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462 Cards in this Set
- Front
- Back
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What is hydrostatic pressure
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pressure of a liquid at rest
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what is hydrodynamic pressure
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pressure generated by viscosity and by a pump
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How does Compliance relate to volume and pressure
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C= Dv/Dp. a very compliant vessel will have very large changes in V for a given change in P
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How does laplaces law relate to blood vessels
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A very large Radius vessel will need much more tension to contain a given pressure than a smaller vessel. P=R/T
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How does CO relate to resistance
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CO=dP/R. pressure and flow are directly proportional. smaller vessels will have greater pressure and flow.
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How does radius affect Flow
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any change in R will affect flow proportionally to the 4th power. in comparison to L which is 1:1 inversely.
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what happens to R as tubes are added in parallel
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"decreases TPR, 1/R+1/R+1/R etc"
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How do tubes in parallel affect conductance
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conductance increases
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how do you get MABP
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(Pdias +(Psyst-Pdias))/3
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When does flow go from laminar to turbulent
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"when velocity and diameter get larger, or when viscosity increases. Reynauds number >2000"
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Ficks equation
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CO= VO2/ (O2pvein- O2partery)
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equation for dulution technique
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Dye mg/(avg [dye]/dL blood * (T2-T1)
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what is preload
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the amount in the ventricle before contracting
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what is afterload
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force against which the heart must pump
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what is the relationship between Ca and sarcomere length
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as sarcomere length increases they become more responsive to Ca. and as a result force increases
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why is titin important
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keeps cardiac muscle from stretching beyond plateau
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If you increase preload what will happen?
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"Increase SV, increase SBP, "
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What factors affect preload
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"Blood volume, CVP****, muscle pumping, intrathoracic pressure, body position, pericardium, ventricular compliance"
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what happens when afterload is increased
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SV decreases
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what affects afterload
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"aortic pressure, aortic compliance, aortic valve resistance"
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what happens if you increase contractility
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"increase SV, shift filling curve, preload will decrease and afterload will increase"
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what happens to CO as Venous pressure increases
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CO will also increase
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What happens to venous pressure as CO increases
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Venous pressure will fall
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what happens during the A wave
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atrial systole
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what happens during the C wave
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isovolumetric contraction
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what happens on the X decent
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rapid ejection (systole)
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V wave
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"ventricular systole, atrial pressure rises"
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Y descent
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"Mitral valve opens, atrial pressure drops"
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What causes the first heart sound and what point does it correspond to on the EKG
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it is blood flow causing mitral valve to shut and occurs during the QRS complex
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What causes the 2nd heart sound and when does it happen in relation to the EKG
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the sound is caused by blood flow against the aortic valve and occurs during the T wave
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what causes the 3rd sound
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blood beginning to rapidly fill the ventricles
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what is the 4th heart sound
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atrial systole
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what occurs during phase 0-1 in cardiac AP
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"Sodium channels open, Na pours into cells"
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what happens in phase 2
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Ca enters leading to contraction
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what happens in phase 3
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"repolarization, K exits the cells"
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If HR increases too much what happens
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"Heart has less time to fill, preload goes down and so does SV, leading to a lower BP (can be chicken/egg: low BP can trigger tachy too)"
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what is pulse pressure
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the difference between systolic and diastolic pressures
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How does MABP relate to CO
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CO x R= MABP
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TPR is
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the difference in pressure between the aorta and the right atrium. should be around 20 mmHg/L/min
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Decreasing compliance
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"increases pulse pressure, (inc systole, dec diastole) "
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increasing resistance
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increases systolic BP and diastolic BP about the same amounts.
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increase resistance and decreasing compliance
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will greatly increase systolic pressure and increase diastolic some.
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what is a major determinant of capillary pressure
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venous pressure (has 1/4 resistance of arterial side)
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how is the relationship of venous pressure and capillary pressure important
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very small changes in pressure in the pulmonary veins due to left ventricle problems can cause capillaries to back up and flood lungs with fluid
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what determines if capillaries filter or absorb material
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"Capillary hydrostatic pressure, interstitial fluid pressure, plasma colloid pressure, interstitial colloid pressure"
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If NFP is positive which direction is material travelling
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Fluid will filter into the interstitium
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how is NFP calculated
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"NFP=Pc+∏if-Pif-∏c
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How do you get from A to B
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decrease in CTY (MI)
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How do you get from B to B'
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Preload increases via reflex to compensate for decreased CTY
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B to C
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increase preload through renal function (Na and H2O)
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C to D
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iontropic drugs
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What is occurring during the PR interval
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SA node has fired and the signal is traveling to the AV node where there is a delay to let the ventricles fill. should be less than 5 boxes (form beginning of P to R)
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How long should QRS be
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3 boxes (.12 sec)
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What is the beginning and end of the ST interval
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from S to the end of T
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What is the QT interval
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From Q to the end of T.
