from Oklahoma State University
Determine Need for Rural Doctor
Videoconferencing Presentation
2008 Economics of Health Care TP
Non-Physician Clinicians in Workforce TP
Standards of Medical Care in Diabetes - 2008
Collection of free Downloadable Medical Videos,
Lecture Notes, Literature & PowerPoint Presentations
30 May 2009
Emergency Medicine Video Lectures and Slides
Emergency Medicine Video Lectures
from Oklahoma State University
from Oklahoma State University
- Stop, Look, and Listen: Assessment of Domestic Violence (370) Kathy Bell, R.N.
- ED Management of Epistaxis (374) Tom Hamilton, D.O.
- Geriatric Trauma (370) Michele Fowler, D.O.
- Hand and Wrist Injuries (371) Brent Nossaman, D.O.
- Treatment of Hypertension in the ER (373) Richard Blubaugh, D.O.
- Managing the Burn Victim (372) Billy Bryan, D.O.
- Stroke Complications (375) Harvey Drapkin, D.O.
Emergency Medicine Video Lectures
Emergency Medicine Video Lectures
from Oklahoma State University
from Oklahoma State University
- Burn and Inhalation Injury by Dr. Billy Bryan, D.O. - Part 1
- Burn and Inhalation Injury by Dr. Billy Bryan, D.O. - Part 2
- Airway Control and the Trama Patient by Dr. Jimmy Morgan, D.O. - Part 1
- Airway Control and the Trama Patient by Dr. Jimmy Morgan, D.O. - Part 2
- Occular Emergency by Dr. Anthony Economou, D.O.
- Te Rapid Neurologic Exam in the Emergency Department by John T. Main, D.O.
- Recognition and Documentation of Injuries by Ronald F. Distefano, D.O.
- Coping with a Tramatic Event - Mass Casualties by Dr. Billy Bryan, D.O.
29 May 2009
Heart Rhythm Abnormalities video(Part 2)
Heart Rhythm Abnormalities video(Part 2)
Millions of people have irregular heart rhythms, also called arrhythmias. Their hearts either beat too fast or too slow. These problems can be benign or they can also signal a life-threatening condition--sudden cardiac death-which is the number-one cause of death in the U.S. This program covers different kinds of heart rhythm problems and treatments.
Part Two:
Medical treatments for arrhythmias
Cardiac ablation-how it works
Different types of ablation
PET/CT cardiac imaging
Many are unaware of arrhythmias
Guest:
Dr. Stephen Shorofsky, a cardiologist and director of cardiac electrophysiology at the University of Maryland Medical Center. Dr. Shorofsky is also a professor of medicine at the University of Maryland School of Medicine.
Millions of people have irregular heart rhythms, also called arrhythmias. Their hearts either beat too fast or too slow. These problems can be benign or they can also signal a life-threatening condition--sudden cardiac death-which is the number-one cause of death in the U.S. This program covers different kinds of heart rhythm problems and treatments.
Part Two:
Medical treatments for arrhythmias
Cardiac ablation-how it works
Different types of ablation
PET/CT cardiac imaging
Many are unaware of arrhythmias
Guest:
Dr. Stephen Shorofsky, a cardiologist and director of cardiac electrophysiology at the University of Maryland Medical Center. Dr. Shorofsky is also a professor of medicine at the University of Maryland School of Medicine.
Heart Rhythm Abnormalities video(Part 1)
Heart Rhythm Abnormalities video(Part 1)
Millions of people have irregular heart rhythms, also called arrhythmias. Their hearts either beat too fast or too slow. These problems can be benign or they can also signal a life-threatening condition--sudden cardiac death-which is the number-one cause of death in the U.S. This program covers different kinds of heart rhythm problems and treatments.
Part One:
Irregular heart rhythms
Causes of arrhythmias
Symptoms of arrhythmia
Testing for arrhythmia - ECG/EKG
Sudden cardiac death
Implanted defibrillators
Pacemakers
Guest:
Dr. Stephen Shorofsky, a cardiologist and director of cardiac electrophysiology at the University of Maryland Medical Center. Dr. Shorofsky is also a professor of medicine at the University of Maryland School of Medicine.
Millions of people have irregular heart rhythms, also called arrhythmias. Their hearts either beat too fast or too slow. These problems can be benign or they can also signal a life-threatening condition--sudden cardiac death-which is the number-one cause of death in the U.S. This program covers different kinds of heart rhythm problems and treatments.
Part One:
Irregular heart rhythms
Causes of arrhythmias
Symptoms of arrhythmia
Testing for arrhythmia - ECG/EKG
Sudden cardiac death
Implanted defibrillators
Pacemakers
Guest:
Dr. Stephen Shorofsky, a cardiologist and director of cardiac electrophysiology at the University of Maryland Medical Center. Dr. Shorofsky is also a professor of medicine at the University of Maryland School of Medicine.
Heart Failure Advances video(Part 2)
Heart Failure Advances video(Part 2)
About 5 million Americans are living with heart failure, a chronic condition that is the leading cause of hospitalization for people over age 65. There has been a lot of progress in understanding and treating heart failure in recent years, and the latest advances are discussed in this interview.
Part Two:
Range of heart failure severity
Fluid retention/weight monitoring
Beta Blocker medications
Ace Inhibitor medicines
Diuretics
Heart pumps
Guest:
Dr. Mandeep Mehra, the head of cardiology at the University of Maryland Medical Center. Dr. Mehra is also a professor of medicine and head of the division of cardiology at the University of Maryland School of Medicine
About 5 million Americans are living with heart failure, a chronic condition that is the leading cause of hospitalization for people over age 65. There has been a lot of progress in understanding and treating heart failure in recent years, and the latest advances are discussed in this interview.
Part Two:
Range of heart failure severity
Fluid retention/weight monitoring
Beta Blocker medications
Ace Inhibitor medicines
Diuretics
Heart pumps
Guest:
Dr. Mandeep Mehra, the head of cardiology at the University of Maryland Medical Center. Dr. Mehra is also a professor of medicine and head of the division of cardiology at the University of Maryland School of Medicine
Heart Failure Advances video(Part 1)
Heart Failure Advances video(Part 1)
About 5 million Americans are living with heart failure, a chronic condition that is the leading cause of hospitalization for people over age 65. There has been a lot of progress in understanding and treating heart failure in recent years, and the latest advances are discussed in this interview.
Part One:
Definition of heart failure
Symptoms
Diagnosis
Risk factors
Guest:
Dr. Mandeep Mehra, the head of cardiology at the University of Maryland Medical Center. Dr. Mehra is also a professor of medicine and head of the division of cardiology at the University of Maryland School of Medicine
About 5 million Americans are living with heart failure, a chronic condition that is the leading cause of hospitalization for people over age 65. There has been a lot of progress in understanding and treating heart failure in recent years, and the latest advances are discussed in this interview.
Part One:
Definition of heart failure
Symptoms
Diagnosis
Risk factors
Guest:
Dr. Mandeep Mehra, the head of cardiology at the University of Maryland Medical Center. Dr. Mehra is also a professor of medicine and head of the division of cardiology at the University of Maryland School of Medicine
Parkinson's Disease Guidelines video(Part 1)
Parkinson's Disease Guidelines video(Part 1)
Experts in Parkinson's disease have revised the guidelines for diagnosing and treating the disease in order to help people receive the best care. In this program, the Parkinson's disease specialist who was lead author of the guidelines explains what changes were made and why, along with the latest information about Parkinson's disease.
Part One:
Parkinson's symptoms
Diagnosing Parkinson's disease
Progression of Parkinson's disease
Medications - Levodopa
Drugs for motor fluctuations
Guest:
Dr. William Weiner, chief of neurology at the University of Maryland Medical Center where he directs the Parkinson's Disease and Movement Disorders Center. Dr. Weiner is also professor and chairman of Neurology at the University of Maryland School of Medicine.
Experts in Parkinson's disease have revised the guidelines for diagnosing and treating the disease in order to help people receive the best care. In this program, the Parkinson's disease specialist who was lead author of the guidelines explains what changes were made and why, along with the latest information about Parkinson's disease.
Part One:
Parkinson's symptoms
Diagnosing Parkinson's disease
Progression of Parkinson's disease
Medications - Levodopa
Drugs for motor fluctuations
Guest:
Dr. William Weiner, chief of neurology at the University of Maryland Medical Center where he directs the Parkinson's Disease and Movement Disorders Center. Dr. Weiner is also professor and chairman of Neurology at the University of Maryland School of Medicine.
Parkinson's Disease Guidelines video(Part 2)
Parkinson's Disease Guidelines video(Part 2)
Experts in Parkinson's disease have revised the guidelines for diagnosing and treating the disease in order to help people receive the best care. In this program, the Parkinson's disease specialist who was lead author of the guidelines explains what changes were made and why, along with the latest information about Parkinson's disease.
Part Two:
Deep brain stimulation
Complementary therapies
Benefits of exercise
Physical / speech therapy
Emotional effects of Parkinson's disease
Depression / anxiety
Mental / cognitive changes
Clinical trials
Future research - stem cells
Guest:
Dr. William Weiner, chief of neurology at the University of Maryland Medical Center where he directs the Parkinson's Disease and Movement Disorders Center. Dr. Weiner is also professor and chairman of Neurology at the University of Maryland School of Medicine.
Experts in Parkinson's disease have revised the guidelines for diagnosing and treating the disease in order to help people receive the best care. In this program, the Parkinson's disease specialist who was lead author of the guidelines explains what changes were made and why, along with the latest information about Parkinson's disease.
Part Two:
Deep brain stimulation
Complementary therapies
Benefits of exercise
Physical / speech therapy
Emotional effects of Parkinson's disease
Depression / anxiety
Mental / cognitive changes
Clinical trials
Future research - stem cells
Guest:
Dr. William Weiner, chief of neurology at the University of Maryland Medical Center where he directs the Parkinson's Disease and Movement Disorders Center. Dr. Weiner is also professor and chairman of Neurology at the University of Maryland School of Medicine.
Surgery for Lung Cancer video (Part 2)
Surgery for Lung Cancer (Part 2)
More than 85 percent of lung cancer cases are smoking-related. In this interview, we hear from a chest surgeon who specializes in treating lung and esophageal cancer about the trends in smoking in the United States. The interview also covers lung cancer, including how it develops and how it is treated.
Part Two:
Diagnosing lung cancer
Types of lung cancer
Lung cancer symptoms
Staging
Lobectomy
Recurrence Rate
Dr. Richard Battafarano, head of thoracic surgery at the University of Maryland Medical Center. Dr. Battafarano is also an associate professor of surgery at the University of Maryland School of Medicine.
More than 85 percent of lung cancer cases are smoking-related. In this interview, we hear from a chest surgeon who specializes in treating lung and esophageal cancer about the trends in smoking in the United States. The interview also covers lung cancer, including how it develops and how it is treated.
Part Two:
Diagnosing lung cancer
Types of lung cancer
Lung cancer symptoms
Staging
Lobectomy
Recurrence Rate
Dr. Richard Battafarano, head of thoracic surgery at the University of Maryland Medical Center. Dr. Battafarano is also an associate professor of surgery at the University of Maryland School of Medicine.
Surgery for Lung Cancer video (Part 1)
Surgery for Lung Cancer (Part 1)
More than 85 percent of lung cancer cases are smoking-related. In this interview, we hear from a chest surgeon who specializes in treating lung and esophageal cancer about the trends in smoking in the United States. The interview also covers lung cancer, including how it develops and how it is treated.
Part One:
Cancer death rates
Trends in smoking
Lung cancer
Pack years
Second hand smoke
Dr. Richard Battafarano, head of thoracic surgery at the University of Maryland Medical Center. Dr. Battafarano is also an associate professor of surgery at the University of Maryland School of Medicine.
View here
More than 85 percent of lung cancer cases are smoking-related. In this interview, we hear from a chest surgeon who specializes in treating lung and esophageal cancer about the trends in smoking in the United States. The interview also covers lung cancer, including how it develops and how it is treated.
Part One:
Cancer death rates
Trends in smoking
Lung cancer
Pack years
Second hand smoke
Dr. Richard Battafarano, head of thoracic surgery at the University of Maryland Medical Center. Dr. Battafarano is also an associate professor of surgery at the University of Maryland School of Medicine.
View here
Uterine Fibroid Embolism Video-2
Uterine Fibroid Embolism and Interventional Radiology (Part 2)
Radiologists are known for looking inside the body to diagnose health problems. And now, many of these same doctors now use advanced
imaging equipment, not just to diagnose, but also to treat a wide range of problems. In this program, you'll learn how interventional
radiologists use minimally invasive techniques to help people with many conditions, including uterine fibroids and cancer.
Part Two:
Uterine fibroids - what are they?
Uterine fibroid symptoms
Uterine fibroid embolization
Treating pelvic pain
Guest:
Dr. Howard Richard, an interventional radiologist at the University of Maryland Medical Center. Dr. Richard is also an assistant professor of diagnostic radiology at the University of Maryland School of Medicine
Radiologists are known for looking inside the body to diagnose health problems. And now, many of these same doctors now use advanced
imaging equipment, not just to diagnose, but also to treat a wide range of problems. In this program, you'll learn how interventional
radiologists use minimally invasive techniques to help people with many conditions, including uterine fibroids and cancer.
Part Two:
Uterine fibroids - what are they?
Uterine fibroid symptoms
Uterine fibroid embolization
Treating pelvic pain
Guest:
Dr. Howard Richard, an interventional radiologist at the University of Maryland Medical Center. Dr. Richard is also an assistant professor of diagnostic radiology at the University of Maryland School of Medicine
Uterine Fibroid Embolism Video-1
Uterine Fibroid Embolism and Interventional Radiology (Part 1)
Radiologists are known for looking inside the body to diagnose health problems. And now, many of these same doctors now use advanced
imaging equipment, not just to diagnose, but also to treat a wide range of problems. In this program, you'll learn how interventional
radiologists use minimally invasive techniques to help people with many conditions, including uterine fibroids and cancer.
Part One:
What is interventional radiology (IR)?
Technological advances to see inside the body
Overview of conditions that can be treated with IR
SIR-Spheres treatment for liver cancer
Radio frequency ablation for tumors
Guest:
Dr. Howard Richard, an interventional radiologist at the University of Maryland Medical Center. Dr. Richard is also an assistant professor of diagnostic radiology at the University of Maryland School of Medicine
Radiologists are known for looking inside the body to diagnose health problems. And now, many of these same doctors now use advanced
imaging equipment, not just to diagnose, but also to treat a wide range of problems. In this program, you'll learn how interventional
radiologists use minimally invasive techniques to help people with many conditions, including uterine fibroids and cancer.
Part One:
What is interventional radiology (IR)?
Technological advances to see inside the body
Overview of conditions that can be treated with IR
SIR-Spheres treatment for liver cancer
Radio frequency ablation for tumors
Guest:
Dr. Howard Richard, an interventional radiologist at the University of Maryland Medical Center. Dr. Richard is also an assistant professor of diagnostic radiology at the University of Maryland School of Medicine
Neurobiology of Fear, Anxiety and Extinction video
Neurobiology of Fear, Anxiety and Extinction: Implications for Psychotherapy
by:Dr. Michael Davis, Video from MIT
About the Lecture
Few scientists have charted the grim territory of fear and anxiety with the same doggedness and precision as Michael Davis.
