This document discusses the pathogenesis and complications of diabetes mellitus. It describes the autoimmune destruction of pancreatic beta cells in type 1 diabetes and genetic and environmental factors leading to insulin resistance and beta cell dysfunction in type 2 diabetes. The three main mechanisms underlying diabetic complications are non-enzymatic glycosylation, activation of protein kinase C, and disturbances in the polyol pathway due to intracellular hyperglycemia. Late complications discussed include nephropathy, retinopathy, neuropathy, and vascular disease.
Pathophysiology of Diabetes Mellitus (Harrison’s Principles of Internal Medic...Batoul Ghosn
This presentation talks about the Pathophysiology part of Diabetes Mellitus I & II as well as Diabetic Ketoacidosis & Hyperglycemic Hyperosmolar State and Finally with Medical Nutrition Therapy in DIabetes Mellitus. It is made entirely from the Harrsion's Book 19th edition.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
Atherosclerosis - Definition - Risk Factors - Lesser and Non Quantitated risk factors - Arterial wall - The development of Atherosclerosis - Many Features of the injury Hypothesis - The process of Atherogenesis - Pathogenesis in short - Morphology of Atheroma - Components of Atheromatous Plaque (MP) - Complications and clinical significance - Cardiovascular risk and its assessment.
Diabetes mellitus -INTRODUCTION,TYPES OF DIABETES MELLITUSvarinder kumar
INTRODUCTION
TYPES OF DIABETES MELLITUS
DIAGNOSE TEST FOR DIABETES MELLITUS
MECHANISM OF ACTION OF INSULIN (IDDM)
HERBAL DRUG TREATMENT FOR DIABETES
LIFESTYLE FOR TYPE 1 AND TYPE 2 DM
NEW ANTI DIABETIC DRUGS
Pathophysiology of Diabetes Mellitus (Harrison’s Principles of Internal Medic...Batoul Ghosn
This presentation talks about the Pathophysiology part of Diabetes Mellitus I & II as well as Diabetic Ketoacidosis & Hyperglycemic Hyperosmolar State and Finally with Medical Nutrition Therapy in DIabetes Mellitus. It is made entirely from the Harrsion's Book 19th edition.
Diabetes mellitus (DM) has routinely been described as a metabolic disorder characterized by hyperglycemia that develops as a consequence of defects in insulin secretion, insulin action, or both.
Such a deficiency results in increased concentrations of glucose in the blood, which in turn damage many of the body's systems, in particular the blood vessels and nerves.
1. Microvascular (due to damage to small blood vessels).
2. Macrovascular (due to damage to larger blood vessels).
Atherosclerosis - Definition - Risk Factors - Lesser and Non Quantitated risk factors - Arterial wall - The development of Atherosclerosis - Many Features of the injury Hypothesis - The process of Atherogenesis - Pathogenesis in short - Morphology of Atheroma - Components of Atheromatous Plaque (MP) - Complications and clinical significance - Cardiovascular risk and its assessment.
Diabetes mellitus -INTRODUCTION,TYPES OF DIABETES MELLITUSvarinder kumar
INTRODUCTION
TYPES OF DIABETES MELLITUS
DIAGNOSE TEST FOR DIABETES MELLITUS
MECHANISM OF ACTION OF INSULIN (IDDM)
HERBAL DRUG TREATMENT FOR DIABETES
LIFESTYLE FOR TYPE 1 AND TYPE 2 DM
NEW ANTI DIABETIC DRUGS
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. Learning Outcomes
Identify the morphological changes in different tissues and organs due to
long standing diabetes mellitus
Describe pathogenesis of diabetes mellitus and its complications
Describe autoimmune insulitis and amyloidosis of pancreas due to DM
Describe macro and microvascular disease due to DM
Identify diabetic nephropathy, retinopathy and neuropathy
3. Pathogenesis of Type -1 DM
Autoimmune factors:
Failure of self tolerance in T cells specific for beta cell antigens.
Autoantibodies react against β-cell antigens and cause β-cell damage by
release of IFN-γ from CD8+T cells and production of TNF and IL-1 from
activated macrophages.