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where do leads V1 and V2 go
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4th intercostal space on either side of the sternum
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What are the 4 characteristics of myocardium
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"Excitability, Contractility, automaticity, conductivity"
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What happens to TPR during sympathetic activation
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"goes up, constrict peripheral vessels in bowel, increase blood flow to skeletal muscle"
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What is ANCA
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anti-endothelial cell antibodies
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What is C-anca
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"cytoplasmic staining
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What is P-ANCA
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"Perinuclear staining for MPO
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Polyarteritis Nodosa
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"Small-Medium Arteries
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Histological features of PAN
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"thick walls, transmural involvment, necrosis, almost complete lumen obliteration"
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Microscopic Polyangiitis
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"Arteries, Caps, Venules
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What causes microscopic polyangiitis
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immune reaction or tumors
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Churg-Strauss
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"GI
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(Temporal arteritis)"
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"Large-small arteries
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Takayasu Arteritis
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"HLA: A24, B52, DR2
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What will an angiogram show in Takayasu
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"areas without filling. aorta, brachiocephalic, subclavian"
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Histology of Takayasu
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"Thickened lumen, giant cells, tunica media beginning to be fragmented, patchy irregularities"
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Infectious Arteritis
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"mycotic aneurysms, can cause thrombi, many PMNs, thrombi in lumen"
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Kawasaki Disease
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"Conjunctivitis
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Wegener Granulomatosis
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"Vessel necrosis
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(Buerger's disease)"
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"Thombi and inflammation occluding lumen
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Cavernous Hemangioma
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"Skin, Mucosa, sharp demarcated margins, cells in the vessels are benign"
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Capillary Hemangioma
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"small dots, small mass, on mucosal surfaces, benign"
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Glomus Tumor
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"neurovascular origin
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Hemangioendothelioma
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"intermediate benign-malignant
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Angiosarcoma
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"can look like rhabdo, anaplastic spindle shaped cells, poorly grown vessels"
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What causes angiosarcoma
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"Vinyl Chloride
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Kaposi Sarcoma
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"spindle shaped cells, high N:C, herpes occlusions, plaque like purple lesions"
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von-Hippel Lindau
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"autosomal dominant, VHL gene, can involve brainstem, retina, liver, kidney, or pancreas"
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Osler Weber
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"autosomal dominant
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Sturge Weber
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"port wine stain face, glaucoma, hemangiomatoma in meninges"
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Pralidoxime
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antidote for irreversible cholinergics
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Overall what are the effects of cholinergics
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"Miosis, Stim GI, Micturation, increases fluid secretion, bronchoconstriction, "
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Miochol
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intraocular use. used for pupillary constriction
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Carbachol
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"topical use for glaucoma,
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Bethanechol
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"increases peristalsis, micturition,"
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Pilocarpine
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"Can be used in an insert for glaucoma, also used to reverse mydriatics for eye exams"
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Inhibitors of cholinesterase
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"Physostigmine
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Physostigmine
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"open angle glaucoma, reversible cholinesterase inhibitor
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Demecarium
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"powerful miotic
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what is used as an antidote to OD of nondepolarizing skeletal muscle relaxants
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edrophonium
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Neostigmine
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"myasthenia, nondepol skel musc relax poisoning"
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isoflurophate"
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irreversible cholinesterase inhibs
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Muscarinic Blockers
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inhibit cholinergic signalling at postganglionic parasympathetic receptors
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Ganglionic blockers
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block cholinergic signalling at autonomic ganglia both parasympathetic and sympathetic
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neuromuscular blockers
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work at synapse at skeletal muscle
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Actions of anticholinergic drugs
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"Decrease GI motility
