際際滷shows by User: AhmedMandour37 / http://www.slideshare.net/images/logo.gif 際際滷shows by User: AhmedMandour37 / Thu, 14 Sep 2023 15:53:37 GMT 際際滷Share feed for 際際滷shows by User: AhmedMandour37 dkadrsyed2584-190602083813 (1).pptx /slideshow/dkadrsyed2584190602083813-1pptx/260957116 dkadrsyed2584-1906020838131-230914155337-bf56c01d
Diabetes mellitus, often referred to simply as DIABETES. Diabetes is a condition in which the body: Does not produce enough insulin, and/or Does not properly respond to insulin Insulin is a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. Type 1 diabetes: Diagnosed in children and young adults Previously known as Juvenile Diabetes Type 2 diabetes: Typically diagnosed in adulthood Also found in overweight children Complications of blood glucose alterations Hypoglycemia Hyperglycemia Ketosis Acidosis DKA (Hyperglycemia + Ketosis + Acidosis) Normal fasting blood glucose level 4-6 mmol/L definition: A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. 160,000 Admissions to private hospitals/year Cost = over 1 billion $ annually 65% = <19 years old Main cause of death in children with diabetes (approximately 85%) Cerebral edema in 69% Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis The biochemical criteria for the diagnosis of DKA3,4 Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism AETIOLOGY: No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes: Stressful precipitating event that results in increased cate]]>
Diabetes mellitus, often referred to simply as DIABETES. Diabetes is a condition in which the body: Does not produce enough insulin, and/or Does not properly respond to insulin Insulin is a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. Type 1 diabetes: Diagnosed in children and young adults Previously known as Juvenile Diabetes Type 2 diabetes: Typically diagnosed in adulthood Also found in overweight children Complications of blood glucose alterations Hypoglycemia Hyperglycemia Ketosis Acidosis DKA (Hyperglycemia + Ketosis + Acidosis) Normal fasting blood glucose level 4-6 mmol/L definition: A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. 160,000 Admissions to private hospitals/year Cost = over 1 billion $ annually 65% = <19 years old Main cause of death in children with diabetes (approximately 85%) Cerebral edema in 69% Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis The biochemical criteria for the diagnosis of DKA3,4 Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism AETIOLOGY: No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes: Stressful precipitating event that results in increased cate]]> Thu, 14 Sep 2023 15:53:37 GMT /slideshow/dkadrsyed2584190602083813-1pptx/260957116 AhmedMandour37@slideshare.net(AhmedMandour37) dkadrsyed2584-190602083813 (1).pptx AhmedMandour37 Diabetes mellitus, often referred to simply as DIABETES. Diabetes is a condition in which the body: Does not produce enough insulin, and/or Does not properly respond to insulin Insulin is a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. Type 1 diabetes: Diagnosed in children and young adults Previously known as Juvenile Diabetes Type 2 diabetes: Typically diagnosed in adulthood Also found in overweight children Complications of blood glucose alterations Hypoglycemia Hyperglycemia Ketosis Acidosis DKA (Hyperglycemia + Ketosis + Acidosis) Normal fasting blood glucose level 4-6 mmol/L definition: A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. 160,000 Admissions to private hospitals/year Cost = over 1 billion $ annually 65% = <19 years old Main cause of death in children with diabetes (approximately 85%) Cerebral edema in 69% Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis The biochemical criteria for the diagnosis of DKA3,4 Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism AETIOLOGY: No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes: Stressful precipitating event that results in increased cate <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/dkadrsyed2584-1906020838131-230914155337-bf56c01d-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Diabetes mellitus, often referred to simply as DIABETES. Diabetes is a condition in which the body: Does not produce enough insulin, and/or Does not properly respond to insulin Insulin is a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy. Type 1 diabetes: Diagnosed in children and young adults Previously known as Juvenile Diabetes Type 2 diabetes: Typically diagnosed in adulthood Also found in overweight children Complications of blood glucose alterations Hypoglycemia Hyperglycemia Ketosis Acidosis DKA (Hyperglycemia + Ketosis + Acidosis) Normal fasting blood glucose level 4-6 mmol/L definition: A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. 160,000 Admissions to private hospitals/year Cost = over 1 billion $ annually 65% = &lt;19 years old Main cause of death in children with diabetes (approximately 85%) Cerebral edema in 69% Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis The biochemical criteria for the diagnosis of DKA3,4 Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors: Age &lt;12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism AETIOLOGY: No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes: Stressful precipitating event that results in increased cate
dkadrsyed2584-190602083813 (1).pptx from AhmedMandour37
]]> 72 0 https://cdn.slidesharecdn.com/ss_thumbnails/dkadrsyed2584-1906020838131-230914155337-bf56c01d-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 ibd-191006070029 (1).pptx /slideshow/ibd191006070029-1pptx/260912427 ibd-1910060700291-230913211424-c9432644
Clinically, inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines that is marked by remission and relapses due to inappropriate mucosal immune response . TYPICAL IBD : (2 Major Types): Ulcerative Colitis (Colitis Ulcerosa) Crohns Disease (Regional Enteritis) ATYPICAL IBD: Lymphocytic Colitis Collagenous Colitis Ischaemic Colitis Diversion Colitis Indeterminate Colitis Bachets Disease Watery stools, blood or mucus in the stool Diarrhoea - persisting for more than 4 weeks Crampy abdominal pain, Nocturnal defecation Fever. Weight loss is significant. Anal fissures, anal fistulae, frank bleeding per rectum Abdominal masses can occur Symptoms are generally recurrent. The pathogenesis of EIM in IBD is not well understood. Diseased gastrointestinal mucosa may trigger immune responses at the extraintestinal site due to shared epitopes. E.g.: intestinal bacteria and the synovia : bacteria that are translocated across the leaky intestinal barrier trigger an adaptive immune response that finally is unable to discriminate between bacterial epitopes and epitopes of joints or the skin. Triggers of the autoimmune responses in certain organs seem to be influenced by genetic factors. EIM in patients with CD are more frequently observed in patients with HLA-A2, HLA-DR1, and HLA-DQw5 EIM in patients with UC are more likely to appear when the HLA-DR103 genotype is present. HLA-B8/DR3 is associated with an increased risk of PSC in UC. HLA-DRB1-0103, HLA-B-27, and HLA-B-58 are associated with EIM of joints, the skin, and eyes, respectively, in patients with IBD. HLA-B*27 itself does not seem to be associated with IBD, but HLA-B*27 shows a strong association with the development of ankylosing spondylitis, as 50% to 90% of patients with IBD are positive for this marker. 15% in CD & 10% in UC Skin lesions develop after the onset of bowel symptoms Concomitant active peripheral arthritis EN are hot, red, tender nodules measuring 15 cm in diameter and are found on the anterior surface of the lower legs, ankles, calves, thighs, and arms 112% of UC patients and less commonly in Crohns colitis May occur years before the onset of bowel symptoms Run a course independent of the bowel disease Respond poorly to colectomy Usually associated with severe disease Begins as a pustule and then spreads concentrically Lesions then ulcerate, with violaceous edges surrounded by a margin of erythema Centrally, they contain necrotic tissue with blood and exudates Lesions may be single or multiple and grow as large as 30 cm Pyoderma Vegetans Pyostomatitis Vegetans Sweet Syndrome Psoriasis Perianal Skin Tag Aphthous Stomatitis Arthritis Develops In 1520% Of IBD Patients Common In CD > UC Worsens With Exacerbations Of Bowel Activity Asymmetric, Polyarticular, And Migratory And Most Often Affects Large Joints Of The Upper And Lower Extremities Colectomy frequently Cures The Arthritis ankylosing spondylitis: 10% Of ]]>
Clinically, inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines that is marked by remission and relapses due to inappropriate mucosal immune response . TYPICAL IBD : (2 Major Types): Ulcerative Colitis (Colitis Ulcerosa) Crohns Disease (Regional Enteritis) ATYPICAL IBD: Lymphocytic Colitis Collagenous Colitis Ischaemic Colitis Diversion Colitis Indeterminate Colitis Bachets Disease Watery stools, blood or mucus in the stool Diarrhoea - persisting for more than 4 weeks Crampy abdominal pain, Nocturnal defecation Fever. Weight loss is significant. Anal fissures, anal fistulae, frank bleeding per rectum Abdominal masses can occur Symptoms are generally recurrent. The pathogenesis of EIM in IBD is not well understood. Diseased gastrointestinal mucosa may trigger immune responses at the extraintestinal site due to shared epitopes. E.g.: intestinal bacteria and the synovia : bacteria that are translocated across the leaky intestinal barrier trigger an adaptive immune response that finally is unable to discriminate between bacterial epitopes and epitopes of joints or the skin. Triggers of the autoimmune responses in certain organs seem to be influenced by genetic factors. EIM in patients with CD are more frequently observed in patients with HLA-A2, HLA-DR1, and HLA-DQw5 EIM in patients with UC are more likely to appear when the HLA-DR103 genotype is present. HLA-B8/DR3 is associated with an increased risk of PSC in UC. HLA-DRB1-0103, HLA-B-27, and HLA-B-58 are associated with EIM of joints, the skin, and eyes, respectively, in patients with IBD. HLA-B*27 itself does not seem to be associated with IBD, but HLA-B*27 shows a strong association with the development of ankylosing spondylitis, as 50% to 90% of patients with IBD are positive for this marker. 