Cardiovascular Miscellany 1 (Nichols) Flashcards
Cardiomyocytes viewed under the microscope after reperfusion following an MI may show:
Contraction banding due to calcium influx following ATP depletion, enhancing actin-myosin interaction, resulting in hypercontraction.
Describe what is going on in cardiac Raynaud.
Coronary artery hyper-reactivity, causing a syndrome of chest pain identical in quality to chest pain from atherosclerotic CAD (angina pectoris)
What may result, is coronary artery vasospasm due to the bleed vessel hyper-reactivity –> contraction band necrosis seen under scope.
What is Variant Angina aka Prinzmetal Angina?
a clinical entity characterized by episodes of angina pectoris, usually at rest and often between midnight and early morning, in association with ST-segment elevation.
Vascular smooth muscle hyper-reactivity thought to be central to the pathogenesis.
Major risk factor: smoking
More frequent in Japan
Dx often make in indiv. <50yo
Pain generally lasts 5-15 mins.
Character: same as angina pectoris
What is Takotsubo cardiomyopathy?
“Broken heart syndrome”
angina due to extreme stress caused by vasospasm –> Myocardial ischemia, infarction, possibly death.
What’s going on in Karposi Sarcoma?
In immune suppressed or compromised pts, erythematous, plaquey lesions appear on the distal lower extremities and with time, move proximally. Can be treated by discontinuing immunesuppression, antivirals (for HHV8), or resection/radiation/chemotherapy. It is a low grade tumor, bordering benign-malignancy.
Usually asymptomatic.
Virally encoded G protein induces VEGF production. Viral homologue of cyclin D drives proliferation and multiple KSHV-encoded proteins inhibit p53.
Histology: jagged, vascular channels, monocytosis, spindle cells, extravasation of erythrocytes, hemosiderin deposition. Small hemorrhages.
Tell me about deep vein thrombosis.
Common. 400,000 cases/yr in US
Serious, can be fatal if embolizes.
100,000 deaths due to embolization of DVT in US
Higher incidence in men than women, older than younger.
Cancer, HOSPITALIZATION, surgery, major trauma, pregnancy, oral contraceptives, CHF, obesity, inherited coagulation defects, are risk factors
MOST IMPORTANT RISK FACTOR: PROLONGED IMMOBILIZATION
Proximal thrombosis: popliteal veins Major problem
Distal thrombosis: calf veins
Look for edema, erythema, superficial venous dilation
Asymmetry over 2cm of calf circumference + screen for DVT (mederate sens. and spec.)
D-dimer: high sens. moderate spec. (Neg. D-dimer? Not a DVT)
What is Homans sign?
forcefully dorsiflexing the food in a pt suspected of having a DVT may cause calf pain
Poor sens. and moderate spec.
Risk of dislodging more thrombus in calf
What is venous stasis dermatitis?
Presents with erythematous, scaling, and eczematous patches or plaques, hyperpigmentation, maybe hemosiderin accumulation, affecting the lower extremities.
Medial ankle most freq. and severely involved.
Due to chronic venous insufficiency.
Risk factors: age, fam. Hx, female, standing occupation, obesity, DVT Hx.
CHF and hypertension aggravate.
What is the most common cause of lower extremity ulcers?
Chronic venous disease.
Ulcers usually located low on the medial ankle, never above the knee. Very tender, shallow, exudative, granulation base.
What is Trousseau syndrome?
migratory thrombophlebitis due to elaboration of procoagulant factors from malignant tumors resulting in evanescent (quickly fading or disappearing) thromboses in different vascular beds at different times.
What is Sturge-Weber syndrome?
also called encephalotrigeminal angiomatosis.
Uncommon congenital disorder associated with facial port wine nevi, ipsilateral venous angiomas, mental retardation, seizures, hemiplegia, and radiopacities of the skull.
What is superior vena cava syndrome?
usually caused by neoplasms that compress or invade the superior vena cava. Resulting obstruction produces marked dilation of veins of head, neck, arms, chest, associated with cyanosis.
What is Osler-Weber-Rendu disease?
Aka Hereditary hemorrhagic telangectasia
Autosomal dominant disorder caused by mutations in genes that encode components of the TGF-B signaling pathway in endothelial cells.
Telangectasias present at birth.
Lesions can spontaneously rupture, causing serious epistaxis (nosebleed), GI bleeding, or hematuria.
How does portal venous hypertension present?
caput medusae (distended veins radiating from umbilicus) gastro-esophageal varices, hemorrhoids. G-E varices most important bc they can rupture leading to airway compromise or massive upper GI hemorrhage.
