Renal Disorders: Why Dialysis Can Help Your Kidneys “Let It Go”

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Kidneys are a good example of the saying, “you don’t know what you’ve got ‘till it’s gone”. This is primarily because most people genuinely do not know they have reached an irreversible loss of kidney function until it is too late. You may be wondering how such a drastic decline in kidney function can silently progress under the radar. To answer why and how renal dysfunction typically goes undetected, it is important to first understand what makes the kidneys unique to other aspects of the body.

Your vital organs are all special with their own unique abilities and superpowers. For example, the liver is the only organ in your body with the capacity to regenerate itself. The key quality to remember when it comes to kidneys is they like to both work together as a team. Working together may not seem as much of a superpower, but it is incredibly useful when one kidney compensates for the impaired function of the other kidney. Even alone, a single kidney’s working nephrons can also compensate for the loss or degeneration of other nephrons within the organ itself.4 The kidneys are so highly adaptable they do a stellar job of making a sinking ship look like it is sailing, but this also means trying to identify declining renal function early to prevent progression of disease can be very challenging. Many patients will find themselves in this position and although we can screen for risk factors, a decline in renal function will likely remain silent and unrecoverable.

Outlined above are the differences between acute kidney injury (AKI) and chronic kidney disease (CKD). Since kidney damage is irreversible, prevention of AKI and CKD is paramount. For renal disorders, there is no real cure as therapy is typically supportive and dependent on the etiology.1 With this in mind, you may be wondering how we can go about being more proactive towards kidney disease. Clinical surveillance is an example of an effort that serves this very cause. If we take a look at the Nephrotoxic Injury Negated by Just-in-time Action (NINJA) project, we can see a 38% decrease in AKI exposure (estimated 633 cases avoided) and a 64% decrease in AKI (398 cases avoided) due to surveillance providing a timelier approach in identifying AKI.2

Although we have medications in place to treat the secondary complications and further progression of CKD, patients who do progress to end stage renal disease will find themselves dependent on dialysis in the absence of a kidney transplant.1 So, what happens to patients who officially progress to end stage renal disease and require dialysis? Well, the good news is there are some options. Patients can decide between hemodialysis (HD) or peritoneal dialysis (PD).1 HD requires several visits a week to a HD center and may cause further decline in residual renal function as compared to PD, which may be conveniently performed at home but has a higher risk of peritonitis.1

The title of this post references Frozen because that’s exactly how dialysis works: by letting all the toxins in your body go. When your kidneys are damaged, they cannot filter out all the toxins in your body as well so waste products and fluid can accumulate to a fatal degree.3 Dialysis helps prevent this accumulation by allowing toxins to essentially move from the blood to the dialysate, thereby filtering the blood and acting in place of the kidneys.1

References

  1. DiPiro, Joseph T. Pharmacotherapy: A Pathophysiologic Approach. New York: McGraw-Hill Medical, 2020. Print.
  2. Goldstein SL, Mottes T, Simpson K, et al. A sustained quality improvement program reduces nephrotoxic medication-associated acute kidney injury. Kidney Int. 2016;90(1):212-221. doi:10.1016/j.kint.2016.03.031.
  3. Dialysis. NHS. Accessed January 25, 2021. https://www.nhs.uk/conditions/dialysis/.
  4. Fattah H, Layton A, Vallon V. How Do Kidneys Adapt to a Deficit or Loss in Nephron Number?. Physiology (Bethesda). 2019;34(3):189-197. doi:10.1152/physiol.00052.2018.
  5. Bynum W. When kidneys fail. Lancet. 2014;383(9931):1798-1799.

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Thyroid Disorders: When Your Glands Go to the Dark Side

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If you are familiar with the Star Wars franchise, you know there is a light side and a dark side of the force. These sides represent either the selfless or the selfish and essentially act to hold the galaxy together. If you consider our galactic friends and their adventures for a second, you may be able to see there is a large parallel between the galaxy and the human body. After all, the goal for all Jedi is to keep the force within balance, or in the context of the human body and for our purposes, within homeostasis.