15% in CD & 10% in UC Skin lesions develop after the onset of bowel symptoms Concomitant active peripheral arthritis EN are hot, red, tender nodules measuring 15 cm in diameter and are found on the anterior surface of the lower legs, ankles, calves, thighs, and arms 112% of UC patients and less commonly in Crohns colitis May occur years before the onset of bowel symptoms Run a course independent of the bowel disease Respond poorly to colectomy Usually associated with severe disease Begins as a pustule and then spreads concentrically Lesions then ulcerate, with violaceous edges surrounded by a margin of erythema Centrally, they contain necrotic tissue with blood and exudates Lesions may be single or multiple and grow as large as 30 cm Pyoderma Vegetans Pyostomatitis Vegetans Sweet Syndrome Psoriasis Perianal Skin Tag Aphthous Stomatitis Arthritis Develops In 1520% Of IBD Patients Common In CD > UC Worsens With Exacerbations Of Bowel Activity Asymmetric, Polyarticular, And Migratory And Most Often Affects Large Joints Of The Upper And Lower Extremities Colectomy frequently Cures The Arthritis ankylosing spondylitis: 10% Of ]]> Wed, 13 Sep 2023 21:14:24 GMT /slideshow/ibd191006070029-1pptx/260912427 AhmedMandour37@slideshare.net(AhmedMandour37) ibd-191006070029 (1).pptx AhmedMandour37 Clinically, inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines that is marked by remission and relapses due to inappropriate mucosal immune response . TYPICAL IBD : (2 Major Types): Ulcerative Colitis (Colitis Ulcerosa) Crohns Disease (Regional Enteritis) ATYPICAL IBD: Lymphocytic Colitis Collagenous Colitis Ischaemic Colitis Diversion Colitis Indeterminate Colitis Bachets Disease Watery stools, blood or mucus in the stool Diarrhoea - persisting for more than 4 weeks Crampy abdominal pain, Nocturnal defecation Fever. Weight loss is significant. Anal fissures, anal fistulae, frank bleeding per rectum Abdominal masses can occur Symptoms are generally recurrent. The pathogenesis of EIM in IBD is not well understood. Diseased gastrointestinal mucosa may trigger immune responses at the extraintestinal site due to shared epitopes. E.g.: intestinal bacteria and the synovia : bacteria that are translocated across the leaky intestinal barrier trigger an adaptive immune response that finally is unable to discriminate between bacterial epitopes and epitopes of joints or the skin. Triggers of the autoimmune responses in certain organs seem to be influenced by genetic factors. EIM in patients with CD are more frequently observed in patients with HLA-A2, HLA-DR1, and HLA-DQw5 EIM in patients with UC are more likely to appear when the HLA-DR103 genotype is present. HLA-B8/DR3 is associated with an increased risk of PSC in UC. HLA-DRB1-0103, HLA-B-27, and HLA-B-58 are associated with EIM of joints, the skin, and eyes, respectively, in patients with IBD. HLA-B*27 itself does not seem to be associated with IBD, but HLA-B*27 shows a strong association with the development of ankylosing spondylitis, as 50% to 90% of patients with IBD are positive for this marker. 15% in CD & 10% in UC Skin lesions develop after the onset of bowel symptoms Concomitant active peripheral arthritis EN are hot, red, tender nodules measuring 15 cm in diameter and are found on the anterior surface of the lower legs, ankles, calves, thighs, and arms 112% of UC patients and less commonly in Crohns colitis May occur years before the onset of bowel symptoms Run a course independent of the bowel disease Respond poorly to colectomy Usually associated with severe disease Begins as a pustule and then spreads concentrically Lesions then ulcerate, with violaceous edges surrounded by a margin of erythema Centrally, they contain necrotic tissue with blood and exudates Lesions may be single or multiple and grow as large as 30 cm Pyoderma Vegetans Pyostomatitis Vegetans Sweet Syndrome Psoriasis Perianal Skin Tag Aphthous Stomatitis Arthritis Develops In 1520% Of IBD Patients Common In CD > UC Worsens With Exacerbations Of Bowel Activity Asymmetric, Polyarticular, And Migratory And Most Often Affects Large Joints Of The Upper And Lower Extremities Colectomy frequently Cures The Arthritis ankylosing spondylitis: 10% Of <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/ibd-1910060700291-230913211424-c9432644-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Clinically, inflammatory bowel disease (IBD) is a chronic inflammatory condition of the intestines that is marked by remission and relapses due to inappropriate mucosal immune response . TYPICAL IBD : (2 Major Types): Ulcerative Colitis (Colitis Ulcerosa) Crohns Disease (Regional Enteritis) ATYPICAL IBD: Lymphocytic Colitis Collagenous Colitis Ischaemic Colitis Diversion Colitis Indeterminate Colitis Bachets Disease Watery stools, blood or mucus in the stool Diarrhoea - persisting for more than 4 weeks Crampy abdominal pain, Nocturnal defecation Fever. Weight loss is significant. Anal fissures, anal fistulae, frank bleeding per rectum Abdominal masses can occur Symptoms are generally recurrent. The pathogenesis of EIM in IBD is not well understood. Diseased gastrointestinal mucosa may trigger immune responses at the extraintestinal site due to shared epitopes. E.g.: intestinal bacteria and the synovia : bacteria that are translocated across the leaky intestinal barrier trigger an adaptive immune response that finally is unable to discriminate between bacterial epitopes and epitopes of joints or the skin. Triggers of the autoimmune responses in certain organs seem to be influenced by genetic factors. EIM in patients with CD are more frequently observed in patients with HLA-A2, HLA-DR1, and HLA-DQw5 EIM in patients with UC are more likely to appear when the HLA-DR103 genotype is present. HLA-B8/DR3 is associated with an increased risk of PSC in UC. HLA-DRB1-0103, HLA-B-27, and HLA-B-58 are associated with EIM of joints, the skin, and eyes, respectively, in patients with IBD. HLA-B*27 itself does not seem to be associated with IBD, but HLA-B*27 shows a strong association with the development of ankylosing spondylitis, as 50% to 90% of patients with IBD are positive for this marker. 15% in CD &amp; 10% in UC Skin lesions develop after the onset of bowel symptoms Concomitant active peripheral arthritis EN are hot, red, tender nodules measuring 15 cm in diameter and are found on the anterior surface of the lower legs, ankles, calves, thighs, and arms 112% of UC patients and less commonly in Crohns colitis May occur years before the onset of bowel symptoms Run a course independent of the bowel disease Respond poorly to colectomy Usually associated with severe disease Begins as a pustule and then spreads concentrically Lesions then ulcerate, with violaceous edges surrounded by a margin of erythema Centrally, they contain necrotic tissue with blood and exudates Lesions may be single or multiple and grow as large as 30 cm Pyoderma Vegetans Pyostomatitis Vegetans Sweet Syndrome Psoriasis Perianal Skin Tag Aphthous Stomatitis Arthritis Develops In 1520% Of IBD Patients Common In CD &gt; UC Worsens With Exacerbations Of Bowel Activity Asymmetric, Polyarticular, And Migratory And Most Often Affects Large Joints Of The Upper And Lower Extremities Colectomy frequently Cures The Arthritis ankylosing spondylitis: 10% Of
ibd-191006070029 (1).pptx from AhmedMandour37
]]> 62 0 https://cdn.slidesharecdn.com/ss_thumbnails/ibd-1910060700291-230913211424-c9432644-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 NASH risk factors and management.pptx /AhmedMandour37/nash-risk-factors-and-managementpptx nashriskfactorsandmanagement-230913204420-37436d63
INTRODUCTION: Most common among all Liver disorders & the cause of CLD Commonest cause of asymptomatic abnormal LFTs Most common cause of End stage liver disease requiring liver transplantation Present in 75% of the individuals with Obesity and Type 2DM NAFLD exists as a spectrum from simple steatosis to cirrhosis Hepatic steatosis describes accumulation of fat >5% of liver weight Commonest cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease NAFLD -DEFINITION: Evidence of hepatic steatosis (Imaging/Histology) No cause for secondary fat accumulation (significant alcohol consumption, drugs, hereditary conditions) Working Classification of NAFLD NNFL(Non NASH Fatty Liver) Type 1 : Only steatosis Type 2 : Steatosis + non specific lobular inflammation NASH( Non alcoholic Steatohepatitis) Type 3 : Steatosis + Inflammation +/- Fibrosis of variable levels Type 4 : Steatosis + Inflammation + Hepatocyte ballooning + Fibrosis/Mallory Denk bodies Nonalcoholic Fatty Liver Disease (NAFLD) Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis. Nonalcoholic Fatty Liver (NAFL) Presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes or no evidence of fibrosis. The risk of progression to cirrhosis and liver failure is minimal. Nonalcoholic steatohepatitis (NASH) Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. This can progress to cirrhosis, liver failure and rarely liver cancer. NASH Cirrhosis Presence of cirrhosis with current or previous histological evidence of steatosis or steatohepatitis Cryptogenic Cirrhosis Presence of cirrhosis with no obvious etiology. Patients with cryptogenic cirrhosis are heavily enriched with metabolic risk factors such as obesity and metabolic syndrome. DIAGNOSIS: NAFLD/NASH is a diagnosis of exclusion, and liver biopsy will often be required to confirm the diagnosis, stage the disease, rule out other liver diseases, and determine the need for and urgency of aggressive therapy DIAGNOSIS WHEN TO SUSPECT NAFLD??? History : no symptoms ,fatigue, malaise and abdominal discomfort. The presence of any of the following, especially with a history of abnormal AST/ALT, should lead to a work-up for NAFLD/NASH: Presence of obesity, especially morbid obesity (BMI > 35) Diagnosis of type 2 diabetes mellitus Diagnosis of metabolic syndrome History of obstructive sleep apnea Presence of insulin resistance Chronic elevation of AST/ALT, otherwise unexplained Detailed patient history of alcohol consumptionthreshold < 20 g/day in women, < 30 g/day in men. Physical examination : Central obesity correlates with severity of inflammation on biopsy dorsocervical lipohypertrophy (buffalo hump) correlates with hepatocyte injury. advanced liver disease: spider ang]]>
