A

Markedly elevated aldosterone

Stimulates Na-H Antiporter and HCO3- reabsorption

26
Q

What kinds of things can cause metabolic acidosis?

A

Ingestion of Acids or acid forming compounds

Losing HCO3- (diarrhea)

Non-volatile acid accumulation (lactic acid, other endogenous produced acids, etc)

Renal HCO3- recovery is reduced

Excretion of titratable acid and NH4+ is reduced

27
Q

What is going on with Type I (distal) renal tubular acidosis?

A

H+ ATPase activity is reduced in the distal nephron

Or there’s a generalized failure of Type A intercalated cells

28
Q

What is the major cation we use to calculate the anion gap?

A

Na+

29
Q

With Type II (Proximal) renal tubular acidosis, is the anion gap normal?

A

Yes

30
Q

What is going on with Type IV Renal tubular acidosis?

A

It starts with an aldosterone deficiency that causes HYPERkalemia.

The extra K+ will be absorbed by cells, and in exchange they will release H+ into the ECF, causing an acidosis.

The H+ATPase in the Collecting duct will also be inhibited, so you’re retaining more H+.

All the extra K+ inside the cells will inhibit renal glutaminase, which impairs the formation of NH4+ as well as Bicarb.

This all helps to cause a metabolic acidosis.

31
Q

How do you treat saline-resistant metabolic alkalosis (like the one caused by Conn’s syndrome aka aldosterone-secreting tumor)?

A

Two options:
Remove the tumor

Give an aldosterone antagonist (Spironolactone)

32
Q

How is it possible that a metabolic alkalosis caused by vomiting or diuretics can be made even worse by the kidneys?

A

Because the loss of fluid (ECF contraction) will stimulate the Renin-angiotensin II-Aldosterone system

Angiotensin II will stimulate the Na-H+ antiporter and HCO3- reabsorption (losing even more H+)

Aldosterone will stimulate the secretion of H+ using the H+ATPase from type A intercalated cells and K+ from principal cells

33
Q

What is a renal tubular acidosis?

A

A metabolic acidosis caused by diminished H+ secretion in the kidneys

(3 types)

34
Q

Will the anion gap increase if you have a metabolic acidosis caused by an excess of non-volatile (fixed) acids?

A

Yes!

Fixed acids will liberate H+ which is buffered by HCO3- without changing Cl- levels!

Bicarb decreases because it’s COMBINING with H+ to neutralize it!! You’re not “losing” bicarb in body secretions or anything like that.
Cl- will NOT change

Anion Gap= Na - Cl - HCO3

35
Q

What are the major anions used to calculate anion gap?

A

Cl-

HCO3-

36
Q

Does the anion gap calculation take into account EVERY anion in the body?

A

No, several anions are omitted from routine blood chemistry analyses (sulfate, phosphate, etc)

37
Q

Is renal compensation fast or slow?

A

Slow, but powerful

Compensates for respiratory problems and metabolic problems if they don’t involve the kidney

38
Q

What kind of metabolic alkalosis will not respond to giving saline?

A

Metabolic alkalosis that is caused by an aldosterone secreting tumor (like Conn’s syndrome)

39
Q

What types of renal tubular acidosis are associated with a hypokalemia?

A

Type I

Severe Type II

Physiology Exam 1(Lauren) (12 decks)

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