Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
171 Cards in this Set
- Front
- Back
|
t/f
most pt's are asymptomatic before disease clinically evident |
t
|
|
|
metabolic syndrome more than or equal ---- issues
|
3
|
|
|
metabolic sydrome more than or equal 3 of the following
|
abd obesity
elevated tg increased bp elevated glucose low hdl proinflammatory state |
|
|
waist size of abd obesity
|
women >/= 35
men >/= 40 |
|
|
elevated tg in metabolic syn
|
>/= 150
|
|
|
elevated fasting glucose value in metablic syndrome
|
>/= 100 mg/dl
|
|
|
HDL </= in metablolic syndrome
|
men: 40 mg/dl
women: 50 mg/dl |
|
|
symptoms
|
none
severe cp sweating anxiety sob loss of consciousness speech or movement difficulty abd pain sudden death |
|
|
signs
|
none
severe abd pain eruptive xanthomas pancreatitis peripheral polyneuropathy htn bmi >30 kg/m^2 waist size > 40 men waist size > 35 women |
|
|
desirable cholesterol
|
< 200
|
|
|
borderline high cholesterol
|
200-239
|
|
|
high cholesterol
|
240
|
|
|
opitmal ldl
|
< 100
|
|
|
near or above optimal ldl
|
100-129
|
|
|
borderline high ldl
|
130-159
|
|
|
high ldl
|
160-189
|
|
|
very high ldl
|
190
|
|
|
low hdl
|
< 40
|
|
|
high hdl
|
60 mg/dl
|
|
|
normal tg
|
< 150
|
|
|
borderline high tg
|
150-199
|
|
|
high tg
|
200-499
|
|
|
very high tg
|
500
|
|
|
major risk factors that modify ldl goals
|
age men >/= 45 women >/= 55
family hx of premature chd cigarette smoking htn low hdl |
|
|
family hx of preamature chd
male age? women? |
male>/= 45 yrs
women >/= 55 yrs |
|
|
hdl >/= ---- substract 1
|
60
|
|
|
chd/chd equivalents
|
other atherosclerotic disease: pvd, AAA, symptomatic carotid aretery disease
DM multiple risk factors that confer a 10 yr risk for CHD > 20 % |
|
|
what does the framingham risk score look at
|
age
total cholesterol smoking status hdl cholesterol systolic bp |
|
|
t/f
you will use the framingham risk score if the pt has DM |
f
cuz it's a risk equivalent |
|
|
primary tx target
|
LDL
|
|
|
more CHD risk factors or higher framingham global risk score:
|
more stringent LDL goal
|
|
|
good candidates for for goal LDL < 70 mg/dl
|
people w/ IHD/CAD
initial or recurrent ACS dm current tobacco use diffuse vascular disease metabolic syndrome |
|
|
circumstances against aggressvie tx
|
money
ClCr < 30ml/min age > 80 yrs small body frame/frailty life expectancy < 2 yrs recent comorbitiy/instablity critical drug interactions ~ 40% reduction and close to goal |
|
|
w/ TLC how many times do you evaluate LDL response before you cang the f/u to q 4-6 mo or add drug tx
|
twice (6 weeks apart)
|
|
|
% decrease in LDL for rosuvastatin
|
45-55%
|
|
|
atorvastatin % decrease in LDL
|
40-60 %
|
|
|
% decrease in LDL for fluvastatin
|
20-40 %
|
|
|
% decrease in LDL for simvastatin
|
30 - 50 %
|
|
|
% decrease in LDL for lovastatin
|
20 - 40%
|
|
|
% decrease in LDL for pravastatin
|
20-40 %
|
|
|
% increase in HDL for niacin
|
15-35%
|
|
|
% decrease in TG for rosuvastatin
|
20-30%
|
|
|
which two drugs has a 20 - 50 % decrease in TG
|
niacin
fibrates |
|
|
this is not the 1st line of tx if TG's are elevated at baseline
|
bile acid resins
(no change in tg or increase in TG) |
|
|
VLDL =
|
TG/5
|
|
|
statins reduce --- cholesterol synthesis, lowering intracellar choleserol, which stimulates upregulation of LDL receptors and increase the uptake of ----- particles fromt eh systemic circulation
