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    Pathology AH Slides

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    The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.

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    Pathology AH Slides

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    b9p6vmfnc4
    5 views34 pages
    The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.

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    Pathology AH slides

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    The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    5 views34 pages

    Pathology AH Slides

    Uploaded by

    b9p6vmfnc4
    The document summarizes the pathophysiology of arterial hypertension. It describes how blood pressure is regulated through factors like cardiac output, total peripheral resistance, and circulating blood volume. It then discusses the classification, causes, risk factors, clinical signs and symptoms, end-organ damage, and established diseases associated with arterial hypertension. The neurogenic, renal, and local vascular mechanisms involved in blood pressure regulation are also summarized.

    Copyright:

    © All Rights Reserved
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    Download as pptx, pdf, or txt
    of 34

    Arterial hypertension

    2024
    Biophysical model of the blood pressure (BP) regulation

    BP

    VCB
    CO TPR

    BP = f (CO, TPR, VCB)


    • CO – cardiac output
    • VCB – volume of the circulating blood
    • TPR – total peripheral resistance
    Arterial hypertension
    - systolic blood pressure >140 mmHg or diastolic blood pressure > 90 mmHg
    AH is a major cause mortality because it is a major risk factor for:
    - Stroke
    - heart failure
    - renal failure
    - Atherosclerosis
    - Dementia
    Classification:
    1. Primary (or essential) hypertension 85% - 95% of all human cases (we
    don’t know underlying conditions)
    2. secondary hypertension
    Systemic blood pressure regulation
    Systemic regulation
    - Neurogenic (SNS, PSNS)
    - Vasopressin
    - Kidney: RAAS, Na+-uresis, volume blood circulation
    - Heart: system of Na+uretic peptide (A and B)
    - Adrenimedullin (powerful vasodilator)
    - Immune system
    Local BP regulation
    Vasoconstiction Vasodilation
    • Na+uretic peptide (C)
    • Angiotensin 2 • NO
    • Endothelin-1 • Bradykinin
    • Acetylcholine
    • Serotonin • Adenosine
    • Thromboxane А2 • Histamine
    • Prostaglandin F2α • Prostaglandin E2
    • Prostacyclin (PGI2)
    • Leukotrienes • NO
    • EDHF
    Neurogenic control

    1). Baroreceptors (mechanoRc)


    2). Vasomotor center:
    - the nucleus tractus solitarius
    in the dorsal medulla
    (baroreceptors integration)
    - the rostral part of the ventral
    medulla (pressor region)
    - centers in the pons and
    midbrain.
    3). SNS / PSNS activity
    Kidneys mechanism BP regulation
    1. the production of renin - RAAS
    2. renal pressure natriuresis mechanism (macula densa)
    3. modulate systemic sympathetic tone by generating impulse via
    renal afferent nerves.
    Regulation of RAAS activity
    This apparatus senses:
    - the renal perfusion pressure
    - the sodium concentration in the distal tubular fluid (macula densa)
    - renin release is stimulated by β- and decreased by α-adrenoceptor
    stimulation.
    - High angiotensin II concentrations suppress renin secretion via a
    negative feedback loop.
    Kallikrein-kinin systems
    Tissue kallikreins
    (kininogen - vasoactive
    peptides).
    The most important –
    bradykinin –
    vasodilation, water and
    Na+ uresis .
    Renomedullary vasodepression

