HTN, dyslipidemia, obesity, metabolic disorder Flashcards
What is the definition of hypertension?
Defined by determining the levels of BP that cause target organ damage, morbidity, and mortality as material flow is delivered
- CO x PVR = BP
How would a provider diagnose HTN?
Two elevated BP readings on two separate occasions at least two weeks apart
Primary vs secondary HTN
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)
What should the provider do if primary HTN is diagnosed in children at 10 years old?
Order initial labs (CBC, ESR, CRP, UA, renal function panel)
- Start screening at 3 years old or earlier if there is a clinical concern
How does DBP change later in life?
DBP levels off or drops in the 50th decade of life
How does SBP change later in life?
SBP rises with advanced age
- If SBP is =/> 160 in the elderly (older than 85 years old), will have increased risk of stroke
True/false: HTN symptoms usually only occur after end organ damage
True - may also be asymptomatic
- End organ damage signs: diabetic nephropathy, Cushing’s syndrome
HTN risk factors
- 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
HTN physical exam components
- 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
HTN diagnostic studies
- UA
- CBC, potassium, BUN, serum creatinine, calcium, uric acid
- Fasting blood glucose
- Lipoprotein
- EKG (to identify LVH)
JNC 8 HTN diagnostic criteria
- Under 60 years - BP >140/90
- +60 years - BP >150/90
ASH/ISH HTN guidelines
BP >130/80 in adults and elders
African Americans respond better to what classification of BP medication? Asian Americans?
African Americans - diuretics (thiazides), CCB
Asian Americans - CCB, ARB
First line HTN medication for patients with diabetes and CKD
ACE inhibitor (including black patients)
If patient’s BP continues to be >160/100, they will need to start combo therapy with which two medication classes?
Thiazide and ACE inhibitors
When should a patient with HTN go to the ED?
- BP >180/120
- Individual has signs of target organ dysfunction
When is a specialist referral indicated for patients with HTN?
If HTN is resistant to therapy (failure of three full dose, or maximally tolerated, antihypertensive drugs, including a diuretic)
Non pharmacologic management of HTN
- Lifestyle modifications
- Regular exercise
- Healthy weight
- Tobacco cessation
- Reduction of daily dietary sodium to <2,300 mg
- Moderation of alcohol intake
Four common medication classes used to treat HTN
- ACE inhibitors
- ARBs
- Thiazide diuretics
- CCB
True/false: For non-orthostatic patients whose BP are >160 or 100 mmHg diastolic, two drug therapy is suggested as initial pharmacological treatment
True - If BP not at goal, may increase initial drug dose or add a new drug
What labs should be ordered to monitor the patient on ACE inhibitors or ARBs?
Serum potassium
Expected normal values for LDL, TGs, and HDLs
- LDL: <130 (book says <100)
- TGs: <150
- HDL: females >50, males >40
When is universal screening for dyslipidemia indicated for pediatric patients?
Universal screening in children 9-11 years old
Four target population groups for statin therapy
- CV disease (HTN, CAD, HF, etc.)
- LDL 190 mg/dL or higher
- Type 2 DM who are ages 40-75 years old
- Estimated 10 year risk of CV disease of 7.5% or higher who are 40-75 years of age
What medication can be started for patients who cannot tolerate statin therapy?
Ezetimibe (especially for patients with DM)
What intensity of statin therapy (high, moderate, low) should be prescribed to patients with very high risk ASCVD (>20%)?
High intensity or maximal statin
Name two high intensity statins
- Atorvastatin 40-80 mg
- Rosuvastatin 20-40mg
Dyslipidemia clinical presentation
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
Dyslipidemia PMH components
- 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
Dyslipidemia physical exam components
- 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
Dyslipidemia diagnostic labs
Fasting lipid panel (total blood cholesterol, LDL, HDL, TGs) for all adults >20 years of age, every 5 years
After starting lipid lowering drugs, should a second lipid panel be obtained?