|
hepatic
non-HDL |
|
|
dose of hmg-coa reductase inhibitors
|
once daily in evening
|
|
|
exceptions to once daily evening
|
atorvastatin
rosuvastatin |
|
|
------- requires dosage adjustment in severe renal impairment and hepatic disease
|
rosuvastatin
|
|
|
AE of statins
|
elevated transaminases
myalgia myopathy rhabodmyalgia flu like symptoms mild GI disturbances |
|
|
when will you see a reduction in LDL-C
|
days
|
|
|
when will you see cardiac events reduced
|
years
|
|
|
most effective drug at lowering LDL-C
|
statins
also very well tolerated |
|
|
when shoud you test statins/liver safetly
|
before
12 wks after after dose increase periodically |
|
|
s/s of liver toxicity in statins
|
jaundice
malaise fatigue lethargy |
|
|
if objective evidence such as Labs and S/S show liver toxicity what do you do
|
d/c statin
ID etiology |
|
|
isolated asymptomatic AST/ALT 1-3 x ULN:
|
don't d/c
|
|
|
isolated asymtomatic AST/ALT > 3 x ULN:
|
repeat, r/o other etiologies
continue, reduce dose, or d/c |
|
|
statins are CI in decompensated ----
|
cirrhosis
|
|
|
for every 5 mg dose of statin there's a ---% reduction in total cholesterol for doubling dose
|
5
|
|
|
double dose decrease LDL by --%
|
7
|
|
|
when do u check a baseline CK
|
high risk pt
|
|
|
t/f
routine CK in asymptomatic pts not recommended |
true
|
|
|
symptoms monitoring w/ ck measurement on in --- individuals
|
symptomatic
|
|
|
what other diseases can cause elevated ck
|
hypothyroidism
trauma falls seizures rigourous exercise infection |
|
|
what can exacerbate ck levels w/ statins
|
grapefruit juice consumption
concomittant meds herbals |
|
|
if there's unexplained -- or cognitive impairment d/c statin for ---- mo (PN) or 1-3 mo (CI)
|
PN
3-6 |
|
|
w/ pn or CI if there's improvement:
no improvement: |
risk/benefit
no improvement: restart |
|
|
BAR
|
cholestyramine
colestipol colesevelam |
|
|
cholestyramine dose
|
4-16 g/d
|
|
|
colestipol dose
|
5-20 g/d
|
|
|
colesevelam dose
|
625 mg tabs
6-7 tabs/day |
|
|
BAR reduce --- events
|
coronary
|
|
|
AE of BAR
|
GI: constipation, bloating, ab pain, flatulence
Lack of systemic toxicity |
|
|
DI of BAR
|
bind other neg charged drugs
impede absorption of drugs and/or fat-soluable vits must give other drugs 1 hrs before 4-6 hrs after |
|
|
when must you give other drugs w/ BAR
|
1 hr before or 4-6 hrs after
|
|
|
BAR impede ---- soluable vits
|
fat
|
|
|
t/f
BAR is usu an add-on tx to statin |
t
|
|
|
t/f
statins are the safest of all lipid lowering agents |
f
BAR |
|
|
t/f
BAR well tolerated by patients |
f
poorly tolerated esp at higher doses only moderately effective at cholesterol reduction with monotherapy |
|
|
bar may aggravate ------
|
hypertriglyceridemia
|
|
|
caution w/ bars and TG > --- mg/dL
|
200
|
|
|
BAR CI w/ TG > -- mg/dL
|
400
|
|
|
primary mechanism of bar in the ----
|
terminal ileum
|
|
|
bar increase ---- BA excretion
|
fecal
|
|
|
bar increase:
|
LDL receptors
VLDL and LDL removal cholesterol 7-a hydroxylase conversion of cholesterol to BA BA secretion |
|
|
AE of BAR
|
gi distress/constipation
hypernatremia hypercholestermia impair fat soluable vit absorption reduce bioavailability of other meds |
|
|
to prevent bar
|
titrate slowly
increase fluid intake increase dietary bulk stool softeners |
|
|
fat soluable vit absorption
|
A
D E K |
|
|
what meds will have reduced bioavailability w/ BAR
|
warfarin
