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acid base disorder specifics Flashcards

1
Q

What is aldosterone?

A

a steroid hormone

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2
Q

where is aldosterone produced?

A

produced exclusively in the zona glomerulosa of the adrenal cortex.

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3
Q

What is the major circulating mineralocorticoid in humans?

A

Aldosterone

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4
Q

Basic (more common) causes of metabolic alkalosis?

A

Vomiting, NG suctioning

Diuretic administration
Hyperaldosteronism

NaHCO3 administration

Lactate, acetate, citrate administration (massive blood transfusion)

Alkali administration to patients with renal failure

Abrupt correction of chronic hypercapnia

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5
Q

What PH and HCO3 would tell you someone has Met. Alk?

A

PH greater than 7.45

HCO3 greater than 26

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6
Q

Compensatory mechanism for Met.Alk?

A

hypoventilation

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7
Q

Would someone with Met. Alk have high or low blood potassium?

A

low blood potassium (from the hydrogen coming out of the cell trying to make things more acidic, thus potassium goes into the cell making the serum level of potassium low)

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8
Q

physiologic effects of Met. Alk?

A

tachycardia, potentiate of digoxin toxcicity.
decreased ionized calcium.
compensatory hypoventilation.
leftward shift in the oxyhemoglobin curve (alkalosis)
decreased CO

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9
Q

Treatment of Met. Alk?

A

fix the underlying issue and surrounding complications. Bc of loss of volume due to diuretics or GI losses you want to give fluid, typically NS, this also helps renal perfusion.
Give potassium to reverse hypokalemia.
decrease min. vent if on the vent.
You can give ammonium chloride or any med that acts as H+ to increase acidity.
Give acetazolamide (diamox) to inhibit carbonic anhydrase so no more bicarb can be made and it enhances excretion of bicarbonate.

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10
Q

Less common causes of metabolic alk?

A

increased mineralocorticoid activity

Primary hyperaldosteronism

Cushing’s syndrome

Licorice ingestion

Bartter’s syndrome
Bartter’s: Elevated renin, angiotensin II, and aldosterone

Milk-alkali syndrome
glucose feeding after starvation
sodium penicillins
Bone metastases

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11
Q

principal site of action of aldosterone is

A

distal nephron

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12
Q

principal regulators of aldosterone synthesis and secretion are the

A

renin-angiotensin system and the potassium ion concentration.

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13
Q

Hyperaldosteronism is characterized by?

A

excessive secretion of aldosterone, which causes increases in sodium reabsorption and loss of potassium and hydrogen ions.

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14
Q

What is responsible for Cushings syndrome, excessive level of what hormone?

A

Cortisol

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15
Q

Where is cortisol produced?

A

adrenal glands

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16
Q

What does cortisol do in the body?

A

regulate your blood pressure and keeps your cardiovascular system functioning normally.
Cortisol also helps your body respond to stress and regulates the way you convert (metabolize) proteins, carbohydrates and fats in your diet into usable energy.

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17
Q

When levels of cortisol are too high in your body you may develop?

A

Cushing syndrome

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18
Q

If your body overproduces cortisol it is known as?

A

endogenous Cushing syndrome.

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19
Q

what can cause endogenous Cushing syndrome?

A

excess production by one or both adrenal glands (known as adrenal adenoma)
or overproduction of the adrenocorticotropic hormone (ACTH), which normally regulates cortisol production.

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20
Q

pituitary gland tumor (pituitary adenoma) is associated with what disorder? (Most common endogenous reason for this disorder)

A

Cushing DISEASE

A noncancerous (benign) tumor of the pituitary gland, located at the base of the brain, secretes an excess amount of ACTH, which in turn stimulates the adrenal glands to make more cortisol. When this form of the syndrome develops, it’s called Cushing disease. It occurs much more often in women

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21
Q

when a tumor develops in an organ that normally does not produce ACTH, the tumor will begin to secrete this hormone in excess, resulting in

A

Cushing syndrome

These tumors, which can be noncancerous (benign) or cancerous (malignant), are usually found in the lungs, pancreas, thyroid or thymus gland.

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22
Q

symptoms of cushing syndrome?

A

Buffalo hump, ruddy, moonface, balance issues, vertigo, blurred vision, acne, female baldness, water retention, menstrual cycle out of wack, (mimics diabetes), sleep disorders, depression
Hyperglycemia, guys develop breast, fat on the back, dumpy looking middle with skinny arms and legs

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23
Q

characterized byhypokalemia, hypochloremia,metabolic alkalosis, and hyperreninemia with normal blood pressure…. what syndrome is this?

