Comprehensive Material Flashcards
What is the different between the contractile (structural) components of smooth muscle and skeletal muscle?
Smooth muscle,,,
- No troponin
- Myosin heads point in various directions, which allows for multi-directional contraction
- Contains dense bodies instead of z-discs
- Smooth muscle cells can shrink and bulge
Skeletal
- z-discs instead of dense bodies
Describe the actomyosin regualtion of skeletal muscle contraction
- ATP binds to the myosin when it is associated with the actin, resulting in the myosin unbinding from the actin
- The ATP is hydrolyzed, resulting in the return of the myosin to its resting conformation and formation of a cross-bridge
- Phosphate is released, resulting in power stroke, ADP is released, and cycle repeats
- . In order for myosin to bind, Ca2+ must bind to TnC (troponin), resulting in a conformational change that reveals the myosin binding site
Describe the actomyosin regulation of smooth muscle contraction
- Ca2+ comes into cell the from ECM (main source is NOT SR) and binds to calmodulin, activates MLCK, phosphorylates myosin
- Cross bridge sequence occurs that is the same as skeletal muscle, except the power strokes can continue so long as the myosin is phosphorylated
- Ca2+ decreases, MLCK downregulated, dephosphorylation of myosin, which results in relaxation
How does calcium participate in both smooth muscle mechanical events and smooth muscle electrical events
Mechanical was described above
For the electrical events of smooth muscle, Ca2+, which comes from the ECM for smooth muscle, can influx into the cell resulting in depolarization, or it can efflux out of the cell, resulting in repolarization
Type I diabetes: cause, signs, symptoms
Can detect autoantibodies many years before onset of disease (autoimmune disease)
Polyuria, thirst, blurred vision, wt loss, weakness, dizzy, sensory nerve dysfunction (paresthiasis), level of consciousness
Type II diabetes: cause, signs, symptoms
High insulin and normal plasma glucose. Metabolic syndrome (see below). Asymptomatic initially. Infections (from elevated glucose), neuropathy (retinal, peripheral), polyuria, thirst, etc, obesity and metabolic syndrome.
Therapy for Type I diabetes
Diet, patient education, and INSULIN
Therapy for type II diabetes
Diet, pt. education, lots of pharmacological strategies (increase insulin secretion/action by mimicking GLP1, inhibit degradation of GLP1. Inhibit K secretion, etc. etc.) Insulin can be used when other strategies don’t work well
Hypoglycemia symptoms
ANS symptoms - tachycardia, sweating, tremors, nausea, hunger
Neurologic symptoms - confusion, irritable, blurred vision, tired
Hypoglycemia treatment
Glucose/glucagon
Describe ketoacidosis
Insulin deficiency causes mobilization of energy stores which includes ketogenesis and thus metabolic acidosis.
More common in Type I.
Treat by restoring plasma vol., reduce glucose, correct acidosis, replenish electrolytes.
Describe flow, velocity of flow and surface area throughout the vascular system
- The volume of flow is equal at all levels.
- As total cross sectional area increases(arteries to arterioles), the flow velocity decreases. Flow is proportional to pressure gradient, the 4th power of the radius and inversely proportional to viscosity and length of the capillary. Radius has a great impact on the flow. The greater the radius, the greater the flow.
- Capillaries have the maximum surface area with the minimum velocity.
Describe in the form of an equation the relationship between flow, pressure and resistance (Ohm’s Law and Poiseuille’s Law).
Flow=(Pi-Po )/Resistance
Pi = pressure coming in Po = pressure going out
List the parameters that need to be known in order to calculate total peripheral resistance
Total peripheral resistance:
Pi=aortic pressure
Po=right atrial pressure
Cardiac output
TPR=(Pi-Po)/(cardiac output)
List the parameters that need to be known in order to calculate the resistance of the pulmonary circuit
Pulmonary circuit resistance:
Pulmonary artery pressure
Left atrial pressure
Cardiac output
Explain piloerection
Piloerection, “Goosebumps”-arrector pilli muscles will be activated via alpha one receptors and increased sympathetic tone. These are attached to cutaneous hair follicles
What mediates shivering?
Shivering is mediated by primary motor center for shivering in the posterior hypothalamus
How does sympathetic chemical thermogenesis work?
Sympathetic chemical thermogenesis: Norepinephrine and epinephrine stimulate brown fat, which produces heat by oxidative phosphorylation. It doesn’t produce ATP. Sympathetic activation via beta one receptors, possibly beta 3.
What part of the hypothalamus is activated in exposure to cold?
Exposure to cold –> mechanisms for heat gain
Posterior hypothalamus is activated. There is cutaneous vasoconstriction with increased sympathetic tone and alpha one activation
What part of the hypothalamus is activated during heat loss?
Heat Loss: Anterior hypothalamus activated
What are the results of anterior hypothalamus activation?
- Cutaneous dilation occurs, which is mediated by decreased adrenergic tone (decreased norepinephrine), which is decreased activation of Alpha-one receptors.
- Cutaneous blood flow represents the exception to the rule for control, which is normally that organs control their blood flow according to local factors and events, and don’t pay attention to the brain.
- The skin is under central control because it is used for overall regulation of temperature.
What part of the nervous system is involved in thermoregulatory sweating?
General thermoregulatory sweating: sympathetic cholinergic event
