DIT review - Cardiology 6 Flashcards
1
Q
What are the treatment options for primary (essential) HTN?
A
Thiazide diuretics
Dihydropyridine CCBs
ACEI / ARBs
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
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
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
5
Q
What drugs can be used for hypertension in pregnancy
A
THINK: Hypertensive Mothers Like Nifedipine
Hydralazine, Methyldopa, Labetalol, Nifedipine
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
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
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)
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
- Direct arteriolar vasodilator with little or no effect on venous circulation
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
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
12
Q
What drugs cause drug-induced lupus?
A
- SHIPP-E
- S – sulfa drugs
- H – Hydralazine
- I – Isoniazid
- P – Procainamide
- P – Phenytoin
- E – Etanercept
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
- Vasodilation via nitric oxide
14
Q
Adverse effects of Nitroprusside
A
- NO is metabolized to cyanide (poison)
- = blue cyanide exhaust pipe
- Cyanide toxicity is associated with seizures
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
- Selective dopamine 1 receptor agonist
16
Q
What are the type of arteriosclerosis
A
(1) Arteriolosclerosis
(2) Monckeberg medial calcific sclerosis
(3) Atherolsclerosis
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
- Hyaline
- Results in reduced vessel caliber with end-organ damage
18
Q
Describe microscopic appearance of hyaline arteriolosclerosis
A
- Protein seen as pink hyaline on microscopy
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
What is the most common coronary artery to be occluded
Left anterior descending (LAD)
26
What is the most posterior part of the heart and how can it cause complications
* 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
What will you see on EKG in Prinzmetal angina and how do you treat it?
Transient ST elevation
Treat with Dihydropyridine CCBs
28
MOA of statins
* 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
Effects of statins on LDL, HDL, and TGs
* 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
Adverse effects of statins
* 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
Describe the production/use of bile acids
* 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
MOA of Cholestyramine
* 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
Effects of bile acid resins on LDL, HDL, and TG
20% reduction in LDL (not first-line, Statins are)
Minimal increase in HDL and TG
34
Adverse effects of Bile acid resins
* 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
MOA of Ezetimibe
* 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
Effects of Ezetimibe on LDL, HDL, and TG
Causes LDL reduction (but should be used in conjunction with statins)
No effect on HDL or TAG
37
Adverse effects of Ezetimibe
* Increase in transaminases – Increased LFTs
* =raised LFT flag
* Diarrhea/steatorrhea
* = oily water coming from eel in water
38
39
MOA of fibrates
* 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
Effects of Fibrates on LDL, HDL, and TAG
First line treatment for lowering TAG
Minimally elevates HDL and lowers LDL
41
Adverse effects of fibrates
* 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
MOA of Niacin
* 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
Effects of Niacin on LDL, HDL, and TAG
First line treatment for raising HDL
Minimally lowers TAG and LDL
44
Adverse effects of Niacin
* 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
Effect of fish oil
Lower TAG
46
What are the 3 types of acute coronary syndrome (ACS)
* ST segment elevation MI (STEMI)
* Non-ST segment elevation MI (NSTEMI)
* Unstable angina