So then, what happens when the body is no longer in homeostasis? If you go back to our simplified analogy, you’ll find it suggests some aspect within the body has pulled a Darth Vader and gone to the dark side which can predictably have devastating consequences. This Star Wars analogy is also a stellar example for the pathogenesis of cancer as a cancerous cell is in essence simply a Darth Vader cell, but we will dive further into cancer a couple weeks from now (so stay tuned).

The thyroid gland is situated at the base of the neck and plays an important role in metabolism and development within the human body.1 The thyroid is glandular in nature meaning it secretes hormones and can therefore be categorized under dysfunctions of the endocrine system. Specifically, we can identify the type of thyroid dysfunction or disease by looking a little closer at where exactly regulation goes haywire. Regulation of the thyroid occurs through the hypothalamic-pituitary-thyroid (HPT) axis.1 It is important to understand the HPT axis encompasses the hypothalamus, anterior pituitary and thyroid gland which also stores the hormones T3 (triiodothyronine) and T4 (thyroxine).1 An appropriate feedback loop for the HPT axis is illustrated below:

As annotated in the figure, the hypothalamus releases thyrotropin-releasing hormone (TRH) allowing for positive feedback to the pituitary gland. The pituitary gland then produces thyroid-stimulating hormone (TSH) allowing for positive feedback to the thyroid gland. Lastly, the thyroid gland produces T3 and T4 allowing for negative feedback on hypothalamus and pituitary gland to decrease levels of TRH + TSH so homeostasis and balance is upheld within the body.

In the context of a thyroid gland, an appropriate regulation of homeostasis like the example above would be referred to as euthyroid, meaning everything is working as it should be and the force is in balance. When the force is unbalanced, we see cases of hypothyroidism and hyperthyroidism where your glands officially go to the dark side. The good thing about thyroid dysfunction is these processes are entirely predictable if you understand what goes wrong in what part of the loop.

I hope our little galactic journey through primary thyroid disorders has been informative and helpful. Notice how in both cases of primary hyperthyroidism and primary hypothyroidism, the negative feedback loop is still trying to work, it just does not matter because there is an autoimmune issue with the gland itself. Although the negative feedback loop is still there, the process fails due to either the destruction or dysfunction of the gland itself.

References

  1. DiPiro JT, Talbert RL, Yee GC, et al, eds. Pharmacotherapy: A Pathophysiologic Approach. 11th ed. McGraw-Hill; 2020.

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Hypertension: Why You Shouldn’t Take Your Stress With a Grain of Salt

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Although an estimated ~90% of high blood pressure cases are likely to be classified under the term “primary” or “essential” hypertension, we still have a very poor understanding of the etiology as a whole. As such, primary hypertension is often labeled as idiopathic, which is medical terminology for no identifiable cause that we are aware of at this time. We do, however, have an inkling for several risk factors which are associated with the development of hypertension.

In this post, we will attempt to break them down using a mnemonic that helps tie everything together. Can you think of what might be a good mnemonic for this cause? If you thought stress, you would be correct. We’ve all experienced stress at some point in our lives. Imagine yourself in peak rush hour traffic, the time is now 7:45 AM and your final starts at 8:00 AM. Can you feel your heart racing? The point stands that stress can exacerbate blood pressure and we think it is an excellent way to outline the following known risk factors:

As you soak in all these risk factors and suggested lifestyle changes, remember to consider the following: hypertension tends to be a disease state where adherence to therapy can be particularly troublesome. This is understandable as hypertensive patients generally feel no different but may still be expected to take several classes of medications, follow up routinely, and tolerate various adverse effects of medications that can interfere with their overall quality of life. Therefore, hypertension is known as a silent killer and as with any disease state, a solid line of communication is vital to ensuring appropriate therapy and patient satisfaction.

References

  1. Hypertension. IBM Micromedex. Truven Health Analytics/IBM Watson Health; 2020. Accessed December 26, 2020. http://www.micromedexsolutions.com.
  2. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71(6):1269-1324.

