Ipapburke Cardio Test 1- Hypertension

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DEFINITION OF HYPERTENSION

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A PROGRESSIVE CV SYNDROME WITH MANY CAUSES THAT RESULT IN BOTH FUNCTIONAL AND STRUCTURAL CHANGES TO THE HEART AND VASCULAR SYSTEM

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HYPERTENSION WITH NO CLEARLY IDENTIFIABLE CAUSE (95%)

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PRIMARY

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TYPE OF HTN ASSOCIATED WITH SOME CLEARLY IDENTIFIABLE CAUSE

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SECONDARY

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NORMAL BP FOR ADULTS

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<120 SBP; <80 DBP

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PREHYPERTENSION

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120-139 SBP OR 80-89

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STAGE 1 HYPERTENSION

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140-159 SBP OR 90-99

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STAGE 2 HYPERTENSION

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>160 OR >100

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IDENTIFIABLE CAUSES OF HYPERTENSION

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CHRONIC KIDNEY DZ, COARCTATION OF AORTA, CUSHING'S SYNDROME, DRUG INDUCED, PHEO, OBSTRUCTIVE UROPATHY, PRIMARY ALDOSTERONISM, RENOVASCULAR HYPERTENSION, SLEEP APNEA, THYROID OR PARATHYROID DISEASE

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MOST COMMON FORM OF SECONDARY HYPERTENSION

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RENAL PARENCHYMA DISEASE (ANY KIDNEY IMPAIRMENT MAY ALSO IMPACT BP CONTROL)

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POSSIBLE CAUSES OF RENAL PARENCHYMA DISEASE

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DIABETIC NEUROPATHY, GLOMERULONEPHRITIS, HYPERTENSIVE RENAL DISEASE (CULPRIT AND PROBLEM); DRUG INDUCED RENAL DZ, AND POLYCYSTIC KIDNEY DZ

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CONSIDER FIBROMUSCULAR DYSPLASIA OF THE KIDNEYS IN WHAT PRESENTING PATIENTS?

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YOUNG PEOPLE WITH ACUTE OR NEW ONSET OF RENAL FAILURE

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WHAT ARE THE TWO PRIMARY MECHANISMS OF RENAL ARTERY STENOSIS?

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ATHEROSCLEROSIS AND FIBROMUSCULAR DYSPLASIA

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HOWD OES DIMINISHED RENAL BLOOD FLOW AFFECT THE BLOOD PRESSURE?

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STIMULATES THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM, LEADNG TO INCREASED VOLUME RETENTION AND INCREASED BP

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WHAT DOES RISING CREATININE AFTER INITIATION OF ACE INHIBITOR INDICATE?

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RENAL ARTERY STENOSIS

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WHAT DO YOU MONITOR WITHIN ONE MONTH OF PRESCRIBING ACE-I? WHY?

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MONITOR BUN/CREATININE B/C ACE-I CAN INCREASE BP AND CAUSE KIDNEY FAILURE

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HOW CAN RENAL ARTERY STENOSIS BE TREATED?

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BALLOON OPEN ATHEROSCLEROTIC PLAQUE AND PLACE A STENT

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WHAT IS COARCTATION OF THE AORTA?

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RARE CONGENITAL NARROWING OF THE PROXIMAL AORTA NEAR THE ORIGIN OF THE LEFT SUBCLAVIAN ARTERY WHICH MAY LEAD TO HTN

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WHAT WILL BE THE CHANGE IN THE UPPER EXTREMITY PULSES IN COARCTATION?

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THE UPPER IMPULSES WILL BE BOUNDING

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WHAT ARE THE CLASSICAL CLINICAL FINDINGS FOR COARCTATION?

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RIB NOTCHING ON XRAY AND DIMINISHED FEMORAL PULSES

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HOW DOES COARCTATION LEAD TO HTN?

