Sodium Homeo Flashcards

(41 cards)

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?

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
why is interstitial hydrostatic pressure usually negative?
drainage of interstitial fluid into lymphatics
26
what is the most common cause of increased movement of fluid from the intravascular compartment to the interstitium?
increased hydraulic pressure
27
what is the main mechanism for edema formation in heart, liver, and kidney dz?
increased hydrostatic pressure in the intravascular compartment that comes from the venous end (where there is no sphincter to control flow)
28
decreased plasma protein would result in?
decreased oncotic pressure and thus edema (increased fluid in interstitium)
29
edema due to increased capillary permeability occurs in?
pregnancy, inflammatory and allergic reactions, sepsis, ARDS
30
name three safeguards to prevent severe edema
increase in hydrostatic pressure of interstitium, increase in lymphatic flow, decrease in interstitial oncotic pressure (diluted by fluid entry)
31
examples of high output heart failure
hyperthyroidism, AV fistula (output bypasses large sections of circulation)
32
in the early phases of heart failure, RAAS and SNS activation are balanced out by ___ and ___
vasodilatory prostaglandins and atrial natriuretic peptide
33
the SNS system stimulates nuclei in the ____ resulting in non-osmotic release of ADH
hypothalamus
34
name 4 causes of ascites in liver disease
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
tx of sodium retention seen with liver disease
strict sodium and water restriction; careful use of diuretics
36
overuse of diuretics in liver disease will result in metabolic ____ and ___kalemia
alkalosis; hypo-
37
nephrotic syndrome is usually caused by disorders of the?
glomerulus
38
what is the cause of protein permeability and loss in nephrotic syndrome?
loss of fixed negative charges in the glomerular capillary wall (with or without structural changes in the wall)
39
cardinal features of nephrotic syndrome include?
hypoalbuminemia; peripheral edema; lipiduria; dyslipidemia (and associated atherosclerosis, venous thrombosis)
40
the majority of evidence suggests that edema secondary to the nephrotic syndrome is primarily due to the (underfill/overfill) mechanism
overfill; unexplained increase in salt and water retention in the distal portions of the nephron occurs FIRST
41
tx of nephrotic syndrome
reverse glomerular dz (corticosteroids, cytotoxic agents), sodium restriction, ?cautious use of diuretics, occasional infusion of albumin, ACE inhibitors to reduce proteinuria