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A Brief Review on Dyslipidemia for Pharmacists

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  • General information:
    • Dyslipidemia is defined as a condition in which an individual has elevated cholesterol or lipids in an individual’s blood such as the following:
      • HDL: “Good” cholesterol
      • LDL: “Bad” cholesterol
      • Triglycerides (TGs)
    • LDL cholesterol can form plaques in vessels
    • HDL cholesterol helps remove LDL
    • TGs are formed in fat cells when calories are not burned right away
  • Symptoms:
    • Regarded as a silent disease in which patients are unaware of having it
  • Types and causes:
    • Primary dyslipidemia:
      • Inherited through genetics
    • Secondary dyslipidemia
      • Caused by lifestyle factors such as the following:
        • Obesity
        • Diabetes
        • Hypothyroidism
        • Alcoholism
  • Risk factors:
  • Review of lab values**:
 Total cholesterolHDL  LDLTGs
Desirable< 200> 40 (men) > 50 (women)  < 100< 150
Borderline200 – 239   130-159150-199
High  > 240     160-189  200-499  
Very high      > 190> 500

**All units are in mg/dL

  • Treatment options:
Class and Mechanism of ActionGeneric (Brand) NamesSide EffectsBlack Box WarningsContraindications
Statins: Inhibits the rate-limiting step for cholesterol synthesis by inhibiting HMG-CoA reductase   **first-line**Atorvastatin (Lipitor) Rosuvastatin (Crestor) Simvastatin (Zocor) Pravastatin (Pravachol) Pitavastatin (Livalo) Fluvastatin (Lescol) Lovastatin (Mevacor) Simvastatin + Ezetimibe (Vytorin)  Myalgia Arthralgia Myopathy Diarrhea Cognitive impairmentSkeletal muscle effects  

Hepatotoxicity (increased LFTs)		Pregnancy Breastfeeding  

Use with cyclosporine  

Active liver disease
Bile Acid Sequestrants: Inhibits absorption of bile acids into blood which ultimately aids in reducing LDL  Cholestyramine (Questran) Colesvelam (Welchol) Colestipol (Colestid)  Abdominal pain Cramping Flatulence Constipation Increased TGs Increased LFTs   Esophageal obstruction   Cholestyramine: Biliary obstruction  
Colesvelam: Bowel obstruction and TGs > 500
Fibrates: PPAR-α agonist; inhibits TG synthesis and decreases VLDLGemfibrozil (Lopid) Fenofibrate (Tricor)  Abdominal pain Dyspepsia Increased LFTs  
Upper respiratory tract infection (URTI)  		Risk of myopathy with concurrent statin use   Increased serum creatinine   CholelithiasisLiver disease Renal disease Gallbladder disease  

Use with repaglinide
PCSK-9 Inhibitors: Monoclonal antibodies that decrease LDLAlirocumab (Oraluent) Evolocumab (Repatha)Flu Cold URTI Injection site reaction   Urinary tract infection (UTI)    
2-Azetidinones: Inhibits absorption of cholesterol at the small intestineEzetimibe (Zetia)Myalgia Arthralgia Diarrhea URTI  Skeletal muscle effectsAvoid in patients with hepatic impairment
Fish Oils: Unknown mechanism of action    Omega-3 Acid (Lovaza) Icosapent Ethyl (Vascepa)Dyspepsia Flatulence Burping Increased LDLCaution in those with a fish/shellfish allergy 
Nicotinic acid/Vitamin B3: Decreases synthesis of VLDL, LDL, and TGs  Niacin (Niacor, Niaspan)Flushing Pruritis Nausea Vomiting Diarrhea Cough

