W2 Cardiovascular Disease Flashcards

Question

What are the updated cholesterol guidelines [know] What is the main goal now? What is the recommended therapy for low, borderline, intermediate and high?

Answer 1

**lower is better** **aim for % decrease** —low risk **<5%** = lifestyle improvements —borderline **5-7.5%** = consider moderate intensity statin —intermediate **7.5 - 20%** = consider moderate intensity statin to reduce LDL by >30% —if ineffective, consider adding **ezetimibe** or **bile acid sequestrant** —high **>20%** = moderate/high intensity statin to achieve >50% reduction in LDL

Answer 2

Genetic abnormality in the LDL receptor clearance mechanism that **allows LDL to accumulate in the circulation since it cannot be removed**. It can be heterozygous or homozygous These patients will have a propensity to develop early onset CAD/Ischemic. **Statins don’t work on these patients**

Answer 3

**ASCVD** —high intensity statin: >50 LDL reduction —if remains high, add ezetimibe —if remains high still, add **PCSK9 inhibitor** **LDL >190** —high intensity statin: >50 LDL reduction —if remains high, add ezetimibe —if remains high still, **add bile acid sequestrant** **Diabetes** —age 40-75 —regardless ASCVD risk —moderate statin for >30% reduction —high intensity statin for >50% reduction —+ezetimibe **Ezetimibe** — a cholesterol absorption inhibitor that targets uptake at the jejunal enterocyte brush border **Bile acid sequestrants** — These medicines work by blocking bile acid in your stomach from being absorbed in your blood. Your liver then needs the cholesterol from your blood to make more bile acid. This reduces your cholesterol level

Answer 4

if the dose of a statin is doubled then there is an approximate 6% increase in LDL lowering efficacy by doubling the dose - the so-called 6 percent rule

Answer 5

**BP = cardiac output x total peripheral resistance** CO = volume of blood ejected from the ventricular per minute, ~5 litres **CO= stroke volume x HR** SV = volume of blood ejected from ventricle during systole SV depends on preload, afterload, and cardiac contractility

Answer 6

+contractility +preload (like the gas tank) - afterload (what the LV is pushing against)

Answer 7

1. **Heart**: pumping pressure/contractility 2. **Vascular/vessel tone**: determines peripheral resistance 3. **Kidney**: regulates intra vascular volume and peripheral resistance *no matter how high the cardiac output or total peripheral resistance, renal excretion or volume can return BP to normal* *pressure natriuresis (urine volume and sodium excretion) is blunted in HTN due to microvascular and tubulointerstitial injury* 4. **Hormones** : module the functions of the other systems: RAS, adrenal hormones and CNS catecholamines

Answer 8

**baroreceptor reflex** Located in **aortic arch and carotid sinuses** Not involved in long term regulation or prevention of chronic HTN as the **baroreceptor reset themselves to high pressures and inhibit feedback**.

Answer 9

“Essential HTN” = 90% of patients! We don’t know what’s causing it —genetics —environmental —behavioural factors **need _two separate visits_ AND and ambulatory blood pressure monitor at home to confirm the diagnosis (white coat syndrome)** 10% has an underlying cause, this is known as “secondary HTN”

Answer 10

**—genetics** No singular genetic marker for HTN has been discovered, likely a complex, polygenic disorder **—environmental** High sodium diet, alcohol intake, poor exercise **—systemic abnormalities** RAAS dysfunction in kidney/adrenal catecholamine mal regulation Abnormal stress response or increased basal sympathetic tone in the CNS Blood vessel hyper responsiveness to catecholamines/increased endothelial **—insulin resistance and obesity** —increases sympathetic activation —increased vasc resistance —obesity increases blood volume related to increased body mass and blood viscosity **—natural history or age** —younger people have higher BP —as age, CO declines and vascular resistance increases from hypertrophy related to prolonged pressure stress

Answer 11

**Exogenous:** —prescribed: OCPs, NSAIDs, epogen —recreational stimulate use and chronic alcohol consumption/withdrawal **Renal causes:** —**renal artery stenosis** > atherosclerosis and fibromuscluar dysplasia reduces renal blood flow therapy secreting renin secondary to low perfusion —**CKD** > damaged nephrons are unable to excrete normal amounts of Na and H2O leading to a rise in intravascular volume, elevated CO, and increased BP

