أسئلة المحاضرة الرابعة CVS باثولوجي
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أسئلة المحاضرة الرابعة CVS باثولوجي

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Questions and Answers

What is the primary classification of hypertension that accounts for most cases?

  • Secondary Hypertension
  • Benign Hypertension
  • Essential Hypertension (correct)
  • Malignant Hypertension

    • Which factor is not considered a common cause of primary hypertension?

  • Genetic factors
  • Endocrine disorders (correct)
  • Stress and obesity
  • Increased dietary sodium intake

    • Which condition is considered a secondary cause of hypertension?

  • Toxemia of pregnancy (correct)
  • Physical inactivity
  • Liddle Syndrome
  • Increased heart rate

    • How is blood pressure primarily determined in the vascular system?

    <p>Cardiac output and peripheral resistance</p> Signup and view all the answers

    Which of the following is NOT a humoral vasodilator?

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

    In primary hypertension, what happens to the sensitivity of baroreceptors to elevated blood pressure?

    <p>They become less sensitive.</p> Signup and view all the answers

    Which of the following is a common environmental factor contributing to hypertension?

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

    What percentage of hypertension cases is classified as secondary hypertension?

    <p>5%</p> Signup and view all the answers

    What is the primary physiological effect of autoregulation in hypertension?

    <p>Vasoconstriction to protect tissues</p> Signup and view all the answers

    In benign hypertension, how does cardiac output change over time?

    <p>It returns to normal</p> Signup and view all the answers

    Which age group is most likely to develop malignant hypertension?

    <p>30-40 years</p> Signup and view all the answers

    What is a characteristic feature of decompensated stage in benign hypertension?

    <p>Dilated left ventricle with thin walls</p> Signup and view all the answers

    Which type of arteriolosclerosis is associated with malignant hypertension?

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

    What distinguishes renal changes in benign nephrosclerosis from malignant nephrosclerosis?

    <p>Kidneys in benign nephrosclerosis are small and contracted</p> Signup and view all the answers

    What is a common progression of pressure in malignantly affected individuals?

    <p>Pressure rises rapidly over 200/120</p> Signup and view all the answers

    How does the presence of atheroma in benign versus malignant arteriolosclerosis differ?

    <p>Atheroma is less severe in malignant arteriolosclerosis</p> Signup and view all the answers

    What is a significant microscopic change observed in the afferent arterioles during hypertensive pathology?

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

    Which of the following is NOT a characteristic of malignant hypertensive encephalopathy?

    <p>Retinal exudate</p> Signup and view all the answers

    In malignant hypertension, what consequence may arise from retinal hemorrhage?

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

    Which finding is typically associated with benign hypertensive nephropathy?

    <p>Mild compensatory dilatation</p> Signup and view all the answers

    What is a common finding seen in both benign and malignant hypertensive retinopathy?

    <p>Retinal hemorrhage</p> Signup and view all the answers

    Which of the following describes a change specific to malignant hypertension?

    <p>Progressive uremia</p> Signup and view all the answers

    What type of aneurysms are related to benign hypertensive changes in the brain?

    <p>Intracerebral microaneurysms</p> Signup and view all the answers

    Which of the following vascular changes is associated with the base of the pyramids in cases of hypertension?

    <p>Thickening and dilation</p> Signup and view all the answers

    What primarily contributes to the elevation of blood pressure in terms of cardiac output?

    <p>Increased stroke volume</p> Signup and view all the answers

    Which of the following factors is most closely associated with primary hypertension?

    <p>Genetic predisposition</p> Signup and view all the answers

    What characterizes secondary hypertension compared to primary hypertension?

    <p>It has a known underlying cause.</p> Signup and view all the answers

    Which hormonal factor contributes to increased peripheral resistance in hypertension?

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

    What environmental factor is NOT recognized as contributing to the development of primary hypertension?

    <p>Chronic end-stage renal disease</p> Signup and view all the answers

    Which physiological mechanism primarily regulates blood pressure through sensitivity of baroreceptors?

    <p>Neural factors</p> Signup and view all the answers

    Which condition may lead to a secondary form of hypertension due to hormonal imbalances?

