Endocrinology - Lipids and Hypertension Flashcards
Discuss screening for dyslipidemia
- men >40 and women >50 or post-menopausal Regardless of Age Conditions - evidence of arthersclerosis - AAA - diabetes - hypertension - cigarette smoking - stigmata of dyslipidemia (arcus cornea, xanthelasma or xanthoma) - Family history of cardiovascular disease or dysplipidemia - Chronic kidney disease - Obesity - IBD - HIV - Erectile dysfunction - COPD - hypertension in pregnancy
Discuss screening risk using Framingham Risk Score, LDL, Non-HDL and Apo-B screening
No Pharmacology - low risk: FRS <10% Primary Prevention - Intermediate risk: FRS 10-19% and LDL >=3.5 or Non-HDL >=4.3 or Apo-B >=1.2 or men >50, women >60 with one component of metabolic syndrome - High risk: FRS: >20% Statin-Indicated Condition - Clinical artherosclerosis - AAA - Diabetes: age >40, Age >30 with type 1 for >15 years, microvascular disease - Chronic kidney disease LDL >=5 (genetic)
Discuss dyslipidemia therapy and targets
Targets following Initiation of Statin - LDL <2.0 or >50% reduction or ApoB <0.8 or non-HDL <2.6 - Every doubling of dose of statin result in 6% decrease in LDL Target Not Achieved Add on - Ezetimibe 1st line - PCSK9 inhibitor as 2nd line Non Pharmacological Therapy - Smoking cessation - Diet - Exercise
Discuss valid blood pressure check in clinic
Patient - back and arm supported - seated comfortably with legs uncrossed, feet on ground shoulder width apart - no talking - sitting for 5 minutes Cuff - 3cm above elbow crease - width 40% of arm circumference - length 80-100% of arm circumference Measurement - inflate to 30 mmHg above radial pulse obliteration - deflate slowly for average of 2 readings 60 seconds apart
Discuss criteria for diagnosis of hypertension
First Visit
- BP >180/110 then hypertension
- BP automatic >135/85 or office >140/90 then move to second visit
At Home Automatic Blood Pressure
- daytime automatic is >135/85 then hypertension
- if no home monitoring available and BP >140/90 then hypertension
List the target blood pressures
- <140/90
- <130/80 for diabetes
- <150/90 for elderly
Discuss lifestyle modifications for hypertension
Diet - DASH diet - limit sodium to 1.5-2.3g Exercise - 30-60min 4-7x/week Smoking Cessation Relaxation and Stress Management Healthy BMI and Waist Circumference
Discuss the indications to begin medication for hypertensions
- diastolic >90 with target organ damage or cardiovascular risk factors
- diastolic >100 or systolic >160
- systolic >140 with end organ damage
Discuss the medications used for hypertension
1st Line - Thiazide diuretics - ACE inhibitors - ARB - Long acting calcium channel blockers - Beta blockers Add-On - caution CCB and BB - caution ACEi and ARB - caution hypokalemia with thiazides
Discuss secondary causes of hypertension and potential investigations
Hyperthyroidism - TSH Aortic Coartation - CXR - CT angiogram Cushing Syndrome - 24-hr urine cortisol Obstructive Sleep Apnea - Overnight polysomnogram Renal Disease - Renal ultrasound Pheochromocytoma - 24hr urine fractionated metanephrines and catecholamines Medications - NSAIDs - OCP - Steroids - Cocaine
Discuss the Framingham risk score
- completed every 3-5 years in those 40-75 Components - Gender - Age - HDL-C - total cholesterol - SBP - Smoking - Diabetes Double - Family with cardiovascular disease in male <55 or female <55
Differentiate between hypertensive crisis and malignant hypertension
Crisis
- asymptomatic hypertension >=210/130
Malignant Hypertension
- BP >180/110 with acute target ongoing organ damage
- hypertensive encephalopathy with papilledema
- acute ischemic stroke
- intracranial hemorrhage
- acute LV failure
- ACS
- Acute aortic dissection
- Acute Kidney Injury
- EclampsiaDiscuss the causes of malignant hypertension
Essential Hypertension Secondary Hypertension - renovascular - endocrine: hypo/hyperthyroid, hyperaldosteronism, pheochromocytoma - chronic kidney disease CNS - stroke - mass - epilepsy Vascular - aortic dissection Medication - MAOI - beta blocker withdrawal Substance - alcohol withdrawal - cocaine/amphetamine intoxication - pregnancy
Discuss the presentation and management of hypertensive crisis
Presentation
- blurred vision
- headache
- nausea/vomiting
- focal neurological deficit
- dyspnea
- angina
Investigations
- CBC, electrolytes, creatinine, BUN, glucose
- CXR
- ECG
- Urinalysis
- possible troponin or CT head if concerned
Management
- ABC
- Treat underlying cause
- Reduce blood pressure
- reduce MAP by 10-20% in first hour then by 25% gradually over next 23hr, target <170/110
- IV labetalol bolus 20mg followed by 20-80mg every 10 min for total dose of 300mg
- IV nitroprusside 0.25-0.5mcg/kg per minute increased to 8-10mcg/kg if needed
- Address target organ damage
- hypokalemia then PO KClDiscuss signs of secondary hypertension
