cardio 1 Flashcards
causes of viral myocarditis
parvovirus B19, HHV-6, HIV, and adenovirus.
picorna (coxsackie)
signs of MI but no cardio markers elevated
unstable angina
which beta blockers from the selective type has an effect on B2 rec too
labetolol
pulsus parodoxus
seen in cardiac tamponade or constrictive pericarditis
decrease in pressure on deep insp
pulsus parvus et tardus
aortic stenosis
he patient’s history of pharyngitis 2 weeks ago and the palpable non-blanching skin lesions with arthritis and abdominal pain are classic signs of
HSP
small cell vasculitis
blood brain barrier composed of
Composed of three layers: pedicles (foot processes of astrocytes), a basal membrane, and capillary endothelial cells bound by tight junctions.
damage to tight junctions can lead to edema
what is the function of PDGF in atherosclerosis
binds to tyrosine kinase receptors and stimulates the transition of cells from the G1 phase to the S phase. PDGF is released at atherosclerotic lesion sites by platelets and macrophages and stimulates proliferation and migration of smooth muscles cells in the tunica intima,
how is the thrombus formed after atheroma
matrix metalloproteinases is thought to be responsible for breaking down the fibrous cap of an atheroma. Matrix metalloproteinases, which are secreted by inflammatory cells in the atheroma (e.g., macrophages), weaken the fibrous cap by breaking down the extracellular matrix. Subsequently, minor stress can rupture the fibrous cap and expose the atheroma’s highly thrombogenic lipid core. It is this event that then causes the acute, total obstruction of the vessel and subsequent myocardial infarction.
bronchial artery originates
from internal thoracic arteries
branch of thoracic aorta
LEFT originates directly from thoracic aorta
what happens in ischemic muscle
dysfunction of sarcoplasmic ca channel
production of lactid acid due to anaerobic resp
inc in H+…. this gets throw out and Na+ is absp in
Na brings water along —– cell swelling
idarucizumab
dabigatran reversal
direct thrombin inhibitor
used fro —- venous thromboembolism and a fib
drug prescribed in anaphylactic shock
how does it affect the pacemaker action potential
catecholamines
increase Na and ca influx in PHASE 4
adenosine also works on PHASE 4 —- increases the K conductance —– decreases HR
what phase determines Heart rate
PHASE 4
Nonbacterial verrucous thrombi on the undersurface of the mitral valve are suggestive of
licman sack
SLE
subacute endocarditis
strept viridians
opt res, alpha hemolytic…
staph epidermis … venous catethers
infective endocarditis
most common staph aureus
damage to which artery in cervial esophagus dissection
The inferior thyroid artery originates from the thyrocervical trunk (left) or subclavian artery (right). It supplies the cervical portion of the esophagu
freidrich ataxia
deg of lateral corticospinal tract ( spastic paralysis)
deg of spinocerebellar tract ( ataxia)
dorsal columns (dec vib sense proprioception)
common cause of death —– HF
Autosomal recessive
fredreich ataxia gene
fraxatin ch 9
mitochondrial dysfunction
most common consequence of pt with right sided IE
pulomary embolism
Bacterial colonization of the heart valves can lead to the formation of thrombi and subsequent bacterial emboli.
he patient’s early-onset coronary heart disease and marfanoid habitus (tall and thin stature with increased arm span, arachnodactyly) in combination with a history of deep vein thromboses (DVTs) and learning disability raise concern
homocystinuria
Fever, pleuritic chest pain, pericardial friction rub (high-pitched scratching sound), and a pericardial and unilateral pleural effusion occurring 3 weeks after an MI
dressler
immune complex-mediated damage (type III hypersensitivity reaction) to the pericardium.
nitrate tolerance
Development of tolerance is a typical side-effect of chronic nitrate therapy. The mechanism underlying nitrate tolerance is not completely understood but is thought to involve decreased sensitivity of the vascular endothelium to nitrates. The most effective strategy to prevent this is intermittent therapy with nitrate-free intervals of at least 8 hours, which would be accomplished by avoiding isosorbide dinitrate at night.
free wall rupure after mi
within 2 weeks
can lead to cardiac tamponade
previous MI is protective
time line for ventricular anneurysm post MI
few weeks to months
interventricular septal rupture
due to macrophages
3-5 days
pt under treatment for afib and heart failure
attempts suicide
abd pain, hyperkalemia, blurry vision
digoxin toxicity
cholinergic = diarrhea vomiting nausea yellow vision
hyperkalemia
BBlockers overdose
verdose would likely cause hypotension, bradycardia, bronchospasm, and hypoglycemia
woman has a pruritic, red-brown rash over the medial ankles, varicose veins, and bilateral lower extremity edema. Her occupation likely requires her to stand for prolonged periods. These findings suggest
stasis dermatitis due to chronic venous insuff
Dermal deposition of hemosiderin is a key feature of stasis dermatitis.
differentiate ulcers caused bby PAD
they are well demarcated
painful
claudication, hair loss on the leg, or nail changes.
pt undergoes cardiac catheterization and 2 weeks later returns with low urinary output
high creatinine levels
mottle purple discoloration of feet and ischemic changes on big toe
cholestrol embolization syndrome
skin description is livedo reticularis due to vessel spasm
very high Cr due to AKI
txt stop anticoag therapy and begin statins
physiological effect of sotalol
BB with K channel blocking ability
decreased conduction through AV node
how do BB lead to decrease in AV node conduction
blocking b1 rec leads to DECREASED sympathetic tone —– decrease in HR
K+ blocking effect of sotalol …. increased myocyte AP duration due to delayed efflux of K+.—— increased ERP and prolonged QT
slow av cond is eveident by increase PR interval on ecg
prolonged repolarization caused in which classes of antiarrythmic drugs
2 and 4
2- BB
4- calcium cb
both act on pacemaker action potention
which class of antiarythmics works by decreased conduction in cardiac myocytes and purkinje fiber
Decreased conduction in cardiac myocytes and Purkinje fibers is the mechanism by which sodium channel blockers (class I antiarrhythmics) function.