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Review / Wrong Answers > DIT review - Cardiology 6 > Flashcards

DIT review - Cardiology 6 Flashcards

1
Q

What are the treatment options for primary (essential) HTN?

A

Thiazide diuretics

Dihydropyridine CCBs

ACEI / ARBs

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2
Q

What treatment do blacks and elderly respond better to for primary HTN

A

CCBs

  • Skethcy = elderly black man with calci-yum ice cream in the dippin pool
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3
Q

What drugs should be used with caution in patients with HTN and heart failure

A

Beta-blockers

Must be used with caution and contraindicated in cardiogenic shock

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4
Q

What is the problem with using beta-blockers in patients with HTN and DM?

A

Beta-blockers may mask the symptoms of hypoglycemia

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5
Q

What drugs can be used for hypertension in pregnancy

A

THINK: Hypertensive Mothers Like Nifedipine

Hydralazine, Methyldopa, Labetalol, Nifedipine

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6
Q

What drugs can be used to treat Hypertensive emergency

A
  • Labetalol (alpha and beta blocker)
  • Calcium channel blockers (Clevildipine and Nicardipine)
  • Hydralazine
  • Nitroprusside
  • Fenoldopam
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7
Q

What is the MOA of Labetalol treating hypertensive emergency

A
  • Labetalol is an alpha and beta antagonist
    • = alpha and beta buttons on organ
  • Beta-blockers lower BP by directly decreased HR and contractility
  • Alpha-1 antagonists lead to vasodilation
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8
Q

Describe the MOA of CCBs in treating HTN emergency

A
  • Remember that dihydropyridines CCBs cause arteriolar dilation which reduces systemic resistance (e.g. afterload)
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9
Q

Describe the MOA of Hydralazine

A
  • Mechanism of action:
    • Direct arteriolar vasodilator with little or no effect on venous circulation
      • = dilated red hose
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10
Q

Describe the main adverse effect of Hydralazine and what can be done to minimize the effect

A
  • Can cause hypotension
    • = pregnant lady fainting
  • Hydralazine induced reflex tachycardia can worsen angina
    • = anvil anchoring hydroboat
  • Because of worsening angina, a beta-blocker is co-administered
    • = beta-1 bugler leaving to get on hydro boat and pushing over the reflex tachycardia hammer doc
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11
Q

What drug can be combined with Hydralazine to treat heart failure

A
  • Hydralazine combine with nitrate (e.g. Nitroglycerine) can treat heart failure
    • Hydralazine is an arteriolar dilator to decrease afterload
    • Nitrates act as venous dilators to decrease preload
      • = dynamite = stick of nitroglyceri
      • = failing heart balloon
    • This combo provides mortality benefit for certain patients in heart failure
      • = guardian angel life preserver sign
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12
Q

What drugs cause drug-induced lupus?

A
  • SHIPP-E
    • S – sulfa drugs
    • H – Hydralazine
    • I – Isoniazid
    • P – Procainamide
    • P – Phenytoin
    • E – Etanercept
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13
Q

Describe the MOA of nitroprusside

A
  • Mechanism of action:
    • Vasodilation via nitric oxide
      • = nitric oxide exhaust
    • Nitric oxide promotes smooth muscle relaxation by increasing GMP
      • = Grumpy guy near nitro boat
    • Leads to both venous and arteriolar vasodilation (decreased preload and afterload)
      • = sailor of nitro-boat with dilated red sleeves and blue pants
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14
Q

Adverse effects of Nitroprusside

A
  • NO is metabolized to cyanide (poison)
    • = blue cyanide exhaust pipe
  • Cyanide toxicity is associated with seizures
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15
Q

MOA of Fenoldopam

A
  • Sketchy = old lady Pam
  • Mechanism of action
    • Selective dopamine 1 receptor agonist
      • = old lady propelling from a single rope
    • Results in a rise in cAMP
      • = camping tent
    • cAMP causes vasodilation in arteries
      • = dilated red sleeves
    • Can also cause coronary vasodilation
      • = dilated coronary crown
    • Dilation of renal arteries, increasing renal perfusion
      • = kidney shaped thing attached to rope
    • Dopamine also leads to increased Na+ and water excretion
      • = salty peanuts falling into water = natriuresis
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16
Q

What are the type of arteriosclerosis

A

(1) Arteriolosclerosis
(2) Monckeberg medial calcific sclerosis
(3) Atherolsclerosis

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17
Q

Describe the 2 type of arteriolosclerossi

A
  • (1) Arteriolosclerosis
    • Affects small arteries and arterioles
    • 2 types:
      • Hyaline
        • Caused by protein leaking into vessel wall, producing vascular thickening
        • Consequence of benign HTN or diabetes
      • Hyperplastic
        • Thickening of vessel wall caused by hyperplasia of smooth muscle
        • Consequence of severe HTN
    • Results in reduced vessel caliber with end-organ damage
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18
Q

