CV Exam (random stuff I need to improve) Flashcards
ranges for desirable, borderline, and high cholesterol?
- Desirable: < 200
- Borderline: 200-240
- High: > 240
NCEP ATP III ranges for optimal/desirable, near/above optimal, borderline high, high, and very high levels of LDL?
- Optimal/desirable: < 100
- Near/above optimal: 100-129
- Borderline high: 130-159
- High: 160-189
- Very high: 190+
List 5 predictive factors used to assess 10-year coronary heart disease risk based on the NCEP’s ATP III guidelines.
Age Diabetes Smoking Blood pressure categories NCEP total cholesterol categories LDL cholesterol categories
Statin effects on % reductions/increases of serum lipids:
v LDL (20-60%), v TG (10-20%), ^ HDL (5-10%)
What is SREBP?
TS factor activated by statin’s action, which increases LDL-receptor expression (binds B100)
Which statins are affected by CYP3A4 inducers/inhibitors?
LSA:
Lovastatin, sivastatin, atorvastatin
Which statins are affected by CYP2C9 inducers/inhibitors?
FR
Fluvastatin, rosuvastatin
Which statin is unaffected by CYP450 metabolism?
Pravastatin
Which statins does gemfibrozil affect, and how?
v OATP2/v Glucoronidation –> ^[all Statins]
Bile acid-binding resins (coles) effects on % reductions/increases of serum lipids:
v LDL (10-25%), small increase in TG
What enzyme is upregulated with use of bile acid-binding resins?
Cholesterol 7alpha-hydroxylase
rate-limiting step of bile acid synthesis
What is NCPL1?
Membrane protein that mediates intestinal cholesterol absorption, inhibited by ezetimibe.
Ezetimibe’s effects on % reductions/increases of serum lipids:
v LDL (~18%)
What is PCSK9?
Protease, produced by the liver, that leads to the degradation of hepatocyte LDL receptors. Inhibited by PCSK9 inhibitors evolocumab, alirocumab.
PCSK9 inhibitors’ effects on % reductions/increases of serum lipids:
v LDL (> 50%)
What is PPAR-alpha? (give detail)
Fibrates are ligands for the PPAR-alpha receptor. Leads to:
A. Decreased ApoC3/increased LPL expression –> increased FA oxidation –> decreased VLDL synthesis –> increased VLDL clearance.
B. Increased apoA1 expression –> increased HDL production.
Fibrates effects on % reductions/increases of serum lipids:
v TG (40-60%), v LDL (10-20%), ^ HDL (10-20%)
How does Niacin act?
A. Decreased lipolysis in adipocytes –> decreased FFA –> decreased VLDL.
B. Inhibits DGAT2 –> decreased VLDL synthesis.
C. ApoCIII –> increased LPL –> increased VLDL clearance.
D. Increased apoAI expression –> increased HDL production.
E. Decreased Lp(a) –> decreased thrombosis.
Niacin’s effects on % reductions/increases of serum lipids:
Effect on serum lipids: v TG (30-80%), v LDL (10-20%), ^ HDL (10-30%)
What are the names of 2 drugs used to treat homozygous FH?
give MoA of each
Lomitapide: Inhibits MTP in both erythrocytes and liver –> decreased production of chylomicrons, VLDL, and LDL
Mipomerson: Antisense oligonucleotide specific for apoB48/100 –> decreased expression of apoB48/100 –> decreased VLDL & LDLs.
What is the major side effect of lomitapide and mipomerson?
Hepatotoxicity.
Optimal triglyceride level?
Very high level?
< 150
> 500
Optimal HDL level in men? Women?
Men: >40
Women: >50
Name the 2 large vessel vasculides and their differentiating factors.
- Temporal/Giant Cell Arteritis: > 50 y/o
2. Takayasu Arteritis: Adults < 50 y/o
Read everything important about Giant Cell Arteritis.
