This document discusses diabetic cranial and autonomic neuropathies. It covers the clinical spectrum and treatments. Key points include:
- Diabetic neuropathies can affect 30-50% of people with diabetes and uncontrolled blood sugar levels can worsen symptoms over time.
- Cranial neuropathies most commonly involve cranial nerves III, IV, VI and the facial nerve. Symptoms include diplopia, ptosis, and facial weakness. Treatment focuses on blood sugar control.
- Autonomic neuropathies can impact the heart, gastrointestinal tract, genitourinary system and sweat glands. Symptoms vary by the nerves affected but treatments aim to control blood sugar and use medications
A presentation made to laboratory medicine professionals on 10 December 2016 during the Zimbabwe Association of Clinical Biochemistry and Laboratory Medicine (ZACBLM) symposium held at Parirenyatwa Group of Hospitals, Harare, Zimbabwe
This document outlines a presentation on hepatic encephalopathy. It begins with an introduction defining hepatic encephalopathy and its clinical spectrum. It then covers the epidemiology, classification, etiopathogenesis including theories around ammonia and GABA, clinical features, differential diagnosis, investigations including blood tests and EEG, and treatment including lactulose, antibiotics, and dietary changes. The presentation concludes with references.
complete and detail study on the topic of anti epileptic drugs . the topic contain drugs of epilepsy with their uses, side effect, mechanism of action, classification of epileptic drugs.
basic information of receptors
Hepatic encephalopathy, short review & updateRushdanZakariah
This document provides an overview of hepatic encephalopathy. It describes hepatic encephalopathy as a complex neuropsychiatric syndrome characterized by disturbances in consciousness and personality changes. Acute episodes can be reversible while chronic cases may progress to coma or death. Precipitating factors include constipation, surgery, and progressive liver disease. Ammonia plays a central role in pathogenesis, as the liver is unable to metabolize and excrete nitrogenous waste products, leading to accumulation of ammonia in the blood and brain. Treatment aims to remove precipitating factors, reduce nitrogenous load from the gut, and manage symptoms. Options include nutritional management, laxatives, antibiotics like rifaximin, and lactulose to produce
Management of Diabetic Autonomic Neuropathy Shinjan Patra
This document discusses the management of autonomic neuropathy in patients with diabetes. It begins with an overview of the autonomic nervous system and outlines the evaluation and testing of cardiac, gastrointestinal, genitourinary, sudomotor and neurovascular involvement in diabetic autonomic neuropathy. Specific tests are described to assess cardiovascular autonomic function, gastric emptying, bladder function and sweating. Management focuses on tight glycemic control, drug therapies for symptomatic hypotension, and treatments tailored to individual organ system involvement such as prokinetic agents for gastroparesis or alpha-blockers for erectile dysfunction.
Autonomic neuropathy and anesthetic implicationsRichie Sanam
Diabetic patients have increased risk of complications during surgery due to microvascular and macrovascular changes caused by the disease. Autonomic neuropathy is common and affects the cardiovascular, gastrointestinal, genitourinary systems. It is important to assess for autonomic dysfunction preoperatively using tests like heart rate variability, gastric emptying tests, urodynamic studies to guide anesthesia management and reduce risks. Regional anesthesia is preferred over general anesthesia for patients with autonomic neuropathy due to the risk of hypotension, but careful titration is needed to avoid it. Strict glycemic control and protocols to reduce aspiration risk must also be followed in these high risk patients.
This document provides an overview of hepatic encephalopathy. It defines hepatic encephalopathy as a complex metabolic disorder seen in patients with liver dysfunction, characterized by disturbances in consciousness and behavior. It discusses the pathogenesis, including the ammonia and false neurotransmitter hypotheses. Precipitating factors and clinical manifestations ranging from mild cognitive changes to coma are described. Diagnosis involves ruling out other causes and elevated ammonia levels. Treatment focuses on reducing ammonia through dietary changes, lactulose, antibiotics, and other supportive measures. Prognosis depends on the severity and underlying liver disease.
A presentation made to laboratory medicine professionals on 10 December 2016 during the Zimbabwe Association of Clinical Biochemistry and Laboratory Medicine (ZACBLM) symposium held at Parirenyatwa Group of Hospitals, Harare, Zimbabwe
This document outlines a presentation on hepatic encephalopathy. It begins with an introduction defining hepatic encephalopathy and its clinical spectrum. It then covers the epidemiology, classification, etiopathogenesis including theories around ammonia and GABA, clinical features, differential diagnosis, investigations including blood tests and EEG, and treatment including lactulose, antibiotics, and dietary changes. The presentation concludes with references.
complete and detail study on the topic of anti epileptic drugs . the topic contain drugs of epilepsy with their uses, side effect, mechanism of action, classification of epileptic drugs.
basic information of receptors
Hepatic encephalopathy, short review & updateRushdanZakariah
This document provides an overview of hepatic encephalopathy. It describes hepatic encephalopathy as a complex neuropsychiatric syndrome characterized by disturbances in consciousness and personality changes. Acute episodes can be reversible while chronic cases may progress to coma or death. Precipitating factors include constipation, surgery, and progressive liver disease. Ammonia plays a central role in pathogenesis, as the liver is unable to metabolize and excrete nitrogenous waste products, leading to accumulation of ammonia in the blood and brain. Treatment aims to remove precipitating factors, reduce nitrogenous load from the gut, and manage symptoms. Options include nutritional management, laxatives, antibiotics like rifaximin, and lactulose to produce
Management of Diabetic Autonomic Neuropathy Shinjan Patra
This document discusses the management of autonomic neuropathy in patients with diabetes. It begins with an overview of the autonomic nervous system and outlines the evaluation and testing of cardiac, gastrointestinal, genitourinary, sudomotor and neurovascular involvement in diabetic autonomic neuropathy. Specific tests are described to assess cardiovascular autonomic function, gastric emptying, bladder function and sweating. Management focuses on tight glycemic control, drug therapies for symptomatic hypotension, and treatments tailored to individual organ system involvement such as prokinetic agents for gastroparesis or alpha-blockers for erectile dysfunction.
Autonomic neuropathy and anesthetic implicationsRichie Sanam
Diabetic patients have increased risk of complications during surgery due to microvascular and macrovascular changes caused by the disease. Autonomic neuropathy is common and affects the cardiovascular, gastrointestinal, genitourinary systems. It is important to assess for autonomic dysfunction preoperatively using tests like heart rate variability, gastric emptying tests, urodynamic studies to guide anesthesia management and reduce risks. Regional anesthesia is preferred over general anesthesia for patients with autonomic neuropathy due to the risk of hypotension, but careful titration is needed to avoid it. Strict glycemic control and protocols to reduce aspiration risk must also be followed in these high risk patients.
This document provides an overview of hepatic encephalopathy. It defines hepatic encephalopathy as a complex metabolic disorder seen in patients with liver dysfunction, characterized by disturbances in consciousness and behavior. It discusses the pathogenesis, including the ammonia and false neurotransmitter hypotheses. Precipitating factors and clinical manifestations ranging from mild cognitive changes to coma are described. Diagnosis involves ruling out other causes and elevated ammonia levels. Treatment focuses on reducing ammonia through dietary changes, lactulose, antibiotics, and other supportive measures. Prognosis depends on the severity and underlying liver disease.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure and characterized by changes in cognition, behavior, and personality. It ranges from minor alterations in brain function to deep coma. The main causes are thought to be increased levels of ammonia and other toxins in the blood due to the liver's inability to remove them. Treatment focuses on reducing ammonia production in the gut through dietary changes, antibiotics, and lactulose. Managing precipitating factors and providing supportive care are also important. For severe or recurrent cases, procedures to bypass the liver such as TIPSS or liver transplantation may be considered.