INTRODUCTION: Most common among all Liver disorders & the cause of CLD Commonest cause of asymptomatic abnormal LFTs Most common cause of End stage liver disease requiring liver transplantation Present in 75% of the individuals with Obesity and Type 2DM NAFLD exists as a spectrum from simple steatosis to cirrhosis Hepatic steatosis describes accumulation of fat >5% of liver weight Commonest cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease NAFLD -DEFINITION: Evidence of hepatic steatosis (Imaging/Histology) No cause for secondary fat accumulation (significant alcohol consumption, drugs, hereditary conditions) Working Classification of NAFLD NNFL(Non NASH Fatty Liver) Type 1 : Only steatosis Type 2 : Steatosis + non specific lobular inflammation NASH( Non alcoholic Steatohepatitis) Type 3 : Steatosis + Inflammation +/- Fibrosis of variable levels Type 4 : Steatosis + Inflammation + Hepatocyte ballooning + Fibrosis/Mallory Denk bodies Nonalcoholic Fatty Liver Disease (NAFLD) Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis. Nonalcoholic Fatty Liver (NAFL) Presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes or no evidence of fibrosis. The risk of progression to cirrhosis and liver failure is minimal. Nonalcoholic steatohepatitis (NASH) Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. This can progress to cirrhosis, liver failure and rarely liver cancer. NASH Cirrhosis Presence of cirrhosis with current or previous histological evidence of steatosis or steatohepatitis Cryptogenic Cirrhosis Presence of cirrhosis with no obvious etiology. Patients with cryptogenic cirrhosis are heavily enriched with metabolic risk factors such as obesity and metabolic syndrome. DIAGNOSIS: NAFLD/NASH is a diagnosis of exclusion, and liver biopsy will often be required to confirm the diagnosis, stage the disease, rule out other liver diseases, and determine the need for and urgency of aggressive therapy DIAGNOSIS WHEN TO SUSPECT NAFLD??? History : no symptoms ,fatigue, malaise and abdominal discomfort. The presence of any of the following, especially with a history of abnormal AST/ALT, should lead to a work-up for NAFLD/NASH: Presence of obesity, especially morbid obesity (BMI > 35) Diagnosis of type 2 diabetes mellitus Diagnosis of metabolic syndrome History of obstructive sleep apnea Presence of insulin resistance Chronic elevation of AST/ALT, otherwise unexplained Detailed patient history of alcohol consumptionthreshold < 20 g/day in women, < 30 g/day in men. Physical examination : Central obesity correlates with severity of inflammation on biopsy dorsocervical lipohypertrophy (buffalo hump) correlates with hepatocyte injury. advanced liver disease: spider ang]]> Wed, 13 Sep 2023 20:44:20 GMT /AhmedMandour37/nash-risk-factors-and-managementpptx AhmedMandour37@slideshare.net(AhmedMandour37) NASH risk factors and management.pptx AhmedMandour37 INTRODUCTION: Most common among all Liver disorders & the cause of CLD Commonest cause of asymptomatic abnormal LFTs Most common cause of End stage liver disease requiring liver transplantation Present in 75% of the individuals with Obesity and Type 2DM NAFLD exists as a spectrum from simple steatosis to cirrhosis Hepatic steatosis describes accumulation of fat >5% of liver weight Commonest cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease NAFLD -DEFINITION: Evidence of hepatic steatosis (Imaging/Histology) No cause for secondary fat accumulation (significant alcohol consumption, drugs, hereditary conditions) Working Classification of NAFLD NNFL(Non NASH Fatty Liver) Type 1 : Only steatosis Type 2 : Steatosis + non specific lobular inflammation NASH( Non alcoholic Steatohepatitis) Type 3 : Steatosis + Inflammation +/- Fibrosis of variable levels Type 4 : Steatosis + Inflammation + Hepatocyte ballooning + Fibrosis/Mallory Denk bodies Nonalcoholic Fatty Liver Disease (NAFLD) Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis. Nonalcoholic Fatty Liver (NAFL) Presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes or no evidence of fibrosis. The risk of progression to cirrhosis and liver failure is minimal. Nonalcoholic steatohepatitis (NASH) Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. This can progress to cirrhosis, liver failure and rarely liver cancer. NASH Cirrhosis Presence of cirrhosis with current or previous histological evidence of steatosis or steatohepatitis Cryptogenic Cirrhosis Presence of cirrhosis with no obvious etiology. Patients with cryptogenic cirrhosis are heavily enriched with metabolic risk factors such as obesity and metabolic syndrome. DIAGNOSIS: NAFLD/NASH is a diagnosis of exclusion, and liver biopsy will often be required to confirm the diagnosis, stage the disease, rule out other liver diseases, and determine the need for and urgency of aggressive therapy DIAGNOSIS WHEN TO SUSPECT NAFLD??? History : no symptoms ,fatigue, malaise and abdominal discomfort. The presence of any of the following, especially with a history of abnormal AST/ALT, should lead to a work-up for NAFLD/NASH: Presence of obesity, especially morbid obesity (BMI > 35) Diagnosis of type 2 diabetes mellitus Diagnosis of metabolic syndrome History of obstructive sleep apnea Presence of insulin resistance Chronic elevation of AST/ALT, otherwise unexplained Detailed patient history of alcohol consumptionthreshold < 20 g/day in women, < 30 g/day in men. Physical examination : Central obesity correlates with severity of inflammation on biopsy dorsocervical lipohypertrophy (buffalo hump) correlates with hepatocyte injury. advanced liver disease: spider ang <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/nashriskfactorsandmanagement-230913204420-37436d63-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> INTRODUCTION: Most common among all Liver disorders &amp; the cause of CLD Commonest cause of asymptomatic abnormal LFTs Most common cause of End stage liver disease requiring liver transplantation Present in 75% of the individuals with Obesity and Type 2DM NAFLD exists as a spectrum from simple steatosis to cirrhosis Hepatic steatosis describes accumulation of fat &gt;5% of liver weight Commonest cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease NAFLD -DEFINITION: Evidence of hepatic steatosis (Imaging/Histology) No cause for secondary fat accumulation (significant alcohol consumption, drugs, hereditary conditions) Working Classification of NAFLD NNFL(Non NASH Fatty Liver) Type 1 : Only steatosis Type 2 : Steatosis + non specific lobular inflammation NASH( Non alcoholic Steatohepatitis) Type 3 : Steatosis + Inflammation +/- Fibrosis of variable levels Type 4 : Steatosis + Inflammation + Hepatocyte ballooning + Fibrosis/Mallory Denk bodies Nonalcoholic Fatty Liver Disease (NAFLD) Encompasses the entire spectrum of fatty liver disease in individuals without significant alcohol consumption, ranging from fatty liver to steatohepatitis and cirrhosis. Nonalcoholic Fatty Liver (NAFL) Presence of hepatic steatosis with no evidence of hepatocellular injury in the form of ballooning of the hepatocytes or no evidence of fibrosis. The risk of progression to cirrhosis and liver failure is minimal. Nonalcoholic steatohepatitis (NASH) Presence of hepatic steatosis and inflammation with hepatocyte injury (ballooning) with or without fibrosis. This can progress to cirrhosis, liver failure and rarely liver cancer. NASH Cirrhosis Presence of cirrhosis with current or previous histological evidence of steatosis or steatohepatitis Cryptogenic Cirrhosis Presence of cirrhosis with no obvious etiology. Patients with cryptogenic cirrhosis are heavily enriched with metabolic risk factors such as obesity and metabolic syndrome. DIAGNOSIS: NAFLD/NASH is a diagnosis of exclusion, and liver biopsy will often be required to confirm the diagnosis, stage the disease, rule out other liver diseases, and determine the need for and urgency of aggressive therapy DIAGNOSIS WHEN TO SUSPECT NAFLD??? History : no symptoms ,fatigue, malaise and abdominal discomfort. The presence of any of the following, especially with a history of abnormal AST/ALT, should lead to a work-up for NAFLD/NASH: Presence of obesity, especially morbid obesity (BMI &gt; 35) Diagnosis of type 2 diabetes mellitus Diagnosis of metabolic syndrome History of obstructive sleep apnea Presence of insulin resistance Chronic elevation of AST/ALT, otherwise unexplained Detailed patient history of alcohol consumptionthreshold &lt; 20 g/day in women, &lt; 30 g/day in men. Physical examination : Central obesity correlates with severity of inflammation on biopsy dorsocervical lipohypertrophy (buffalo hump) correlates with hepatocyte injury. advanced liver disease: spider ang
NASH risk factors and management.pptx from AhmedMandour37
]]> 44 0 https://cdn.slidesharecdn.com/ss_thumbnails/nashriskfactorsandmanagement-230913204420-37436d63-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 DKA by Dr. A. Mandour.pptx /slideshow/dka-by-dr-a-mandourpptx/259757654 dkabydr-230809195657-d8c72a9b
DIABETIC KETOACIDOSIS (DKA): A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis Classic Triad of DKA: Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors for DKA at onset: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism Why do ketones develop? No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes of DKA/HHS: Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis Symptoms include: Deep, rapid breathing Fruity breath odor Very dry mouth Nausea and vomiting Lethargy/drowsiness DKA is life-threatening and needs immediate treatment Symptoms of DKA/HHS Polyuria Polydypsia Blurred vision Nausea/Vomiting Abdominal Pain Fatigue Confusion Obtundation Physical Examination in DKA/HHS: Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness Treatment of DKA: Fluids and Electrolytes Fluid replacement Restores perfu]]>