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INCREASED BP IN THE AORITC ARCH AND UPPER EXTREMITIES ACCELERATES ATHEROSCLEROSIS AND IMPAIRS BARORECEPTORS IN THE AORTIC ARCH; ALSO THERE IS IMPAIRED BLOOD FLOW TO DISTAL TO THE COARCTATION CAUSING IMPAIRED RENAL PERFUSION

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WHAT IMAGING IS DONE FOR COARCTATION OF THE AORTA?

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ANGIOGRAPHY

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WHAT CAUSES RIB NOTCHING?

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DILATED INTERCOSTAL ARTERIES (COARCTATION)

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CATECHOLAMINE SECRETING TUMORS OF NEUROENDOCRINE CELLS, USUALLY LOCATED IN THE ADRENAL MEDULLA

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PHEOCHROMOCYTOMA

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HOW DOES A PHEO AFFECT BP?

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THERE IS EPISODIC SECRETION OF CATECHOLAMINES THAT LEAD TO ACTIVATION OF THE SYMPATHETIC NERVOUS SYSTEM

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CHARACTERISTIC SYMPTOMS OF A PHEO

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EPISODIC HEADACHES, PALPITATIONS, AND DIAPHORESIS

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MEN SYNDROMES TYPE 2A AND 2B ASSOCIATED WITH PHEOS USUALLY INVOLVE WHAT THREE CONDITIONS

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MEDULLARY THYROID CARCINOMA; HYPERPARATHYROIDISM; AND RET ONCOGENE

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WHAT IS CONN SYNDROME?

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CAUSE OF HYPERALDOSTERONISM; ADRENAL ADENOMA THAT SECRETES EXCESS MINERALCORTICOIDS THAT INCREASED BP

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TWO CAUSES OF HYPERALDOSTERONISM

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CONN SYNDROME (ADRENAL ADENOMA) OR BILATERAL HYPERPLASIA ("PRIMARY" ALDOSTERONISM)

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WHAT MECHANISM IN HYPERALDOSTERONISM CAUSES HYPERTENSION?

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INCREASED SODIUM RETENTION DUE TO EXCESS OF ALDOSTERONE

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CLASSIC FINDING OF HYPERALDOSTERONISM

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UNPROVOKED HYPOKALEMIA (IN ABSENCE OF DIURETIC OR LATROGENIC CAUSE)

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DIAGNOSIS FOR ALDOSTERONISM

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ELEVATED 24 HR URINE ALDOSTERONE LEVEL; SERUM ALDOSTERONE: RENIN RATIO > 25:1

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CUSHING'S DISEASE

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PITUITARY ADENOMA THAT OVERPRODUCES ACTH

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HOQ DOES CUSHING'S DISESE CAUSE HYPERTENSION?

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EXCESS GLUCOCORTICOIDS (FROM ANY CAUSE) LEAD TO INCREASED BLOOD VOLUME AND RENIN PRODUCTION

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DIAGNOSTIC TESTS FOR CUSHING'S SYNDROME

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DEXAMETHASONE SUPPRESSION TEST; 24 HR URINE FREE CORTISOL LEVELS

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HOW DOES HYPERTHYROIDISM LEAD TO HYPERTENSION?

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EXCESS METABOLIC ACTIVITY LEADS TO CARDIAC HYPERACTIVITY AND INCREASED BLOOD VOLUME (BECAUSE THE TISSUES NEED MUCH MORE OXYGEN)

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WHAT TYPE OF HYPERTENSION IS HYPERTHYROIDISM CLASSICALLY ASSOCIATED WITH?

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SYSTOLIC HYPERTENSION

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HYPOTHYROIDISM IS CLASSICALLY ASSOCIATED WITH?

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DIASTOLIC HYPERTENSION

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HOW DOES HYPERPARATHYROIDISM CAUSE HTN?

