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This document discusses changes to the kidneys that can result from hypertension. It describes two conditions: nephrosclerosis and malignant nephrosclerosis. Nephrosclerosis is a renal pathology associated with sclerosis of renal arterioles and small arteries. It is strongly linked to hypertension and involves thickening of arterial walls and hyalinization. Malignant nephrosclerosis is a more severe vascular disorder seen in accelerated or malignant hypertension. It involves endothelial injury, fibrinoid necrosis of arterioles, and hyperplastic arteriolitis characterized by intimal thickening of arterial walls. Both conditions can lead to ischemic damage and alterations to the glomeruli and tubules of the kidneys.
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Renal Hypertension
Renal hypertension is high blood pressure caused by kidney disease. It can be caused by renal stenosis where the renal arteries narrow, decreasing blood flow to the kidneys, or chronic glomerulonephritis where inflammation damages the glomeruli. This causes increased renal vascular resistance and decreased glomerular filtration, stimulating the renin-angiotensin system which increases blood pressure. Investigations include blood and urine tests, ultrasound, CT scan, and biopsy. Treatments depend on the cause but may include angioplasty, stenting, medications, or controlling blood pressure and protein intake.
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Hypertension and kidney
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This document discusses two types of nephrosclerosis: benign and malignant. Benign nephrosclerosis is caused by thickening of renal arterioles over time from aging, hypertension, or diabetes. It can cause scarring and loss of renal function. Malignant nephrosclerosis involves a worsening of hypertension that damages renal vessels, causing ischemia and sudden loss of function. The pathology involves fibrinoid necrosis and intimal thickening of arteries. Aggressive treatment of high blood pressure is needed to prevent permanent kidney damage in malignant nephrosclerosis.
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Glomerular disease with histopathology
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Renal pathology. Lecture 1 acute kidney injury, sufia husain 2020
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1) Nearly all renal diseases secondarily involve the renal blood vessels, with the main diseases affecting the kidneys' blood vessels being benign nephrosclerosis, malignant nephrosclerosis, and thrombotic microangiopathies.
2) Benign nephrosclerosis is characterized by hyaline thickening of small arteries and arterioles causing ischemic atrophy, while malignant nephrosclerosis features hyperplastic "onion skin" thickening of arterioles and fibrinoid necrosis.
3) Thrombotic microangiopathies include hemolytic uremic syndrome and thrombotic thrombocytopenic purpura, characterized by microangiopathic hemolytic anemia
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THIS PRESENTATION COVERS ALL ASPECTS OF HTN RETINOPATHY - EPIDEMIOLOGY , PATHOPHYSIOLOGY , CLINICAL FEATURES AND TREATMENT
Renal manifestations of systemic disease(s).
Systemic diseases that commonly present with renal manifestations: diabetic and hypertensive nephropathy, lupus nephritis, congestive heart failure (Cardiorenal Syndromes), liver disease, and paraproteinemia , infections (HCV, HIV, COVID-19,..), other rheumatological disorders (Rhod A., Gout, SCL), HSP, Vasculitis, hereditary kidney diseases, Familial Mediterranean Fever (FMF), and Malignancy.
Vascular Kidney Diseases.pdf
Vascular Kidney Diseases Notes discusses several conditions:
1. Nephrosclerosis is renal pathology associated with hypertension, causing sclerosis of renal arterioles and small arteries. It is characterized by a leather grain appearance, hyaline arteriolosclerosis, and glomerulosclerosis.
2. Malignant nephrosclerosis is due to very high blood pressure (>200/120) and is characterized by pinpoint hemorrhages, hyperplastic arteriolosclerosis, and fibrinoid necrosis of small renal arteries.
3. Thrombotic microangiopathy includes conditions like hemolytic uremic syndrome and thrombotic thrombocytopenic purpura that involve small vessel thrombosis leading
L5 & 6 effects of htn on vessels & heart 20 (2)
This document discusses the effects of hypertension on vessels and the heart. It defines various types of hypertension and their causes. Essential or primary hypertension accounts for 95% of cases and results from genetic and environmental factors that increase blood volume and peripheral resistance. This causes pathological changes in vessels like hyaline arteriolosclerosis and hyperplastic arteriolosclerosis. Hypertension can also lead to hypertensive heart disease, causing left ventricular hypertrophy and eventually heart failure if not controlled. Pulmonary hypertension from lung diseases can cause right ventricular hypertrophy known as cor pulmonale. Long term hypertension increases the risks of stroke, heart disease, and renal failure.
disorders of veins.pptx
This document discusses common disorders of arteries and veins, focusing on hypertensive vascular disease and atherosclerosis. It defines hypertension and outlines the pathogenesis of essential hypertension. Complications include stroke, heart disease, and renal failure. The document describes hyaline and hyperplastic arteriolosclerosis seen in hypertension. It also summarizes the risk factors, pathogenesis, and morphology of atherosclerosis, noting its role in cardiovascular diseases.
