Hypertension and Atherosclerosis Overview
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Questions and Answers

An arterial wall affected by atheronitis is characterized by which of the following features?

  • Fatty streaks and multiple 1-2mm yellowish dots. (correct)
  • The presence of calcified nodules exceeding 5mm in diameter.
  • Absence of endothelial layer due to complete denudation.
  • A thickness greater than 0.5mm with densely packed collagen.

Which of the following sequences accurately describes the progression of atherosclerosis?

  • Aneurysm formation → Fibrous plaque → Fatty streak.
  • Fatty streak → Complications → Fibrous plaque.
  • Calcification → Fatty streak → Fibrous plaque.
  • Fatty streak → Fibrous plaque → Complications. (correct)

In the pathogenesis of atherosclerosis, how does oxidized LDL contribute to plaque formation?

  • By converting into HDL, thus raising the HDL:LDL ratio.
  • By inhibiting smooth muscle migration, preventing connective tissue synthesis.
  • By attracting monocytes via chemotactic signals, leading to foam cell formation. (correct)
  • By directly stimulating the proliferation of endothelial cells.

What is the primary mechanism by which familial hypercholesterolemia accelerates atherosclerosis?

<p>Reduced functional LDL receptors, causing elevated blood LDL levels. (C)</p> Signup and view all the answers

How does the growth of atherosclerotic plaques affect the arterial lumen, and what is the consequence of this change?

<p>Decreases lumen size; restricts blood flow. (D)</p> Signup and view all the answers

A patient's blood pressure consistently reads 142/92 mm Hg during multiple appointments. What is the most appropriate course of action?

<p>Refer the patient to their general practitioner (GP) for further evaluation and management. (C)</p> Signup and view all the answers

Which of the following factors is LEAST likely to be associated with primary hypertension?

<p>Chronic kidney disease (A)</p> Signup and view all the answers

A patient presents with hypertension and a known history of Cushing's syndrome. This hypertension is MOST likely classified as:

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

Which of the following lifestyle modifications would be LEAST beneficial for a patient newly diagnosed with primary hypertension?

<p>Increasing consumption of processed foods (C)</p> Signup and view all the answers

A patient taking nifedipine for hypertension presents with noticeable gingival overgrowth. Which medication is MOST likely responsible for this oral manifestation?

<p>Calcium channel blockers (A)</p> Signup and view all the answers

Which of the following potential complications of untreated hypertension carries the HIGHEST risk of sudden, life-threatening events?

<p>Stroke (cerebrovascular accident) (C)</p> Signup and view all the answers

A dentist notices lichenoid reactions in a patient's mouth. The patient's medical history includes hypertension managed with medication. Which class of antihypertensive drugs is MOST likely contributing to this oral manifestation?

<p>ACE inhibitors or Beta blockers (C)</p> Signup and view all the answers

In the context of atherosclerosis, what is the primary difference between large elastic arteries and large muscular arteries concerning the development of the condition?

<p>Atherosclerosis affects the intimal layer in both types of arteries. (A)</p> Signup and view all the answers

Flashcards

Fatty Streaks

Early stage of atherosclerosis characterized by 1-2mm yellowish dots.

Aorta, Carotid, Coronary Arteries

Atherosclerosis commonly occurs in these three arteries.

LDL's role in Atherosclerosis

LDL enters the intima, oxidizes, attracts monocytes, which ingest oxidized LDL forming foam cells, stimulating smooth muscle migration and accumulation leading to plaque formation.

Effect of Atherosclerosis on Lumen Size

Fibrous and fatty tissue build up and take up space.

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Familial Hypercholesterolemia

Genetic disorder leading to high LDL levels due to decreased LDL receptors.

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Hypertension Threshold

140/90 mm Hg or higher

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Primary vs. Secondary Hypertension

Primary: No identifiable cause. Secondary: Caused by another condition.

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Secondary Hypertension Causes

Renal disease, endocrine disorders, pregnancy, drugs, coarctation of the aorta.

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Lifestyle Changes for Hypertension

Weight loss, exercise, reduced alcohol/salt, stop smoking, healthy diet.

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Hypertension Medications

ACE inhibitors, ARBs, beta-blockers, calcium channel blockers, diuretics.