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CAUSE AND EFFECT IS UNCLEAR; MAY BE ATTRIBUTED TO HYPERCALCEMIA AND POTENTIAL COEXISTING RENAL DYSFUNCTION

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COMMON DRUGS THAT CAUSE HTN

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ESTROGENS, CORTICOSTEROIDS, CYCLOSPORINE, ERYTHROPOIETIN, SYMPATHOMIMETIC DRUGS (PSEUDOEPHEDRINE, OTC COUGH SYRUPS), ALCOHOL, AND COCAINE

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WHAT AMOUNT OF ALCOHOL CONSUMPTION HAS BEEN ASSOCIATED WITH HTN?

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MORE THAN 2 DRINKS PER DAY

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NEW ONSET OF HTN IN AN OLD PERSON IS PROBABLY DUE TO WHAT?

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RENAL ARTERY STENOSIS OR DRUG INDUCED

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WHAT IS DIAGNOSIS OF RESISTANT OR DIFFICULT-TO-CONTROL HTN BASED ON?

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CONSISTENTLY ELEVATED BP MEASUREMENTS DESPITE ADHERENCE TO TREATMENT REGIMENTS CONTAINING 3 MEDS

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WHAT IS AMBULATORY BP MONITORING USED FOR?

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TO EVALUATE WHITE COAT HYPERTENSION; HYPOTENSIVE SYMPTOMS WITH ANTIHYPERTENSIVE MEDS, EPISODIC HYPERTENSION, AUTONOMIC DYSFUNCTION

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AN ABSENCE OF 10-20 BP DROP WHILE SLEEPING MAY INDICATE WHAT?

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INCREASED CVD RISK

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FOLLOWUP FOR PATIENT WITH NORMAL BP WITH NO ACUTE END ORGAN DAMAGE

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2 YEARS

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FOLLOWUP FOR PATIENT WITH PREHYPERTENSION WITH NO ACUTE END ORGAN DAMAGE

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RECHECK IN 1 YEAR

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FOLLOWUP FOR PATIENT WITH STAGE 1 HYPERTENSION WITH NO ACUTE END ORGAN DAMAGE

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CONFIRM WITHIN 2 MONTHS

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FOLLOWUP FOR PATIENT WITH STAGE 2 HYPERTENSION WITH NO ACUTE END ORGAN DAMAGE

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EVALUATE OR REFER FOR CARE WITHIN 1 MONTH; FOR THOSE WITH HIGHER PRESSURES, EVALUATE AND TREAT IMMEDIATELY (WITHIN 1 WEEK)

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WHAT CAN BASELINE CHEST XRAY DONE IN HTN SHOW?

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CARDIAC SILHOUETTE, RIB NOTCHING, PULMONARY OVERLOAD (HF), GREAT VESSEL ANOMALIES

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WHY WOULD YOU DO ECHOCARDIOGRAPHY ON HTN PATIENT?

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USED IN YOUNGER PATIENTS WHEN YOU HEAR A MURMUR AND SEE LVH ON EKG

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WHAT IS THE BP GOAL FOR ALL PATIENTS WITH RENAL DYSFUNCTION?

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130/80

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FIRST LINE DRUG FOR HTN

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THIAZIDE DIURETIC (UNLESS COMPELLING INDICATION)

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FIRST LINE DRUG FOR HTN WITH DM/ RENAL DISEASE

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ACE-I

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FIRST LINE DRUG FOF HTN POST MI

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BETA BLOCKER OR ACE-I (THEN ADD THIAZIDE)

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FIRST LINE DRUG FOR HTN AND HF

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BETA BLOCKER OR ACE-I

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FIRST LINE DRUG FOR HTN AND STROKE PREVENTION

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ACE-I AND A THIAZIDE

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MOST EFFECTIVE LIFESTYLE MODIFICATION FOR HTN

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WEIGHT LOSS

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LIFESTYLE MODIFICATIONS FOR HTN

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WEIGHT LOSS, DASH EATING PLAN, DIETARY SODIUM REDUCTION, AEROBIC PHYSICAL ACTIVITY, AND MODERATION OF ALCOHOL CONSUMPTION

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WHAT LABS MUST BE MONITORED IN PATIENTS TAKING HYPERTENSIVE MEDS?