CVS pathology -4 Hypertension (HTN) 2019, sufia husain
The document discusses hypertension (high blood pressure), including its definition, risk factors, causes, classification, pathogenesis, effects on organs, and complications. It notes that hypertension has no symptoms in early stages but can damage organs over time, leading to heart disease, stroke, kidney failure, and retinal damage. Uncontrolled high blood pressure is also defined as malignant hypertension, which can cause rapid organ damage within years.
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This document discusses angiogenesis, which is the growth of new blood vessels from pre-existing vessels. It occurs in both health and disease as a normal process to meet metabolic demands, but can also enable tumor growth and progression. The document outlines the history of angiogenesis research, mechanisms of healthy and pathological angiogenesis, roles in conditions like cancer and wound healing, therapeutic applications and limitations. Angiogenesis-targeting treatments like bevacizumab are FDA-approved but many clinical trials of other anti-angiogenic therapies have failed due to tumor complexity and resistance mechanisms. Combination therapies may be more effective approaches.
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This document provides an overview of secondary glomerular disorders, including definitions and key details about specific conditions like diabetic nephropathy, hypertensive nephropathy, lupus nephropathy, membranoproliferative glomerulonephritis, post-streptococcal glomerulonephritis, Goodpasture syndrome, dysproteinemias, sickle cell nephropathy, HIV nephropathy, granulomatosis with polyangiitis, and polyarteritis nodosa. It discusses the pathophysiology, clinical features, diagnostics, and management of each condition. Terminology related to glomerular diseases and the structure of the glomerular
L87- Renal 111.ppt
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by anti-nuclear antibodies that can cause renal involvement in 65% of cases, presenting as hematuria, nephritis, nephrotic syndrome or chronic renal failure. Lupus nephritis is classified from Class I to VI based on glomerular pathology. Henoch–Schönlein purpura can cause renal abnormalities like hematuria, nephritic syndrome or nephrotic syndrome in one-third of patients. Vasculitis and ANCA nephropathy often present as rapidly progressive glomerulonephritis. Diabetic nephropathy is characterized by glomerular basement
AKI - Basics
Acute kidney injury (AKI) is a major public health problem associated with high mortality and morbidity. It can occur in 1-2% of hospitalized patients and up to 50-65% of patients in the ICU. AKI is defined based on changes in serum creatinine and urine output using the RIFLE, AKIN, and KDIGO criteria. The causes of AKI include sepsis, surgery, cardiogenic shock, nephrotoxins, obstruction and hepatorenal syndrome. The pathology involves tubular injury, endothelial dysfunction, inflammation and vasoconstriction. Evaluation of AKI includes assessing volume status, potential causes, urine analysis and imaging. Management involves treating the underlying cause, fluid
Hypertensive Retinopathy
Hypertension can damage the eye and lead to hypertensive retinopathy. Chronic high blood pressure causes gradual changes to the retinal blood vessels including arteriolar narrowing, nicking at arteriovenous crossings, and changes to the light reflex seen in the vessels. Malignant or acute hypertension can additionally cause retinal hemorrhages, cotton wool spots, and exudates due to damage to the small blood vessels in the retina. Strict control of blood pressure is important to prevent further eye damage and risk of other end-organ complications.
CHRONIC KIDNEY DISEASE.docx
This document defines chronic kidney disease (CKD) and describes its stages based on glomerular filtration rate (GFR). The main causes of CKD are then discussed, including hypertension, diabetes, glomerulonephritis, and urinary tract obstructions. For each cause, the document explains the pathophysiological changes that occur at the glomerular and tubular levels to reduce kidney function over time. Symptoms and complications of decreased GFR are also outlined. Finally, the document reviews treatment approaches for CKD including tight blood pressure and glucose control, avoidance of nephrotoxins, diet modification, and management of complications.
General medicine update for every doctor hypertension
Hypertension is a leading global cause of death and disability. It doubles the risk of cardiovascular diseases like heart disease and stroke. While treating hypertension reduces these risks, many hypertensive patients remain untreated or inadequately treated. Hypertension affects the eyes by damaging blood vessels in the retina, optic nerve, and choroid which can lead to vision loss if uncontrolled. Doctors are advised to gradually lower blood pressure using recommended first-line drug classes and monitor for associated organ damage.
