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Block 2 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

What is acidosis and alkalosis?

What is acidemia and alkalemia?

A

Pathological process/condition that causes pH to change

Blood pH altered

Acidemia pH < 7.35
Alkalemia pH >7.45

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2
Q

Cause for respiraotry acidosis or alkalosis?

Cause for metabolic acidosis or alkalosis?

A

Pathological change in PaCO2:

Often due to the lung function, but can be also due to CO2 poisoning.

Pathological change in [HCO3-]

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3
Q

What types of acid/bases are buffered by:

Non-votile buffers (e.g. Hb)?

Bicarbonate system (volatile)?

A

CO2

Metabolic acid products / Gastrointestinal acid products

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4
Q

Clinical causes for respiratory acidosis?

Non-pulmonary?

Pulmonary?

A

Non-Pulmonary:

Disruption in neural linkage driving breathing

Central nervous system depression (drug overdose, anesthesia)

External environment preventing nromal breathing (heavy weight)

Pulmonary:

Upper airway obstruction

Severe asthma attack

COPD (bronchitis especially)

Severe pneumonia

Severe pulmonary edema

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5
Q

Clinical causes for respiratory alkalosis?

Non-pulmonary?

Pulmonary?

A

Arterial hypoxemia or hypoxia

Direct stimulation of pulmonary mechano- and chemo-receptors by lung disease

Psychological factors

Chemical or physical factors that directly stimulate the medullary respiratory center

Pulmonary: Bacterial pneumonia, Pulmonary embolus, Acute asthma (all first three)

Non-pulmonary: sepsis, liver disease, pregnancy, psychogenic hyperventilation

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6
Q

When oxygen begins to drive breathing?

A

When PaO2 is less than 60 mmHg

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7
Q

Causes for metabolic acidosis

A

Gastrointestinal acid production (GAP)

Diarrhea or laxative abuse (loss og HCO3- and H+ absorption)

Metabolic acid production (MAP)

Imbalance between organic acid production and consumption (incomplete metabolism of carbons that forms acid because of lack of oxygen during hypoxia)

e.g. lactic acidosis (exercise), ketoacidosis (type I diabetes)

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8
Q

Causes for metabolic alkalosis

What does it require?

What will happen eventually to HCO3-?

A

Vomiting or nasogastric drainage (loss of H+)

Generation and maintenance mechanism (volume depletion, hypokalemia, aldosterone excess)

Spill of HCO3- urine

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9
Q

Values for acute respiratory acidosis and alkalosis

A

Acute respiratory acidosis

pH down by 0.07

HCO3- up slightly (~1 mM)

Acute respiratory alkalosis

pH up by 0.08

HCO3- down slightly (~2 mM)

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10
Q

Values for metabolic acidosis and alkalosis

A

Acidosis

PaCO2 = 1.5 x [HCO3-] + 8 ± 2 (Winter’s Formula)

Alkalosis

PaCO2 = 0.7 [HCO3-] + 20 (+/- 5)

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11
Q

Which electrolytes are measured?

A

Sodium Na+ (140 mM)
Potassium K+(4 mM)
Chloride Cl- (100 mM)
“Bicarbonate HCO3- “ (24-30 mM)(really total CO2)

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12
Q

Anion gap equation

A

Anion gap = [Na+]-([Cl-] + [CO2])

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13
Q

[HCO3-] vs. total CO2

A

[HCO3-] is in arteries (calculated from pH and PaCO2)

rules of thumb for acid base disturbances

venous total CO2 equals CO2 dissolved + [HCO3-]

Anion gap calculation

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14
Q

Normal ion gap

A

12mM +-4

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15
Q

Types of ion gaps

A

Normal

Anion gap metabolic acidosis or normochloremic

Non-anion gap metabolic acidosis or hyperchloremic

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16
Q

Three disorders account for most cases of anion gap metabolic acidosis

A
17
Q

Lactic acidosis (gap acidosis)

Result of?

Common causes?

A

Anareobic metabolism (increases with hypoxia)

Circulatory failure (cardiogenic shock) ; Sepsis (septic shock)

18
Q

Ketoacidosis (gap acidosis)

Causes?

