Ambulatory Med Chapter Flashcards
Two major types of HTN?
Essential (no ID cause–95%) and Secondary
Most common cause of secondary HTN?
Renal artery stenosis.
Most common cause of secondary HTN in young woman?
OCPs.
Causes of secondary HTN?
1) Renal/renovascular,
2) Endocrine,
3) Meds,
4) Coarctation of the aorta,
5) Cocaine,
6) Sleep Apnea
What effect does HTN have on heart?
Increased afterload–>concentric LV hypertrophy–>decreased LV function. Chamber dilates–>fail.
What are the major organs damaged by HTN? Effects?
Heart--LVH, MI, CHF, aortic dissectoin, Brain--Stroke and TIA Chronic kidney disease Peripheral vascular disease Retinopathy
Risk factors for HTN?
Age (old) Gender (men) Race (African American 2x white risk) Obesity Fam history Hi sodium intake Alcohol (2 + drinks per day)
What is the cutoff for hypertension? Prehypertension?
HTN: 140/90 general, 130/80 in diabetes/renal pts.
Pre-HTN–120-139/80-89
How to test for HTN? Immediate follow up?
BP–5 min rest before measurement, no caffeine or cigs for 30 mins pre measurement. 2 readings >4 weeks apart.
F/u: Urinalysis, Chem panel, Fasting glucose, Lipids and EKG.
bHCG in women before starting drugs.
Lifestyle changes for HTN?
Decrease salt Wt loss Exercise Avoid alcohol Cut saturated fat Stop complicating meds Cut stress
Pharmacological management of HTN. Who is each recommended for?
1A) Thiazide diuretics–best for black, non diabetics.
1Bi) ACE inhibs–best for diabetics
1Bii) ARBs–best for those who cant tolerate ACE
1C) Ca channel blockers
(all great first choices)
1D) Beta blockers
2) Alpha blockers–second or third line
3) Vasodilators (hydralazine/minoxidil)–for very refractory
What can act as a secondary cause of hyperlipidemia?
Endocrine--hyperthyroid, DM, Cushings Renal--Nephrotic, uremia Liver--chronic liver disease Meds--Beta blockers, thiazides, glucocorticoids, estrogen Pregnancy
Risk factors for hyperlipidemia?
Diet (saturated fat, high calorie for TGs, Alcohol for TGs and HDL) Age Activity level Family hx, genetics Gender (men > women until menopause) Meds
Which lipid correlates w CAD risk?
LDL > 160
Goal levels for Lipids?
Chol < 200
LDL <125
How good is HDL?
Great. Increase in HDL by 10–>50 % CAD risk reduction.
Chol to HDL ratio <4.5 is ideal.
Clinical symptoms of hyperlipidemia?
Normally asymptomatic.
Xanthelasma–on eyelid
Xanthoma–on tendon
Pancreatitis w really high TGs.
Dx of hyperlipidemia?
Fasting TG panel. Also check TSH, LFTs, BUN/Cr, Glucose.
What classes of meds are used to treat hyperlipidemia?
HMGCoA Reductase inhibs (statins)
Niacin
Bile acid binding resins
Fibrates
How do statins work? What lab values will they change? What side effects should you watch out for?
Inhibit HMG COA reductase. Also have antioxidant effect on Cornary Arteries.
Reduces LDL–>reduction in CV events and mortality
Liver toxicity–watch for elevated LFTs.
Rhabdo very rare but CPK elevates.
What does niacin do to lab values? Who should/should it not be used in? Side effects?
All good–lower TG, lower LDL, raises HDL.
Do not use in diabetics.
Facial flushing. Check LFTs and CPK as w statin.
What effect do bile acid resins have on lab values? Who should it be used in? Commonly used?
Lower LDL, higher TGs.
Used in combo w statins or niacin.
Bad GI side effects, so uncommon to use.
What effect do fibrates have on lab values? Side effects?
Lower TGs.
Mild GI side effects. Higher LFTs, some myopathies, gynecomastia, wt gain and gallstones.
How should you approach the tx of high TGs only?
1) Lifestyle–wt loss, diet, exercise, glycemic control
2) Fibrates, nictonic acid, fish oil
3) Statin just bc of cardioprotection.
Differential for a headache?
VOMIT:
Vascular–subarachnoid hemorrhage, subdural or epuidural hematoma, intraparenchymal hemorrhage, temporal arteritis
Other–malignant HTN, post-LP, pheo, pseudomotor cerebri
Medication related–nitrates, EtOH withdrawal, painkiller abuse
Infection–meningitis, encephalitis, abscess, sinusitis, herpes
Tumor
Risk factors for CAD?
Cigarette smoking HTN DM Low HDL Age (M>45, W>55) Male Family history of premature CAD
What is the emergency eval for a headache?
1) Noncontrast CT
2) LP for small bleed
What is a tension headache?
Worsens throughout day, precipitated by stress/anxiety/depression
Vise-like around head and tightness in posterior neck
How should you treat a tension headache?
1) ID and address causal factor
2) NSAID, acetaminophen and/or aspirin
3) Consider migraine meds
How common are cluster headaches? Who gets them?
Rare, occurs in middle-aged men. Comes in episodic–2-3 mos w remissions (90%) and chronic–1-2 years w/o remission (10%)
What are the clinical features of a cluster headache?
Unilateral, behind the eye.
Deep, burning or stabbing pain.
Ipsilateral lacrimation, stuffiness, facial flushing.
Begins after bedtime, worse w sleep and alcohol.
How should you treat a cluster headache?
Sumatriptan
O2
How should you prevent cluster headaches?
Verapamil.
How does one get migraines?
What causes migraines?
Who gets them?
Types?
Inherited.
Serotonin depletion?
More common in women than men.
w/aura (15%) or w/o aura (85%); can be menstrual or status migrainosus (72 hrs straight)
What are the clinical features of a migraine?
Prodrome -excitation or inhibition of CNS -sweets craving -depression, irritability or fatigue Severe throbbing unilateral headache -4-72 hours -worse w cough, physical activity, bending May have nausea/vomiting, photophobia or sensitivity to smell
What is commonly misdiagnosed as migraines w more frequent headaches? Tx?
Rebound analgesic headaches. Headache occurs every day or 2.
Wean patient off painkillers
How should you treat migraines?
Mild–NSAID, acetaminophen
Dihydroergotamine (DHE)–serotonin agonist
Sumatriptan–more selective serotonin agonist
Is there a way to prevent migraines?
Beta-blocker (propranolol) or TCA (amitriptyline)