    • Renomedullary interstitial cells, located mainly in the renal papilla,


    secrete an inactive substance medullipin I. This lipid is transformed in
    the liver into medullipin II.
    • This substance exerts a prolonged hypotensive effect, possibly by
    direct vasodilatation, inhibition of sympathetic drive in response to
    hypotension, and a diuretic action.
    The Role of the Vasculature in
    Hypertension
    It depends on vascular caliber, reactivity, elasticity.
    1. vasoconstrictor hormone: Ang II, catecholamines, and vasopressin,
    2. Impairment of endothelium – dependent vasodilation - to inhibit NO
    production and prostacyclin, and endothelium-derived
    hyperpolarizing factor
    3. ↑ endothelin – 1 and thromboxane A2
    4. Larger vessels predominantly use NO, whereas smaller arteries and
    arterioles are also modulated by endothelium-dependent
    hyperpolarization and vasodilator prostaglandins
    5. traverse MEJs (myoendothelial junctions)
    In normal condition. Elastic large aorta reflect the pressure wave
    • In the youth: the pulse pressure is relatively low and the waves
    reflected by the peripheral vasculature and elastic aorta
    • With ageing, stiffening of the aorta increases the pulse pressure. It is
    lead to AH, left ventricular afterload, and contributes to left
    ventricular hypertrophy..
    Immune system
    • cytokine IL-17A (interleukin 17A) produced by a subset of T cells, innate
    lymphocytes, histiocytes, and renal tubular cells.
    • IL-17A affects renal tubular handling of sodium and seems to modulate
    pressure natriuresis
    • this cytokine stimulates vascular superoxide production, causes
    inhibitory phosphorylation of the endothelial NOS, and therefore,
    reduces the caliber of blood vessels.
    • Over the long term, IL-17A promotes vascular fibrosis and impairs
    vascular elasticity.
    • In contrast, regulatory T cells and anti-inflammatory cytokines, such as
    IL-10, have antihypertensive effects mediated, in part, by counteracting
    IL-17A.
    Arterial hypertension
    Primary (or essential) Secondary hypertension
    hypertension 1. Renal
    • 85% - 95% of all human cases 2. Endocrine
    • we don’t know underlying 3. Hemodynamic
    conditions
    4. Medicines
    5. CNS
    Risk factors
    modifiable Non - modifiable
    - Smoking (now or in the past)
    - Dyslipidemia - Male sex
    - Total cholesterol >190 mg/dL and/or HDL-
    cholesterol ♂<40 mg/dL; ♀<46 mg/dL and/or - Age (♂≥ 55 years; ♀≥ 65 years)
    - Fasting blood glucose 102–125 mg/dL - Cardiovascular disease in a first-
    - Hyperuricemia
    degree relative (♂ <55 years; ♀ <65
    - Obesity (BMI ≥ 30 kg/m² and/or, abdominal
    years)
    obesity (waist circumference ♂ ≥ 102 cm; ♀ ≥
    88 cm) - Family history of early onset of
    - Premature menopause arterial hypertension
    - Sedentary lifestyle
    - Psychosocial and socioeconomic factors
    - Heart rate >80/min at rest
    Clinical symptoms
    • Headache in the occiput
    • dizziness
    • floaters in the eyes or other visual disturbances
    • Nausea
    Asymptomatic end-organ damage
    - Pulse pressure (in an elderly individual) ≥ 60 mm Hg
    - Carotid-femoral pulse wave velocity >10 m/s
    - Left-ventricular hypertrophy: electrocardiographic signs (Sokolow–Lyon
    index >3.5 mV, etc.) and/or echocardiographic signs (left-ventricular
    mass index: ♂ >115 g/m²; ♀ ≥95 g/m²)
    - Advanced retinopathy (hemorrhges or exudates, papilledema)
    - Ankle–arm index <0.9
    - Renal failure, moderate (eGFR >30–59 mL/min/1.73 m2)
    - Microalbuminuria (30–300 mg/24 hr or 30–300 mg/g creatinine)
    - Diabetes mellitus (Fasting blood glucose ≥ 126 mg/dL in at least two
    measurements and/or HbA1c >7% and/or Postprandial blood glucose
    ≥199 mg/dL)
    Established cardiovascular and kidney
    disease
    - Cerebrovascular disease: ischemic stroke, cerebral hemorrhage, TIA
    - Coronary artery disease: myocardial infarction, angina, myocardial
    revascularization
    - Presence of hemodynamically significant atheromatous plaque (stenosis) on
    imaging
    - Heart failure, including heart failure with preserved ejection fraction
    - Peripheral artery disease
    - Atrial fibrillation
    - Severe albuminuria > 300 mg/24 h or ACR (preferably in morning urine) >300
    mg/g
    - CKD stage 4 and 5, eGFR < 30 mL/min/1.73m2

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