HTN, dyslipidemia, obesity, metabolic disorder Flashcards

1
Q

What is the definition of hypertension?

A

Defined by determining the levels of BP that cause target organ damage, morbidity, and mortality as material flow is delivered

  • CO x PVR = BP
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2
Q

How would a provider diagnose HTN?

A

Two elevated BP readings on two separate occasions at least two weeks apart

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3
Q

Primary vs secondary HTN

A

Primary - 95% of all HTN, there is no known cause (due to genetics, environment)

Secondary - directly attributable to structural, circulatory, or chemical abnormalities (e.g. pheochromocytoma)

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4
Q

What should the provider do if primary HTN is diagnosed in children at 10 years old?

A

Order initial labs (CBC, ESR, CRP, UA, renal function panel)

  • Start screening at 3 years old or earlier if there is a clinical concern
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5
Q

How does DBP change later in life?

A

DBP levels off or drops in the 50th decade of life

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6
Q

How does SBP change later in life?

A

SBP rises with advanced age

  • If SBP is =/> 160 in the elderly (older than 85 years old), will have increased risk of stroke
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7
Q

True/false: HTN symptoms usually only occur after end organ damage

A

True - may also be asymptomatic

  • End organ damage signs: diabetic nephropathy, Cushing’s syndrome
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8
Q

HTN risk factors

A
  • Genetics
  • Obesity
  • Dyslipidemia, LVH, glucose intolerance, OSA, family history
  • Metabolic syndrome
  • High dietary fat and sodium
  • Lower potassium and magnesium intake
  • Physical inactivity
  • Excessive alcohol intake
  • Smoking
    • Stress
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9
Q

HTN physical exam components

A
  • Obtain BP and HR in each arm twice
  • Auscultate carotid and aortic arteries
  • Perform fundoscopy
  • Obtain height and weight
  • Assess for evidence of end organ impairment and secondary causes for HTN
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10
Q

HTN diagnostic studies

A
  • UA
  • CBC, potassium, BUN, serum creatinine, calcium, uric acid
  • Fasting blood glucose
  • Lipoprotein
  • EKG (to identify LVH)
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11
Q

JNC 8 HTN diagnostic criteria

A
  • Under 60 years - BP >140/90
  • +60 years - BP >150/90
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12
Q

ASH/ISH HTN guidelines

A

BP >130/80 in adults and elders

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13
Q

African Americans respond better to what classification of BP medication? Asian Americans?

A

African Americans - diuretics (thiazides), CCB

Asian Americans - CCB, ARB

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14
Q

First line HTN medication for patients with diabetes and CKD

A

ACE inhibitor (including black patients)

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15
Q

If patient’s BP continues to be >160/100, they will need to start combo therapy with which two medication classes?

A

Thiazide and ACE inhibitors

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16
Q

When should a patient with HTN go to the ED?

A
  • BP >180/120
  • Individual has signs of target organ dysfunction
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17
Q

When is a specialist referral indicated for patients with HTN?

A

If HTN is resistant to therapy (failure of three full dose, or maximally tolerated, antihypertensive drugs, including a diuretic)

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18
Q

Non pharmacologic management of HTN

A
  • Lifestyle modifications
  • Regular exercise
  • Healthy weight
  • Tobacco cessation
  • Reduction of daily dietary sodium to <2,300 mg
  • Moderation of alcohol intake
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19
Q

Four common medication classes used to treat HTN

A
  • ACE inhibitors
  • ARBs
  • Thiazide diuretics
  • CCB
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20
Q

True/false: For non-orthostatic patients whose BP are >160 or 100 mmHg diastolic, two drug therapy is suggested as initial pharmacological treatment

A

True - If BP not at goal, may increase initial drug dose or add a new drug

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21
Q

What labs should be ordered to monitor the patient on ACE inhibitors or ARBs?

A

Serum potassium

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22
Q

Expected normal values for LDL, TGs, and HDLs

A
  • LDL: <130 (book says <100)
  • TGs: <150
  • HDL: females >50, males >40
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23
Q

When is universal screening for dyslipidemia indicated for pediatric patients?

A

Universal screening in children 9-11 years old

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24
Q

Four target population groups for statin therapy

A
  1. CV disease (HTN, CAD, HF, etc.)
  2. LDL 190 mg/dL or higher
  3. Type 2 DM who are ages 40-75 years old
  4. Estimated 10 year risk of CV disease of 7.5% or higher who are 40-75 years of age
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25
Q

What medication can be started for patients who cannot tolerate statin therapy?

A

Ezetimibe (especially for patients with DM)

26
Q

What intensity of statin therapy (high, moderate, low) should be prescribed to patients with very high risk ASCVD (>20%)?

A

High intensity or maximal statin

27
Q

Name two high intensity statins

A
  • Atorvastatin 40-80 mg
  • Rosuvastatin 20-40mg
28
Q

Dyslipidemia clinical presentation

A

S/s do not appear unless other co-morbidities are associated with elevated lipids (e.g. heart disease)

  • Xanthomas - present only when the disease is severe and prolonged
  • Signs of exertion angina or claudication
29
Q

Dyslipidemia PMH components

A
  • Perform complete medical and family history (HTN, diet and exercise patterns, smoking, drug and alcohol history, etc.)
  • Screen for obesity, DM, hypothyroidism, liver and renal disease
  • Document any known arterial sclerotic CVD
  • Assess lifetime risk of ASCVD
30
Q

Dyslipidemia physical exam components

A
  • Serial measurement of cardiac rate and rhythm
  • BP
  • Height and weight
  • Waist-to-hip ratio
  • BMI indicated in hyperlipidemia and ASCVD
  • Xanthomas may be present on areas such as Achilles tendon and on elbows, knees, and metacarpal joints
31
Q

Dyslipidemia diagnostic labs

A

Fasting lipid panel (total blood cholesterol, LDL, HDL, TGs) for all adults >20 years of age, every 5 years

32
Q

After starting lipid lowering drugs, should a second lipid panel be obtained?