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what are the belladonna alkaloids
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atropine and scopolamine
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Dicyclomine
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"IBS, antispasmodic, tertiary amine (good lipid solubility)"
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Oxybutinin
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"Bladder instability
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Tropicamide
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"mydriatic
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clindinium
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"quaternary amine
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glycopyrrolate
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"preanesthetic med
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Nondepolarizing ganglionic blocks
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"Stop sympathetics- get vasodilation
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mecamylamine
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"nondepolarizing, secondary amine
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Trimethaphan
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"release histamine
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Indicator of LVH
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V1 +V5 R wave >35 mm
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Indicator of RVH
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+R wave in V1
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1st degree block
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PR interval is longer than 5 boxes or .2 sec in each beat
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Wenckebach
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PR interval gets longer and longer until there is a missing qrs
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Mobitz
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"atria firing regularly on own rate, ventricles responding to some not to others. 2:1, 3:1 fashion "
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3rd degree block
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atria and ventricles beating entirely on their own rhythms
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slurred QRS
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WPW syndrome
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Atrial rate >250
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flutter
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Atrial rate >350
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fibrillation
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Junctional rhythm
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"no P wave, AV node fires on own"
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Atrial enlargment
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biphasic p waves
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How is Epi made
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Tyrosin>LDopa> Dopamine>NE>Epi
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How is NE converted to Epi
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phenylethanolamine N methyltransferase in the chromafin cells of the adrenals
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where do you find MAO
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in mitochondria and nerve terminal
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how does MAO degrade epi/NE
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deaminates the alpha carbon
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COMT is found
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"in cytoplasm, lots in liver, some in synapse"
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COMT degrades NT by
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puts on a methyl on the 3 oxygen
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what is the most imporant mechanism for stopping NE signalling
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reuptake (80%)
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Alpha 1 receptor
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"inc TPR (vasoconstrict), mydriasis, pilomotor, inc BS, decrease secretions"
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Alpha 2
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"presynaptic, negative feedback"
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Beta1
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"in heart, increases CTY, HR"
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Beta 2
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"dilation in pulm and skel musc
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relative strength of NT on alpha receptors
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Epi>NE>DA>Isop
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relative strength of NT on beta1 receptors
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Isop>Epi=NE
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relative strength of NT on beta2 receptors
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Isop>Epi>NE>DA
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ADR of alpha agonists
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"Anxiety, Resp diff, forceful CTY, HA, HTN, rebound congestion"
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Clonadine
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"Alpha2 receptor in brain stem. hypotension, sedation, bradycardia"
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2ndary msgr for alpha
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IP3
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2ndary msgr for beta
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adenylyl cyclase
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Isoproteronal
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"Beta 1 and 2
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Dobutamine
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Increases CO
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Beta 2 agonists
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"albuterol, metaproterenol, terbutaline"
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DA
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"low dose - D1, vasodilation in kidney
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alpha blockers
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"decrease vasc resist, increase HR (reflex), increase NE release"
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phenoxybenzamine
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"irreversible uptake inhibitor
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Prazosin
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"Dec TPR
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yohimbine
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"inc bp, HR, antagonize 5HT recept."
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How do beta blockers work
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decrease conduction from SA to AV nodes
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Non selective beta blockers
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"Propanolol
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Pindolol
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"NS
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Selective Beta 1
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"Metoprolol
