Hypertension Quiz: Causes and Complications

True (A)

Atherosclerosis

<p>80</p> Signup and view all the answers

<p>Primary aldosteronism (B)</p> Signup and view all the answers

<p>High HDL levels (A)</p> Signup and view all the answers

<p>Primary hypertension = 90% of cases, no identifiable cause Secondary hypertension = 10% of cases, identifiable underlying causes Malignant hypertension = Severe pressure elevations with high risk of death Hypertensive heart disease = Cardiac complications caused by chronic hypertension</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Hyaline arteriolosclerosis</p> Signup and view all the answers

<p>neural and hormonal inputs</p> Signup and view all the answers

<p>nephrosclerosis</p> Signup and view all the answers

<p>Hyaline arteriolosclerosis = Homogeneous, pink hyaline thickening Hyperplastic arteriolosclerosis = Onion-skin appearance of vessel walls Pulmonary hypertension = Increased blood pressure in pulmonary arteries</p> Signup and view all the answers

<p>Aortic dissection (B)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Angiotensin II (B)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>ACE</p> Signup and view all the answers

<p>vascular</p> Signup and view all the answers

<p>Aldosterone = Increases sodium resorption Prostaglandins = Counterbalance vasopressor effects ANP = Inhibits sodium resorption Catecholamines = Induces vasoconstriction</p> Signup and view all the answers

<p>Angiotensin II (A)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>It increases.</p> Signup and view all the answers

<p>angiotensin I</p> Signup and view all the answers

<p>Hormonal signals (A), Local metabolic conditions (C)</p> Signup and view all the answers

<p>Genome-wide association studies (B)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>An increase in blood pressure</p> Signup and view all the answers

<p>vasoconstriction</p> Signup and view all the answers

<p>Genetic factors = Contribute minimally to blood pressure levels Renal sodium excretion = Key initiating event in hypertension Vasoconstrictive influences = Increase peripheral resistance Fluid volume = Affects cardiac output and blood pressure</p> Signup and view all the answers

<p>Alters fluid volume and cardiac output (A)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Insufficient renal sodium excretion</p> Signup and view all the answers

<p>resetting of pressure natriuresis</p> Signup and view all the answers

<p>Increased peripheral resistance (B)</p> Signup and view all the answers

<p>Angiotensin II (D)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Primary hyperaldosteronism</p> Signup and view all the answers

<p>aldosterone</p> Signup and view all the answers

<p>Renovascular hypertension = Caused by renal artery stenosis leading to increased renin Primary hyperaldosteronism = Chronic excess aldosterone secretion causing hypertension Liddle syndrome = Distal tubular reabsorption of sodium in response to aldosterone Essential hypertension = Majority caused by genetic and environmental factors</p> Signup and view all the answers

<p>Mutations in aldosterone synthase (D)</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>It increases aldosterone secretion.</p> Signup and view all the answers

<p>renin</p> Signup and view all the answers

<p>Congestive heart failure (D)</p> Signup and view all the answers

A condition where blood pressure is consistently high, exceeding 120/80 mmHg.

Hypertension caused by an identifiable underlying medical condition, such as adrenal disease or renal disease.

Adrenal disease including primary aldosteronism, Cushing syndrome, and pheochromocytoma. Renal disease including renal artery stenosis.

Hypertension with no identifiable underlying cause, also known as essential hypertension.

A rapidly progressive and severe form of hypertension, characterized by very high blood pressure and potential organ damage.

Severe pressure elevations (systolic > 200 mmHg, diastolic > 120 mmHg), renal failure, retinal hemorrhages and exudates.

The amount of blood pumped by the heart per minute, determined by stroke volume and heart rate.

Mainly by filling pressure, which is regulated by sodium homeostasis.

Vascular tone reflects a balance between vasoconstrictors (including angiotensin II, catecholamines, and endothelin) and vasodilators (including kinins, prostaglandins, and NO).

Resistance vessels show autoregulation, whereby increased blood flow induces vasoconstriction to protect tissues against hyperperfusion.

Blood pressure is fine-tuned by tissue pH and hypoxia to accommodate local metabolic demands.

The kidneys and heart contain cells that sense changes in blood pressure or volume.

Renin is a proteolytic enzyme produced by renal juxtaglomerular cells (myoepithelial cells adjacent to the glomerular afferent arterioles).

Renin is released in response to low blood pressure in afferent arterioles, elevated levels of circulating catecholamines, and low sodium levels in the distal convoluted renal tubules.