Autoantibodies, detected in the blood of 70-80% of cases
Genetic susceptibility Principal genetic susceptibility locus resides in the
(HLA-D) region in chromosome 6, several non-HLA genes also confer
susceptibility, resulting in excessive T cell activation and cell damage
Environmental factors Viral infections, (mumps, rubella, and coxsackie B)
as some of viral antigens, antigenically similar to β cell antigens leading to
islets damage
4. Pathogenesis of Type 2 DM
A complex multifactorial disease which involves interactions of genetics,
environmental risk factors and inflammation with no autoimmune basis
Genetic factors; More than a dozen “diabetogenic” genes identified
(both parents diabetic; 50% risk to the child)
Environmental factors; Sedentary life style, dietary habits and obesity
Insulin resistance; Decreased ability of peripheral tissues to respond
to insulin
Beta cell dysfunction; Manifested as inadequate insulin secretion in the
face of insulin resistance and hyperglycemia
5. Type 2 DM: Insulin Resistance
Insulin resistance is influenced by;
Genetic defects of Insulin receptor
Genetic defects of Insulin signaling pathway (inactivating mutations)
Obesity
7. Obesity and Insulin Resistance
Role of free fatty acids (FFAs);
In obese, increased intracellular TG’s in muscle and liver
and products of FFAs metabolism are potent inhibitors of
insulin signaling pathways
Role of Adipokines
Released by adipose tissue into systemic circulation (like;
leptin, adiponectin, and resistin), changes in their levels
associated with insulin resistance as for example;
Adiponectin levels reduced in states of obesity causing
insulin resistance where as its normal levels contributes to
insulin sensitivity in peripheral tissues where as; Resistin
levels increased in obesity which contributes to insulin
resistance
Inflammation
Pro-inflammatory cytokines secreted in response to FFAs
results in both insulin resistance and beta cell dysfunction
8. β-Cell Dysfunction
Qualitative; when secretary defect progresses to involve all phases of
insulin secretion
Quantitative; a decrease in β-cell mass, islet degeneration with deposition
of islet amyloid protein (amylin) ,a characteristic finding in individuals with
Type 2 DM.
Pathogenesis: In peripheral insulin resistance, insulin secretion is initially
higher for each level of glucose in order to compensate for peripheral
resistance and results in β-cell hyperplasia (as seen in the pre-diabetic
state) later; followed by decrease in β-cell mass that progress to diabetes
due to adverse effects of high circulating FFAs ("lipotoxicity") or chronic
hyperglycemia ("glucotoxicity“)
9. Etiologic Classification of Diabetes Mellitus
Type 1 Diabetes
β-cell destruction - absolute insulin deficiency
Type 2 Diabetes
Insulin resistance with relative insulin deficiency
Genetic Defects of β-Cell Function
Maturity onset diabetes of the young (MODY)
caused by mutations in MODY1 to MODY6
Mitochondrial DNA mutations
Genetic Defects in Insulin Processing or Insulin
Action
Defects in proinsulin conversion, Insulin gene
mutations, Insulin receptor mutations
Exocrine Pancreatic Defects
Chronic pancreatitis, Pancreatectomy, Neoplasia,
Cystic fibrosis, Hemochromatosis
Endocrinopathies
Growth hormone excess, Cushing syndrome,
Hyperthyroidism, Pheochromocytoma,
Glucagonoma
Infections
Mumps, CMV and Coxsackievirus B
Drugs
Glucocorticoids , Thyroid hormone and
β-adrenergic agonists
Genetic Syndromes Associated with Diabetes
Down syndrome, Kleinfelter syndrome and
Turner syndrome
Gestational Diabetes Mellitus
11. Pathogenesis of Complications of DM
The long-term complications of DM are similar in both types of DM
and involve three underlying mechanisms
1- Non-enzymatic glycosylation
2- Activation of protein kinase C
3- Intracellular hyperglycemia- disturbances in polyol pathways
12. 1- Non-enzymatic glycosylation
In this process glucose chemically attaches to free amino groups of proteins
without the aid of enzymes and is directly related to blood glucose level
Glycosylated hemoglobin; its levels in the blood provides an index of the
average blood glucose levels over the 120-day life span of erythrocytes
Advanced glycosylation end products (AGEs); formed as a result of non-
enzymatic reaction between intracellular glucose precursors and amino
groups of proteins
13. ADVANCED GLYCOSYLATION END PRODUCTS (AGEs)
AGEs bind to a specific receptor (RAGE), which is expressed on
inflammatory cells (macrophages & T cells), endothelial cells and on
vascular smooth muscle
Early glycosylation products of collagen and other long lived proteins in the
interstitial tissues and blood vessel walls undergo chemical rearrangements
to form irreversible AGEs which may trap non-glycosylated plasma and
interstitial proteins
In large vessels, trapping LDL, for example, retards its efflux from the vessel
wall and enhances the deposition of cholesterol in the intima, thus
accelerating atherogenesis
In capillaries, including those of renal glomeruli, plasma proteins such as
albumin bind to the glycated basement membrane, resulting in basement
membrane thickening characteristic of diabetic glomerulopathy
14. AGEs
Effects of the AGE-RAGE signaling axis within the vascular
compartment includes;
Release of pro-inflammatory cytokines and growth factors from intimal
macrophages
Generation of reactive oxygen species in endothelial cells
Increased procoagulant activity on endothelial cells and macrophages
Enhanced proliferation of vascular smooth muscle cells and synthesis of
extracellular matrix
