Step 1 - CV 3

denniskwinn's version from 2015-04-25 15:59


Question Answer
Wegener’sCharacterized by triad of focal necrotizing vasculitis, necrotizing granulomas in the lung and upper airway, and necrotizing glomerulonephritis
Wegener’s symptomsHemoptysis, hematuria, perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea.
Wegener’s findingsc-ANCA is a strong marker of disease; chest x-ray may reveal large nodular densities; hematuria and red cell casts.
Wegener’s treatmentCyclophosphamide and corticosteroids
Microscopic polyangiitisLike Wegener’s but lacks granulomas (p-ANCA) - small vessels
Primary pauci-immune crescentic glomerulonephritisVasculitis limited to kidney - Pauci-immune= paucity of antibodies
Churg-Strauss syndromeGranulomatous vasculitis with eosinophilia - most often presents with asthma, sinusitis, skin lesions and peripheral neuropathy (wrist/foot drop) - can also involve heart, GI, and kidneys - p-ANCA
Sturge-Weber diseaseCongenital vascular disorder that affects capillary sized blood vessels. Manifests with port-wine stain (aka nevus flammeus) on face, ipsilateral leptomeningeal angiomatosIs (intracerebral AVM), seizures, and early-onset glaucoma.
Henoch-Schonlein purpuraMost common form of childhood systemic vasculitis. Skin rash on buttocks and legs (palpable purpura), arthralgia, intestinal hemorrhage, abdominal pain, and melena. Follows URis. IgA immune complexes. Association with IgA nephropathy - common triad of skin,joints, GI, multiple lesions of same age
Buerger’s diseaseaka thromboangiitis obliterans; idiopathic segmental, thrombosing vasculitis of small and medium peripheral arteries and veins - seen in heavy smokers - small and medium vessels
Buerger’s symptomslntermittent claudication, superficial nodular phlebitis, cold sensitivity (Raynaud's phenomenon), severe pain in affected part. May lead to gangrene and autoamputation of digits
Buerger’s treatmentsmoking cessation
Kawasaki diseaseAcute, self-limiting necrotizing vasculitis in infants/children. Association with Asian ethnicity - small and medium vessels
Kawasaki symptomsFever, conjunctivitis, changes in lips/oral mucosa (strawberry tongue), lymphadenitis, desquamative skin rash. May develop coronary aneurysms
Kawasaki treatmentIV immunoglobulin, aspirin
Polyarteritis nodosaImmune complex- mediated transmural vasculitis with fibrinoid necrosis. - small and medium arteries
Polyarteritis nodosa symptomsFever, weight loss, malaise, abdominal pain, melena, headache, myalgia, hypertension, neurologic dysfunction, cutaneous eruptions - typicall renal and visceral vessels (NOT pulm arteries)
Polyarteritis nodosa findingsHBV+ in 30% patients, multiple aneurys and constrictions on arteriogram - lesion are of different ages
Polyarteritis nodosa treatmentCorticosteroids, cyclophosphamide
Takayasu’s arteritisgranulomatous thickening of aortic arch and/or proximal great vessels. Associated with an ↑ ESR. Primarily affects asian females < 40 years of age - pulseless
Takayasu’s symptomsFever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in upper extremities - FAN MY SKIN On Wednesday
Temporal arteritisMost common vasculitis affecting medium and large arteries, usually branches of carotid artery. - focal, granulomatous inflammatoin, affects elderly females
Temporal arteritis symptomsUnilateral headache, jaw claudication, impaired vision (occlusion of ophthalmic artery that may lead to irreversible blindness).
Temporal arteritis findingsAssociated with ↑ ESR, half of patients have systemic involvement and polymyalgia rheumatica
Temporal arteritis treatmentHigh-dose steroids


Question Answer
Strawberry hemangIoma BenIgn capillary hemangioma of Infancy. Initially grows wIth child, then spontaneously regresses.
Cherry hemangiomaBenign capillary hemangIoma of the elderly Does not regress. Frequency ↑ with age.
Pyogenic granulomaPolypoid capillary hemangioma that can ulcerate and bleed. Assoclated with trauma and pregnancy.
Cystic hygromaCavernous lymphangioma of the neck. Associated with Turner's syndrome.
