Cardiology Flashcards

1
Q

What is atherosclerosis?

A

A progressive inflammatory disorder of the arterial walls characterized by lipid rich deposits (atheromas)

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2
Q

What risk factors contribute to Atherosclerosis?

A

Modifiable: HTN, DM, Hyperlipidemia, Smoking, Alcohol consumption, obesity (esp truncal), Exercise

Non-modifiable: Age, Sex, FH (HTN, DM, Hyperlipidemia)

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3
Q

Preventative measures for atherosclerosis?

A

Primary prevention:

a) Modify the risk of the entire population through diet and lifestyle advice (Balanced diet, regular exercise, avoid smoking, maintain ideal BMI)
b) Targeted strategy: High risk groups

Secondary prevention: Pts who already have evidence of atheromatous plaques & have high risk of cardiovascular events

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4
Q

Preventative measures for atherosclerosis?

A

Primary prevention:

a) Modify the risk of the entire population through diet and lifestyle advice (Balanced diet, regular exercise, avoid smoking, maintain ideal BMI)
b) Targeted strategy: High risk groups

Secondary prevention: Pts who already have evidence of atheromatous plaques & have high risk of cardiovascular events

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5
Q

Unstable vs Stable atheromatous plaques?

A

Unstable plaque: Thin fibrous cap, large lipid core, increased inflammation

Stable plaque: Thick fibrous cap, negligible atheromatous core, minimal inflammation

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6
Q

Clinical consequences of Atherosclerosis include:

A
  1. Ischemia distal to plaque–> MI, stroke, PAOD
  2. Plaque erosion/rupture–> Thrombosis, Embolus, Haemorrhage into plaque
  3. Weakening of media of vessel wall–> aneurysm formation
  4. Critical stenosis–> angina, claudication
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7
Q

Arteriolosclerosis (characteristics)

A

This is a type of arterosclerosis. Affects small arteries & arterioles. May cause ischaemic injury distally. Hyaline or Hyperplastic. Associated with HTN & DM

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8
Q

Monckeburg medial sclerosis (characteristics)

A

This is a type of arterosclerosis. Char by calcific deposits in muscular arteries. Lesions don’t encroach the vessel lumen. Usually not clinically significant

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9
Q

What is HTN?

A

Elevated blood Pressure of >/= 140/90mmHg on at least two readings on at least two separate visits

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10
Q

Predisposing Factors for developing HTN?

A
NON-MODIFIABLE
o	Ethnicity (African Americans >Asians or Whites)
o	Family History
o	Age >30
o	Male

MODIFIABLE
o Diet (excessive salt intake/fatty diet)
o Exercise –Sedentary Lifestyle; Obesity (especially abdominal)
o Alcohol consumption
o Smoking
o DM (suspected that insulin resistance in hyperinsulinemia leads to renal sodium retention and proliferation of vascular muscle cells; both lead to increased BP)
o Dyslipidemia
o Psychological Stress

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11
Q

Causes of HTN?

A
  1. Essential HTN (90%, undetermined cause)
  2. Secondary HTN (10%, known cause)
    “RECENT”
    o Renal: Renal artery stenosis, PKD, Renal failure, Glomerulonephritis, SLE, Renal tumours
    o Endocrine: Acromegaly; Hyperthyroidism; Primary Hyperparathyroidism; Primary hyperaldosteronism [Conn Syndrome] (most common); Hypercortisolism [Cushing syndrome]; Phaeochromocytoma; CAH
    o Coarctation of the Aorta
    o Estrogen: OCPs
    o Neurologic: Incr ICP, Psychostimulant use
    o Treatment: NSAIDs, Steroids
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12
Q

What is HTN Urgency?

A

SBP>210 or DBP >120 with minimal or no target organ damage

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13
Q

What is Accelerated HTN?

A

significant recent increase in BP over previous Hypertensive levels associated with evidence of vascular damage on fundoscopy but without papilledema

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14
Q

What is Malignant HTN?

A

Sufficient elevation in BP to cause papilledema and other manifestations of vascular damage (retinal haemorrhages, bulging discs, mental status changes, increasing creatinine)

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15
Q

What is HTN Emergency?

A

Severe HTN (DBP >120) + acute target organ damage

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16
Q

Discuss ACE inhibitors

A

Anti-hypertensive Drug

E.g. Captopril, Enalopril, Lisinopril

MOA: Reversibly inhibits ACE; Prevents inactivation of bradykinin (a potent vasodilator) by ACE

USE: 1st line agent in patients with HTN, IHD, CCF, DM, Renal Dx

ADVERSE EFFECTS: ACEi induced cough, angioedema, hyperkalemia, hypotension, acute renal failure

ABSOLUTE C/I: Hypersensitivity, Pregnancy, breastfeeding, anuria, H/o ACEi induced angioedema

RELATIVE C/I: Aortic Stenosis, Renal dysfxn (alter dose), Bilateral renal artery stenosis, solitary kidney, drug interactions (other anti-HTN, NSAIDs, K+ sparing diuretic)

17
Q

Discuss ARBs

A

Anti-HTN

E.g. Losartan, Candesartan, Valsartan

MOA: Competetive Angiotensin II receptor antagonist

USE: HTN, CCF

ADVERSE EFFECTS: Angioedema, Hyperkalemia

ABSOLUTE C/I: Hypersensitivity, Pregnancy, breastfeeding, anuria, H/o ARB induced angioedema

RELATIVE C/I: Aortic Stenosis, Renal dysfxn (alter dose), Bilateral renal artery stenosis, solitary kidney, drug interactions (other anti-HTN, NSAIDs, K+ sparing diuretic)

18
Q

What is Aliskiren used for?

A

It is a direct renin inhibitor used to treat HTN

MOA: Targets RAAS at point of activation by binding renin

ADVERSE EFFECTS: Rash, Diarrhea, Cough, Angioedema, Gout, Renal Stones

C/I: Hypersensitivity, Pregnancy, Bilateral renal artery stenosis

Drug Interactions with P-glycoprotein inhibitors e.g. (ketoconazole, verapamil, clarithromycin, amiodarone)

19
Q

Calcium Channel blockers can be divided into:

A

Dihydropyridines (e.g. Nifedipine, Clevidipine, Nicardipine, Amlodipine). These act primarily on the vascular smooth muscle

Non-Dihydropyridine:
a) Benzothiazepine e.g. Diltiazem
b) Phenylalkylamines e.g. Verapamil
These act on the heart

20
Q

MOA of Calcium channel blockers

A

CCBs bind to L-type calcium channels on the heart and vascular smooth muscle)–>decr frequency of Ca2+ channel opening in response to cell depolarization

EFFECTS

  1. Vascular smooth muscle relaxation–>vasodilation–>decr PVR, decr afterload–>decr BP
  2. Decr cardiac muscle contractility–>Decr Cardiac output –>decr BP
  3. Decr SAN discharge–>decr HR–>Decr CO–>decr BP
  4. Decr AVN conduction–> termination of supraventricular arrhythmias