CASE PRESENTATION ON HEPATIC ENCEPHALOPATHY DUE TO ALCOHOLISMRahman Khan
- The patient, a 43-year-old male, presented with altered sensorium since the previous evening.
- He has a history of end-stage liver disease and portal hypertension with recurrent hepatic encephalopathy.
- On examination, he appeared drowsy and irritable. Investigations confirmed hepatic encephalopathy.
- He was diagnosed with hepatic encephalopathy due to alcoholism and prescribed medications including cefotaxime, pantoprazole, ondansetron, lactulose, ursodeoxycholic acid, rifaximin, and L-ornithine-L-aspartic acid to treat the condition and its symptoms.
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunts. Gut-derived toxins such as ammonia cross the blood-brain barrier and cause neurological or psychiatric abnormalities. Treatment involves removing precipitating causes, lowering ammonia levels through antibiotics, lactulose, and BCAA supplementation, and correcting nutritional deficiencies. For refractory or recurrent cases, transplantation may be required.
This document discusses hepatic encephalopathy, which is a reversible neuropsychiatric complication of severe liver disease. It can be caused by cirrhosis, portal-systemic bypass, or acute liver failure. The pathogenic mechanisms involve ammonia toxicity and false neurotransmitters. Clinical manifestations range from sleep disturbances and confusion to coma. Treatment focuses on identifying and removing precipitating factors, reducing ammonia production, correcting amino acid imbalances, and managing complications. Prognosis depends on the underlying liver disease.
Pre-operative assessment, evaluation and preparation of a patient of Diabetes...Saptaparni Hazra
This document provides guidance on preoperative evaluation and preparation of patients with diabetes mellitus undergoing surgery. Key points include determining the type and control of the patient's diabetes, assessing for complications, identifying high-risk patients, and optimizing diabetes management in the perioperative period. Intraoperative glucose should be managed between 140-180 mg/dL to minimize risk, and subcutaneous or intravenous insulin may be used depending on the surgical scenario and hemodynamic stability of the patient. Thorough preoperative evaluation and careful perioperative glucose management are essential in patients with diabetes.
This 85-year-old lady presented with involuntary movements of her left upper and lower limbs for one week. MRI brain showed degenerative changes in the caudate nucleus and putamen. She was diagnosed with hemichorea, also known as senile chorea, and started on treatment with haloperidol and trihexyphenidyl. Hemichorea is caused by lesions in the caudate nucleus and presents with non-rhythmic, rapid flinging movements that are exacerbated by activity and emotion.
This document discusses renal and hepatic encephalopathy. It defines uremic encephalopathy as a brain disorder that occurs in patients with untreated or inadequately treated kidney disease. Symptoms range from mild to severe and fluctuate depending on kidney function. Uremic toxins that accumulate due to renal dysfunction are a primary cause. Treatment involves optimizing dialysis to adequately remove toxins. Other types of encephalopathy discussed include dialysis dementia, central pontine myelinolysis, seizures, and restless leg syndrome. Causes, clinical features, diagnosis and management are described for each condition.
This document discusses diabetic neuropathy, including its definition, prevalence, risk factors, clinical presentations, investigations, and types. Some key points:
- Diabetic neuropathy is nerve dysfunction in people with diabetes after other causes have been excluded. It has a prevalence of 5-100% and is the most common neuropathy in developed countries.
- Risk factors include poor glycemic control, hypertension, smoking, alcohol, and longer duration of diabetes. Clinical presentations include distal symmetrical polyneuropathy, proximal diabetic neuropathy, truncal neuropathy, and mononeuropathies.
- Investigations include blood tests to assess glucose levels, vitamin deficiencies and organ function. Types include chronic sensorimotor neuropathy, autonomic neuropathy
Hepatic encephalopathy is a disorder of brain function caused by liver failure and the buildup of toxic substances. Ammonia produced during protein breakdown in the gut cannot be removed by the damaged liver and crosses into the brain. Symptoms range from confusion to coma. Treatment aims to reduce ammonia levels through a low-protein diet, lactulose to increase ammonia excretion, antibiotics to treat gut infections, and medications to stimulate ammonia metabolism. Prognosis depends on the severity and reversibility of the underlying liver disease.
This document discusses neonatal metabolic encephalopathy and its causes. It describes neonatal encephalopathy as a clinically defined syndrome of disturbed neurologic function in the earliest days of life, manifested by subnormal consciousness, seizures, and difficulties with breathing and muscle tone. The main causes are listed as hypoxic-ischemic encephalopathy, perinatal stroke, progressive encephalopathy of metabolic, infectious or toxic origin, brain anomalies, hemorrhage, genetic mutations or maternal toxins. Metabolic disorders presenting with encephalopathy are divided into those with significant biochemical abnormalities like hyperammonemia, metabolic acidosis or hypoglycemia, and those without clear abnormalities. Specific metabolic disorders are discussed in detail, along with their
This document provides information on causes and treatment of hypoglycemia. It defines hypoglycemia and outlines symptoms. It describes various causes of hypoglycemia including insulin excess, critical illness, hormone deficiencies, drugs, and tumors. It discusses diagnostic criteria and treatment approaches. Hypoglycemia is a common side effect of diabetes treatment that physicians must work to prevent and address promptly when it occurs.
Hypoglycemia, or low blood sugar, is caused by very low levels of blood glucose, below 3.0 mmol/L. It is common in type 1 diabetes and can occur due to overdose of insulin or diabetes medications, excessive alcohol consumption, or certain illnesses. Symptoms range from irregular heartbeat and sweating to confusion and loss of consciousness. Treatment involves giving the person glucose tablets, juice, or an IV glucose solution to quickly raise their blood sugar levels. Preventing hypoglycemia requires education on recognizing symptoms early and always having access to fast-acting carbohydrates.
Hepatic encephalopathy is a complex, reversible neuropsychiatric disorder seen in patients with severe liver dysfunction. It ranges from mild cognitive impairment (minimal HE) to coma (overt HE). Precipitating factors like infections, GI bleeding, and high protein intake can trigger episodes. Treatment focuses on removing triggers, lowering ammonia with lactulose/rifaximin, and considering liver transplant for persistent cases. Diet, lactulose, antibiotics, and surgery to reduce portosystemic shunting are used to manage and prevent recurrent episodes of hepatic encephalopathy.
Diabetic neuropathy- a Precise Insight , by RxVichuZ!! ;) ;)RxVichuZ
Hello members....this is my 40th powerpoint...published in GOOGLE SLIDESHARE!! :) :)
I wish to thank each and everyone who have supported me all the way...!!!
This presentation deals with DIABETIC NEUROPATHY ...the causes, epidemiological statistics, pathogenesis.
A deeper insight into manifestations, complications, management & natural remedies have been provided....!!
Do go through this...and let me know you reviews!!!
When you THINK DIFFERENTLY, it becomes an INNOVATION,
When u infuse DEDICATION into that INNOVATION, it becomes an INVENTION..!!
HAPPY READING!!
