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IEMR > (IEMR9)Water and Electrolytes > Flashcards

(IEMR9)Water and Electrolytes Flashcards

1
Q

What is the TBW for males percentage?

A

60%

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2
Q

What is the TBW for women percentage?

A

50%

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3
Q

What is the equation for TBW?

A

ICF + ECF

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4
Q

ICF is what percentage of TBW?

A

2/3rd

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5
Q

ECF is what percentage of TBW?

A

1/3rd

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6
Q

Interstitial fluid volume is what percentage of ICF?

A

0%

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7
Q

Vascular fluid volume is what percentage of ICF?

A

0%

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8
Q

Interstitial fluid volume is what percentage of ECF?

A

2/3rd

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9
Q

Vascular fluid volume is what percentage of ECF?

A

1/3rd

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10
Q

If you provide a patient with 3 L of saline, what is the volume distribution?

A

1L to the ECF and 2 L to the ICF. .333 L will go to the vascular volume and .666 L will go to the interstitial volume.

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11
Q

If a person lost 1L of blood, how many L of normal saline are you going to provide to that patient?

A

9L of normal saline

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12
Q

What is the equation to calculate normal plasma osmolality?

A

Plasma osmolality = 2*[Na] + [Glucose]/18 + [BUN]/2.8

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13
Q

What is the normal concentration of BUN?

A

8-20 mg/dL

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14
Q

If a person has a dramatic increase in plasma glucose, you should be thinking what as a good differential diagnosis?

A

diabetes mellitus

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15
Q

If a person has a dramatic increase in BUN, you should be thinking what as a good differential diagnosis?

A

kidney failure

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16
Q

What is the equation for total body osmolality?

A

ECF osmolality + ICF osmolality

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17
Q

What is the equation for ECF osmoles?

A

ECF osmolality*ECF volume

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18
Q

What is the equation for ICF osmoles?

A

ICF osmolality*ICF volume

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19
Q

What are the main hormones for salt and water regulation?(3 points)

A

ADH, aldosterone and natriuretic hormones

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20
Q

ADH has a high affinity for what type of receptor in the kidneys?

A

V2

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21
Q

ADH has a low affinity for what receptor in the body

A

V1

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22
Q

What is the purpose of the V3 and V4 receptors?

A

ADH modifies drinking behavior by interacting with the V3 and V4 receptors in the pituitary and the hypothalamus, respectively speaking

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23
Q

Where is ADH synthesized?

A

It is synthesized in the supraoptic nuclei of the hypothalamus

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24
Q

What type of hormone is ADH?

A

peptide hormone

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25
Q

What assist the transfer of ADH to the posterior pituitary gland?

A

neurophysins

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26
Q

Main hormone involved in regulation of water balance and only hormone that increase reabsorption of solute-free water int he kidney collecting duct - by increase AQP-2 channels

A

ADH

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27
Q

What are the effects of ADH besides reabsorption of water in the collecting duct?(5)

A

secondarily increase the reabsorption of NaCl in the thick ascending limb, acts on V1 receptors on vasculature causing vasoconstriction in larger doses, stimulates ACTH secretion by acting on V3 receptors in the pituitary, has an affect on memory and cognition and stimulates gluconeogenesis

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28
Q

How does ADH affect urine osmolality?

A

It increases urine osmolality

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29
Q

How does ADH affect urine flow rate?

A

it decreases flow rate

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30
Q

How is ADH secretion regulated?(2 points)

A

Tonically inhibited by normal arterial pressure and the primary regulator is the normal osmolality state

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31
Q

What are potent stimulator of ADH secretion?(2 points)

A

nausea and vomiting

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32
Q

What are examples of physiological changes that decrease ADH/VP secretion?(5 points)

A

decreased plasma osmolality, increased inhibition due to increase firing of low volume receptors(by increasing the ECF volume), cold, drugs and glucocorticoids

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33
Q

What are examples of drugs that affect ADH secretion?(3 points)

A

alcohol, α-adrenergic agonist, opiate antagonist

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34
Q

How is ADH secretion affected during pregnancy?

A
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35
Q

How does ADH release change during trauma?

A
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36
Q

What happens if there is a deficiency of ADH?

A

diabetes insipidus: nephrogenic of hypothalmic

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37
Q

What are the types of diabetes insipidus?

A

nephrogenic or hypothalmic

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38
Q

What is SIADH?

A

excess release of ADH

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39
Q

SIADH usually leads to what?(3 points)

A

hyponatremia, water retention and significant increase in urine osmolality

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40
Q

How does SIADH affect urine osmolality?

A

significant increase in urine osmolality

41
Q

How does SIADH affect electrolyte balance?

A

hyponatremia

42
Q

What drug is a known cause of nephrogenic diabetes insipidus?