- Granulomatous (giant cells, epitheloid cells, exudate/necrosis) vasculitis, classically involves carotid a. (headaches), but also ophthalmic (visual disturbances, jaw claudication)
- *>50 y/o, usually females
- Polyarthralgia rheumatica (morning stiffness)
- Elevated ESR, CRP
- Mutation in HLA-DR4; T cell mediated (IL-6)
- Bx reveals inflamed vessel w/giant cells, intimal fibrosis (destruction of IEL)
- MR Angio useful when larger vessel
- Tx: corticosteroids, high risk blindness w/o, anti-IL-6 AB
Read everything important about Takayasu Arteritis.
- Granulomatous (monocytes, giant cells), vasculitis, often involves aortic arch at branch pts (*collaterals form, more common than in GCA)
- Intimal hyperplasia, adventitial fibrosis
- *Adults < 50 y/o (young azn females)
- Visual sx, weak/absent pulse (“pulseless dz”), visual/neuro sx
- HTN when renal a. involved
- ESR elevated, but no specific marker
- Tx: corticosteroids, anti-IL-6 AB
Name the 2 medium vessel vasculides and their differentiating factors.
- Polyarteritis nodosa: GI, hep. B
2. Kawasaki disease: kids, heart
Read everything important about Polyarteritis Nodosa.
- Necrotizing vasculitis, multiple organs, lungs are spared
- Classically presents in young adults as HTN (renal a.), abd pain w/melena (*mesenteric a.), mononeuritis multiplex (sensory + motor; eg wrist drop), skin: livedo reticularis (rash)
- Higher incidence in hep. B pts
- Early lesion: transmural inflammation w/fibrinoid necrosis, will heal w/fibrosis (nodosa)–“string of pearls” on x-ray.
- Fatal if untreated
- Tx: corticosteroids, cyclophosphamide, long term: methotrexate
Read everything important about Kawasaki Disease.
- AKA mucocutaneous lymph node syndrome
- Typically azn children <4
- Nonspecific signs: fever, conjunctivitis, erythema to palms/soles, enlarged cervical nodes, strawberry tongue, desquamation
- *Coronary a. commonly involved: risk for thrombosis w/MI; aneurysm w/rupture
- CBC, ESR, CRP, LFT, albumin (show inflam.), echo
- Similar to PAN- less severe fibrosis
- Likely microbial agent cause; self-limited
- Tx: ASA + IV IG (but never give child w/viral syndrome ASA)
Name the 5 small vessel vasculides and their differentiating factors.
ANCA-ASSOCIATED
1. Granulomatosis w/ Polyangiitis: c-ANCA, nasopharynx
2. Eosinophilic Granulomatosis w/Polyangiitis: pANCA, asthma
3. Microscopic polyangiitis: pANCA
IMMUNE COMPLEX
1. IgA Vasculitis: antecedent infection, mostly kids
2. Cryoglobulinemic vasculitis: Hep. C
Read everything important about Granulomatosis w/Polyangiitis.
- Formerly Wegener’s Granulomatosis (“c”)
- Nectrotizing, granulomatous
- Commonly involves *nasopharynx, lungs, kidneys (“C”)
- Classic: middle-aged male w/sinusitis/nasopharyngeal ulcer, hemoptysis, bil. nodular lung infiltrates, and hematuria due to rapid progressing glomerulonephritis (can become crescentic- obliterates glumerulus)
- *c-ANCA (correlates w/dz activity)
- Also a/w saddle-nose deformity, mononeuritis multiplex, necrotizing scleritis, palpable purpura, orbital pseudotumor, etc., arthritis
- Tx: corticosteroids w/cyclophosphamide, relapses common (“c”)
Read everything important about Eosinophilic Granulomatosis w/Polyangiitis.
- Formerly Churg-Strauss Syndrome
- Nectrotizing granulomatous inflammation w/eosinophils involving multiple organs, esp. lungs + heart
- Similar to GPA, but no upper resp tract involvement (still affects triad)
- *Asthma and peripheral eosinophilia present
- *p-ANCA (correlates w/dz activity)
- Phases
1. Atopy, allergic rhinitis, asthma
2. Eosinophilia
3. Systemic vasculitis - Can also be a/w coronary arteritis (leading cause of death), cardiomyopathy, gastroenteritis
Read everything important about Microscopic Polyangiitis.
