HYPERLIPIDEMIA, ACUTE CORONARY SYNDROME, ANGINA Flashcards
types of hyperlipidemia
- mixed hyperlipidemia (combo of elevated HDL, LDL, or triglycerides)
- hypercholesterolemia (high LDL)
- hypertriglyceridemia (high TG)
Hyperlipidemia- definition
inc levels of lipids/fats in the blood
risk factors of HLD
- diet (alcohol, saturated fats)
- age
- sedentary lifestyle
- fam Hx
- gender (men>women)
- genetic mutations (familial hypercholesterolemia)
HLD clinical features
- asymp
- xanthoma in SEVERE HLD (hard yellow plaque/nodules of tendons and skin)
- pancreatitis w/hypertriglyceridemia
fasting lipid panel goals for pt with HLD
- cholesterol <200
- LDL <100, <70 for DM, CAD
- HDL >40 men, >50 women
- triglycerides <150
LDL is most important for CAD!!!
HLD Tx names
statins, PSK9 inhibitors, niaotinic acid, fenofibrates, bile acid binding resins
HLD- statins
HMG-CoA reductase inhibitor
- Rosuvastatin, atorvastatin, simvastatin, pravastatin
- inhibiting cholesterol synth by inhibiting HMG-CoA reducates in the liver
- this INC LDL receptors–>promotes LDL clearance
- reduces progressions of plaque, reduce mortality
MOST POTENT
crestor, lipitor, zocor, pravachol
HLD- statins side effects
rhabdomyolysis, myalgia, arthralgia, elevated ALT/AST
HLD- PSK9 Inhibitors
- Alirocumab (praluent), avolocumab (repatha)
- inhibit degradation of LDL receptors–> inc LDL clearance
indications
- familial hypercholesterolemia
- CAD
HLD- PSK9 Inhibitors side effects
headaches, diarrhea, URI symptoms
HLD- Niaotinic acid
& side effects
- niacin
- lowers triglycerides
- CAN inc HDL
side effects: facial flushing, pruritis, n/v
HLD- Fenofibrates
& side effects
- gemfibrozil
- lower triglycerides
side effects: n/d, abdominal pain
HLD- bile acid binding resins
- cholestyramine colestipol, colesevelam
- lowers LDL
- Does not change triglycerides
GI side effects
RARELY USED
which HLD medication is the most potent?
statins
Angina Pectoris- definition and types
inadequate tissue perfusion of the myocardium
- imbalance in cardiac demand and tissue perfusion
- CP originates from heart
- typical or atypical
MC is CAD
typical Angina Pectoris- clin features
- men
- mid sternal or L sided
- squeezing, tightness, pressure
- “sitting on chest”
-
levine sign–> CLENCHES FIST OVER STERNUM
- radiation to LEFT ARM
Atypical Angina Pectoris- clin features
- females, elderly, DM, immuncomp
- Jaw, right shoulder pain
- radiation to RIGHT or BIL arms, back
Angina Pectoris- causes
what is the MC?
CAD IS MC
- embolus
- arteritis
- dissection
- congenital abnormality
- vasospasm (cocaine or prinzmetals)
Stable Angina
characteristics and tx
exacerbated with activity/emotion, relieved with REST
- predictable and last less than 3 mins
- relieved with sublingual nitroglycerin
reproducible
unstable angina
characteristics and tx
grouped with acute coronary syndrome
- angina that WORSENS
1 of the following: angina at rest, new onset of angina symptoms, inc pain in stable pts
- less responsive to sublingual nitro
- indicates stenosis that ENLARGED
prinzmetal angina
characteristic, when does it occur, caused by
vasospasm at REST
- MC in FEMALES
- 75% with atherosclerotic lesion
- occurs early morning
- exercise capacity preserved
- from cocaine use
what kind of angina can happen from cocaine use?
prinzmetal/vasospastic angina
Acute Coronary Syndrome- definition
SUDDEN dec coronary blood flow
these grouped conditions may occur when blood flow is blocked to myocardium
- unstable angina
- NSTEMI (partial thickness necrosis)
- STEMI (full thickness necrosis)
MI- MC cause
- thrombosis (ruptured plaque–thrombus formed–occlusion)
- MI can be silent, common w pt that has atypical symptoms
ACS- symptoms
- typical or atypical CP
- diaphoresis
- SOB/dyspnea
- n/v
- dizzy/lightheaded
- syncope
- anxiety
ACS- signs
- HTN
- hypotension
- tachycardia
- bradycardia/heart block (inferior wall MI)
- murmur
- friction rub
- bibasilar rales
ACS- Dx with EKG
12 lead EKG
STEMI-> st elevation >1 mm in 2 leads
NSTEMI and unstable angina–> ST depressions or T wave inversions
- POS CARDIAC ENZYMES = NSTEMI
positive cardiac enzymes indicate?