Describe microscopic appearance of hyaline arteriolosclerosis

A
  • Protein seen as pink hyaline on microscopy
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19
Q

Describe microscopic appearance of hyperplastic arteriolosclerosis

A
  • “Onion skin” on microscopy (too many muscle layers)
20
Q

Describe the presentation of Monckeberg medial calcific sclerosis

A
  • Calcifications in the media of medium-sized arteries
  • Non-obstructive – clinically benign
21
Q

Rank the affected vessels of atherosclerosis in order

A
  • Abdominal aorta > coronary artery > popliteal artery > carotid artery
22
Q

Describe the pathogenesis of atherosclerosis

A
  • Endothelial damage = lipids leak into intima = macrophage oxidize and consume lipids = result in foam cell = fatty streak (collection of macrophages with lipids within them) = smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition à fibrous plaque = complex atheroma
23
Q

What is the diagnosis of this classic presentation: palpable, pulsatile abdominal mass

A

Abdominal aortic aneurysm

24
Q

What does it mean to have a R dominant heart

A
  • Posterior descending/interventricular artery arises from RCA
  • This occurs in 80% of population
25
Q

What is the most common coronary artery to be occluded

A

Left anterior descending (LAD)

26
Q

What is the most posterior part of the heart and how can it cause complications

A
  • Left atrium is the most posterior part of the heart
    • Enlargement can cause dysphagia due to compression of esophagus or hoarseness due to compression of L recurrent laryngeal nerve
27
Q

What will you see on EKG in Prinzmetal angina and how do you treat it?

A

Transient ST elevation

Treat with Dihydropyridine CCBs

28
Q

MOA of statins

A
  • Mechanism of action:
    • Main action is lowering of LDLs
    • Statins inhibit HMG CoA reductase, and thus prevent endogenous cholesterol production
      • = pirate knocking over HMG crude ore-reducer
    • In response to decreased hepatic cholesterol synthesis, hepatocytes will increase LDL receptor expression on their surface, thus clearing LDL from circulation
      • = statin-punk pirate threatening workers to pull in LDL ship
29
Q

Effects of statins on LDL, HDL, and TGs

A
  • Most powerful drug for lowering LDL cholesterol (30-60%)
  • Mild effect of lowering triglycerides (Statins are not first line)
  • Mild increase in HDL (Statins are not first line)
30
Q

Adverse effects of statins

A
  • Teratogenic (maybe)
    • = tarantula
  • Myopathy (muscle weakness/soreness) – occurs weeks to months after starting therapy
    • = king with it out of crispy chicken leg
  • May cause elevations in serum CK
    • = Crispy chicKen bucket
  • Hepatotoxicity – Mild elevations in liver function tests (LFTs) are common (reversible with discontinuous of drug)
    • = raised LFT flag
31
Q

Describe the production/use of bile acids

A
  • Bile acids (derived from cholesterol) are released into the intestinal lumen
    • = sea “gall” droppings covering cholesterol gold bars = bile acids
  • The liver metabolizes cholesterol into bile acids (conjugated to become water soluble aka bile salts)
    • = liver station worker loading sea “galls”
  • Bile acids are secreted and stored in the gallbladder and then released into the intestine to aid in the absorption of fat
    • sea gull exiting liver to go to green “gallbladder” station
  • Within the intestines, 95% of bile acids in the ileum are recycled back to the liver through enterohepatic circulation
    • = sea gull dropping swept back into liver station
32
Q

MOA of Cholestyramine

A
  • Sketchy = Cho”lobster”amine
    • MOA - precent intestinal reabsorbtion of bile acids so that the liver must use up cholesterol to make more
  • Bile acid resins bind bile acids in the intestinal lumen and prevent the absorption of bile, thus preventing recycling of bile acids back to the liver
    • = lobster disabling the sea gull droppings sweeper from sending bile acids back to liver
  • The bind to bile acids and then bring them to the colon to be excreted
  • Because there is a decrease in bile acids, the liver must promote synthesis of new bile acids (derived from cholesterol), depleting the liver cholesterol stores
    • = empty gold chest in the liver port
  • Liver will compensate by:
    • Increasing activity of HMG CoA reductase to synthesize more cholesterol
      • = crude ore reducer
    • Upregulated expression of LDL receptors, decreased circulating LDL
      • = activating LoaD-L receptor
33
Q

Effects of bile acid resins on LDL, HDL, and TG

A

20% reduction in LDL (not first-line, Statins are)