levothyroxine digoxin dose 6 hrs from other meds |
|
|
-- dose of bar well tolerated
|
low
|
|
|
which formulation of bar may increase ----
|
palatability
but, tablets are large |
|
|
what do you mix bar w/
|
mix w/ liquids or food such as OJ, oatmeal, applesauce
|
|
|
which is odorless and tasteless
|
Colestipol
|
|
|
DI of ezetimibe
|
cholestyramine
fibrates cyclosporine |
|
|
t/f
significant drug interactions w/ statins |
f
no signi pharmocokineti interaction |
|
|
where does ezettimibe work
|
jejunum
|
|
|
indications for ezetimibe
|
hypercholesterolemia
homozygous familial hypercholesterolemia homozygous sitosterolemia |
|
|
ezetimibe selectively inhibits --- cholesterol absorption
|
intestinal
|
|
|
eze decreases ---- delivery of cholesterol to the liver
|
intestinal
|
|
|
eze increases expression of hepatic---- ---
|
LDL receptors
|
|
|
eze decreases cholesterol content of ---- particles
|
artherogenic
|
|
|
eze and its active ---- metabolite circulate enterohepatically
|
glucoronide
|
|
|
eze and its active glucuronide metabolite delivers agent back to the site of action and limits --- exposure
|
systemic
|
|
|
eze CI
|
hypersensitiviy
unexplained or mod to severe liver enzyme elevation preg c category as monotherapy all statins are CI in pregnancy and nursing women |
|
|
all -- are ci in pregnancy
|
statins
|
|
|
in combo tx what dose of BAS do you give e/ statin
|
low dose
|
|
|
t/f
there's HDL benefits w/ BAS and statin |
f
no benefits |
|
|
when is BAS and statin CIed
|
in high TG
|
|
|
statin and niacin combo esp desired in
|
pts w/ abnorm HDL-C ad or TG not corrected w/ statin alone
|
|
|
statin and niacin combo have an increased risk of ---- and ---
|
hepatoxicity
myopathy |
|
|
statin and fibrate are desirable in pt's w/ abnl ---- and/or ---
|
HDL-C
TG |
|
|
statin and fibrate increased risk of ------
|
myopathy
more risk than statin/niacin |
|
|
in pt w/ TG > ---- mg/dl consider ------- goal in addition to LDL goal
|
200
non-HDL |
|
|
Non-HDL = Total ----- - HDL
|
cholesterol
approximates LDL + VLDL |
|
|
t/f
for pts w/ very high TG (> 500), control of TG can take primary focus, to reduce risk of abd pain and ----- |
t
pancreatitis |
|
|
pros of adding niacin or fibrate to a statin
|
better decrease in TG and increase in HDL
may decrease LDL-C more decrease Lp(a) (niacin) increase LDL particle size decrease fibrinogen (fibrate) agiographic data |
|
|
cons of adding niacin or fibrate to a statin
|
increased cost and complexity
increased myositis risk increase hepatitis risk (niacin) potential for drug interaction minimal outcome data |
|
|
targets for tx after LDL-C goal i pts w/ TG >/= 200 mg/dL
|
know chart
|
|
|
normal fasting tg's
|
< 150 mg/dl
|
|
|
borderline - high tg's (fasting)
|
150 - 199 mg/dl
|
|
|
high fasting tg
|
200-499
|
|
|
very high tg's (fasting)
|
>/= 500 mg/dl
|
|
|
high --- are an independent risk factor for chd, but much less strong than ---
|
TG
LDL |
|
|
in diabetics, good --- control is central to controlling ------
|
glycemic
triglycerides |
|
|
tx of mixed hyperlipidemia
|
TLC
Drug tx: achieve LDL-C goal achieve non-HDL-C goal |
|
|
fibric acids AE
|
GI complaints
raskh myalgia HA fatigue transient increase in transaminase and alkaline phosphate gallstones enchanced hypoglycemicc effects in pts on sulfonylureas may potentiate effects of oral anticoagulants: monitor PT/INR |
|
|
