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FNP I Final Review Powerpoint Questions

HTN
● What is the difference between HTN and White Coat HTN?
○ White coat HTN is when the patient is hypertensive in the office setting, but normotensive
outside of the office setting. Recommend home blood pressure monitoring before prescribing
anti-hypertensives and consider 24-hour ambulatory monitoring.
HLD
● What are the causes of hyperlipidemia?
○ Primary
■ Genetics
■ Genetic mutation (single gene); Heterozygous
■ Chol levels are usually 2-3x the normal LDL levels
● in adults, > 190 and in children, > 160
■ Prevalence is 1:200
■ Usually don't require genetic testing unless uncertainty in dx
○ Secondary
■ Lifestyle: diet high in saturated fat (affects mostly the LDL), exercise, ETOH (biggest

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effect on HDL - can have a positive effect on HDL unless excessive intake; will also

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increase triglyceride levels), smoking, obesity

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■ Chronic diseases: DM, hypothyroidism, nephrotic syndrome (lowers HDL), menopause

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(accelerate increase of LDL in year following menopause), obstructive liver disease, CRF
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■ Drugs: anabolic steroids and HIV drugs can cause low HDL; progestins, synthetic
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steroids, glucocorticoids, amiodarone or protease inhibitors, and thiazides (high doses)
can cause increased LDL
● How would you work a patient up for these causes?
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○ UA (proteinuria)
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○ TSH
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○ LFTs
○ HgbA1c and fasting blood glucose
● What medication and at what dose would you start a patient on with hyperlipidemia?
○ Statins remain 1st line therapy
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○ Pts with DM do not need a ASCVD - they just get started on a moderate dose statin
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○ Someone 40 - 75 yrs who isn't being tx'ed for hyperlipidemia, do 10 yrs ASCVD risk. If > 7.5%
then TREAT; if 5 - 7.5% then consider treat w/ moderate dose statins.
○ Pediatrics - Lifestyle modification first; Then start LOW and titrate SLOW unlike w/ adults who
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have high LDL or have ASCVD risk > 7.5% where you would start with high dose statin.
○ Elderly - Start with a moderate dose statin therapy for secondary prevention (pt who has known
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heart disease and elevated cholesterol levels) instead of a high dose statin.
● How would you treat a patient with hypertriglyceridemia?
○ Drugs Affecting Lipoprotein Metabolism -
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■ Fibric Acid (Gemfibrozil, fenofibrate, etc) Indicated for ppl w/ severe


hypertriglyceridemia > 500.
■ Long Chain Omega 3 Fatty Acids - At 4 gm / day, trigs can be lowered 45%; will also
have an effect on LDL and can raise HDL.
○ Statins
■ Lower trigs by 7-30%
○ Nicotinic Acid
■ Lowers trigs by 7-30%
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● Diet changes for a person with hypertriglyceridemia?
○ Decrease ETOH
● Diet changes for a person with elevated LDL?
○ Decreased intake of cholesterol and/or trans fatty acids. Decreased intake of animal products
and red meat.
● Diet changes for a person with low HDL
○ Increased intake of vegetables, fruits, low fat dairy products, whole grains, fish, poultry, beans,
non-tropical vegetable oils, and nuts. Avoidance of red meat, sugary drinks, and sweets. Limit
sodium intake and intake of saturated and trans fat.
● What if a patient has both elevated cholesterol and triglycerides?
○ For hypertriglyceridemia, add fenofibrate, niacin, or omega-3 fatty acid to medication regimen,
along with statin therapy
● What are the non-pharm options for treatment?
○ Lose weight if obese or overweight (maintain health BMI)
○ Healthier diet with more fruits and vegetables and less red meat and animal products. Limit
saturated and trans fat to less than 5-6% of calories. Limit sodium to 2,400 mg/day.
○ Less ETOH consumption or no ETOH consumption
○ Start exercise program (moderate-vigorous aerobic activity, atleast 40 minutes, 2-4 times a
week)

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○ Tobacco cessation

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● Understand the side effects of statins, from mild to severe

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○ Statins - mainstay; no evidence that combo/monotherapy with other meds effective in decreasing

