This document discusses diabetic retinopathy, including:
- Criteria for diagnosing diabetes and risk factors for type 2 diabetes such as family history, obesity, and hypertension.
- Diabetic retinopathy is the leading cause of blindness in working-age adults and risk increases with duration of diabetes and poor blood sugar control.
- Pathogenesis involves microvascular occlusion leading to ischemia, hypoxia, and new abnormal blood vessel growth which can cause vision loss if left untreated.
- Stages include background, pre-proliferative, and proliferative retinopathy each with characteristic signs.
- Treatment depends on stage but may include anti-VEGF drugs or laser photocoagulation surgery to prevent
COMPLICATIONS OF DIABETES BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE...Prof Dr Bashir Ahmed Dar
The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels.Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.
GESTATIONAL DIABETES BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPO...Prof Dr Bashir Ahmed Dar
The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels.Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.
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
COMPLICATIONS OF DIABETES BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE...Prof Dr Bashir Ahmed Dar
The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels.Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.
GESTATIONAL DIABETES BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPO...Prof Dr Bashir Ahmed Dar
The complications of diabetes mellitus are far less common and less severe in people who have well-controlled blood sugar levels.Wider health problems accelerate the deleterious effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.
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
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
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STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
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Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
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disorder called alcohol use disorder (AUD), with mild, moderate,
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In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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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
3. Criteria for the Diagnosis of Diabetes Mellitus
• Symptoms of diabetes plus random blood
glucose concentration 11.1 mmol/L (200
mg/dL)or
• Fasting plasma glucose 7.0 mmol/L (126
mg/dL)or
• Two-hour plasma glucose 11.1 mmol/L (200
mg/dL) during an oral glucose tolerance test
4. Risk Factors for Type 2 Diabetes
Mellitus
•Family history of diabetes (i.e., parent
or sibling with type 2 diabetes)
•Obesity (BMI 25 kg/m2)
•Habitual physical inactivity
•Race/ethnicity (e.g.,African American,
Latino, Native American,Asian
American, Pacific Islander)
•Previously identified IFG or IGT
5. •History of GDM or delivery of baby >4
kg (>9 lb)
•Hypertension (blood pressure 140/90
mmHg)
•HDL cholesterol level <35 mg/dL (0.90
mmol/L) and/or a triglyceride level
>250 mg/dL (2.82 mmol/L)
•Polycystic ovary syndrome or
acanthosis nigricans
•History of vascular disease
7. DIABETIC RETINOPATHY
Diabetes – sustained hyperglycemia secondary to
lack, or diminished efficacy of endogenous insulin
2 main types of diabetes
• Insulin dependent diabetes (IDD)
• 10 -20 years of age
• Non-insulin dependent diabetes (NIDD)
• 50 – 70 years old
8. Diabetic retinopathy
• Leading cause of legal blindness in individuals between
the ages of 20 and 65 years
Risk factors for diabetic retinopathy
1.Duration of diabetes – most important factor
2.Poor metabolic control
3.Other factors – pregnancy, hypertension, renal
disease, anemia
9. Pathogenesis of DR
DR is a microangiopathy affecting the retinal
precapillary arterioles, capillaries and venules.
Large vessels may also be involved. Retinopathy
has features of both microvascular occlusion
and leakage.
10. Microvascular occlusion:
• Thickening of basement membrane
• Capillary endothelial cell damage and
proliferation
• Changes in red blood cells leading to defective
oxygen transport
• Increased stickiness and aggregation of
platelets
11. Pathogenesis of DR
Microvascular occlusion
↓
Retinal capillary non-perfusion
↓
Retinal ischemia
↓
Retinal hypoxia
↓
AV shunts (IRMA) & neovascularization
15. The hard exudates are composed of lipid
and proteinaceous material, such as
fibrinogen and albumin that leak from the
impaired blood–retinal barrier. They are
deposited primarily in the outer plexiform
layer of the retina.
16.
17. Microvascular leakage
Pathogenesis
The cellular elements of retinal capillaries consists
of endothelial cells and pericytes.These elements
are responsible for the structural integrity of the
vessel wall.
In DM there is reduction of pericytes which causes
distention of capillary walls and breakdown of
blood retinal barrier, leading to leakage of plasma
constituents into the retina (increased vascular
permeability) leading to retinal edema.
18. Reduction in number of pericytes
↓
Distended capillary walls
& breakdown of blood retinal barrier
↓
Leakage of plasma constituents into the retina
↓
Retinal edema
↓
Exudates
PATHOGENESIS OF DIABETIC RETINOPATHY
20. SIMPLE BACKGROUND DR
1. Microaneurysms (saccular pouches due to capillary
distention)
- First clinically detectable lesion of DR
- Small round dots usually temporal to the macula
2. Hemorrhages
3. Hard exudates – yellow waxy appearance with
distinct margins
4. Retinal edema
21.
22.
23. Signs of background diabetic retinopathy
Microaneurysms usually
temporal to fovea
Intraretinal dot and
blot haemorrhages
Hard exudates
frequently
arranged in clumps or
rings
Retinal oedema seen as
thickening on biomicroscopy
24. PREPROLIFERATIVE DR
- Lesions are caused by retinal ischemia
1. Vascular changes
2. Dark blot hemorrhages (hemorrhagic retinal infarcts)
3. Cotton wool spots caused by capillary occlusion
4. Intraretinal microvascular abnormalities
25. Preproliferative diabetic retinopathy
Treatment - not required but watch for proliferative disease
• Cotton-wool spots
• Venous irregularities
• Dark blot haemorrhages
• Intraretinal microvascular
abnormalities (IRMA)
Signs
27. Indications for treatment of proliferative
diabetic retinopathy
NVD > 1/3 disc in area Less extensive NVD
+ haemorrhage
NVE > 1/2 disc in area
+ haemorrhage
28. TREATMENT
1. Medicine
anti-VEGF medicine: aflibercept, bevacizumab, or ranibizumab.
These medicines block the growth of abnormal blood vessels in the eye.
These can stop further vision loss and may improve vision in some people.
2. Laser photocoagulation
aim: to induce involution of new vessels and prevent recurrent vitreous
hemorrhage
COMPLICATIONS
1. Persistent intragel vitreous hemorrhage
2. Retinal detachment
3. Opaque membranes
4. Burnt-out stage – increase in fibrous component and decrease in vascular
component
5. Rubeosis iridis
29. • Spot size (200-500 m)
depends
on contact lens magnification
• Gentle intensity burn (0.10-0.05 sec)
• Follow-up 4 to 8 weeks
• Area covered by complete PRP
• Initial treatment is 2000-3000 burns
Laser panretinal photocoagulation
30. Indications for vitreoretinal surgery
Retinal detachment involving
macula
Severe persistent vitreous
haemorrhage
Dense, persistent premacular
haemorrhage
Progressive proliferation
despite laser therapy