A pathophysiology diagram titled 'Impact of hypertension on viral immunity' comparing cellular immune responses under normal and hypertensive conditions. The top panel, 'Normal blood pressure,' illustrates a dendritic cell presenting antigens to a T cell via receptor-ligand interactions and cytokine release. This stimulation leads to robust T-cell activation and proliferation, resulting in a large cluster of effector T cells essential for viral clearance. The bottom panel, 'Hypertension,' depicts the same initial dendritic cell-T cell interaction but highlights the presence of elevated Angiotensin II. Angiotensin II binds to Angiotensin II receptors expressed on the activated T cell. This signaling inhibits sustained proliferation and instead promotes a T-cell contraction phase, resulting in a significantly reduced population of T cells. The diagram indicates that this hypertensive state leads to an impaired effector response and delayed viral clearance. Key components labeled include dendritic cells, T cells, cytokines, Angiotensin II, and Angiotensin II receptors.

This pathophysiology diagram illustrates the anti-hypertensive mechanism of Lactiplantibacillus plantarum (Lb. plantarum) in functional foods. The process begins with Lb. plantarum fermenting milk, which produces bioactive hydrolysates. These hydrolysates function as Angiotensin-Converting Enzyme (ACE) inhibitors, targeting the zinc-binding (Zn2+) site of the ACE protein. The diagram depicts two physiological pathways influenced by this inhibition: 1) The Bradykinin Pathway: Typically, ACE degrades the vasodilator bradykinin into inactive products. By inhibiting ACE, hydrolysates prevent bradykinin degradation, promoting vasodilation and relieving hypertension. 2) The Renin-Angiotensin Pathway: Normally, ACE transforms Angiotensin I into the potent vasoconstrictor Angiotensin II, leading to vascular contraction and hypertension. The hydrolysates inhibit this transformation, preventing pathological vasoconstriction. The visual contrast emphasizes the transition from constricted, hypertensive blood vessel states to relaxed, dilated states through the modulation of enzymatic activity. This diagram serves as a model for how probiotic-derived peptides can mitigate cardiovascular risk factors by interfering with the biochemical pathways responsible for systemic blood pressure regulation.

An anatomical and pathophysiology diagram illustrating the brain regions and neural pathways involved in neurogenic hypertension. The illustration features a sagittal view of the human brain with key regulatory centers labeled, including the hypothalamus, paraventricular nucleus (PVN), and components of the brainstem: the rostral ventrolateral medulla (RVLM), nucleus of the solitary tract (NTS), caudal ventrolateral medulla (CVLM), and the intermediolateral cell column (IML). Purple stars denote the locations of circumventricular organs (CVOs) distributed near the hypothalamus and brainstem. The diagram maps the functional connectivity between these regions and the heart. A green line represents the parasympathetic input originating from the RVLM/brainstem area, while a red line represents the sympathetic input originating from the IML, both descending to the cardiac target. This illustration highlights the neuroregulatory network responsible for blood pressure control and the autonomic imbalance (increased sympathetic and decreased parasympathetic tone) characteristic of neurogenic hypertension.

This pathophysiology diagram illustrates the mechanism of action of imidazoline receptor agonists on blood pressure regulation. The visual is divided into a sagittal brain anatomical diagram and a secondary physiological flowchart. On the left, the diagram highlights the 'I1 imidazoline receptors' located within the Rostral Ventrolateral Medulla (RVLM) of the brainstem, situated inferior to the cerebrum and anterior to the cerebellum. Below this, three pharmacological agents—Clonidine, Moxonidine, and Rilmenidine—are listed as imidazole agonists that target these receptors. To the right, a downward flowchart depicts the systemic consequences of receptor activation: stimulation of the RVLM leads to the 'Inhibition of sympathetic nerve activity,' followed by the 'Inhibition of norepinephrine' release. This progression results in 'Decreased vasoconstriction,' visually represented by an illustration of a dilated blood vessel with reduced smooth muscle tension. The final clinical outcome is identified as 'Reduced blood pressure.' The content is designed for intermediate medical education, focusing on neuropharmacology and cardiovascular physiology.