Glomus tumorBenign, painful, red-blue tumor under fingernails. Arises from modified smooth muscle cells of glomus body.
Bacillary angiomatosisBenign capillary skin papules found in AlDS patients. Caused by Bartonella henselae infections. Frequently mistaken for Kaposi' sarcoma.
AngiosarcomaHighly lethal malignancy of the lover. Associated with vinyl chloride, arsenic, and Th02 (Thorotrast) exposure.
LymphangiosarcomaLymphatic malignancy assocIated with persistent lymphedema (e.g., postradical mastectomy).
Kaposi’s sarcomaEndothelial malignancy of the skill associated WIth HHV-8 and HIV - Frequently mistaken for bacillary angiomatosis


Question Answer
Therapy for essential hypertensionDiuretics, ACE lnhibitors, angiotensin Il, receptor blockers (ARBs), calcium channel blockers.
Therapy for CHFDiuretics, ACE inhibitors/ARBs, Beta blockers (compensated but not for decompensated), K+-sparing diuretics.
Therapy for HTN in DMACE inhibitors/ARBs, calcium channel blockers, diuretics, Beta blockers, a-blockers
Hydralazine mechanism ↑ cGMP→ smooth muscle relaxation. Vasodilates arterioles> veins; afterload reduction.
Hydralazine clinical useSevere hypertension, CHF. First-line therapy for hypertension In pregnancy, with methyldopa. Frequently coadministered with a Beta-blocker to prevent reflex tachycardia.
Hydralazine toxicityCompensatory tachycardIa (contraindlcated in angina/CAD), fluid retention, nausea. headache, angIna. Lupus-like syndrome.
Minoxidil mechanismK+ channel opener - hyperpolarizes and relaxes vascular smooth muscle
Minoxidil clinical useSevere hypertension
Minoxidil toxicityHypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retentIon
Ca channel blockersNifedipine, verapamil, diltiazem
Ca channel blocker mechanismBlock voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility - -
Ca channel blocker Vascular smooth muscle targetingNifedlpine > diltiazem > verapamil
Ca channel blocker heart targetingVerapamil >diltiazem > nifedipine
Ca channel blocker clinical useHypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.
Ca channel blocker toxicityCardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation
Nitroglycerin, isosorbide dinitrate mechanismVasodilate by releasing nitric oxide in smooth muscle, causing ↑ in cGMP and smooth muscle relaxation. Dilate veins>> arteries. ↓ preload
Nitroglycerin clinical useAngina, pulmonary edema. Also used as an aphrodisiac and erection enhancer
Nitroglycerin toxicityReflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial exposure; development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia,dizziness, and headache on reexposure.
Malignant HTN treatmentNItroprusside, Fenoldopam, Diazoxide
NitroprussideShort acting; ↑ cGMP via direct release of NO. Can cause cyanide toxicity (releases CN)
FenoldopamDopamine D1 receptor agonist- relaxes renal vascular smooth muscle.
DiazoxideK+ channel opener- hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia (reduces insulin release).
Goal of antiaginal therapyreduction of myocardial O2 consumption (MV02) by decreasing 1 or more of the determinants of MVO2: end diastolic volume, blood pressure, heart rate, contractility, ejection time
Nitrates effects for antianginal therapy(affect preload) - ↓ end diastolic volume, ↓ BP, ↑ contractility (reflex response), ↑HR, ↓Ejection time, ↓MVO2 (O2 consumption) - nifedipine similar in effect
Beta blocker effects for antianginal therapy(affect afterload) - ↑ end diastolic volume, ↓BP, ↓ contractility, ↓HR, ↑ Ejection time, ↓MVO2 (O2 consumption) - verapamil similar effect
Nitrates and betablockers together for anginano effect or ↓ end diastolic volume, ↓BP, little effect on contractility, ↓ HR, little effect on ejection time, ↓↓ MVO2
Cardiac glycosideDigoxin-75% bioavailability, 20-40% protein bound, tl l2 = 40 hours, urinary excretion
Cardiac glycosides mechanismDirect inhibition of a+/K+ ATPase leads to indirect Inhibltion of Na+/CaZ+ exchanger/antiport. ↑ [Ca2+]→ positive inotropy. Stimulates vagus nerve.