#RxVichuZ-alwz4uh!! :)
This document discusses the management of portosystemic encephalopathy. It begins by describing the different types and classifications of hepatic encephalopathy. It then discusses the effects of ammonia and various treatments to reduce ammonia levels, including lactulose, antibiotics like rifaximin, L-ornithine L-aspartate, and probiotics. It notes that while lactulose and protein restriction have no effect on mortality, rifaximin reduces risks of breakthrough hepatic encephalopathy episodes and hospitalizations. The document also briefly discusses other management strategies, adjunctive treatments, and notes that liver transplantation is the ultimate management goal for overt hepatic encephalopathy.
1. The document discusses the medical management of congenital heart disease, focusing on congestive heart failure, cyanotic spells, duct dependent lesions, and PDA in preterm infants.
2. Key treatments for congestive heart failure include diuretics, ACE inhibitors, ionotropes like digoxin, and newer drugs like carvedilol. For cyanotic spells, oxygen, morphine, bicarbonate, ketamine, and propranolol are used.
3. Duct dependent lesions require prostaglandin E1 infusion to maintain ductal patency. Complications of cyanosis like anemia, polycythemia, and hyperuricemia are also addressed
learn about excellent case article published in NEJM regarding celiac disease,its rare presentation and approach for the same along with discussion ..we should always think about this rare presentations
1) Diabetic neuropathy is a syndrome comprising separate clinical disorders that affect the peripheral nervous system, with a prevalence of 66% for type 1 diabetes and 59% for type 2 diabetes.
2) Risk factors include hyperglycemia, longer duration of diabetes, age, hypertension, and smoking.
3) The most common form is distal symmetrical sensorimotor polyneuropathy, which involves small and large fiber sensory, autonomic, and motor nerves in various combinations.
Hypoglycemia is defined as a glucose level below 55 mg/dL with symptoms relieved by raising glucose levels. It can occur in diabetes due to excessive insulin or missed meals, and in non-diabetics due to drugs, critical illness, or tumors. Symptoms include autonomic symptoms like sweating and tremors, and neuroglycopenic symptoms like confusion and drowsiness. Treatment involves oral glucose if able, or IV glucose and glucagon injections. Prevention focuses on glucose monitoring, education, flexible regimens, and glycemic goals tailored to each individual.
1. Encephalopathy refers to diffuse brain dysfunction due to systemic, metabolic, or toxic derangements and can be caused by conditions like sepsis, organ failure, medications, or electrolyte disturbances.
2. Status epilepticus refers to continuous seizures or repetitive discrete seizures with impaired consciousness between seizures. It requires acute anticonvulsant treatment if lasting more than 15-30 minutes as it can cause permanent neurological injury or death.
3. Prolonged seizures can cause respiratory, hemodynamic, metabolic, and thermal alterations like hypoxia, hypotension, hypoglycemia, and hyperthermia which exacerbate neuronal injury. Timely management includes securing the airway, treating metabolic derangements,
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver failure and characterized by changes in cognition, behavior, and personality. It ranges from minor alterations in brain function to deep coma. The main causes are thought to be increased levels of ammonia and other toxins in the blood due to the liver's inability to remove them. Treatment focuses on reducing ammonia production in the gut through dietary changes, antibiotics, and lactulose. Managing precipitating factors and providing supportive care are also important. For severe or recurrent cases, procedures to bypass the liver such as TIPSS or liver transplantation may be considered.
CASE PRESENTATION ON HEPATIC ENCEPHALOPATHY DUE TO ALCOHOLISMRahman Khan
- The patient, a 43-year-old male, presented with altered sensorium since the previous evening.
- He has a history of end-stage liver disease and portal hypertension with recurrent hepatic encephalopathy.
- On examination, he appeared drowsy and irritable. Investigations confirmed hepatic encephalopathy.
- He was diagnosed with hepatic encephalopathy due to alcoholism and prescribed medications including cefotaxime, pantoprazole, ondansetron, lactulose, ursodeoxycholic acid, rifaximin, and L-ornithine-L-aspartic acid to treat the condition and its symptoms.
Hepatic encephalopathy is a brain dysfunction caused by liver disease or portosystemic shunts. Gut-derived toxins such as ammonia cross the blood-brain barrier and cause neurological or psychiatric abnormalities. Treatment involves removing precipitating causes, lowering ammonia levels through antibiotics, lactulose, and BCAA supplementation, and correcting nutritional deficiencies. For refractory or recurrent cases, transplantation may be required.
This document discusses hepatic encephalopathy, which is a reversible neuropsychiatric complication of severe liver disease. It can be caused by cirrhosis, portal-systemic bypass, or acute liver failure. The pathogenic mechanisms involve ammonia toxicity and false neurotransmitters. Clinical manifestations range from sleep disturbances and confusion to coma. Treatment focuses on identifying and removing precipitating factors, reducing ammonia production, correcting amino acid imbalances, and managing complications. Prognosis depends on the underlying liver disease.
Pre-operative assessment, evaluation and preparation of a patient of Diabetes...Saptaparni Hazra
This document provides guidance on preoperative evaluation and preparation of patients with diabetes mellitus undergoing surgery. Key points include determining the type and control of the patient's diabetes, assessing for complications, identifying high-risk patients, and optimizing diabetes management in the perioperative period. Intraoperative glucose should be managed between 140-180 mg/dL to minimize risk, and subcutaneous or intravenous insulin may be used depending on the surgical scenario and hemodynamic stability of the patient. Thorough preoperative evaluation and careful perioperative glucose management are essential in patients with diabetes.
This 85-year-old lady presented with involuntary movements of her left upper and lower limbs for one week. MRI brain showed degenerative changes in the caudate nucleus and putamen. She was diagnosed with hemichorea, also known as senile chorea, and started on treatment with haloperidol and trihexyphenidyl. Hemichorea is caused by lesions in the caudate nucleus and presents with non-rhythmic, rapid flinging movements that are exacerbated by activity and emotion.
This document discusses renal and hepatic encephalopathy. It defines uremic encephalopathy as a brain disorder that occurs in patients with untreated or inadequately treated kidney disease. Symptoms range from mild to severe and fluctuate depending on kidney function. Uremic toxins that accumulate due to renal dysfunction are a primary cause. Treatment involves optimizing dialysis to adequately remove toxins. Other types of encephalopathy discussed include dialysis dementia, central pontine myelinolysis, seizures, and restless leg syndrome. Causes, clinical features, diagnosis and management are described for each condition.
This document discusses diabetic neuropathy, including its definition, prevalence, risk factors, clinical presentations, investigations, and types. Some key points:
- Diabetic neuropathy is nerve dysfunction in people with diabetes after other causes have been excluded. It has a prevalence of 5-100% and is the most common neuropathy in developed countries.
- Risk factors include poor glycemic control, hypertension, smoking, alcohol, and longer duration of diabetes. Clinical presentations include distal symmetrical polyneuropathy, proximal diabetic neuropathy, truncal neuropathy, and mononeuropathies.
- Investigations include blood tests to assess glucose levels, vitamin deficiencies and organ function. Types include chronic sensorimotor neuropathy, autonomic neuropathy
Hepatic encephalopathy is a disorder of brain function caused by liver failure and the buildup of toxic substances. Ammonia produced during protein breakdown in the gut cannot be removed by the damaged liver and crosses into the brain. Symptoms range from confusion to coma. Treatment aims to reduce ammonia levels through a low-protein diet, lactulose to increase ammonia excretion, antibiotics to treat gut infections, and medications to stimulate ammonia metabolism. Prognosis depends on the severity and reversibility of the underlying liver disease.