A

lithium

43
Q

What is the firs thing you do to treat nephrogenic diabetes insipidus?

A

correct the hypercalcemia and/or the hyperkalemia

44
Q

What are the three things you do to treat nephrogenic diabetes insipidus?(3 points)

A

correct the hyperkalemia and/or the hypercalcemia, discontinue the use of a drug that is causing the nephrogenic diabetes insipidus and provide the patient with hyrochlorothiazide and amiloride

45
Q

What is the most important mineral corticoid in humans?

A

aldosterone

46
Q

Where is aldosterone specifically synthesized in the body?

A

zona glomerulosa in the adrenal cortex

47
Q

What is Star?

A

Steroid Acute Regulatory protein that plays a critical role in steroid synthesis by binding to cholesterol, mobilizing it into the mitochondria and performing a side cleave enzymatic reaction to produce pregnenolone

48
Q

How does steroid synthesis produce the main three classes of steroids in the body? What are the precursors and the final product?

A

Pregnenolone goes through a couple steps to become alodsterone. 17-OH pregnenolone is converted to glucocorticoid and DHEA is converted to androgenstendione

49
Q

How does cortisol synthesis and secretion into the bloodstream affect ACTH synthesis and secretion?

A

negative feedback resulting in decrease synthesis and secretion of ACTH

50
Q

What is the action of aldosterone?(2 points)

A

It increse the number of ENaC sodium channels all over the body and it increase the reabsortion of sodium in the collecting duct.

51
Q

Why does aldosterone lead to the increase absorption of sodium and the secretion of potassium?

A

The ENaC channels in the principal cells in the connecting tubule and the cortical connecting lead to a very negative charge on the lumen side of the principal cell which drives a secretion of potassium via a potassium channel on the lumenal side. An increase in the ENaC channels is going to increase the negative charge on the lumenal side; therefore, leading to a significant increase in secretion of potassium in the principal cells of the connecting tubule and the cortical collecting tubule

52
Q

Where are general locations you find the ENaC channel in your body?(3)

A

salivary glands, colon and kidney

53
Q

How does aldosterone secretion change the electrolyte balance in feces?

A

increase potassium secretion and sodium retention

54
Q

What are the probelms that result from hypoaldosteronism?(3 points)

A

decreased sodium reabsorption, decrease chloride reabsorption, increased potassium reabsorption, increase hyrdrogen ion reabsorption and GI probelms

55
Q

What does decrease sodium and chloride reabsorption do to the body?(7 points)

A

hyponatremia, decrease ECF volume, natriuresis, polyuria, dehydration, hypotension and then fatal shock

56
Q

What are the probelms to the body that result in retension of potassium and hydrogen ions?(2 points)

A

hyperkalemia and metabolic acidosis

57
Q

What are examples of GI probelms caused by hypoaldosteronism?(3 points)

A

nausesa, vomitting and diarrhea

58
Q

How do you treat hypoaldosteronism?

A

salt supplementation and replacement therapy

59
Q

What is Conn’s disease?

A

primary hyperaldosteronism due to adrenal tumor or hyperplasia

60
Q

How does Conn’s disease affect the body?(5 points: aldosterone levels, ECF volume, plasma volume, blood pressure, potassium level and extra)

A

aldosterone is high, expanded ECF and plasma volumes, increased blood pressure, hypokalemia and escape from sodium-retaining effects

61
Q

What is a hyperfunction mineralcorticoid disease state?

A

secondary hyperaldosteronism

62
Q

Secondary hyperaldosteronism is seen in what type of patients?(3 points)

A

CHF failure patients, liver cirrhosis and nephrosis

63
Q

Why is congestive heart failure a cause of secondary hyperaldosteronism?

A

there is an decrase in CO, leading to an decrease(perceived, because there is an increase in the inteterstitial fluid) in blood volume, deccreasing GFR leading to an increase in renin, ANG-II and aldosterone

64
Q

Why is liver cirrhosis associated with secondary hyperaldosteronism?

A

there is a decrease in the onctic pressure due to the lack of the liver’s ability to synthesize plasma proteins, leading to a decrease in blood volume, leading to decrease GFR, leading to the release of renin, ang-II and aldosterone

65
Q

What are some iatrogenic syndromes leading to hyperaldosteronism?(2 points)

A

consuming licorice or taking any steroid medication similar to mineral corticoids

66
Q

What is glycyrrhiza?

A

Active ingredient in licorice that cause hyperaldosteronism

67
Q

How does licorice hyperaldosteronism?

