Sodium Homeo Flashcards

1
Q

changes in water secretion are controlled by?

A

ADH only

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2
Q

changes in sodium secretion are determined by?

A

a variety of overlapping features in concert

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3
Q

compared to water secretion, sodium secretion occurs more?

A

slowly

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4
Q

you gain 1kg of water weight for every ____ sodium you retain

A

140 mEq

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5
Q

if you increase sodium intake, it will take ___ days for your body to adjust and begin excreting equal to ingestion

A

4 days (slower than water excretion response to added H2O)

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6
Q

when does ECF volume return to baseline after increased salt intake?

A

not until 4 days after reducing salt intake back to normal level (stays up if salt intake remains high)

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7
Q

the body attempts to retain salt when?

A

the EABV is low (usually correlates with the ECF but is specific to organ blood flow)

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8
Q

what detect changes in EABV?

A

high pressure baroreceptors in aortic arch, carotid sinus, LV of heart, JG apparatus in afferent arterioles of kidney (low pressure receptors less important)

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9
Q

what percent of filtered sodium is reabsorbed in each region of the collecting duct

A

67% in proximal tubules, 25% ascending loops, 5% distal tubules, 3% collecting ducts

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10
Q

normally about ___% of filtered sodium is reabsorbed

A

99.40%

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11
Q

increased hydrostatic pressure from increased sodium intake results in?

A

increased glomerular filtration rate, increased pressure in peritubular capillaries (pressure natriuresis)–> increased sodium excretion (at higher body weight)

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12
Q

increased EABV sensed by the JGA results in?

A

decreased renin, angiotension, and aldosterone

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13
Q

increased EABV sensed by the aortic arch and carotid sinus results in?

A

decreased catecholamines and decreased sympathetic outflow

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14
Q

increased EABV sensed by the cardiac atria results in?

A

increased atrial natriuretic factor

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15
Q

how does angiotensin II increase sodium reabsorption?

A

directly at proximal tubule, indirectly by peripheral vasoconstriction which increases vascular resistance, stimulates production of aldosterone

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16
Q

from where is aldosterone released?

A

cortex of adrenal gland

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17
Q

where does aldosterone act?

A

promotes sodium reabsorption in exchange for potassium by activating sodium channels in CCT

18
Q

renin is released from?

A

juxtaglomerular cells in afferent arteriole

19
Q

how is release of renin controlled?

A

negative feedback through three major components: baroreceptors in afferent arterioles, chemoreceptors in macula densa, EABV and sympathetic nervous system

20
Q

how does the macula densa work?

A

located in the distal tubule where it detects the concentration of sodium in the urine and acts on JG cells that are right next door

21
Q

name 3 ways in which renal efferent nerves influence excretory function

A

regulation of GFR; release of renin; reabsorption from proximal and distal nephron segments

22
Q

at what point does an increase in ECF show signs of edema?

A

3L

23
Q

generalized edema is suggestive of an increase in ECF volume of ____ liters and a corresponding increase in sodium content of _____

A

4-5 L; 500-700mEq

24
Q

name three causes of salt and water retention by the kidneys that could occur in a state of normal or high ECF

A

heart disease, kidney disease, liver disease (perceived decreased in EABV due to increased fluid in venous system)

25
Q

why is interstitial hydrostatic pressure usually negative?

A

drainage of interstitial fluid into lymphatics

26
Q

what is the most common cause of increased movement of fluid from the intravascular compartment to the interstitium?

A

increased hydraulic pressure

27
Q

what is the main mechanism for edema formation in heart, liver, and kidney dz?

A

increased hydrostatic pressure in the intravascular compartment that comes from the venous end (where there is no sphincter to control flow)

28
Q

decreased plasma protein would result in?

A

decreased oncotic pressure and thus edema (increased fluid in interstitium)

29
Q

edema due to increased capillary permeability occurs in?

A

pregnancy, inflammatory and allergic reactions, sepsis, ARDS

30
Q

name three safeguards to prevent severe edema

A

increase in hydrostatic pressure of interstitium, increase in lymphatic flow, decrease in interstitial oncotic pressure (diluted by fluid entry)

31
Q

examples of high output heart failure

A

hyperthyroidism, AV fistula (output bypasses large sections of circulation)

32
Q

in the early phases of heart failure, RAAS and SNS activation are balanced out by ___ and ___

A

vasodilatory prostaglandins and atrial natriuretic peptide

33
Q

the SNS system stimulates nuclei in the ____ resulting in non-osmotic release of ADH

A

hypothalamus

34
Q

name 4 causes of ascites in liver disease

A
  1. increased sinusoidal pressure and pooling of blood in splanchnic venous system; 2. peripheral vasodilation (increase NO); 3. hepatorenal reflex? (neural response to sinusoidal pressure); 4. hypoalbuminemia
35
Q

tx of sodium retention seen with liver disease

A

strict sodium and water restriction; careful use of diuretics

36
Q

overuse of diuretics in liver disease will result in metabolic ____ and ___kalemia

A

alkalosis; hypo-

37
Q

nephrotic syndrome is usually caused by disorders of the?

A

glomerulus

38
Q

what is the cause of protein permeability and loss in nephrotic syndrome?

A

loss of fixed negative charges in the glomerular capillary wall (with or without structural changes in the wall)

39
Q

cardinal features of nephrotic syndrome include?

A

hypoalbuminemia; peripheral edema; lipiduria; dyslipidemia (and associated atherosclerosis, venous thrombosis)

40
Q

the majority of evidence suggests that edema secondary to the nephrotic syndrome is primarily due to the (underfill/overfill) mechanism

A

overfill; unexplained increase in salt and water retention in the distal portions of the nephron occurs FIRST

41
Q

tx of nephrotic syndrome

A

reverse glomerular dz (corticosteroids, cytotoxic agents), sodium restriction, ?cautious use of diuretics, occasional infusion of albumin, ACE inhibitors to reduce proteinuria