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A high school biology teacher comes to you with high blood pressure. Tests show that she also has increased levels of renin in her blood and atherosclerotic plaques that have nearly blocked/occluded blood flow through her renal arteries. She does not understand. It would be clinically accurate to explain to her that the (decreased or increased?) blood flow in her renal arteries could have caused an excessive increase in renin secretion via activation of the renin-angiotensin system (RAS) pathway, and that the resulting chronically (decreased or increased?) blood pressure has likely led to the formation of the atherosclerotic plaque, given it is such a great risk factor.

When oxygen levels are (above or below) 60 mmHg, the primary stimulus for the peripheral chemoreceptors is (pH or CO2).

Why would a patient with a disease that causes excess aldosterone secretion (called hyperaldosteronism) develop secondary hypertension?

On an ECG (clinically referred to using the German abbreviation EKG since when spoken ECG sound like EEG), the QRS complex is the largest wave and is indicative of atrial repolarization.

You go to do a standard median cubital (MC) venipuncture blood draw and accidentally stabbed the patient’s high pressure radial artery, and now blood is leaking out of the resultant arterial hole rapidly and blood volume is dropping. The patient is now hypotensive. The baroreceptor-mediated reflexive response here will include: 

Both an albuterol inhaler and an EpiPen can help someone dealing with an asthmatic attack by (constricting or dilating) the bronchioles due to excess ACh and histamine stimulation, among other agents.

A dislodged blood clot that traveled in circulation and obstructed a vessel is a clinical condition called a thromboembolism.

Other than the breakdown of platelet APD, what other consistent processes normally prevent the positive feedback loop of platelet plug formation from occurring abnormally, i.e., in the absence of damaged vessels?

A normal average arterial blood value for the partial pressure of oxygen taken by ABG (arterial blood gas) should be

With respect to the first step in hemostasis – vasoconstriction, when a vessel is cut paracrine molecules which are vasoconstrictive are released to slow blood flow/blood loss and this is similar to what you are trying to achieve more drastically by applying a tourniquet to a hemorrhage site. Say someone goes to draw blood from a patient’s superficial lower pressure MC (median cubital) vein but punctures the deeper higher pressure brachial artery accidently (they never learned their surface anatomy…). Does vasoconstriction and thus the indicated site for a tourniquet need to occur superior/proximal or inferior/distal to the vessel break? Hint: think about flow from the left side of the heart out to the systemic circulation.