Summary : This figure illustrates the organ-specific and vascular effects of hypertension, detailing pathological changes in the eye, heart, kidney, brain, large and medium arteries, and microcirculation. Each organ system is listed with its associated hypertensive complications. diagram: # Organ Systems and Hypertensive Effects : ## Eye : • Microvascular remodelling • Hypertensive retinopathy ## Heart : • LVH (left ventricular hypertrophy) • LA and LV dilatation (left atrial and left ventricular) • AF (atrial fibrillation) • Obstructive and non-obstructive CAD (coronary artery disease) • Myocardial infarction • Diastolic and/or systolic heart failure ## Kidney : • Glomerular arteriolar hypertension • Glomerulosclerosis • Albuminuria/Proteinuria • ↓ GFR (glomerular filtration rate) ## Brain : • White matter lesions • Silent microinfarcts • Microbleeds • Brain atrophy • Cognitive impairment • Vascular dementia • Ischaemic stroke • Cerebral haemorrhage ## Large and Medium Arteries : • Atherosclerosis • Vascular calcification • Arterial stiffness ## Microcirculation : • Endothelial dysfunction • ↑ Vasoreactivity • Vascular remodelling • Fibrosis and inflammation • ↑ Peripheral vascular resistance # Layout : • Central human figure with icons representing each organ system. • Each organ system is connected to a text box listing its hypertensive complications. • Colour-coded circles and boxes for each organ/vascular system. # Additional Information : • Footnote mentions sex-differences (not detailed in the figure). • ESC (European Society of Cardiology) logo at the bottom right. # Analysis : • The figure demonstrates that hypertension affects multiple organ systems, with distinct pathological changes in each. • Both macrovascular (large arteries) and microvascular (small vessels, microcirculation) complications are highlighted. • The heart, brain, and kidney are shown to be particularly vulnerable, with a wide range of structural and functional consequences. • The diagram visually emphasises the systemic nature of hypertensive disease and its multi-organ impact.

This clinical photograph displays a retinal fundus image highlighting hypertension-mediated end-organ damage (EOD), specifically hypertensive retinopathy. The image is annotated with numerical markers indicating key diagnostic features: (1) points to blurred optic disc margins and papilloedema, signaling severe intracranial pressure or grade IV hypertensive changes; (2) identifies multiple cotton wool spots, which are small, fluffy, whitish lesions representing focal retinal ischemia; and (3) demonstrates generalized arteriolar attenuation and increased vascular tortuosity, where the retinal vessels appear narrowed and more winding than normal. The anatomical focus includes the optic nerve head, the retinal nerve fiber layer, and the retinal vasculature. This material is pedagogically relevant for ophthalmology and internal medicine, illustrating the ocular manifestations of malignant or accelerated hypertension and the importance of fundoscopic examination in assessing systemic cardiovascular risk and subclinical target organ damage.

Summary : This figure provides a structured overview of how to measure and diagnose hypertension-mediated organ damage (HMOD) in the kidney, heart, and arteries, including what to measure, diagnostic criteria, and clinical indications for assessment. flowchart/table hybrid: # Why measure? : • Support decision to start or intensify blood pressure (BP)-lowering treatment for: – Individuals with elevated BP and SCORE2/SCORE2-OP risk of 5–<10% – Uncertain situations (BP/risk close to thresholds, masked/white-coat hypertension, non-traditional CVD risk factors) – Individuals <40 years old with elevated BP – Assistance overcoming patient/physician inertia # Which organ? : • Kidney • Heart • Arteries # What to measure? : ## Kidney : • eGFR (estimated glomerular filtration rate) • ACR (albumin-to-creatinine ratio) ## Heart : • ECG • Echocardiography • Cardiac biomarkers ## Arteries : • Carotid or femoral ultrasound • Pulse wave velocity • Cardiac CT # How to diagnose HMOD? : ## Kidney : • Moderate-to-severe kidney disease: – eGFR <60 mL/min/1.73 m² (irrespective of albuminuria) – Albuminuria ≥30 mg/g (irrespective of eGFR) ## Heart : • LVH (left ventricular hypertrophy) by ECG: – Sokolow–Lyon: SV1+RV5 >35 mm – RaVL ≥11 mm – Cornell voltage: SV3+RaVL >28 mm (men), >20 mm (women) • LVH by echocardiography: – LV mass/height².⁷ (g/m².⁷): >50 (men), >47 (women) – LV mass/BSA (g/m²): >115 (men), >95 (women) – LV concentric geometry: RWT ≥0.43 • Diastolic dysfunction: – LA volume/height² (mL/m²): >18.5 (men), >16.5 (women) – LA volume index (mL/m²): 34 – e’ <7cm; E/e’ >14 • Cardiac biomarkers: – hs-cTnT or >99th percentile upper reference limit – NT-proBNP >125 pg/mL (<75 years) or >450 pg/mL (≥75 years) ## Arteries : • Carotid/femoral ultrasound: Plaque (focal wall thickening >1.5 mm) • Pulse wave velocity: – Carotid-femoral PWV >10 m/s – Brachial-ankle PWV >14 m/s • Cardiac CT: Coronary artery calcium score >100 Agatston units # Design Encodings : • Organ sections are colour-coded: kidney (purple), heart (light purple), arteries (blue). • Icons represent each organ and measurement modality. • Diagnostic criteria are listed in shaded boxes for each organ. # Layout : • Four main columns: Why measure?, Which organ?, What to measure?, How to diagnose HMOD? • Rows for kidney, heart, and arteries, each with corresponding measurements and criteria. # Analysis : • The figure provides a comprehensive, organ-based approach to diagnosing HMOD, with clear measurement modalities and diagnostic thresholds for kidney, heart, and arterial damage. • It highlights the importance of tailored assessment based on clinical context and risk, and provides actionable criteria for each organ system. • The use of colour and icons aids rapid identification of organ systems and measurement types.