Hyperglycemia Hyperuricemia  
Orthostatic hypotension  		Hepatotoxicity  

Rhabdomyolysis with concurrent statin use		Liver disease  

Arterial bleed  

Peptic ulcer disease
High-Intensity Statin Therapy (Lowers LDL on average by > 50%)Moderate-Intensity Statin Therapy (Lowers LDL on average by 30-49%)  
Atorvastatin 40-80 mg Rosuvastatin 20-40 mgAtorvastatin 10-20 mg
Rosuvastatin 5-10 mg
Simvastatin 20-40 mg
Pravastatin 40-80 mg
Lovastatin 40 mg
Fluvastatin 40 mg
Pitavastatin 2-4 mg  
  • Additional notes:
    • Statins
      • Patient must contact their doctor for any muscle symptoms or dark urine
      • Simvastatin, lovastatin, and fluvastatin must be taken at bedtime
      • Avoid gemfibrozil, niacin (> 1 gram), and colchicine
      • Simvastatin and lovastatin:
        • Avoid strong CYP3A4 inhibitors such as azoles, erythromycin, clarithromycin, HIV protease inhibitors, cobicistat, nefazodone, cyclosporine, grapefruit juice
    • Bile Acid Sequestrants
      • Take with food and water (colesevelam)
      • Space out with multivitamins
        • At least 4 hours of one another
      • ACC/AHA guidelines do not recommend use if TGs are > 300
    • Fibrates
      • Can increase LDL when TGs are high
      • Patient must contact their doctor for any muscle symptoms, dark urine, abdominal pain, nausea, or vomiting
    • PCSK-9 Inhibitors
      • Store in fridge
      • Prior to administration allow for syringe to warm up to room temperature for 30-45 minutes
        • Inspect for any particles and/or color changes
      • Rotate injection sites
        • Alirocumab and evolocumab: Subcutaneous injections given in the thigh, upper arm, or abdomen (except within 2 inches from belly button)
    • 2-Azetidinones (Zetia):
      • Avoid concurrent use with gemfibrozil
      • Monitor LFTs with concurrent statin or fibrate use
      • Give 2 hours before or 4 hours after bile acid sequestrants
      • Patient must contact their doctor for any muscle symptoms or dark urine
      • Concurrent use with cyclosporine may increase levels of both drugs
    • Nicotinic acid/Vitamin B3
      • Must be taken with food
      • Monitor LFTs
      • Niaspan:
        • IR: Flushing/itching
        • ER: Less flushing than IR; take at bedtime
      • Avoid spicy food and ethanol
      • Take 4-6 hours after bile sequestrant acids
  • Treatment algorithm:
Prevention type  SituationTreatment
        Primary preventionLDL > 190 mg/dLHigh-intensity statin  
Primary preventionAge 40-75LDL 70-189 mg/dLPatients with diabetesModerate-intensity statin, unless 10-year ASCVD risk > 7.5%  
Primary preventionEvaluating 10-year clinical atherosclerotic cardiovascular disease (ASCVD) score  ASCVD risk > 7.5%: high intensity statin
 
ASCVD risk > 5% but <7.5%: moderate-intensity statin  
Secondary preventionPatients with clinical ASCVD< 75 years old: high intensity statin 
> 75 years old: moderate-intensity statin  

We hope this review helped refresh your clinical knowledge on dyslipidemia!

Best of luck,

Sam Tamjidi

RxPharmacist Team

References:

  1. Micromedex Solutions. Greenwood Village, CO: Truven Health Analytics. http://micromedex.com/. Accessed October 30, 2020.

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What Pharmacists Need to know about Diabetes

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As per the Centers for Disease Control and Prevention (CDC), 34.2 million people, or 1 in every 10, in the United States have diabetes. Diabetes is 7th on the list of leading causes of death while the total estimated medical costs and costs associated with lost work and wages equates to an estimated $327 billion.

