Flashcards in Cardiovascular UWorld Deck (81)
A 78 year old man dies and autopsy of his heart reveals cardiac myocytes with intracytoplasmic inclusions of yellow-brown granules. What causes this?
This is lipofuscin, it forms with age due to long term free radical injury and lipid peroxidation. Very common in heart and liver in aged, malnourished and cachectic patients.
Why do patients with B12 deficiency get posterior column and other neurologic symptoms?
B12 deficiency results in accumulation of methyl-malonly CoA due to inability to convert it to succinyl CoA. This results in incorporation of non-physiologic fatty acids into neurons.
How can folic acid and B12 supplementation decrease levels of homocysteine in an attempt to minimize thrombosis?
Folic acid and B12 make it possible for methionine synthetase to function and convert homocysteine to methionine.
What bugs might be involved in a patient with suspect endocarditis and labs that show gram-positive cocci that can synthesize dextran from sucrose?
Strep viridians (mutans and sanguinis). Dextran is insoluble which allows them to adhere to teeth and prosthetic heart valves.
Most important mediators in auto regulation of coronary blood flow? Where do they come from?
NO and adenosine. NO and citrulline are synthesized from arginine and oxygen by eNOS in the coronary endothelium. NO then activates guanylate cyclase, increasing cGMP levels, causing vasodilation. Adenosine comes from ATP metabolisms and vasodilates the small coronary vessels.
Treatment for niacin-related flushing and pruritus?
Aspirin 30-60 minutes prior to administration will inhibit the prostaglandins (PGD2 and PGE2) that mediate the reaction to niacin.
Only class III anti-arrhythmic with additional beta-blocking properties?
Sotalol. You'll know to pick this because the patient will have long QT and bradycardia.
Cardiac medication that can cause gingival hyperplasia and hyperprolactinemia?
Treatment of a patient with endocarditis and labs showing gram positive, catalase positive, coagulase negative cocci? What if cultures come back methicillin-sensitive?
80% of coagulase negative staph are methicillin resistant and should be treated with vancomycin. If cultures return methicillin sensitive, you may treat with a beta-lactamase resistant PCN like nafcillin or oxacillin.
When can the Purkinje system assume a pacemaker role?
Severe bradycardia less than 40 beats per minute.
How is it that a patient with aortic stenosis has a steady state of flow through the capillary beds, which have a much smaller diameter than the aorta?
The steady state velocity of blood flow at any given point in the vasculature is inversely proportional to the diameter of the vessel through which the blood flows:
Vol(in) = A1*V1 = Vol(out) = A2*V2
Artery likely lacerated in a patient with a skull fracture at the junction of the frontal, temporal, parietal and sphenoid bones?
This location is the "pterion", which is where the middle meningeal artery lies. This is a branch of the maxillary artery, from the external carotid.
Coagulation labs used to monitor Warfarin and Heparin?
Warfarin = PT/INR. Heparin = aPTT.
How is calcium efflux prior to myocardial relaxation accomplished?
Sarcoplasmic reticulum's Ca ATPase pump and sarcolemmal 3Na/Ca exchanger.
Why do CCBs only work in cardiac and smooth muscle and not skeletal muscle.
The L-type Ca channels in skeletal muscle causes mechanical opening of the RyR receptor of the sarcoplasmic reticulum and no Ca influx is required to open the sarcoplasmic reticulum as is necessary in cardiac and smooth muscle.
Where does Ca go in the cardiac, skeletal and smooth muscle myocytes after it is release from the sarcoplasmic reticulum?
Cardiac and skeletal = troponin C, then allowing actin and myosin to bind. Smooth muscle = calmodulin -> myosin light chain kinase phosphorylation -> myosin phosphorylation -> myosin binds to actin.
What makes an atheroma more prone to rupture than other atheromas?
Progressive plaque enlargement leads to vascular smooth muscle cell death. These cells secrete collagen and fibrin to form the fibrous cap of the atheroma, and when they die the atheroma becomes unstable.
Collagen subtypes. Which types are deposited after a patient has an MI?
1) Dermis, bone, tendons, ligaments, dentin, cornea, blood vessels and scar tissue
2) Cartilage, vitreous humor and nucleus pulposus
3) Skin, lungs, intestines, blood vessels, bone marrow, lymphatics and granulation tissue (7 days after MI, eventually replaced by type I scar tissue)
4) Basement membrane
Conditions that cause pulsus paradoxus?
Those that impair the RV ability to expand in the pericardial space (tamponade, asthma, COPD and constrictive pericarditis) leading the inter ventricular septal shift towards the LV, reducing SBP during inspiration.
How do beta-agonists cause bronchial wall dilation?
They bind to Gs -> adenylate cyclase activation -> increased cAMP
Heart sound in a non-stenotic bicuspid aorta?
Early systolic, high pitched click in the RUSB.
Cause of fluid overload and cardiac remodeling in patients with CHF
Compensatory activation of the RAAS and sympathetic nervous system increase after load and cause cardiac remodeling.
How does milrinone increase cardiac contractility?
It is a PDE3 inhibitor, which increases cAMP concentrations. This results in increased Ca efflux from the sarcoplasmic reticulum, allowing for stronger myocyte contraction.
How does NE cause vasoconstriction?
Alpha-1 stimulation results in IP3 pathway mediated vasoconstriction.
How does NE cause increased heart rate and contractility?
Beta-1 stimulation results in Gs pathway mediated increased cAMP. Note that the heart rate typically remains unchanged due to reflex bradycardia after NE induces alpha-1 mediated vasoconstriction.
What happens when you stimulate an alpha-2 receptor?
There is decreased cAMP and release of NE and insulin is inhibited.
Statin side effects
Hepatotoxicity and myopathy
Fibrate side effects
Gallstones and myopathy
Bile acid sequestrant side effects
GI upset and malabsorption