Nearly four decades ago, researchers learned that animals, including humans, startle more when fearful. A sudden noise in a dark, creepy alley provokes a greater reaction than in a well-lit room, for instance. That got Davis and his colleagues wondering what neural mechanisms underlie the startle reflex, and how fear plays a part in the response.
In his talk, Davis describes the meticulous experiments he and others have conducted over many years. Starting with the fear potentiated startle test -- where animals are trained to pair a stimulus such as light, or sound, with a shock -- researchers began to track the pathways that mediate the response in the nervous system. Using chemical tracers that could follow electrical activity in the brain, Davis found a group of cells in the central nucleus of the amygdala that are critical for fear conditioning. “It was a nice day in the laboratory,” he says. When he knocked out this part of the amygdala with drugs or a lesion, it selectively decreased fear potentiated startle.
by:Dr. Michael Davis, Video from MIT
About the Lecture
Few scientists have charted the grim territory of fear and anxiety with the same doggedness and precision as Michael Davis.
Nearly four decades ago, researchers learned that animals, including humans, startle more when fearful. A sudden noise in a dark, creepy alley provokes a greater reaction than in a well-lit room, for instance. That got Davis and his colleagues wondering what neural mechanisms underlie the startle reflex, and how fear plays a part in the response.
In his talk, Davis describes the meticulous experiments he and others have conducted over many years. Starting with the fear potentiated startle test -- where animals are trained to pair a stimulus such as light, or sound, with a shock -- researchers began to track the pathways that mediate the response in the nervous system. Using chemical tracers that could follow electrical activity in the brain, Davis found a group of cells in the central nucleus of the amygdala that are critical for fear conditioning. “It was a nice day in the laboratory,” he says. When he knocked out this part of the amygdala with drugs or a lesion, it selectively decreased fear potentiated startle.
Kanas University Video Lecture Library part2
Kanas University Video Lecture Library part2
Liver Transplantation Part A
J. Kinscher, MD
Monitoring Part A | Part B
T. Davis, CRNA, 2000
Monitored Anesthesia Care Part A
H. Mathewson, MD, 2001
Neurosurgical Anesthesia Part A
H. Mathewson, MD, 2001
Pain Management / Regional Blocks 1
Part A | Part B | Part C | Part D | Part E
H. Mathewson, MD, 2000
Positioning Part A | Part B
C. Weber CRNA, 2001
Preoperative Evaluation Part A | Part B | Part C
M. Hutchinson, MD, 2001
Obstretrics I Part A | Part B
G. Shih, MD, 2001
Obstetrics II Part A | Part B
P. Steer, MD, 2000
Otorhinolaryngology Part A | Part B
G Unruh, MD, 2001
Pediatric Anesthesia I Part A
R. Torline, MD, 2001
Pediatric Anesthesia II Part A | Part B
T Davis, CRNA, 2000
Pulmonary Disease Part A | Part B
H. Mathewson, MD, 2002
Regional Anesthesia / Spinal Part A | Part B
H. Mathewson, MD, 2001
Respiratory Function & Anesthesia Part A
H. Mathewson, MD, 2001
Trauma Part A | Part B
H. Mathewson, MD, 2001
Thoracic Anesthesia Part A | Part B
H. Mathewson, MD, 2001
Vascular Surgery Part A | Part B
H. Mathewson, MD
All videos are copyright 2006 by the University of Kansas and may not be duplicated, displayed, broadcast or otherwise used without permission.
Liver Transplantation Part A
J. Kinscher, MD
Monitoring Part A | Part B
T. Davis, CRNA, 2000
Monitored Anesthesia Care Part A
H. Mathewson, MD, 2001
Neurosurgical Anesthesia Part A
H. Mathewson, MD, 2001
Pain Management / Regional Blocks 1
Part A | Part B | Part C | Part D | Part E
H. Mathewson, MD, 2000
Positioning Part A | Part B
C. Weber CRNA, 2001
Preoperative Evaluation Part A | Part B | Part C
M. Hutchinson, MD, 2001
Obstretrics I Part A | Part B
G. Shih, MD, 2001
Obstetrics II Part A | Part B
P. Steer, MD, 2000
Otorhinolaryngology Part A | Part B
G Unruh, MD, 2001
Pediatric Anesthesia I Part A
R. Torline, MD, 2001
Pediatric Anesthesia II Part A | Part B
T Davis, CRNA, 2000
Pulmonary Disease Part A | Part B
H. Mathewson, MD, 2002
Regional Anesthesia / Spinal Part A | Part B
H. Mathewson, MD, 2001
Respiratory Function & Anesthesia Part A
H. Mathewson, MD, 2001
Trauma Part A | Part B
H. Mathewson, MD, 2001
Thoracic Anesthesia Part A | Part B
H. Mathewson, MD, 2001
Vascular Surgery Part A | Part B
H. Mathewson, MD
All videos are copyright 2006 by the University of Kansas and may not be duplicated, displayed, broadcast or otherwise used without permission.
Kanas University Video Lecture Library part1
Kanas University Video Lecture Library
Acid-Base & Electrolyte Balance Part A
H. Mathewson, MD, 2001
Acid-Base Balance Part A | Part B
T. Davis, CRNA, 2000
Acute/Chronic Pain Part A (acute) | Part B (chronic)
Principles of Acute Pain Mgmt
Special Considerations - Chronic Pain
Twillman, PhD
Burns and Anesthesia Part A | Part B
C. Elliott, CRNA, PhD, 2000
Cardiothoracic Surgery & Anesthesia Part A | Part B
Peter Hild, MD
Cardiovascular Disorders Part A | Part B
H. Mathewson, MD, 2002
Cardiovascular Anesthesia I Part A | Part B | Part C
H. Mathewson, MD, 2001
Cardiovascular Anesthesia II Part A | Part B
H. Mathewson, MD, 2001
Cardiovascular Anesthesia - Cardiac Abnormalities/Arhythmias Part A | Part B
H. Mathewson, MD, 2002
Dilemmas & Controversies in Intubation Part A Part B
A. Kovac, MD
Ear, Nose & Throat Anesthesia Part A | Part B
G. Unruh, MD
Electrocardiology Part A | Part B
H. Mathewson, MD, 2000
Fluids and Electrolytes Part A | Part B
T Davis, CRNA, 2000
Genitourinary Part A | Part B
H. Mathewson, MD, 2001
Hemostasis Part A | Part B | Part C
J. Kinscher, MD, 2000
HIV/Infection Control Part 1
S. Shaffer RN, MSN, 2000
HIV Part 2
C. Elliott, CRNA, PhD
Laser Safety in the Operating Room Part A | Part B
G. Unruh, MD
All videos are copyright 2006 by the University of Kansas and may not be duplicated, displayed, broadcast or otherwise used without permission.
Acid-Base & Electrolyte Balance Part A
H. Mathewson, MD, 2001
Acid-Base Balance Part A | Part B
T. Davis, CRNA, 2000
Acute/Chronic Pain Part A (acute) | Part B (chronic)
Principles of Acute Pain Mgmt
Special Considerations - Chronic Pain
Twillman, PhD
Burns and Anesthesia Part A | Part B
C. Elliott, CRNA, PhD, 2000
Cardiothoracic Surgery & Anesthesia Part A | Part B
Peter Hild, MD
Cardiovascular Disorders Part A | Part B
H. Mathewson, MD, 2002
Cardiovascular Anesthesia I Part A | Part B | Part C
H. Mathewson, MD, 2001
Cardiovascular Anesthesia II Part A | Part B
H. Mathewson, MD, 2001
Cardiovascular Anesthesia - Cardiac Abnormalities/Arhythmias Part A | Part B
H. Mathewson, MD, 2002
Dilemmas & Controversies in Intubation Part A Part B
A. Kovac, MD
Ear, Nose & Throat Anesthesia Part A | Part B
G. Unruh, MD
Electrocardiology Part A | Part B
H. Mathewson, MD, 2000
Fluids and Electrolytes Part A | Part B
T Davis, CRNA, 2000
Genitourinary Part A | Part B
H. Mathewson, MD, 2001
Hemostasis Part A | Part B | Part C
J. Kinscher, MD, 2000
HIV/Infection Control Part 1
S. Shaffer RN, MSN, 2000
HIV Part 2
C. Elliott, CRNA, PhD
Laser Safety in the Operating Room Part A | Part B
G. Unruh, MD
All videos are copyright 2006 by the University of Kansas and may not be duplicated, displayed, broadcast or otherwise used without permission.
PREVENTIVE GERIATRICS
PREVENTIVE GERIATRICS
Dr.I.Selvaraj,I.R.M.S
B.Sc., M.B.B.S.,(M.D Community medicine).,
D.P.H.,D.I.H.,P.G.C.H&FW (NIHFW, New Delhi)
Sr.D.M.O (Selection Grade Officer)
INDIAN RAILWAYS MEDICAL SERVICE
It is the art and science of preventing disease in the geriatric population and promoting their health and efficiency
* Hippocrates noted conditions common in later life
* Aristotle offered theory of ageing based on loss of heat
* The word geriatrics was invented by Ignatz L. Nascher, a vienna born immigrant to the united states
* Geriatric medicine was a product of the British NHS
* Nascher was the father of geriatrics and Majory Warren was its Mother
* The 1st Geriatric service was started in U.K in 1947.
* Geriatric department at GH, Chennai was established in 1978.
* Post Graduate course in Geriatric medicine has been started in 1996 at Madras medical college.
* Prof. V.S. Natarajan was the first Geriatric professor in India
* The study of physical and psychological changes that occur in old age is called “gerontology”.
* Geriatrics is the branch of general medicine concerned with clinical, preventive, medical and social aspects of illness in the elderly.
* The old age is defined as the age of retirement. In our country it is fixed at 60 years and above.
Present scenario in INDIA
* Cataract &Visual impairment- 88%
* Arthritis &locomotion disorder-40%
* CVD &HT – 18%
* Neurological problems- 18%
* Respiratory problems including Chronic bronchitis- 16%
* GIT problems- 9%
* Psychiatric problems- 9%
* Loss of Hearing – 8%
Theory of aging
* Somatic mutation theory
* Autoimmune theory
* Hayflick’s theory of aging
Geriatrics
* Senility
* Decline in sexual prowess
* Diminution in endocrine activity
* Loss of elasticity of blood vessels
* Rise in B.P
RISK OF GERIATRICS
* PRONE FOR INFECTIONS
* PRONE FOR INJURIES
* NEED SPECIAL ASSISTANCE
* PRONE FOR PSYCHOLOGICAL PROBLEMS
* PRONE FOR DEGENERATIVE DISORDERS
* INCREASED RISK FOR DISEASE
* INCREASED RISK OF DISABILITY
* INCRASED RISK OF DEATH
AIM OF GERIATRIC MEDICINE
* Maintenance of health in old age by high levels of engagement and avoidance of disease
* Early detection and appropriate treatment of disease
* Maintenance of maximum independence consistent with irreversible disease and disability
* Sympathetic care and support during terminal illness
GERIATRIC PEOPLE PROBLEMS
* HEALTH PROBLEMS
1.Joint problems
2.Impairment of special senses
3. Cardio vascular disease
4.Hypothermia
5.Cancer, Prostate enlargement, Diabetes& Accidental falls
* Psychological problems
1. Emotional problems
2. Suicidal tendency
3. Senile dementia, Alzheimer’disease
* Social problems
* Poverty, Loneliness, Dependency, Isolation, Elder abuse, Generation Gap
GERIATRIC TEAM
* Geriatricians
* Nurses
* Physiotherapist
* Social worker
* And Health worker
* Investigation is an essential tool in the diagnosis of elderly patients.
* Under or over investigations to be avoided.
* Know the age related variables while interpreting the results.
* Non-invasive tests are preferred than invasive.
* The objective of the investigations is to improve the quality of life.
* One must try to get the diagnosis right, as wrong diagnosis is harbinger of wrong treatment
* Polypharmacy should be avoided whenever possible
* Regular review of medication is a must
* Poor drug compliance could be due to poor advice
* Proper nutrition is vital for healthy living
* A well balanced nutritious diet is ideal for older age
* It is not the quantity but the quality
Indicators of health status of aged
* Age proportional mortality rate
* Age specific death rate persons over 55 years
* Age specific prevalence rates for cvd, cancers and accidents.
* % elders taking three or more drugs/day
* Cumulative percentage of elders undergone cataract surgery
* Proportion of elders admitted to the hospital in the past one year
PREVENTION
* Primordial prevention
* Pre geriatric care
* Primary prevention
* Health education
* Exercise
* Secondary prevention
* Annual medical check-up
* Early detection ( Universal approach, Selective approach)
* Treatment
* Tertiary prevention
* Counseling and Rehabilitation
* Welfare activities (Sanjay Niradhar Yojana, Vridhashrama)
* Chiropody services
* Improving quality of life
* Cultural programme
* Old age club
* Meals-on wheel service
* Home help
* Old age home
PREVENTIVE GERIATRICS.ppt
Dr.I.Selvaraj,I.R.M.S
B.Sc., M.B.B.S.,(M.D Community medicine).,
D.P.H.,D.I.H.,P.G.C.H&FW (NIHFW, New Delhi)
Sr.D.M.O (Selection Grade Officer)
INDIAN RAILWAYS MEDICAL SERVICE
It is the art and science of preventing disease in the geriatric population and promoting their health and efficiency
* Hippocrates noted conditions common in later life
* Aristotle offered theory of ageing based on loss of heat
* The word geriatrics was invented by Ignatz L. Nascher, a vienna born immigrant to the united states
* Geriatric medicine was a product of the British NHS
* Nascher was the father of geriatrics and Majory Warren was its Mother
* The 1st Geriatric service was started in U.K in 1947.
* Geriatric department at GH, Chennai was established in 1978.
* Post Graduate course in Geriatric medicine has been started in 1996 at Madras medical college.
* Prof. V.S. Natarajan was the first Geriatric professor in India
* The study of physical and psychological changes that occur in old age is called “gerontology”.
* Geriatrics is the branch of general medicine concerned with clinical, preventive, medical and social aspects of illness in the elderly.
* The old age is defined as the age of retirement. In our country it is fixed at 60 years and above.