Diabetes, otherwise known as increased sugar levels (hyperglycemia) may be a result of decreased insulin secretion, decreased insulin sensitivity, or both. It can present itself in one of two forms of the following:

  • Type 1
    • Autoimmune destruction of beta cells
    • Loss of insulin production
    • Must use insulin injections
  • Type 2
    • Insulin resistance
    • Decreased insulin production over time
    • Associated with obesity, physical inactivity, family history
  • Signs and symptoms of diabetes include:
Signs and Symptoms of Diabetes
  • Risk factors:
Risk Factors for Diabetes
  • General Screening Criteria:
    • All patients with BMI greater than or equal to 25 kg/m2 + 1 risk factor
    • Children/adolescents with obesity + 1 risk factor
    • 45 years old if no risk factors are present
    • Pregnant women at 24-48 weeks
PrediabetesDiabetes
->Fasting plasma glucose (FPG) 100-125 mg/dL; or
->2-hour glucose after glucose tolerance test 140-199 mg/dL; or
->A1c 5.7-6.4%  		->Symptoms + random plasma glucose > 200 mg/dL; or
->2-hour glucose after glucose tolerance test > 200 mg/dL; or
->FPG > 126 mg/dL; or
->A1c > 6.5%  
  • Glycemic targets (per ADA guidelines):
    • A1c < 7%
    • 80-130 mg/dL pre-prandial plasma glucose
    • < 180 mg/dL post-prandial plasma glucose
    • A1c should be measured quarterly if not at goal
      • Or twice yearly if at goal
      • (A1c – 2) x 30 = average blood glucose
  • Drugs that may increase blood glucose levels:
Drugs that may increase blood glucose levels
  • Non-drug treatment options:
    • Smoking cessation
    • Weight loss
      • 3500 kcal weekly reduction = 1 lb weight loss
      • Waist circumference < 35 inches for females and < 40 inches for males
    • Nutrition
      • Carbs from vegetables, fruits, grains, and dairy
      • Omega-3 fatty acids and fiber
      • Limit saturated fat, cholesterol, and sodium
      • 15 g = 1 serving of carbohydrates
    • Physical activity
      • 150 min/week, moderate intensity
      • No more than 2 consecutive days off
      • Resistance training at least 2x/week
Drug treatments (oral medications)
  • Additional notes on oral drug classes:
    • Biguanides
      • Take with food
      • Use of alcohol increases the risk of lactic acidosis
      • Discontinue before any imaging with iodinated contrast; resume after 48 hrs
    • Meglitinides
      • Take 1-30 minutes before meals
      • If skipping a meal, skip dose as well
    • Sulfonylureas
      • Take with breakfast
        • Exception: Glipizide IR 30 minutes before breakfast
      • Glyburide – avoid in elderly and patients with renal impairment
    • Thiazolidinediones
      • Take with meals
      • May take weeks to take effect
      • Additional warnings:
        • Bladder cancer (pioglitazone only)
        • Risk of macular edema
        • Fracture risk
        • Hepatic failure
        • Resumption of ovulation
    • SGLT-2 Inhibitors
      • Caution when taking with diuretics and NSAIDs (due to risk of hypotension and acute kidney injury)
      • Additional warnings:
        • Genital infections
        • Hypotension
        • Increased LDL
        • Renal insufficiency
        • Ketoacidosis
      • Monitor K+ with Canagliflozin
    • DPP-4 Inhibitors
      • Take in the morning
Drug treatments (injectable medications)

Additional notes on injectable drug classes:

  • GLP-1 Agonists:
    • Exenatide and lixisenatide are administered 60 minutes before a meal
    • All others given without regard to food
  • Amylin Analog
    • Used in treatment of both type I and II diabetes
    • Reduce mealtime insulin by 50%