A

Bartter syndrome

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24
Q

Why do people with Bartter syndrome lose Na, Cl, and K ?

A

autosomal recessive renal tubular disorders

The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium.

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25
What would licorice poisoning look like? | what is the treatment?
regular licorice ingestion can result in hypokalemia, hypernatremia, and water retention. Emergency treatment of licorice poisoning is largely supportive and consists primarily of monitoring for electrolyte abnormalities (especially of potassium) and other complications, with correction if necessary.
26
what is it in the black licorice that causes issues?
glycyrrhizin
27
the main acid base imbalance from massive blood transfusion is what and what would you treat it with?
metabolic alk. | treat with calcium chloride bc you will be low in calcium levels.
28
symptoms of low calcium?
Cramps, muscle spasms, and aches
29
What causes Milk-alkali syndrome? and what imbalance ultimately occurs?
ingestion of large amounts of calcium and absorbable alkali, with resulting hypercalcemia
30
if milk alkali syndrome is left untreated what can happen?
can lead to metastatic calcification and renal failure.
31
Why were people all of a sudden getting Milk alkali syndrome in the 1920s?
Sippy regimen, consisting of milk and bicarbonate, for treatment of peptic ulcer disease.
32
what stopped milk alkali syndrome even though people were still treating their peptic ulcers? Why have we seen a resurgence?
With the development of nonabsorbable alkali and histamine-2 blockers for treatment of peptic ulcer disease, milk-alkali syndrome became a rare cause of hypercalcemia; however, with the increased use and promotion of calcium carbonate for dyspepsia and for calcium supplementation, a resurgence of milk-alkali syndrome has occurred.
33
What would resp. alk look like in realation to the PH and CO2?
PH > 7.45 | PaCO2 < 35
34
What does the acronym ROME mean?
Respiratory opposite metabolic equal. stating that when the bicarb moves down or up the PH moves in the same direction down or up. When the CO2 moves down or up the PH moves in the opposite direcetion down or up.
35
What would someone in resp. alk. look like? S/S?
``` Deep rapid breathing hyperventilation tachycardia decreased or normal BP hypokalemia numbness and tingling of extremities lethargy and confusion light headedness could be nausea, vomiting. ```
36
Normal Causes of Resp. Alk?
``` centrally stimulating things can give you resp. alk high altitudes hyperventilation anxiety, fear, PE Mechanical ventilation ischemia stroke fever Hypoxemia Pulmonary dz Severe anemia sepsis ```
37
drugs that can cause resp. alk?
salicylates progesterone (pregnancy) analeptics (doxapram)
38
Effects of Resp. Alk?
``` low potassium low calcium cardiac dysrhythmias Bronchoconstriction Hypotension Potentiates toxicity of digoxin Doubling minute ventilation decreases cerebral blood flow by half ```
39
during neurosurgery some times they like to do what to decrease the ICP? and what would the target level be? and what level is dangerous?
decreases ICP to decrease the PaCO2 (to decrease PaCO2 you make the patient breath more). 20-30 but not lower than 20 bc that can cause cerebral ischemia.
40
how long after instituting hyperventilation does cerebral blood flow return to previous levels? (also the CSF HCO3 returns to normal)
8-24 hours
41
analeptics are a drug that can cause Resp Alk, what type of drugs would this be?
analeptics are drugs that stimulate the CNS. Used with ADHD, for depression, with respiratory depression. Doxapram is one but not used much today.
42
What would be the PH and PaCO2 with Resp. Acidosis?
pH less than 7.35 | PaCO2 greater than 45
43
what ventilation status would cause Resp. acidosis?
hypoventilaiton | when minute ventilation is insufficient to eliminate CO2 production without an increased capillary-alveolar CO2 gradient
44
Who is the prime dz for Resp. acidosis?
COPD
45
What would someone with Resp. acidosis look like? (effects of it)
``` rapid shallow resp. decreased BP skin/mucous pale to cyanotic HA hyperkalemia dysrhythmias due to increased K drowsiness, dizziness disorientation muscle weakness hyperreflexia "I can't catch my breath" cardiovascular depression that is offset by catecholamines increased secretion. CNS depression-CO2 narcosis hypovolemia ```