- Necrotizing vasculitis, multi-organ, esp. kidney, lung
- Fibrinoid necrosis of media; leukocytoclastic
- Similar presentation to GPA, but no nasopharyngeal involvement, no granulomas, and + *p-ANCA levels correlated w/dz activity.
- Also similar to PAN, but smaller vessels
- Tx: corticosteroids w/cyclophosphamide, relapses common. Use rituximab when severe.
Read everything important about IgA Vasculitis.
- Formerly Henoch-Schonlein Purpura
- IgA complex deposition –> complement activation
- *Mostly affects children
- *Recent antecedent infection common (usually upper respiratory tract- IgA protects mucosal sites)
- P/w palpable purpura in buttocks/legs, GI pain/bleeding, hematuria (IgA nephropathy)
- Self-limited, may recur. Steroids for severe tx.
What is ANCA?
Explain the 2 types
Anti-neutrophil cytoplasmic antibody
- ABs directed against neutrophilic granules (mostly against enzymes)
pANCA: anti-myeloperoxidase
cANCA: anti-proteinase 3
- ANCA formation induced by drugs or cross-reactive microbial antigen (autoimmune, infections, malignancies).
ANCA binds these cells, further activating. ANCA activated neutrophils –> release lytic granules and ROS–> vascular dmg.
What is the “triad” of areas that small vessel vasculides typically affect?
Skin, lung, kidneys
Read everything important about Cryoglobulinemic Vasculitis.
- Three types of cryoglobulinemia
Type I: Monoclonal Ig, immunoproliferative disorders
Type II: Mixed (poly & monoclonal), chronic infection
Type III: Mixed, autoimmune disorders - Typically type II or III
- *Underlying hep. C common
- Viral triggered, immune-complex mediated
- Palpable purpura, weakness, Reynaud’s, multiplex mononeuritis
Name the 4 consequences of cardiac remodeling, as occurs w/overproduction of renin.
- Myocyte hypertrophy
- Re-expression of fetal isoforms
- Myocyte apoptosis
- Changes in the interstitial matrix
3 drugs that prevent ventricular remodeling:
- ACE Inhibitors/ARBs/LCZ696
- Beta Blockers
- Aldosterone Antagonists
(same + hydralazine w/nitrates)
- ACE Inhibitors/ARBs/LCZ696
- Hydralazine + Nitrates
- Beta Blockers (carvedilol, metoprolol, bucindolol)
- Aldosterone antagonists (spironolactone, eplerenone)
3 types of tissue found in heart valves?
- Spongiosa: more matrix and GAGs
- Fibrosa: mostly fibrosis
- Reticularis: more elastic fibers
3 sequelae from calcific aortic stenosis?
- CHF
- Ischemia
- Syncope
What is the pathology of MVP?
Unknown
- Usually asymptomatic
Give the 3 examples of noninfected vegetations?
Acute Rheumatic Fever
Endocarditis of System Lupus Erythematosus
(Liebman-Sacks Endocarditis)
Nonbacterial Thrombotic Endocarditis
(Marantic Endocarditis)What are the killer chest pains?
- ACS
- Tension PTX
- PE
- Dissecting aneurysm
What comprises ACS?
Unstable angina
nonSTEMI
STEMI
Stress tests are ___% sensitive, maybe ___% specific
60
80
Non-genetic causes of dilated cardiomyopathy?
- Myocarditis
- Peri partum
- Toxic (eg alcohol)
- Idiopathic
Causes of restrictive cardiomyopathy?
Idiopathic Radiation fibrosis (lymphomas that require radiation to heart) Amyloidosis Sarcoidosis Inborn errors of metabolism Endocardial fibroelastosis Loeffler endomyocarditis
What is congo red staining used to see?
Beta-amyloid (apple-green birefringence under polarized light)
Most common cause of myocarditis in US?
Coxsakie A & B viruses
(also cytomegalovirus, HIV, bacteria, parasites)
- There is also immune-mediated (drug rxns, rheumatic fever), giant cell myocarditis, and sarcoidosis (noncaseating granulomas)
Define: pulsus paradoxis, beck’s triad, and kussmaul sign.