DIABETIC KETOACIDOSIS (DKA): A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis Classic Triad of DKA: Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors for DKA at onset: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism Why do ketones develop? No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes of DKA/HHS: Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis Symptoms include: Deep, rapid breathing Fruity breath odor Very dry mouth Nausea and vomiting Lethargy/drowsiness DKA is life-threatening and needs immediate treatment Symptoms of DKA/HHS Polyuria Polydypsia Blurred vision Nausea/Vomiting Abdominal Pain Fatigue Confusion Obtundation Physical Examination in DKA/HHS: Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness Treatment of DKA: Fluids and Electrolytes Fluid replacement Restores perfu]]> Wed, 09 Aug 2023 19:56:57 GMT /slideshow/dka-by-dr-a-mandourpptx/259757654 AhmedMandour37@slideshare.net(AhmedMandour37) DKA by Dr. A. Mandour.pptx AhmedMandour37 DIABETIC KETOACIDOSIS (DKA): A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis Classic Triad of DKA: Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors for DKA at onset: Age <12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism Why do ketones develop? No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes of DKA/HHS: Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis Symptoms include: Deep, rapid breathing Fruity breath odor Very dry mouth Nausea and vomiting Lethargy/drowsiness DKA is life-threatening and needs immediate treatment Symptoms of DKA/HHS Polyuria Polydypsia Blurred vision Nausea/Vomiting Abdominal Pain Fatigue Confusion Obtundation Physical Examination in DKA/HHS: Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness Treatment of DKA: Fluids and Electrolytes Fluid replacement Restores perfu <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/dkabydr-230809195657-d8c72a9b-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> DIABETIC KETOACIDOSIS (DKA): A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Not commonly associated with ketonaemia and acidosis Classic Triad of DKA: Hyperglycemia - blood glucose greater than 11.1 mmol/L Ketosis - ketones present in blood and/or urine Acidosis - pH less than 7.3 and/or bicarbonate less than 15 mmol/L DKA is generally categorized by the severity of the acidosis. MILD Venous pH less than 7.3 and/or bicarbonate concentration less than 15 mmol/L MODERATE Venous pH less than 7.2 and/or bicarbonate concentration less than 10 mmol/L SEVERE Venous pH less than 7.1 and/or bicarbonate concentration less than 5 mmol/L Risk factors for DKA at onset: Age &lt;12 yrs No first degree diabetic relative Lower socioeconomic status High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs Poor access to medical care Uninsured Usage of SGLT-2 inhibitor euglycaemic DKA SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism Why do ketones develop? No carbohydrate intake fasting gastroenteritis Atkins diet, neonates fed high-fat milk Prolonged exercise, pregnancy Lack of insulin activity onset of diabetes (insufficient secretion) interruption of insulin delivery in established pt Increase in insulin resistance infection, illness, surgery, stress Alcohol, salicylate ingestion, inborn metabolic errors Causes of DKA/HHS: Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis Symptoms include: Deep, rapid breathing Fruity breath odor Very dry mouth Nausea and vomiting Lethargy/drowsiness DKA is life-threatening and needs immediate treatment Symptoms of DKA/HHS Polyuria Polydypsia Blurred vision Nausea/Vomiting Abdominal Pain Fatigue Confusion Obtundation Physical Examination in DKA/HHS: Hypotension, tachycardia Kussmaul breathing (deep, labored breaths) Fruity odor to breath (due to acetone) Dry mucus membranes Confusion Abdominal tenderness Treatment of DKA: Fluids and Electrolytes Fluid replacement Restores perfu
DKA by Dr. A. Mandour.pptx from AhmedMandour37
]]> 232 0 https://cdn.slidesharecdn.com/ss_thumbnails/dkabydr-230809195657-d8c72a9b-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 AB policy.pptx /slideshow/ab-policypptx/259311506 abpolicy-230720085546-aac43936
CDC Key Prevention Strategies for Antimicrobial Resistance Prevent Infection Step 1: Vaccinate Fact: Influenza and pneumococcal vaccination of at-risk hospital patients and influenza vaccination of healthcare personnel will prevent infections. Step 2: Get the catheters out Fact: Catheters and other invasive devices are the # 1 exogenous cause of hospital-onset infections. Diagnose & Treat Infection Effectively Step 3: Target the pathogen Fact: Appropriate antimicrobial therapy saves lives. Step 4: Access the experts Fact: Infectious diseases expert input improves the outcome of serious infections. Use Antimicrobials Wisely Step 5: Practice antimicrobial control Fact: Programs to improve antimicrobial use are effective. (Antimicrobial Stewardship) Step 6: Use local data Fact: The prevalence of resistance can vary by locality, patient population, hospital unit, and length of stay. Step 7: Treat infection, not contamination Fact: A major cause of antimicrobial overuse is treatment of contaminated cultures. Step 8: Treat infection, not colonization Fact: Step 9: Know when to say no to vancomycin Fact: Vancomycin overuse promotes emergence, selection,and spread of resistant pathogens. Step 10: Stop antimicrobial treatment Fact: Failure to stop unnecessary antimicrobial treatment contributes to overuse and resistance. Prevent Transmission Step 11: Isolate the pathogen Fact: Patient-to-patient spread of pathogens can be prevented. Step 12: Break the chain of infection Fact: Healthcare personnel can spread antimicrobial-resistant pathogens from patient to patient Antimicrobial stewardship; is an activity that includes appropriate selection, dosing, route, and duration of antimicrobial therapy.. Why is Antimicrobial Stewardship Important? 200-300 million antibiotics are prescribed annually.45% for outpatient use 25-40% of hospitalized patients receive antibiotics 10-70% are unnecessary or suboptimal 5% of hospitalized patients who receive antibiotics experience an Adverse reaction. Health insurance companies will no longer reimburse for hospital acquired conditions deemed preventable. Why is an antibiotic policy necessary? To improve patient care by considered use of antibiotics for prophylaxis and therapy. To rationalize the use of antibiotics. To prevent or retard the emergence of resistant strains. To improve education of junior doctors by providing guidelines for appropriate therapy What are the clinical uses of antibiotics : 1. Therapeutic use:- It is administration of an antimicrobial agent where substantial microbial infection has occurred. 2. Prophylactic Use:- It is the use of antimicrobial agent before any infection has occurred to prevent a subsequent infection. The Antimicrobial Stewardship Program (ASP) should be administered by multidisciplinary team (AST) composed of: an infectious diseases (ID)physician a clinical pharmacist with ID training, a clinical microbiologist, an IC professional, Antibioti]]>
CDC Key Prevention Strategies for Antimicrobial Resistance Prevent Infection Step 1: Vaccinate Fact: Influenza and pneumococcal vaccination of at-risk hospital patients and influenza vaccination of healthcare personnel will prevent infections. Step 2: Get the catheters out Fact: Catheters and other invasive devices are the # 1 exogenous cause of hospital-onset infections. Diagnose & Treat Infection Effectively Step 3: Target the pathogen Fact: Appropriate antimicrobial therapy saves lives. Step 4: Access the experts Fact: Infectious diseases expert input improves the outcome of serious infections. Use Antimicrobials Wisely Step 5: Practice antimicrobial control Fact: Programs to improve antimicrobial use are effective. (Antimicrobial Stewardship) Step 6: Use local data Fact: The prevalence of resistance can vary by locality, patient population, hospital unit, and length of stay. Step 7: Treat infection, not contamination Fact: A major cause of antimicrobial overuse is treatment of contaminated cultures. Step 8: Treat infection, not colonization Fact: Step 9: Know when to say no to vancomycin Fact: Vancomycin overuse promotes emergence, selection,and spread of resistant pathogens. Step 10: Stop antimicrobial treatment Fact: Failure to stop unnecessary antimicrobial treatment contributes to overuse and resistance. Prevent Transmission Step 11: Isolate the pathogen Fact: Patient-to-patient spread of pathogens can be prevented. Step 12: Break the chain of infection Fact: Healthcare personnel can spread antimicrobial-resistant pathogens from patient to patient Antimicrobial stewardship; is an activity that includes appropriate selection, dosing, route, and duration of antimicrobial therapy.. Why is Antimicrobial Stewardship Important? 200-300 million antibiotics are prescribed annually.45% for outpatient use 25-40% of hospitalized patients receive antibiotics 10-70% are unnecessary or suboptimal 5% of hospitalized patients who receive antibiotics experience an Adverse reaction. Health insurance companies will no longer reimburse for hospital acquired conditions deemed preventable. Why is an antibiotic policy necessary? To improve patient care by considered use of antibiotics for prophylaxis and therapy. To rationalize the use of antibiotics. To prevent or retard the emergence of resistant strains. To improve education of junior doctors by providing guidelines for appropriate therapy What are the clinical uses of antibiotics : 1. Therapeutic use:- It is administration of an antimicrobial agent where substantial microbial infection has occurred. 2. Prophylactic Use:- It is the use of antimicrobial agent before any infection has occurred to prevent a subsequent infection. The Antimicrobial Stewardship Program (ASP) should be administered by multidisciplinary team (AST) composed of: an infectious diseases (ID)physician a clinical pharmacist with ID training, a clinical microbiologist, an IC professional, Antibioti]]> Thu, 20 Jul 2023 08:55:46 GMT /slideshow/ab-policypptx/259311506 AhmedMandour37@slideshare.net(AhmedMandour37) AB policy.pptx AhmedMandour37 CDC Key Prevention Strategies for Antimicrobial Resistance Prevent Infection Step 1: Vaccinate Fact: Influenza and pneumococcal vaccination of at-risk hospital patients and influenza vaccination of healthcare personnel will prevent infections. Step 2: Get the catheters out Fact: Catheters and other invasive devices are the # 1 exogenous cause of hospital-onset infections. Diagnose & Treat Infection Effectively Step 3: Target the pathogen Fact: Appropriate antimicrobial therapy saves lives. Step 4: Access the experts Fact: Infectious diseases expert input improves the outcome of serious infections. Use Antimicrobials Wisely Step 5: Practice antimicrobial control Fact: Programs to improve antimicrobial use are effective. (Antimicrobial Stewardship) Step 6: Use local data Fact: The prevalence of resistance can vary by locality, patient population, hospital unit, and length of stay. Step 7: Treat infection, not contamination Fact: A major cause of antimicrobial overuse is treatment of contaminated cultures. Step 8: Treat infection, not colonization Fact: Step 9: Know when to say no to vancomycin Fact: Vancomycin overuse promotes emergence, selection,and spread of resistant pathogens. Step 10: Stop antimicrobial treatment Fact: Failure to stop unnecessary antimicrobial treatment contributes to overuse and resistance. Prevent Transmission Step 11: Isolate the pathogen Fact: Patient-to-patient spread of pathogens can be prevented. Step 12: Break the chain of infection Fact: Healthcare personnel can spread antimicrobial-resistant pathogens from patient to patient Antimicrobial stewardship; is an activity that includes appropriate selection, dosing, route, and duration of antimicrobial therapy.. Why is Antimicrobial Stewardship Important? 