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Labetalol
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"Beta2 with some alpha1
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Order a chest xray
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"Angina, MI, PTX, PE, Aortic diss, esoph rupture"
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order arteriogram
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"angina, PE"
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CT scan
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"PTX, PE, dissection, esoph"
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Monckeberg
|
"asymptomatic calcifications of the media in muscular arteries. may falsely elevate systolic pressure
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Hyaline arteriosclerosis
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"hyaline thickening of the walls
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Hyperplastic arteriolosclerosis
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"Onion skin thickening of the wall, narrowing lumen
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What is the sequence of events in atherosclerosis
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"1. Injury/inflammation
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What are the key cells in the formation of an atheroma
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T cells
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what are the consequences of chronic hyperlipidemia
|
"impaired endothelium function
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Where are the most common sites of plaques
|
"Abd Aorta
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Diabetes affect on micro vasculature
|
"retinopathy, kindeys, peripheral nerves"
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Diabetes and macro vasc
|
"MI, stroke, gangrene"
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what are the 3 metabolic pathways of atherosclerosis in diabetics
|
"Advanced glycation end products
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AGEs
|
cause cross linking in ECM and cause sclerosis and decrease elasticity
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How do AGEs interfere with circulating proteins
|
AGE/protein bind to macrophages. cytokines released can result in nephropathy
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How does intracellular hyperglycemia relate
|
"increases oxidative injury in cytoplasm, depletes cell NADPH, cannot make glutathione"
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Most common occlusion in a non diabetic pt
|
superficial femoral artery
|
|
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most common occlusion in a diabetic pt
|
"popliteal artery
|
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what does a ABI of <.90 mean
|
"PAD dx, 50% cross sectional occlusion in the leg"
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at what ABI do symptoms begin
|
".65-.79
|
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Severe PAD
|
".5-.64
|
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resting ischemia
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".50-0
|
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ApoB48
|
Bad
|
|
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ApoB100
|
Bad
|
|
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ApoCII
|
Good
|
|
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ApoCIII
|
Bad
|
|
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ApoE
|
good
|
|
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LPL
|
Good
|
|
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PCSK9
|
Bad
|
|
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ApoA
|
Bad
|
|
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HDL
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good
|
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ABCA1
|
good
|
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PLTP
|
Bad
|
|
|
Syphilitic Aortitis
|
"Tertiary Syphilis
|
|
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Type A dissection
|
ascending aorta
|
|
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Type B dissection
|
does not involve the ascending
|
|
|
What is used to treat stable angina
|
"Ca channel blockers, Nitrates, Beta blockers"
|
|
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What is used against unstable angina
|
beta blockers and nitrates
|
|
|
tx for variant angina
|
nitrates
|
|
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What is the physiologic response to nitrates
|
"vasodilation
|
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Verapamil/Diltiazem
|
"Ca channel blocker
|
|
|
Amlidipine, Nicardipine"
|
"Reflex tachy, vasodilation
|
|
|
"Metrapolol, Propanolol"
|
"Beta2 blockers
|
|
|
Rapid Decline"
|
aortic regurg
|
|
|
Delayed Decline"
|
IHSS
|
|
|
Slow decline"
|
aortic stenosis
|
|
|
"how do you seperate S1, 3, and 4"
|
"S1 is enhanced by inspiration
|
|
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How do you split S2
|
"Inspiration
|
|
|
major risk factos for CAD/Angina
|
"Smoking, HTN, Diabetes, High cholesterol,"
|
|
|
minor factors for CAD/MI
|
"obesity, fam hx, gout, CRP"
|
|
|
Positive Hepatojugular reflex is evidence for
|
RIght ventricular overload
|
|
|
Kussmaul Sign
|
Sign of pericardial effusions
|
|
|
Right coronary feeds
|
posterior ventricles
|
|
|
what is myocardial bridging
|
"CA can dip into the myocardium, can occlude during contraction"
|
|
|
when does irreversible injury begin in MI
|
20-40 min
|
|
|
4-12 Hrs
|
Coagulation necrosis
|
|
|
12-24 hrs
|
"darkening/mottling, pyknosis
|
|
|
1-3 days
|
"Lots of neutrophils lots of necrosis
|
|
|
3-5 days
|
"hyperemic border
|
|
|
7-10 Days
|
"Macrophages, granulation tissue"
|
|
|
10-14 days
|
"depressed infarct borders, new vessels and collagen depositiion"
|
|
|
2-8 weeks
|
"fibrosis, grey white scarring"
|
|
|
2 mo- years
|
"dense collagenous scar, remodeling"
|
|
|
increasing viscosity will
|
"Decrease flow, decrease turbulance"
|
|
|
How are BABRs used in therapy
|
used alongside statins or niacin or fibrates
|
|
|
Colesvelam
|
does not inhibit other drug absorbtion
|
|
|
Cholestramine
|
"BABR
|
|
|
Colestipol
|
"BABR
|
|
|
MOA of HMG CoA reductase inhibitors
|
"competitively inhibit HMGCoA-R
|
|
|
Pravastatin
|
does not need food for absorbtion
|
|
|
ADR of statins
|
"Increase AST, ALT, CPK
|
|
|
Ezetimibe
|
"inhibits Cholesterol intake from GI tract, used along with statins"
|
|
|
Niacin
|
"B3
|
|
|
Gemfibrozil
|
"Fibric Acid derivative
|
|
|
Left sided heart failure results in
|
pulmonary congestion and edema
|
|
|
What are heart failure cells
|
"hemosiderin laden macrophages
|
|
|
Right sided hear failure will result in
|
"Congestion of the viscera, Cardiac cirrhosis, soft tissue edema"
|
|
|
Clinically what how will a CHF pt present
|
"Dyspnea, orthopnea, rales, edema"
|
|
|
What is the most common CMP
|
"Dilated
|
|
|
How does the heart appear in DCMP
|
Left ventricle and atrium dilated
|
|
|
How does the heart appear in HCMP
|
"Thick septum and ventricular walls, sometimes has dilated left atrium"
|
|
|
How does the heart appear in RCMP
|
"Ventricles normal looking, but stiff
|
|
|
What genetics are involved in DCMP
|
"mutated cytoskeleton genes
|
|
|
What mutation is common in children with CMP
|
mitochondrial mutations
|
|
|
What genes are usually mutated in HCMP
|
Sarcomeric protiens and energy transfer
|
|
|
What can cause DCMP
|
"Genetics, alcohol, pregnancy, immunologic, nutrition, HTN"
|
|
|
How does DCMP appear histologically
|
cells are hypertrophied or stretched and elongated with fibrotic interstitium.