Present scenario in INDIA
* Cataract &Visual impairment- 88%
* Arthritis &locomotion disorder-40%
* CVD &HT – 18%
* Neurological problems- 18%
* Respiratory problems including Chronic bronchitis- 16%
* GIT problems- 9%
* Psychiatric problems- 9%
* Loss of Hearing – 8%
Theory of aging
* Somatic mutation theory
* Autoimmune theory
* Hayflick’s theory of aging
Geriatrics
* Senility
* Decline in sexual prowess
* Diminution in endocrine activity
* Loss of elasticity of blood vessels
* Rise in B.P
RISK OF GERIATRICS
* PRONE FOR INFECTIONS
* PRONE FOR INJURIES
* NEED SPECIAL ASSISTANCE
* PRONE FOR PSYCHOLOGICAL PROBLEMS
* PRONE FOR DEGENERATIVE DISORDERS
* INCREASED RISK FOR DISEASE
* INCREASED RISK OF DISABILITY
* INCRASED RISK OF DEATH
AIM OF GERIATRIC MEDICINE
* Maintenance of health in old age by high levels of engagement and avoidance of disease
* Early detection and appropriate treatment of disease
* Maintenance of maximum independence consistent with irreversible disease and disability
* Sympathetic care and support during terminal illness
GERIATRIC PEOPLE PROBLEMS
* HEALTH PROBLEMS
1.Joint problems
2.Impairment of special senses
3. Cardio vascular disease
4.Hypothermia
5.Cancer, Prostate enlargement, Diabetes& Accidental falls
* Psychological problems
1. Emotional problems
2. Suicidal tendency
3. Senile dementia, Alzheimer’disease
* Social problems
* Poverty, Loneliness, Dependency, Isolation, Elder abuse, Generation Gap
GERIATRIC TEAM
* Geriatricians
* Nurses
* Physiotherapist
* Social worker
* And Health worker
* Investigation is an essential tool in the diagnosis of elderly patients.
* Under or over investigations to be avoided.
* Know the age related variables while interpreting the results.
* Non-invasive tests are preferred than invasive.
* The objective of the investigations is to improve the quality of life.
* One must try to get the diagnosis right, as wrong diagnosis is harbinger of wrong treatment
* Polypharmacy should be avoided whenever possible
* Regular review of medication is a must
* Poor drug compliance could be due to poor advice
* Proper nutrition is vital for healthy living
* A well balanced nutritious diet is ideal for older age
* It is not the quantity but the quality
Indicators of health status of aged
* Age proportional mortality rate
* Age specific death rate persons over 55 years
* Age specific prevalence rates for cvd, cancers and accidents.
* % elders taking three or more drugs/day
* Cumulative percentage of elders undergone cataract surgery
* Proportion of elders admitted to the hospital in the past one year
PREVENTION
* Primordial prevention
* Pre geriatric care
* Primary prevention
* Health education
* Exercise
* Secondary prevention
* Annual medical check-up
* Early detection ( Universal approach, Selective approach)
* Treatment
* Tertiary prevention
* Counseling and Rehabilitation
* Welfare activities (Sanjay Niradhar Yojana, Vridhashrama)
* Chiropody services
* Improving quality of life
* Cultural programme
* Old age club
* Meals-on wheel service
* Home help
* Old age home
PREVENTIVE GERIATRICS.ppt
28 May 2009
MusculoSkeletal Imaging Teaching Files Part2
Musculoskeletal Case Forty One - Aneurysmal Bone Cyst
Musculoskeletal Case Forty Two - Pulmonary Osteoarthropathy
Musculoskeletal Case Forty Three - Melorheostosis
Musculoskeletal Case Forty Four - Brown Tumors Secondary to Hyperparathyroidism
Musculoskeletal Case Forty Five - Frostbite
Musculoskeletal Case Forty Six - Erosive Osteoarthritis
Musculoskeletal Case Forty Seven - Disuse Osteoporosis
Musculoskeletal Case Forty Eight - Scleroderma
Musculoskeletal Case Forty Nine - Articular Muscle of the Knee
Musculoskeletal Case Fifty - Sacral Stress Fracture
Musculoskeletal Case Fifty One - Condensing Osteitis
Musculoskeletal Case Fifty Two - Bucket Handle Tear of Lateral Meniscus
Musculoskeletal Case Fifty Three - Scleroderma with acroosteolysis
Musculoskeletal Case Fifty Four - Fluid in the Medial Collateral Ligament Bursa
Musculoskeletal Case Fifty Five - Partial Rupture of Tendon on Radial Tuberosity
Musculoskeletal Case Fifty Six - Synovial Osteochondramatosis
Musculoskeletal Case Fifty Seven - Unilateral Locked Facet
Musculoskeletal Case Fifty Eight - Ankylosing Spondylitis
Musculoskeletal Case Fifty Nine - Supracondylar Process of the Humerus
Musculoskeletal Case Sixty - Linear & Non displaced Fracture of Radial Head
Musculoskeletal Case Sixty One - Neurofibroma
Musculoskeletal Case Sixty Two - Lunatriquetral Coalition
Musculoskeletal Case Sixty Three - Dorsal Trans-radial Styloid Perilunate Dislocation
Musculoskeletal Case Sixty Four - Fibroxanthoma
Musculoskeletal Case Sixty Five - Secondary Hyperparathyroidism
Musculoskeletal Case Sixty Six - Transient Lateral Patellar Dislocation
Musculoskeletal Case Sixty Seven - Volar Intercalated Segmental Instability (VISI)
Musculoskeletal Case Sixty Eight - Calcaneal Cyst
Musculoskeletal Case Sixty Nine - Infection of Intervertebral Disc Cages
Musculoskeletal Case Seventy - Pelligrini - Stieda Disease
Musculoskeletal Case Seventy One - Bone Infarct
Musculoskeletal Case Seventy Two - Lymphoma
Musculoskeletal Case Seventy Three - Lisfranc Fracture / Dislocation of Foot
Musculoskeletal Case Seventy Four - Fracture through Solitary Bone Cyst
Musculoskeletal Case Seventy Five - Chondrosarcoma
Musculoskeletal Case Seventy Six - Posterior Dislocation with Impaction Fracture of the Humeral Head
Musculoskeletal Case Seventy Seven - Complete Rupture of the Hamstring Tendons
Musculoskeletal Case Seventy Eight - Aneurysmal Bone Cyst
Musculoskeletal Case Seventy Nine - Bilateral Subcapital Femoral Epiphyses
Musculoskeletal Case Eighty - Meniscal Ossicle
Musculoskeletal Case Eighty One - Lateral Patellar Dislocation
Musculoskeletal Case Eighty Two- Tear of Anterior Cruciate Ligament
Musculoskeletal Case Eighty Three- Soft Tissue Hemangioma
Musculoskeletal Case Eighty Four - Osteoid Osteoma
Musculoskeletal Case Eighty Five - Bucket Handle Tear of Medial Meniscus
MusculoSkeletal Imaging Teaching Files Part1
Musculo Skeletal Imaging Teaching Files
Musculoskeletal Case One - Insufficiency Fractures
Musculoskeletal Case One - Insufficiency Fractures
Musculoskeletal Case Two - Subacute Hematoma
Musculoskeletal Case Three - Blount's Disease
Musculoskeletal Case Four - Ankylosing Spondylitis
Musculoskeletal Case Five - Quadriceps Tendon Rupture
Musculoskeletal Case Six - Tarsal Coalition
Musculoskeletal Case Seven - Bilateral Glenoid Hypoplasia
Musculoskeletal Case Eight - Disruption of the Anterior Cruciate Mechanism
Musculoskeletal Case Nine - Bucket Handle Tear
Musculoskeletal Case Ten - Insufficiency Stress Fractures
Musculoskeletal Case Eleven - Infectious Tenosynovitis/Palmar Abscess
Musculoskeletal Case Twelve - Discoid Lateral Meniscus With a Tear
Musculoskeletal Case Thirteen - Melorheostosis of Phalanges
Musculoskeletal Case Fourteen - Melorheostosis
Musculoskeletal Case Fifteen - Talocalcaneal Subtalar Coalition
Musculoskeletal Case Sixteen - Uncorrected Developmental Dysplasia of the Left Hip
Musculoskeletal Case Seventeen - Infectious Spondylitis
Musculoskeletal Case Eighteen - Tillaux Fracture
Musculoskeletal Case Nineteen - Sarcoidosis of Hands
Musculoskeletal Case Twenty - Synovial Osteochondromatosis
Musculoskeletal Case Twenty One - Necrotizing Fasciitis
Musculoskeletal Case Twenty Two - Benign Giant Cell Tumor With a Pathological Fracture
Musculoskeletal Case Twenty Tree - SLAP Lesion
Musculoskeletal Case Twenty Four - Dracunculiasis (Guinea Worm Disease)
Musculoskeletal Case Twenty Five - Multiple Hereditary Exostoses
Musculoskeletal Case Twenty Six - Monteggia Fracture-Dislocation (Type 1)
Musculoskeletal Case Twenty Seven - Ruptured Baker’s Cyst
Musculoskeletal Case Twenty Eight - Myositis Ossificans
Musculoskeletal Case Twenty Nine - Flexion-Distraction Fracture at L1 Vertebral Body
Musculoskeletal Case Thirty - Calcium Pyrophosphate Dihydrate (CPPD) Arthropathy
Musculoskeletal Case Thirty One - Neuromuscular Arthropathy Secondary to Poliomyelitis
Musculoskeletal Case Thirty Two - Giant Cell Tumor With Pathologic Fracture
Musculoskeletal Case Thirty Three - Type IV SLAP Lesion of the Glenoid Labrum
Musculoskeletal Case Thirty Four - Melorheostosis
Musculoskeletal Case Thirty Five - Fractured Talar Lateral Process
Musculoskeletal Case Thirty Six - Osteopetrosis
Musculoskeletal Case Thirty Seven - Discitis / Osteomyelitis
Musculoskeletal Case Thirty Eight - Insufficiency Fracture of the Femoral Neck
Musculoskeletal Case Thirty Nine - Osgood Schlatter's Disease
Musculoskeletal Case Forty - Osteochondroma of L3 Spinous Process
Routes of Drug Administration
Routes of Drug Administration
By:Robert L. Copeland, Ph.D.
Department of Pharmacology, Howard University
Drug Absorption
* Absorption is the process by which a drug enters the bloodstream without being chemically altered or
* The movement of a drug from its site of application into the blood or lymphatic system
* Factors which influence the rate of absorption
* The rate at which a drug reaches it site of action depends on:
* Mechanisms of solute transport across membranes
Ion Trapping:
Kidney:
Lipid-Water Partition Coefficient
Enteral Routes
Sublingual/Buccal
Oral
First-pass Effect
Parenteral Routes
Intravascular
Absorption phase is bypassed
Intramuscular
Subcutaneous
Inhalation
Topical
Time-release preparations
Routes of Drug Administration.ppt
By:Robert L. Copeland, Ph.D.
Department of Pharmacology, Howard University
Drug Absorption
* Absorption is the process by which a drug enters the bloodstream without being chemically altered or
* The movement of a drug from its site of application into the blood or lymphatic system
* Factors which influence the rate of absorption
* The rate at which a drug reaches it site of action depends on:
* Mechanisms of solute transport across membranes
Ion Trapping:
Kidney:
Lipid-Water Partition Coefficient
Enteral Routes
Sublingual/Buccal
Oral
First-pass Effect
Parenteral Routes
Intravascular
Absorption phase is bypassed
Intramuscular
Subcutaneous
Inhalation
Topical
Time-release preparations
Routes of Drug Administration.ppt
SEDATIVE/HYPNOTICS ANXIOLYTICS
SEDATIVE/HYPNOTICS ANXIOLYTICS
By:Martha I. Dávila-García, Ph.D.
Department of Pharmacology, Howard University
Optimal Performance Nervous Breakdown
Performance Anxiety GOAL
SEDATIVE/HYPNOTICS ANXIOLYTICS
Manifestations of anxiety:
Pathological Anxiety
Causes of Anxiety
1). Medical:
o Respiratory
o Endocrine
o Cardiovascular
o Metabolic
o Neurologic.
2). Drug-Induced:
o Stimulants
+ Amphetamines, cocaine, TCAs, caffeine.
o Sympathomimetics
+ Ephedrine, epinephrine, pseudoephedrine phenylpropanolamine.
o Anticholinergics\Antihistaminergics
+ Trihexyphenidyl, benztropine, meperidine diphenhydramine, oxybutinin.
o Dopaminergics
+ Amantadine, bromocriptine, L-Dopa, carbid/levodopa.
o Miscellaneous:
+ Baclofen, cycloserine, hallucinogens, indomethacin.
3). Drug Withdrawal:
Anxiolytics
Sedative/Hypnotics
Properties of Sedative/Hypnotics in Sleep
1) The latency of sleep onset is decreased (time to fall asleep).
2) The duration of stage 2 NREM sleep is increased.
3) The duration of REM sleep is decreased.
4) The duration of slow-wave sleep (when somnambulism and nightmares occur) is decreased.
Other Properties of Sedative/Hypnotics
GABAergic SYSTEM
Benzodiazepines
* Diazepam
* Triazolam
* Lorazepam
* Alprazolam
* Clorazepate => nordiazepam
* Halazepam
* Clonazepam
* Oxazepam
* Prazepam
Barbiturates
* Phenobarbital
* Pentobarbital
* Amobarbital
* Mephobarbital
* Secobarbital
* Aprobarbital
Respiratory Depression
Coma/Anesthesia
Ataxia
Sedation
Anxiolytic
Anticonvulsant
DOSE
RESPONSE
BARBS
BDZs
ETOH
GABAergic SYNAPSE
GABA
glutamate
glucose
GAD
GABA-A Receptor
GABA AGONISTS BDZs
Mechanisms of Action
Benzodiazepines
PHARMACOLOGY
* BDZs potentiate GABAergic inhibition at all levels of the neuraxis.
* BDZs cause more frequent openings of the GABA-Cl- channel via membrane hyperpolarization, and increased receptor affinity for GABA.
* BDZs act on BZ1 (1 and 2 subunit-containing) and BZ2 (5 subunit-containing) receptors.
* May cause euphoria, impaired judgement, loss of cell control and anterograde amnesic effects.
Pharmacokinetics of Benzodiazepines
CNS Effects
Lipid solubility
Biotransformation of Benzodiazepines
Properties of Benzodiazepines
Side Effects of Benzodiazepines
Toxicity/Overdose with Benzodiazepines
Drug-Drug Interactions with BDZs
Pharmacokinetics of Barbiturates
Properties of Barbiturates Mechanism of Action.
Toxicity/Overdose
Miscellaneous Drugs
* Buspirone
* Chloral hydrate
* Hydroxyzine
* Meprobamate (Similar to BARBS)
* Zolpidem (BZ1 selective)
* Zaleplon (BZ1 selective)
Properties of Other drugs.
OTHER USES
ANXYOLITICS
Alprazolam
Chlordiazepoxide
Buspirone
Diazepam
Lorazepam
Oxazepam
Triazolam
Phenobarbital
Halazepam
Prazepam
HYPNOTICS
Chloral hydrate
Estazolam
Flurazepam
Pentobarbital
Lorazepam
Quazepam
Triazolam
Secobarbital
Temazepam
Zolpidem
References:
SEDATIVE/HYPNOTICS ANXIOLYTICS.ppt
By:Martha I. Dávila-García, Ph.D.
Department of Pharmacology, Howard University
Optimal Performance Nervous Breakdown
Performance Anxiety GOAL
SEDATIVE/HYPNOTICS ANXIOLYTICS
Manifestations of anxiety:
Pathological Anxiety
Causes of Anxiety
1). Medical:
o Respiratory
o Endocrine
o Cardiovascular
o Metabolic
o Neurologic.
