cardio: HLD Flashcards

1
Q

statins that must be taken at night

A

lovastatin, simvastatin, pravastatin, fluvastatin

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2
Q

statin that must be taken with food

A

lovastatin

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3
Q

lipophilic statins

A

atorvastatin, pitavastatin, simvastatin, fluvastatin, lovastatin

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4
Q

high intensity statin

A

atorvastatin 40-80mg, rosuvastatin 20-40mg

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5
Q

moderate intensity statin

A

atorvastatin 10-20mg, rosuvastatin 5-10mg, simvastatin 20-40mg

pravastatin 40-80mg, lovastatin 40-80mg, fluvastatin XL 80mg, fluvastatin 40mg BD, pitavastatin 1-4mg

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6
Q

low intensity statin

A

simvastatin 10mg

pravastatin 10-20mg, lovastatin 20mg, fluvastatin 20-40mg

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7
Q

statin potency

A

fluvastatin, pravastatin, lovastatin < simvastative < atorvastatin < rosuvastatin

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8
Q

exogenous cholesterol pathway

A

chylomicrons transport TG and cholesterol from intestine to the tissues > subsequently stored, oxidized to bile acids or secreted in bile unchanged

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9
Q

endogenous cholesterol pathway

A

cholesterol and newly synthesised TG are transported from liver as VLDL to muscle and adipose tissue > TG are hydrolysed and resulting fatty acids enter the tissues > during this process, lipoprotein particles become LDL > cells take up LDL by endocytosis via LDL receptors that recognise LDL apolipoproteins

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10
Q

are statins safe in pregnancy and lactation?

A

no!!!

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11
Q

SAMS: myalgias

A

muscle aches and pain, CK normal

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12
Q

SAMS: myositis/myopathy

A

muscle pain and weakness interfering with daily activities, CK > 10xULN with concerning sx or objective weakness

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13
Q

SAMS: rhabdomyolysis

A

muscle breakdown, CK>40xULN + renal injury

  • occurs when damaged muscle tissue releases its proteins and electrolytes into the blood. These substances can damage the heart and kidneys and cause permanent disability or even death
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14
Q

SAMS: statin-associated autoimmune myopathy

A

HMGCR antibodies, incomplete resolution

  • very rare form of muscle damage caused by the immune system in people who take statin medications
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15
Q

risk factors for SAMS

A
  • age > 75yo
  • female
  • low BMI
  • Asian descent
  • impaired kidney function (CKD stage 3-5) or liver impairment
  • surgery with high metabolic demands, consider holding off before
  • acute infection
  • high level of physical activity
  • excess alcohol
  • drug abuse
  • dietary effects (excessive grapefruit, cranberry juice)
  • hypothyroidism: untreated or undertreated
  • genetic factors: CYP450 or drug transporter related mutations
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16
Q

myoglobinuria

A

myoglobin (muscle proteins broken down) > goes to kidney and bound to renal tubules

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17
Q

if no muscle sx present but CK is raised

A

consider checking thyroid function or muscle related
?clinical significance

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18
Q

DDI with statins: amiodarone

A

do not exceed:
- simvastatin 20mg
- lovastatin 40mg

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19
Q

DDI with statins: macrolide antibiotics

A

do not exceed:
- atorvastatin 20mg, with clarithromycin
- pravastatin 40mg, with clarithromycin
- pitavastatin 1mg, with erythromycin

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20
Q

DDI with statins: amlodipine

A

do not exceed simvastatin 20mg

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21
Q

DDI with statins: colchicine

A

caution with lovastatin, simvastatin, fluvastatin, pitavastatin, pravastatin

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22
Q

DDI with statins: gemfibrozil

A

CI with simvastatin
avoid with: L,P,P,A,F
do not exceed R 10mg (use only if needed, avoidance recommended)

23
Q

DDI with statins: other fibrates

A

caution with all statins

24
Q

DDI with statins: verapamil

A

do not exceed:
- simvastatin 10mg
- lovastatin 20mg

25
Q

niacin and fibric acid drugs can rarely cause rhabdomyolysis or liver failure when used alone, but…

A
  • combining them with statins incr risk of rhabdo or liver failure
  • gemfibrozil should not be combined with statins
  • other fibric acids and niacin are used, with caution, in combi with statins
26
Q

coadm of statins with bile salt binding resins, how is it done?