200-300 million antibiotics are prescribed annually.45% for outpatient use 25-40% of hospitalized patients receive antibiotics 10-70% are unnecessary or suboptimal 5% of hospitalized patients who receive antibiotics experience an Adverse reaction. Health insurance companies will no longer reimburse for hospital acquired conditions deemed preventable. Why is an antibiotic policy necessary? To improve patient care by considered use of antibiotics for prophylaxis and therapy. To rationalize the use of antibiotics. To prevent or retard the emergence of resistant strains. To improve education of junior doctors by providing guidelines for appropriate therapy What are the clinical uses of antibiotics : 1. Therapeutic use:- It is administration of an antimicrobial agent where substantial microbial infection has occurred. 2. Prophylactic Use:- It is the use of antimicrobial agent before any infection has occurred to prevent a subsequent infection. The Antimicrobial Stewardship Program (ASP) should be administered by multidisciplinary team (AST) composed of: an infectious diseases (ID)physician a clinical pharmacist with ID training, a clinical microbiologist, an IC professional, Antibioti <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/abpolicy-230720085546-aac43936-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> CDC Key Prevention Strategies for Antimicrobial Resistance Prevent Infection Step 1: Vaccinate Fact: Influenza and pneumococcal vaccination of at-risk hospital patients and influenza vaccination of healthcare personnel will prevent infections. Step 2: Get the catheters out Fact: Catheters and other invasive devices are the # 1 exogenous cause of hospital-onset infections. Diagnose &amp; Treat Infection Effectively Step 3: Target the pathogen Fact: Appropriate antimicrobial therapy saves lives. Step 4: Access the experts Fact: Infectious diseases expert input improves the outcome of serious infections. Use Antimicrobials Wisely Step 5: Practice antimicrobial control Fact: Programs to improve antimicrobial use are effective. (Antimicrobial Stewardship) Step 6: Use local data Fact: The prevalence of resistance can vary by locality, patient population, hospital unit, and length of stay. Step 7: Treat infection, not contamination Fact: A major cause of antimicrobial overuse is treatment of contaminated cultures. Step 8: Treat infection, not colonization Fact: Step 9: Know when to say no to vancomycin Fact: Vancomycin overuse promotes emergence, selection,and spread of resistant pathogens. Step 10: Stop antimicrobial treatment Fact: Failure to stop unnecessary antimicrobial treatment contributes to overuse and resistance. Prevent Transmission Step 11: Isolate the pathogen Fact: Patient-to-patient spread of pathogens can be prevented. Step 12: Break the chain of infection Fact: Healthcare personnel can spread antimicrobial-resistant pathogens from patient to patient Antimicrobial stewardship; is an activity that includes appropriate selection, dosing, route, and duration of antimicrobial therapy.. Why is Antimicrobial Stewardship Important? 200-300 million antibiotics are prescribed annually.45% for outpatient use 25-40% of hospitalized patients receive antibiotics 10-70% are unnecessary or suboptimal 5% of hospitalized patients who receive antibiotics experience an Adverse reaction. Health insurance companies will no longer reimburse for hospital acquired conditions deemed preventable. Why is an antibiotic policy necessary? To improve patient care by considered use of antibiotics for prophylaxis and therapy. To rationalize the use of antibiotics. To prevent or retard the emergence of resistant strains. To improve education of junior doctors by providing guidelines for appropriate therapy What are the clinical uses of antibiotics : 1. Therapeutic use:- It is administration of an antimicrobial agent where substantial microbial infection has occurred. 2. Prophylactic Use:- It is the use of antimicrobial agent before any infection has occurred to prevent a subsequent infection. The Antimicrobial Stewardship Program (ASP) should be administered by multidisciplinary team (AST) composed of: an infectious diseases (ID)physician a clinical pharmacist with ID training, a clinical microbiologist, an IC professional, Antibioti
AB policy.pptx from AhmedMandour37
]]> 130 0 https://cdn.slidesharecdn.com/ss_thumbnails/abpolicy-230720085546-aac43936-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 null-5.pptx /slideshow/null5pptx/255089621 null-5-221230153517-845b9a01
Mechanism action of Antibiotic Resistance Denied access: membrane becomes impermeable for antibiotic: e.g. Imipenem Antibiotic modification: some bacteria have enzymes that cleave or modify antibiotics: e.g. beta lactamase inactivates penicillin Altered target site: antibiotic cannot bind to its intended target because the target itself has been modified Pumping out the antibiotic faster than it gets in: e.g. tetracyclines Alternative target (typically enzyme): e.g. Alternative penicillin binding protein (PBP2a) in MRSA Newly invented antibiotic resistance bacteria The World Health Organisation has published a list of the 12 bacteria built-in abilities to find new ways to resist treatment and can pass along genetic material that allows other bacteria to become drug-resistant as well. They are- Pseudomonas aeruginos,: carbapenem-resistant. Enterobacteriaceae ,carbapenem-resistant Acinetobacter baumannii: carbapenem-resistant. Enterococcus faecium, vancomycin-resistant Staphylococcus aureus, methicillin-resistant Helicobacter pylori:clarithromycin-resistant. Campylobacter: fluoroquinolone-resistant. Neisseria gonorrhoeae: cephalosporin-resistant Streptococcus pneumonia.penicillin-non-susceptible Haemophilus influenzae, ampicillin-resistant Several species of Shigella, fluoroquinolone-resistant Enterobacteriaceae ,carbapenem-resistant Carbapenem-resistant enterobacteriaceae (CRE )usually infects patients who are already ill - for example, those in long-term or intensive care units. It is typically spread from person to person, in this case during an endoscopic procedure. Salmonellae, fluoroquinolone-resistant Salads are the second most common sourceof foodborne illness, responsible for anumber of salmonella and E coli outbreakin the US and Europe. Prevention and control of Antibiotic Resistance Antibiotic resistance is accelerated by the misuse and overuse of antibiotics, as well as poorinfection prevention and control. Steps can be taken at all levels of society to reduce the impactand limit the spread of resistance. Antibiotics Asubstances produced by various species of living microorganisms. Inhibit pathogens by interfering with intracellular process. Kill bacteria and treat infections Example : Ampicillin, Actinonin. Bacteria have a remarkable genetic plasticity that allows them to respond to a wide array of environmental threats, including the presence of antibiotic molecules that may jeopardize their existence. Bacteria sharing the same ecological niche with antimicrobial-producing organisms have evolved ancient mechanisms to withstand the effect of the harmful antibiotic molecule and, consequently, their intrinsic resistance permits them to thrive in its presence. Therefore, to understand development of antibiotic resistance in pathogens, we need to consider important reservoirs of resistance genes, which may include determinants that confer self-resistance in antibiotic producing soil bacteria and genes]]>
Mechanism action of Antibiotic Resistance Denied access: membrane becomes impermeable for antibiotic: e.g. Imipenem Antibiotic modification: some bacteria have enzymes that cleave or modify antibiotics: e.g. beta lactamase inactivates penicillin Altered target site: antibiotic cannot bind to its intended target because the target itself has been modified Pumping out the antibiotic faster than it gets in: e.g. tetracyclines Alternative target (typically enzyme): e.g. Alternative penicillin binding protein (PBP2a) in MRSA Newly invented antibiotic resistance bacteria The World Health Organisation has published a list of the 12 bacteria built-in abilities to find new ways to resist treatment and can pass along genetic material that allows other bacteria to become drug-resistant as well. They are- Pseudomonas aeruginos,: carbapenem-resistant. Enterobacteriaceae ,carbapenem-resistant Acinetobacter baumannii: carbapenem-resistant. Enterococcus faecium, vancomycin-resistant Staphylococcus aureus, methicillin-resistant Helicobacter pylori:clarithromycin-resistant. Campylobacter: fluoroquinolone-resistant. Neisseria gonorrhoeae: cephalosporin-resistant Streptococcus pneumonia.penicillin-non-susceptible Haemophilus influenzae, ampicillin-resistant Several species of Shigella, fluoroquinolone-resistant Enterobacteriaceae ,carbapenem-resistant Carbapenem-resistant enterobacteriaceae (CRE )usually infects patients who are already ill - for example, those in long-term or intensive care units. It is typically spread from person to person, in this case during an endoscopic procedure. Salmonellae, fluoroquinolone-resistant Salads are the second most common sourceof foodborne illness, responsible for anumber of salmonella and E coli outbreakin the US and Europe. Prevention and control of Antibiotic Resistance Antibiotic resistance is accelerated by the misuse and overuse of antibiotics, as well as poorinfection prevention and control. Steps can be taken at all levels of society to reduce the impactand limit the spread of resistance. Antibiotics Asubstances produced by various species of living microorganisms. Inhibit pathogens by interfering with intracellular process. Kill bacteria and treat infections Example : Ampicillin, Actinonin. Bacteria have a remarkable genetic plasticity that allows them to respond to a wide array of environmental threats, including the presence of antibiotic molecules that may jeopardize their existence. Bacteria sharing the same ecological