2). Drug-Induced:
o Stimulants
+ Amphetamines, cocaine, TCAs, caffeine.
o Sympathomimetics
+ Ephedrine, epinephrine, pseudoephedrine phenylpropanolamine.
o Anticholinergics\Antihistaminergics
+ Trihexyphenidyl, benztropine, meperidine diphenhydramine, oxybutinin.
o Dopaminergics
+ Amantadine, bromocriptine, L-Dopa, carbid/levodopa.
o Miscellaneous:
+ Baclofen, cycloserine, hallucinogens, indomethacin.
3). Drug Withdrawal:
Anxiolytics
Sedative/Hypnotics
Properties of Sedative/Hypnotics in Sleep
1) The latency of sleep onset is decreased (time to fall asleep).
2) The duration of stage 2 NREM sleep is increased.
3) The duration of REM sleep is decreased.
4) The duration of slow-wave sleep (when somnambulism and nightmares occur) is decreased.
Other Properties of Sedative/Hypnotics
GABAergic SYSTEM
Benzodiazepines
* Diazepam
* Triazolam
* Lorazepam
* Alprazolam
* Clorazepate => nordiazepam
* Halazepam
* Clonazepam
* Oxazepam
* Prazepam
Barbiturates
* Phenobarbital
* Pentobarbital
* Amobarbital
* Mephobarbital
* Secobarbital
* Aprobarbital
Respiratory Depression
Coma/Anesthesia
Ataxia
Sedation
Anxiolytic
Anticonvulsant
DOSE
RESPONSE
BARBS
BDZs
ETOH
GABAergic SYNAPSE
GABA
glutamate
glucose
GAD
GABA-A Receptor
GABA AGONISTS BDZs
Mechanisms of Action
Benzodiazepines
PHARMACOLOGY
* BDZs potentiate GABAergic inhibition at all levels of the neuraxis.
* BDZs cause more frequent openings of the GABA-Cl- channel via membrane hyperpolarization, and increased receptor affinity for GABA.
* BDZs act on BZ1 (1 and 2 subunit-containing) and BZ2 (5 subunit-containing) receptors.
* May cause euphoria, impaired judgement, loss of cell control and anterograde amnesic effects.
Pharmacokinetics of Benzodiazepines
CNS Effects
Lipid solubility
Biotransformation of Benzodiazepines
Properties of Benzodiazepines
Side Effects of Benzodiazepines
Toxicity/Overdose with Benzodiazepines
Drug-Drug Interactions with BDZs
Pharmacokinetics of Barbiturates
Properties of Barbiturates Mechanism of Action.
Toxicity/Overdose
Miscellaneous Drugs
* Buspirone
* Chloral hydrate
* Hydroxyzine
* Meprobamate (Similar to BARBS)
* Zolpidem (BZ1 selective)
* Zaleplon (BZ1 selective)
Properties of Other drugs.
OTHER USES
ANXYOLITICS
Alprazolam
Chlordiazepoxide
Buspirone
Diazepam
Lorazepam
Oxazepam
Triazolam
Phenobarbital
Halazepam
Prazepam
HYPNOTICS
Chloral hydrate
Estazolam
Flurazepam
Pentobarbital
Lorazepam
Quazepam
Triazolam
Secobarbital
Temazepam
Zolpidem
References:
SEDATIVE/HYPNOTICS ANXIOLYTICS.ppt
ANTIEPILEPTIC DRUGS
ANTIEPILEPTIC DRUGS
By:Martha I. Dávila-García, Ph.D.
Department of Pharmacology, Howard University
Epilepsy
A group of chronic CNS disorders characterized by recurrent seizures.
* Seizures are sudden, transitory, and uncontrolled episodes of brain dysfunction resulting from abnormal discharge of neuronal cells with associated motor, sensory or behavioral changes.
Causes for Acute Seizures
* Trauma
* Encephalitis
* Drugs
* Birth trauma
* Withdrawal from depressants
* Tumor
* High fever
* Hypoglycemia
* Extreme acidosis
* Extreme alkalosis Hyponatremia
* Hypocalcemia
* Idiopathic
Seizures
* The causes for seizures can be multiple, from infection, to neoplasms, to head injury. In a few subgroups it is an inherited disorder.
* Febrile seizures or seizures caused by meningitis are treated by antiepileptic drugs, although they are not considered epilepsy (unless they develop into chronic seizures).
* Seizures may also be caused by acute underlying toxic or metabolic disorders, in which case the therapy should be directed towards the specific abnormality.
Neuronal Substrates of Epilepsy
The Brain
The Synapse
The Ion Channels/Receptors
ions
Cellular and Synaptic Mechanisms of Epileptic Seizures
I. Partial (focal) Seizures
II. Generalized Seizures
Classification of Epileptic Seizures
Scheme of Seizure Spread
Simple (Focal) Partial
Contralateral spread
I. Partial (Focal) Seizures
Scheme of Seizure Spread
Complex Partial Seizures
Complex Secondarily Generalized Partial Seizures
I. Partial (focal) Seizures
II. Generalized Seizures
* Generalized Tonic-Clonic Seizures
* Absence Seizures
* Tonic Seizures
* Atonic Seizures
* Clonic and Myoclonic Seizures.
* Infantile Spasms
II. Generalized Seizures
Neuronal Correlates of Paroxysmal Discharges
B. Absence Seizures (Petite Mal)
Treatment of Seizures
Goals:
* Block repetitive neuronal firing.
* Block synchronization of neuronal discharges.
* Block propagation of seizure.
Strategies:
* Modification of ion conductances.
* Increase inhibitory (GABAergic) transmission.
* Decrease excitatory (glutamatergic) activity.
Actions of Phenytoin on Na+ Channels
* Resting State
* Arrival of Action Potential causes depolarization and channel opens allowing sodium to flow in.
* Refractory State, Inactivation
Sustain channel in this conformation
GABAergic SYNAPSE
Drugs that Act at the GABAergic Synapse
* GABA agonists
* GABA antagonists
* Barbiturates
* Benzodiazepines
* GABA synthesizing enzymes
* GABA uptake inhibitors
* GABA metabolizing enzymes
GLUTAMATERGIC SYNAPSE
* Excitatory Synapse.
* Permeable to Na+, Ca2+ and K+.
* Magnesium ions block channel in resting state.
* Glycine (GLY) binding enhances the ability of GLU or NMDA to open the channel.
* Agonists: NMDA, AMPA, Kianate.
Chemical Structure of Classical Antiseizure Agents
Treatment of Seizures
* Hydantoins: phenytoin
* Barbiturates: phenobarbital
* Oxazolidinediones: trimethadione
* Succinimides: ethosuximide
* Acetylureas: phenacemide
* Other: carbamazepine, lamotrigine, vigabatrin, etc.
* Diet
* Surgery, Vagus Nerve Stimulation (VNS).
* Most classical antiepileptic drugs exhibit similar pharmacokinetic properties.
* Good absorption (although most are sparingly soluble).
* Low plasma protein binding (except for phenytoin, BDZs, valproate, and tiagabine).
* Conversion to active metabolites (carbamazepine, primidone, fosphenytoin).
* Cleared by the liver but with low extraction ratios.
* Distributed in total body water.
* Plasma clearance is slow.
* At high concentrations phenytoin exhibits zero order kinetics.
Pharmacokinetic Parameters
Effects of three antiepileptic drugs on high frequency discharge of cultured neurons
Block of sustained high frequency repetitive firing of action potentials.
PHENYTOIN (Dilantin)
* Oldest nonsedative antiepileptic drug.
* Fosphenytoin, a more soluble prodrug is used for parenteral use.
* “Fetal hydantoin syndrome”.
* Manufacturers and preparations.
* It alters Na+, Ca2+ and K+ conductances.
* Inhibits high frequency repetitive firing.
* Alters membrane potentials.
* Alters a.a. concentration.
* Alters NTs (NE, ACh, GABA)
Toxicity:
* Ataxia and nystagmus.
* Cognitive impairment.
* Hirsutism
* Gingival hyperplasia.
* Coarsening of facial features.
* Dose-dependent zero order kinetics.
* Exacerbates absence seizures.
* At high concentrations it causes a type of decerebrate rigidity.
CARBAMAZEPINE (Tegretol)
* Tricyclic, antidepressant (bipolar)
* 3-D conformation similar to phenytoin.
* Mechanism of action, similar to phenytoin. Inhibits high frequency repetitive firing.
* Decreases synaptic activity presynaptically.
* Binds to adenosine receptors (?).
* Inh. uptake and release of NE, but not GABA.
* Potentiates postsynaptic effects of GABA.
* Metabolite is active.
Toxicity:
* Autoinduction of metabolism.
* Nausea and visual disturbances.
* Granulocyte supression.
* Aplastic anemia.
* Exacerbates absence seizures.
OXCARBAZEPINE (Trileptal)
* Closely related to carbamazepine.
* With improved toxicity profile.
* Less potent than carbamazepine.
* Active metabolite.
* Use in partial and generalized seizures as adjunct therapy.
* May aggravate myoclonic and absence seizures.
* Mechanism of action, similar to carbamazepine It alters Na+ conductance and inhibits high frequency repetitive firing.
Toxicity:
* Hyponatremia
* Less hypersensitivity and induction of hepatic enzymes than with carbamazepine
PHENOBARBITAL (Luminal)
* Except for the bromides, it is the oldest antiepileptic drug.
* Although considered one of the safest drugs, it has sedative effects.
* Many consider them the drugs of choice for seizures only in infants.
* Acid-base balance important.
* Useful for partial, generalized tonic-clonic seizures, and febrile seizures
* Prolongs opening of Cl- channels.
* Blocks excitatory GLU (AMPA) responses. Blocks Ca2+ currents (L,N).
* Inhibits high frequency, repetitive firing of neurons only at high concentrations.
Toxicity:
* Sedation.
* Cognitive impairment.
* Behavioral changes.
* Induction of liver enzymes.
* May worsen absence and atonic seizures.
PRIMIDONE (Mysolin)
* Metabolized to phenobarbital and phenylethylmalonamide (PEMA), both active metabolites.
* Effective against partial and generalized tonic-clonic seizures.
* Absorbed completely, low binding to plasma proteins.
* Should be started slowly to avoid sedation and GI problems.
* Its mechanism of action may be closer to phenytoin than the barbiturates.
Toxicity:
* Same as phenobarbital
* Sedation occurs early.
* Gastrointestinal complaints.
VALPROATE (Depakene)
ETHOSUXIMIDE (Zarontin)
CLONAZEPAM (Klonopin)
VIGABATRIN
LAMOTRIGINE (Lamictal)
FELBAMATE (Felbatrol)
TOPIRAMATE (Topamax)
TIAGABINE (Gabatril)
ZONISAMIDE (Zonegran)
GABAPENTIN (Neurontin)
Status Epilepticus
Treatment of Status Epilepticus in Adults
DIAZEPAM (Valium) AND
LORAZEPAM (Ativan)
Treatment of Seizures
PRIMARY GENERALIZED TONIC-CLONIC SEIZURES (Grand Mal)
GENERALIZED ABSENCE SEIZURES
ATYPICAL ABSENCE, MYOCLONIC, ATONIC* SEIZURES
INFANTILE SPASMS
Treatment of Seizures in Pregnancy
INTERACTIONS BETWEEN ANTISEIZURE DRUGS
ANTISEIZURE DRUG INTERACTIONS
With other drugs:
ANTIEPILEPTIC DRUGS.ppt
http://www.med.howard.edu/pharmacology/handouts/ANTIEPILEPTICS_OL2003.ppt
By:Martha I. Dávila-García, Ph.D.
Department of Pharmacology, Howard University
Epilepsy
A group of chronic CNS disorders characterized by recurrent seizures.
* Seizures are sudden, transitory, and uncontrolled episodes of brain dysfunction resulting from abnormal discharge of neuronal cells with associated motor, sensory or behavioral changes.
Causes for Acute Seizures
* Trauma
* Encephalitis
* Drugs
* Birth trauma
* Withdrawal from depressants
* Tumor
* High fever
* Hypoglycemia
* Extreme acidosis
* Extreme alkalosis Hyponatremia
* Hypocalcemia
* Idiopathic
Seizures
* The causes for seizures can be multiple, from infection, to neoplasms, to head injury. In a few subgroups it is an inherited disorder.
* Febrile seizures or seizures caused by meningitis are treated by antiepileptic drugs, although they are not considered epilepsy (unless they develop into chronic seizures).
* Seizures may also be caused by acute underlying toxic or metabolic disorders, in which case the therapy should be directed towards the specific abnormality.
Neuronal Substrates of Epilepsy
The Brain
The Synapse
The Ion Channels/Receptors
ions
Cellular and Synaptic Mechanisms of Epileptic Seizures
I. Partial (focal) Seizures
II. Generalized Seizures
Classification of Epileptic Seizures
Scheme of Seizure Spread
Simple (Focal) Partial
Contralateral spread
I. Partial (Focal) Seizures
Scheme of Seizure Spread
Complex Partial Seizures
Complex Secondarily Generalized Partial Seizures
I. Partial (focal) Seizures
II. Generalized Seizures
* Generalized Tonic-Clonic Seizures
* Absence Seizures
* Tonic Seizures
* Atonic Seizures
* Clonic and Myoclonic Seizures.
* Infantile Spasms
II. Generalized Seizures
Neuronal Correlates of Paroxysmal Discharges
B. Absence Seizures (Petite Mal)
Treatment of Seizures
Goals:
* Block repetitive neuronal firing.
* Block synchronization of neuronal discharges.
* Block propagation of seizure.
Strategies:
* Modification of ion conductances.
* Increase inhibitory (GABAergic) transmission.
* Decrease excitatory (glutamatergic) activity.
Actions of Phenytoin on Na+ Channels
* Resting State
* Arrival of Action Potential causes depolarization and channel opens allowing sodium to flow in.
* Refractory State, Inactivation
Sustain channel in this conformation
GABAergic SYNAPSE
Drugs that Act at the GABAergic Synapse
* GABA agonists
* GABA antagonists
* Barbiturates
* Benzodiazepines
* GABA synthesizing enzymes
* GABA uptake inhibitors
* GABA metabolizing enzymes
GLUTAMATERGIC SYNAPSE
* Excitatory Synapse.
* Permeable to Na+, Ca2+ and K+.
* Magnesium ions block channel in resting state.
* Glycine (GLY) binding enhances the ability of GLU or NMDA to open the channel.
* Agonists: NMDA, AMPA, Kianate.
Chemical Structure of Classical Antiseizure Agents
Treatment of Seizures
* Hydantoins: phenytoin
* Barbiturates: phenobarbital
* Oxazolidinediones: trimethadione
* Succinimides: ethosuximide
* Acetylureas: phenacemide
* Other: carbamazepine, lamotrigine, vigabatrin, etc.
* Diet
* Surgery, Vagus Nerve Stimulation (VNS).
* Most classical antiepileptic drugs exhibit similar pharmacokinetic properties.
* Good absorption (although most are sparingly soluble).
* Low plasma protein binding (except for phenytoin, BDZs, valproate, and tiagabine).
* Conversion to active metabolites (carbamazepine, primidone, fosphenytoin).
* Cleared by the liver but with low extraction ratios.
* Distributed in total body water.
* Plasma clearance is slow.
* At high concentrations phenytoin exhibits zero order kinetics.