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

    Which factor is least likely to enhance peripheral resistance in patients with hypertension?

    <p>Humoral vasodilators</p> Signup and view all the answers

    What is a hallmark characteristic of the compensated stage in benign hypertension?

    <p>Concentric left ventricular hypertrophy with bulge of interventricular septum.</p> Signup and view all the answers

    Which type of arteriolosclerosis is characterized by onion skin appearance of the vessels?

    <p>Hyperplastic arteriolosclerosis.</p> Signup and view all the answers

    In malignant hypertension, what effect does it typically have on renal size?

    <p>Results in nephromegaly with a normal or enlarged size.</p> Signup and view all the answers

    How does the progression of blood pressure in malignant hypertension typically manifest?

    <p>Rapidly escalates to levels over 200/120.</p> Signup and view all the answers

    What type of renal changes is specifically associated with benign nephrosclerosis?

    <p>Small and contracted kidneys.</p> Signup and view all the answers

    Which condition indicates that malignant hypertension may develop in previously normotensive individuals?

    <p>Immediate onset of a hypertensive crisis.</p> Signup and view all the answers

    How does the formation of atheroma in benign arteriosclerosis compare to malignant arteriosclerosis?

    <p>Less severe in malignant conditions.</p> Signup and view all the answers

    What is the likely outcome of hypertension on the left atrium in benign cases?

    <p>Hypertrophy followed by dilation.</p> Signup and view all the answers

    What is a likely outcome of malignant hypertensive retinopathy?

    <p>Complete blindness</p> Signup and view all the answers

    Which change is indicative of necrosis in the nephron due to malignant hypertension?

    <p>Necrotising arteriolitis</p> Signup and view all the answers

    Which characteristic is shared between benign and malignant hypertension in terms of heart failure?

    <p>Left ventricular failure</p> Signup and view all the answers

    In the context of cerebral impacts from malignant hypertension, what is a common consequence?

    <p>Cerebral edema</p> Signup and view all the answers

    Which finding is more indicative of benign than malignant hypertensive nephropathy?

    <p>Minimal fibrosis with few lymphocytes</p> Signup and view all the answers

    What type of vascular changes occurs at the base of the pyramids in cases of hypertension?

    <p>Thick and dilated arteries</p> Signup and view all the answers

    What type of microscopic vessel changes is associated with benign hypertension?

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

    Which pathological change is seen in malignant hypertensive encephalopathy that is not typically found in benign cases?

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

    Study Notes

    Definition

    • Persistent elevation of systemic blood pressure above 140/90 mmHg.

    Classification

    • Primary (Essential) Hypertension: Unknown cause, accounts for 95% of cases.
      • Etiology:
        • Genetic Factors:
          • Gene defects affecting enzymes involved in aldosterone metabolism.
          • Mutation in proteins affecting renal sodium reabsorption.
        • Environmental Factors:
          • Increased dietary sodium intake.
          • Stress, obesity, smoking, physical inactivity.
    • Secondary Hypertension: 5% of cases, due to other diseases.
      • Causes:
        • Renal: Renal diseases, renal ischemia.
        • Endocrine: Hyperaldosteronism, pheochromocytoma, Cushing’s Syndrome.
        • Coarctation of the aorta.
        • Polycythemia rubra vera.
        • Toxemia of pregnancy.
        • Contraceptive pills

    Blood Pressure

    • BP is the function of cardiac output and peripheral vascular resistance.
    • Cardiac Output:
      • Increased by:
        • Increased blood volume.
        • Increased heart rate.
        • Increased cardiac contractility.
    • Peripheral Resistance:
      • Determined mainly at the level of arterioles.
      • Regulated by:
        • Humoral vasoconstrictors: Angiotensin II, catecholamines, endothelin.
        • Humoral vasodilators: Kinin, prostaglandins, nitric oxide (NO).
        • Neural factors: Through arterial baroreceptors. In primary hypertension, baroreceptors become less sensitive to elevated BP.
        • Autoregulation: Increased blood flow leads to vasoconstriction to protect tissue from overperfusion.