46
Causes of Resp. Acidosis?
resp. depression (anesthesia, overdose, Increased ICP) Airway obstruction decreased alveolar capillary diffusion (pneumonia, COPD, ARDS, PE) Opioid induced "wooden chest syndrome" stroke, trauma flail chest from MVA (paradoxical chest rise)
47
increased CO2 productions (which would lead to resp. acidosis) can be caused by?
``` Large carbohydrate loads Malignant hyperthermia Intensive shivering Prolonged seizure activity Thyroid storm Extensive thermal injury (burns) ```
48
Treatment of ACUTE Resp. Acidosis?
Mechanical ventilation
49
Treatment of CHRONIC resp. acidosis?
improvement of pulmonary function to permit more effective elimination of CO2
50
What would Metabolic Acidosis look like in relation to the pH and HCO3?
PH less than 7.35 | HCO3 less than 22
51
What compensatory mechanism normally accompanies metabolic acidosis?
Hperventilation
52
With metabolic acidosis if you have a significant reduction of pH what might you see? s/s
Increased PVR Reduced myocardial contractility Decreased SVR Impaired response of CV system to endogenous or exogenous catecholamines
53
what would someone with metabolic acidosis look like? s/s
``` HA decreased BP hyperkalemia muscle twitching warm, flushed skin (vasodilation) nausea vomiting diarrhea confusion, increased drowsiness KUSSMAUL respiration (compensatory hyperventilation) rapid shallow respirations ```
54
how do you calculate anion gap?
Na - (HCO3 + Cl)
55
What is a normal anion gap value ?
The book state 8-12 | Hammon states 10-14
56
Why do clinicians use the anion gap formula?
to identify the cause of metabolic acidosis.
57
what creates the largest anion gaps?
ketoacidosis and lactic acidosis. bc the kidneys are not excreting the acids like they should.
58
what occurs when the body losses bicarbonate and replaces it with chloride ions?
hyperchloriemic acidosis or normal anion gap acidosis. | also diarrhea
59
Causes of metabolic acidosis?
increased anion gap increased production of acids through renal failure, ketoacidosis (starvation, diabetic) lactic acidosis alcoholic rhabdomylosis (crush injury) injestion of toxin (salicylate, mehanol, ethylene glycol, paraldehyde, toluene, sulfur)
60
what can cause lactic acidosis?
sever tissue hypoxia followed by hypoxemia, hypoperfusion (ischemia) or inability to utilize oxygen (cyanide) can result in lactic acidosis.
61
When old people are obsessed with BM and take milk of mag all the time to poop what acid base imbalance do they have?
metabolic acidosis?
62
causes of metabolic acidosis with normal anion gap (hyperchloremic) ?
Diarrhea ingestion of CaCl2, MgCl2 Fistulae ileal loop obstruction carbonic anhydrase inhibitors LOW aldosterone large amount of bicarbonate free solutions (NS) TPN Increased intake of ammonium chloride, lysine HCL Arginine HCL (any of the opposites to fix metabolic alk.)
63
How much does min. ventilation increase for every 1mmHg increase in PaCO2
Minute ventilation increases (vol expelled from lungs) 1-4 L/min for every 1mmHG increase in PaCO2 (to blow off acid)
64
Pulmonary compensation during metabolic acidosis, mediated by what and changes made based on what?
Mediated by chemoreceptors within brain stem | Receptors respond to changes in CSF pH
65
Decreases in arterial blood pH stimulates medullary respiratory centers and increases?
alveolar ventilation and restores pH toward normal
66
how long does it take pulmonary response to reach a steady state?
12-24 hours
67
can respiratory response to change in pH restore it back to normal?
PH is never completely restored to normal
68
What is intracellular hydrogen concentration and what pH is it equal to?
160 nmol/L intracellular which is equivalent to 6.8 pH
69
Increases in arterial blood PH depress?
respiratory centers
70
what would elevate the PaCO2 and restore arterial pH towards normal?
alveolar hypoventilation
71
hypoventilation can lead to hypoxia, which stimulates oxygen sensitive chemoreceptors. theses receptors stimulate ventilation . if someone is on room air the paCO2 does not usually rise above?
greater than 55mmHg
72
for every 1mEq/L increase in HCO3 your paCO2 will increase how much?
.25-1mmHg

Basics exam 2 (6 decks)

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