- age of onset before puberty
- age <30 in non-obese and non-black with negative family history
- severe or resistant hypertension
- acute rise in BP in previously stable individual
- malignant or accelerated hypertension
Discuss Renal Artery Stenosis as secondary cause of hypertension
Risk Factors - Age >50 - other arthersclerotic disease - smoking Presentation - severe and refractory - asymmetric renal size - flank bruit - spontaneous hypokalemia - >30% increase in creatinine with ACE - flash pulmonary edema Diagnosis - Doppler ultrasound confirmed with CTA Management - percutaneous angioplasty with stent - ACEi for unilateral
Discuss hyperaldosteronism for cause of secondary hypertension
Definition - primary: increased adrenal aldosterone production - secondary: increase renin-angiotensin stimulating increased aldosterone production Primary Causes - adrenal adenoma (Conn) - bilateral idiopathy adrenal hyperplasia - familial hyperaldosteronism - aldosterone producing carcinoma Secondary Causes - renin-producing tumour - decreased renal perfusion Presentation - fatigue, weakness - metabolic abnormality: hypernatremia, hypokalemia, hypomagnesia, metabolic alkalosis Diagnosis - plasma aldosterone >400 - plasma aldosterone:renin ratio >140 in primary, normal in secondary Treatment - underlying cause - K sparing diuretic (spironolactone)
Discuss Cushing’s syndrome for secondary cause of hypertension
- increase glucorticoid in syndrome
- ACTH secreting pituitary adenoma increasing adrenal glucorticoid production in disease
ACTH Dependent - ACTH secreting pituitary tumour
- etopic ACTH secreting tumour
ACTH Independent - exogenous glucocorticoid use
- primary adrenocortical tumour
- alcoholism
Presentation - Facies: red cheeks, acne, moon face
- dorsal fat pad
- purple striae
- central obesity with thin arms/legs
- easy bruising
Diagnosis - 24hr urinary free cortisol 4x normal
- lack cortisol suppression with dexamethasone use
Management - treat underlying cause
- mitotane to reduce cortisol
Discuss pheochromocytoma as cause of secondary hypertension
- catelcholmine secreting adrenal tumour
- sporadic or familial with MEN2A, 2B, von Hippel-Lau, neurofibromatosis
Presentation - symptoms triggered by stress, exertion
- triad: episodic pounding headache, palpitation, diaphoresis
- tremor, anxiety, blurry vision
- orthostatic hypotension
Diagnosis - high urinary metanephrine and normetanephrine
Management - pre-operative preparation
- alpha blockade with phenoxybenzamine
- beta blockade with propranolol
- metyrosine to inhibit catelcholmine synthesis - surgical remove
Discuss the pathophysiology, presentation, and diagnosis of Familial Hypercholesterolemia
Pathophysiology
- Autosomal dominant condition resulting in increased LDL due to ApoB100 mutation which affects interaction with LDL receptor
- Increased destruction of PCSK9-receptor
Presentation
- Tendinous xanthomas
- Xanthelasmas
- Corneal Arcus
- Very high risk for coronary vascular disease
Diagnosis
- Any of the following: LDL >=5 if >40 or >=4.5 if 18-39 or <=4 if <18 plus
- Any of the following
- DNA Mutation
- Tendon xanthoma
- LDL >=8.5
- If none then:
- 1st degree relative with high LDL
- 1st degree relative with early coronary vascular disease
Discuss the pathophysiology and phenotype of Familial Combine Hyperlipidemia and Polygenic hypercholesterolemia
Pathophysiology - Autosomal dominance resulted in increased secretion of ApoB Phenotypes - Increased VDLD and increased triglycerides - Increased LDL alone - Increase VLDL and LDL - Increase Apo B Polygenic Hypercholesterolemia - high LDL, most individuals
Discuss the pathophysiology of lipoprotein (a) hypercholesterolemia
- LDL with Apo(a) present
- Apo(a) resemble plasminogen - Increased risk of coronary artery disease due to increased thrombogenesis and decreased thrombolysis
Discuss the pathophysiology, presentation, and management of Familial Dysbetalipoproteinemia
Pathophysiology
- Have ApoE E2/E2 (normal E3/E3) so have decreased affinity for LDL-R and LRP resulting in decreased uptake of VLDL and chylomicron
- Increase formation of atheroma and xanthoma
- Increased triglyceride
- Have incomplete penetrance so require second to result in dyslipidemia
Presentation
- Early cardiovascular disease
- Elevated IDL and chylomicron remnants
- Tuberous xanthomas and xanthoma striata palmaris
Discuss chylomicronemia syndrome
Pathophysiology
- Autosomal recessive condition where have LPL or ApoCII deficiency
- Require diabetes or alcohol use for complete penetrance
- Result in increased triglyceride levels
Presentation
- Recurrent pancreatitis
- Eruptive xanthomas
- Centrifuged serum appears milky
Discuss hypoalphalipoproteinemia
- Heterogeneous group of low HDL-C disorders
- autosomal recessive
Defect - ApoA1
- ABCA1 in Tangier (yellow infiltrates in tonsils)
- LCAT in fish eye disease