|
|
|
DCMP Genetics
|
"Autosomal dominant, x linked recessive seen in 20 yo, mitochondrial in children"
|
|
|
DCMP-Myocarditis
|
"Common in young pts
|
|
|
DCMP-ETOH
|
"acetylaldehyde has toxic affect on myocardium
|
|
|
DCMP- Pregnancy
|
"Peripartum CMP
|
|
|
Arrhythmogenic right Ventricular dysplasia
|
"DCMP subtype
|
|
|
Hypertrophic CMP
|
"abnormal diastolic filling, thickened flabby and hypercontracting heart
|
|
|
How does the septum appear in HCMP
|
"enlarged, bulging into left vent (banana shaped)"
|
|
|
Histologically how does HCMP appear
|
myocytes look like stars or crosses
|
|
|
HCMP genetics
|
"Mutations in genes for sarcomeres
|
|
|
HCMP Clinical Features
|
"Reduced chamber size
|
|
|
Restrictive CMP
|
"Stiff Ventricles
|
|
|
Causes of RCMP
|
"Idiopathic, radiation, fibrosis, amyloid, sarcoid, metastasis"
|
|
|
Morphology of RCMP
|
"ventricles normal size
|
|
|
Restrictive endomyocardial fibrosis
|
"common in africa/tropical areas
|
|
|
Loeffler Endomyocarditits
|
"large mural thrombi
|
|
|
Endocardial Fibroelastosis
|
"Uncommon
|
|
|
Which CMP is a systolic dysfunction
|
DCMP
|
|
|
Hypertensive Heart Disease
|
"increase demand on the heart results in pressure overload and hypertrophy
|
|
|
Right sided HTN disease
|
"can arise from emphysema, pulmonary HTN, COPD, portal HTN
|
|
|
Infective causes of Myocarditis
|
"Viral: coxsackievirus-most common
|
|
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Other causes of myocarditis
|
"Sarcoid, SLE, Drugs, Radiation, Giant cell myocarditis"
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Gross findings in myocarditis
|
"Heat dilated with soft focal hemorrhage, areas of necrosis mononuclear cell infiltration"
|
|
|
hypersensitivity myocarditis
|
"Older people
|
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Cardiac Sarcoidosis
|
"asymptomatic
|
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Other causes of myocarditis
|
"chemo, lithium, phenothiazides, chloroquine, cocaine
|
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Amyloidosis
|
"deposition of beta pleated sheets of protein in myocardium
|
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Iron overload
|
"dilated heart, iron deposited in the ventricles, inducing ROS damage, heart has rusty brown color, hemosiderin in perinuclear spaces of myocytes"
|
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Long QT syndrome
|
"autosomal dominant
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Brugada Syndrome
|
"Ion channelopathy resulting in sudden death
|
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Catecholaminergic polymorphic ventricular tachycardia
|
"Sudden death w exercise
|
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Short QT syndrome
|
"Premature Afib (adolescence)
|
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Commotio Cordis
|
"Sudden Blunt trauma to the chest resulting in VFib
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Symptoms of Valvular Heart Disease
|
"Asymptomatic
|
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|
What problems present with a holosystolic murmur
|
"Mitral regurg, ventricular septal defect, and Tricuspid regurg"
|
|
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Mitral Regurg
|
"Common
|
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|
Mitral Valve Prolapse
|
"Congenital and common
|
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|
what can cause mitral regurg
|
"lupus, papillary muscle dysfunction, papillary rupture, rheumatic fever, MVP"
|
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Mitral Stenosis
|
"seen in rheumatic disease
|
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Radiologic Dx of mitral stenosis
|
"in a barium swallow you will see partial occlusion of esophagus due to atrial enlargement
|
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Aortic Stenosis
|
"Get hypertrophied ventricle, leading to ischemia and reduced diastolic filling"
|
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Aortic regurg murmur
|
High pitched early diastolic murmur
|
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Causes of aortic regurg
|
"rheumatic fever, syphilis, takayasu, marfan, ehlers danlos, endocarditis"
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|
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What class of bacteria is typically responsible for endocarditis and why
|
Gram + because they can bind to fibrin
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What bacteria can cause very rapid endocarditis
|
Staph Aureus
|
|
|
Typically how long does IE take to manifest symptoms
|
2-3 months
|
|
|
What is the course of IE
|
"turbulant flow causing an inflammatory response which induces plt activation and sticking, followed by thrombin, fibrin and bacteria stick, layering of this process makes the lesion"
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What are the typical sites of IE
|
"Aortic valve or mitral valve
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What are the major pathogens for Native valves
|
"Staph
|
|
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What are the major pathogens for prothetic valve
|
"First 60 days: Staph epi.