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L5 & 6 effects of htn on vessels & heart 20 (2)
L5 & 6 effects of htn on vessels & heart 20 (2)
CVS pathology -4 Hypertension (HTN) 2019, sufia husain
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General medicine update for every doctor hypertension
General medicine update for every doctor hypertension
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This document provides an overview of nitrates, beta-blockers, calcium channel blockers, and potassium channel openers used to treat angina. It describes their mechanisms of action, pharmacokinetics, adverse drug reactions, drug interactions, and uses. The drugs work to reduce cardiac workload and oxygen demand or increase myocardial blood flow. Their effects include vasodilation, reduced heart rate, contractility and blood pressure. Common side effects are headache, flushing, and hypotension due to vasodilation. Drug interactions and dependence are concerns, requiring gradual withdrawal from nitrates. The document references essential pharmacology textbooks for further information.
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This document discusses different methods used to classify malnutrition, including their strengths and limitations. It describes Gomez's classification, which is based on weight-for-age and has the strengths of being simple and easy to measure but assumes all children of the same age have the same weight. Waterlow's classification uses weight-for-height and height-for-age to identify stunted, wasted, or stunted and wasted children. Mid-upper arm circumference is a quick field measurement of muscle mass but is not applicable for children under 1 year or over 5 years. The WHO classification uses z-scores to define levels of malnutrition but its standard values may not be appropriate for low- and middle-income countries.
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mechanism of hearing
The document summarizes the mechanism of hearing and the auditory pathway. It describes how sound is captured by the pinna and amplified through the external ear canal and middle ear bones. This causes vibrations that are transduced into electrical signals by hair cells in the cochlea. These signals travel along the auditory nerve and pathway in the brainstem and temporal lobe to the auditory cortex. Deafness can occur from damage to the peripheral structures of the external and middle ear (conductive) or the inner ear and auditory nerve (sensorineural).
visual pathways
The visual pathway contains the retinogeniculate pathway which projects from the retina to the lateral geniculate nucleus and onto the primary visual cortex. The lateral geniculate nucleus contains magnocellular, parvocellular, and koniocellular layers which project to different areas of the visual cortex and are involved in motion perception, color vision, and visual acuity. The optic radiation carries signals from the lateral geniculate nucleus to the occipital lobe via Meyer's loop. The dorsal and ventral visual pathways in the occipital lobe are involved in motion detection and object identification respectively. Lesions at different points in the visual pathway can cause specific visual field defects such as right eye vision loss or left hom
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The document discusses the vascular supply of the brain. There are two vertebral arteries and two internal carotid arteries that supply the brain. The middle cerebral artery, which branches from the internal carotid artery, supplies most of the lateral surface of the brain including the motor and sensory areas. The anterior cerebral artery supplies the medial surface including the leg area. The posterior cerebral artery branches from the basilar artery and supplies the temporal and occipital lobes. Strokes can occur from issues with these arteries, including ischemic strokes from embolisms or hemorrhagic strokes from ruptured aneurysms.
The functions of vestibular apparatus
The vestibular apparatus consists of the otolith organs and semicircular canals and detects sensations of equilibrium and acceleration. The saccule and utricle contain sensory hair cells oriented to detect upward/downward and side-to-side movement respectively. The three semicircular canals arranged orthogonally detect angular acceleration. Vestibular nuclei process sensory input to coordinate reflexes like vestibulo-ocular for gaze and vestibulo-spinal for posture. Together the vestibular system provides spatial orientation and senses self-motion.
acute pyelonephritis ab. d
1. Acute pyelonephritis is a bacterial infection of the kidney that is usually associated with a urinary tract infection. It is characterized microscopically by patchy inflammation, neutrophils in the tubules, and tubular necrosis.
2. Complications of acute pyelonephritis include papillary necrosis, pyonephrosis, and perinephric abscess. Hydronephrosis is dilation of the renal pelvis and calyces due to urinary outflow obstruction.
