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Discussion

HELP with Pathophys of Hypertension

Hey everyone I need help with the patho phys of HTN. Here is what I have so far

Pathophysiology of HTN: Cardiac output is raised with normal total peripheral resistance (TRP) over time the cardiac output drops to normal levels but the TRP levels increase. The kidney plays a role since it excretes sodium and increases fluid reabsorption. This excess fluid causes BP to rise. Decreasing pressure in the renal artery causes the secretion of renin enzyme. Renin in turn causes the formation of Angiotensin I, which causes the kidneys to retain sodium and water. Angiotensin I is converted to Angiotensin II by angiotension converting enzyme found in the lungs. Angiotension II causes vasoconstricts of the arterioles which further increases TRP and elevates the BP further.

My instructor is very hard and i need to know if this will be enough to correctly describe it. Any help or input would be greatly appreciated.

Thanks!

Andrea:nurse:

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Thats good now think of it in terms of concepts. what happens when you give vaso constrictors, how much harder does the heart have to work in order to pump all that fluid through those tiny vessles. what will that do to the tiny vessels in the kidneys. what will eventually happen to the heart when the volumes starts backing up, i.e. CHF. those are the kinds of concepts you will need to know for your exam. I love HTN feel free to PM me.

that is definately ONE of the causes of HTN, but u have to consider the patho behind other causes/risk factors like age, PVD, CAD, weight, etc. i actually did a patho on HTN last semester, im new to this site so i dunno if there's a way to post it up here for or not but i'll try to help if i can.

  • Experts

hypertension is due to

  • increased cardiac output
    • any condition that increases heart rate or stroke volume

    [*]increased total peripheral resistance

    • any factor that increases blood viscosity or reduces vessel diameter

    [*]both increased cardiac output and total peripheral resistance

with total peripheral resistance. . .vasoconstriction or high pressures in vessels when prolonged over time will cause vessels to thicken and strengthen in order to tolerate the stress. the smooth muscle of the arteries will hypertrophy and sustain hyperplasia. the tunica intima and tunica media of the arteries will experience fibromuscular thickening that results in permanent narrowing of the vessel's lumen. these changes aggravate an inflammatory response resulting in biochemical mediators entering the areas where these changes are actively occurring (see https://allnurses.com/forums/f50/histamine-effect-244836.html for a description of the pathophysiology of the inflammatory response) which results in the permeability of the vascular endothelium. with this permeability, sodium, calcium, water, plasma proteins and other substances enter the vessel causing further vessel wall thickening and increasing the smooth muscle responsiveness to vasoconstriction.

renin, an enzyme produced and secreted from the kidney becomes angiotensin i which, according to my references does nothing until it is converted to angiotensin ii which stimulates the secretion of aldosterone which, in turn, causes the reabsorption of sodium in the kidneys. this renin-angiotensin system helps to regulate blood pressure. if it goes on the fritz, as it does in renal disease, and the kidneys fail to synthesize renin, the blood pressure becomes elevated.

  • Author

So if she is on a calcium channel blocker then the HTN is usually due to total peripheral resistance??

She has no signs of being overweight. She is 5ft 8 inches and weighs 144 pounds. Does not smoke and as of now does not have any other medical conditions that can cause and alteration in her blood pressure.

About the Ca channel blocker question, that is not necessarily the only reason. one of the types of HTN is primary or idiopathic, there is no known reason for the cause of the HTN, then there is secondary which is attributed to the risk factors i.e. age, gender, diet, sedentary lifestyle, comorbidities, medications etc. then theres malignant which is a rapid uncontrollable rise in BP. its possible that ur patient has primary HTN and although she doesn't have many of the risk factors, she still has elevated BP. therefore maybe shes on Ca Channel blockers because it is the only type of drug that her BP responds to, or perhaps beta blockers and ACE inhibitors aren't compatible with other meds shes taking. without knowing her history i couldn't say for sure, but don't assume they're using one form of BP med because they have a certain cause of HTN.

Pathophysiology

Essential hypertension develops from renal system dysfunction. The kidney is a filtering organ that retains vital blood components and excretes excess fluid. If too much fluid is retained, BP rises. If too little fluid is retained, BP decreases. Arterial pressure within the renal artery triggers a feedback loop. The kidneys excrete sodium, which osmotically draws fluid into the excretory system in a process called pressure diuresis. This causes a decrease in blood fluid volume and arterial pressure.

As pressure within the renal artery decreases, the kidneys reflexively secrete an enzyme called renin. This enzyme causes the formation of a protein called Angiotensin I. Angiotensin I directly stimulates the kidneys to retain sodium and fluid. Angiotensin I is converted in the lungs, via the enzyme angiotensin converting enzyme (ACE) to Angiotensin II. Angiotensin II is a potent vasoconstrictor which increases total peripheral vascular resistance and hence elevates BP.

As BP elevates, the whole system begins again with pressure diuresis. In healthy individuals, this feedback loop maintains a constant blood pressure with only minor fluctuations. In patients with essential hypertension, this feedback loop fails for undiscovered reasons. The result is a higher than normal level of pressure within the renal artery necessary for pressure diuresis to occur.

Also, this site http://www.bmj.com/cgi/content/full/322/7291/912 was VERY in depth on it, i liked it a lot, hope it helps!

  • Experts

so if she is on a calcium channel blocker then the htn is usually due to total peripheral resistance??

i think this would be a good question for you to ask a cardiologist. how would the doctor know that the physical changes in the arteries had occurred? i don't know if they can adequately detect this unless there is some sophisticated testing that does it. i think they pretty much have to go by the symptomatic evidence they collect. but, i would ask a doctor.

calcium channel blockers suppress calcium ions from crossing over the cell membranes of cardiac and the smooth muscle of the blood vessels. the result is relaxation of the vascular smooth muscle of the heart, dilation of the coronary arteries, dilation of peripheral arteries and slowing of the sa and av node electrical impulse conduction in the heart which will slow the heart rate. this would work to increase vessel diameter thus decreasing total peripheral resistance. result: lowering of the blood pressure by increasing vessel diameter if the vessels are compliant.

she has no signs of being overweight. she is 5ft 8 inches and weighs 144 pounds. does not smoke and as of now does not have any other medical conditions that can cause and alteration in her blood pressure.

there are many more factors than overweight and smoking that enter into this. there is a lot about hypertension and why it occurs that they do not know. when i was looking up the pathophysiology for you in a pathophysiology textbook this was something that they talked about. they know how tpr works and the renin-angiotensin system, but there's a lot of other stuff that enters into the picture that is still a puzzle and only theory and conjecture.

what is the connection of the increased fasting blood glucose to hypertension?

  • Experts
what is the connection of the increased fasting blood glucose to hypertension?

I think researchers have found that chronically high blood sugars are also associated with high LDL cholesterol levels as well. How this is related is too complicated for me to understand. It is the high cholesterol levels that are the underlying factors causing atherosclerosis which leads to the hypertension in diabetes.

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