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What pt groups should receive prophylaxis for IE
|
"Prosthetic valve
|
|
|
what groups are at moderate risk for IE
|
"PDA, VSD, ASD, Coarcation of Aorta, Bicuspid Aortic Valve, IHSS, Valvular dysfunction, MVP w regurg"
|
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What is Low risk for IE
|
"isolated secundum ASD, greater than 6 mo after repair of ASD, VSD or PDA, benign heart murmurs"
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|
|
Strep bovis endocarditis is an indication of
|
underlying carcinoma (5-8% association w colon cancer)
|
|
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What are the clinical manifestations of endocarditis
|
"FROM JANE
|
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|
what are osler nodes
|
very painful white circular lesions with surrounding erythema
|
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what are janeway lesions
|
"petechial lesions, not painful"
|
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what is a roth spot
|
a central circular discoloration seen on a fundoscopic exam
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Mycotic aneurysm
|
"CNS aneurysm associated with endocarditis
|
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Major Duke criteria
|
"Echo w visible abnormality w a regurgitant jet. persistant pos blood culture. ESR, CRP, Rheumatoid factor, RBC in urine"
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What organisms are part of the Duke Major criteria
|
"Strep Viridians, Staph, Strep bovis, HACEK organisms, enterocci without focus"
|
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What are the HACEK organisms
|
"Haemophilus
|
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what are minor duke criteria
|
"predisposition to disease
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What puts someone at risk for Group B strep IE
|
"diabetes, etoh, neoplasm, chronic infection, invasive medical instruments, cirrhosis, spina bifida"
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What other bacteria cause IE (rare)
|
"Pneumo, bartonella, coxiella, chlamydia, mycoplasma, T. whippeli"
|
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what is the tx course for endocarditis
|
"4-8 weeks of IV abx
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|
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Nonbacterial thrombotic endocarditis
|
associated with adenocarcinoma. produces hypercoagulable state
|
|
|
Who can a valve become incompetent indirectly
|
"Ventricle dilation, dilation of the pulmary artery or aorta"
|
|
|
what determines the severity of the disease in valvular pathology
|
rate of development of disease along with rate of compensation from the heart
|
|
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What are possible etiologies of valvular disease
|
"Tensor apparatus fibrosis or rupture
|
|
|
What can cause aortic stenosis
|
"Age (senile calcification)
|
|
|
What is the underlying mechanism of calcified valvular degeneration
|
usually a dystrophic calcification
|
|
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What is the most common acquired valvular abnormality
|
Aortic Stenosis
|
|
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What is the most common congenital valvular defect
|
Bicuspid Aortic Valve
|
|
|
Mitral annular calcification
|
"calcium deposits on the circular ring around the valve, usually does not affect function but can cause a stenosis or regurg"
|
|
|
what is a secondary risk of valvular calcification
|
emboli
|
|
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Myxomatous Degeneration of the Mitral Valve
|
"aka Mitral Valve Prolapse
|
|
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Secondary changes in MVP
|
"Fibrotic thickening of the leaflets and L vent endocardium
|
|
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Rheumatic Fever
|
Antibodies to group A strep (pyrinogens) cross react with endocardium
|
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What is the most common sequelae in Rheumatic fever
|
Mitral Stenosis
|
|
|
Acute Rheumatoid carditis
|
"All 3 layers of heart (pancarditis)
|
|
|
Aschoff Bodies
|
areas of fibrinoid necrosis with surrounding mononuclear cell inflammation
|
|
|
Anitschokow Cells
|
"Large histocytes/macrophages w a vesicular nuclei and basophilic cytoplasm
|
|
|
How can RF present
|
"Migratory Polyarthritis of large joints
|
|
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What is the most common cause of mitral stenosis
|
Rheumatic heart disease
|
|
|
How does the mitral valave appear in rheumatic heart disease
|
"""Fish mouth""
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|
|
Chronic aorta valvulitis
|
"More common in males
|
|
|
In general what is the MOA of Class I antiarrythmics
|
"block sodium channels, slowing the rate of depolarization (phase 0) "
|
|
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MOA"
|
"Binds open and inactivated Na channels. Slows Phase 0.
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Indications for Quinidine
|
"Tachyarrythmias, "
|
|
|
Quinidine ADR
|
"Tinnitus, vertigo, Torsades, Thrombocytopenia, hepatitis, decreases Dig clearance"
|
|
|
MOA Procanimide
|
"Binds open and inactivated Na channels. Slows Phase 0.
|
|
|
Procainamide ADR
|
"Lupus like syndrome, asystole, arrhythmia, depression, hallucinations"
|
|
|
How does procainamide block K channels
|
has an active metabolite that blocks K
|
|
|
MAO Disopyramide
|
"Negative Ionotrope
|
|
|
ADR Disopyramide
|
"Anticholinergic activity
|
|
|
What are the Class Ia drugs
|
"Quinidine
|
|
|
What will increase Class Ia toxicity
|
Hyperkalemia
|
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|
Class Ib agents
|
Lidocaine
|
|
|
MOA of Lidocaine
|
"rapid association/dissociation with Na Channels, shorten phase 3. Shortens QT but increases refractory period"
|
|
|
Lidocaine ADR
|
"Cardiac depression, CNS stimulant/seizures"
|
|
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Flecainide
|
"Suppresses Phase 0, widens QRS and PR. only used for serious Afib and SVT. Has high mortality in post MI pts"
|
|
|
Lidocaine Indications
|
Ventricular arrhythmia
|
|
|
Class II
|
"Beta Blockers
|
|
|
Propanolol
|
"SVT, VT, post MI care"
|
|
|
Esmolol
|
"good for acute aflutter/fib
|
|
|
Metoprolol
|
"good alternative for propanolol
|
|
|
Amiodarone
|
"has actions of I, II, III, and IV
|
|
|
Amiodarone ADR
|
"analog to thyroxine (thyroid issues)
|
|
|
Sotalol
|
"Beta blocker w Class III properties
|
|
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Bretylium
|
"Blocks catecholamine release and K channels
|
|
|
Ibutilide
|
"Class III
|
|
|
Dofetilide
|
"Class III
|
|
|
Class IV
|
"Ca channel blockers, decrease phase 4, also slow phase 0 by slowing AV conduction."
