FR Review 9 - Hyperlipidemia, Antihistamines, Steroids, Chemo Flashcards

1
Q

In summary, what is the major effect of each class of the hyperlipidemia medications?

A

Statins: decrease LDL
Bile Acid Sequestering Agents: decrease LDL
Niacin: increases HDL with some decrease in triglycerides
Fibrates: decrease triglycerides
Omega-3 Fatty Acids: decrease triglycerides
Cholesterol Absorption Inhibitors: as an adjunct only to help decrease LDL

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2
Q

What drug class is the most effective at lowering LDL?

A

Statin drugs

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3
Q

What effect do statin drugs have on LDL, HDL, and triglycerides?

A

LDL: decrease
HDL: slight increase
Triglycerides: decrease

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4
Q

What is the benefit of increasing HDL?

A

HDL is responsible for transporting other cholesterols back to the liver to be recycled

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5
Q

Why is it theorized that statin drugs may reduce inflammation?

A

Statins cause a reduction in CRP. CRP is a marker of inflammation.

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6
Q

Differentiate older statins from newer statins in terms of how they are administered?

A

Older: should be taken at night because they have a short half-life and cholesterol is mostly made during sleep
Newer: can be taken at any time because they have a longer half life

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7
Q

Describe the AEs of statin drugs

A

Few AEs –> they are generally well tolerated
Statins can cause myalgias and cause rhabdomyolysis –> less common than most people believe
GI complaints: dyspepsia, heartburn, abdominal pain –> most frequent AE
AST and ALT can rise depending on dose

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8
Q

What is the mechanism of action of Bile Acid Sequestering Agents?

A

They bind to and sequester bile acids in the colon so they are not absorbed. The subsequent decrease in bile acids causes the liver to attempt to make more bile acids. In this process, the liver consumes more cholesterol and LDL decreases.

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9
Q

In what way do bile acid sequestering agents negatively impact lipids?

A

They increase triglycerides –> Triglycerides cannot be processed without bile acids.

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10
Q

What two drugs do bile acid sequestering agents interact with and how is this managed?

A
  • Warfarin and Levothyroxine –> they stick to the bile acid sequestering agents and are not absorbed.
  • Space administration of bile acid sequestering agents from drugs they interact with.
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11
Q

How is niacin used?

A

As an adjunct with another lipid lowering agent to raise HDL.

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12
Q

What side effects might patients complain of after taking niacin and why and how might this be mitigated?

A

Facial flushing and headaches because niacin causes release of prostaglandins.
Take an NSAID with niacin to lessen release of prostaglandins

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13
Q

What three conditions can be exacerbated by taking niacin?

A

Hepatotoxicity, Hyperglycemia, Peptic Ulcer Disease

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14
Q

Describe the use of cholesterol absorption inhibitors?

A

Always used as an adjunct with another lipid agent to decrease LDL

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15
Q

Name the only cholesterol absorption inhibitor available.

A

Ezetimibe

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16
Q

What are the AEs of cholesterol absorption inhibitors?

A

Not well tolerated –> GI distress, abdominal pain, diarrhea, steatorrhea

17
Q

Describe the mechanism of action of PSK9 inhibitors.

A

PSK9 is an enzyme that metabolizes LDL receptors in the liver. By inhibiting the enzyme, LDL receptors in the liver increase and more LDL is pulled into the liver for recycling and elimination.

18
Q

What are the disadvantages of PSK9 inhibitors?

A

They are expensive and must be injected sub-Q

19
Q

Differentiate allergic rhinitis from non-allergic rhinitis?

A

Allergic rhinitis is caused by an increase in histamine (HST)
Colds cause rhinitis due to an increase in Ach

20
Q

If someone has a cold, would a sedating or non-sedating antihistamine be more effective?

A

Sedating because they have anti-Ach properties and Ach is the cause of rhinitis in a cold.

21
Q

What are the two primary indications for hydroxyzine?

A

Anxiety and pruritis –> used a lot in the ED for poison ivy

22
Q

When an antihistamine product is followed by the letter D (Ex, Claritin D) what does this mean and what two drugs are added?

A

The antihistamine is coformulated with a decongestant.

The antihistamine is combined with either pseudoephedrine or phenylephrine.

23
Q

In what patients would you want to avoid use of antihistamine-D products and why?

A

Patients with HTN because decongestants are alpha-1 agonists that provide vasoconstriction.

24
Q

Describe 7 AEs of steroids administration.

A

Hyperglycemia from gluconeogenesis and decreased use of glucose in the periphery
Catabolism and reduced anabolism
Osteoporosis with increased calcium excretion
Delayed growth in children
Fat deposition in the shoulders, face, and abdomen
Reduced healing
Suppress allergic responses and Ab production

25
Q

What dose of steroids is required to suppress the HPA axis and decrease endogenous steroid production?

A

At least 20mg of prednisone or equivalent for at least 14 days

26
Q

If a patient is on enough steroids to suppress their HPA axis, what will result from rapid withdrawal of the drug?

A

Acute adrenocortical insufficiency

27
Q

In patients on enough steroids to suppress their HPA axis, when might a clinician need to increase their dose?

A

During the course of stressful events (surgery for ex) - aka stress dose steroids

28
Q

What is the typical dose for stress dose steroids and what would the dose be for a minor procedure?

A

Typical: 50-100mg hydrocortisone IV

Minor procedure: 20mg hydrocortisone PO

29
Q

What differentiates leukocytosis due to demargination from leukocytosis due to an infection?

A

Infection shows a left shift –> increase in immature WBCs called bands

30
Q

List the hydrophilic steroids and their uses.

A

Triamcinolone - joint injections and topical agents

Beclomethasone, budesonide, fluticasone, mometasone, ciclesonide –> inhaled

31
Q

What is the most lipophilic steroid?

A

Dexamethasone

32
Q

What is the overriding goal of cytotoxic chemotherapy?

A

Drugs kill healthy and cancerous cells - goal is to kill the cancer without killing the patient

33
Q

T/F: Cytotoxic agents kill healthy cells at the same rate they kill cancer cells.

A

False: They tend to kill cancer cells faster because cancer cells are replicating more quickly.

34
Q

Of healthy cells, which will be affected first by cytotoxic drugs.

A

Rapidly dividing cells –> bone marrow, GI, hair, etc.

35
Q

Describe how dosing of cytotoxic agents is different than most other drugs.

A

Typically, drugs are dosed to efficacy - we give as much as possible to have the most positive effect. Cytotoxic drugs are dosed to toxicity - we give the max amount we can give without the drug killing you.

36
Q

What is another name for targeted therapy agents and how is this clinically relevant?

A

Cytostatic agents because they mostly inhibit cancer cell growth signals.
They prevent tumor growth rather than destroying the tumors. Only cytotoxic agents destroy tumors.

37
Q

Describe how cytostatic drugs are administered?

A

They are usually given continuously rather than in on-off cycles like cytotoxic agents.

38
Q

Other than simply being targeted agents, state why cytostatic agents are less toxic than cytotoxic agents.

A

They are dosed based on efficacy as opposed to cytotoxic agents which are dosed to toxicity.

39
Q

What are the common AEs associated with cytostatic agents?

A

EGFR - receptor blocked by cytostatic agents that cause skin rashes and other effects (including conjunctivitis and dry eyes)
VEGF - receptor blocked by cytostatic agents that inhibits angiogenesis (CV effects)