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ASCVD risk

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○ **Do not add gemfibrozil to statin therapy; increased risk of myositis/rhabdomyolysis
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○ Statins - headache, rash, fatigue, myalgia, myositis → rhabdomyolysis,
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elevated liver enzymes/liver dysfunction, increased risk of DM
○ Bile acid sequestrants - can interfere with absorption of other meds; constipation,
bloating/fullness, flatulence, nausea; contraindicated if triglycerides >300
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○ Nicotinic acid - flushing sensation; may be reduced by taking 325 mg ASA prior to taking med;
low compliance with multiple doses/day; check uric acid - may elevate, peptic ulcers, GI
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disturbances
○ Fibric acids - may increase LDL; well tolerated, work especially for triglycerides >500;
contraindicated if GFR <30, GI disturbances, cholelithiasis, hepatitis
○ Cholesterol absorption inhibitors - check liver function, discontinue if ALT elevated >3x
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baseline; diarrhea, arthralgia, rhabdomyolysis, hepatitis, pancreatitis, thrombocytopenia


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○ Long chain omega 3 FA - 2-4 gram/daily to be effective; nausea, dyspepsia, rash, increased
bleeding time, elevated fasting BG, unpleasant aftertaste
● Be aware of drug interactions with statins - which drugs can particularly have a serious
interaction with statins.
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○ Do NOT add gemfibrozil (Lopid) to statin therapy due to increased risk of myocitis and
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rhabdomyelitis.
○ Other medications that interact with statins and increase patient’s risk for
myopathy/rhabomylosis include Macrolides, Itraconazole, Gemfibrozil, Cyclsporine, Niacin, and
Danazol.
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● What would be your physical and lab findings if a patient has a side effect of a statin?
○ Muscle aches and weakness
○ Elevated CK
○ ***CPK is preferred test in patients presenting with muscle signs/symptoms, because CPK is
more sensitive and specific than other labs***
● Myopathy vs Rhabdo
○ Myalgia
■ Muscle aches or weakness WITHOUT elevated CK

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■ Least severe and most common presentation
■ Patients can be reassured and remain on statin therapy
○ Myositis
■ Myalgia or weakness WITH elevated CK < 10 times upper level normal (ULN)
■ Statin should be discontinued
■ Once statin is discontinued, CK will return to normal and there is no long-term adverse
effects
■ Statin therapy should be reinitiated once CK levels return to normal
○ Rhabdomyolysis
■ Muscle symptoms with VERY HIGH (>10 times ULN), increased serum Creatinine, and
myoglobinuria
■ Most severe and least common presentation
■ May lead to renal failure
■ Risk from statins is < 0.5%
■ Present with urinary myoglobin and renal insufficiency
■ CK and myoglobin is released into the circulation
■ More common in patients on combination therapy, especially in patients on statin and
gemfibrozil
● How would you evaluate?
○ To evaluate for adverse muscle symptoms related to statins, check CK, LFT’s, Creatinine

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(serum), and do a urinalysis (check for urinary myoglobin and renal insufficiency).
○ Some patients may have a mild CK elevation that is unrelated to statin therapy.

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○ Mild elevations of CK can occur following exercise, especially in patients who run.
○ Mild elevations of CK are also common in patients who experience blunt force trauma or muscle

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cramping, so always evaluate patients for secondary causes of muscle symptoms.
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● What would you do? Stop it, change it, change the dose?
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○ Discontinue the statin until symptoms can be evaluated and until the cause of symptoms can be
determined.
○ If muscle symptoms, or elevated CK do not resolve after 2 months off of statin, consider other
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causes of muscle symptoms.


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○ If muscle symptoms resolve and no contraindications exist, restart the patient on the same or
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lower dose of original statin to establish a causal relationship


○ If causal relationship exists, discontinue original statin and use lower dose of another statin
○ Once low dose of statin is tolerated, gradually increase the dose as tolerated to the maximum
tolerated dose
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○ If persistent muscle symptoms are unrelated to statin therapy or the predisposing condition has
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been treated, resume statin therapy at original dose


● Evaluation and management
Diabetes
● Understand the pathophysiology of Type 2 Diabetes
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● Physiologically how type 2 DM changes over time and what can affect the changes
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● What is the diagnostic criteria for pre-diabetes


○ Impaired fasting glucose (IFG) result of 100-125 mg/dl
○ Impaired glucose tolerance (IGT) result of greater than/equal to 140, 2 hours after glucose drink
and < 199 mg/dl
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○ A1C of 5.7-6.4%
● What are the indications of pre-diabetes in history, physical and lab results
● What are your management options for patients dx’d with pre-diabetes (when if ever would you
decide to start meds? What lifestyle changes would you recommend?)
○ Diet should be well balanced and consist of complex carbohydrates
○ Consider having patient see a dietician