This document discusses neonatal metabolic encephalopathy and its causes. It describes neonatal encephalopathy as a clinically defined syndrome of disturbed neurologic function in the earliest days of life, manifested by subnormal consciousness, seizures, and difficulties with breathing and muscle tone. The main causes are listed as hypoxic-ischemic encephalopathy, perinatal stroke, progressive encephalopathy of metabolic, infectious or toxic origin, brain anomalies, hemorrhage, genetic mutations or maternal toxins. Metabolic disorders presenting with encephalopathy are divided into those with significant biochemical abnormalities like hyperammonemia, metabolic acidosis or hypoglycemia, and those without clear abnormalities. Specific metabolic disorders are discussed in detail, along with their
This document provides information on causes and treatment of hypoglycemia. It defines hypoglycemia and outlines symptoms. It describes various causes of hypoglycemia including insulin excess, critical illness, hormone deficiencies, drugs, and tumors. It discusses diagnostic criteria and treatment approaches. Hypoglycemia is a common side effect of diabetes treatment that physicians must work to prevent and address promptly when it occurs.
Hypoglycemia, or low blood sugar, is caused by very low levels of blood glucose, below 3.0 mmol/L. It is common in type 1 diabetes and can occur due to overdose of insulin or diabetes medications, excessive alcohol consumption, or certain illnesses. Symptoms range from irregular heartbeat and sweating to confusion and loss of consciousness. Treatment involves giving the person glucose tablets, juice, or an IV glucose solution to quickly raise their blood sugar levels. Preventing hypoglycemia requires education on recognizing symptoms early and always having access to fast-acting carbohydrates.
Hepatic encephalopathy is a complex, reversible neuropsychiatric disorder seen in patients with severe liver dysfunction. It ranges from mild cognitive impairment (minimal HE) to coma (overt HE). Precipitating factors like infections, GI bleeding, and high protein intake can trigger episodes. Treatment focuses on removing triggers, lowering ammonia with lactulose/rifaximin, and considering liver transplant for persistent cases. Diet, lactulose, antibiotics, and surgery to reduce portosystemic shunting are used to manage and prevent recurrent episodes of hepatic encephalopathy.
Diabetic neuropathy- a Precise Insight , by RxVichuZ!! ;) ;)RxVichuZ
Hello members....this is my 40th powerpoint...published in GOOGLE SLIDESHARE!! :) :)
I wish to thank each and everyone who have supported me all the way...!!!
This presentation deals with DIABETIC NEUROPATHY ...the causes, epidemiological statistics, pathogenesis.
A deeper insight into manifestations, complications, management & natural remedies have been provided....!!
Do go through this...and let me know you reviews!!!
When you THINK DIFFERENTLY, it becomes an INNOVATION,
When u infuse DEDICATION into that INNOVATION, it becomes an INVENTION..!!
HAPPY READING!!
#RxVichuZ-alwz4uh!! :)
This document discusses the management of portosystemic encephalopathy. It begins by describing the different types and classifications of hepatic encephalopathy. It then discusses the effects of ammonia and various treatments to reduce ammonia levels, including lactulose, antibiotics like rifaximin, L-ornithine L-aspartate, and probiotics. It notes that while lactulose and protein restriction have no effect on mortality, rifaximin reduces risks of breakthrough hepatic encephalopathy episodes and hospitalizations. The document also briefly discusses other management strategies, adjunctive treatments, and notes that liver transplantation is the ultimate management goal for overt hepatic encephalopathy.
1. The document discusses the medical management of congenital heart disease, focusing on congestive heart failure, cyanotic spells, duct dependent lesions, and PDA in preterm infants.
2. Key treatments for congestive heart failure include diuretics, ACE inhibitors, ionotropes like digoxin, and newer drugs like carvedilol. For cyanotic spells, oxygen, morphine, bicarbonate, ketamine, and propranolol are used.
3. Duct dependent lesions require prostaglandin E1 infusion to maintain ductal patency. Complications of cyanosis like anemia, polycythemia, and hyperuricemia are also addressed
learn about excellent case article published in NEJM regarding celiac disease,its rare presentation and approach for the same along with discussion ..we should always think about this rare presentations
1) Diabetic neuropathy is a syndrome comprising separate clinical disorders that affect the peripheral nervous system, with a prevalence of 66% for type 1 diabetes and 59% for type 2 diabetes.
2) Risk factors include hyperglycemia, longer duration of diabetes, age, hypertension, and smoking.
3) The most common form is distal symmetrical sensorimotor polyneuropathy, which involves small and large fiber sensory, autonomic, and motor nerves in various combinations.
Hypoglycemia is defined as a glucose level below 55 mg/dL with symptoms relieved by raising glucose levels. It can occur in diabetes due to excessive insulin or missed meals, and in non-diabetics due to drugs, critical illness, or tumors. Symptoms include autonomic symptoms like sweating and tremors, and neuroglycopenic symptoms like confusion and drowsiness. Treatment involves oral glucose if able, or IV glucose and glucagon injections. Prevention focuses on glucose monitoring, education, flexible regimens, and glycemic goals tailored to each individual.
1. Encephalopathy refers to diffuse brain dysfunction due to systemic, metabolic, or toxic derangements and can be caused by conditions like sepsis, organ failure, medications, or electrolyte disturbances.
2. Status epilepticus refers to continuous seizures or repetitive discrete seizures with impaired consciousness between seizures. It requires acute anticonvulsant treatment if lasting more than 15-30 minutes as it can cause permanent neurological injury or death.
3. Prolonged seizures can cause respiratory, hemodynamic, metabolic, and thermal alterations like hypoxia, hypotension, hypoglycemia, and hyperthermia which exacerbate neuronal injury. Timely management includes securing the airway, treating metabolic derangements,
It is one of the hardest subjects to grasp initially. I have read this thoroughly during the initial years of my anesthesia training. This presentation on the pharmacology of anesthesia addresses the key concepts any anesthetist should have on his fingertips.
1362405305 neuropathy reversal and limiting impact skkedfsimedia
This document discusses evidence for halting progression and causing reversal of diabetic neuropathy. It outlines 11 hopes for achieving this, including tight glucose control, pancreas transplantation, controlling oxidative stress with supplements like alpha lipoic acid and gamma linolenic acid, vasodilation, nerve growth factors, and C-peptide administration. Strategies for limiting neuropathy's impact include symptomatic relief, preventing foot ulcers and amputations through regular inspection and early treatment of issues like corns, calluses, and infections. Education of patients is emphasized.
1362576429 neuropathy reversal and limiting impact skkedfsimedia
This document discusses evidence for halting progression and causing reversal of diabetic neuropathy. It outlines 11 hopes or strategies that show promise based on studies: 1) tight blood glucose control, 2) pancreas transplantation, 3) controlling oxidative stress with alpha lipoic acid, 4) controlling oxidative stress with gamma linolenic acid, 5) controlling oxidative stress with vitamin E, 6) vasodilation with cilostozol, 7) preventing vasoconstriction, 8) chronic intermittent intravenous insulin therapy, 9) experimental nerve growth factors, 10) C-peptide seems useful for halting/reversing Type 1 neuropathy, 11) PKC inhibitors. It also outlines strategies for limiting the impact of diabetic neuropathy through symptomatic
1) Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a motor neuron disease characterized by both upper and lower motor neuron signs resulting in spasticity, muscle atrophy, and weakness.
2) Diagnosis involves excluding other potential causes through examination, testing, imaging, and electrodiagnostic studies to determine if signs are consistent with ALS.
