FLUIDS LYTES

Question 1

osmoreceptors

Answer 1

detect changes in plasma osmolality

and therefore Changes in volume..

responsible for day-to-day fine tuning of volume.

Question 2

baroreceptors

Answer 2

sensitive to changes in pressure

“barometer” are used in a storm - only used for big pressure problem

The baroreceptors contribute relatively little to control of fluid balance under normal conditions.

Question 3

Changes in effective circulating volume are sensed by

Answer 3

volume receptors of the

intrathoracic capacitance vessels and atria,

the pressure receptors of the aortic arch and carotid arteries,

the intrarenal baroreceptors, and, to a lesser extent, the hepatic and cerebrospinal volume receptors.

These baroreceptors control volume by means of sympathetic and parasympathetic connections.

The atria also appear to serve as endocrine organs capable of directing responses to volume changes with elaboration of the hormone atrial natriuretic peptide.

Question 4

the renin-angiotensin system

Answer 4

The main hormonal mediator of baroreceptor modulation of volume control is the renin-angiotensin system. The result of this complex system of receptors or messengers is a change in sodium and water balance mediated by the kidneys. It is through changes in sodium and water reabsorption that volume and pressure ultimately normalize. Renin is a proteolytic enzyme released in response to changes in arterial pressure, changes in delivery of sodium to the macula densa of the distal convoluted renal tubule, increases in β-adrenergic activity, and increases in cellular levels of cyclic adenosine monophosphate. Renin cleaves angiotensin I from circulating angiotensinogen. Angiotensinogen is abundant, so this reaction is enzyme dependent rather than substrate dependent. Angiotensin I is further cleaved to angiotensin II, which acts locally and systemically to increase vascular tone. Angiotensin II affects sodium reabsorption by decreasing renal plasma flow and the glomerular filtration coefficient. Finally, angiotensin II increases sodium reabsorption by means of direct tubular action and stimulation of aldosterone release from the adrenal cortex.

Question 5

Hypoaldosteronism anion gap and effect on K and H

Answer 5

Hypoaldosteronism results in defective distal hydrogen and potassium secretion in the kidney and causes a

hyperkalemic

metabolic acidosis associated

normal anion gap.

Question 6

Metabolic alkalosis typically occurs secondary to a loss of

Answer 6

anions.

Question 7

A common chloride responsive alkalosis is secondary to

Answer 7

gastrointestinal loss from prolonged gastric drainage, similar to that which can occur from excessive vomiting.

Question 8

Renal tubular acidoses (both proximal and distal) are associated with what acid base problem

Answer 8

non-anion gap acidosis.

Question 9

While duodenal fistulae and large amount of ileostomy output can result in what acid base problem

Answer 9

metabolic acidosis,

do not result in the large anion loss which leads to metabolic alkalosis.

Question 10

list order from most to least of Potassium secretion in the gi tract

Answer 10

colon
salivary (CAREFUL, highest amylase)
gastric
bile, 
pancreatic, 
duodenum, 
 ileum.

Question 11

electrolyte abnormality associated wiht multiple premature ventricular contractions (PVC), then wide complex tachycardia, then cardiac arrest.

Answer 11

HYPER K

makes the heart hyper

WIDE complex TACHY then dead

high potassium concentration of the cardioplegia extracellular prevents repolarization.