Rx_1.13 (Cardio) Flashcards
Histologic description of Aschoff bodies
- aschoff body = indicates rheumatic heart dz
- aschoff body = non-caseating granuloma w/multi-nucleated giant cells
Anatomical location of jugular vein
- within carotid sheath
- lateral to the carotid artery
- anterior to the vagus nerve
Young girl w/hypertension @ extremities + narrowing of thoracic aorta on aortogram ==> dx?
- coarctation of aorta
- possibly Turner Syndrome (XO), esp. if other features present
Common features of Turner’s Syndrome
- short stature
- webbed neck
- coarctation of aorta
- bicuspid aortic valve
- streak ovaries
- primary amenorrhea
Fick principle (for calculation of CO)
CO = (total O2 body consumption)/(arterial O2 - venous O2)
Intact right hemidiaphram elevated above left on (inspiratory) xray ==> dx?
damaged right phrenic nerve
Possible severe consequence of untreated UTI
- pyelonephritis
- sepsis
- acute kidney failure ==> hyperkalemia
Common dangerous feature of acute kidney failure
- indicators = high BUN, high creatinine
- consequence = hyperkalemia ==> cardiac arrhytmias
ECG finding in hyperkalemia
- peaked T waves
Presentation of Staph Aureus endocarditis
- acute onset
- IV drug user
- tricuspid valve ==> systolic murmur
- septic emboli from right side ==>
- cough
- pleuritic chest pain
- diffuse pulmonary infiltrates
- pyoneumothorax
Characteristics of S. aureus
- gram +, facultative, cluster-forming anaerobe
- catalase +, coagulase +
- beta-hemolytic
- produces golden yellow pigment in culture
Fxn of carotid sinus baroreceptors
- facilitate response to hypotension
- sends afferent signals via glossopharyngeal nerve to medulla to control sympathetic outflow
- hypotension ==> decreased firing ==> increased sympathetic outflow
- transduce pressures from 50-180mmHg
Fxn of aortic arch baroreceptors
- respond to increases in blood pressure
- less sensitive than carotid sinus
- respond to stretch caused by BP @ 110-200 mmHg
- receptors do not fire in hypotensive state
Characteristics of phases 1-4 of ventricular AP
- 0 = rapid upstroke and depolarization
- voltage-gated Na channels open
- 1 = initial repolarization
- inactivation of voltage-gated Na channels
- K channels begin to open
- 2 = plateau
- Ca influx from volt-gate Ca channels balances K efflexu
- Ca influx triggers release of Ca from sarc reticulum and myocyte contraction
- 3 = rapid repolarization
- massive K efflux due to opening of slow K channels and close of Ca channels
- 4 = resting
- high K permeability through K channels
fixed and widely split S2 ==> dx? (+mechanism)
- Atrial Septal defect
- normal cause for splitting:
- inspiration ==> decreased intrathoracic pressure ==> increased venous return @ RA/RV ==> delayed closure of pulmonic valve
- in ASD:
- shunt ==> constant blood flow across from L => R leads to increased flow into RA/RV ==> constant delay of pulmonic valve independent of breath