A

It inhibits 11-β-hydroxy steroid dehydrogenase which allows cortisol to bind to the mineral corticoid target cells

68
Q

What are general categories that cause endocrine hypertension?(4 points)

A

endocrine hypertension as a result of chronic renal failure, generla hypertension resulting from a pathology in a number of endocrine ograns, natriuretic factors/hormones and other endocrine aspects of kidney function

69
Q

What natriuretic factors are known to cause endocrine hypertension in particular circumstances?(3 points)

A

atrial natriuretic peptide(ANP), brain derived natriuretic peptide and others

70
Q

What synthesizes and releases ANP?

A

cardiomyocytes in the atria

71
Q

What generally stimulates the release of ANP?

A

atrial stretch

72
Q

What specifically causes the synthesis and release of ANP?

A

increased intravascular volume and increased intravascular pressure

73
Q

How does ANP affect the kidneys?(renal arteries, GFR, renin secretion, ANGII, aldosterone)

A

vasodilation of renal arteries, small increase in GFR, inhibition of renin secretion and effects secondary t inhibition of ANG II and aldosterone

74
Q

ANP is what type of hormone?(what is it’s composition)

A

peptide hormone

75
Q

What is the specific mechanism of action of ANP?

A

It binds to guanylate cyclase, gunayl cyclase converts ATP to cGMP and there is a decrease in Na-K ATPase activity

76
Q

How does brain derived natriuretic peptide work?

A

it is an endogenous sodium potassium ATpase inhibitor

77
Q

How does dopamine assist in the prevention of hypertension?

A

it is a vasodilator and it increases sodium excretion

78
Q

How does bradykinin and prostaglandins assist in the prevention of hypertension?

A

they inhibit the reabsorption of sodium in the distal tubule by affecting the ENaC channels

79
Q

How does blood pressure change with age?

A

blood pressure increases with age

80
Q

What is a pheochromocytoma?

A

tumor of the adrenal medulla

81
Q

What type of primary germ layer cause a pheochromocytoma?

A

neuroectodermal

82
Q

What are the most sifnificant symptoms of pheochromocytoma?(3 points)

A

hypertension, sustained or paroxysmal

83
Q

What is the classic triad of paroxysmal episodes that’s associated with pheochromocytomas?(3 points)

A

palpitations, diaphoresis and severe headaches

84
Q

What special pathological condition is experienced by patients with untreated pheochromocytoma?(vasculature)

A

lability of blood pressure

85
Q

What causes the lability of the blood pressure for a patient with pheochromocytoma?**(2) **How does this affect the heart?

A

there is chronic loss of blood volume and there is constant catecholamine release. There is also cardiomyopathy.

86
Q

Why do patients with untreated pheochromocytoma experience chronic bood volume loss?

A

The chronic blood volume depletion is due to the inhibition of the renin-angiotensin-aldosterone system being inhibited by the excessive release of catehcolamines from the tumor of the adrenal medulla

87
Q

How is a person blood sugar affected with pheochromocytoma?

A

hyperglycemia

88
Q

Why does a person with untretead pheochromocytoma experience hyperglycemia?

A

because the excessive catechoalamine release leads to increase lipolysis which results in excessive amounts of free fatty acids in the blood and the subsequent inbhibition of glucose by muscle cells

89
Q

If myocytes, hepatocytes and adipocytes become resistant to insulin, what happens to the level of insulin?

A

the level of circulating insulin increases in the blood

90
Q

If the level of circulating insulin increase in the blood, how does this affect the adrenergic nervous system, sodium levels and muscle?

A

It causes activation of hte adrenergic nervous system, it causes sodium retention and it leads to smooth muscle hypertrophy

91
Q

How does glucocorticoid excess effect cardiac output and hepatic production of angiotensinogen?

A

it increases cardiac output and it increases hepatic production of angiotensinogen

92
Q

How does glucocorticoids excess affect the synthesis of prostaglandins? What is the genearl mechanism of action?

A

It decreases the syntehsis of prostaglandins by blocking phospholipase

93
Q

Does excess glucocorticoid release acuse vasoconstriction or vasodilation?

A

it causes vasoconstriction

94
Q

The most common cause of end-stage renal disease is what?

A

diabetes mellitus

95
Q

The second most common cause of end stage renal disease is what?

A

hypertension

96
Q

How does low concentration of phosphate in the blood influence parathyroid hormone release?

A

There would be an increase in the parathyroid hormone to incrase the level of phosphate being secreted into the bloodstream as a result of the osteoclastic breakdown of bone

97
Q

What are the symptosm of hypokalemia?(5 points)

A

muscle cramps, muscle weakness, palpitations, paralysis and parathesia

98
Q

A 58 yof weighing 105 # and 50 inches tall whose father had colon cancer decides that she needs to be checked out. She schedules a colonoscopy and does the usual prep. After the procedure she is sent home but develops tremor and has trouble breathing. In the ER they give her a breathing treatment which induces cramping and palpitations.
What’s up? And how do we go about fixing it?

A

IEMR (19 decks)

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