Thiazide diuretics NCLEX pharmacology review for nursing students!
Thiazide diuretics are medications that help remove extra fluid volume from the blood through increased urination. This review will discuss the mechanism of action of thiazide diuretics, what conditions they treat, nursing implications, side effects, and patient education.
Don’t forget to take the thiazide diuretics quiz after reviewing this material.
Thiazide Diuretics Review Lecture
Thiazide Diuretics NCLEX Pharmacology Review
Always ask yourself these 5 questions when you see a drug name to help you understand how the drug works, your role as a nurse, and what information will be asked on an exam about the drug:
Name (specifically the family name)? This will tell how the drug works.
Used for? This will tell you WHY the drug was ordered…what condition is this medication treating in your patient?
Responsibilities as the nurse? This will tell you what your role is as the nurse and what you need to monitor in the patient.
Side effects? Know the common side effects of the medications
Education pieces for the patient? As the nurse we play a HUGE role in educating our patients on how to take the drug, what to watch out for, and when to call the doctor.
Now, using those 5 questions let’s go over what you need to know about thiazide diuretics for exam:
Name?
This category of medications is known as the thiazide diuretics.
- Thiazide: this tells us it works to inhibit the thiazide sensitive sodium-chloride cotransporter (NCC) in the early part of the distal convoluted tubule (DCT).
- Diuretic: this tells us it increases urinary output by decreasing the amount of sodium reabsorption (remember water loves sodium and will always follow it).
- The result: sodium and chloride stay in the filtrate at this specific point in the nephron and will not be reabsorbed into the blood, which causes water to stay in the filtrate rather than being reabsorbed back into the blood.
- This leads to increased urination and removes extra fluid from the blood.
- The result: sodium and chloride stay in the filtrate at this specific point in the nephron and will not be reabsorbed into the blood, which causes water to stay in the filtrate rather than being reabsorbed back into the blood.
Thiazides are not as powerful as loop diuretics, but get the job done for providing diuresis effects.
Why? This is because most of the sodium in the filtrate is already reabsorbed within the thick ascending limb of the loop of Henle, which is where loop diuretics work and this makes them more powerful. Remember the loop of Henle accounts for about 25% of sodium reabsorption.
Therefore, when the filtrate reached the DCT it is not as high in sodium (the DCT normally reabsorbed about 5-7% of sodium in the filtrate) so they aren’t as powerful as loop diuretics.
Plus, thiazides do not work well if the glomerular filtration rate (GFR) is less than 30 (when compared to loop diuretics). Therefore, if a patient has renal failure with a fluid volume overload issue, loop diuretics are more effective for them. GFR tells us how well the kidneys are working to filter the blood.
Example of thiazide diuretics: unfortunately you can’t go by the ending of the generic name like with other medications…but some do end with “thiazide”
- Hydrochlorothiazide (HCTZ)
- Indapamide
- Chlorothiazide
- Metolazone
- Chlorthalidone
To understand how these drugs work we have to review the basic anatomy and physiology of the nephron:
Review of the Anatomy and Physiology of the Nephron
Nephrons are structures within the kidneys that allow them to function and without them working properly the kidneys fail to work properly.
There are millions of nephron units in each kidney. They function to filter the blood and manage the amount of water, ions, and waste in the blood. These substances filtered by the nephron will either be reabsorbed into the blood or stay in the filtrate where they will be excreted as urine.
The nephron is divided into several parts, and each part has its own unique role for tweaking the filtrate created by the glomerulus until it is just what the body needs and what it doesn’t need it will be excreted as urine.
The parts of the nephron are:
- afferent arteriole: delivers blood via the renal artery to the nephron so it can be filtered
- efferent arteriole: takes filtered blood away from the nephron after it has been filtered
- glomerulus: filters the blood and creates the filtrate which contains ions, water, and waste
- bowman’s capsule: collects the filtrate as it drips down from the glomerulus
- proximal convoluted tubule: the first tubule that starts tweaking the filtrate by reabsorbing ions, water, etc.
- NOTE: so far all of these parts of the nephron hang out in the renal cortex of the kidneys. This provides an isotonic environment where the sodium concentration in equal inside the nephron (hence the filtrate) and outside of it.
- However, as the filtrate progresses and enters into the loop of Henle, it enters into the renal medulla, which is a very salty (HYPERtonic) environment. This environment is necessary for water reabsorption by descending loop of Henle and the collecting ducts.
- loop of Henle: it has a descending and ascending limb and it responsible for about 25% of sodium reabsorption…
- The descending limb of the loop of Henle is only permeable to water (not ions). While the ascending limb (mainly the thick ascending limb) is only permeable to ions rather than water.
- distal convoluted tubule: the filtrate is now back in the renal cortex (an isotonic environment) for some more tweaking:
- some functions of the DCT is to reabsorb sodium, chloride, and calcium, and the secretion of potassium into the filtrate, which is under the influence of aldosterone.
- collecting ducts: this is the last part of the nephron where the filtrate is finally tweaked. Ions and water will be reabsorbed. The last part of the collecting duct is found in the medulla interstitum and will play a role in one last function of water reabsorption.
