MSF Exam 2 Practice Test Questions And Answers Verified 100% Correct

MSF Exam 2 Practice Test Questions And Answers Verified 100% Correct A. Increased venous return, increased stroke volume Decreased venous capacitance means venoconstriction has occurred. Venoconstriction causes less blood to be held on the venous side and increases venous return to the heart. This would increase preload and increase stroke volume Decreased venous capacitance or compliance would cause which of the following: A. Increased venous return, increased stroke volume B. Increased venous return, decreased mean arterial pressure C. Decreased venous return, decreased volume D. Increased right atrial pressure, decreased mean arterial pressure Third spacing is excess fluid filtration into the interstitial space that is picked up by the lymphatics leading to edema. This can be attributed mostly to a high Pc (capillary hydrostatic pressure) that favors filtration out of the capillary and due to a decreased capillary oncotic pressure that could be related to a lack of proteins that means less is absorbed into the capillaries. You could also see heart failure related to increased filtration out of the capillaries. Arteriolar dilation leads to venous constriction and increased venous pressure d/t volume expansion. What is the biggest player of Starling Forces related to "third spacing" and why? What other clinical symptoms could you see with this? Jv = Kf (Pc + interstitial oncotic pressure - capillary oncotic pressure - Pi) Jv = 12(20 + 6 - 15 - 2) Jv = 108 Given the values below, what is the fluid flux? Kf = 12 Pi = 2 Pc = 20 interstitial oncotic pressure = 6 capillary oncotic pressure = 15 This is describing the myogenic mechanism that is used to explain autoregulation, or the intrinsic ability of blood vessels to detect changes If the blood vessels are too rigid or don't have tension, autoregulation is not good What does this process describe? What would impede this? When the driving pressure increases the vessel is stretched. Intrinsic properties of the vessel detect the change and cause smooth muscle contraction -> reduced radius of vessel -> increases resistance and prevents a rise in blood flow. B. Prostaglandin is an agonist of vasodilation E. Epinephrine is an agonist of vasodilation and binds the beta-2-receptor (GPCR) adenylyl cyclase that increases cAMP and reduces the Ca sensitivity of contractile mechanisms Which two of these are not an agonist of vasoconstriction? A. Serotonin B. Prostaglandin C. Angiotensin II D. Endothelin E. Epinephrine A. Heat generating mechanisms like activating motor nerves on skeletal muscle You are an EMT and you come to a call where a patient has fallen into a pool in the dead of winter. What physiological process is occurring in his body to maintain his core temperature at "set point" when his hypothalamus senses its deviation below normal? A. Heat generating mechanisms like activating motor nerves on skeletal muscle B. Heat generating mechanisms like decreasing thyroid hormone production C. Heat generating mechanisms like water evaporating off of the body D. Heat dissipating mechanisms like peripheral vasodilation B. Heat stroke caused by severe tissue damage due to impaired heat dissipating mechanisms You are working in the ED and your patient works on construction sites during the middle of the summer. He is normally sure to drink plenty of fluids but today, the hottest day on record in Oklahoma, he does not have any water or Gatorade. What are you most likely treating him for right now in your ED after he lost consciousness on site after complaining of a terrible headache? A. Heat exhaustion due to loss of blood volume from excessive sweating B. Heat stroke caused by severe tissue damage due to impaired heat dissipating mechanisms C. Heat exhaustion caused by abnormally regulated Ca channels D. Heat stroke caused by inhibition of COX and prostaglandins C. Inotropic; cardiac glycosides (Oubain, digoxin) Positive inotropic effects increase tension and increased muscle force/contraction by increasing amount of intracellular calcium (stimulating sympathetic nervous system). Increases in a staircase-like fashion aka Bowditch Cardiac glycosides induce positive inotropic effects by inhibiting Na-K-ATPase in plasma membrane so sodium stays in the cell. This means the Na-Ca exchanger then slows down bc of altered gradient and keeps Ca in the cell to increase contractility. Chronotropic effects are related to heart rate Dromotropic effects are related to conduction velocity Which of the below is synonymous with contractility? What is a drug class that increases this? A. Chronotropic; diuretics B. Dromotropic; beta-blockers C. Inotropic; cardiac glycosides D. Chronotropic; beta-blockers E. Dromotropic; cardiac glycosides F. Inotropic; diuretics B. Preload is the end-diastolic volume. It puts the ventricle at a good length to later contract. This is also the first heart sound during auscultation A. Afterload is the aortic pressure. It's what the heart has to overcome to pump blood out aka the diastolic pressure C. Is when the second heart sound is heard Where is the preload and what does it correlate with? Where is the afterload and what does it correlate with? Stroke volume is the volume ejected from left ventricle in one heartbeat. It is the width of the P-V loop (SV = EDV - ESV). Positive inotropic effects increase the SV and therefore the width of the P-V loop