|
|
|
verapamil and diltiazem
|
"bind to open Ca channels and prevent repolarization.
|
|
|
Class IV ADR
|
"negative inotropes
|
|
|
Adenosine
|
"Hyperpolarization of cells by increasing K efflux
|
|
|
Marantic Endocarditis
|
"Non bacterial thrombotic endocarditis, underlying adenocarcinoma. Aortic Valve.
|
|
|
Acute Endocarditis
|
"occurs in a few days, dyspnea
|
|
|
subacute endocarditis
|
"low grade fever, occurs on abnormal valves, takes a long time to develop"
|
|
|
What murmur is heard w IE
|
systolic murmur that progresses to a diastolic murmur
|
|
|
Morphology of endocarditis
|
"ring abscess
|
|
|
Endocarditis of SLE
|
"Libman Sacks endocarditis
|
|
|
Carcinoid Heart Disease
|
"well circumscribed, monotonous nuclei, aggressive or not
|
|
|
S. viridans
|
"coag neg
|
|
|
why would a pt with IE have negative blood cultures
|
prior administration of antibiotics
|
|
|
S. pyogenes
|
"can cause rheumatic fever
|
|
|
What is the most common congenital cardiac defect
|
VSD
|
|
|
What can cause cardiac congenital defects
|
"developmental abnormalities
|
|
|
Digeorge Syndrome
|
"ch22
|
|
|
Rubella infection can result in
|
PDA
|
|
|
Left to Right shunts
|
"ASD
|
|
|
ASD
|
"LtR
|
|
|
Secundum ASD
|
"more common
|
|
|
Primum ASD
|
"Next to aortic valve
|
|
|
VSD
|
"more common than ASD
|
|
|
Right to Left shunts
|
"Tetralogy of Fallot
|
|
|
PDA
|
"association w Rubella
|
|
|
Atrioventricular Septal Defect
|
"inadequate formation of the AV valves
|
|
|
Tetralogy of Fallot
|
"Had VSD and obstruction of the R vent outflow tract, Aorta overides the VSD and you get RVH"
|
|
|
How does ToF present
|
"depends on the severity of subpulmonary stenosis, can lead to cyanosis and R heart failure"
|
|
|
Morphology ToF
|
"boot shaped xray
|
|
|
Transposition of the Great Arteries
|
"Incompatible with life
|
|
|
Truncus Arteriosis
|
"Aorta and Pulmonary artery are the same vessel, underylying VSD
|
|
|
Tricuspid atresia
|
"occlusion of tricuspid valve. RVH, R heart failure, passive edema"
|
|
|
Total anomalous pulmonary venous connection
|
"pulmonary veins don't attach to the LA, get systemic veins from lungs drain to the coronary sinus
|
|
|
Coarcation of the aorta
|
"Associated w Turner's (45 XO)
|
|
|
Coarctation of the Aorta without PDA
|
"HTN in upper extremities
|
|
|
Eisemengers
|
"When shunt switches r-l or vice versa
|
|
|
What is Stage 1 HTN
|
90-99 diastolic
|
|
|
what are the etiologies of HTN
|
"Heart pump based
|
|
|
Stepped care approach to HTN
|
"1: diuretics, B block, or ACE-Inhib
|
|
|
Thiazides
|
"Mild to moderate HTN
|
|
|
Loop/K sparing Diuretics
|
More severe HTN
|
|
|
Propanolol ADR
|
"crazy dreams, impotence, increase in cholesterol, fatigue"
|
|
|
Carvedilol"
|
"Block a and b receptors
|
|
|
Prazosin
|
"Alpha 1 block
|
|
|
Clonidine
|
"Alpha 2 agonist
|
|
|
Methyldopa
|
"Alpha 2 agonist
|
|
|
Hydralazine
|
"arteriolar dilator
|
|
|
Minoxidil
|
"Ateriolar dilator
|
|
|
Nitroprusside
|
"NO activates cGMP, kills MLC kinases->dilation"
|
|
|
MOA ACE-inhibs
|
"block ACE, decrease aldosterone, increase bradykinin, dec sympathetics, increase vasodilation"
|
|
|
ACE inhibs ADR
|
"Dec prostaglandins result in coughing
|
|
|
ACE inhibs
|
"Captopril
|
|
|
Angiotensin II blockers
|
"Lasartan
|
|
|
What is Tubuloglomerular feedback
|
"Macula densa cells detect decreases in Na, results in constriction of afferent arteriole. ADH levels increased"
|
|
|
Where does most reabsorption happen
|
PCT
|
|
|
Acetazolamide
|
"Carbonic anhydrase inhibitors
|
|
|
