Cardio CB / Histo Flashcards
Which protein is responsible for the elasticity of striated muscle?
Titin. It binds the thick filament to the Z disk.
Mutations in titin can produce what type of disease?
Dilated cardiomyopathy. Titin defects result in overstretching of cardiac muscle during diastole, which in turn causes decreased overlap between actin and myosin, and impaired systolic function
Malignant hyperthermia can be brought on by what?
General anesthesia. Typically succinylcholine.
What is malignant hyperthermia?
Genetic condition. Susceptibility can occur due to at least six genetic mutations, with the most common one being of the RYR1 gene. In susceptible individuals, the medications induce the release of stored calcium ions within muscle cells. The resulting increase in calcium concentrations within the cells cause the muscle fibers to contract.[1] This generates excessive heat and results in metabolic acidosis.
Treatment for malignant hyperthermia?
Dantrolene sodium & rapid cooling.
What is SERCA and what regulates it?
ATP driven Ca pump found in the SR membrane Regulated by phospholamban
Is SR more abundant in skeletal muscle or cardiac muscle?
Skeletal
Dystrophin, dystroglycan, desmin, syntrophin, dystrobrevin…what do these all have in common?
All involved in molecular anchoring at the costamere
What is stained red in this picture?
Dystrophin
A key component of the mechanical anchorage of successive cardiomyocytes in the intercalated disk is the?
fascia adherens
membrane anchorage is always via the plus end actin (thin) filaments, and not thick (myosin) filaments. In striated types of muscles, this means the terminal hemi I-band. The intercalated disk is where the next Z-line of the aligned myofibrils should be.
Where are connexins?
In gap junctions at intercalated disc.
What is stained green here?
connexin
Notice stepladder pattern. The majority of gap junctions are located at the lateral (longitudinal) component. Gap junctions function as electrical synapses.
What is pictured here?
Gap junction. It is a zipper-like structure where connexons embedded in the adjoining cell membranes are perfectly aligned to form tunnels connecting the cytosols. Connexons are composed of connexins.
All components of blood vessels are derived from?
mesenchyme
How does smooth muscle respond to hypercalcemia?
What about skeletal muscle? How does it respond to hypocalcemia?
Unlike skeletal muscle, smooth muscle responds to hypercalcemia by increased and sustained contraction.
Skeletal muscle displays tetany in response to hypocalcemia (the increased excitability results in release of Ca2+ from the extensive sarcoplasmic reticulum).
What layer of the heart is this?
Epicardium.
The outer surface of the heart lacks crevices. In the epicardial connective tissue, ample white adipose tissue is present, and so are nerves (N) and larger diameter branches of coronary arteries and cardiac veins (blue arrows). From the pericardium, connective tissue shoots toward the endocardium. These septum-like connective tissue structures house blood vessels and nerves (red arrow), and contribute to the mechanical properties of the ventricular wall. They may become excessive (fibrosis) and rigid (due to accumulation of advanced glycosylation end products [AGEs]) making the wall of the heart stiff, less compliant.
What are heart valves made of?
Valves are endocardium doublings (folds). They are covered by endothelium, and their core is connective tissue (CT). Note the conspicuous absence of blood vessels in the CT of the valve in the image. Normal valves are mostly avascular (like the cornea), except at their anchorage, where a few blood vessels are present.
Progression of atherosclerosis
THE PROGRESSION OF ATHEROSCLEROSIS
Monocytes initially roll on, then adhere to, and finally migrate across the activated endothelium (diapedesis). Oxidized LDL is taken up by these monocyte-derived macrophages via the scavenger LDL receptor and become foam cells. Smooth muscle cells enter the intima from the media, and secrete ECM. With disintegration of foam cells, insoluble cholesterol is deposited extracellularly. The released fat binds calcium and hardens (calcification of the plaque). Removal of cholesterol from the intimal deposits is aided by HDL.