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BUN/CR, HYDRATION STATUS, AND ELECTROLYTES (DO BMP)

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LABETOLOL USED FOR?

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HTN URGENCY

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SEVERELY ELEVATED BP WITH CLINICALLY EVIDENT END ORGAN DAMAGE THAT REQUIRES IMMEDIATE THERAPY VIA IV

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HYPERTENSIVE EMERGENCY

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WHAT DIASTOLIC BP INDICATES HYPERTENSIVE CRISIS

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GREATER THAN 130- BEWARE

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WHAT IS THE CAUSE OF MOST HYPERTENSIVE CRISES?

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CONSEQUENCE OF PROLONGED INADEQUATE CONTROL OF CHRONIC HYPERTENSION, OFTEN WITH SUPERIMPOSED ACUTE HEMODYNAMIC INSULT

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WHY DO WE AVOID OVERLY RAPID REDUCTION OF BP IN HYPERTENSIVE CRISES?

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IT MAY INDUCE WORSENED END ORGAN ISCHEMIA IF ELEVATED BP WAS A PHYSIOLOGIC COMPENSATION FOR A COEXISTING PATHOLOGIC PROCESS

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THERAPEUTIC GOAL IN HYPERTENSIVE CRISES MANAGEMENT

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PROMPT REDUCTION OF 20-25% AND A DIASTOLIC PRESSURE UNDER 100

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WHAT DO PATIENTS WITH TRUE HYPERTENSIVE EMERGENCY REQUIRE?

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ICU ADMISSION, PARENTERAL MEDICATIONS, CONTINUOUS CARDIAC MONITORING, INVASIVE BP MONITORING (RADIAL ARTERY LINE)**, ADJUSTMENT OF BP MEDICATION REGIMEN WHILE IN A CONTROLLED SETTING

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HOW ARE PATIENTS WITH HYPERTENSIVE URGENCY WHO ARE NOT ADMITTED MANAGED?

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ORAL MEDICATIONS BUT REQUIRE EXTENDED MONITORING PRIOR TO RELEASE AND CLOSE FOLLOW UP

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APPROPRIATE INTERVENTIONS IN HYPERTENSIVE URGENCY WHEN PATIENTS ARE ALREADY BEING TREATED FOR HYPERTENSION

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INCREASE DOSE OF EXISTING MEDICATIONS OR ADD ANOTHER AGENT; REINSTITUTE MEDS IN NON-ADHERENT PATIENTS; ADD DIURETIC AND EMPHASIZE SODIUM RESTRICTIONS

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IF HYPERTENSIVE URGENCY IN A PREVIOUSLY UNTREATED PATIENT, WHAT CAN BE DONE?

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ORAL FUROSEMIDE IF PT IS NOT VOLUME DEPLETED; ORAL CLONIDINE; OBSERVE FOR A FEW HOURS TO A REDUCTION OF 20 TO 30 MM HG; PRESCRIBE LONG ACTING AGENT AND FOLLOW UP WITH PCP WITHIN A FEW DAYS

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DRUGS USED IN HYPERTENSIVE EMERGENCY

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NITROPRUSSIDE, NICARDIPINE, LABETALOL, FENDOLDOPAM

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HOW DOES NITROPRUSSIDE WORK IN HYPERTENSIVE EMERGENCY?

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IT IS AN ARTERIOLAR AND VENOUS DILATOR; IS GIVEN VIA IV INFUSION AND WORKS IN A MATTER OR SECONDS WITH A QUICK HALF LIFE (CAUTIONS LONG TERM USE B/C OF CHANCE OF CYANIDE POISOINING)

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WHAT CLASS OF DRUG IS FENOLDOPAM?

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PERIPHERAL DOPAMINE-1 RECEPTOR AGONIST

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2 MOST COMMONLY USED DRUGS IN HYPERTENSIVE EMERGENCY

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IV SODIUM NITROPRUSSIDE AND RAPDI ACTING BETA BLOCKER