niche with antimicrobial-producing organisms have evolved ancient mechanisms to withstand the effect of the harmful antibiotic molecule and, consequently, their intrinsic resistance permits them to thrive in its presence. Therefore, to understand development of antibiotic resistance in pathogens, we need to consider important reservoirs of resistance genes, which may include determinants that confer self-resistance in antibiotic producing soil bacteria and genes]]> Fri, 30 Dec 2022 15:35:17 GMT /slideshow/null5pptx/255089621 AhmedMandour37@slideshare.net(AhmedMandour37) null-5.pptx AhmedMandour37 Mechanism action of Antibiotic Resistance Denied access: membrane becomes impermeable for antibiotic: e.g. Imipenem Antibiotic modification: some bacteria have enzymes that cleave or modify antibiotics: e.g. beta lactamase鐃 inactivates penicillin Altered target site: antibiotic cannot bind to its intended target because the target itself has been modified鐃緒 Pumping out the antibiotic faster than it gets in: e.g. tetracyclines Alternative target (typically enzyme): e.g. Alternative penicillin binding protein (PBP2a) in MRSA Newly invented antibiotic resistance bacteria The World Health Organisation has published a list of the 12 bacteria built-in abilities to find new ways to resist treatment and can pass along genetic material that allows other bacteria to become drug-鐃resistant as well. They are- Pseudomonas aeruginos,: carbapenem-resistant. Enterobacteriaceae ,鐃carbapenem-resistant Acinetobacter baumannii: carbapenem-resistant. Enterococcus faecium,鐃 vancomycin-resistant Staphylococcus aureus,鐃 methicillin-resistant Helicobacter pylori:clarithromycin-resistant. Campylobacter: fluoroquinolone-resistant. Neisseria gonorrhoeae: cephalosporin-resistant Streptococcus pneumonia.鐃penicillin-non-susceptible Haemophilus influenzae,鐃 ampicillin-resistant Several species of Shigella,鐃 fluoroquinolone-resistant Enterobacteriaceae ,carbapenem-resistant Carbapenem-resistant enterobacteriaceae (CRE )usually鐃 infects patients who are already ill - for example, those in鐃 long-term or intensive care units. It is typically spread from鐃 person to person, in this case during an endoscopic鐃 procedure. Salmonellae, fluoroquinolone-resistant Salads are the second most common source鐃of foodborne illness, responsible for a鐃number of salmonella and E coli outbreak鐃in the US and Europe. Prevention and control of Antibiotic Resistance Antibiotic resistance is accelerated by the misuse and overuse of antibiotics, as well as poorinfection prevention and control. Steps can be taken at all levels of society to reduce the impact鐃and limit the spread of resistance. Antibiotics Asubstances produced by various鐃 species of living microorganisms.鐃緒 Inhibit pathogens by interfering鐃 with intracellular process. Kill bacteria and treat infections鐃緒 Example : Ampicillin, Actinonin. Bacteria have a remarkable genetic plasticity that allows them to respond to a wide array of environmental threats, including the presence of antibiotic molecules that may jeopardize their existence. Bacteria sharing the same ecological niche with antimicrobial-producing organisms have evolved ancient mechanisms to withstand the effect of the harmful antibiotic molecule and, consequently, their intrinsic resistance permits them to thrive in its presence. Therefore, to understand development of antibiotic resistance in pathogens, we need to consider important reservoirs of resistance genes, which may include determinants that confer self-resistance in antibiotic producing soil bacteria and genes <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/null-5-221230153517-845b9a01-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Mechanism action of Antibiotic Resistance Denied access: membrane becomes impermeable for antibiotic: e.g. Imipenem Antibiotic modification: some bacteria have enzymes that cleave or modify antibiotics: e.g. beta lactamase鐃 inactivates penicillin Altered target site: antibiotic cannot bind to its intended target because the target itself has been modified鐃緒 Pumping out the antibiotic faster than it gets in: e.g. tetracyclines Alternative target (typically enzyme): e.g. Alternative penicillin binding protein (PBP2a) in MRSA Newly invented antibiotic resistance bacteria The World Health Organisation has published a list of the 12 bacteria built-in abilities to find new ways to resist treatment and can pass along genetic material that allows other bacteria to become drug-鐃resistant as well. They are- Pseudomonas aeruginos,: carbapenem-resistant. Enterobacteriaceae ,鐃carbapenem-resistant Acinetobacter baumannii: carbapenem-resistant. Enterococcus faecium,鐃 vancomycin-resistant Staphylococcus aureus,鐃 methicillin-resistant Helicobacter pylori:clarithromycin-resistant. Campylobacter: fluoroquinolone-resistant. Neisseria gonorrhoeae: cephalosporin-resistant Streptococcus pneumonia.鐃penicillin-non-susceptible Haemophilus influenzae,鐃 ampicillin-resistant Several species of Shigella,鐃 fluoroquinolone-resistant Enterobacteriaceae ,carbapenem-resistant Carbapenem-resistant enterobacteriaceae (CRE )usually鐃 infects patients who are already ill - for example, those in鐃 long-term or intensive care units. It is typically spread from鐃 person to person, in this case during an endoscopic鐃 procedure. Salmonellae, fluoroquinolone-resistant Salads are the second most common source鐃of foodborne illness, responsible for a鐃number of salmonella and E coli outbreak鐃in the US and Europe. Prevention and control of Antibiotic Resistance Antibiotic resistance is accelerated by the misuse and overuse of antibiotics, as well as poorinfection prevention and control. Steps can be taken at all levels of society to reduce the impact鐃and limit the spread of resistance. Antibiotics Asubstances produced by various鐃 species of living microorganisms.鐃緒 Inhibit pathogens by interfering鐃 with intracellular process. Kill bacteria and treat infections鐃緒 Example : Ampicillin, Actinonin. Bacteria have a remarkable genetic plasticity that allows them to respond to a wide array of environmental threats, including the presence of antibiotic molecules that may jeopardize their existence. Bacteria sharing the same ecological niche with antimicrobial-producing organisms have evolved ancient mechanisms to withstand the effect of the harmful antibiotic molecule and, consequently, their intrinsic resistance permits them to thrive in its presence. Therefore, to understand development of antibiotic resistance in pathogens, we need to consider important reservoirs of resistance genes, which may include determinants that confer self-resistance in antibiotic producing soil bacteria and genes
null-5.pptx from AhmedMandour37
]]> 67 0 https://cdn.slidesharecdn.com/ss_thumbnails/null-5-221230153517-845b9a01-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 bad news2022MILITARY (1).ppt /slideshow/bad-news2022military-1ppt/252826368 badnews2022military1-220904210932-17989316
It is part of the job to regularly break bad news, yet training for doctors and nurses on how to disclose distressing news to patients or relatives is markedly unappreciated, until now. Most professionals develop their own appropriate techniques for breaking such news . Studies in the child disability field in USA and other western countries reveal that about 50% of parents are dissatisfied with the way news of their son's or daughter's disability was given to them How to break bad news 1- Getting started: a. Get the physical setting right b. Ensure family support at the time of breaking the news c. Fire a warning shot 2- Find out how much the patient already knows 3- Find out how much the patient wants to know 4- Decide on your objectives 5- Share the information a. Give the information in small chunks b. Use English, not medispeak c. Reinforce and clarify the information frequently d. Listen for the patients feelings e. Blend your agenda with the patients agenda f. Offer hope Bad news may be: Sudden death & unexpected complications and changes in the course of illness. Hopeless cases & No resuscitation decision (minimal medical interference ) Genetic disorders & congenital anomalies Brain damage & long term Prognosis HOW TO DELIVER A BITTER PILL GENERAL RULES: Introduce yourself if you have not met the parents Private room , a curtain drawn around patient if not possible to move to private room Sit down on the same level as the parents & the patient. Free from interruptions, checking that pagers & mobile phones are switched off. Doctors are encouraged to allow patients or relatives the feeling that they have their unlimited consultation time & attention. Good eye contact Sensitivity and honesty are paramount Correct names are used. Note questions or topics avoided. Respect the patient's right to "denial". They will often "selectively perceive" information they can cope with. Appreciate that patients can, and do, cope positively with truth about illness. Tell staff what has been said. They might be involved in future discussions. Realize that most patients become aware of their situation gradually, rather than during one meeting. Arrange for a second interview between the parents within 24-48 hours THE MANNER OF TELLING Honestly -- with uncertainties acknowledged. Straightforward, without embarrassment. Explanations should be clear and not overly technical Invite parents to ask questions Offer to introduce parents to another parent with a child with similar condition ??????? What If...The parents start crying ??????????You should pause and say soothing statements like : I am sorry to have to give you this news. It is not easy for me. I know that this is not what you were expecting to hear this. I understand and appreciate deeply your feelingsetc Dont say Cheer up. Things could be worse What If The patient becomes angry? I am sorry ]]>
