Electrolyte and pH balance (Ch. 26 Part II) Flashcards

1
Q

Na+ Balance and aldosterone

A

Body tries to hang onto Na+, reabsorbs it in kidneys and that helps us reabsorb water too 65% in PCT (majority of reabsorption occurs in PCT, filtrate volume decreases a lot) 25% in loops of Henle,

High [aldosterone]: The rest (10%) is absorbed in the DCT & CD,

Low [aldosterone]: Na+ is not actively reabsorbed- lost to urine, water follows

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2
Q

aldosterone’s effects on K+ balance

A

since Na+ gets reabsorbed in higher amounts with aldosterone due to more Na-K pumps, K+ goes the other way and we urinate it out

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3
Q

ANP’s effects at kidney

A

opposite of aldosterone, increases urine output, decreases BP because it increases urine output to bring BV down

eliminates sodium from the body, water follows

[effect on GFR as it relates to contractile activity of glomerular mesangial cells]

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4
Q

estrogen

A
  • High [aldosterone]:
  • The rest (10%) is absorbed in the DCT & CD
  • Low [aldosterone]:
  • Na+ is not actively reabsorbed- lost to urine, water follows
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5
Q

Progesterone

A
  • Progesterone decreases Na+ reabsorption (blocks aldosterone)•
  • Promotes Na+ and H2O loss
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6
Q

K+’s importance in APs and RMP

A

affects RMP and generation APs in neurons and muscle cells (so does sodium and calcium)

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7
Q

hyperkalemia

A

high ECF [K+] causes depolarization & hyperexcitability, RMP closer to threshold potential, too many APs quickly fired during period of hyperexcitability, so reduced excitability follows and can lead to cardiac arrhythmia → arrest

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8
Q

reversal potential review

A

charge difference at which you start reversing the flow of potassium because the cell is so negative inside that for every K+ that exits, another is pulled in (-90 for K+, +55 for Na+)

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9
Q

hypokalemia

A

very dangerous because can easily lead to unresponsiveness and sudden cardiac arrest

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10
Q

Regulation of K+ Balance

A

K+ balance is controlled in cortical collecting ducts by regulating amount secreted into filtrate

  • Most important factor affecting K+ secretion is its concentration in ECF, which is determined by diet
  • K+ controls its own ECF concentration via feedback regulation of aldosterone release
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11
Q

how can acidosis lead to hyperkalemia

A

lots of hydrogen ions moving into cell, H+ wants to bind to P-, potassium leaves cell to balance charge, hyperkalemia

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12
Q

PTH (parathyroid hormone)

A

released from parathyroid gland in response to Ca2+ dropping, because we need to get more Ca2+ into blood

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13
Q

3 ways PTH increases Ca2+ in blood

A

increase osteoclast activity in bone to cause Ca2+ and PO43- release into blood, increase Ca2+ reabsorption in kidney tubule, higher activation of vitamin D by kidney which increases Ca2+ absorption from food in small intestine

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14
Q

where each buffer plays its biggest role

A
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15
Q

understand bicarbonate buffer system intimately

A
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16
Q

3 ways to rid body of acid

A

chemical buffering systems, lungs can eliminate volatile acids, kidneys can eliminate nonvolatile fixed acids/bases

17
Q

You are examining a patient’s bloodwork, which indicates the following:

pH: 7.4

PCO2: 4.1 mm Hg

HCO3-: 20 mEq/L

a. Is this patient’s condition acidosis or alkalosis? b.Is the source of this condition respiratory or metabolic? Is compensation occurring (yes or no)?

normal ranges are pH: 7.35-7.45

pCO2: 4.7-6

HCO3: 22-24

A
18
Q

Laxix (Furosemide) is a loop diuretic that is commonly prescribed to patients with hypertension or congestive heart failure. These patients are at an increased risk of cardiac arrhythmias and/or arrest. Why? Hint: think movement of charged ions into/out of cell

A
19
Q

change pco2 to 7 on question 24 of study guide

A
20
Q

Hypersecretion of aldosterone results in hypokalemia, which causes …

A

hyperpolarization of neurons and the need for a stronger than normal stimulus to trigger an action potential

21
Q

Mr. Heyden’s low blood pressure will trigger certain compensatory mechanisms. Which statement below best reflects the changes in hormone levels that will occur?

A

Mr. Heyden’s ADH, aldosterone, and renin will increase.

22
Q

would hypokalemia make it easier or harder to generate an AP?

A

harder, because less ECF K+ makes the difference between RMP and threshold too great

23
Q

Which of these combinations of values would indicate that a patient was suffering from metabolic acidosis?

A

Increased blood HCO3- levels and decreased pH

24
Q

Which of the hormones results in increased sodium reabsorption (and therefore water reabsorption also)?

A

aldosterone

25
Q

ANP’s effects on BP through kidneys’ granular cells

A

atrial cells detect high BP and release ANP; ANP makes its way to the kidneys’ granular cells to tell them to decrease secretion of renin → less angiotensin II → more vasodilation → lower BP

26
Q

ANP’s effects on BP through CD

A

ANP from atrial cells → hypothalamus and posterior pituitary → stimulate ADH release → kidneys’ CD has fewer aquaporins → less water reabsorption → higher urine output → lower BP;

OR directly to CD to decrease Na+ & therefore water reabsorption

27
Q

ANP’s effect on BP after it reaches the adrenal cortex

A

decrease aldosterone release → inhibit CD in kidney → lower Na+ reabsorption, more Na+ lost in urine, water follows, lower BV → lower blood pressure

28
Q

Na+ and estrogen & progesterone

A

Estrogen

Increases NaCl reabsorption (like aldosterone)••Leads to H2O retention during menstrual cycles and pregnancy

Progesterone

Progesterone decreases Na+ reabsorption (blocks aldosterone)••Promotes Na+ and H2O loss

29
Q

would hyperkalemia make it easier or harder to generate an AP?

A

easier, because extra K+ in ECF is more positive, so the difference between RMP and threshold is less

30
Q

Explain how acidosis can lead to hyperkalemia

A

acidosis → more H+ ions in ECF move down their gradient into cells → K+ leaves cells to balance that charge → more K+ in ECF

31
Q

What happens to K+ levels with alkalosis?

A

ECF K+ levels fall with alkalosis, hypokalemia

32
Q

how is K+ balance controlled

A

high circulating K+ → stimulate aldosterone release in kidneys → more Na-K+ pumps in cortical collecting ducts → more Na+ absorbed and more K+ secreted in urine

33
Q

how is K+ balance controlled

A
34
Q

ECF and ADH

A

An increase in ECF osmolality prompts ADH release by stimulating the hypothalamic osmoreceptors.

35
Q

What happens when the body senses decreased stretch in afferent arterioles?

A

Granular cells of kidneys release renin → convert angiotensin I-II

36
Q

what does angiotensin II activate/target (name 4 things)

A

→ thirst mechanism, adrenal cortex, posterior pituitary, systemic arterioles