Pharmacokinetic Parameters
Effects of three antiepileptic drugs on high frequency discharge of cultured neurons
Block of sustained high frequency repetitive firing of action potentials.
PHENYTOIN (Dilantin)
* Oldest nonsedative antiepileptic drug.
* Fosphenytoin, a more soluble prodrug is used for parenteral use.
* “Fetal hydantoin syndrome”.
* Manufacturers and preparations.
* It alters Na+, Ca2+ and K+ conductances.
* Inhibits high frequency repetitive firing.
* Alters membrane potentials.
* Alters a.a. concentration.
* Alters NTs (NE, ACh, GABA)
Toxicity:
* Ataxia and nystagmus.
* Cognitive impairment.
* Hirsutism
* Gingival hyperplasia.
* Coarsening of facial features.
* Dose-dependent zero order kinetics.
* Exacerbates absence seizures.
* At high concentrations it causes a type of decerebrate rigidity.
CARBAMAZEPINE (Tegretol)
* Tricyclic, antidepressant (bipolar)
* 3-D conformation similar to phenytoin.
* Mechanism of action, similar to phenytoin. Inhibits high frequency repetitive firing.
* Decreases synaptic activity presynaptically.
* Binds to adenosine receptors (?).
* Inh. uptake and release of NE, but not GABA.
* Potentiates postsynaptic effects of GABA.
* Metabolite is active.
Toxicity:
* Autoinduction of metabolism.
* Nausea and visual disturbances.
* Granulocyte supression.
* Aplastic anemia.
* Exacerbates absence seizures.
OXCARBAZEPINE (Trileptal)
* Closely related to carbamazepine.
* With improved toxicity profile.
* Less potent than carbamazepine.
* Active metabolite.
* Use in partial and generalized seizures as adjunct therapy.
* May aggravate myoclonic and absence seizures.
* Mechanism of action, similar to carbamazepine It alters Na+ conductance and inhibits high frequency repetitive firing.
Toxicity:
* Hyponatremia
* Less hypersensitivity and induction of hepatic enzymes than with carbamazepine
PHENOBARBITAL (Luminal)
* Except for the bromides, it is the oldest antiepileptic drug.
* Although considered one of the safest drugs, it has sedative effects.
* Many consider them the drugs of choice for seizures only in infants.
* Acid-base balance important.
* Useful for partial, generalized tonic-clonic seizures, and febrile seizures
* Prolongs opening of Cl- channels.
* Blocks excitatory GLU (AMPA) responses. Blocks Ca2+ currents (L,N).
* Inhibits high frequency, repetitive firing of neurons only at high concentrations.
Toxicity:
* Sedation.
* Cognitive impairment.
* Behavioral changes.
* Induction of liver enzymes.
* May worsen absence and atonic seizures.
PRIMIDONE (Mysolin)
* Metabolized to phenobarbital and phenylethylmalonamide (PEMA), both active metabolites.
* Effective against partial and generalized tonic-clonic seizures.
* Absorbed completely, low binding to plasma proteins.
* Should be started slowly to avoid sedation and GI problems.
* Its mechanism of action may be closer to phenytoin than the barbiturates.
Toxicity:
* Same as phenobarbital
* Sedation occurs early.
* Gastrointestinal complaints.
VALPROATE (Depakene)
ETHOSUXIMIDE (Zarontin)
CLONAZEPAM (Klonopin)
VIGABATRIN
LAMOTRIGINE (Lamictal)
FELBAMATE (Felbatrol)
TOPIRAMATE (Topamax)
TIAGABINE (Gabatril)
ZONISAMIDE (Zonegran)
GABAPENTIN (Neurontin)
Status Epilepticus
Treatment of Status Epilepticus in Adults
DIAZEPAM (Valium) AND
LORAZEPAM (Ativan)
Treatment of Seizures
PRIMARY GENERALIZED TONIC-CLONIC SEIZURES (Grand Mal)
GENERALIZED ABSENCE SEIZURES
ATYPICAL ABSENCE, MYOCLONIC, ATONIC* SEIZURES
INFANTILE SPASMS
Treatment of Seizures in Pregnancy
INTERACTIONS BETWEEN ANTISEIZURE DRUGS
ANTISEIZURE DRUG INTERACTIONS
With other drugs:
ANTIEPILEPTIC DRUGS.ppt
http://www.med.howard.edu/pharmacology/handouts/ANTIEPILEPTICS_OL2003.ppt
Antiviral Agents
Antiviral Agents
By:Jillian H. Davis
Department of Pharmacology, Howard University
Viruses
* Obligate intracellular parasites
* Consist of a core genome in a protein shell and some are surrounded by a lipoprotein
* lack a cell wall and cell membrane
* do not carry out metabolic processes
* Replication depends on the host cell machinery
* Steps for Viral Replication
Sites of Drug Action
Antiviral Agents
Antiherpes Agents
* Acyclovir- prototype
* Valacyclovir
* Famciclovir
* Penciclovir
* Trifluridine
* Vidarabine
Mechanism of Action Acyclovir
* an acyclic guanosine derivative
* Phosphorylated by viral thymidine kinase
* Di-and tri-phosphorylated by host cellular enzymes
* Inhibits viral DNA synthesis
* Alteration in viral thymidine kinase
* Alteration in viral DNA polymerase
* Cross-resistance with valacyclovir, famciclovir, and ganciclovir
Clinical Uses Acyclovir
* Oral, IV, and Topical formulations
* Cleared by glomerular filtration and tubular secretion
* Uses:
o Herpes Simplex Virus 1 and 2 (HSV)
o Varicella-zoster virus (VZV)
* Side Effects: nausea, diarrhea, headache, tremors, and delirium
Valacyclovir
* L-valyl ester of acyclovir
* Converted to acyclovir when ingested
* M.O.A.: same as acyclovir
* Uses:
o 1) recurrent genital herpes
o 2) herpes zoster infections
* Side Effects: nausea, diarrhea, and headache
Famciclovir
* Prodrug of penciclovir (a guanosine analog)
* M.O.A.: same as acyclovir
* does not cause chain termination
* Uses: HSV-1, HSV-2, VZV, EBV, and hepatitis B
* Side Effects: nausea, diarrhea, and headache
Trifluridine
* Trifluridine- fluorinated pyrimidine
o inhibits viral DNA synthesis same as acyclovir
o incorporates into viral and cellular DNA
o Uses: HSV-1 and HSV-2 (topically)
Vidarabine
* An adenosine analog
* inhibits viral DNA polymerase
* incorporated into viral and cellular DNA
* metabolized to hypoxanthine arabinoside
* Side Effects: GI intolerance and myelosuppression
Anti-Cytomegalovirus Agents
* Gancyclovir
* Valgancyclovir
* Cidofovir
* Foscarnet
* Fomivirsen
Ganciclovir
* An acyclic guanosine analog
* requires triphosphorylation for activation
* monophosphorylation is catalyzed by a phosphotransferase in CMV and by thymidine kinase in HSV cells
* M.O.A.: same as acyclovir
* Uses: CMV*, HSV, VZV,and EBV
* Side Effect: myelosuppression
Valgancyclovir
* Monovalyl ester prodrug of gancyclovir
* Metabolized by intestinal and hepatic esterases when administered orally
* M.O.A.: same as gancyclovir
* Uses: CMV*
* Side Effect: myelosuppression
Cidofovir
* A cytosine analog
* phosphorylation not dependent on viral enzymes
* Uses: CMV*, HSV-1, HSV-2, VZV, EBV, HHV-6, adenovirus, and human papillomavirus
* Side Effects: nephrotoxicity (prevented by admin. of probenecid)
* Resistance: mutation in DNA polymerase gene
Foscarnet
* An inorganic pyrophosphate
* inhibits viral DNA polymerase, RNA polymerase, and HIV reverse transcriptase
* does not have to be phosphorylated
* Uses: HSV, VZV, CMV, EBV, HHV-6, HBV, and HIV
* Resistance due to mutations in DNA polymerase gene
* Side Effects: hypo- or hypercalcemia and phosphotemia
Fomivirsen
* An oligonucleotide
* M.O.A.: binds to mRNA and inhibits protein synthesis and viral replication
* Uses: CMV retinitis
* Side effects: iritis and increased intraocular pressure
Antiretroviral Agents
1) Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
2) Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
3)Protease inhibitors
Reverse Transcriptase Inhibitors
* Zidovudine (AZT)
* Didanosine- causes pancreatitis*
* Lamivudine- causes pancreatitis
* Zalcitabine- causes peripheral neuropathy*
* Stavudine- causes peripheral neuropathy*
* Abacavir
Mechanism of Action Zidovudine (AZT)
* A deoxythymidine analog
* enters the cell via passive diffusion
* must be converted to the triphosphate form by mammalian thymidine kinase
* competitively inhibits deoxythymidine triphosphate for the reverse transcriptase enzyme
* causes chain termination
Mechanism of Resistance Zidovudine
* Due to mutations in the reverse transcriptase gene
* more frequent after prolong therapy and in persons with HIV
Clinical Uses Zidovudine
* Available in IV and oral formulations
* activity against HIV-1, HIV-2, and human T cell lymphotropic viruses
* mainly used for treatment of HIV, decreases rate of progression and prolongs survival
* prevents mother to newborn transmission of HIV
Side Effects Zidovudine
* Myelosuppression, including anemia and neutropenia
* GI intolerance, headaches, and insomnia
Other NRTIs
* Didanosine- synthetic deoxy-adenosine analog; causes pancreatitis*
* Lamivudine- cytosine analog
* Zalcitabine- cytosine analog; causes peripheral neuropathy*
* Stavudine- thymidine analog;causes peripheral neuropathy*
* Abacavir- guanosine analog; more effective than the other agents; fatal hypersensitivity reactions can occur
Nucleotide Inhibitors
* Tenofovir
* Adefovir
Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
* Nevirapine
* Delavirdine
* Efavirenz
Mechanism of Action NNRTIs
Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Protease Inhibitors
Indinavir and Ritonavir
Saquinavir
Nelfinavir and Amprenavir
Fusion Inhibitors
Anti-Hepatitis Agents
Interferons
Ribavirin
Anti-Influenza Agents
Amantadine and Rimantadine
Zanamivir and Oseltamivir
Antifungal Agents
Fungal Infections
Systemic Antifungals
Amphotericin B
Flucytosine
Azoles
Differences in Azoles
Mucocutaneous Antifungals
Topical Antifungals
Antiviral Agents.ppt
By:Jillian H. Davis
Department of Pharmacology, Howard University
Viruses
* Obligate intracellular parasites
* Consist of a core genome in a protein shell and some are surrounded by a lipoprotein
* lack a cell wall and cell membrane
* do not carry out metabolic processes
* Replication depends on the host cell machinery
* Steps for Viral Replication
Sites of Drug Action
Antiviral Agents
Antiherpes Agents
* Acyclovir- prototype
* Valacyclovir
* Famciclovir
* Penciclovir
* Trifluridine
* Vidarabine
Mechanism of Action Acyclovir
* an acyclic guanosine derivative
* Phosphorylated by viral thymidine kinase
* Di-and tri-phosphorylated by host cellular enzymes
* Inhibits viral DNA synthesis
* Alteration in viral thymidine kinase
* Alteration in viral DNA polymerase
* Cross-resistance with valacyclovir, famciclovir, and ganciclovir
Clinical Uses Acyclovir
* Oral, IV, and Topical formulations
* Cleared by glomerular filtration and tubular secretion
* Uses:
o Herpes Simplex Virus 1 and 2 (HSV)
o Varicella-zoster virus (VZV)
* Side Effects: nausea, diarrhea, headache, tremors, and delirium
Valacyclovir
* L-valyl ester of acyclovir
* Converted to acyclovir when ingested
* M.O.A.: same as acyclovir
* Uses:
o 1) recurrent genital herpes
o 2) herpes zoster infections
* Side Effects: nausea, diarrhea, and headache
Famciclovir
* Prodrug of penciclovir (a guanosine analog)
* M.O.A.: same as acyclovir
* does not cause chain termination
* Uses: HSV-1, HSV-2, VZV, EBV, and hepatitis B
* Side Effects: nausea, diarrhea, and headache
Trifluridine
* Trifluridine- fluorinated pyrimidine
o inhibits viral DNA synthesis same as acyclovir
o incorporates into viral and cellular DNA
o Uses: HSV-1 and HSV-2 (topically)
Vidarabine
* An adenosine analog
* inhibits viral DNA polymerase
* incorporated into viral and cellular DNA
* metabolized to hypoxanthine arabinoside
* Side Effects: GI intolerance and myelosuppression
Anti-Cytomegalovirus Agents
* Gancyclovir
* Valgancyclovir
* Cidofovir
* Foscarnet
* Fomivirsen
Ganciclovir
* An acyclic guanosine analog
* requires triphosphorylation for activation
* monophosphorylation is catalyzed by a phosphotransferase in CMV and by thymidine kinase in HSV cells
* M.O.A.: same as acyclovir
* Uses: CMV*, HSV, VZV,and EBV
* Side Effect: myelosuppression
Valgancyclovir
* Monovalyl ester prodrug of gancyclovir
* Metabolized by intestinal and hepatic esterases when administered orally
* M.O.A.: same as gancyclovir
* Uses: CMV*
* Side Effect: myelosuppression
Cidofovir
* A cytosine analog
* phosphorylation not dependent on viral enzymes
* Uses: CMV*, HSV-1, HSV-2, VZV, EBV, HHV-6, adenovirus, and human papillomavirus
* Side Effects: nephrotoxicity (prevented by admin. of probenecid)
* Resistance: mutation in DNA polymerase gene
Foscarnet
* An inorganic pyrophosphate
* inhibits viral DNA polymerase, RNA polymerase, and HIV reverse transcriptase
* does not have to be phosphorylated
* Uses: HSV, VZV, CMV, EBV, HHV-6, HBV, and HIV
* Resistance due to mutations in DNA polymerase gene
* Side Effects: hypo- or hypercalcemia and phosphotemia
Fomivirsen
* An oligonucleotide
* M.O.A.: binds to mRNA and inhibits protein synthesis and viral replication
* Uses: CMV retinitis
* Side effects: iritis and increased intraocular pressure
Antiretroviral Agents
1) Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
2) Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
3)Protease inhibitors
Reverse Transcriptase Inhibitors
* Zidovudine (AZT)
* Didanosine- causes pancreatitis*
* Lamivudine- causes pancreatitis
* Zalcitabine- causes peripheral neuropathy*
* Stavudine- causes peripheral neuropathy*
* Abacavir
Mechanism of Action Zidovudine (AZT)
* A deoxythymidine analog
* enters the cell via passive diffusion
* must be converted to the triphosphate form by mammalian thymidine kinase
* competitively inhibits deoxythymidine triphosphate for the reverse transcriptase enzyme
* causes chain termination
Mechanism of Resistance Zidovudine
* Due to mutations in the reverse transcriptase gene
* more frequent after prolong therapy and in persons with HIV
Clinical Uses Zidovudine
* Available in IV and oral formulations
* activity against HIV-1, HIV-2, and human T cell lymphotropic viruses
* mainly used for treatment of HIV, decreases rate of progression and prolongs survival
* prevents mother to newborn transmission of HIV
Side Effects Zidovudine
* Myelosuppression, including anemia and neutropenia
* GI intolerance, headaches, and insomnia
Other NRTIs
* Didanosine- synthetic deoxy-adenosine analog; causes pancreatitis*
* Lamivudine- cytosine analog
* Zalcitabine- cytosine analog; causes peripheral neuropathy*
* Stavudine- thymidine analog;causes peripheral neuropathy*
* Abacavir- guanosine analog; more effective than the other agents; fatal hypersensitivity reactions can occur
Nucleotide Inhibitors
* Tenofovir
* Adefovir
Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
* Nevirapine
* Delavirdine
* Efavirenz
Mechanism of Action NNRTIs
Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
Protease Inhibitors
Indinavir and Ritonavir
Saquinavir
Nelfinavir and Amprenavir
Fusion Inhibitors
Anti-Hepatitis Agents
Interferons
Ribavirin
Anti-Influenza Agents
Amantadine and Rimantadine
Zanamivir and Oseltamivir
Antifungal Agents
Fungal Infections
Systemic Antifungals
Amphotericin B
Flucytosine
Azoles
Differences in Azoles
Mucocutaneous Antifungals
Topical Antifungals
Antiviral Agents.ppt
Anticoagulant, Antithrombotic and Anti-Platelet Drugs
Anticoagulant, Antithrombotic and Anti-Platelet Drugs
By:Robert Taylor, MD, Ph.D.
