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Therapeutics > Exam 3 lecture 9 > Flashcards

Exam 3 lecture 9 Flashcards

1
Q

Normal PH of body?

A

7.35-7.45

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2
Q

What is it called when PH <7.35? WHat about when it is greater than 7.45?

A

less than 7.35 is acidemia
more than 7.45 is alkalemia

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3
Q

Acid base imbalances can be either ______ or _____

A

Metabolic or respiratory

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4
Q

Metabolic acid base imbalances are more reflective of which organ

A

Kidney is metabolic

Lung is respiratory

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5
Q

What compounds are changed in metabolic imbalances? What about on the respiratory imbalances

A

metabolic imbalances- Hydrogen and HCO3 (bicarb)

respiratory imbalances- involve changes in CO2

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6
Q

How do compensations occur in our body? Which one is faster?

A

lungs compensate metabolic disorders (lung compensation is much faster)
Kidneys compensate respiratory disorders

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7
Q

What are normal blood gas values to remmeber? best source for these values

A

PaCO2- 40
HCO3- 24
PaO2- 95-100
SaO2- > or = 95%

arterial blood gases are our best sources for obtaining these values

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8
Q

What are adverse consequences of acidemia

A
  1. CV
    -decreased CO
    - impairememnt of cardiac contractility
    - increased pulmonary vascular resistance
    -Increased arrhythmias (due to hyperkalemia)
  2. Metabolic
  • insulin resistance
    -inhibition of anaerobic glycolysis\
  • hyperkalemia
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9
Q

How does acidemia affect the CNS? lungs?

A

Coma or altered mental status

hyperventilation

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10
Q

adverse consequences of alkalemia

A
  1. CV
    - decreased coronary blood flow
    - arteriolar constriction
    - decreased anginal threshold
    - arrhythmias
  2. Metabolic
    - decreased K+, Ca and Mg
    -Stimulation of anaerobic glycolysis (increase of ATP causes metabolic remodeling, could cause HF)
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11
Q

How does alkalemia affect ventilation

A

Hypoventilation (decreased respiration)

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12
Q

Where is acid coming from in our body?

A
  1. Diet (1 mEq/kg/day consumed)
  2. Wemake some by breaking down carbohydrates (glucose)
  3. non volatile acids formed constantly
    - Anaerobic metabolism- lactic acid, pyruvic acid
    - Triglyceride oxidation- acetoaceti acid
    - metabolism of cysteine/methionine- sulfuric/phosphoric acid
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13
Q

3 mechanisms that bpdy has to deal with acid

A
  1. buffering
  2. renal regulation
  3. ventilator regulation
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14
Q

What is the 1st line of defense for acidosis

A

Buffering system

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15
Q

Define buffer? What are the main buffers in body?

A

Buffer- ability of a solution containing a weak acid and its anion (base) to resist change in PH with addition of a strong acid or base

main buffers
- bicarb/carbonic acid
-phosphate
-protein

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16
Q

What is the first thing that happens when acid increases

A

Bicarb buffer (rapid onset with intermediate capacity)

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17
Q

Why is bicarb so good at being a buffer for body

A

HCO3 present in largest concentration extracellularly over any other buffer
- supply of CO2 is unlimited
- acidity can be controlled by HCO3 or pCO2

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18
Q

Our abilities to use bicarb as buffer depends on two things. What are they?

A

Ability of kidney and lungs to excrete and retain HCO3 and CO2 respectively

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19
Q

MOA of how bicarb acts as a buffer when acid is added

A

HCO3 becomes H2CO3 and later CO2 and H20 with carbonic anhydrase
Large quantites of CO2 can be exhaled rapidly
Body needs HCO3 added to the system in an amount equivakent to the H loas ingested every day

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20
Q

What is the seocnd buffer that acts after bicarb buffer?

A

Phosphate buffer

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21
Q

Onset and capacity of phospahte buffer compared to bicarb buffer

A

Intermediate onset and capacity (not fast at all)

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22
Q

What are our last buffers after bicarb and phosphate

A

Protein buffr

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23
Q

Onset and capacity of protein buffer?

A

rapid onset and limited capacity

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24
Q

Key protein buffers

A

albumin and hemoglobin
More effective intracellular buffers vs extracellular

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25
Q

After buffers what is another method of acid regulation

A

Renal regulation

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26
Q

Role of kidneys for acid base management

A

Reabsorb bicarb
Make new bicarb (through hydrogen excretion)

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27
Q

How does bicarb reabsorption occur

A
  1. filtered Bicarb in urine combines with hydrogen ion and makes H2CO3
  2. Carbonic anhydrase dissociates that into H20 and CO2
  3. Water and CO2 go into proximal tubule and get converted back into H2CO3.
  4. Bicarb and hydrogen form and Bicarb goes into blood stream (no net loss of hydrogen)
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28
Q

How does limiting H+ secretion into proximal tubule affect acid-base balance?