A

Diabetic (type 1)

Starvation

Alcoholic (drinking/vomiting)

19
Q
A
20
Q

How kideny can respond to acidemia?

How kideny can respond to alkalemia?

A

Acidemia

Conserve filtered bicarbonate

Make “new” bicarbonate

Excrete fixed acid

Alkalemia

Excrete bicarbonate (alkalosis)

21
Q

Whereis bicarbonate absorbed?

How much bicarbonate is excreted? “The biggest job the kideny perform”

How much bicarbonate is excteted during alkalosis?

A

80% in PCT

15% Thick asending limb

5% Collecting duct

0% excreted

1-2%

22
Q

How proximal tubules are reabsorbing HCO3-?

A
23
Q

What is important function of a-intercalated cells?

How low pH can go in distal collecting duct?

How is that accomplished?

A

To secrete acid

4.4

Instead of Na+/H+ exchanger, direct K+/H+ pump and H+ is used in these cells

24
Q

How high elevation affects pH due to respiration?

What is Diamox?

A

Respiratory alkalosis

Carbonic anhydrase inhibitor (allows more bicarbonate excretion)

25
Q

What are the methods by which the kideny eleminate fixed acid?

A

Formation of titratable acid

Formation of ammonium

26
Q

How fixed (metabolic) acid can be removed from the body through ammonium ion (NH4+)?

How is that processs different in PCT vs. collecting duct?

Where is amonia made?

A

Glutamine is split into NH4+ HCO3

NH4+ is exported to lumen by NH4+/Na+ exchanger

H+ ATP pump will drive H+ and NH3 will follow

In PCT

27
Q

Pathway for ammonia in kidneys

How aldosterone affects NH3 secretion?

A

Aldosterone stimulates H+ secretion

28
Q

Net acid excretion

A

New Acid Excretion = TA + NH4+ + HCO3 in urine

29
Q

What is more of reabsorbed or new bicarbonate?

A

Reabsorbed 4147 mM/day > 59 mM/day

30
Q

What is required for bicarbonate reabsorption?

A

Hydrogen ion secretion

31
Q

How different diuretics affect H+ secretion?

A
32
Q

Respecitve movement of H+/K+ in most of cells

A
33
Q

Difference between addition of inorganic acid vs. organic acid (diabetic ketoacidosis)

A

Inorganic acid

Anion cannot leak in cell inhibit H+/Na+ pump (buildup of H+ in only ECF)

Less sodium lowers the activity of Na/K+ pump

Metabolic acidosis -> Hyperkalemia

Ketoacidosis (organic acid)

Anion leaks in cell and does not inhibit H+/Na+ pump (buildup of H+ in both compartments)

No change to Na+/K+ pump due to that fact

BUT Na+/K+ pump not active because lack of insulin

K+ is lost with urine

BE CAREFUL WITH ADDITION OF ALDOSTERONE -> hypokalemia

34
Q

Metabolic Acidosis due to kidney problems

A

Renal failure (chronic)

Renal tubular acidosis (RTA)

35
Q

Two types of renal tubular acidosis

Effect on urine HCO3-, pH, K+ , Cl-

Side effects?

Treatment?

A

Distal (type I) RTA

Impaired H+atpase, H+/K+ atpase, or basolateral HCO3-/Cl- exchange

pH > 5.5

Proximal (type II) RTA e.g. Fanconi Syndrome

Impaired , H+/K+ atpase, or basolateral HCO3-/Cl- exchange

Uringe HCO3- (+) ; pH (+) ; K (+) ; Cl (-)

Bone demineralisation, urinary stoone, nephrocalcinosis

Base + Potassium

36
Q

Single episode of vomiting vs. prolonged vomitting

A

Single event (+) K+ ; (+) HCO3- ; (+) pH

Multiple events (+) TA ; (+) NH4 ; (-) pH and hypokalemia

Aldosterone not only stimulates sodium absorption but also activates H+ pump in intestitial cells

37
Q

WHat is the effect of hyperaldosteronemia

A

(+) H+ secretion

(+) K+ secretion

(+) Increased Na+ reabsorption

Block 2 (7 decks)

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