3) While there is no cure for ALS, treatment focuses on managing symptoms through exercise, nutrition, medications, rehabilitation, and respiratory support to prolong survival and quality of life.
The document discusses the parasympathetic nervous system and cholinergic drugs. It describes how the parasympathetic nervous system works to rest and digest functions like decreasing heart rate and increasing GI motility. It then explains cholinergic drugs, which mimic acetylcholine, as either direct acting agonists that bind receptors or indirect acting drugs that inhibit acetylcholinesterase. Side effects result from overstimulation of the parasympathetic nervous system and can include things like increased secretions, bronchospasm, and bradycardia.
This document provides an overview of depression, including its definition, types, epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, investigations, and treatment. Depression is a common mental disorder characterized by depressed mood and loss of interest or pleasure. It affects over 350 million people globally and is the leading cause of disability for those aged 15-44 in the U.S. Depression has genetic, environmental, biochemical, and physical illness-related causes and is treated through antidepressants, psychotherapy, lifestyle changes, and in severe cases, electroconvulsive therapy. The document covers various antidepressant classes and their mechanisms of action and side effects.
This document provides an overview of depression, including its definition, types, epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, investigations, and treatment. Depression is defined as a common mental disorder characterized by depressed mood, loss of interest, feelings of guilt, sleep disturbances, low energy, and poor concentration. Major types include major depressive disorder, bipolar disorder, dysthymic disorder, and situational depression. Depression affects over 350 million people globally and is a leading cause of disability. Causes may include genetic, environmental, biochemical and neurological factors. Treatment involves antidepressant medications like SSRIs, TCAs, and MAOIs as well as psychotherapy and other non-pharmacological approaches.
Unconsciousness implies that is a stage of depressed cerebral function that result impairment in response to sensory stimuli; abnormal loss of awareness of self & surroundings.
Diabetic neuropathy is a common complication of diabetes that affects the peripheral nervous system. It is defined as a disorder of peripheral nerves in the setting of diabetes without other causes. Up to 90% of patients with diabetes may develop neuropathy. The risk increases with age, duration of diabetes, poor glycemic control, and other factors like smoking. Neuropathy can cause pain, numbness, weakness and autonomic dysfunction. Treatment involves managing blood sugar levels, identifying other contributing factors, and medications to relieve pain or autonomic symptoms. Proper diagnosis and management of neuropathy and its risk factors can help prevent progression of nerve damage in diabetes patients.
Dr. Prosper's presentation covered the approach to proteinuria. It began with background on proteinuria and the basic physiology of the glomerular filtration barrier (GFB). Proteinuria was defined as excessive proteins in urine over 150mg/24hrs. Measurement methods including dipstick tests and 24hr urine collections were discussed. The etiology of proteinuria was classified as benign, glomerular, tubular, overflow or post renal. A thorough history, physical exam, labs, urine studies and renal ultrasound were recommended in the evaluation. A renal biopsy may be indicated in persistent cases. Treatment focuses on controlling underlying causes like diabetes or hypertension and reducing cardiovascular risk factors.
This document discusses pseudotumor cerebri (PTC), also known as idiopathic intracranial hypertension. PTC is characterized by increased intracranial pressure without a tumor or other mass. It most commonly affects obese young women. Symptoms include headache, vision changes like transient visual obscurations, and papilledema. Treatment involves weight loss, medication like acetazolamide, repeated lumbar punctures, and sometimes surgical procedures like shunt placement or optic nerve sheath fenestration if other treatments fail to prevent vision loss. Prognosis depends on factors like severity of papilledema and rate of visual decline.
Peripheral neuropathy is a condition that results from damage to the peripheral nerves outside of the brain and spinal cord. It can cause numbness, tingling, pain or weakness in the hands, feet or other areas. There are several types including peripheral, autonomic and focal neuropathies. The most common cause is diabetes, through mechanisms such as increased aldose reductase activity and oxidative stress damaging nerves over time. Diagnosis involves physical exams, nerve conduction tests and ruling out other potential causes. Treatment focuses on managing pain, slowing progression, and preventing complications through good glucose control, medications, physical therapy and foot care.
Diabetic neuropathy is a type of nerve damage that can occur if you have diabetes. High blood sugar (glucose) can injure nerves throughout the body. Diabetic neuropathy most often damages nerves in the legs and feet.
Epilepsy is simply aberrant electrical activity spreading throughout an area of, or the whole of, the brain.
Antiepileptic medications limit the propagation of this spread and inhibit development of symptoms.
Drugs used to treat epilepsy are termed antiepileptics.
Aim of pharmacological treatment of epilepsy is to minimize seizure activity / frequency, without producing adverse drug effects.
1) A 55-year-old woman suddenly developed left-sided weakness after stopping her warfarin, raising concern for hemorrhagic stroke. Rapid diagnosis with CT and attention to reversing any coagulopathy is important.
2) A 20-year-old male student experiencing prolonged seizure requires immediate treatment to stop the seizure and prevent future seizures, given risk of neuronal injury.
3) A 35-year-old woman presented with the worst headache of her life and symptoms concerning for aneurysmal subarachnoid hemorrhage, requiring urgent CT to rule out this neurological emergency.
therapies in psychiatry 1111111111111111MaryemSafdar2
The document discusses various treatment modalities in psychiatry including somatic (physical) therapies like psychopharmacology, electroconvulsive therapy, and psychosurgery. It focuses on psychopharmacology, describing different classes of psychotropic drugs including antipsychotics, antidepressants, mood stabilizers, anxiolytics, and their indications, mechanisms of action, dosages, side effects, and the nurse's role when administering them. Electroconvulsive therapy is also summarized briefly.
1. The document discusses emerging drugs for the treatment of epilepsy, providing details on mechanisms of action, pharmacokinetics, clinical trials and adverse effects for several promising new anti-epileptic drugs.
2. These include brivaracetam, carisbamate, eslicarbazepine acetate, retigabine, perampanel, ganaxolone, and stiripentol. Drugs like brivaracetam and carisbamate are in Phase III trials as adjunctive therapies for partial onset seizures.
3. The newer drugs offer advantages over older anti-epileptics like fewer drug interactions and less toxicity profiles. They expand treatment options for
Similar to 1362571948 diab cranial auto neuropathy (20)
This document discusses diabetic neuropathy, including its etiology, risk factors, prevalence, and mechanisms. Some key points:
- Hyperglycemia is a major risk factor and can lead to nerve damage through vascular closure, fatty acid abnormalities, and advanced glycation end products.
- Neuropathy that causes foot ulceration may affect 40% of diabetics, especially elderly patients with type 2 diabetes.
- Loss of sensation can lead to repeated trauma and abnormal foot loading, while motor neuropathy causes muscle wasting and foot deformities. Together these increase pressure points and risk of foot ulcers and infections.
- Autonomic neuropathy damages sweat glands and blood vessels, causing dry, cracked skin that is more prone
1) Regional anesthesia is well-suited for patients with diabetes as it avoids many risks associated with general anesthesia such as aspiration and hypotension.
2) Proper preparation such as applying an elastic bandage before surgery and counseling the patient can improve the success of regional blocks.
3) Different types of regional blocks like sciatic, femoral, ankle, and high/mid-leg blocks are described which can provide anesthesia for lower limb procedures while avoiding the risks of other anesthesia methods.
4) Careful technique and practice are important for successful regional blocks in patients with diabetes.
- Screening with ABI should be conducted in all diabetic patients older than 50 years and those younger than 50 with risk factors like hypertension, smoking, and diabetes duration over 10 years.