It is part of the job to regularly break bad news, yet training for doctors and nurses on how to disclose distressing news to patients or relatives is markedly unappreciated, until now. Most professionals develop their own appropriate techniques for breaking such news . Studies in the child disability field in USA and other western countries reveal that about 50% of parents are dissatisfied with the way news of their son's or daughter's disability was given to them How to break bad news 1- Getting started: a. Get the physical setting right b. Ensure family support at the time of breaking the news c. Fire a warning shot 2- Find out how much the patient already knows 3- Find out how much the patient wants to know 4- Decide on your objectives 5- Share the information a. Give the information in small chunks b. Use English, not medispeak c. Reinforce and clarify the information frequently d. Listen for the patients feelings e. Blend your agenda with the patients agenda f. Offer hope Bad news may be: Sudden death & unexpected complications and changes in the course of illness. Hopeless cases & No resuscitation decision (minimal medical interference ) Genetic disorders & congenital anomalies Brain damage & long term Prognosis HOW TO DELIVER A BITTER PILL GENERAL RULES: Introduce yourself if you have not met the parents Private room , a curtain drawn around patient if not possible to move to private room Sit down on the same level as the parents & the patient. Free from interruptions, checking that pagers & mobile phones are switched off. Doctors are encouraged to allow patients or relatives the feeling that they have their unlimited consultation time & attention. Good eye contact Sensitivity and honesty are paramount Correct names are used. Note questions or topics avoided. Respect the patient's right to "denial". They will often "selectively perceive" information they can cope with. Appreciate that patients can, and do, cope positively with truth about illness. Tell staff what has been said. They might be involved in future discussions. Realize that most patients become aware of their situation gradually, rather than during one meeting. Arrange for a second interview between the parents within 24-48 hours THE MANNER OF TELLING Honestly -- with uncertainties acknowledged. Straightforward, without embarrassment. Explanations should be clear and not overly technical Invite parents to ask questions Offer to introduce parents to another parent with a child with similar condition ??????? What If...The parents start crying ??????????You should pause and say soothing statements like : I am sorry to have to give you this news. It is not easy for me. I know that this is not what you were expecting to hear this. I understand and appreciate deeply your feelingsetc Dont say Cheer up. Things could be worse What If The patient becomes angry? I am sorry ]]> Sun, 04 Sep 2022 21:09:32 GMT /slideshow/bad-news2022military-1ppt/252826368 AhmedMandour37@slideshare.net(AhmedMandour37) bad news2022MILITARY (1).ppt AhmedMandour37 It is part of the job to regularly break bad news, yet training for doctors and nurses on how to disclose distressing news to patients or relatives is markedly unappreciated, until now. Most professionals develop their own appropriate techniques for breaking such news . Studies in the child disability field in USA and other western countries reveal that about 50% of parents are dissatisfied with the way news of their son's or daughter's disability was given to them How to break bad news 1- Getting started: a. Get the physical setting right b. Ensure family support at the time of breaking the news c. Fire a warning shot 2- Find out how much the patient already knows 3- Find out how much the patient wants to know 4- Decide on your objectives 5- Share the information a. Give the information in small chunks b. Use English, not medispeak c. Reinforce and clarify the information frequently d. Listen for the patients feelings e. Blend your agenda with the patients agenda f. Offer hope Bad news may be: Sudden death & unexpected complications and changes in the course of illness. Hopeless cases & No resuscitation decision (minimal medical interference ) Genetic disorders & congenital anomalies Brain damage & long term Prognosis HOW TO DELIVER A BITTER PILL GENERAL RULES: Introduce yourself if you have not met the parents Private room , a curtain drawn around patient if not possible to move to private room Sit down on the same level as the parents & the patient. Free from interruptions, checking that pagers & mobile phones are switched off. Doctors are encouraged to allow patients or relatives the feeling that they have their unlimited consultation time & attention. Good eye contact Sensitivity and honesty are paramount Correct names are used. Note questions or topics avoided. Respect the patient's right to "denial". They will often "selectively perceive" information they can cope with. Appreciate that patients can, and do, cope positively with truth about illness. Tell staff what has been said. They might be involved in future discussions. Realize that most patients become aware of their situation gradually, rather than during one meeting. Arrange for a second interview between the parents within 24-48 hours THE MANNER OF TELLING Honestly -- with uncertainties acknowledged. Straightforward, without embarrassment. Explanations should be clear and not overly technical Invite parents to ask questions Offer to introduce parents to another parent with a child with similar condition ??????? What If...鐃The parents start crying ??????????You should pause and say soothing statements like : I am sorry to have to give you this news. It is not easy for me. I know that this is not what you were expecting to hear this. I understand and appreciate deeply your feelingsetc Dont say Cheer up. Things could be worse What If The patient becomes angry? I am sorry <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/badnews2022military1-220904210932-17989316-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> It is part of the job to regularly break bad news, yet training for doctors and nurses on how to disclose distressing news to patients or relatives is markedly unappreciated, until now. Most professionals develop their own appropriate techniques for breaking such news . Studies in the child disability field in USA and other western countries reveal that about 50% of parents are dissatisfied with the way news of their son&#39;s or daughter&#39;s disability was given to them How to break bad news 1- Getting started: a. Get the physical setting right b. Ensure family support at the time of breaking the news c. Fire a warning shot 2- Find out how much the patient already knows 3- Find out how much the patient wants to know 4- Decide on your objectives 5- Share the information a. Give the information in small chunks b. Use English, not medispeak c. Reinforce and clarify the information frequently d. Listen for the patients feelings e. Blend your agenda with the patients agenda f. Offer hope Bad news may be: Sudden death &amp; unexpected complications and changes in the course of illness. Hopeless cases &amp; No resuscitation decision (minimal medical interference ) Genetic disorders &amp; congenital anomalies Brain damage &amp; long term Prognosis HOW TO DELIVER A BITTER PILL GENERAL RULES: Introduce yourself if you have not met the parents Private room , a curtain drawn around patient if not possible to move to private room Sit down on the same level as the parents &amp; the patient. Free from interruptions, checking that pagers &amp; mobile phones are switched off. Doctors are encouraged to allow patients or relatives the feeling that they have their unlimited consultation time &amp; attention. Good eye contact Sensitivity and honesty are paramount Correct names are used. Note questions or topics avoided. Respect the patient&#39;s right to &quot;denial&quot;. They will often &quot;selectively perceive&quot; information they can cope with. Appreciate that patients can, and do, cope positively with truth about illness. Tell staff what has been said. They might be involved in future discussions. Realize that most patients become aware of their situation gradually, rather than during one meeting. Arrange for a second interview between the parents within 24-48 hours THE MANNER OF TELLING Honestly -- with uncertainties acknowledged. Straightforward, without embarrassment. Explanations should be clear and not overly technical Invite parents to ask questions Offer to introduce parents to another parent with a child with similar condition ??????? What If...鐃The parents start crying ??????????You should pause and say soothing statements like : I am sorry to have to give you this news. It is not easy for me. I know that this is not what you were expecting to hear this. I understand and appreciate deeply your feelingsetc Dont say Cheer up. Things could be worse What If The patient becomes angry? I am sorry
bad news2022MILITARY (1).ppt from AhmedMandour37
]]> 14 0 https://cdn.slidesharecdn.com/ss_thumbnails/badnews2022military1-220904210932-17989316-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 Risk factors of diabetes.pptx /slideshow/risk-factors-of-diabetespptx/252826003 riskfactorsofdiabetes-220904200315-38592780
Diabetes is a world-wide public health problem. About 422 million people worldwide have diabetes, the majority living in low-and middle-income countries, and 1.5 million deaths are directly attributed to diabetes each year. Both the number of cases and the prevalence of diabetes have been steadily increasing over the past few decades in countries of all income levels. Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys and nerves. The most common is type 2 diabetes, usually in adults, which occurs when the body becomes resistant to insulin or doesn't make enough insulin. In the past 3 decades the prevalence of type 2 diabetes has risen dramatically in countries of all income levels. Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin by itself. For people living with diabetes, access to affordable treatment, including insulin, is critical to their survival. There is a globally agreed target to halt the rise in diabetes and obesity by 2025. Symptoms of type 1 diabetes include the need to urinate often, thirst, constant hunger, weight loss, vision changes and fatigue. These symptoms may occur suddenly. Symptoms for type 2 diabetes are generally similar to those of type 1 diabetes but are often less marked. As a result, the disease may be diagnosed several years after onset, after complications have already arisen. For this reason, it is important to be aware of risk factors. Type 1 diabetes cannot currently be prevented. Effective approaches are available to prevent type 2 diabetes and to prevent the complications and premature death that can result from all types of diabetes. These include policies and practices across whole populations and within specific settings (school, home, workplace) that contribute to good health for everyone, regardless of whether they have diabetes, such as exercising regularly, eating healthily, avoiding smoking, and controlling blood pressure and lipids. The starting point for living well with diabetes is an early diagnosis the longer a person lives with undiagnosed and untreated diabetes, the worse their health outcomes are likely to be. Easy access to basic diagnostics, such as blood glucose testing, should therefore be available in primary health care settings. Patients will need periodic specialist assessment or treatment for complications. A series of cost-effective interventions can improve patient outcomes, regardless of what type of diabetes they may have. These interventions include blood glucose control through a combination of diet, physical activity and, if necessary, medication; control of blood pressure and lipids to reduce cardiovascular risk and other complications; and regular screening for damage to the eyes, kidneys and feet to facilitate early treatment]]>