Department of Pharmacology, Howard University
Clinical Thrombosis
Indications For Antithrombotic Therapy
* Venous thromboembolic disease
o Deep venous thrombosis (DVT)
o Pulmonary embolism (PE)
o Primary prophylaxis of DVT or PE
* Arterial thromboembolic disease
o Prosthetic heart valves
o Mitral valve disease, especially with atrial fibrillation
o Congestive cardiomyopathies, especially with atrial fibrillatio
o Atrial fibrillation
o Mural cardiac thrombi
o Transient ischemic attacks
o Stroke in evolution
* Disseminated intravascular coagulation
* Maintenance of patency of vascular grafts, shunts, bypasses
Recombinant Human Activated Protein C
* Drotrecogin alfa (activated)- Xigris
* Indicated for Severe Sepsis in Adults with Acute Organ Dysfunction with High Risk of Death
* Reduction in Death as Primary End Point
* Antithrombotic, Antiinfammatory, Profibrinolytic Properties
* Serious Bleeding is Major Side Effect
Antithrombin III Inhibits the Following Serine Proteases
* Coagulation
* Factor XIIa
* Factor XIa
* Factor IXa
* Factor Xa
* Thrombin
* Fibrinolysis
* Plasmin
Inhibitory activity against all these enzymes is substantially accelerated by heparin
Heparin
Anticoagulant Properties of Heparin
* Inhibits the thrombin-mediated conversion of fibrinogen to fibrin
* Inhibits the aggregation of platelets by thrombin
* Inhibits activation of fibrin stabilizing enzyme
* Inhibits activated factors XII, XI, IX, X and II
* Biologic Sources
* Bioavailability
* Metabolism
* Elimination
* Side Effects
* Overdose
* Contraindications
* Pregnancy- YES
Unfractionated Heparin
* High Dose
Monitoring of Anticoagulant Therapy
Heparin
Low Dose Unfractionated Heparin
Indications for and Contraindications to Parenteral Anticoagulant Agents
Regional anesthesia
Pregnancy
Prosthetic Heart Valves
Regional anesthesia
Antithrombin III inhibitor
Low-molecular-weight heparin
Unfractionated heparin
Enoxaparin(Lovenox)
Dalteparin(Fragmin)
Tinzaparin(Innohep)
Contraindication
Approved & Appropriate Indications
Class
Anticoagulant Agent
Thrombocytopenia other than heparin-induced thrombocytopenia
Direct thrombin inhibitor
Heparinoid
Hirudin derivative
Synthetic factor Xa inhibitor
Ardeparin
Lepirudin
Argatroban
Danaparoid
Bivalirudin
Fondaparinux(Arixtra)
Heparin-Antibiotic Interactions
Mechanisms of HIT
Therapy of HIT
Warfarin
* Bioavailability
* Metabolism
* Serum Protein Binding
* Vitamin K Status
* Protein C Effects
* Elimination
* Side Effects
* Overdose
* Contraindications
* Pregnancy- NO
Contraindications to Antithrombotic Therapy
Platelet Receptor Mediated Pathways: Drugs
GP IIB/IIIA Inhibitors
Abciximab (ReoPro)
Eptifibatide (Integrilin)
Tirofiban
Thrombin
-Final Common Pathway
-Promotes Platelet Adhesion (Fibrinogen, vWF)
Ticlopidine
Clopidogrel
ADP
ASA
NSAIDs
Arachidonic Acid
Anti Platelet Drugs
CAD
Stroke-TIAs
Permanently inhibits COX-1 and COX-2
Aspirin
TIAs;Stroke
CAD;PVD
Inhibits ADP PlatAg;active metabolite
Ticlopidine
Clopidrgrel
TIAs
Inhibits PDE; increases cAMP
Dipyridamole
Limited Reversibly inhibits COX-1
NSAIDs
Uses
Mechanism
Drug
Anticoagulant, Antithrombotic and Anti-Platelet Drugs.ppt
By:Robert Taylor, MD, Ph.D.
Department of Pharmacology, Howard University
Clinical Thrombosis
Indications For Antithrombotic Therapy
* Venous thromboembolic disease
o Deep venous thrombosis (DVT)
o Pulmonary embolism (PE)
o Primary prophylaxis of DVT or PE
* Arterial thromboembolic disease
o Prosthetic heart valves
o Mitral valve disease, especially with atrial fibrillation
o Congestive cardiomyopathies, especially with atrial fibrillatio
o Atrial fibrillation
o Mural cardiac thrombi
o Transient ischemic attacks
o Stroke in evolution
* Disseminated intravascular coagulation
* Maintenance of patency of vascular grafts, shunts, bypasses
Recombinant Human Activated Protein C
* Drotrecogin alfa (activated)- Xigris
* Indicated for Severe Sepsis in Adults with Acute Organ Dysfunction with High Risk of Death
* Reduction in Death as Primary End Point
* Antithrombotic, Antiinfammatory, Profibrinolytic Properties
* Serious Bleeding is Major Side Effect
Antithrombin III Inhibits the Following Serine Proteases
* Coagulation
* Factor XIIa
* Factor XIa
* Factor IXa
* Factor Xa
* Thrombin
* Fibrinolysis
* Plasmin
Inhibitory activity against all these enzymes is substantially accelerated by heparin
Heparin
Anticoagulant Properties of Heparin
* Inhibits the thrombin-mediated conversion of fibrinogen to fibrin
* Inhibits the aggregation of platelets by thrombin
* Inhibits activation of fibrin stabilizing enzyme
* Inhibits activated factors XII, XI, IX, X and II
* Biologic Sources
* Bioavailability
* Metabolism
* Elimination
* Side Effects
* Overdose
* Contraindications
* Pregnancy- YES
Unfractionated Heparin
* High Dose
Monitoring of Anticoagulant Therapy
Heparin
Low Dose Unfractionated Heparin
Indications for and Contraindications to Parenteral Anticoagulant Agents
Regional anesthesia
Pregnancy
Prosthetic Heart Valves
Regional anesthesia
Antithrombin III inhibitor
Low-molecular-weight heparin
Unfractionated heparin
Enoxaparin(Lovenox)
Dalteparin(Fragmin)
Tinzaparin(Innohep)
Contraindication
Approved & Appropriate Indications
Class
Anticoagulant Agent
Thrombocytopenia other than heparin-induced thrombocytopenia
Direct thrombin inhibitor
Heparinoid
Hirudin derivative
Synthetic factor Xa inhibitor
Ardeparin
Lepirudin
Argatroban
Danaparoid
Bivalirudin
Fondaparinux(Arixtra)
Heparin-Antibiotic Interactions
Mechanisms of HIT
Therapy of HIT
Warfarin
* Bioavailability
* Metabolism
* Serum Protein Binding
* Vitamin K Status
* Protein C Effects
* Elimination
* Side Effects
* Overdose
* Contraindications
* Pregnancy- NO
Contraindications to Antithrombotic Therapy
Platelet Receptor Mediated Pathways: Drugs
GP IIB/IIIA Inhibitors
Abciximab (ReoPro)
Eptifibatide (Integrilin)
Tirofiban
Thrombin
-Final Common Pathway
-Promotes Platelet Adhesion (Fibrinogen, vWF)
Ticlopidine
Clopidogrel
ADP
ASA
NSAIDs
Arachidonic Acid
Anti Platelet Drugs
CAD
Stroke-TIAs
Permanently inhibits COX-1 and COX-2
Aspirin
TIAs;Stroke
CAD;PVD
Inhibits ADP PlatAg;active metabolite
Ticlopidine
Clopidrgrel
TIAs
Inhibits PDE; increases cAMP
Dipyridamole
Limited Reversibly inhibits COX-1
NSAIDs
Uses
Mechanism
Drug
Anticoagulant, Antithrombotic and Anti-Platelet Drugs.ppt
27 May 2009
Foot and Ankle Complaints
Foot and Ankle Complaints
By:Allyson Howe, MD
Major USAF MC
Capital Conference 2007
INTRODUCTION
* Anatomy and Function
o Foot
o Ankle
* Common complaints
* Common diagnoses
FOOT AND ANKLE ANATOMY
* 26 bones and 2 sesamoids
* Forefoot
o Metatarsals
o phalanges
* Midfoot
o 5 tarsals
* Rearfoot
o Talus and Calcaneus
FOOT AND ANKLE
* FUNCTIONS
o Absorb impact loading forces
o Adapt to uneven ground
o Allow efficient propulsion
FOOT AND ANKLE COMPLAINTS
HISTORICAL CLUES
* Previous injury?
* New shoes?
* New sport/activity?
* Sudden increase in mileage?
* Long term training without rest?
FOOT AND ANKLE COMMON COMPLAINTS
* Heel pain
* Forefoot pain
* Ankle pain
* Numbness/tingling/burning
* Ankle swelling
* Heel pain
* Forefoot pain
* Ankle pain
* Numbness/tingling/burning
* Ankle swelling
HEEL PAIN
* Determine location
o Plantar surface
+ Plantar fasciitis
+ Heel pad atrophy
+ Distal tarsal tunnel syndrome
+ Calcaneal stress fracture
o Posterior heel
+ Retrocalcaneal bursitis
+ Achilles tendinopathy
+ Sever’s disease
+ Stress fracture
+ Lateral Plantar Nerve entrapment
Consider inflammatory conditions also:
Gout
Reiter’s
Psoriasis
PLANTAR FASCIITIS
* Pain at the most anterior portion of the heel pad
* Medial tubercle
* Worst with first step in the morning or after inactivity
* Pain increases with active dorsiflexion of first toe
* Treatment
o ICE
o Stretching
o NSAIDs
o Correction of arch abnormalities
o Improved shoe quality
o Training adjustment
o Night splints
o Injections
HEEL PAD ATROPHY
TARSAL TUNNEL SYNDROME
RETROCALCANEAL BURSITIS
ACHILLES TENDINOPATHY
SEVER’S DISEASE aka. Calcaneal Apophysitis
LATERAL PLANTAR NERVE ENTRAPMENT
FOREFOOT PAIN
* Acute
* Trauma
* Chronic
5th METATARSAL FRACTURE
METATARSAL FRACTURE
GOUT
LIS FRANC SPRAIN
METATARSALGIA
STRESS FRACTURE
ANKLE PAIN
OSTEOCHONDRAL DEFECT
ANKLE SPRAIN
OTTAWA ANKLE AND FOOT RULES
Ottawa Ankle Rules
Radiographs
A-P View of Ankle
Lateral View of Ankle
Mortise View of Ankle
Mortise View Normals
CLASSIFICATION OF LATERAL ANKLE SPRAINS
Instability testing
Grade II
Grade I
OTHER (THAN LATERAL) ANKLE SPRAINS
ANKLE SPRAIN TREATMENT
NON-HEALING ANKLE SPRAINS
NUMBNESS/TINGLING/BURNING
Peripheral Neuropathy
Diabetes
Nutritional deficiency
Alcoholism
Heavy metal exposure
Chemotherapy
Renal disease
INH therapy
HIV
JOGGER’S FOOT
MORTON’S NEUROMA
ATRAUMATIC ANKLE SWELLING
TAKE HOME POINTS
RHEUMATOID ARTHRITIS
* ANKLE
o Ankle sprains- medial and lateral and high
+ Ottawa ankle rules
o Achilles tendonitis
o Retrocalcaneal bursitis
o Posterior tibial tendonitis
o Sever’s disease (calcaneal apophysitis)
o Tarsal tunnel syndrome
o OCD
* FOOT
o Plantar fasciitis
o Metatarsalgia
o Morton’s neuroma
o Tarsal tunnel
o Toe fracture
o Navicular stress fracture
o Freiberg’s infarction
Foot and Ankle Complaints.ppt
By:Allyson Howe, MD
Major USAF MC
Capital Conference 2007
INTRODUCTION
* Anatomy and Function
o Foot
o Ankle
* Common complaints
* Common diagnoses
FOOT AND ANKLE ANATOMY
* 26 bones and 2 sesamoids
* Forefoot
o Metatarsals
o phalanges
* Midfoot
o 5 tarsals
* Rearfoot
o Talus and Calcaneus
FOOT AND ANKLE
* FUNCTIONS
o Absorb impact loading forces
o Adapt to uneven ground
o Allow efficient propulsion
FOOT AND ANKLE COMPLAINTS
HISTORICAL CLUES
* Previous injury?
* New shoes?
* New sport/activity?
* Sudden increase in mileage?
* Long term training without rest?