Minimal increase in HDL and TG

34
Q

Adverse effects of Bile acid resins

A
  • Increase in serum triglycerides
    • Increased endogenous production of cholesterol will also cause increase in hepatic production TAG and VLDL
      • = lobster pushing out VLDL (hypertriglyceridemia)
    • So should not be used in hypercholesterol patients who also have hypertriglycerides
  • Cholesterol gall stones (liver is throwing too much cholesterol into biliary tract
    • = sea gull standing on stones
  • GI upset (constipation and bloating)
    • = lobster clamping GI pipe
  • Steatorrhea (can lead to reduced absorption of fat soluble vitamins, ADEK)
    • = DEcK-A
  • Bile-acid binding resins decrease statin absorption (Must be given 4 hours apart)
    • = lobster clashing with statin pirate
35
Q

MOA of Ezetimibe

A
  • Sketchy = Z-shaped eel
  • Mechanism of action:
    • Binds cholesterol in the GI tract, preventing their absorption
      • = eel blocking gold delivery to chylomicron hot air balloon at intestinal lumen
    • No delivery of cholesterol to liver via chylomicrons (restricted access to exogenous cholesterol)
      • = empty chest deliver from hot air balloon
    • This will lead to:
      • Increasing activity of HMG CoA reductase to synthesize more cholesterol
        • = crude ore reducer
      • Upregulated expression of LDL receptors, decreased circulating LDL
        • = activating LoaD-L receptor
36
Q

Effects of Ezetimibe on LDL, HDL, and TG

A

Causes LDL reduction (but should be used in conjunction with statins)

No effect on HDL or TAG

37
Q

Adverse effects of Ezetimibe

A
  • Increase in transaminases – Increased LFTs
    • =raised LFT flag
  • Diarrhea/steatorrhea
    • = oily water coming from eel in water
38
Q
A
39
Q

MOA of fibrates

A
  • Decreases serum VLDL (35-50% and decreased triglycerides by activating PPAR-alpha at liver and peripheral tissues
    • = news PPAR of light house attendant, being used as a signal
  • When activated, PPAR-alpha upregulates LPL at extra-hepatic sites
  • This means increased hydrolysis of chylomicron and VLDL TG’s at peripheral tissues – aka decreased serum TGs
    • = Jellyfish taking down VLDL ship
    • = trident passengers escaping from ships that were trapped by jellyfish
  • Less VLDLs means less conversion into LDLs (very mild effect )
    • = jelly fish sinking LDL ship
  • Elevate HDLs
    • Fibrates activate the synthesis of Apolipoproteins A1 and A2 by hepatocytes, which are necessary for production of nascent HDLs
      • = jelly fish raising HDL submarine
40
Q

Effects of Fibrates on LDL, HDL, and TAG

A

First line treatment for lowering TAG

Minimally elevates HDL and lowers LDL

41
Q

Adverse effects of fibrates

A
  • Myopathy
    • = bit chicken leg
    • Risk is even more elevated when combined with statins
  • Increased risk for cholesterol gallstones
    • = sea gull balancing on stones
      • Inhibition of cholesterol 7a-hydroxylase, which catalyzes the rate limiting step in the synthesis of bile acids
      • Reduced bile acid production results in decreased cholesterol solubility in bile
      • Leads to increased formation of cholesterol stones
42
Q

MOA of Niacin

A
  • Mechanism of action:
    • Unknown
    • Raises HDL (30%)
      • Most effective drug for increasing serum HDL
        • = elevated HDL submarine on top of monster
      • Decreases HDL cholesterol transfer and delaying HDL clearance
    • Decreases VLDL, and thus decreased TG
      • Acts at the liver to inhibit VLDL secretion
        • = Monster grabbing on to VLDL ship
        • = trident passengers escaping airship held by monster
      • Also reduces TG release from adipose tissue
    • Decreased LDL (mild) due to lowering of VLDL
      • = monster sinking LDL ship
43
Q

Effects of Niacin on LDL, HDL, and TAG

A

First line treatment for raising HDL

Minimally lowers TAG and LDL

44
Q

Adverse effects of Niacin

A
  • Cutaneous vasodilation and sensation of warmth (flushing)
    • = red fiery furnace
    • This effect is mediated by prostaglandins
      • = pro-slugger bat
    • Effect is counter-acted by NSAIDs (including aspirin) – take aspirin 30 min before niacin
      • = fire extinguishers
  • Hyperglycemia
    • = guy sitting on monster throwing candy into mouth
  • Hyperuricemia = gout precipitation
    • = yellow knitting needles
  • Elevated LFTs leading to severe hepatotoxicity (requires monitoring)
    • = raised LFT flag on flaming liver
45
Q

Effect of fish oil

A

Lower TAG

46
Q

What are the 3 types of acute coronary syndrome (ACS)

A
  • ST segment elevation MI (STEMI)
  • Non-ST segment elevation MI (NSTEMI)
  • Unstable angina

Review / Wrong Answers (140 decks)

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