  • Drug treatments (Insulin)
    • For all insulins:
      • Side effects: weight gain
      • Warnings; hypoglycemia, hypokalemia
      • Never use pens for more than one individual
      • Most are 100 units/mL concentration
      • High risk medications
    • Dosing strategies
      • Basal insulin
        • Long or intermediate acting
        • Mainly affect fasting blood glucose
      • Bolus insulin
        • Rapid or short acting
        • Two purposes:
          • Prandial (mealtime) & correction (acute elevation)
Drug treatments (Insulin medications)
  • Insulins that do not require a prescription:
    • Regular insulin, NPH, and the premixed 70/30 combination
  • Insulin dosing for Type I diabetes:
    • Rapid-acting and basal insulin preferred
    • If using NPH and regular insulin
      • 2/3 NPH, 1/3 regular
    • Initiating basal/bolus insulin:
      • Calculate total daily dose (TDD)
        • 0.6 units/kg/day using TBW
      • Step 2: Divide TDD
        • 50% basal
        • 50% bolus
      • Step 3: Divide the bolus among 3 meals
    • Based on the amount of carbohydrates in a meal, meal-time insulin can be adjusted using rule of 500 (rapid-acting insulin) or rule of 450 (regular insulin)
      • (500 or 450)/TDD = g of carbs covered by 1 unit of insulin
  • Correction factor/dose
    • Factor:
      • Determines how much blood sugar will drop for every 1 unit of insulin. Uses the rule of 1800 (rapid-acting insulin) or rule of 1500 (regular insulin)
        • (1800 or 1500)/TDD = correction factor for 1 unit of insulin
  • Dose:
    • Amount of insulin required to bring blood glucose back to normal: [(blood glucose now) – (target blood glucose)]/   correction factor = correction dose
  • General treatment algorithm for Type II Diabetes:
General treatment algorithm for Type II Diabetes
  • For A1c greater than or equal to 8.5%: Jump straight to dual treatment
  • A1C > 10%: Think insulin
  • Cardiovascular benefit:
    • GLP1 agonists: liraglutide, semaglutide, exenatide
    • SGLT2 inhibitors: empagliflozin, canagliflozin
  • Patient-specific factors
    • Drugs that minimize hypoglycemia:
      • DPP4 inhibitor, GLP1 agonist, SGLT2 or TZD
    • Drugs that promote weight loss:
      • GLP1 agonist or SGLT2 inhibitors
    • Drugs with cost concerns:
      • Sulfonylurea or TZD
  • Combinations to avoid:
    • DPP4 inhibitors + GLP1
    • Sulfonylureas + insulin
  • Insulin dosing for Type II diabetes:
    • Initiate basal insulin after patient fails to reach or maintain goal on multiple oral therapies
    • Starting dose: 0.1-0.2 units/kg/day or 10 units/day
    • Titrate by 10-15% or 2-4 units once or twice weekly until fasting blood glucose at goal
    • If patient reaches fasting blood glucose goal but their A1c is still above goal:
      • Consider the addition of rapid acting mealtime insulin or GLP-1 agonist
  • Insulin administration:
    • Abdomen is the injection site (avoid belly button)
    • May also inject in thighs, buttocks, arms
      • Be consistent with administrations
    • Prime before each dose
    • Rotate sites
  • Hypoglycemia is common with insulin products, thus important to be aware of what to look out for and how to treat it
    • Defined as a blood glucose < 70 mg/dl
    • Symptoms: sweating, pallor, irritable, hunger, lack of coordination, sleepy
      • Beta blockers mask most except hunger and sweating
    • Treatment
      • Consume 15-20 g of glucose/simple carbohydrates
      • Recheck glucose levels after 15 minutes
      • Repeat if needed
      • Eat a small meal/snack to prevent recurrence
    • Glucagon is used only if patient is unconscious
  • Diabetes in pregnancy
    • Gestational diabetes: during pregnancy
      • Risks
        • Macrosomia
        • Hypoglycemia at birth
        • Obesity and type 2 diabetes
      • Management
        • Lifestyle modifications
        • Insulin added if needed (preferred)
        • Metformin and glyburide used
      • Goals:
        • Fasting < 95 mg/dL
        • 1-hour post-meal less than or equal to 140
        • 1-hour post-meal less than or equal to 120

We hope this review helped refresh your clinical knowledge on diabetes. Next up, we will take a look at dyslipidemia.

Best of luck,

Sam Tamjidi

RxPharmacist Team

References:

  1. National Diabetes Statistics Report, 2020. Centers for Disease Control and Prevention. https://www.cdc.gov/diabetes/data/statistics-report/index.html. Accessed October 26, 2020.
  2. Micromedex Solutions. Greenwood Village, CO: Truven Health Analytics. http://micromedex.com/. Accessed October 26, 2020.

