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Kidneys > L5-L6- Acid Base Disorders > Flashcards

L5-L6- Acid Base Disorders Flashcards

1
Q

Normal Value and Range for Bicarbonate?

A

[HCO3] = 26 +/- 4 mmol/liter

22-30

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2
Q

ARterial blood gas listing and normal values?

A

pH/PaCO2/PaO2

pH normal = 7.36-7.44

PaCO2= 36-44

PaO2 = 60-90

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3
Q

What/s the HH equation for pH homeostasis?

A

pH = 6.10 + Log ( [HCO3] / 0.03 PaCO2)

pH = [HCO3] / PaCO2

pH = Kidney/Lung

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4
Q

Acidemia vs ACidosis?

Alkalosis vs alkalemia?

A

Acidosis - decrease pH

Acidemia - measured pH is <7.36

Alkalosis - increase pH

Alkalemia - measured pH >7.44

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5
Q

What are the three adaptive responses to changes in pH?

A

**1) Buffer –> hide it! **

  • HCO3 binds free H+ and gets consumed so have to make more of it

2) Compensation

  • generate secondary disorder to minimize changes in pH
  • NEVER brings pH back to normal
  • should go away when primary goes away (*except Maintained Metab Alkalosis)
  • HCO3 and PaCO2 always change in parallel

3) Elimination in Kidney - takes a while

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6
Q

How does the kidney eliminate H+? In what three areas? when does the urine become acidic? How low can it go?

A

1) Proximal Convoluted tubule: Urine pH = Serum pH; all bicarb filtered and then H+ secreted and binds it. Brush Border CA eliminates and makes CO2 and H20. Then Reclaim and remake HCO3 bc H+ secretion linked to bicarb creation.

2) Distal Convoluted Tubule: Titratable Acids (Phosphates and Sulfates) increase H+ secretion and make urine slightly more acidic now

3) Collecting Duct: Ammonia Production!!! Excess H+ Secreted here (majority of it!) by CD - I.C. cells and urine becomes very acidic

Lowest pH of urine is 4.4

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7
Q

How can you tell if it is a primary metabolic change or a primary respiratory change?

A

Primary Metabolic - Changes in pH and Bicarb happen in parallel

Primary Respiratory - changes in pH and Bicarb happen in opposite directions

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8
Q

How can you tell Simple AB disorders?

A

Simple - single AB disorders and compensation continues only as long as primary does, compensation does NOT return pH to normal, and Compensation MUST be within predicted range!!

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9
Q

How do you know if it’s a mixed disorder?

A

Mixed - 2 or more primary AB disorders

_Violates the rules of simple: _

  • can bring pH back to normal
  • Bicarb abd PaCo2 do NOT move in parallel
  • compensation persists
  • compensaiton NOT in predicted range
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10
Q

How does the GI tract contribute to AB disorders? What does vomiting cause? What does Diarrhea cause?

A

Normally, Gastric Cells secrete HCl into lumen and Bicarb into blood and Colon Cells secrete Bicarb into lumen and HCl in to blood

Vomiting therefore leads to Alkalosis

Diarrhea therefore leads to Acidosis

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11
Q

What is Metabolic Acidosis? What is the compensation? What are the effects?

How can you tell if renal cause or not?

A

MA = Decrease in [HCO3} and Decrease pH

Compensation = Decrease PaCO2

_Effects: _

  • Oxygen Dissoc crve shifts right and more distributed to tissues
  • CNS depression
  • Hyperkalemia, Less Cardiac Contractility, Arrhythnmia
  • Decreased pulmonary Blood flow
  • Renal increase NH3 production and HCO3 production

_URINE PH _

  • Acid = non-renal cause
  • Alkaline = Renal Cause = Paradoxical Alk Urine = RTA
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12
Q

How do you calculate Anion Gap? What is the normal range for anion gap?

A

AG = Na - {HCO3 + Cl]

Normal range is 9-13

>13 = High Anion Gap

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13
Q

In General, what are the causes of Metabolic ACidosis? (not specific ones yet)

A

H+ Gain from either increased production or decreased secretion

  • CKD disease and less nephrons
  • RTA and H+ impaired

HCO3 Losses from either Diarrhea or RTA!!!

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14
Q

What are the causes of Non-AG Metabolic Acidosis aka Hyperchloremic MA? causes?

A

HEART CCU

Hyperalimentation - SO4/PO4

Expansion of volume - Saline given

Acetazolamide - Renal cause

RTA - Renal Cause

Diarrhea - GI

Cholestyramine - GI

Carbonic Anhydrase Inhibitor - Renal

Uterosigmoidoscopy - Renal/GI

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15
Q

What are the causes of high anion gap Metabolic acidosis? Biomarkers?

A

MUDPILES

Methanol - formaldehyde

Uremia - creatinine

Diabetes - ketones

Propylene glycol (given w/drugs for Status Epilepticus)- Increased Osmotic Gap

Lactate

INH/INfection - Medication levels

Ethylene Glycol - Oxalate/Increased Osmotic Gap

Salicylates

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16
Q

What is Renal Tubular Acidosis? What are the 3 types and what is unique about each type?

A

RTA is a problem where nephrons can’t secrete H+

_Type 1 = Distal Nephron _

  • Urine pH not max acidic (>5.3) - can’t acidify urine
  • Low serum K
  • Complication is Nephrocalcinosis - bc can’t reabsorb calcium

Type 2 = Proximal Nephron

  • Urine acidic bc distal tubule makes up
  • Low Serum K
  • Rickets!!

