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What is the primary classification of hypertension that accounts for most cases?
What is the primary classification of hypertension that accounts for most cases?
Which factor is not considered a common cause of primary hypertension?
Which factor is not considered a common cause of primary hypertension?
Which condition is considered a secondary cause of hypertension?
Which condition is considered a secondary cause of hypertension?
How is blood pressure primarily determined in the vascular system?
How is blood pressure primarily determined in the vascular system?
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Which of the following is NOT a humoral vasodilator?
Which of the following is NOT a humoral vasodilator?
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In primary hypertension, what happens to the sensitivity of baroreceptors to elevated blood pressure?
In primary hypertension, what happens to the sensitivity of baroreceptors to elevated blood pressure?
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Which of the following is a common environmental factor contributing to hypertension?
Which of the following is a common environmental factor contributing to hypertension?
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What percentage of hypertension cases is classified as secondary hypertension?
What percentage of hypertension cases is classified as secondary hypertension?
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What is the primary physiological effect of autoregulation in hypertension?
What is the primary physiological effect of autoregulation in hypertension?
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In benign hypertension, how does cardiac output change over time?
In benign hypertension, how does cardiac output change over time?
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Which age group is most likely to develop malignant hypertension?
Which age group is most likely to develop malignant hypertension?
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What is a characteristic feature of decompensated stage in benign hypertension?
What is a characteristic feature of decompensated stage in benign hypertension?
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Which type of arteriolosclerosis is associated with malignant hypertension?
Which type of arteriolosclerosis is associated with malignant hypertension?
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What distinguishes renal changes in benign nephrosclerosis from malignant nephrosclerosis?
What distinguishes renal changes in benign nephrosclerosis from malignant nephrosclerosis?
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What is a common progression of pressure in malignantly affected individuals?
What is a common progression of pressure in malignantly affected individuals?
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How does the presence of atheroma in benign versus malignant arteriolosclerosis differ?
How does the presence of atheroma in benign versus malignant arteriolosclerosis differ?
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What is a significant microscopic change observed in the afferent arterioles during hypertensive pathology?
What is a significant microscopic change observed in the afferent arterioles during hypertensive pathology?
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Which of the following is NOT a characteristic of malignant hypertensive encephalopathy?
Which of the following is NOT a characteristic of malignant hypertensive encephalopathy?
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In malignant hypertension, what consequence may arise from retinal hemorrhage?
In malignant hypertension, what consequence may arise from retinal hemorrhage?
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Which finding is typically associated with benign hypertensive nephropathy?
Which finding is typically associated with benign hypertensive nephropathy?
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What is a common finding seen in both benign and malignant hypertensive retinopathy?
What is a common finding seen in both benign and malignant hypertensive retinopathy?
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Which of the following describes a change specific to malignant hypertension?
Which of the following describes a change specific to malignant hypertension?
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What type of aneurysms are related to benign hypertensive changes in the brain?
What type of aneurysms are related to benign hypertensive changes in the brain?
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Which of the following vascular changes is associated with the base of the pyramids in cases of hypertension?
Which of the following vascular changes is associated with the base of the pyramids in cases of hypertension?
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What primarily contributes to the elevation of blood pressure in terms of cardiac output?
What primarily contributes to the elevation of blood pressure in terms of cardiac output?
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Which of the following factors is most closely associated with primary hypertension?
Which of the following factors is most closely associated with primary hypertension?
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What characterizes secondary hypertension compared to primary hypertension?
What characterizes secondary hypertension compared to primary hypertension?
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Which hormonal factor contributes to increased peripheral resistance in hypertension?
Which hormonal factor contributes to increased peripheral resistance in hypertension?
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What environmental factor is NOT recognized as contributing to the development of primary hypertension?
What environmental factor is NOT recognized as contributing to the development of primary hypertension?
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Which physiological mechanism primarily regulates blood pressure through sensitivity of baroreceptors?