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A Brief Review on Hypertension for Pharmacists

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With so many organ systems, disease states, and medications to remember, preparation for the NAPLEX may often times seem like a daunting task. While there can be a considerable amount of material to go over for each clinical module, there are certainly some things that deserve more focus than others. This brief review will cover some of the most important information you need to know about hypertension when preparing for your upcoming exam.

General information:

  • Hypertension (HTN) is asymptomatic
  • HTN increases the risk for heart attacks, strokes, and kidney failure
  • Risk factors include the following:
    • High sodium and fat diet, physical inactivity, obesity, tobacco use, excessive alcohol consumption, genetics and family history, age, sex (women more likely than men), and race (African Americans more likely than any other race)
    • Drugs can also increase blood pressure, including the following:
      • Amphetamines, cocaine, pseudoephedrine, immunosuppressants, Nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, ethanol, caffeine, serotonin and norepinephrine reuptake inhibitors (SNRIs), oral contraceptives, erythropoietin

Blood pressure categories:

 Ultimate blood pressure goal:

  • 130/80 mmHg

Treatments:

Four preferred drug classes for the following patient subgroups:

  • Non-African American: Thiazide diuretic, CCB, ACE inhibitor or ARB
  • African American: Thiazide diuretic
  • Patients with chronic kidney disease or diabetes with albuminuria ACE inhibitor or ARB
  • Initiate two drugs regimens if blood pressure is > 150/90 mmHg

Additional information:

  • ACE inhibitors, ARBs, Aliskiren
    • Do not use with Entresto
    • Do not use any combination of ACE inhibitors, ARBs, and aliskiren for treatment
  • CCBs
    • CYP3A4 substrates, avoid CYP3A4 inhibitors (eg, grapefruit)
    • Caution with ankle swelling and/or irregular heartbeat
    • Amlodipine and felodipine are the safest to use in patients with HF
  • BBs
    • No longer preferred for HTN treatment
      • Primarily used first-line for heart disease, post myocardial infarction, and HF
    • Use with caution when taking other drugs that decrease HR
    • Mask symptoms of hypoglycemia
  • Diuretics
    • Take doses in the morning or afternoon to avoid frequent urination symptoms at night
    • Provide K+ supplementation to compensate for decreased K+ levels
      • This does not remain true for K+ sparing diuretics
  • Hypertensive emergency
    • Blood pressure > 180/120 mmHg
    • Acute organ damage
    • IV medication used for treatment
      • Clevidipine, nicardipine, diltiazem, verapamil, enalaprilat, esmolol, labetalol, metoprolol tartrate, propranolol, nitroglycerin, nitroprusside, chlorothiazide
    • Goal is to decrease blood pressure by < 25% within first hour
  • Hypertensive urgency
    • Blood pressure > 180/20 mmHg
    • No organ damages
    • Oral medication for treatment
  • Pregnancy
    • Treatment with labetalol, methyldopa or nifedipine XR

Treatments (non-pharmacological):

  • Lifestyle modifications
    • DASH diet, limit salt intake (<1,500 mg/day), exercise, limit alcohol consumption, maintain proper weight (BMI between 18.5 – 24.9)

Be on the look-out for our next review, which will focus on diabetes.

Best of luck,

Sam Tamjidi

RxPharmacist Team

References: Micromedex Solutions. Greenwood Village, CO: Truven Health Analytics. http://micromedex.com/. Accessed October 12, 2020.

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Creating an edge over other PharmD graduates

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It has always been my top-priority goal to gain experiences that would further my personal and professional development which made this position an especially enticing one. Throughout pharmacy school, my unique experiences in diverse work settings and industries helped create a necessary edge over other Doctor of Pharmacy graduates. Although my post-doctoral fellowship was cancelled due to COVID-19, RxPharmacist allowed me to continue to have a productive summer as I developed new skills to become a more marketable Doctor of Pharmacy graduate.

My experience aligned perfectly with my growth mindset as I grew to overcome obstacles that came with completing new projects. Beyond the expected technical skills from content creation and remote communication, I was also exposed to start-up culture and entrepreneurship. My cohort was able to participate in brainstorming sessions on business and marketing strategy that management provided instant feedback on. The mentorship and network development also made it easy for my cohort to connect and support each other in their career trajectory.