    Early Events Leading to Established Hypertension

    • Salt & water retention leads to increased blood volume and cardiac output.
    • Additional sodium is excreted by the kidneys to match intake and prevent further fluid retention.
    • Cardiac output returns to normal.
    • Increased peripheral resistance (increased arteriolar tone) develops.

    Benign Hypertension

    • Incidence: 90-95%
    • Age of onset: Usually after 40 years old.
    • Course: Prolonged for many years, gradual rise in pressure to 180/100 mmHg.

    Malignant Hypertension

    • Incidence: 5-10%
    • Age of onset: 30-40 years old.
    • Course: Rapid rise in pressure over 200/120 mmHg, can occur on top of existing benign HTN.

    Cardiac Changes

    • Benign Hypertension:
      • Compensated Stage:
        • Concentric left ventricular hypertrophy with bulging of the interventricular septum.
      • Decompensated Stage:
        • Left ventricular dilation with a thin wall.
        • Left atrial hypertrophy then dilation, pulmonary hypertension, and right-sided heart failure.
    • Malignant Hypertension: Minimal effect due to the short course, unless superimposed on pre-existing benign HTN.

    Vascular Changes

    • Benign Hypertension:
      • Hyaline arteriolosclerosis.
      • Elastosis.
      • Atheroma is more severe.
    • Malignant Hypertension:
      • Necrotizing arteriolitis (fibrinoid necrosis).
      • Cellular hyperplasia (hyperplastic arteriolosclerosis with "onion skin" appearance of the vessels).
      • Atheroma is less severe.

    Renal Changes

    • Benign Nephrosclerosis:
      • Gross:
        • Size: Small (primary contracted kidney).
        • Capsule: Adherent, strips easily and shows areas of subcapsular hemorrhage.
        • C/S: Reduced cortex and medulla, not demarcated from each other. Arteries at the base of the pyramids are thick and dilated.
      • Microscopic:
        • Blood vessels: Hyaline arteriolosclerosis of afferent arterioles.
        • Nephrons: Non-functioning: Atrophy, fibrosis, and hyalinization. Functioning: Compensatory hypertrophy.
        • Interstitium: Fibrosis and few lymphocytes.
    • Malignant Nephrosclerosis:
      • Gross:
        • Size: Normal or enlarged.
        • Capsule: Strips easily, noticeable areas of subcapsular hemorrhage.
        • C/S: Areas of hemorrhage, arteries at the base of the pyramids are dilated.
      • Microscopic:
        • Blood Vessels: Necrotizing arteriolitis of afferent arterioles.
        • Nephrons: Non-functioning: Necrosis and fibrosis. Functioning: Mild compensatory dilatation.
        • Interstitium: Minimal fibrosis and hemorrhage.

    Brain Changes

    • Benign Hypertensive Encephalopathy:
      • Intracerebral microaneurysms, related to small vessels of the basal ganglia, multiple and small.
      • May rupture and cause massive spontaneous cerebral hemorrhage.
    • Malignant Hypertensive Encephalopathy:
      • Arterial spasm leads to:
        • Cerebral edema.
        • Papilledema.
        • Encephalomalacia (liquefactive necrosis due to ischemia).
      • Massive spontaneous cerebral hemorrhage.

    Retinal Changes

    • Benign Hypertensive Retinopathy: Retinal hemorrhage and exudate.
    • Malignant Hypertensive Retinopathy: Retinal hemorrhage, edema, and necrosis, may lead to blindness.

    Late Complications

    • Benign Hypertension: Left ventricular failure, cerebral hemorrhage, chronic uremia.
    • Malignant Hypertension: Progressive uremia, left ventricular failure, cerebral hemorrhage.

    Hypertension

    • Persistent elevation of systemic blood pressure above 140/90 mmHg.
    • Classified into two main types: Primary (essential) and Secondary hypertension.
    • Primary hypertension is the most common (95%) while secondary hypertension is less common (5%).
    • Primary hypertension has unknown cause, while secondary hypertension is caused by other diseases.