A

Results in urinary bicarb loss

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29
Q

What do carbonase anhydrase inhibitors do?

A

inhibits carbonic anhydrase, leads to decreased entry of CO2 and H20 for reabsorption. This leads to metabolic acidosis (if we want to correct alkilosis this is good)

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30
Q

Bicarb generation is also referred to as

A

Enhanced H+ excretion

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31
Q

where does H excretion occur (exam)

A

distal tubule

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32
Q

How long does bicarb generation (h+ excretion) take? Capacity?

A

24 hours (delayed onset), but has large capacity

33
Q

What are the two proccesses for making new bicarb (excreting H+)

A
  1. ammonium excretion
  2. titrateable acidity
34
Q

Describe steps in ammonium excretion (how new bicarb is made)

A
  1. secreted H+ in distal tubule combines with ammonia to make ammonium (too big) and is excerted
  2. Bicarb generated from breakdown of carbonic acid is able to cross into capillary. (new bicarb made)

also called ammoniagenesis

35
Q

describe steps in titratable acidity

A
  1. phosphoric acid combines with H+ in distal tubule and turns to dihydrogen phosphate (too big) and is excreted
  2. Hydrogen ion lost in process and bicarb created. New bicarb created in capillary
36
Q

capacity of titrateable acidity

A

Capacity is small and can not be increased (because it depends on phosphates and phosphates do not have great access)

37
Q

what percent of net acid excretion does distal tubule H+ secretion comprise of

A

50% of net acid excretion

38
Q

simple way to put distal tubule actions

A

CO2 combines with H20 in presence of Carbonic anhydrase form H2CO3 which breaksdown into H and HCO3

The H is transported back into urine

HCO3 crosses into capillary

39
Q

after buffering and renal regulation, what is the third way we control acid base in out body

A

Ventilatory regulation

40
Q

onset and capacity of ventilatory regulation

A

Rapid onset and large capacity

41
Q

what do chemoreceptors detect and do in ventilatory regulation

A

Detect an increase in PaCO2 and increase rate and depth of ventilation

42
Q

When its metabolic what compound should we always check?

A

Always bicarb (HCO3)

42
Q

In ventilatory regulation, what are peripheral chemoreceptors activated by? what about central chemoreceptors?

A

Peripheral chemoreceptors activated by arterial acidosis, hypercapnia (high Pco2 levels) and hypoxia
Central chemoreceptors activated by CSF acidosis

43
Q

What are the 4 different acid-base imbalances and what are their compensation characteristics

A

Metabolic acidosis
caused by- decrease in HCO3
Compensated with- decrease in PaCO2

Metabolic alkilosis
caused by- increase in HCO3
Compensated by increase in PaCO2

Respiratory acidosis
-caused by- increase in PaCO2
compensated with increase in HCO3

Respiratory alkilosis
- caused by decrease in PaCO2
compensated with decrease in HCO3

44
Q

PH and HCO3 of of metabolic acidosis? compensatory action?

A

low pH (<7.35), low serum HCO3 (<24) and a compensatory decrease in PaCO2

45
Q

What should we always calculate for all metabolic acidosis

A

Anion gap

46
Q

Anion gap formula? What is a normal anion gap? What does the values mean if they are high or low or normal

A

Na- (cl+HCO3)

Normal anion gap- 3-11

if normal or low, it is considered non anion gap metabolic acidosis
If anion gap is high, it is anion gap metabolic acidosis

47
Q

non anion gap acidosis is also known as? why?

A

Hyperchloremic acidosis

overall there is a loss of plasma HCO3 and replaced by Cl-

48
Q

common causes of non anion gap acidosis

A
  1. GI bicarb losses
  2. renal bicarb wasting
  3. exogenous acid given to patient
49
Q

What are some GI bicarb losses

A
  1. diarrhea
  2. pancreatic fistulas/billiary drainage (these fluids are rich in HCO3)
50
Q

What are some renal bicarb losses

A
  1. Type II renal tubular acidosis (RTA)
    problem with proximal tubule (reabsorption site for bicarb)
51
Q

What are causes of RTA (issues with proximal tubule) that cause renal bicarb losses

A

heavy metal toxicity
carbonic anhydrase inhibitors
topiramate
Faconis syndrome

reabsorption of bicarb is reduced. HCO3 will be lost

52
Q

What is urine PH is patients that have RTA? why?

A

PH often <5.3

When HCO3 is lost in RTA, this also results in Na and fluid loss, which will then activate the renin angiotensin system

Aldosterone increases Na/H20 reabsorption and augments K+ excretion

53
Q

Other than type II RTA, what causes impaired renal acid excretion?