Cardiac glycosides clinical useCHF (↑ contractility); atrial fibrillation (↓ conduction at AV node and depression of SA node).
Cardiac glycoside toxicityCholinergic- nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG - ↑PR, ↓QT, scoopIng,T-wave inversion, arrhythmia, hyperrkalemia. . Worsened by renal failure (↓ excretion), hypokalemia (permissive for digoxin binding at K+ binding site on a+/K+ ATPase), quinidine (↓ digoxin clearance, displaces digoxin from tissue-binding sites).
Cardiac glycoside antitodeslowly normalize K+, lidocain, cardiac pacer, anti-dig Fab fragments, Mg2+
Antiarrhythmics (Na channel blockers) Local anesthetics. low or block (↓) conduction (especially In depolarized cells). ↓ slope of phase 0 depolanzation and ↑ threshold for firing in abnormal pacemaker cell . Are state dependent (selectively) depress tissue that is frequently depolarized, e.g., fast tachycardia ).
Class IA antiarrhythmicsQuinidine, Procainamide, Disopyramide. ↑ AP duration, ↑ effective refractory period (ERP), ↑ QT interval. Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.
quinidine toxicity(cinchonism - headache, tinnitus; thrombocytopenia; torsades de pointe due to ↑ QT interval);
procainamide toxicity(reversible SLE-like syndrome).
Class IB antiarrhythmicsLidocaine, Mexiletine, Tocainide, ↓ AP duration. Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrhythmias (especially post-MI ) and in digitalis-induced arrhythmias.
Class IB antiarrhythmics toxicitylocal anesthetic. C S stimulation/depression, cardiovascular depression
Class IC antiarrhythmicsFlecainide, Encainide, Propafenone. No effect on AP duration. Useful in V-tachs that progress to VF and in intractable SVt. Usually used only as last resort in refractory tachyarrhythmia . For patients without structural abnormality
Class IC antiarrhythmics toxicityproarrhythmic, especially post-MI, (contraindicated). Significantly prolongs refractory period in AV node.
Hyperkalemia and class I antiarrhythmicsincrease toxicity of all
Class II antiarrhythmics (Beta blockers ) Propanolol, esmolol, metoprolol, atenolol, timolol
Class II antiarrhythmics (Beta blockers ) mechanism↓ cAMP, ↓Ca currents. Suppress abnormal pacemakers by'" slope of phase 4. AV node particularly sensitive ↑ PR interval. Esmolol very short acting.
Class II antiarrhythmics (Beta blockers ) clinical useV-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
Class II antiarrhythmics (Beta blockers ) toxicityImpotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). lay mask the signs of hypoglycemia. Metoprolol can cause dyslipidemia. Treat overdose wIth glucagon.
Class III antiarrhythmics (K+ channel blockers)Sotalol, ibutilide, bretylium, dofetilide, amiodarone
Class III antiarrhythmics mechanism↑AP duration, ↑ ERP. Used when other antiarrhythmics fail. ↑ QT interval.
Sotalol toxicitytorsades de pointes, excessive Beta block
Ibutilide toxicityTorsades de pointes
Bretylium toxicitynew arrythmias, hypotension
Amiodarone toxicitypulmonary fibrosis, hepatotoxicity, hypothyroid/hyperthyroid, corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF
Class IV antiarrhythmics (CA channel blockers)Verapamil, Diltiazem
Class IV antiarrhythmics mechanismPrimarily affect AV nodal cell . ↓ conduction velocity, ↑ ERP, ↑ PR interval. Used in prevention of nodal arrhythmias (e.g" SVT)
Class IV antiarrhythmics toxicityConstipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
Adenosine as antiarrhythmic↑ K+ out of cells → hyperpolarizing the cell + ↓Ca - Drug of choice in diagnosing/abolishing supraventricular tachycardia. Very short acting (-15 sec),Toxicity includes Rushing, hypotension, chest pain. Effects blocked by theophylline
K+ as antiarrhythmicDepresses ectopic pacemakers in hypokalemia (e.g. Digoxin toxicity)
Mg2+ as antiarrhythmicEffective in torsades de pointes and digoxin toxicity