Jessica, a physiology student who takes a diuretic drug for high blood pressure,
ID: 3508078 • Letter: J
Question
Jessica, a physiology student who takes a diuretic drug for high blood pressure, says she drinks water constantly and yet is constantly thirsty. During lab exercise, she discovers that her urine contains glucose. Alarmed, she goes to her physician, who tests her blood and urine and obtains an electrocardiogram (ECG)
Some of the new terms and concepts you will encounter include:
Hyperglycemia, glycosuria, and hypokalemia
Osmolality and osmotic pressure
Jessica took a diuretic that promotes urinary water loss, and had glucose in her urine.
How would loss of water because of the diuretic affect her plasma concentration and osmotic pressure?
How would the presence of an extra solute—glucose—in the urine affect the urine's osmotic pressure and tendency to draw water by osmosis?
Jessica's plasma osmolality was higher than normal, and she complained of being constantly thirsty.
How does her high plasma osmolality cause her thirst?
How does her high plasma osmolality relate to her taking a diuretic drug and having glucose in her urine?
Jessica had an abnormal electrocardiogram (ECG) and mild hypokalemia.
What is hypokalemia, and how might it have been produced?
How would hypokalemia affect the resting membrane potential of Jessica's heart and her ECG?
Explanation / Answer
How does her high plasma osmolality cause her thirst?
There are two main mechanisms by which the body combats dehydration. Dehydration leads to a decrease in blood volume (hypovolemia) and, consequently, an increase in plasma osmolality (increased solute concentration). The increase in osmolality, in turn, is detected by osmoreceptor neurons in the hypothalamus. Increases in sodium (Na+) and chloride (Cl) are potent stimulators of hypothalamic osmoreceptors. Hypothalamic osmoreceptors are located in the circumventricular organ referred to as the organum vasculosum of the lamina terminalis (OVLT). Hypothalamic osmoreceptors then stimulate other hypothalamic neurons (magnocellular neurons), whose cells bodies are in the supraoptic and paraventricular nuclei of the anterior hypothalamus, but whose axon terminals are in the posterior pituitary, to release the antidiuretic hormone (ADH; also known as vasopressin) into the bloodstream. Circulating ADH reaches the kidney collecting ducts to increase water reabsorption and hence water retention. Increased water retention increases the extracellular fluid volume (and blood volume), ultimately bringing plasma osmolality back down to its normal set point of about 295 mOsm/kg. Note that that at the normal plasma osmolality of 295 mOsm/kg, there is baseline secretion of ADH, thus, allowing for dynamic control of ADH release when plasma osmolality increases or decreases.
What is hypokalemia?
Hypokalemia is when blood’s potassium levels are too low. Potassium is an important electrolyte for nerve and muscle cell functioning, especially for muscle cells in the heart. our kidneys control our body’s potassium levels, allowing for excess potassium to leave the body through urine or sweat.
how might hypokalemia have been produced?
Low potassium can occur for many reasons. Use of water pills (diuretics), diarrhoea, and chronic laxative abuse are the most common causes of low potassium levels.
Illness and other medications may also lower potassium levels. but in this case, it is due to the prolonged intake of diuretics.
How would hypokalemia affect the resting membrane potential of Jessica's heart and her ECG
In summary, the early effect of mild hyperkalemia on myocyte function is to increase myocyte excitability by shifting the resting membrane potential to a less negative value and thus closer to threshold potential; but as potassium levels continue to rise, myocyte depression occurs and Vmax continues to decrease.
ECG should be done on patients with hypokalemia. Cardiac effects of hypokalemia are usually minimal until serum potassium concentrations are < 3 mEq/L. Hypokalemia causes sagging of the ST segment, depression of the T wave, and elevation of the U wave. With marked hypokalemia, the T wave becomes progressively smaller and the U wave becomes increasingly larger. Sometimes, a flat or positive T wave merges with a positive U wave, which may be confused with QT prolongation. Hypokalemia may cause premature ventricular and atrial contractions, ventricular and atrial tachyarrhythmias, and 2nd- or 3rd-degree atrioventricular block. Such arrhythmias become more severe with increasingly severe hypokalemia; eventually, ventricular fibrillation may occur. Patients with significant preexisting heart disease and patients receiving digoxin are at risk of cardiac conduction abnormalities as a result of even mild hypokalemia.
How would loss of water because of the diuretic affect her plasma concentration and osmotic pressure?
Secretion of ADH occurs in the hypothalamus. It is synthesised and packaged into granules within the neurones to be released when required. Its release is regulated by hypothalamic osmoreceptors which swell or shrink in response to plasma osmolarity. The granules are transported down the axons where they are released from nerve terminals in the posterior pituitary gland. ADH release is also effected by baroreceptors to a small extent as obviously decreasing blood volume decreases blood pressure and vice versa.
Effect on plasma osmolarity
ADH increases the permeability of the collecting duct to water. It's mechanism is tonically active i.e. it will respond to a low or high plasma osmolarity. Should your osmolality fall below 280mOsmol/kg H2O then ADH release will cease entirely. This makes the collecting duct entirely impermeable to water so the large amount of very dilute urine coming in from the loop of henle and the distal convoluted tubule will remain dilute. You will lose water and thus blood plasma osmolality will rise as it becomes more concentrated.
In health you will always have some ADH released but a change in 1% of the body's plasma osmolarity will cause a large shift in ADH release. Should your blood become too concentrated more ADH will be released therefore more water will be reabsorbed as the collecting duct will be more permeable to water. This results in smaller amounts of much more concentrated urine being produced and water being conserved. Note that the amount of solute being excreted does not change a huge amount (solvent drag can occur occasionally) only the amount of water reabsorbed.
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