FOOT AND ANKLE COMMON COMPLAINTS
* Heel pain
* Forefoot pain
* Ankle pain
* Numbness/tingling/burning
* Ankle swelling
* Heel pain
* Forefoot pain
* Ankle pain
* Numbness/tingling/burning
* Ankle swelling
HEEL PAIN
* Determine location
o Plantar surface
+ Plantar fasciitis
+ Heel pad atrophy
+ Distal tarsal tunnel syndrome
+ Calcaneal stress fracture
o Posterior heel
+ Retrocalcaneal bursitis
+ Achilles tendinopathy
+ Sever’s disease
+ Stress fracture
+ Lateral Plantar Nerve entrapment
Consider inflammatory conditions also:
Gout
Reiter’s
Psoriasis
PLANTAR FASCIITIS
* Pain at the most anterior portion of the heel pad
* Medial tubercle
* Worst with first step in the morning or after inactivity
* Pain increases with active dorsiflexion of first toe
* Treatment
o ICE
o Stretching
o NSAIDs
o Correction of arch abnormalities
o Improved shoe quality
o Training adjustment
o Night splints
o Injections
HEEL PAD ATROPHY
TARSAL TUNNEL SYNDROME
RETROCALCANEAL BURSITIS
ACHILLES TENDINOPATHY
SEVER’S DISEASE aka. Calcaneal Apophysitis
LATERAL PLANTAR NERVE ENTRAPMENT
FOREFOOT PAIN
* Acute
* Trauma
* Chronic
5th METATARSAL FRACTURE
METATARSAL FRACTURE
GOUT
LIS FRANC SPRAIN
METATARSALGIA
STRESS FRACTURE
ANKLE PAIN
OSTEOCHONDRAL DEFECT
ANKLE SPRAIN
OTTAWA ANKLE AND FOOT RULES
Ottawa Ankle Rules
Radiographs
A-P View of Ankle
Lateral View of Ankle
Mortise View of Ankle
Mortise View Normals
CLASSIFICATION OF LATERAL ANKLE SPRAINS
Instability testing
Grade II
Grade I
OTHER (THAN LATERAL) ANKLE SPRAINS
ANKLE SPRAIN TREATMENT
NON-HEALING ANKLE SPRAINS
NUMBNESS/TINGLING/BURNING
Peripheral Neuropathy
Diabetes
Nutritional deficiency
Alcoholism
Heavy metal exposure
Chemotherapy
Renal disease
INH therapy
HIV
JOGGER’S FOOT
MORTON’S NEUROMA
ATRAUMATIC ANKLE SWELLING
TAKE HOME POINTS
RHEUMATOID ARTHRITIS
* ANKLE
o Ankle sprains- medial and lateral and high
+ Ottawa ankle rules
o Achilles tendonitis
o Retrocalcaneal bursitis
o Posterior tibial tendonitis
o Sever’s disease (calcaneal apophysitis)
o Tarsal tunnel syndrome
o OCD
* FOOT
o Plantar fasciitis
o Metatarsalgia
o Morton’s neuroma
o Tarsal tunnel
o Toe fracture
o Navicular stress fracture
o Freiberg’s infarction
Foot and Ankle Complaints.ppt
Hormone Replacement Therapy
Hormone Replacement Therapy… and other options
By:Marc Childress, MD
Risks vs. Benefits in a post-WHI world
* Cancer Risk
* Osteoporosis
* Dementia
* Vasomotor Symptoms
* Urogenital Symptoms
* Cardiovascular Disease
Breast Cancer
* Mixed Results
* Excess risk approx ½ of anticipated
* Question of prognosis, timeframe of concern
Gratuitous Perspective Slide
* Increased risk of breast CA with 10% weight gain (2 add’l cases per 1000 pt-years)
* Increased risk of breast CA with combined tx (0.8 add’l cases per 1000 pt-years)
Endometrial Cancer
* Known increase in risk with unopposed estrogen
* WHI showed no signif risk of CA with combined tx
Ovarian Cancer
* No overt correlation b/w combined HRT and ovarian CA risk
* There IS a signif risk reduction associated with OCPs
Colorectal Cancer
* Signif Risk Reduction of Colon CA with combined Est/Pro
* While less cases, trend toward worse prognosis (nodal spread)
* No risk reduction observed with estrogen alone
Osteoporosis
* Well established
* Risk reduced at hip, vertebrae, and wrist over placebo
* Similar numbers for estrogen alone vs combined tx.
Dementia
* Presumed correlation with long-term estrogen and cognitive fxn
* WHIMS (memory study)
Vasomotor Symptoms
* Signif Reduction in hot flashes
* Mod improvement in sleep
* Well-known and unchanged
Urogenital Symptoms
* Can preclude occurrence of atrophic vaginitis
* Thought to prevent urinary incontinence, contradicted by WHI and HERS
Cardiovascular Disease
* Counter to previous belief, very small increase in risk of CV events with combined tx
* Estrogen alone did not show increase in risk of CV events,
* Stroke
* Venous Thromboembolism
* Which one of the following would be accurate advice regarding these risks and benefits?
* The incidence of stroke is decreased
* The incidence of myocardial infarction is decreased
* The incidence of pulmonary embolism is decreased
* The risk of breast cancer is increased
* The incidence of colorectal cancer is increased
Overview
* Current indications (brief? Tx)
o Vasomotor sxs
o Sleep disturbance
o Urogenital changes
* Additional benefits
o Osteoporosis prevention
* Risks include
o Increase in ischemic stroke
o Increase in DVT, PE
o Mild increase in breast CA risk for combined tx
o Increase in inconclusive mammograms
o Increase in GB dz with combined tx
Osteoporosis
Vasomotor Symptoms
* Pharmacologic Therapies
Vasomotor Symptoms
* Pharmacologic Therapies
Herbal Options
Vasomotor Symptoms
* Herbal/Complementary Compounds
Vasomotor Symptoms
* Not Helpful
Urogenital Symptoms
Hormone Replacement Therapy.ppt
By:Marc Childress, MD
Risks vs. Benefits in a post-WHI world
* Cancer Risk
* Osteoporosis
* Dementia
* Vasomotor Symptoms
* Urogenital Symptoms
* Cardiovascular Disease
Breast Cancer
* Mixed Results
* Excess risk approx ½ of anticipated
* Question of prognosis, timeframe of concern
Gratuitous Perspective Slide
* Increased risk of breast CA with 10% weight gain (2 add’l cases per 1000 pt-years)
* Increased risk of breast CA with combined tx (0.8 add’l cases per 1000 pt-years)
Endometrial Cancer
* Known increase in risk with unopposed estrogen
* WHI showed no signif risk of CA with combined tx
Ovarian Cancer
* No overt correlation b/w combined HRT and ovarian CA risk
* There IS a signif risk reduction associated with OCPs
Colorectal Cancer
* Signif Risk Reduction of Colon CA with combined Est/Pro
* While less cases, trend toward worse prognosis (nodal spread)
* No risk reduction observed with estrogen alone
Osteoporosis
* Well established
* Risk reduced at hip, vertebrae, and wrist over placebo
* Similar numbers for estrogen alone vs combined tx.
Dementia
* Presumed correlation with long-term estrogen and cognitive fxn
* WHIMS (memory study)
Vasomotor Symptoms
* Signif Reduction in hot flashes
* Mod improvement in sleep
* Well-known and unchanged
Urogenital Symptoms
* Can preclude occurrence of atrophic vaginitis
* Thought to prevent urinary incontinence, contradicted by WHI and HERS
Cardiovascular Disease
* Counter to previous belief, very small increase in risk of CV events with combined tx
* Estrogen alone did not show increase in risk of CV events,
* Stroke
* Venous Thromboembolism
* Which one of the following would be accurate advice regarding these risks and benefits?
* The incidence of stroke is decreased
* The incidence of myocardial infarction is decreased
* The incidence of pulmonary embolism is decreased
* The risk of breast cancer is increased
* The incidence of colorectal cancer is increased
Overview
* Current indications (brief? Tx)
o Vasomotor sxs
o Sleep disturbance
o Urogenital changes
* Additional benefits
o Osteoporosis prevention
* Risks include
o Increase in ischemic stroke
o Increase in DVT, PE
o Mild increase in breast CA risk for combined tx
o Increase in inconclusive mammograms
o Increase in GB dz with combined tx
Osteoporosis
Vasomotor Symptoms
* Pharmacologic Therapies
Vasomotor Symptoms
* Pharmacologic Therapies
Herbal Options
Vasomotor Symptoms
* Herbal/Complementary Compounds
Vasomotor Symptoms
* Not Helpful
Urogenital Symptoms
Hormone Replacement Therapy.ppt
Thyroid Disease Facts
Thyroid Disease Facts
By:Jeffrey Medland
Lt Col, USAF, MC, SFS
Chief, Endocrinology
MGMC, Andrews AFB, MD
Capital Conference-June 2007
Outline
* Thyroid Testing
* Hypothyroidism
o Causes
o Signs/symptoms
o Treatment
* Hyperthyroidism
o Causes
o Signs/symptoms
o Treatment
* Thyroid Nodules/ Cancer
* Thyroid Disease and Pregnancy
o Hypothyroidism
o Hyperthyroidism (Hyperemesis Gravidarum, Graves’)
o Thyroiditis
* Factors affecting Thyroid function, LT4
Thyroid
Colloid
Apical Membrane
Basal Membrane
Thyroid Peroxidase (TPO)
“Iodination Reaction”
“Coupling Reaction”
Thyroid Testing
* TSH
o Best test for screening for thyroid dysfunction!
o Log/linear response w/ FT4
+ A 2-fold change in FT4 produces a 100-fold change in TSH
o Not specific for a particular thyroid disease.
+ Don’t use TSH alone for diagnosis!
o Also useful in
+ Assessing LT4 tx in 1° hypothyroidism
+ Monitoring TSH-suppressive tx in thyroid Ca
* FT4
o Testing methods:
+ Equilibrium dialysis
+ Analog assays
o Abnormal TSH check this next
o Indications:
+ In conjunction w/ TSH for diagnosing hyperthyroidism or hypothyroidism.
+ Monitoring LT4 replacement in central hypothyroidism (TSH not helpful)
+ Assessing response to tx following 131-RAIA (Graves, toxic nodules)
+ Monitoring ATD tx in pregnant females
* FT3
o Abnormal TSH + normal FT4, then check this (T3 Thyrotoxicosis)
Pituitary Hypothyroidism
Subclinical Hyperthyroidism, Autonomous nodules
Thyrotoxicosis, Thyroiditis (stage 1)
Pituitary Hyperthyroidism
Subclinical Hypothyroidism
Primary Hypothyroidism, Thyroiditis (stage 3)
Clinical Status
FT4
Overview of Thyroid Function Tests
* Thyroid Antibodies (TPO, Tg, TSI, TRAb)
* Thyroglobulin (Tg)
* Radioactive Iodine Uptake and Scan (RAIU/Scan)
* Tc99m-Pertechnetate Scan
* Fine Needle Aspiration (FNA)
* Ultrasound
* Calcitonin
Hypothyroidism
Thyroiditis
Hypothyroidism (Treatment)
Hypothyroidism (treatment in general)
Indications for LT4 replacement
Hypothyroidism + surgery
Hypothyroidism + elderly
Combined LT4/LT3 tx
Hyperthyroid Eye Disease
Does131-RAIA worse ophthalmopathy?
Graves’ Dermopathy Thyroid Dermopathy
Thyroid Acropachy
RAIU/Scan
Increased RAIU
Decreased RAIU
Surgery (sub-total thyroidectomy)
Apathetic Hyperthyroidism
Thyroid Storm
Subclinical Hyperthyroidism
Thyroid Nodules
Red Flags concerning for Cancer
FNA Results:
Thyroid Nodules “Mimickers”
Thyroid Cancer
MTC
Thyroid Disease in Pregnancy
Four factors alter thyroid function in pregnancy
1) Transient ↑ in hCG, during the 1st trimester can stimulate the TSH-R
2) E2-induced ↑ in TBG during the 1st trimester, which is sustained during pregnancy.
3) Alterations in immune function leading to onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease.
4) urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine deficiency (<50 µg/d).
Known Hypothyroidism already on LT4
Stage 1 to 4
Hyperemesis Gravidarum (HG)
Hyperemesis Gravidarum vs. Graves’
Causes of Increased LT4 requirement
Drugs Affecting Thyroid Function
Somatostatin, Glucocorticoids
Dopamine
Amiodarone Effect on Thyroid Function
Amiodarone and the Thyroid
Iodine Effect
Direct Toxic Effect
* Thyroiditis (AIT type 2)
“Innocent Changes”
Jod-Basedow phenomenon (Historical)
* Definition- Hyperthyroidism induced by excess Iodine.
* Coindet (French physician) in 1821 published his cases about Hyperthyroidism.
* In the English speaking world this became known as Graves’ disease (1835), and in the German speaking world as von Basedow’s disease (1840).
* Coindet’s cases of hyperthyroidism were actually Iodine-induced, hence it came to be known as the Iodine-Basedow phenom.
* Jod is German for Iodine, hence the Jod-Basedow phenom!
* Coindet was deprived of credit for not only describing Hyper- thyroidism, but also the variant of hyperthyroidism caused by excess Iodine
* The credit was given to Dr “Jod” who never existed!
Conditions affecting Thyroid Function
Autoimmune Polyglandular Syndromes 2
Hypokalemic Periodic Paralysis
Hyperthyroid Eye Disease
Cutis Aplasia
Cutis Aplasia Keloid
Cutis Aplasia
Thyroid Binding Globulin (TBG)
Increased TBG
Decreased TBG
Thyroid Regulation
Amiodarone the Thyroid
Amiodarone Effects on Thyroid
Thyroid Hormone
* There is no absorption from the stomach. Absorption occurs in the small bowel.
* The main absorptive sites appear to be the proximal and mid-jejunum.
* Progressively decreasing degrees of absorption occur along the distal bowel and proximal colon.
* Hypothyroidism can lead to a slight increase in absorption.
Thyroid Disease Facts.ppt
By:Jeffrey Medland
Lt Col, USAF, MC, SFS
Chief, Endocrinology
MGMC, Andrews AFB, MD
Capital Conference-June 2007
Outline
* Thyroid Testing
* Hypothyroidism
o Causes
o Signs/symptoms
o Treatment
* Hyperthyroidism
o Causes
o Signs/symptoms
o Treatment
* Thyroid Nodules/ Cancer
* Thyroid Disease and Pregnancy
o Hypothyroidism
o Hyperthyroidism (Hyperemesis Gravidarum, Graves’)
o Thyroiditis
* Factors affecting Thyroid function, LT4
Thyroid
Colloid
Apical Membrane
Basal Membrane
Thyroid Peroxidase (TPO)
“Iodination Reaction”
“Coupling Reaction”
Thyroid Testing
* TSH
o Best test for screening for thyroid dysfunction!
o Log/linear response w/ FT4
+ A 2-fold change in FT4 produces a 100-fold change in TSH
o Not specific for a particular thyroid disease.
+ Don’t use TSH alone for diagnosis!
o Also useful in
+ Assessing LT4 tx in 1° hypothyroidism
+ Monitoring TSH-suppressive tx in thyroid Ca
* FT4
o Testing methods:
+ Equilibrium dialysis
+ Analog assays
o Abnormal TSH check this next
o Indications:
+ In conjunction w/ TSH for diagnosing hyperthyroidism or hypothyroidism.
+ Monitoring LT4 replacement in central hypothyroidism (TSH not helpful)
+ Assessing response to tx following 131-RAIA (Graves, toxic nodules)
+ Monitoring ATD tx in pregnant females
* FT3
o Abnormal TSH + normal FT4, then check this (T3 Thyrotoxicosis)
Pituitary Hypothyroidism
Subclinical Hyperthyroidism, Autonomous nodules
Thyrotoxicosis, Thyroiditis (stage 1)
Pituitary Hyperthyroidism
Subclinical Hypothyroidism
Primary Hypothyroidism, Thyroiditis (stage 3)
Clinical Status
FT4
Overview of Thyroid Function Tests
* Thyroid Antibodies (TPO, Tg, TSI, TRAb)
* Thyroglobulin (Tg)
* Radioactive Iodine Uptake and Scan (RAIU/Scan)
* Tc99m-Pertechnetate Scan
* Fine Needle Aspiration (FNA)
* Ultrasound
* Calcitonin
Hypothyroidism
Thyroiditis
Hypothyroidism (Treatment)
Hypothyroidism (treatment in general)
Indications for LT4 replacement
Hypothyroidism + surgery
Hypothyroidism + elderly
Combined LT4/LT3 tx
Hyperthyroid Eye Disease
Does131-RAIA worse ophthalmopathy?