Yes - should be obtained in 4-12 weeks to ensure adherence and efficacy followed by case dependent quarterly to yearly lab testing
Should baseline LFTs be obtained BEFORE statin therapy is initiated?
Yes - stop statin therapy if LFTs increase 2-2.5 times during therapy
- Do not need to check LFTs for bile acid sequestrants
True/false: Therapeutic lifestyle changes remain the first and most important intervention for dyslipidemia
True - heart healthy diet, exercise, weight loss, avoidance of tobacco
Is it recommended to titrate stain drugs?
Titrating statin drugs is no longer recommended to achieve goal levels of LDL
What is next in terms of dyslipidemia management after therapeutic lifestyle changes are made?
Moderate to high intensity statin drugs to lower total cholesterol and LDL, and to prevent coronary heart disease
What is the definition of BMI?
Surrogate measure of adiposity calculated by weight (kg) divided by height (m) squared
- Screening tool
What is the definition of bioimpedance analysis (BIA)?
Non-invasive alternating current predictor of body fat and lean mass (frequently used in weight loss research)
What is the definition of anthropometric measures?
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
Obesity: pathophysiology (multifactorial causes)
- 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
Obesity: pathophysiology (maternal influences)
- Leptin in breast milk supports neonate satiety
- Formula fed infants have higher serum ghrelin (hunger hormone) levels
Obesity: pathophysiology (other causes)
- Smoking cessation (average of 10 lbs weight gain)
- Nicotine is a stimulant → when patients stop smoking they tend to gain 10 lbs
How do insulin and insulin analogues cause obesity?
- Increase recovery of glycosuria calories
- Inhibits lipolysis
- Upregulate TG cholesterol and glucose storage in adipocytes
- Increase appetite
- Increase anabolic protein and adipose synthesis
How do antidepressants lead to obesity?
- TCAs decrease resting metabolic rate
- SSRIs induce carb cravings
How to neuroleptic medications lead to obesity?
Lithium increases carb cravings, increase storage of carbs and lipids, and lower BMR
How to seizure medications lead to obesity?
Atypical antipsychotics stimulate appetite and cause insulin resistance
How to antihistamines cause obesity?
Blocks H1 receptor activity → increasing appetite and carb craving
How to hormonal preparations cause obesity?
Cause insulin resistance
How to cardiac medications (e.g. beta blockers) cause obesity?
- Inhibit satiety and lipolysis
- Reduces BMR
- Increase insulin resistance
- Increases TGCs
How to antiretroviral medications cause obesity?
Causes redistribution of fat to visceral organs
How does tamoxifen cause obesity?
Causes visceral and intra-abdominal fat accumulation
How do corticosteroids cause obesity?
Impairs glucose tolerance
Obesity diagnostic studies
- 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)
Obesity management
- Reduce energy intake
- Eating for weight loss “diets”
- Weight loss maintenance diets
- Medication and/or dietary supplements
- Bariatric surgery
What medications are available for patients with obesity and wish for weight loss?
If BMI >30 or >27 with co-morbidities
- Orlistat
- Controlled substances: lorcacerin, naltrexone/bupropion
What is metabolic syndrome?
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
Metabolic syndrome clinical presentation
Based on clinical findings and lab studies
- Abdominal obesity
- Increased TGs
- Low HDL cholesterol
- HTN
- Acanthosis nigricans
- Skin tags
Metabolic syndrome physical exam components
- Obtain BP, height, weight, BMI
- Ratio of waist to hip
- Fat distribution pattern
- Acanthosis nigricans
If a patient presents with (+) features of metabolic syndrome, screen annual for…
- Hyperglycemia
- Glucose intolerance
- Type 2 DM
Metabolic syndrome lab studies
- Fasting glucose
- Microalbumin level
- CRP level
Metabolic syndrome management
- Exercise for 30 minutes for 5 days/week
- Weight reduction
- Medication (as indicated)
- Antihypertensives
- Antidyslipidemics
- Aspirin → reduce inflammation
- Antidiabetics
- Surgery