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Untreated Hypertension Risks

Heart failure, stroke, coronary artery disease, renal failure, peripheral vascular disease.

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Hypertension Referral Criteria

Uncontrolled (≥140/90 mmHg) or severe (≥180/100 mmHg).

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Atherosclerosis

Buildup of fats/cholesterol in artery walls, affecting the intima.

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Study Notes

  • Study notes on hypertension and atherosclerosis are detailed below focusing on diagnostic criteria, aetiology, treatment, and potential complications.

Hypertension

  • Hypertension is indicated by blood pressure readings of 140/90 mm Hg or higher.
  • Primary hypertension has no identifiable cause, while secondary hypertension results from underlying conditions.
  • Primary hypertension's aetiology involves genetic factors, environmental influences (obesity, alcohol, salt intake, stress), humoral mechanisms, and insulin resistance, which can lead to diabetes.
  • Secondary hypertension's aetiology includes renal disease, pregnancy, endocrine disorders (Conn's syndrome, adrenal hyperplasia, phaeochromocytoma, Cushing's syndrome, acromegaly), certain drugs (corticosteroids, oral contraceptives), and coarctation of the aorta.
  • Diagnosing requires blood pressure measurements on at least three occasions over a 3-month span.
  • Primary hypertension management involves lifestyle adjustments such as weight loss, increased exercise, reduced alcohol and salt intake, smoking cessation, and increased consumption of fruits and vegetables.
  • Secondary hypertension requires medical treatments like ACE inhibitors (e.g., captopril), angiotensin II receptor blockers (e.g., candesartan), beta-blockers (e.g., atenolol), calcium channel blockers (e.g., nifedipine), and diuretics (e.g., bendroflumethiazide).
  • Untreated hypertension may result in heart failure, stroke (cerebrovascular accident), coronary artery disease/myocardial infarction, renal failure, and peripheral vascular disease.
  • Refer patients to a GP if blood pressure is uncontrolled (140/90 mmHg) or urgently if it is severely elevated (180/100 mmHg).

Dental Considerations for Hypertensive Patients

  • Certain hypertension medications can have oral side effects
    • ACE inhibitors may cause loss of taste, angioedema, or lichenoid reactions.
    • Beta-blockers may induce lichenoid reactions.
    • Calcium channel blockers can lead to gingival overgrowth.
    • Diuretics may result in xerostomia (dry mouth).

Atherosclerosis

  • Atherosclerosis develops due to an imbalance in LDL and HDL cholesterol levels.
  • Atherosclerosis involves the buildup of fats, cholesterol, and other substances on artery walls, affecting the intimal layer of large elastic and muscular arteries.
  • Normal intima thickness is less than 0.1mm, consisting of loose fibrous tissue and an endothelial layer.
  • Artery walls with atheronitis exhibit fatty streaks, 1-2mm yellowish dots.
  • Atherosclerosis commonly affects the aorta, carotid, and coronary arteries.
  • The stages of atherosclerosis:
    • Fatty streak formation.
    • Fibrous plaque development.
    • Complications such as rupture, ulceration, thrombosis, haemorrhage, calcification, aneurysm, or embolus formation.
  • LDL's role in atherosclerosis:
    • LDL enters the intima, oxidizes, and attracts monocytes.
    • Fatty tissue on LDL binds to scavenger receptors on monocytes and is ingested.
    • This process stimulates smooth muscle migration and connective tissue synthesis.
    • Macrophage death leads to lipid and cholesterol spillage, causing plaque accumulation.
  • Atherosclerosis reduces the lumen size of arteries due to fibrous and fatty tissue accumulation.

Familial Hypercholesterolaemia

  • Familial hypercholesterolaemia causes hyperlipidaemia and LDL/HDL imbalance.
  • It results in decreased LDL cholesterol receptors, increasing LDL levels in the blood.
    • Heterozygotes may develop the disease in their 40s.
    • Homozygotes may develop the disease in their 20s.
  • The ideal LDL:HDL ratio is 2.99:1.

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Description

Concise study notes on hypertension and atherosclerosis, detailing diagnostic criteria, aetiology, treatment approaches, and potential complications. It covers primary and secondary hypertension, risk factors, and management strategies.

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