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○Patients should exercise, if they don’t currently. Patients may say that their job is exercise, but
the definition of exercise is above/beyond their daily activity. Patients should exercise 5 times a
week for 30-40 minutes as their goal
○ Patients should lose weight and set realistic goals, such as 10% of their body weight over the
next 6 months
○ Patients should control their blood pressure and lipids
○ Therapeutic Drugs
■ Metformin is the medication of choice for pre-diabetes
■ Consider drug therapy after giving the patient atleast three months to make lifestyle
modifications
■ After three months, repeat the patient’s blood work to see how their values have
changed
■ If patient isn’t doing well after three months of lifestyle modifications (A1C or fasting
glucose is worse), add a medication.
■ Medications can be considered right away, without three month trial of lifestyle
modifications, if when you initially diagnose the patient with pre-diabetes, their FBS is
120 or higher (close to being full blown diabetic)
● When should you start pre-conceptual counseling
○ All women of childbearing age (at puberty) and even before that

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○ Do it at every well visit due to the rate of unplanned pregnancies being so high

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○ Pre-conceptual care in women with diabetes appears to reduce the risk of morbidities in infants

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● What are the goals of pre-conceptual counseling in a diabetic patient

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○ Educate patient on the risks of having diabetes and becoming pregnant, which include

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spontaneous abortion, fetal anomalies, fetal demise, pre-eclampsia, macrosomnia, pre-natal
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hypoglycemia, and an increased risk of the baby having diabetes.
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○ Inform patient that major medical malformations remain the leading cause of mortality and
serious morbidity in infants born to mothers with diabetes (either type 1 or type 2)
○ Inform patients that the goal is to keep their A1C as “normal as possible.” For a healthy woman
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who is contemplating becoming pregnant, the more their A1C is controlled, the less their risk of
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complications in the pregnancy.


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○ Inform patient that statins, ACEs, ARBs, and non-insulin therapies are contraindicated in
pregnancy, so if they are on these drugs and don’t want to be pregnant, they should be on a
contraceptive and use it 100% of the time they are sexually active. If planning a pregnancy, and
on these drugs, refer patient to an OB and/or endocrinologist to discuss their options.
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● Diagnosis Criteria - what is the diagnostic criteria to diagnose a patient w/ diabetes?


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○ You have three choices: (What results would you expect to dx someone w/ DM?)
■ Fasting plasma glucose (second best option)
● More sensitive than hemoglobin A1C, but less sensitive than glucose tolerance
test.
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● Make sure the patient is truly fasting for 8 hours before lab draw (only allowed to
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have water and black coffee when fasting for labs)


● Normal: < 100
● Pre-Diabetic: 100-125
● Diabetic: > 126
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■ Hemaglobin A1C (third best option)


● Not great for detecting pre-diabetes, but good for detecting diabetes
● Need elevated blood sugars for over 3 months to get accurate A1C, which
patients might not have with pre-diabetes
● There are also genetic variations with hemoglobin A1C (in African Americans,
Asians, and Mediterranean heritage). Patients with these genetic variations do
not have accurate hemoglobin A1Cs.

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Patients’ A1C can also be inaccurate if they have hemoglobin abnormalities, such
as liver or kidney disease, iron deficiency anemia, or any condition that affects
RBC turnover/count will affect A1C
■ Glucose tolerance test (BEST OPTION*)
● The most accurate test for detecting pre-diabetes and diabetes
● Give the patient a 75 gram carbohydrate load, then test their plasma glucose in 2
hours
● Not diabetic: < 140
● Pre-diabetic: >140- <199
● Full blown diabetes: > 200
● Evaluation - pertinent aspects of the history, ROS (s/s of complications of DM, what would they
exhibit?)
● Management
○ When to start a medication
○ What med would you consider starting
■ Metformin
○ When would you change medications and what would you change to?

○ What if a patient also has HTN?

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○ Goal of treatment

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■ Who should strive for tight control vs loose control?
● Management

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○ Are there special concerns in managing children with diabetes versus adults - growth
and development, self esteem issues etc.

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■ In children, there’s a more rapid progression decline in beta cell function, which means
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children will need insulin sooner than if they were diagnosed with type 2 diabetes as an
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adult. This also means that in children, there is an accelerated development of
complications.
■ With children, there are complex psychosocial/cultural considerations, which make it
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harder to get lifestyle changes going. Need to work with the schools and parents, and
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possibly get social workers involved.


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■ 6% of pediatric patients with diabetes may present with DKA. DKA doesn’t mean the
patient is automatically type 1 diabetic.
■ There are only two medication options for children, which are Metformin and Insulin. All
other hypoglycemics have not been approved for use in children.
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