Answer 12

**Mechanical** —coarctation of the aorta: congenital narrowing of the aorta causing low perfusion to kidney and activation of RAAS as well as elevated pressures proximal to the stenosis blunting the baroreceptor reflex. —finding on CXR: rib notching **Endocrine** —**pheochromocytoma**: catecholamines secreting tumours on the adrenal medulla —**adrenal cortex hormone excess**: mineralocorticoids (hyperaldosteronism) and glucocorticoids (Cushing syndrome) —**mineralocorticoids**: primarily aldosterone, increase blood volume by augmenting reabsorption of sodium in exchange for potassium excretion (hypokalemia) —**glucocorticoids**: mostly cortisol, elevated BP via volume expansion and sodium retention —**hyperthryroidism**: cardiac hyperactivity from sympathetic stimulation with an inc in blood volume —**obstructive sleep apnea**: sympathetic spikes during apneic period

Answer 13

Age : before 20y/o and after 50y/o Severity: dramatic right or refractory to multi drug regimen Onset: abrupt presentation in someone who was normotensive Associated signs/symptoms : renal artery bruits eg Family history : essential HTN often has 1st degree relatives, secondary is more spontaneous

Answer 14

—most cases are **essential HTN 90%** **Other causes** —chronic renal disease —primary aldosteronism —renovascular —pheochromocytoma (A hormone-secreting tumor that can occur in the adrenal glands) —coarctation of the aorta —Cushing syndrome

Answer 15

—generally asymptomatic —LVH, heart failure, MI, Ischemic —cerebri vascular > stroke —aorta & peripheral vascular > aneurysm, dissection and atherosclerosis —kidney > nephrosclerosis and renal failure —retina > arterial narrowing, haemorrhages,exudates, papilledema

Answer 16

—fundoscopic for **retinopathy (disk edema, hemorrhages, arteriolar narrowing)** —neck for **JVD, bruits, goiter** —heart for **murmurs, gallops** —abdomen for **bruits and central obesity** —extremities for **diminished or absent pulses, hair loss, edema**

Answer 17

—**UA** especially for proteinuria —**A1C, lipid panel, TSH, chemistry panel, CBC** —**EKG** for arrhythmias and LVH —**echo** to assess for structure heart disease —possible **renal u/s, thyroid u/s**

Answer 18

—lifestyle modifications first —Start if the pressure is **>130/80** mmHg especially if the patient has CAD risk factors —if the pressure is **>20/10mmHg over goal** after initial therapy, then likely two agents will be needed —re-check pressure after **one month**. If not at goal (120/80), titration dose or add second agent. Once at goal, assess every **3-6 months**

Answer 19

Consider: concomitant diseases, cost, race, and drug-drug interactions _Main classes_ —thiazide diuretics —calcium channel blockers —ace inhibitors or ARB —beta blocker: 4th line agent, not as effective. Side effects in younger people, fatigue. Very useful in pts who have had an MI, good for CAD. **The rest:** —loop diuretics: mostly used for heart failure, volume overload situations —mineralocorticoids receptor antagonist (aldosterone) —alpha blockers (terazosin) —central alpha-2 agonists (colonising, methyldopa) —direct vasodilators (minoxidil, hydralazine)

Answer 20

Diuretics: reduce circulating volume Sympatheolytics: reduce HR, cardiac contractility, renin secretion. Decrease sympathetic tone Vasodilators: reduce vascular resistance Renin-angiotensin system antagonists (ACEI/ARB)

Answer 21

Severe blood pressure is : **180/120** **Emergency** is defined as severe blood pressure **WITH end organ damage** — look at labs. End organ damage could be high troponin, pulmonary edema, papilledema, renal failure **Urgency**: severe BP **without end organ damage**

Answer 22

**Brain**: encephalopathy or signs of stroke/intra cerebral haemorrhage (CT scan) **Eye**: retinopathy (fund.exam) Evidence of damage to heart including **Ischemia**: troponin leak, EKG changes And **heart failure** (echo to assess LV< chest XRay and BNP for pulmonary edema and elevated JVP) Renal damage as eveidenced by **elevated creatinine or proteinuria/hematuria** **Aortic dissection**

Answer 23

—undiagnosed essential HTN and initial visit —non-adherence to anti-HTN and rebound effect —street drugs —CKD —secondary HTN causes including **renal artery stenosis and pheochromocytoma** (small vascular tumour of the adrenal medulla causing irregular secretion of epinephrine and norepinephrine leading to attacks of raised BP, palpitations and headaches) —sleep apnea

Answer 24

Not the same as for essential HTN! Require **IV meds: including CCV, BB, nitrates, direct vasodilators** and **ICU level of care**. Don’t want to drop it too quickly because those organ systems have been used to that pressure for a while. So it can cause Ischemic or stroke if you drop too quickly (hypoperfusion) Goals: —reduce MAP (SBP+2/DBP/3) which is the average arterial blood pressure over one cardiac cycle **by no more than 25% in the first few hours** (know this for critical care!) —if stable, lower to a goal of **160/100 within the next 2-6 hours** followed by adding oral agents and wean off IV meds

W2 Cardiovascular Disease Flashcards

(50 cards)