- Primary prevention is important through addressing risk factors such as smoking, blood pressure and glucose control, antiplatelet therapy, and foot care.
- Cilostazol is preferred over pentoxifylline for treatment of symptomatic PAD to improve walking ability and quality of life.
Peripheral vascular disease can be evaluated and treated using angiography and percutaneous techniques like angioplasty and stenting. Angiography remains the gold standard for vascular evaluation when clinical indications for interventions exist. Percutaneous transluminal angioplasty is a non-surgical technique that uses a balloon to increase vessel lumen and prevent ischemia. It is well-suited for short, non-calcified, solitary lesions in large vessels with good runoff. Thrombolysis can also be used as an alternative in selected cases of acute lower limb ischemia. Stenting and other modalities may be combined as needed for different vascular territories and pathologies.
This document discusses acute ischemia of the lower limb (AILL). It outlines the main causes as embolism (70% from heart), thrombosis on top of stenosis, or popliteal aneurysm. Clinical features include the 5 Ps - pain, pallor, paresthesia, pulselessness, paralysis. Treatment options are intra-arterial thrombolysis, thrombectomy, or surgical embolectomy. Peripheral intra-arterial thrombolysis is a common procedure that rapidly restores blood flow and identifies lesions for intervention. It has better outcomes and fewer bleeding risks than systemic thrombolysis.
1362566341 surgical treatment of diabetic footdfsimedia
This document discusses the surgical treatment of diabetic foot. It provides information on various aspects of diabetic foot including causes of foot problems in diabetes, pathways of diabetic foot ulcer, reasons foot lesions are often missed, importance of high clinical suspicion, concept of plantar spaces, assessment of vascular status, principles of debridement in diabetic foot with vasculopathy, wound healing in diabetes including advantages of moist wound environment and ideal dressing methods, causes of delayed healing, agents that can delay healing, importance of antibiotic therapy and domiciliary wound care services. It also discusses local/regional anesthesia techniques for diabetic foot surgery.
1) The document discusses diabetes mellitus and its implications for anesthesia. It notes that diabetes affects many body systems and can increase surgical risks and complications.
2) Regional anesthesia techniques like nerve blocks are recommended when possible over general anesthesia for diabetic patients due to lower risk of issues like aspiration.
3) Detailed instructions are provided on performing different types of lower leg, mid leg, and high leg nerve blocks for surgeries, with the goal of minimizing surgical stress for diabetic patients.
1362564096 anatomy and spread of foot infectionsdfsimedia
1) The document discusses the anatomy and pathophysiology of diabetic foot infections, including details on the plantar arches and spaces of the foot that can be sites of ulcers and infections.
2) It covers the surgical treatment of diabetic foot infections and complications, such as drainage of midfoot abscesses and gangrene of the toes.
3) Various methods of wound bed preparation are outlined, including sharp debridement to remove necrotic tissue, enzymatic debridement using agents like collagenase, autolytic debridement relying on the body's enzymes, and mechanical debridement through irrigation.
Total contact casting is an effective and ambulatory therapy for healing diabetic neuropathic plantar ulcers. It offloads pressure and shortens healing time to 36-43 days by immobilizing the foot and redistributing pressure. Total contact casting is indicated for grade 1 and 2 plantar ulcers with insensitivity and contraindicated for active infection, ulcers deeper than wide, or excessive swelling. It maintains ambulation while reducing pressure and protecting the foot during healing.
Computer scans of the foot can measure pressure exerted on different areas. The scans quantify peak pressures and can identify pressures beyond tolerable limits, which can be the cause of ulcers. The scans show red areas of abnormally high pressure and reveal how the foot falls and which areas contact the ground. This helps identify areas at risk for future ulcers.
1362465426 mechanism foot injury and ulcer formationdfsimedia
This document provides an overview of the mechanisms that cause diabetic foot ulcers. It discusses several factors that can lead to foot injury and ulcer formation in diabetics including tissue ischemia, neuropathy, trauma, infection, mechanical factors like repetitive force from walking, inflammation, and biomechanical aspects like structural alterations, limited joint mobility, plantar calluses, and footwear. It also covers vascular phenomena where peak plantar pressures can obliterate blood flow and delay healing. The main risk factors for foot ulcers are identified as peripheral neuropathy, minor trauma, deformity, and edema. The document provides recommendations to prevent ulcers like careful foot examination, proper footwear, insoles, keeping feet clean and dry, and cutting toenails properly
The document provides guidance on managing neuropathic foot ulcers in diabetes patients. It recommends daily foot examination for issues like blisters and increased temperature. Treatment includes good glycemic control, managing infections and edema, and offloading pressure through total contact casts. Preventive measures involve regular inspection, education, and careful footwear choice to reduce amputation risk.
The document provides guidance on managing neuropathic foot ulcers in diabetes patients. It recommends daily foot examination for issues like blisters and increased temperature. Treatment includes good glycemic control, managing infections and edema, and offloading pressure through total contact casts. Preventive measures involve regular inspection, footwear choices, and patient education.
The document discusses diabetic foot problems and amputations. It notes that amputation is common, with one occurring every 10 minutes in India and 85% due to untreated or inadequately treated foot ulcers. While amputation seems to quickly address foot issues, it significantly increases mortality risk over time compared to saving the foot through conservative treatment. Amputation is also associated with higher long-term costs, decreased mobility, and loss of independence compared to foot salvage efforts. Overall, the document argues that preventing amputations through proper foot care and conservative treatment strategies has better long-term outcomes than amputation for diabetic foot problems and ulcers.
The document discusses considerations for proper footwear for patients with grade 1 diabetic foot disease. It emphasizes the importance of therapeutic footwear that accommodates, cushions, and stabilizes the foot to prevent ulcers. Key aspects of footwear design discussed include a rigid sole, broad and tough sole, low heel, soft and breathable uppers, and an insole that provides total contact with the foot. Proper fitting and regular inspection of footwear is also highlighted as important for preventing foot problems in diabetic patients.
This document discusses the etiology, pathogenesis, and management of diabetic foot ulcers. It covers methods of off-loading the foot like bedrest, crutches, and special footwear. It describes how small amounts of repeated force can cause skin penetration and ulcer formation over time. It also lists signs of worsening infection and the need for prompt treatment to prevent amputation and other complications. Primary treatments involve evaluation, metabolic control, debridement, off-loading, and corrective footwear.
1362465129 diabetic foot syndrome an indian perspectivedfsimedia
This document discusses diabetic foot syndrome from an Indian perspective. It covers topics such as the classification of diabetic foot types, clinical evaluation of high-risk feet, appropriate technology for diagnosis and management, and solutions for common problems in India. The author emphasizes that clinical evaluation is most important and recommends inspecting the feet of all diabetic patients. Affordable technologies for India include Doppler ultrasound to measure ankle-brachial index and tests of autonomic function like heart rate response to standing.
1362463849 derangement of wound healing in diabetic neuropathydfsimedia
This document discusses factors that impair wound healing in diabetes, including peripheral neuropathy, wound hypoxia, abnormal cellular pathways, excess inflammation, and deficient precursor cells. It then summarizes the results of a study on the role of inflammation in delayed wound healing of diabetic patients. The study found that matrix metalloproteinases MMP-9 and MMP-2, which degrade the extracellular matrix, were overexpressed in the tissue and serum of diabetic patients with infected foot ulcers compared to those without infection. This overexpression contributes to delayed wound healing.