Which physiological mechanism primarily regulates blood pressure through sensitivity of baroreceptors?
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Which condition may lead to a secondary form of hypertension due to hormonal imbalances?
Which condition may lead to a secondary form of hypertension due to hormonal imbalances?
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Which factor is least likely to enhance peripheral resistance in patients with hypertension?
Which factor is least likely to enhance peripheral resistance in patients with hypertension?
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What is a hallmark characteristic of the compensated stage in benign hypertension?
What is a hallmark characteristic of the compensated stage in benign hypertension?
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Which type of arteriolosclerosis is characterized by onion skin appearance of the vessels?
Which type of arteriolosclerosis is characterized by onion skin appearance of the vessels?
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In malignant hypertension, what effect does it typically have on renal size?
In malignant hypertension, what effect does it typically have on renal size?
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How does the progression of blood pressure in malignant hypertension typically manifest?
How does the progression of blood pressure in malignant hypertension typically manifest?
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What type of renal changes is specifically associated with benign nephrosclerosis?
What type of renal changes is specifically associated with benign nephrosclerosis?
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Which condition indicates that malignant hypertension may develop in previously normotensive individuals?
Which condition indicates that malignant hypertension may develop in previously normotensive individuals?
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How does the formation of atheroma in benign arteriosclerosis compare to malignant arteriosclerosis?
How does the formation of atheroma in benign arteriosclerosis compare to malignant arteriosclerosis?
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What is the likely outcome of hypertension on the left atrium in benign cases?
What is the likely outcome of hypertension on the left atrium in benign cases?
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What is a likely outcome of malignant hypertensive retinopathy?
What is a likely outcome of malignant hypertensive retinopathy?
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Which change is indicative of necrosis in the nephron due to malignant hypertension?
Which change is indicative of necrosis in the nephron due to malignant hypertension?
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Which characteristic is shared between benign and malignant hypertension in terms of heart failure?
Which characteristic is shared between benign and malignant hypertension in terms of heart failure?
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In the context of cerebral impacts from malignant hypertension, what is a common consequence?
In the context of cerebral impacts from malignant hypertension, what is a common consequence?
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Which finding is more indicative of benign than malignant hypertensive nephropathy?
Which finding is more indicative of benign than malignant hypertensive nephropathy?
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What type of vascular changes occurs at the base of the pyramids in cases of hypertension?
What type of vascular changes occurs at the base of the pyramids in cases of hypertension?
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What type of microscopic vessel changes is associated with benign hypertension?
What type of microscopic vessel changes is associated with benign hypertension?
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Which pathological change is seen in malignant hypertensive encephalopathy that is not typically found in benign cases?
Which pathological change is seen in malignant hypertensive encephalopathy that is not typically found in benign cases?
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Study Notes
Definition
- Persistent elevation of systemic blood pressure above 140/90 mmHg.
Classification
-
Primary (Essential) Hypertension: Unknown cause, accounts for 95% of cases.
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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.
-
Genetic Factors:
-
Etiology:
-
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
-
Causes:
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.
-
Increased by:
-
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.
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Decompensated Stage:
- Left ventricular dilation with a thin wall.
- Left atrial hypertrophy then dilation, pulmonary hypertension, and right-sided heart failure.
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Compensated Stage:
- 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.
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Malignant Hypertension:
- Necrotizing arteriolitis (fibrinoid necrosis).
- Cellular hyperplasia (hyperplastic arteriolosclerosis with "onion skin" appearance of the vessels).
- Atheroma is less severe.
Renal Changes
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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.
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Microscopic:
- Blood vessels: Hyaline arteriolosclerosis of afferent arterioles.
- Nephrons: Non-functioning: Atrophy, fibrosis, and hyalinization. Functioning: Compensatory hypertrophy.
- Interstitium: Fibrosis and few lymphocytes.
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Gross:
-
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.
-
Gross:
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.
- Arterial spasm leads to:
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
- Increased through:
-
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.
- Determined by:
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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