What dz are they indicative of?
- Pulsus paradoxis: Nlly BP decreases 10 mmHg w/inspiration (low T pressure allows for pulm veins to hold more blood), causing reflex tachy (blood overfills right side, pushing septum into left side). In cardiac tamponade, there’s nowhere for the blood to go because right ventricle is compressed, therefore LV can’t eject as much (?), so BP drops > 10mmHg. Heart sounds heard on chest, but no pulse on inspiration (pulse felt on expiration), and this is the paradox.
Also seen in severe pulm dz - Beck’s triad: In cardiac tamponade: hypotension, quiet heart sounds (fluid covers it up), elevated JVP.
- Kussmaul sign: Increased JVP w/inspiration
Etiologies of pericarditis?
Infections (Viruses, Bacteria, TB, Fungi, Parasites)
Immune-Mediated Reactions (Rheumatic fever, SLE, Post-cardiotomy, Post-MI, drug hypersensitivity)
Uremia
Neoplasia
Trauma
Radiation
Good Combo’s for treating HTN: (may be >1 answer for some)
- Thiazide or Loop diuretic with _________________.
- Thiazide diuretic with _________________.
- CCBs with ___________________.
- K+-sparing diuretics
- Beta-blockers; ACEIs, ARBs (CCB too?)
- ACE-inhibitors, ARBs
Bad Combo’s for treating HTN:
- K+ sparing diuretics with _________________.
- Combo of ACE-inhibitors and _________________ has no advantage in diabetics
- ACE-inhibitors (exacerbate hyperkalemia)
- ARBs (risks of hyperkalemia are increased)
What drug class is DOC for uncomplicated (mild-mod) HTN?
Diuretics (along w/lifestyle mods)
What drug is most effective at treating HTN in African Americans?
- Which would you avoid in this demo? (unless combined w/____)
CCBs (monotherapy) (hint- African Americans need something stronger)
- Beta blockers (+ diuretics)
What anti-hypertensives would you recommend to a pt with DM?
- ACE inhibitors
- CCBs
few effects on carb metabolism
Pts w/what dz should not take acetazolamide?
Cirrhosis (increased urine pH reduces NH3 secretion and thereby increases serum NH3)
Pts w/what dz’s should not take mannitol?
- CHF
- Renal failure (chronic)
- Pulmonary edema (extracts water from cells)
Name the contraindications for each diuretic:
- Thiazides
- Loops
- K+ sparing
- NSAIDs, beta-blocks (raises LDL/HDL ratio)
- NSAIDs, aminoglycosides
- NSAIDs, ARBs, ACEIs (RAS inhibitors)
Name the first-line DOC’s for HTN.
- Diuretics
- CCBs
- ACEIs/ARBs
When are 2 combined HTN drugs recommended, numerically?
When BP >20/10 over
Is a non-dihydropyradine w/a beta-blocker a good or bad combo?
Bad (conduction disturbances)
- “Use w/caution”
Patients taking short-acting nifedipine, diltiazem or verapamil were 1.6 times more
likely to have __________. (dz)
MI
Name the cardioselective BBs.
- Which is lipophilic?
Name the non-selective BBs.
- Which has longer T1/2, and which is used to treat rebound tachy w/hypotensive meds?
Which is a partial non-selective BB?
Name the BBs w/some alpha-blocking activity. Which is lipophilic (given IV), and which is a vasodilator?
(A-M): atenolol, metoprolol (lipo, so sympatholytic)
Propranolol (tx of tachy), nadolol (longer T1/2)
Pindolol
Labetolol (lipophilic, IV), carvedilol (vasodilator)
Name 3 drugs safe to use during pregnancy to treat HTN.
Alpha-methyl DOPA
Beta-blockers
Hydralazine
What patients w/these 3 diseases would benefit from a beta-blocker to treat their HTN.
Diabetes, CHF, MI
Which ACEI allows for once daily dosing?
Which has a shorter T1/2?
Which has a longer T1/2?
Lisinopril
Captopril
Enalapril
- Which thiazide is 1/10th the potency of HCTZ?