- Major amputations should be considered as an option for all patients with diabetic foot disease from the outset. While local treatments aim to preserve the foot, many patients ultimately require amputation due to factors like poor circulation and previous failed treatments.
- The choice between a local amputation and major amputation depends on factors like the patient's age, circulation, mobility, expectations, and preferences. Younger patients with good circulation may be candidates for local treatments, though many will still require subsequent major amputations if local treatments fail.
- Major amputations have advantages like avoiding further surgery and allowing for shorter hospital stays and rehabilitation. However, they also carry disadvantages like reducing independence and being more difficult and expensive to rehabilitate from
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Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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1362571948 diab cranial auto neuropathy
1. Diabetic Cranial and Autonomic
Neuropathies
Clinical spectrum and Treatment
Sanjeev Kelkar
Medical Director
Novo Nordisk Education Foundation
Bangalore
India
2. Diabetic Neuropathy
General:
Incidence – 30 to 50%
Recent Diabcare Asia Statistics – 37%
Diabetic State is the trigger
Uncontrolled diabetes – worsening over time
Good control of diabetes - not the guarantee for –
cure, arrest, reversal
3. Diabetic Neuropathy: Schema
Cranial Neuropathies
Peripheral Neuropathies
Sensory, motor, mixed
Autonomic Neuropathies
Parasympathetic / Sympathetic
Sudomotor
Organ system related
Radiculo-myelopathies with or
without muscle involvement
4. Diabetic Cranial Neuropathies - 1
Isolate involvement known
Older individuals with long standing diabetes
May co-exist with other neuropathies
Groups affected:
Cranial Nerves III, IV & VI
Facial Nerve
Single / Multiple involvement associated with
serious infections
5. Diabetic Cranial Neuropathies - 2
Oculomotor Nerves III, IV and VI
Wide variations on incidence reported.
No hard data.
Gender ratio not reported.
Oculomotor Nerves:
Acute ipsilateral head ache
Refractory to analgesics
Diplopia, ptosis
Pupilary abnormalities +
6. Diabetic Cranial Neuropathies - 3
Pathogenesis:
Focal ischemia
Segmental demyelination
Aberrant remyelination as in any nerve regrowth
7. Diabetic Cranial Neuropathies - 3
Recovery over few days to few months
Recurrence in frequent
Aberrant regeneration uncommon
Laboratory, all cranial imaging and CSF – Normal
Treatment: Good diabetes control
Treatment for the neuropathy – Analgesia, Stop
smoking, vasodilators, omega fatty acids,
anticonvulsants, anti depressants, antioxidants
8. Diabetic Cranial Neuropathies - 4
Facial Neuropathy – Bell’s
Clinical unilateral weakness on the face, upper and
lower
Sensory symptoms in ear less often – pain and
hyperacusis
Gustatory disturbance variable
Complete paralysis supposedly more frequent in
diabetics
9. Diabetic Cranial Neuropathies - 5
Bell’s Palsy:
Treatment control DM
Steroid do not help, merely destabilizes control.
Exposure ketatopathy: Dry cornea due to DM?
Appropriate lubrication
Night taping
Marginal Tasorrhaphy in severe cases
Prognosis: Proportional to initial deficit
10. Diabetes Autonomic Neuropathy: 1
• Must always look for AN
• Development and its worsening to be tracked
• Important to explain –
– Organ system related symptoms
– Avoids unnecessary investigations,
– Help focused treatment
• Scientific explanations help patient reassurance,
relieves doubts
• Has prognostic / danger signal significance
11. Diabetes Autonomic Neuropathy: 2
Pupillary abnormalities:
• Clinically - small sized pupils
• Reduced light reflex - sympathetic dysfunction
• Severe reduction both PNS / SNS involved
12. Diabetes Autonomic Neuropathy: 3
Cardiovascular phenomena –
Sympathetic dysfunction
• Frequent in diabetics
• Responsible for morbidity and higher mortality
rates, can be early in diabetic life
• The balance between the PNS / SNS tones
affects several characteristics of cardiac
function.
• Sometimes PNS abnormalities progresses
simultaneously
13. Diabetes Autonomic Neuropathy: 4
Clinical clues to diagnosis:
Basal Tachycardia 90 – 120 / min.
PNS degeneration
SNS overtone
Basal Bradycardia
SNS dysfunction
(in patients not on cardiovascular drugs, with
heart failure, CHD or hypertension)
14. Diabetes Autonomic Neuropathy: 5
• Absence of beat to beat variations in
inspiration / expiration, change of posture,
stress and mild exercise suggest total
denervation of heart
• Postural hypotension:
Fall of 30/10 mm in supine blood pressure on
standing suggests sympathetic dysfunction
15. Diabetes Autonomic Neuropathy: 6
Cardiac Denervation explains:
Painless MI, vague thoracic abdominal
symptoms be suspect
Sudden cardiac death due to adrenergic super
sensitivity
Important to submit to TMT before putting on
exercises as cardiac output, vascular reflexes
affected
Minor stress variations required in daily life,
16. Diabetes Autonomic Neuropathy: 7
• Gastrointestinal Tract: Symptoms
• Prevalence is high
• Parasympathetic cause peristalsis
• Sympathetic cause sphincter tightening
• Symptoms depend on tonal integrity and
balance of PNS – SNS
• Dominant degeneration decides
• Both PNS / SNS could be involved
17. Diabetes Autonomic Neuropathy: 8
• Gastrointestinal tract – 2
• Gastroparesis – commonest, bloating,
discomfort, heart burn, vomiting
• Vagal denervation critical
• Motor dysfunction due to both ANS degeneration
likely
• Sensory perceptions from gut, increased first,
then bluuted
18. Diabetes Autonomic Neuropathy: 8
• Diabetic Diarrhea, explosive non infective,
painless, abnormal mucosal fluid absorption due
to loss of adrenergic nerve
• Sphincter laxity
• PNS tonal dominance
• Denervation hypersensitivity or loss of
sympathetic brake
19. Diabetes Autonomic Neuropathy: 9
• Gastrointestinal tract – 4
• Diabetic constipation
• Vagal denervation critical
• SNS overtone due to ↓ PNS tone, sphincteric
tightening
• Very common
• Laxative unresponsive
• Erythromycin, cisapride
20. Diabetes Autonomic Neuropathy: 11
• Gastrointestinal tract – 5
• Other mechanisms:
• Pancreatic, exocrine insufficiency
• Insulin deficiency – atrophy of acinar cells
• Reduced enzymatic & bicarbonate output
• Acute hyperglycemia delays gastric emptying if
ANS disturbance is present
21. Treatment Gastroparesis - 1
Restore hydration, electrolyte imbalance
Control hyperglycemia
IV / oral erythromycin
Cisapride orally 5 mg BD to 20 mg thrice – Patient
dependant, now withdrawn.
Enquire for excessive flatulence and frequent
bowel movement
Phenothiazines
22. Treatment Gastroparesis - 2
In severe forms –
Nasogastric decompression
I.V. fluids, correction in metabolic states, hypos,
Removal / disruptions of bezoars through
endoscopy
I.V. Erythromycin – 3 mg / kg body weight / 8 hrly
Oral Erythromycin 250 mg to 500 mg 4 times a day
23. Treatment Gastroparesis - 3
• Liquids initially
• Then blendorised meals, small, frequent ones
• Low fat, low fiber diets
• Paretic stomach also empties liquid,
homogenized meals, vitamins
• Affected is the distal trichurated action for solid
particles
• Jejunostomy feeding in unresponsive
gastroparesis,
• TPN in pan motility disorders
24. Treatment Gastroparesis - 4
Cisapride: Piperidinyl Benzamides Activates
serotonin type 4 receptors, stimulates Ach
relase, smooth muscle contraction.
