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SHADOW HEALTH- ANTIHYPERTENSIVES CONCEPT LAB EXAM 2025|QS & AS|A+ GRADED
Typology: Exams
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Blood pressure (BP) the force applied by circulating blood on the walls of the blood vessels Systolic pressure the pressure against the walls when the hearts ventricles contract Diastolic pressure the pressure exerted when blood is replenished in the heart Normal BP Adults: around 120/80 mmHg When is BP highest when heart muscles contract
When is BP lowest When heart muscles relax, allowing blood back into the heart Factors of Blood pressure
Thiazide diuretics cost-effective, generally tolerated well, and are effective in treating mild to moderate hypertension by reducing blood volume Thiazide MOA Work in the nephron Inhibit reabsorption in the DCT of the nephron Work by inhibiting the reabsorption of Na+ into the blood, and as water tends to follow sodium, its reabsorption is also limited. Water remaining in the filtrate will be excreted as urine. Before vs. after administration of Thiazide diuretics Before: in the DCT of the nephron, Na+ and water (and other molecules), are reabsorbed from the filtrate into the blood
Electrolyte depletion, hypotension, hyponatremia, hyperglycaemia, blood dyscrasias Peripheral Resistance The resistance blood meets as it flows through the blood vessels Peripheral Resistance can be INCREASED by: Vasoconstriction (the narrowing of the blood vessels) Peripheral Resistance can be DECREASED by: Vasodilation (the widening of the blood vessels) Reducing Peripheral Resistance Treating hypertension by reducing peripheral resistance is accomplished by limiting natural vasoconstriction in order to allow blood to flow with less resistance through the vasculature
Vasoconstriction and Vasodilation role in healthy individual -play important role in regulating mean arterial pressure -regulate overall body temperature Vasocontriction: retains heat Vasodilation: allows the body to cool Treating hypertension by reducing peripheral resistance is accomplished by: limiting natural vasoconstriction in order to allow to flow with less restriction through vasculature Mean Arterial Pressure (MAP) the average arterial pressure during the cardiac cycle Drug Classes that reduce peripheral resistance
Calcium Channel Blockers: MOA Prevent Ca2+ from entering arterial smooth muscle cells, thereby promoting relaxation of vascular smooth muscle and vasodilation. Calcium Channel Blockers: Location and explanation of action -work within the cells of cardiac and vascular smooth muscles -the membranes of these cells have channels that allow the influx of calcium ions, which stimulated vasoconstriction Before vs After administration of calcium channel blockers Before: calcium ions enter arterial smooth muscle cells through calcium channels, promoting vasoconstriction After: Calcium channel blockers prevent calcium ions from entering arterial smooth muscle cells (by blocking action of channel), preventing vasoconstriction and promoting vasodilation Calcium Channel Blockers Effects
Reduce peripheral resistance by limiting vasoconstriction and promoting vasodilation Primarily work on arterial smooth muscle to dilate the arteries. As the venous smooth muscle remains unaffected, a pressure and fluid imbalance results, which may lead to edema from fluid pooling in the tissue space between cells. Potential adverse effect of Calcium Channel Blockers ***ones of importance and relevance Peripheral edema of the legs and ankles Common Adverse effects of CCB Flushed skin, headache, dizziness, peripheral edema, lightheadedness, nausea, constipation, fatigue, weakness, myalgia, arthralgia, impotence, sexual dysfunction Serious Adverse effects of CCB
Angiotensin II contracts blood vessels, resulting in increased peripheral resistance and arterial pressure. Angiotensin II also stimulated the adrenal cortex to produce aldosterone (a hormone that increases the kidneys sodium and fluid retention), thereby raising blood volume What Angiotensinogen is produced by The liver What Renin is produced by and what does it form Kidneys, Angiotensin! is formed What is ACE produced by and where? What does it form? Capillary tissue cells, primarly in the lungs. Angiotensiin II is formed What does Angiotensin II stimulate and by what? Aldosterone by the adrenal cortex
What does Angiotensin II bind to causing what? Binds to receptors on blood vessel walls, causing vasoconstriction. What is the role of angiotensin II
Relationship between ACE and angiotensin I & II The production of Angiotensin II heavily relies on ACE's ability to process angiotensin I into angiotensin II Ace inhibitors disrupt this ability, thus preventing angiotensin II from being formed, and preventing vasoconstriction from occurring Bradykinin Peptide chain a powerful vasodilator that is broken down by ACE ACE inhibitors prevent ACE from breaking bradykinin down. When left intact, bradykinin promotes vasodilation of the vasculature--> reducing peripheral resistance ACE inhibitors MOA (simplified) -Since angiotensin II serves as a vasoconstrictor, and is also indirectly responsible for increasing sodium reabsorption in the kidneys, preventing its formation also reduces blood volume
What side effect is associated with the buildup of bradykinin due to ACE inhibitors? Dry cough. What is a vascular effect of ACE inhibitors? Decreased peripheral resistance by inhibiting the production of angiotensin II. What respiratory effect can ACE inhibitors cause? Increased dry cough due to the buildup of bradykinin in the lungs. What renal effect do ACE inhibitors have? Increased urination by limiting aldosterone production and increasing diuresis. Common ACE inhibitors adverse effects
Headache, dizziness, hypotension, rash, cough, taste disturbances Serious ACE inhibitors adverse effects Angioedema, acute renal failure, agranulocytosis, first-dose phenomenon Angiotensin Receptor Blockers (ARBs) a second class of drugs that act on the RAAS to treat hypertension (also first-line therapy) -work similar to ACE inhibitors --> primarily work to reduce vasoconstriction, lowering peripheral resistance and blood volume ARBs Examples