- 10x more potent than HCTZ?
- 20x more potent than HCTZ, but T1/2 10-22 hrs?
- Same potency as HCTZ, but T1/2 44 hrs (longer duration), may be more effective?
- Chlorothiazide
- *Metolazone
- Indapamide
- Chlorthalidone
- Which loop diuretic is 40x more potent than furosemide, but has a shorter T1/2?
- Which has a longer T1/2?
- Bumetanide
2. Torsemide
- Which CA inhibitor is ~ 30x more potent than acetazolamide?
- About 5x more potent than acetazolamide?
- Topical preparation for ocular use–avoids systemic effects?
- Dichlorphenamide
- Methazolamide
- Dorzolamide
Name another vasodilator we need to know besides nitropresside and hydralazine.
Minoxidil (if other drugs are resistant)
What drug class might you combine with a vaso- and arterio-dilators to reduce the reflex tachycardia?
Beta-blockers
What types of angina are Nitrates used in? CCBs?
BBs?
All 3
All 3
Stable and unstable (not variant)
Ranolazine: MoA? Indications? Toxicity? Contraindications?
- Inhibits FA beta oxidation in cardiomyocyte mito. Prevents exercise-induced myocardial ischemia. (unknown mech)
- Originally chronic stable angina unresponsive to other agents; now exercise-induced angina as well.
- Prolonged QT
- Long QT syndrome; contraindicated for use with other drugs that prolong QT interval.
Ivabradine: MoA? Indications? Toxicity? Contraindications?
- Blocks If current in SA nodal fibers. (starts w/letter “I”) Prevents exercise-induced myocardial ischemia.
- Chronic stable angina
- Bradycardia; heart block; luminous phenomenon
- Sick Sinus Syndrome; use with non-dihydropyridine CCBs
Name the drug classes that can be used in the treatment of CHRONIC CHF.
- Diuretics (except CA-inhibitors/mannitol)
- ACEIs/ARBs
- BBs
- Digoxin
Name the drug classes that can be used in the treatment of ACUTE CHF.
- Furosemide
- Nitrates
- Niseritide (synthetic BNP)
- Beta-adrenergic agonists
- PDE-inhibitors (anamrinone, milrinone)
- Digoxin
List the non-pharmacological therapies for ACUTE CHF.
PCI
Ultrafiltration
Intra-aortic balloon pump
LVADs
List the non-pharmacological therapies for CHRONIC CHF.
- Surgical therapy–revascularization for ischemic heart dz–valve repair/replacement for valvular heart dz–aneurysmectomy
- LVADs (bridge to transplant or destination therapy)
- Biventricular pacing: cardiac resynchronization therapy (CRT) +/- implantable cardiac defibrillators (ICDs)
- Cardiac transplantation
In hypertensive emergency, you only wan to lower BP 25-30% in the first 24 hrs. What 2 dz’s are exceptions?
- Dissecting Aneurysm: rapidly (20mins) lowered to 100-120 mmHg
- Acute phase of ischemic stroke: reperfusion candidates
According to JNC 8, what are the maximum systolic and diastolic BP range goals for hypertensive pts under 60?
Over 60?
Age < 60 yrs old
< 140/90 mmHg
Age > 60 yrs old
< 150/90 mmHg
Cutoff for hypertensive urgency/emergency, in mmHg?
> 180/120
200 is # he had for malignant
If aortic stenosis occurs in a pt age 45-50 in the U.S., you should first think what?
Bicuspid valve.
Name the quantitative platelet disorders for your bleeding differential.
- ITP
- TTP-HUS
- Drug-induced
- Hypersplenism
- Neoplasm (invades marrow)
- Virus
- Autoimmune (eg Lupus)
- Gestational
- DIC
Name the acquired clotting factor abnormalities for your bleeding differential.
- Vit K deficiency
- Factor inhibitors
- Liver failure
- Drugs
- DIC
Explain furosemide pharmacokinetics.
Half-life is short (1-1.5 hrs) so duration is only 2-3 hrs. Renal secretion mechanism; organic acid transporter.