Through RxPharmacist, I improved my knowledge of NYS pharmacy law, technical writing, and the test prep start-up industry. I welcome any students and graduates with questions to contact me here: https://www.linkedin.com/in/joan-cheung/

-Joan Cheung

St. John’s University, 2020 PharmD Graduate

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Networking, mentorship, and a preceptor that rocks!

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If you are looking for a great opportunity to jump start your pharmacy career, while gaining valuable firsthand experience and mentorship from an amazing group of people, look no further! The summer graduate internship offered by RxPharmacist is a great program that I would highly encourage to any PharmD student.

When I first joined the team, I was not sure what to expect. I knew that I had a deep interest for medical writing and joining the RxPharmacist team seemed to be the perfect opportunity for post-grad. But, RxPharmacist is so much more than just writing MPJE guides. Being a summer intern afforded me the opportunity to work with amazing pharmacists and other recent graduates. The best part of the program was the mentorship and guidance that I received from my preceptor. While working and studying for your licensure exams FROM HOME, you will also be able to receive the support and guidance you need as you transition from being a student to a true professional!

I would strongly encourage any pharmacist student to consider internship opportunities with RxPharmacist. Not only would you be rewarded as you study for your licensure exams, but you would also be gaining valuable experience and insight to the world of medical writing, marketing, business strategy, and effective networking.

Nnenna I., 2020 RxPharmacist Graduate Summer Intern

Husson University, Class of 2020

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Intern Testimonial- Getting a helping Hand Among COVID-19

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Prior to the completion of pharmacy school there were a lot of questions as to which direction of pharmacy I wanted to pursue. With the many conflicts surrounding job saturation and COVID-19, I was quick to realize it would be in my best interest to become more open-minded towards other career opportunities. Coming across the graduate intern position at RxPharmacist started off as nothing more than curiosity, but now, after completion of the program, I can say with full confidence it was one of the best life decisions I have ever made. 

At RxPharmacist, communication and support is transparent. You work with a team that truly cares about your performance and future career. Not only do they provide constant feedback on your work, but they also create the time to communicate with you to reflect on your resume and cover letter, while assisting you in expanding your professional network. The 10-week program is more than creating a study guide, it’s an opportunity to gain additional insight and hands-on skills that focus on medical writing, entrepreneurship, and marketing. 

The development of your very own study guide will not only aid yourself in passing the MPJE on the first try, but it will also support the pharmacy profession as a whole by helping all other newly graduates succeed as well. I am extremely grateful for the opportunity I had with RxPharmacist and I highly recommend this to anyone seeking experience!

Sam T., 2020 RxPharmacist Graduate Intern

Mercer University, Class of 2020

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Supporting our pharmacy profession: Team Member Testimonial

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My journey with RxPharmacist started with a post on my pharmacy class’s Facebook page asking for help to contribute to their Florida MPJE guide. I reached out and volunteered to help. This experience was very valuable as it helped me develop my writing skills, work within a team with other pharmacy graduates around the State of Florida, and helped me study for the MPJE exam. After I found out I passed the MPJE, there was no way I could take another one.

Little did I know, a year later, I would be moving to Washington, DC. I was researching online for study materials for the DC MPJE, but had little luck in finding materials. That is when I came across RxPharmacist again. I reached out asking if there were any DC MPJE study materials available. Fortunately, I was presented with an opportunity to author a DC MPJE Guide with RxPharmacist. I was already working as a pharmacist and my job was very demanding; however, the RxPharmacist team was very flexible with allowing me to write the guide at my own pace within the time frame requested. This opportunity closely aligned with my goals to help the pharmacy profession and improve my writing skills. Thank you RxPharmacist for another great experience! Best of luck to all current and future pharmacists on your MPJE exams!

Chrissy T., Pharm.D., 2020 Medical Writing Associate

University of Florida College of Pharmacy, Class of 2019

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