Electrolyte and pH balance (Ch. 26 Part II) Flashcards
Na+ Balance and aldosterone
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
aldosterone’s effects on K+ balance
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
ANP’s effects at kidney
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]
estrogen
- High [aldosterone]:
- The rest (10%) is absorbed in the DCT & CD
- Low [aldosterone]:
- Na+ is not actively reabsorbed- lost to urine, water follows
Progesterone
- Progesterone decreases Na+ reabsorption (blocks aldosterone)•
- Promotes Na+ and H2O loss
K+’s importance in APs and RMP
affects RMP and generation APs in neurons and muscle cells (so does sodium and calcium)
hyperkalemia
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
reversal potential review
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+)
hypokalemia
very dangerous because can easily lead to unresponsiveness and sudden cardiac arrest
Regulation of K+ Balance
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
how can acidosis lead to hyperkalemia
lots of hydrogen ions moving into cell, H+ wants to bind to P-, potassium leaves cell to balance charge, hyperkalemia
PTH (parathyroid hormone)
released from parathyroid gland in response to Ca2+ dropping, because we need to get more Ca2+ into blood
3 ways PTH increases Ca2+ in blood
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
where each buffer plays its biggest role
understand bicarbonate buffer system intimately
3 ways to rid body of acid
chemical buffering systems, lungs can eliminate volatile acids, kidneys can eliminate nonvolatile fixed acids/bases
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
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
change pco2 to 7 on question 24 of study guide
Hypersecretion of aldosterone results in hypokalemia, which causes …
hyperpolarization of neurons and the need for a stronger than normal stimulus to trigger an action potential
Mr. Heyden’s low blood pressure will trigger certain compensatory mechanisms. Which statement below best reflects the changes in hormone levels that will occur?
Mr. Heyden’s ADH, aldosterone, and renin will increase.
would hypokalemia make it easier or harder to generate an AP?
harder, because less ECF K+ makes the difference between RMP and threshold too great
Which of these combinations of values would indicate that a patient was suffering from metabolic acidosis?
Increased blood HCO3- levels and decreased pH
Which of the hormones results in increased sodium reabsorption (and therefore water reabsorption also)?
aldosterone
ANP’s effects on BP through kidneys’ granular cells
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
ANP’s effects on BP through CD
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
ANP’s effect on BP after it reaches the adrenal cortex
decrease aldosterone release → inhibit CD in kidney → lower Na+ reabsorption, more Na+ lost in urine, water follows, lower BV → lower blood pressure
Na+ and estrogen & progesterone
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
would hyperkalemia make it easier or harder to generate an AP?
easier, because extra K+ in ECF is more positive, so the difference between RMP and threshold is less
Explain how acidosis can lead to hyperkalemia
acidosis → more H+ ions in ECF move down their gradient into cells → K+ leaves cells to balance that charge → more K+ in ECF
What happens to K+ levels with alkalosis?
ECF K+ levels fall with alkalosis, hypokalemia
how is K+ balance controlled
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
how is K+ balance controlled
ECF and ADH
An increase in ECF osmolality prompts ADH release by stimulating the hypothalamic osmoreceptors.
What happens when the body senses decreased stretch in afferent arterioles?
Granular cells of kidneys release renin → convert angiotensin I-II
what does angiotensin II activate/target (name 4 things)
→ thirst mechanism, adrenal cortex, posterior pituitary, systemic arterioles