A

statins should be taken 1hr before or 4h after bile salt binding resins eg. cholestyramine
- bile salt binding resins bind statins in the intestine and reduce their absorption into the body

27
Q

statins and warfarin, ok?

A

statins incr effect of warfarin
- monitor blood clotting ability carefully

28
Q

statins and red yeast rice, ok?

A

should not be combined!!!
- red yeast rice contains chemical that is similar to statins, can lead to serious side effects such as rhabdomyolysis

29
Q

ezetimibe MOA

A

selective inhibitor of cholesterol transoirt protein, Niemann-Pick-C1-like1 (NPC1L1) protein - in walls of GIT and decr uptake into body
BUT effective in absence of dietary cholesterol: can saturate and still block transporters that takes up biliary cholesterol!!!!!

30
Q

ezetimibe ADR

A

URTI, sinusitis, arthralgia, limb pain, diarrhea

31
Q

PCSK9i

A

Proprotein Convertase Subtilisin/Kexin type 9 inhibitors
- evolocumab, alirocumab

32
Q

PCSK9i MOA

A

bines plasma PCSK9, thus incr LDL receptors on the cell surface > incr cellular uptake of circulating LDL from plasma

33
Q

PCKSK9i adm

A

injectibles, every other week or monthly

34
Q

PCSK9i place in therapy

A

due to exorbitant costs, likely to be cost effective only in the very high-ASCVD

35
Q

evolocumab labelled for

A

homozygous familiar hypercholesterolemia

36
Q

PCSK9i adr

A

itching at site, flu-like sx, early concerns of neurocognitive function changes, incr DM risks shown not to be an issue

37
Q

can PCSK9i be used in pregnancy and lactation?

A

use with caution, unknown!

38
Q

concern with LT use of PCSK9i treatment?

A

autoantibodies

39
Q

cholestyramine MOA

A

bile-acid exchange resins, not absorbed or altered by digestive enzymes
- binds bile acid, prevents reabsorption of drug and cholesterol into body
-> large portion of bile acids removed from enterohepatic circulation
-> liver synthesises more hepatic cholesterol
-> incr hepatic demand for cholesterol
-> incr LDLR expression

40
Q

cholestyramine ADR

A

flatulence, constipation, dyspepsia, nausea: use small doses, ingest ample fluids, incr dose gradually
may cause incr TG

41
Q

niacin

A
  • incr HDL by stimulating production of ApoA1 production in liver
  • upregulate lipoprotein lipase resulting in incr catabolism of VLDL
    WITHDRAWN FROM SG
42
Q

cholestyramine must be adm ____ before and ____ after other drugs

A

4h, 1h

43
Q

metabolic syndrome

A
  • FBG > 5.6mmol/L
  • large waist size (central obesity)
  • high BP>130/85mmHg
  • TG>1.7mmol/L
  • low HDL
44
Q

hallmarks of familial hypercholesterolemia

A

fatty deposits around eye cornea, eye, feet, muscle joints

45
Q

heterogyenous familial hypercholesterolemia (HeFH)

A
  • typically develop CAD before 55yo (M) and 66yo (F)
  • risk for CAD is definite or probably and incr at least 10x
  • critical to diagnose early and treat appropriately
46
Q

homogynous familiar hypercholesterolemia (HoFH)

A
  • develop CAD by 20yo and die before 30yo
  • identification of these children is critical
  • treatment with statins/plasma apheresis
47
Q

what hyperlipidemia meds to use for pregnant women?

A

only bile acid sequestrants
- statins, fibrates, ezetimibe, niacin are ci
- no data with pcsk9i

48
Q

when should we stop statin relative to cessation of contraception?

A

4 weeks prior

49
Q

fibrates MOA

A

incr activity of lipoprotein lipase > incr peripheral clearance

50
Q

how often should we monitor for lipid profile?

A

8+/- 4 wks, after starting tx and after adjustment until goal is reached

51
Q

how often should we monitor for ALT?

A

8-12wks after starting and after dose incr
- routine ALT repeat not reco if on sttatin, consider if on fibrates
- annually will do

52
Q

how often should we monitor for ck?

A

routine monitoring not necessary, recheck if pt develops myalgia
- check for baseline, if ck>4xULN then do not start therapy, recheck

53
Q

how often should we monitor for hba1c?

A

regular checks for pt at high-risk of diabetes or high-dose statins