ADR of Acidazolamide
|
"Cause acidosis
|
|
|
Mannitol
|
"Acts on PCT/Descending loop
|
|
|
Why is mannitol not good for CHFers
|
"Extracts intracellular fluid into the extracellular space, making edema worse"
|
|
|
Indications for mannitol
|
"Increased IOP/ICP, maintaining urine flow in low output conditions, Nephrotoxic drug OD"
|
|
|
Mannitol ADR
|
"Hypernatremia, hyperkalemia, volume depletion"
|
|
|
Furosemide
|
"Loop Diuretic
|
|
|
MOA of Furosemide
|
"increases excretion of Na, K, Cl, Ca, Mg and water. used for severe acute CHF, used in renal failure and hypercalcemia"
|
|
|
Furosemide ADR
|
"Oh Dang
|
|
|
HCTZ
|
"DCT
|
|
|
Effect of HCTZ
|
"increased excretion of Na, K, Cl, Mg, water
|
|
|
Indications for HCTZ
|
"Edema, HTN, Hypocalemia (can increase serum Ca), Hypercalcurema (inhibits Ca secretion into urine (Kidney Stones))"
|
|
|
K sparing diuretics
|
"The K STAys
|
|
|
Where does spironolactone
|
"Collecting Tubule, late DCT
|
|
|
Spironolactone MOA and ADR
|
"antagonist for aldosterone, no Na/K exchange, no K secretion
|
|
|
"Amiloride, Triamterene"
|
"Block Na transport
|
|
|
Conivaptan
|
"Collecting Duct
|
|
|
Demeclocycline
|
"Tetracycline that inhibits ADH action. Oral dosing, used mostly for SIADH
|
|
|
Myxoma
|
Most common tumor of the heart (esp in LA) make up 50%
|
|
|
Sporadic Myxoma
|
"Middle aged females
|
|
|
Familial Type Myxoma
|
"Younger males
|
|
|
Carney's Syndrome
|
"Myxoma, Cushing's, Sertoli cell CA, Fibroadenoma of the breast"
|
|
|
Myxoma Morphology
|
"Big glob of strawberry jelly
|
|
|
Myxoma Histology
|
"Round polygonal cells w a loose mucopolysaccharide background
|
|
|
Rhabdomyoma
|
"Congenital, self regress
|
|
|
Cardiac Fibroma
|
"Solitary, occur 2nd decade of life
|
|
|
Gorlin's Syndrome
|
"Basal cell carcinoma
|
|
|
Sotos Syndrome
|
"Cerebral gigantism
|
|
|
Hamartoma of Cardiac Myocytes
|
"Localized hypertrophy, shares features with HCMP"
|
|
|
Calcified Amorphous tumor of the heart
|
"nodular deposition of Ca with degenerating RBC
|
|
|
Cardiac MICE
|
"Mesothelial Incidental Cardiac Excrescenses
|
|
|
Cystic Tumor of the AV nodal region
|
"Developmental abnormality
|
|
|
Papillary fibroelastoma
|
"grow on endocardium and valves, usually benign, found more often in post cardiac surgical pts, no association with M&M tho"
|
|
|
Paraganglioma
|
"Primary cardiac neoplasm, most common in LA, association with elevated catecholamines in urine"
|
|
|
Fibrosarcoma
|
"CHF symptoms, SVC syndrome
|
|
|
Synovial Sarcoma
|
Biphasic growth: epithelial and mesenchymal
|
|
|
Lymphoma
|
usually spread to heart as 2ndray site
|
|
|
How do you enhance s4
|
hand grip
|
|
|
how do you enhance s1
|
inspiration
|
|
|
how do you enhance S3
|
hand grip lateral recumbant
|
|
|
What makes S1
|
mitral and tricuspid closing
|
|
|
What will increase the sound of S1
|
"mitral stenosis
|
|
|
What can decrease S1
|
"mitral regurg
|
|
|
How do you split S2
|
inhalation
|
|
|
what causes paradoxical splitting
|
"pulm HTN
|
|
|
what is this sound
|
Benign murmur
|
|
|
early to mid murmurs
|
"pulm stenosis
|
|
|
Mid to late murmurs
|
"Aortic Stenosis
|
|
|
Late murmurs
|
"Mitral regurg
|
|
|
Aortic Regurg
|
"At apex, diastolic murmur, use hand grip"
|
|
|
Clicks and snaps
|
"S3, HTN, aortic stenosis"
|
|
|
Mitral Regurg
|
"radiates to base, lateral recumbant do a hand grip"
|
|
|
Aortic Stenosis
|
"left murmu
|
|
|
ASD
|
"Fixed S2, RBBB"
|
|
|
VSD
|
"Increased w grip
|
|
|
PDA
|
"machine gun
|
|
|
Mitral Stenosis
|
"diastolic rumble, click
|