    Primary Hypertension Causes

    • Genetic factors:
      • Gene defects affecting aldosterone metabolism enzymes
      • Mutation in proteins affecting renal sodium reabsorption
    • Environmental factors:
      • Increased dietary sodium intake
      • Stress, obesity
      • Smoking, physical inactivity

    Secondary Hypertension Causes

    • Renal: Renal diseases, ischemia
    • Endocrine: Hyperaldosteronism, pheochromocytoma, Cushing syndrome
    • Coarctation of the aorta
    • Polycythemia rubra vera
    • Toxemia of pregnancy
    • Contraceptive pills

    Blood Pressure Regulation

    • Cardiac Output:
      • Increased through:
        • Increased blood volume
        • Increased heart rate
        • Increased cardiac contractility
    • Peripheral Resistance:
      • Determined by:
        • Humoral vasoconstrictors: angiotensin II, catecholamine, endothelin
        • Humoral vasodilators: kinin, prostaglandins, nitric oxide (NO)
        • Neural factors: through arterial baroreceptors
        • Autoregulation: increased blood flow leading to vasoconstriction to protect tissues
      • In primary hypertension, baroreceptors become less sensitive to elevated blood pressure.

    Early Initiating Events in Primary Hypertension

    • Salt and water retention resulting in increased blood volume and cardiac output
    • Kidneys excrete additional sodium to prevent further fluid retention

    Established Primary Hypertension

    • Cardiac output returns to normal.
    • Increased peripheral resistance (increased arteriolar tone).

    Benign Hypertension

    • Incidence: 90-95%
    • Age: Starts after 40 years.
    • Onset: Pressure rises gradually to 180/100 mmHg.
    • Course: Prolonged for many years.

    Malignant Hypertension

    • Incidence: 5-10%
    • Age: 30-40 years.
    • Onset: Pressure rises rapidly over 200/120 mmHg. Occurs in normotensive individuals or superimposed on existing benign hypertension.
    • Course: Short for months or 1-2 years.

    Cardiovascular Changes in Hypertension

    Benign Hypertension

    • Cardiac: Concentric left ventricular hypertrophy in the compensated stage, followed by dilated left ventricle with thin wall and hypertrophy/dilation of the left atrium in the decompensated stage.
    • Vascular: Hyaline arteriolosclerosis, elastosis, with more severe atheroma.
    • Renal: Small, contracted kidney with adherent capsule, reduced cortex/medulla, and thickened arteries at the base of pyramids. Microscopically, hyaline arteriolosclerosis of afferent arterioles, non-functioning nephrons with atrophy, fibrosis, and hyalinitis. Functioning nephrons show compensatory hypertrophy. Interstitial tissue shows fibrosis and few lymphocytes.

    Malignant Hypertension

    • Cardiac: Minimal effect unless superimposed on benign hypertension.
    • Vascular: Necrotizing arteriolitis with fibrinoid necrosis, cellular hyperplasia (onion skin appearance), with less severe atheroma.
    • Renal: Normal or enlarged kidney with easily stripped capsule, areas of subcapsular hemorrhage. Microscopically, necrotizing arteriolitis of afferent arterioles, non-functioning nephrons with necrosis and fibrosis, mild compensatory dilatation of functioning nephrons. Interstitial tissue shows minimal fibrosis and hemorrhage.

    Brain Changes in Hypertension

    Benign Hypertension

    • Microaneurysms in small vessels of basal ganglia.
    • Multiple, small aneurysms can rupture causing spontaneous cerebral hemorrhage.

    Malignant Hypertension

    • Arterial spasms leading to:
      • Cerebral edema
      • Papilledema
      • Encephalomalcia (liquefactive necrosis due to ischemia)
      • Massive spontaneous cerebral hemorrhage

    Retinal Changes in Hypertension

    Benign Hypertension

    • Retinal hemorrhage and exudate

    Malignant Hypertension

    • Retinal hemorrhage, edema, and necrosis leading to blindness

    Complications of Hypertension

    Benign Hypertension

    • Left ventricular failure
    • Cerebral hemorrhage
    • Chronic uremia

    Malignant Hypertension

    • Progressive uremia
    • Left ventricular failure
    • Cerebral hemorrhage

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