Type 4 = Aldosterone Deficiency/Resistance

  • Urine pH acidic
  • HYPERKALEMIA!!!
17
Q

What is primary Metaboli alkalosis? What is compensation? What are the effects?

GENERALLY what are the causes?

A

Increased HCO3!!!! W/ Increased pH

Compensation = Increase PaCO2 but never above 60

_Effects: _

  • decrase Oxy to tissue - shift curve left
  • decrease cerebral blood flow
  • arrhythmia
  • tetany- Ca
  • SEizures

_Causes: _

**Lower H+ **

  • GI = VOMITING, NG suction, bicarb ingesiton
  • Hypokalemia and transient shift
  • Renal - diuretics

Increased Bicarb - ingest bicarb or Citrate w/ blood transfusions

18
Q

When is MEtabolic Alkalosis Transient and When is it maintained? What are the stimuli to maintain it and where is that done?

A

Transient = No increased bicarb reclamation or H secretion by PCT and so once HCO3 load stops then problem goes away

vs

Maintained = PCT stimulated to increase reclammation and secrete more H+

Stimulus:

- Chloride or Volume Depletion

**- Severe Hypokalemia **

Therefore, extra bicarbonate is retained by the kidney

19
Q

Explain the 3 ways that Metabolic Alkalosis can get maintained.

A

Metabolic Alkalosis maintained when the Kidney secretes more H+ and reclaims more bicarb in these 3 situations:

1) Volume Depletion: increased Na reabsorption in PCT in exchange for H+

2) CL Depletion: Intercalated cells switch from Alpha to Beta when no Cl in urine to exchange for bicarb

3) Hypokalemia (severe): When [K] really low, allowed to leave cells in exhcange for H+ and so get Intracellular Acidosis in Renal Tubular CElls - secrete more

20
Q

How can you get chloride depleted and bicarb loaded together?

A

VOMITING!!! Lose HCL from stomach and increase HCO3 into blood

Vomiting can stop and Metabolic Alkalosis can persist until someone replenishes chloride

21
Q

Causes of Transient MEtabolic Alkalosis?

A

Bicarb Loading

  • Exogenous - Tumor Lysis Syndrome in CLL or CML
  • Endogenous - Bone Dissolution from immobility

Recovery or AO Metabolic Acidosis (Ketoacidosis or Lactic ACid)

Post-Hypercapnic Respiratory Acidosis

22
Q

Cuases of Maintained Metabolic Alkalosis?

A

Chloride and/or Volume depletion

  • VOMITING!!!, NG suction, Diuretics, Post-hypercapnic alkalosis

Potassium <2

  • Mineralcorticoid excess, diuretics, renal failure - decreased GFR

BOTH: K depletion and Cl depletion

- Liddle’s Syndrome - Overactivity of ENAC channels in CD

  • Bartter’s Syndrome - no NKCC cotransporter in TAL
  • Gitelman’s Syndrome - no NaCl Cotransporter in DCT
23
Q

How to use urinalysis to determine how maintained metabolic alkalosis was generated?

A

Urine Cl < 20 - low Cl and Saline responsive from vomiting or NG suction, diuretics, etc

**TX: Give Saline **

Urine Cl > 20 - low Cl and Saline Resistant = Hypokalemias!! from mineralcorticoid excess, diuretics, or renal failure

Then Check Urine Potassium

Low Uk <20 suggests GI loss of K

High Uk >20 suggets Renal +/- hyperaldosteronism loss of K

Treatment w/ Cl and K!

24
Q

Is urine acidic or basic in Metabolic Alkalosis?

A

Urine is ACIDIC!!!!

Net H+ Secretion increases appropriately to balance intake in the face of metabolic alkalosis!

25
Q

what is different about Primary Respiratory AB disorders compared to MEtabolic?

A

Respiratory disorders have 2 HCO3 compensation Confidence Bands to check bc there is both acute and chronic compensation done by the kidneys

26
Q

What are the causes of primary Respiratory acidosis?

A

CNS depressants - like Narcotics

Respiratory Muscle Dysfunctions

Airway Obstruction

Poor gas exchange

27
Q

What can cause both Metabolic Acidosis AND Respiratory Alkalosis?

A

Salicylates!!!

28
Q

What is Respriatory Acidosis? compensation?

A

High PaCO2 leading to low pH

Compensation - renal Incresaes H+ excretion to increase HCO3 reclammations

29
Q

What is one consequence that can occur in Respiratory Acidosis?

A

Can get maintained Metabolic Alkalosis from compensation!!!!

(As cells try to sequester H+ they can leak K)

30
Q

What is Respiratory Alkalosis? Compensation?

A

Decreased PaCO2 and increased pH

Renal Compensation - decrease Bicarb reclammation and decrease renal secretion

31
Q

What are the causes of Primary Resp Alkalosis?

A

Hypoxemia

Lung disease

Sepsis

**SALICYLATES!!!*** (also cause metabolic ACidosis)

CNS stimulants

32
Q

IF there is normal pH, how can you tell if there is a mixed disorder?

A

if BOTH PaCO2 and HCO3 are low or high

And/OR

There is a High anion gap!

33
Q

What if there his an anion gap and the pH is high?

A

THen there is STILL an High Anion Gap Metabolic Acidosis occuring NO MATTER WHAT!!!

More than 1 primary process occurring

Kidneys (13 decks)

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