Renin cleaves plasma angiotensinogen to angiotensin I, which in turn is converted to angiotensin II by ACE (a product of vascular endothelium).

Angiotensin II raises blood pressure by inducing vascular contraction, stimulating aldosterone secretion by the adrenal gland, and increasing tubular sodium resorption.

Aldosterone increases sodium resorption (and thus water) in the distal convoluted tubules, leading to increased blood volume and blood pressure.

Volume expansion releases ANP from atrial and ventricular myocardium, inhibiting sodium resorption in the distal renal tubules, leading to sodium excretion and diuresis. ANP also causes systemic vasodilation.

Certain lifestyle factors like stress, obesity, smoking, lack of physical activity, and high salt intake are associated with an increased risk of developing hypertension.

High blood pressure accelerates atherosclerosis and damages the walls of large and medium arteries, potentially leading to aortic dissection or cerebrovascular hemorrhage.

Three types of small vessel disease are associated with hypertension: hyaline arteriolosclerosis, hyperplastic arteriolosclerosis, and pulmonary hypertension.

This condition involves thickening and narrowing of arterioles due to protein leakage and smooth muscle matrix buildup, impairing blood flow.

Another type of small vessel disease, characterized by onion-like concentric layers of smooth muscle cells in the arteriolar walls.

Chronic hypertension can lead to narrowing of renal arterioles, reducing blood supply to the kidneys, causing scarring and eventually, nephrosclerosis.

Elevated blood pressure in the pulmonary arteries, characterized by thickening and narrowing of the vessels, leading to right heart failure.

Vascular resistance is primarily regulated at the level of the arterioles. This regulation is influenced by neural and hormonal inputs, affecting the diameter of these small blood vessels.

Cardiac output is the volume of blood pumped by the heart per minute. It is determined by two key factors: heart rate, the number of times the heart beats per minute, and stroke volume, the amount of blood ejected by the heart with each beat.

Blood volume is primarily regulated by the kidneys through sodium excretion or resorption. Increased sodium excretion leads to reduced blood volume, while increased resorption leads to increased blood volume.

Renin, an enzyme secreted by the kidneys, plays a crucial role in blood pressure regulation. Released in response to low blood pressure in the afferent arterioles, renin activates the renin-angiotensin-aldosterone system (RAAS).

Angiotensin II, a potent vasoconstrictor, raises blood pressure by increasing vascular smooth muscle (SMC) tone. Additionally, it stimulates the adrenal glands to release aldosterone.

Renovascular hypertension occurs when a narrowing of the renal artery reduces blood flow to the kidney, triggering the RAAS and leading to increased blood pressure.

Primary hyperaldosteronism is a condition where there is excessive production of aldosterone from the adrenal glands. This excess aldosterone leads to increased sodium reabsorption and water retention, causing high blood pressure.

Secondary hyperaldosteronism is caused by conditions outside the adrenal glands that trigger increased aldosterone production. Some common causes include decreased renal perfusion (e.g., renal artery stenosis) and heart failure.

Essential hypertension, the most common type of hypertension, results from complex interactions between multiple genetic and environmental factors. The exact cause is unknown.

Liddle syndrome is a rare genetic disorder caused by mutations in an epithelial sodium channel protein. These mutations cause increased sodium reabsorption in the distal tubule of the kidney, even without aldosterone.

Comparing identical twins (monozygotic) to fraternal twins (dizygotic) helps determine the role of genetics in essential hypertension.

Comparing adopted children to their biological parents versus adoptive parents reveals if genetics or the environment plays a greater role in hypertension.

Rare disorders affecting a single gene can directly cause hypertension by altering how the body handles sodium and regulates blood pressure.

GWAS examine many genes at once to find variations that contribute to hypertension, even if each variation has a small individual effect.

When kidneys don't excrete enough sodium, despite normal blood pressure, it can lead to essential hypertension.

Increased fluid volume due to sodium retention raises cardiac output and peripheral vasoconstriction, contributing to hypertension.

At higher blood pressure, the kidneys eventually excrete enough sodium to balance intake, but only after blood pressure has already risen.

Factors like narrowing of blood vessels (vasoconstriction) or changes in their walls can increase peripheral resistance and contribute to hypertension.

The walls of blood vessels can become thicker and less flexible, contributing to increased peripheral resistance and hypertension.

Increased resistance to blood flow in the peripheral circulation (peripheral resistance) requires the heart to pump harder, leading to higher blood pressure (hypertension).