A

reduced renal H+ excretion

54
Q

What are some causes for impaired renal H+ excretion? Which one is most common

A

Distal tubule RTA (most common)
Type 1 RTA (hypokalemia RTA)
Type IV RTA
chronic renal failure

55
Q

what causes type I RTA

A

distal tubule might have defect

Lupus , myeloma, sickle cell can cause damage to distal tubule

H+ can not be pumped into urine , urine can not be maximally acidified. Since H+ can not be secreted in response to Na+ reabsorption, there is an increase in K+ excretion

56
Q

causes of type IV RTA

A

Low aldosterone (hypo aldosterone state)
Aldosterone stimulates H+ excretion

57
Q

How does chronic renal failure lead to impaired renal acid excretion

A

H secretion is decreases. also less ammonia production (decreases ability to make new CO3 )

58
Q

When does exogenous acid gain occur

A

Administering TPN (just fix TPN)
HCl given for treatment of a condition may cause acidosis
ammonium chloride given for treatment may cause acidosis

59
Q

What are potential causes of anion gap acidosis

A

Calculate anion gap, if high these things could be the cause
(MUDPILES mnemonic)

Methanol intoxication
Uremia
Diabetic ketoacidosis
Poisoning/propylene glycol
intoxication/infection
lactic acidosis
ethylene glycol
salicylates/sepsis

60
Q

difference between anion gap acidosis and non anion gap acidosis

A

Overall HCO3, losses are replaced with another anion besides Cl-

61
Q

when we suspect anion gap metabolic acidosis what do we do

A

we calculate delta gap

62
Q

what is the use of delta gap

A

Used in assessment of anion gap metabolic acidosis to determine if a mixed disorder is present. (only used in anion gap metabolic acidosis)

63
Q

How to calculate delta gap?

A

Difference between patients anion gap and normal value (use 10)

We take the value we get from the above and add it onto the HCO3 (bicarb). It should be normal.

64
Q

What does it mean if we take the delta gap and add it to patients HCO3 and results are elevated?

A

It means there is a mixed disorder (metabolic alkilosis on top of metabolic acidosis)

65
Q

most common cause of anion gap acidosis

A

lactic acidosis

66
Q

What is the normal level of lactic acid in circulation? What is levels are diagnostic for lactic acidosis? What levels have higher than 75% mortality?

A

1 meq/l= normal

> 5 is diagnostic

75% with levels 5-9

67
Q

Are increased levels of lactic acidosis caused by decreased clearence or over production? What is the principal route of conversion of lactic acid? What is it disposed by?

A
  • increased levels are mainly due to decreased clearence

Principal route of elimination is reconversion to pyruvate

Disposal via liver (50%), kidney, muscle and CNS

68
Q

causes of lactic acidosis

A
  1. shock
  2. drugs/toxins (ethanol- decreased blood sugar, ketosis and lactic acidosis)
    metformin
    NRTIs
    linezolid, propofol, isoniazid
    Propylene glycol
  3. seizures (resolves within 2 hrs)
  4. leukemia
  5. hepatic/renal failure
  6. diabetes
  7. malnutrition
  8. rhabdomylosis
69
Q

What are other things besides lactic accidosis that can cause anion gap metabolic acidosis (EXAM)

A

Ketoacidosis
Drug intoxication (salicylate toxicity) (EXAM)

70
Q

how does salicylate toxicity lead to anion gap metabolic acidosis (EXAM)

A

respiratory alkilosis from stimulation of respiratory drive
also metabolic acidosis from accumulatio of acid (Has BOTH Acidosis and alkilosis) PH WILL LOOK NORMAL

71
Q

Drug intoxications other than salicylates that cause acidosis

A

Methanol
Ethylene glycol

72
Q

symptoms of acidosis

A
  • Kussmaul respiration (deep and fast) (compensation to get rid of all that CO2)
  • peripheral vasodilation (tachycardia/ arrhythmia)
  • hyperkalemia
  • bone demineralization
73
Q

When do we consider acute bicarb therapy (giving patient bicarb) in hospital

A

-Hyperkalemia
-PH<7.1 (common in cardiac arrest)
- to reverse overdose

74
Q

How do we dose bicarb? (EXAM) WHat to monitor?

A

(0.5 x IBW) x (12 - bicarb number of patient)

then give 1/3 or 1/2 of what we calculated, monitor ABG (blood gas) and K+ supplement if needed

75
Q

how much bicarb to give during cardiac arrest?

A

1 mEq/kg

76
Q

What are the hazards of bicarb therapy?

A

Overalkylazation can reduce cerebral flow and impair oxygen release from Hgb to tissues

hypernatremia/hyperosmolarity

CSF acidosis (YES ACIDOSIS)

hypokalemia

hypocalcemia

electrolyte shift

77
Q
A

Therapeutics (36 decks)

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