- renal pelvis: filtrate exits the nephron at this location and goes to the ureters and is urinated out.
Now let’s go a little more in depth and talk about how thiazide diuretics affect this process within the nephron…
Thiazide diuretics inhibit the sodium-chloride cotransporter in the early part of the distal convoluted tubule. Remember that the DCT is responsible for about 5-7% of sodium reabsorption. Therefore, if the cotransporter of sodium-chloride is inhibited, it prevents sodium and chloride from being reabsorbed back into the blood. If it’s not going back in the blood, it’s staying in the filtrate and this will cause water to stay within the filtrate…hence, helping provide that diuretic effect. Due to this, watch out for low sodium levels in the blood (hyponatremia).
However, by inhibiting the sodium-chloride cotransporter and increasing the amount of sodium in the filtrate at this point in the nephron, it will affect other channels and transporter within the cells that made up the DCT, and this can lead to electrolyte imbalances that are side effects of this medication:
Hypercalcemia: increased calcium level in the blood (normal 8.5-10.5 mg/L) which means there will be a lower amount of calcium in the filtrate/urine.
- Why? When the NCC cotransporter is inhibited it enhances other channels and transporters that deal with calcium within the cells that make up the DCT. It will cause them to actually increase the reabsorption of calcium to the blood (one of these channels is the trpv5 calcium channel).
- Therefore, thiazides can be helpful in preventing renal stones that consist of calcium (there will be less calcium in the filtrate to create a calcium renal stone). In addition, these medications can help increase calcium levels in the blood, which can increase bone density in susceptible patients.
Hypokalemia: decreased potassium levels in the blood (normal 3.5-5 mEq/L)…loop diuretics can also cause this as well.
- The filtrate in the DCT is now high is sodium because the NCC cotransporter prevented sodium from being reabsorbed back in the blood. Therefore, as it travels down and progresses later in the distal convoluted tubule it will encounter channels that are influenced by aldosterone. Remember aldosterone causes the body to keep sodium and water but EXCRETE potassium…hence potassium and hydrogen ions will be secreted into the filtrate.
- Result: It can lead to HYPOkalemia and metabolic alkalosis (because of the loss of hydrogen ions).
Other miscellaneous causes: increased glucose levels “hyperglycemia” (not truly understood why), increased uric acid levels “hyperuricemia” and it can lead to a gout attack (it alters how the proximal convoluted tubule deals with urate…it increases reabsorption).
Used for?
- Hypertension (usually prescribed first-line for primary hypertension…it helps decrease sodium and water levels in the blood)
- Heart failure (sometimes used with antihypertensive like ACE Inhibitors)
- Renal calculi formed from calcium
Responsibilities of Nurse?
Patient will be losing fluid in the form of urine: watch for signs of dehydration (removing too much fluid)
- Vital Signs (elevated heart rate and low blood pressure SBP <90)
- Monitor closely the patient’s intake and output.
- Daily weight (this is the best indicator of how much fluid the patient is losing). Weigh at the same time every day with the same scale.
Monitor labs:
- Assess for electrolytes imbalances and renal function (BUN and creatinine). Most hospitalized patients will have daily BMP drawn:
- Monitor:
- hypokalemia (normal level is 3.5-5 mEq/L)
- If patient is taking Digoxin, watch out for Digoxin toxicity because a low potassium level can increase this…(normal Digoxin level: 0.5-2 ng/mL)
- hyponatremia (normal level is 135-145 mEq/L)
- If patient is taking Lithium, watch out for Lithium toxicity because low sodium levels in the blood can increase this….. (normal Lithium level: 0.5-1.2 mmol/L)
- hypercalcemia
- metabolic alkalosis
- hypokalemia (normal level is 3.5-5 mEq/L)
- Monitor:
Monitor for signs of gout due to high uric acid levels in the blood.
Monitor glucose levels closely in diabetic patients for hyperglycemia…may need a change insulin or oral diabetic medications as deemed by the physician.
Provide easy access to the bathroom (prevent falls) and avoid giving a dose right before bedtime (this interrupts sleep and increases the risk of falling).
Assess the effectiveness of the medication: decrease in edema, clearer lung fields, decrease weight etc.
Side effects?
Electrolyte imbalances: hyponatremia, hypokalemia….hypercalcemia, hyperglycemia, hyperuricemia, metabolic alkalosis, dehydration, orthostatic hypotension
Education?
- Teach to be aware of signs and symptoms of dehydration (excessive thirst, fatigue, no urination, hypotension), and how to monitor blood pressure and heart rate at home.
- Consuming a healthy diet that includes foods that are high in potassium because this medication can lower potassium levels.
- Changing positions slowly due to orthostatic hypotension that can occur because of the change of fluid volume in the body.
- Monitoring weights daily.
- If diabetic, teach patient to monitor for hyperglycemia because these medication can increase the blood glucose level.
References:
Thiazide Diuretics. Retrieved from https://livertox.nih.gov/ThiazideDiuretics.htm Food and Drug Administration.
Hydrochlorothiazide Tablets, USP [Ebook]. Retrieved from https://www.accessdata.fda.gov/drugsatfda_docs/label/2011/040735s004,040770s003lbl.pdf