NSTEMI
ACS- Dx labs
names
- Cardiac Enzymes
- Creatine Kinase MB (CK-MB)
- myoglobin
ACS- Dx
cardiac enzymes
- names
- released when?
- how often are samples taken
Cardiac Enzymes
- released w necrosis of myocardial tissue
- GOLD STANDARD DX for MI
- 3 sets every 6 hrs
- troponin T and I most specific
might take up to 6 hours for it to be created
ACS- Dx
CK-MB
- when does it inc, peak, normalize
Creatine Kinase MB (CK-MB)
- inc 4-6 hrs
- peaks in 12-24 hrs
- normalizes in 48-72 hrs
ACS- Dx
Myoglobin
- when does it inc, peak, normalize
- inc 1-4 hrs
- peaks 4-6 hrs
- normalizes in 24 hrs
ACS- Tx types
- MONAB (morphine, oxygen, nitroglycerin/NTG, aspirin, beta blocker)
- statins
- UFH or LMWH
- Reperfusion (PCI/percutaneous transluminal coronary angioplasty OR thrombolytics)
what artery corresponds to this wall MI ?
- inferior
- posterior
- septal
- anterior
- lateral
- inferior: R coronary
- posterior: Pos descending
- septal: L anterior descending
- anterior: L anterior descending
- lateral: L anterior descending OR circumflex
ACS Tx- MONAB
Morphine- pain control that isnt controlled w/NTG
Oxygen
NTG
Aspirin- can use adenosine diphosphate receptor inhibitors if allergic (clopidogrel, ticlopidine prasugrel–> inhibit platelet aggregation)
Beta Blocker
caution if bleeding w ADP receptor inhibitors if bleeding or planned CABG within 7 days
ACS Tx- statins
reduce risk of further coronary events
- stabilizes plaque, lowers cholesterol
ACS Tx- UFH or LMWH
UFH- inactivates thrombin by inhibiting fibrin formation
LMWH- binds to and potentiates antithrombin IIIs ability to inactivate factor Xa
ACS Tx- reperfusion
PCTA
- door to cath time
- stents require how long of DAPT
PTCA (percut. transluminal angio)
- PCI is superior
- door to cath time is 90 MINS
- drug eluting stent (DES) and bare metal stents (BMS)
- DES dual antiplatelet therapy x12 months, BMS DAPT x1 month
ACS Tx- reperfusion
Thrombolytics
- door to cath time
- door to cath 30 mins
- reduce mortality and infarction
- tissue plasminogen activators–> alteplase, reteplase, teneceplase
- dissolve clot by activating tissue plasminogen
ACS DX thrombolytic therapy
ABSOLUTE CONTRAINDICATIONS
- previous hemorrhagic CVA
- CVA within last yr
- intracranial neoplasm
- active internal bleeding
- suspected aortic dissection
- trauma or major surgery <2 wks
ACS DX thrombolytic therapy
RELATIVE CONTRAINDICATIONS
- trauma within past 2-4 wks
- major surgery within past 3 wks
- BP >180/110
- bleeding diathesis (inc tendency to bleed)
- prolonged or traumatic CPR
- recent internal bleeding
- noncompressible vascular puncture
- current anticoag use
- active diabetic retinopathy
- pregnancy
- PUD
ACS- MI complications
- V tach, v fib
- cardiogenic shock
- ventricular aneurysm/rupture
- papillary muscle rupture
- HF
- pericarditis
- dressler syndrome (post MI type of pericarditis)
- sudden death
ACS management strategies
Unstable angina needs management strategy
- TIMI scale- thrombolysis in MI
- GRACE- global registry of acute coronary events
LOW score= conservative tx (antiplatelet, anticoag)
HIGH SCORE= invasive tx (cardiac angiogram/plasty)
TIMI- estimates mortality for unstable angina/NSTEMI pts (low is 0-2, high 5-7)
Cocaine induced MI
- definition
- DX
- TX
coronary artery vasospasm secondary to cocaine activation of SNS and a1 receptors
DX- 12 lead EKG (transient diffuse ST elevations), pos troponin, pos utox
TX- CCB and nitrates, ASA and heparin/LMWH until CAD ruled out, BB CI due to inc risk of vasospasm
cocaine causes vasoconstriction