3. Hydronephrosis is caused by various congenital and acquired conditions and can lead to impaired kidney function, fibrosis, and end-stage renal atrophy if long-standing and complete
urine changes
The kidney can excrete urine with a concentration ranging from 50 to 1400 mOsm/L without major changes to solute excretion. Concentrated urine excretion requires a hyperosmotic renal medulla created by a countercurrent multiplier system and increased levels of the antidiuretic hormone vasopressin. The countercurrent multiplier system relies on the anatomical arrangement of loops of Henle and vasa recta to generate tubule-interstitial osmotic gradients as high as 200 mOsm/L. Vasopressin increases water permeability in the late distal convoluted tubule and collecting duct, while urea recirculation within the medulla raises urea concentrations and diffusion. Dilute urine
nephritic and nephrotic syndrome
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
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Diabetes mellitus (ii)
This document provides an overview of type 2 diabetes mellitus (DM), including its pathophysiology, risk factors, clinical presentation, screening and diagnosis, management, and treatment. It discusses DM as characterized by hyperglycemia, insulin resistance, and relative insulin deficiency. Risk factors include genetic susceptibility and environmental exposures. Symptoms result from hyperglycemia and long-term complications can include damage to blood vessels and nerves. Treatment involves lifestyle modifications, glucose monitoring, glycemic control through pharmacotherapy including various oral medications and insulin, and management of cardiovascular risk factors.
Myasthenia gravis
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kidney on hypertension
- 1. KIDNEY ON HYPERTENSION PLB -6 15 sept 2017
- 2. OBJECTIVES # Changes on kidney due to hypertension Aetiopathogenensis and Morphological Features of - Nephrosclerosis - Malignant Nephrosclerosis
- 3. VASCULATURE
- 5. Kidney diseases Both a cause and consequence of
- 6. RENAL VASCULAR DISEASES # Secondary involvement # Mostly smaller vessels are involved Lesions associated with hypertension - Nephrosclerosis (benign) - Malignant Nephrosclerosis
- 7. So, lets see Changes in kidney due to hypertension
- 8. NEPHROSCLEROSIS • Renal pathology associated with sclerosis of renal arterioles and small arteries and is strongly associated with hypertension, which can be both a cause and consequence of of nephrosclerosis. • Also associated with advanced age, more frequent in blacks • Incidence and severity increases in DM and HTN
- 9. PATHOGENESIS • Two process 1. Medial and intimal thickening - As a response to hemodynamic changes, aging, genetic defects, or some combination of these 2. Hyalinization of arteriolar wall - Caused by extravasation of plasma protein (endothelial injury) and increased deposition of BM matrix
- 10. MORPHOLOGY Gross • Cortical scaring and shrinking (fine , even granularity cortical resembling as grain leather)
- 11. • Microscopic Hyaline arteriosclerosis Narrowing of arteries and arterioles lumens Caused by thickening and hyalinization of walls Fibroelastic hyperplasia internal elastic lamina replication and increased myofibroblastic tissue in intima of interlobular and arcuate artery
- 12. # Glomerular alteration Collagen deposition on Bowman’s space Periglomerular fibrosis Total glomerular fibrosis (reduction in GFR)
- 13. # Patchy ischemic atrophy (As a consequence of vascular narrowing) Consists of : a. Tubular atrophy and interstitial fibrosis b. Glomerular alteration
- 14. MALIGNANT NEPHROSCLEROSIS • A renal vascular disorder associated with malignant or accelerated hypertension . • Developed in : preexisting essential hypertension , chronic renal disease(glomerulonephritis) • 1-5% in people with elevated hypertension
- 15. PATHOGENESIS # Vascular lesion as a fundamental lesion Endothelial injury (HTN, Arthritis, coagulopathy) Increased permeability (fibrinogen and other plasma protein, focal cells death of vascular wall and platelet deposition) Fibrinoid necrosis (arterioles and small arteries) # Intravascular thrombosis (activation of platelets and clotting factors)
- 16. Mitogenic factors from paltelets (PDGF),plasma and other cells Hyperplasia of intimal smooth muscle of vessels Hyperplastic arteriosclerosis # Marked increase in plasma renin (angistension II – intrarenal vasoconstriction )
- 17. MORPHOLOGY • Gross Petechial hemorrhage (cortical surfaces) - From rupture of arterioles or glomerular capillaries (flea beaten appearance)
- 18. Microscopic Two histologic alteration : a. Fibrinoid necrosis of arterioles b. Hyperplastic arteriolitis (onion skinning)
- 19. a. Fibrinoid necrosis of arterioles - Eosinophilic appearance of vessel wall due to fibrin deposition - Inflammation (not seen or minimal) - Glomeruli : may become necrotic with neutrophil infiltration
- 20. b. Hyperplastic arteriolitis Onion skinning : Intimal thickening Caused by smooth muscle cells Proliferation with concentric layering of Collagen and pale staining material (proteoglycans plasma proteins)
- 21. References : • Robbins and Cotran Pathologic basis of • Robbins and Cotran atlas of pathology, 3e
- 22. Thank you