A

Yes - should be obtained in 4-12 weeks to ensure adherence and efficacy followed by case dependent quarterly to yearly lab testing

33
Q

Should baseline LFTs be obtained BEFORE statin therapy is initiated?

A

Yes - stop statin therapy if LFTs increase 2-2.5 times during therapy

  • Do not need to check LFTs for bile acid sequestrants
34
Q

True/false: Therapeutic lifestyle changes remain the first and most important intervention for dyslipidemia

A

True - heart healthy diet, exercise, weight loss, avoidance of tobacco

35
Q

Is it recommended to titrate stain drugs?

A

Titrating statin drugs is no longer recommended to achieve goal levels of LDL

36
Q

What is next in terms of dyslipidemia management after therapeutic lifestyle changes are made?

A

Moderate to high intensity statin drugs to lower total cholesterol and LDL, and to prevent coronary heart disease

37
Q

What is the definition of BMI?

A

Surrogate measure of adiposity calculated by weight (kg) divided by height (m) squared

  • Screening tool
38
Q

What is the definition of bioimpedance analysis (BIA)?

A

Non-invasive alternating current predictor of body fat and lean mass (frequently used in weight loss research)

39
Q

What is the definition of anthropometric measures?

A

Low cost easy to use measurement of skin folds, body circumference (waist to hips), height and weight

  • Waist circumference is a strong predictor of CV and cancer outcomes
40
Q

Obesity: pathophysiology (multifactorial causes)

A
  • Increased energy intake and reduced energy expenditure
  • Sedentary environment/insufficient physical activity
  • Genetic predisposition
  • Complex CNS pathways interact with satiety and inhibition threshold
  • Gut hormones
41
Q

Obesity: pathophysiology (maternal influences)

A
  • Leptin in breast milk supports neonate satiety
  • Formula fed infants have higher serum ghrelin (hunger hormone) levels
42
Q

Obesity: pathophysiology (other causes)

A
  • Smoking cessation (average of 10 lbs weight gain)
  • Nicotine is a stimulant → when patients stop smoking they tend to gain 10 lbs
43
Q

How do insulin and insulin analogues cause obesity?

A
  • Increase recovery of glycosuria calories
  • Inhibits lipolysis
  • Upregulate TG cholesterol and glucose storage in adipocytes
  • Increase appetite
  • Increase anabolic protein and adipose synthesis
44
Q

How do antidepressants lead to obesity?

A
  • TCAs decrease resting metabolic rate
  • SSRIs induce carb cravings
45
Q

How to neuroleptic medications lead to obesity?

A

Lithium increases carb cravings, increase storage of carbs and lipids, and lower BMR

46
Q

How to seizure medications lead to obesity?

A

Atypical antipsychotics stimulate appetite and cause insulin resistance

47
Q

How to antihistamines cause obesity?

A

Blocks H1 receptor activity → increasing appetite and carb craving

48
Q

How to hormonal preparations cause obesity?

A

Cause insulin resistance

49
Q

How to cardiac medications (e.g. beta blockers) cause obesity?

A
  • Inhibit satiety and lipolysis
  • Reduces BMR
  • Increase insulin resistance
  • Increases TGCs
50
Q

How to antiretroviral medications cause obesity?

A

Causes redistribution of fat to visceral organs

51
Q

How does tamoxifen cause obesity?

A

Causes visceral and intra-abdominal fat accumulation

52
Q

How do corticosteroids cause obesity?

A

Impairs glucose tolerance

53
Q

Obesity diagnostic studies

A
  • UA, serum glucose
  • Uric acid
  • BUN, creatinine (kidney)
  • CBC, TSH, lipid profile, LFTs
  • Alkaline phosphatase level (2 hour postprandial glucose for hyper insulinemia or insulin resistant patients)
54
Q

Obesity management

A
  • Reduce energy intake
  • Eating for weight loss “diets”
  • Weight loss maintenance diets
  • Medication and/or dietary supplements
  • Bariatric surgery
55
Q

What medications are available for patients with obesity and wish for weight loss?

A

If BMI >30 or >27 with co-morbidities

  • Orlistat
  • Controlled substances: lorcacerin, naltrexone/bupropion
56
Q

What is metabolic syndrome?

A

A cluster of disorders characterized by insulin resistance with…

  • Hyperinsulinemia
  • HTN
  • Abdominal (central or visceral) obesity
  • Dyslipidemia

Additionally can have elevated CRP, increased PAI-1, microalbuminuria

57
Q

Metabolic syndrome clinical presentation

A

Based on clinical findings and lab studies

  • Abdominal obesity
  • Increased TGs
  • Low HDL cholesterol
  • HTN
  • Acanthosis nigricans
  • Skin tags
58
Q

Metabolic syndrome physical exam components

A
  • Obtain BP, height, weight, BMI
  • Ratio of waist to hip
  • Fat distribution pattern
  • Acanthosis nigricans
59
Q

If a patient presents with (+) features of metabolic syndrome, screen annual for…

A
  • Hyperglycemia
  • Glucose intolerance
  • Type 2 DM
60
Q

Metabolic syndrome lab studies

A
  • Fasting glucose
  • Microalbumin level
  • CRP level
61
Q

Metabolic syndrome management

A
  • Exercise for 30 minutes for 5 days/week
  • Weight reduction
  • Medication (as indicated)
    • Antihypertensives
    • Antidyslipidemics
    • Aspirin → reduce inflammation
    • Antidiabetics
    • Surgery