fibric acids may enhance ---- effects in pt w/ sulfonylureas
|
hypoglycemic
|
|
|
important to monitor ----- cuz fibric acids may potentiate effects of oral anticoagulants
|
PT/INR
|
|
|
fibric acids
|
gemfibrozil
fenofibrate clofibrate |
|
|
fibric acids reduce ---
|
tg
reduce hepatic production |
|
|
fibric acids also inhibit synthesis and increase clearance of VLDL carrier and reduces ----- production
|
VLDL
|
|
|
fibric acid result in concurrent increase in -----
|
LDL
|
|
|
--- remains fairly unchanged in fibric acids
|
TC
|
|
|
t/f
fibric acids may increase HDL by >/= 10 to 15 % |
t
|
|
|
fibric acids may reduce LDL by 20 - 25 % in pt's w/ heterozygous ---- ----
|
familial hypercholesterolemia
|
|
|
which is more effective and which is better tolerated
fibric acids or niacin |
more effective: niacin
better tolerated: fibric acid |
|
|
fibric acids used in ---- cuz of better tolerability
|
elderly
|
|
|
fibric acid used in monotherapy due to --- ----
|
low HDL - C
|
|
|
gembibrozil doses -----
|
BID 30 min before meals
|
|
|
t/f
fenofibrate should be taken w/ food |
f
can be taken w/out regard to food |
|
|
fibric acid CI in ------- ---
|
renal failure
|
|
|
combo tx w/ fibric acids w/ ---- or --- increase risk of ---- toxicity
|
niacin
statins muscle |
|
|
diets rich in ---- --- -- from oily fish decrease TC, TG, LDL, increase HDL, and decrease CV events
|
omega 3 fatty acids
|
|
|
rx fish oil:
|
Lovaza
lowers TG 14 - 30 % raises HDL ~ 10 % |
|
|
fda approved as dietary adjuncy for very high --- levels ( > 500 mg/dl)
|
TG
|
|
|
aeof omega 3 fatty acids
|
thrombocytopenia, bleeding disorders
GI disturbances fishy aftertaste worsening glycemic control increased LDL abnorm LFTs |
|
|
safe dose of omega 3 fatty acids
|
</= 3 g/day
|
|
|
-- to -- g of EPA and DHA may be used for very high TG
|
2-4
|
|
|
most fish oil tabs contain --- mg EPA and --- mg of DHA
|
180 mg EPA
120 mg DHA |
|
|
tg's more than --- mg/dl you should take -- to -- g/day DHA and EPA for a 45 % decrease in TG
|
500
3 - 4 g/day |
|
|
modiafiable risk factors contributing to HDL
|
smoking
obesity lack of exercise high carb diet |
|
|
non modifaible risk factor
|
male gender
insulin resistance |
|
|
nicotinic acid decreases hepatic production of ---- and of --- B
|
VLDL
apo B |
|
|
t/f
higher doses of niacin are harder to tolerate and have a smaller effect on LDL |
t
|
|
|
niacin will --- hdl
|
increase
|
|
|
best med to increase HDL
|
nicotinic acid
|
|
|
IR dose of niacin
|
2-4 g/d
|
|
|
extended release (niaspan) dose
|
1-2 g/d
|
|
|
otc products, sustained release of nicotinic acid dose
|
</= 2 g/d
|
|
|
ae of nicotinic acid
|
flushing
itching ha ( IR, Niaspan) hepatotoxicity GI (sustained-release) acitivation of peptic ulcer hyperglycemia reduced insulin insensitivity |
|
|
CI
|
active liver disease
unexplained LFT elevation peptic ulcer disease |
|
|
how do manage flushing se
|
low fat snack and ASA at bedtime
|
|
|
metabolic syndrome:
tg |
>/= 150 mg/dl or tx
|
|
|
HDL-c in met syndrome
|
< 40 in men
< 50 women |
|
|
bp in met syn
|
>/= 130/85
|
|
|
fasting glucose
|
>/= 100 mg/dl
|
|
|
DOC in pt w/ low HDL-C +/- high TG ad high LDL-C
|
niacin
|
|
|
drawback of niacin
|
difficult to take if not ER (BID to TID)
facial flushing gi side effects |
|
|
niacin ci in --- ---- ---
|
chronic liver disease
|
|
|
caution w/ niacin in
|
dm
gout significant hyperuricemia pud |