Not blocked by atropine.
Hence other mechanisms likely
No antidopaminergic effects:
EPS, galactorrhoea, anxiety like metoclopromide
25. Treatment Gastroparesis - 5
Cisapride: No cholinomimetic effects outside gut,
thus better than bethanocol for bladder
frequency.
Dosage: Acute paresis l0 mg QID x 4 weeks
Chronic 10 – 20 mg TDS half hour before meals,
bed time.
Consistent moderate to good symptom relief
score. Excellent safety. No tolerance.
26. Erythromycin
• Inhibits metabolism of other drugs by inhibiting
P-450 cytochrome pathway.
• Should not be co-administered with –
• Cisapride, guanidine, lovastatin, nifedipine,
midazolam, carbomazepine etc.
• High dose – induces ventricular tachycardia
• Non antibiotic, prokinetic macrolides are in the
pipeline
27. Treatment Gastroparesis
Erythromycin:
• Stimulates motilin receptors due to structural
homology with it.
• Stimulates cholinergic mechanism.
• Activates calcium channel
• Raises intracellular calcium and thus
contraction.
• Absorption is formulation dependant
28. Treatment Gastroparesis
• Action Force – Dose dependant – 40 mg to 25
mg close contractions are strong but emptying
can be still poor.
• I.V. doses empty the stomach better with solids,
bezoars help push N.G. tubes in small bowel.
• Help develop migratory motor activity in the
lower bowel.
29. Erythromycin Doses
• IV 3 mg / kg body wt. 8 hrly generally 5 to 7 days
• Tachyphylaxis develops
• Then oral – 250 mg – 500 mg
• Long term efficacy doubted
• Abdominal cramping + ototoxicity in CRF
• Pseudomembranous colitis
30. Diabetes Autonomic Neuropathy: 11
• Sudomotor dysfunction:
(Abnormalities of sweating)
• Sympathetic fiber with cholinergic nerve ending
• Distal loss of sweating 65%
• Dry scaly cracked feet important
• Body segmental loss – 25%
• Single or multiple dermatomes sweat loss – 25%
31. Diabetes Autonomic Neuropathy: 12
• Sexual dysfunction : M : F
• Urinary dysfunction : M : F
• Both SNS PNS denervations common to
• Etiology diabetic
• Tremendous impact on diabetic patients life
• Urinary dysfunction late in realization in males
than sexual dysfunction
32. Diabetes Autonomic Neuropathy: 13
Male sexual dysfunction – 1
• Somatosensory input
– Dorsal nerve of penis
– Perineal nerve to CNS
• Autonomic Nerve supply cavernous nerve from
pelvic plexus, sends afferent impulses
• NO, Ach, VIP released
• Cavernous spaces relax and fill
33. Diabetes Autonomic Neuropathy: 14
Ejaculation:
• Emission – seminal fluid from male adnexa in
posterior urethra
• Needs contraction of the smooth muscles in
male adnexa - sympathetic hypo gastric nerve
innervates
• The same nerve closes bladder neck
• Ejaculation effected by bulbo cavernosus muscle
and perineal muscles – by pudendal branch
34. Diabetes Autonomic Neuropathy: 15
• Abnormalities of functions: Males:
• Impotence – diabetic neuropathy the single most
important cause
• Erectile dysfunction 30 – 59%
• Can be the presenting sign of diabetes
• Poor glucose control associated
• Β blockers, psychotropics, alcohol contribute
• Nocturnal penile tumescence serves as the
simplest, most direct clue
35. Diabetes Autonomic Neuropathy: 16
• Diabetic cystopathy – 1
• Progressive fall in sensations of bladder,
detrusor areflexia and progressively increasing
residual volume
• Seen more in Type I
• Autonomic neuropathy late
• Detrusor afferent abnormality early - common
36. Diabetes Autonomic Neuropathy: 17
• Cystopathy:
• Detrusor afferents do not carry sensation of
fullness to CNS
• Detrusor motor component from S3 – S4
through pelvic nerve not activated
• Bladder trigone and neck innervated by
sympathetic via hypogastric nerve [T11 – 12]
• S3 – S4 degeneration will cause emptying
difficulty
• Hypo gastric nerve damage - incontinence
37. Diabetes Autonomic Neuropathy: 18
• Female cystopathy –
• Additional complicating factors vesical prolapse
• Hypoestrogenised urogenital tract
• Will need surgical correction
• Will need hormone therapy
• Hormones help a great deal in urogenital
syndromes of PMS
38. Treatment of Autonomic Neuropathies - 1
General
• Good diabetes control
• Use of insulin when required earliest
• Smoking x x x
• Blocker drugs?
• Alcohol, overweight, inactivity, over exertion,
mental stresses, preoccupation
• Needs correction, review of one’s own life
39. Neuropathic (n) / Ischemic ulcer (i)
Site Pressure points (n)
Sides / tips of toes (i)
Pain --- ( n ) +++ ( i )
Callus ++ ( n ) --- ( i )
Pulse ++ ( n ) --- ( i )
ABI > 1( n ) < .6 ( i )
Healing ++ ( n ) --- ( i )
40. Autonomic neuropathy - 1
* Damages sympathetic innervation of lower limb
* This results in
Decreased sweating
Results in dry skin fissures / cracks
Super added infection
41. Autonomic neuropathy - 2
Opening of arteriovenous channels
Warm skin ( misleadingly healthy )
Shunting of nutrients and oxygen from
the tissues
Impaired vascular response to infection
45. Neuropathic joint or
Charcot’s arthropathy - 1
1868 French neurologist I.M. Charcot
First described in tabes
Can also be seen in leprosy, syringomyelia,
hereditary sensory neuropathy,
Charcot Marie Tooth disease etc
46. Neuropathic joint or
Charcot’s arthropathy - 2
Relatively rare
Potentially devastating disorder
Long standing diabetes
Dense peripheral neuropathy
Peripheral vascular disease is typically
absent
47. Neuropathic joint or
Charcot’s arthropathy - 1
Sympathetic failure-- increased blood
flow due to arteriovenous anastomosis
Bone demineralisation (diabetic
osteopenia)
Susceptibility to minor, recurrent fractures
49. Neuropathic joint or
Charcot’s arthropathy - 4
Painless disintegration of bone in response to
trivial trauma
Common joints involved are
– Tarso metatarsal
– Metatarso phalangeal
– Ankle joint
– Knee joint
51. Neuropathic joint or
Charcot’s arthropathy - 5
Acute Charcot’s arthropathy may mimic infection
Chronic Charcot’s foot is classically described as
‘bag of bones’
(Gross destruction of joint surfaces and bone with
effusion which is typically painless)
52. Neuropathic joint or
Charcot’s arthropathy - 6
Differentiation from osteomyelitis is difficult
* TC 99 Scan
* Indium labeled white cell scan
* MRI
53. Neuropathic joint or
Charcot’s arthropathy - 7
Early diagnosis and intervention are important to
prevent deformity and loss of function
Treatment includes
*Long term immobilization in plaster of Paris cast, (up to
even 1 year)
*Charcot’s Restraint Orthotic Walker (CROW) which
allows pressure to be off loaded
*Pamidronate - tried as a new treatment of Charcot’s
arthropathy