15. 2- Activation of protein kinase C
Activation of intracellular protein kinase C (PKC) by calcium ions and the
second messenger diacylglycerol (DAG) is an important signal transduction
pathway in many cellular systems
Intracellular hyperglycemia can stimulate the de novo synthesis of DAG from
glycolytic intermediates and hence cause activation of PKC, which induces
production of;
Pro-angiogenic molecules; like, VEGF, involved in neovascularization seen
in diabetic retinopathy
Pro-fibrogenic molecules; like, TGF β, leads to increased deposition of
extracellular matrix and basement membrane material
16. 3- Intracellular hyperglycemia- disturbances in
polyol pathways
Tissues that, do not require insulin for glucose transport (e.g., nerves, lens,
kidneys, blood vessels), hyperglycemia leads to an increase in intracellular
glucose that is then metabolized by enzyme aldose reductase to sorbitol (a
polyol) and to fructose
Accumulated sorbitol and fructose causes cell injury via increased
intracellular osmolarity and water influx, by an increase in cellular
susceptibility to oxidative stress because intracellular antioxidant reserves
are diminished in the course of sorbitol metabolism
17. Morphology of Pancreas in DM
Type 1 DM: Reduced number and size of
islets, and Leukocyte infiltration of the islets,
principally mononuclear cells, an early feature,
but inflammation is often absent by the time the
disease is clinically evident
Type 2 DM: Amyloid replacement of islets,
amyloid deposition occurs around capillaries and
between cells and in advanced stages the islets
may progress to fibrosis
Note: non-diabetic newborns of diabetic mothers,
fetal islets undergo hyperplasia in response to
maternal hyperglycemia
18. Diabetic Arterial Vasculopathy
Macrovascular Disease; accelerated atherosclerosis of aorta, coronary
and renal arteries; results in MI and or gangrene of lower extremities
Hyaline arteriolosclerosis; thickening of arteriolar walls, narrowing of
lumen (as in hypertensive) more prevalent and severe
Microangiopathy; diffuse thickening of vascular and nonvascular
basement membranes, by hyaline material, most evident in capillaries of
skin, skeletal muscle, retina, renal glomeruli, and renal medulla and in
nonvascular structures like, renal tubules, Bowman capsule, peripheral
nerves, and placenta
*Despite increase in thickness of basement membranes, diabetic
capillaries are more leaky than normal to plasma proteins.
19. Diabetic Nephropathy
Three types of renal lesions identified:
Glomerular lesions
Renal vascular lesions
Pyelonephritis and necrotizing papillitis
20. Diabetic - Glomerular Lesions
Basement membrane thickening; of glomeruli & renal tubules
Diffuse mesangial sclerosis; increase in mesangial matrix
along with mesangial cell proliferation (as in old age &
hypertension) associated basement membrane thickening
when marked, present as nephrotic syndrome
Nodular glomerulosclerosis ; Ball-like deposits of a
laminated (PAS-positive) matrix in the periphery of
glomerulus usually contain trapped mesangial cells called
Kimmelstiel-Wilson lesion, pathognomonic of diabetes
and is a major contributor to morbidity and mortality
21. Diabetic Renal Vascular lesions and Pyelonephritis
Renal vascular lesions
Renal atherosclerosis and hyaline
arteriolosclerosis affects both afferent and
efferent arterioles as compare to only
afferent in hypertensive
Pyelonephritis and necrotizing papillitis
Begins as acute or chronic interstitial inflammation,
then spreads to involve tubules, more common in
diabetes
One special pattern of acute pyelonephritis is
necrotizing papillitis (or papillary necrosis), much
more prevalent in diabetics than in non-diabetics
Severe renal hyaline
arteriolosclerosis; note markedly
thickened, (PAS Positive)
tortuous afferent arteriole
22. Diabetic Retinopathy
Nonproliferative retinopathy
Intraretinal or preretinal hemorrhages
Retinal exudates; either “soft”
(microinfarcts) or “hard”(deposits of plasma
proteins and lipids)
Microaneurysms; and venous dilations
Microangiopathy; thickening of the retinal
capillaries
Edema; excessive capillary permeability due
to focal weakening of capillary wall by loss of
capillary pericytes
Edema and retinal exudates that
are "soft" microinfarcts or "hard"
yellowish waxy exudates
23. Retinopathy
Proliferative retinopathy
Neovascularization and
fibrosis leads to blindness, if it
involves the macula
Vitreous hemorrhages can
result from rupture of newly
formed capillaries
Retinal detachment;
organization of the hemorrhage
can pull the retina off its
substratum (retinal detachment)
Neovascularisation near optic disk when bleed,
produces vitreal hemorrhages obscuring vision
Advanced stage with retinal hemorrhages,
exudates, neovascularization, and retinal
detachment
24. Diabetic Neuropathy
Both CNS and PNS are affected
The most frequent pattern of involvement is that of; a peripheral, symmetric
neuropathy of the lower extremities affecting both motor and sensory
function, particularly the latter
Others; autonomic neuropathy, which produces disturbances in bowel and
bladder function and sometimes sexual disorders
Type 1 DM presents in children and require insulin for treatment. The classic manifestations of the disease (hyperglycemia and ketosis) occur late in its course, after more than 90% of the beta cells have been destroyed.
Accelerated atherosclerosis of aorta, coronary and renal arteries; results in myocardial infarction (the most common cause of death in diabetic women and men) as well as gangrene of lower extremities very common