Diabetes is a world-wide public health problem. About 422 million people worldwide have diabetes, the majority living in low-and middle-income countries, and 1.5 million deaths are directly attributed to diabetes each year. Both the number of cases and the prevalence of diabetes have been steadily increasing over the past few decades in countries of all income levels. Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys and nerves. The most common is type 2 diabetes, usually in adults, which occurs when the body becomes resistant to insulin or doesn't make enough insulin. In the past 3 decades the prevalence of type 2 diabetes has risen dramatically in countries of all income levels. Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin by itself. For people living with diabetes, access to affordable treatment, including insulin, is critical to their survival. There is a globally agreed target to halt the rise in diabetes and obesity by 2025. Symptoms of type 1 diabetes include the need to urinate often, thirst, constant hunger, weight loss, vision changes and fatigue. These symptoms may occur suddenly. Symptoms for type 2 diabetes are generally similar to those of type 1 diabetes but are often less marked. As a result, the disease may be diagnosed several years after onset, after complications have already arisen. For this reason, it is important to be aware of risk factors. Type 1 diabetes cannot currently be prevented. Effective approaches are available to prevent type 2 diabetes and to prevent the complications and premature death that can result from all types of diabetes. These include policies and practices across whole populations and within specific settings (school, home, workplace) that contribute to good health for everyone, regardless of whether they have diabetes, such as exercising regularly, eating healthily, avoiding smoking, and controlling blood pressure and lipids. The starting point for living well with diabetes is an early diagnosis the longer a person lives with undiagnosed and untreated diabetes, the worse their health outcomes are likely to be. Easy access to basic diagnostics, such as blood glucose testing, should therefore be available in primary health care settings. Patients will need periodic specialist assessment or treatment for complications. A series of cost-effective interventions can improve patient outcomes, regardless of what type of diabetes they may have. These interventions include blood glucose control through a combination of diet, physical activity and, if necessary, medication; control of blood pressure and lipids to reduce cardiovascular risk and other complications; and regular screening for damage to the eyes, kidneys and feet to facilitate early treatment]]> Sun, 04 Sep 2022 20:03:14 GMT /slideshow/risk-factors-of-diabetespptx/252826003 AhmedMandour37@slideshare.net(AhmedMandour37) Risk factors of diabetes.pptx AhmedMandour37 Diabetes is a world-wide public health problem. About 422 million people worldwide have diabetes, the majority living in low-and middle-income countries, and 1.5 million deaths are directly attributed to diabetes each year. Both the number of cases and the prevalence of diabetes have been steadily increasing over the past few decades in countries of all income levels. Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys and nerves. The most common is type 2 diabetes, usually in adults, which occurs when the body becomes resistant to insulin or doesn't make enough insulin. In the past 3 decades the prevalence of type 2 diabetes has risen dramatically in countries of all income levels. Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin by itself. For people living with diabetes, access to affordable treatment, including insulin, is critical to their survival. There is a globally agreed target to halt the rise in diabetes and obesity by 2025. Symptoms of type 1 diabetes include the need to urinate often, thirst, constant hunger, weight loss, vision changes and fatigue. These symptoms may occur suddenly. Symptoms for type 2 diabetes are generally similar to those of type 1 diabetes but are often less marked. As a result, the disease may be diagnosed several years after onset, after complications have already arisen. For this reason, it is important to be aware of risk factors. Type 1 diabetes cannot currently be prevented. Effective approaches are available to prevent type 2 diabetes and to prevent the complications and premature death that can result from all types of diabetes. These include policies and practices across whole populations and within specific settings (school, home, workplace) that contribute to good health for everyone, regardless of whether they have diabetes, such as exercising regularly, eating healthily, avoiding smoking, and controlling blood pressure and lipids. The starting point for living well with diabetes is an early diagnosis the longer a person lives with undiagnosed and untreated diabetes, the worse their health outcomes are likely to be. Easy access to basic diagnostics, such as blood glucose testing, should therefore be available in primary health care settings. Patients will need periodic specialist assessment or treatment for complications. A series of cost-effective interventions can improve patient outcomes, regardless of what type of diabetes they may have. These interventions include blood glucose control through a combination of diet, physical activity and, if necessary, medication; control of blood pressure and lipids to reduce cardiovascular risk and other complications; and regular screening for damage to the eyes, kidneys and feet to facilitate early treatment <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/riskfactorsofdiabetes-220904200315-38592780-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Diabetes is a world-wide public health problem. About 422 million people worldwide have diabetes, the majority living in low-and middle-income countries, and 1.5 million deaths are directly attributed to diabetes each year. Both the number of cases and the prevalence of diabetes have been steadily increasing over the past few decades in countries of all income levels. Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys and nerves. The most common is type 2 diabetes, usually in adults, which occurs when the body becomes resistant to insulin or doesn&#39;t make enough insulin. In the past 3 decades the prevalence of type 2 diabetes has risen dramatically in countries of all income levels. Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin by itself. For people living with diabetes, access to affordable treatment, including insulin, is critical to their survival. There is a globally agreed target to halt the rise in diabetes and obesity by 2025. Symptoms of type 1 diabetes include the need to urinate often, thirst, constant hunger, weight loss, vision changes and fatigue. These symptoms may occur suddenly. Symptoms for type 2 diabetes are generally similar to those of type 1 diabetes but are often less marked. As a result, the disease may be diagnosed several years after onset, after complications have already arisen. For this reason, it is important to be aware of risk factors. Type 1 diabetes cannot currently be prevented. Effective approaches are available to prevent type 2 diabetes and to prevent the complications and premature death that can result from all types of diabetes. These include policies and practices across whole populations and within specific settings (school, home, workplace) that contribute to good health for everyone, regardless of whether they have diabetes, such as exercising regularly, eating healthily, avoiding smoking, and controlling blood pressure and lipids. The starting point for living well with diabetes is an early diagnosis the longer a person lives with undiagnosed and untreated diabetes, the worse their health outcomes are likely to be. Easy access to basic diagnostics, such as blood glucose testing, should therefore be available in primary health care settings. Patients will need periodic specialist assessment or treatment for complications. A series of cost-effective interventions can improve patient outcomes, regardless of what type of diabetes they may have. These interventions include blood glucose control through a combination of diet, physical activity and, if necessary, medication; control of blood pressure and lipids to reduce cardiovascular risk and other complications; and regular screening for damage to the eyes, kidneys and feet to facilitate early treatment
Risk factors of diabetes.pptx from AhmedMandour37
]]> 56 0 https://cdn.slidesharecdn.com/ss_thumbnails/riskfactorsofdiabetes-220904200315-38592780-thumbnail.jpg?width=120&height=120&fit=bounds presentation Black http://activitystrea.ms/schema/1.0/post http://activitystrea.ms/schema/1.0/posted 0 https://public.slidesharecdn.com/v2/images/profile-picture.png https://cdn.slidesharecdn.com/ss_thumbnails/dkadrsyed2584-1906020838131-230914155337-bf56c01d-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/dkadrsyed2584190602083813-1pptx/260957116 dkadrsyed2584-19060208... https://cdn.slidesharecdn.com/ss_thumbnails/ibd-1910060700291-230913211424-c9432644-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/ibd191006070029-1pptx/260912427 ibd-191006070029 (1).pptx https://cdn.slidesharecdn.com/ss_thumbnails/nashriskfactorsandmanagement-230913204420-37436d63-thumbnail.jpg?width=320&height=320&fit=bounds AhmedMandour37/nash-risk-factors-and-managementpptx NASH risk factors and ...