Graves’ Dermopathy Thyroid Dermopathy
Thyroid Acropachy
RAIU/Scan
Increased RAIU
Decreased RAIU
Surgery (sub-total thyroidectomy)
Apathetic Hyperthyroidism
Thyroid Storm
Subclinical Hyperthyroidism
Thyroid Nodules
Red Flags concerning for Cancer
FNA Results:
Thyroid Nodules “Mimickers”
Thyroid Cancer
MTC
Thyroid Disease in Pregnancy
Four factors alter thyroid function in pregnancy
1) Transient ↑ in hCG, during the 1st trimester can stimulate the TSH-R
2) E2-induced ↑ in TBG during the 1st trimester, which is sustained during pregnancy.
3) Alterations in immune function leading to onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease.
4) urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine deficiency (<50 µg/d).
Known Hypothyroidism already on LT4
Stage 1 to 4
Hyperemesis Gravidarum (HG)
Hyperemesis Gravidarum vs. Graves’
Causes of Increased LT4 requirement
Drugs Affecting Thyroid Function
Somatostatin, Glucocorticoids
Dopamine
Amiodarone Effect on Thyroid Function
Amiodarone and the Thyroid
Iodine Effect
Direct Toxic Effect
* Thyroiditis (AIT type 2)
“Innocent Changes”
Jod-Basedow phenomenon (Historical)
* Definition- Hyperthyroidism induced by excess Iodine.
* Coindet (French physician) in 1821 published his cases about Hyperthyroidism.
* In the English speaking world this became known as Graves’ disease (1835), and in the German speaking world as von Basedow’s disease (1840).
* Coindet’s cases of hyperthyroidism were actually Iodine-induced, hence it came to be known as the Iodine-Basedow phenom.
* Jod is German for Iodine, hence the Jod-Basedow phenom!
* Coindet was deprived of credit for not only describing Hyper- thyroidism, but also the variant of hyperthyroidism caused by excess Iodine
* The credit was given to Dr “Jod” who never existed!
Conditions affecting Thyroid Function
Autoimmune Polyglandular Syndromes 2
Hypokalemic Periodic Paralysis
Hyperthyroid Eye Disease
Cutis Aplasia
Cutis Aplasia Keloid
Cutis Aplasia
Thyroid Binding Globulin (TBG)
Increased TBG
Decreased TBG
Thyroid Regulation
Amiodarone the Thyroid
Amiodarone Effects on Thyroid
Thyroid Hormone
* There is no absorption from the stomach. Absorption occurs in the small bowel.
* The main absorptive sites appear to be the proximal and mid-jejunum.
* Progressively decreasing degrees of absorption occur along the distal bowel and proximal colon.
* Hypothyroidism can lead to a slight increase in absorption.
Thyroid Disease Facts.ppt
Osteoporosis
Osteoporosis
Capital Conference 2007
By:Marc Childress, MD
Osteoporosis
* Epidemiology
* Risk Factors
* Prevention
* Screening
* Diagnosis
* Treatment
* Osteoporosis in Men
* Management
* Falls
* Acute Complications
Osteoporosis
* Average female bone mineral density peaks at age 35, slow decline thereafter
* Density loss is accelerated post-menopausally
Epidemiology
Risk Factors
Predisposing Medical Conditions
* Estrogen Deficiency
* Inflammatory Bowel Disease
* Type 2 Diabetes Mellitus
* Celiac disease
* Cystic fibrosis
* Hyperthyroidism
* Hyperparathyroidism
* Hypogonadism
* Liver Disease
* Corticosteroid use
* Heparin use
* Cyclosporine use
* Depo-Provera use
* Vitamin A (systemic retinoid) use
* No clear increase in risk with carbonated beverages
* Chronic excess thyroid hormone replacement
* diffuse nontoxic goiter
* osteoarthritis
* osteoporosis
* hyperparathyroidism
* Addison’s disease
* Hypothyroidism
* Osteogenesis imperfecta
* Anticonvulsive medication
Prevention
* Adequate total dietary calcium
* Vitamin D
* Regular weight-bearing exercise
* Additional protective factors: increased BMI, African-American ethnicity, moderate EtOH intake
* Which of the following antihypertensives agents may help preserve bone mineral density?
* Atenolol (Tenormin)
* Doxazosin (Cardura)
* Enalapril (Vasotec)
* Hydrochlorothiazide
* Nifedipine (Procardia, Adalat)
* Which one of the following is associated with a reduced risk of post-menopausal osteoporosis?
* Corticosteroid use
* Cigarette smoking
* Diuretic use
* Low BMI
* Asian Ethnicity
Screening
* USPTF/AAFP— “routine screening” above the age of 65, consider between 60-65 for increased risk
* National Osteoporosis Foundation—recommend screening above 65, or in younger with risk factors
* Difficulty with recommendations
Screening Options
* Single Photon absorptiometry
* Dual Photon absorptiometry
* Dual X-ray absorptiometry (DEXA)—MOST POPULAR
* Quantitative CT
* Ultrasound
Diagnosis
Treatment
* Raloxifene (Evista)
* is used to manage hot flashes
* increases bone density
* stimulates breast tissue
* stimulates endometrial proliferation
* raises LDL and total cholesterol levels
Osteoporosis in Men
Chronic Management
Falls
Acute Complications
Osteoporosis.ppt
Capital Conference 2007
By:Marc Childress, MD
Osteoporosis
* Epidemiology
* Risk Factors
* Prevention
* Screening
* Diagnosis
* Treatment
* Osteoporosis in Men
* Management
* Falls
* Acute Complications
Osteoporosis
* Average female bone mineral density peaks at age 35, slow decline thereafter
* Density loss is accelerated post-menopausally
Epidemiology
Risk Factors
Predisposing Medical Conditions
* Estrogen Deficiency
* Inflammatory Bowel Disease
* Type 2 Diabetes Mellitus
* Celiac disease
* Cystic fibrosis
* Hyperthyroidism
* Hyperparathyroidism
* Hypogonadism
* Liver Disease
* Corticosteroid use
* Heparin use
* Cyclosporine use
* Depo-Provera use
* Vitamin A (systemic retinoid) use
* No clear increase in risk with carbonated beverages
* Chronic excess thyroid hormone replacement
* diffuse nontoxic goiter
* osteoarthritis
* osteoporosis
* hyperparathyroidism
* Addison’s disease
* Hypothyroidism
* Osteogenesis imperfecta
* Anticonvulsive medication
Prevention
* Adequate total dietary calcium
* Vitamin D
* Regular weight-bearing exercise
* Additional protective factors: increased BMI, African-American ethnicity, moderate EtOH intake
* Which of the following antihypertensives agents may help preserve bone mineral density?
* Atenolol (Tenormin)
* Doxazosin (Cardura)
* Enalapril (Vasotec)
* Hydrochlorothiazide
* Nifedipine (Procardia, Adalat)
* Which one of the following is associated with a reduced risk of post-menopausal osteoporosis?
* Corticosteroid use
* Cigarette smoking
* Diuretic use
* Low BMI
* Asian Ethnicity
Screening
* USPTF/AAFP— “routine screening” above the age of 65, consider between 60-65 for increased risk
* National Osteoporosis Foundation—recommend screening above 65, or in younger with risk factors
* Difficulty with recommendations
Screening Options
* Single Photon absorptiometry
* Dual Photon absorptiometry
* Dual X-ray absorptiometry (DEXA)—MOST POPULAR
* Quantitative CT
* Ultrasound
Diagnosis
Treatment
* Raloxifene (Evista)
* is used to manage hot flashes
* increases bone density
* stimulates breast tissue
* stimulates endometrial proliferation
* raises LDL and total cholesterol levels
Osteoporosis in Men
Chronic Management
Falls
Acute Complications
Osteoporosis.ppt
Infertility
Infertility
By:Stephanie R. Fugate D.O.
Dewitt Army Community Hospital
Department of OB/GYN
Objectives
* Define primary and secondary infertility
* Describe the causes of infertility
* Diagnosis and management of infertility
Requirements for Conception
* Production of healthy egg and sperm
* Unblocked tubes that allow sperm to reach the egg
* The sperms ability to penetrate and fertilize the egg
* Implantation of the embryo into the uterus
* Finally a healthy pregnancy
Infertility
* The inability to conceive following unprotected sexual intercourse
o 1 year (age < 35) or 6 months (age >35)
o Affects 15% of reproductive couples
+ 6.1 million couples
o Men and women equally affected
* Reproductive age for women
* With the proper treatment 85% of infertile couples can expect to have a child
* Health problems develop
* SAB
* Primary infertility
* Secondary infertility
Conception rates for fertile couples
Age and Pregnancy
Pregnancy
Age and related miscarriage
Causes for infertility
* Male
o ETOH
o Drugs
o Tobacco
o Health problems
o Radiation/Chemotherapy
o Age
o Enviromental factors
* Female
o Age
o Stress
o Poor diet
o Athletic training
o Over/underweight
o Tobacco
o ETOH
o STD’s
o Health problems
* Anovulation (10-20%)
* Anatomic defects of the female genital tract (30%)
* Abnormal spermatogenesis (40%)
* Unexplained (10%-20%)
Evaluation of the Infertile couple
* History and Physical exam
* Semen analysis
* Thyroid and prolactin evaluation
* Determination of ovulation
o Basal body temperature record
o Serum progesterone
o Ovarian reserve testing
* Hysterosalpingogram
Abnormalities of Spermatogenesis
Male Factor
Semen Analysis (SA)
* Obtained by masturbation
* Provides immediate information
o Quantity
o Quality
o Density of the sperm
* Abstain from coitus 2 to 3 days
* Collect all the ejaculate
* Analyze within 1 hour
* A normal semen analysis excludes male factor 90% of the time
* Morphology
* Motility
Normal Values for SA
Volume
Sperm Concentration
Motility
Viscosity
Morphology
pH
WBC
Causes for male infertility
Abnormal Semen Analysis
* Azospermia
* Oligospermia
* Abnormal volume
Evaluation of Abnormal SA
* Repeat semen analysis in 30 days
* Physical examination
o Testicular size
o Varicocele
* Laboratory tests
o Testosterone level
o FSH (spermatogenesis- Sertoli cells)
o LH (testosterone- Leydig cells)
* Referral to urology
Evaluation of Ovulation
Menstruation
* Ovulation occurs 13-14 times per year
* Menstrual cycles on average are Q 28 days with ovulation around day 14
* Luteal phase
* Progesterone causes
* Involution of the corpus luteum causes a fall in progesterone and the onset of menses
Menstrual Cycle
Ovulation
* A history of regular menstruation suggests regular ovulation
* The majority of ovulatory women experience
o fullness of the breasts
o decreased vaginal secretions
o abdominal bloating
* Absence of PMS symptoms may suggest anovulation
o mild peripheral edema
o slight weight gain
o depression
Diagnostic studies to confirm Ovulation
* Basal body temperature
o Inexpensive
o Accurate
* Endometrial biopsy
o Expensive
o Static information
* Serum progesterone
o After ovulation rises
o Can be measured
* Urinary ovulation-detection kits
o Measures changes in urinary LH
o Predicts ovulation but does not confirm it
Basal Body Temperature
* Excellent screening tool for ovulation
o Biphasic shift occurs in 90% of ovulating women
* Temperature
o drops at the time of menses
o rises two days after the lutenizing hormone (LH) surge
* Ovum released one day prior to the first rise
* Temperature elevation of more than 16 days suggests pregnancy
Serum Progesterone
* Progesterone starts rising with the LH surge
o drawn between day 21-24
* Mid-luteal phase
o >10 ng/ml suggests ovulation
Anovulation Symptoms Evaluation
* Irregular menstrual cycles
* Amenorrhea
* Hirsuitism
* Acne
* Galactorrhea
* Increased vaginal secretions
* Follicle stimulating hormone
* Lutenizing hormone
* Thyroid stimulating hormone
* Prolactin
* Androstenedione
* Total testosterone
* DHEAS
* Order the appropriate tests based on the clinical indications
Anatomic Disorders of the Female Genital Tract
Sperm transport, Fertilization, & Implantation
* The female genital tract is not just a conduit
o facilitates sperm transport
o cervical mucus traps the coagulated ejaculate
o the fallopian tube picks up the egg
* Fertilization must occur in the proximal portion of the tube
o the fertilized oocyte cleaves and forms a zygote
o enters the endometrial cavity at 3 to 5 days
* Implants into the secretory endometrium for growth and development
Acquired Disorders
* Acute salpingitis
* Intrauterine scarring
* Endometriosis, scarring from surgery, tumors of the uterus and ovary
* Trauma
Congenital Anatomic Abnormalities
Hysterosalpingogram
* An X-ray that evaluates the internal female genital tract
* Performed between the 7th and 11th day of the cycle
* Diagnostic accuracy of 70%
Hysterosalpingogram
* The endometrial cavity
* Fallopian tubes
* Dye should spill promptly
Unexplained infertility
Treatment of the Infertile Couple
Inadequate Spermatogenesis
Clomid
Superovulatory Medications
Anatomic Abnormalities
Assisted Reproductive Technologies (ART)
Emotional Impact
Conclusion
Test Question Case
Causes for Abnormal SA
* No sperm
o Klinefelter’s syndrome
o Sertoli only syndrome
o Ductal obstruction
o Hypogonadotropic-hypogonadism
* Few sperm
o Genetic disorder
o Endocrinopathies
o Varicocele
o Exogenous (e.g., Heat)
Abnormal Count
* Abnormal Morphology
o Varicocele
o Stress
o Infection (mumps)
* Abnormal Motility
o Immunologic factors
o Infection
o Defect in sperm structure
o Poor liquefaction
o Varicocele
* Abnormal Volume
o No ejaculate
+ Ductal obstruction
+ Retrograde ejaculation
+ Ejaculatory failure
+ Hypogonadism
o Low Volume
+ Obstruction of ducts
+ Absence of vas deferens
+ Absence of seminal vesicle
+ Partial retrograde ejaculation
+ Infection
Infertility.ppt
By:Stephanie R. Fugate D.O.
Dewitt Army Community Hospital
Department of OB/GYN
Objectives
* Define primary and secondary infertility
* Describe the causes of infertility
* Diagnosis and management of infertility
Requirements for Conception
* Production of healthy egg and sperm
* Unblocked tubes that allow sperm to reach the egg
* The sperms ability to penetrate and fertilize the egg
* Implantation of the embryo into the uterus
* Finally a healthy pregnancy
Infertility
* The inability to conceive following unprotected sexual intercourse
o 1 year (age < 35) or 6 months (age >35)
o Affects 15% of reproductive couples
+ 6.1 million couples
o Men and women equally affected
* Reproductive age for women
* With the proper treatment 85% of infertile couples can expect to have a child
* Health problems develop
* SAB
* Primary infertility
* Secondary infertility
Conception rates for fertile couples
Age and Pregnancy
Pregnancy
Age and related miscarriage
Causes for infertility
* Male
o ETOH
o Drugs
o Tobacco
o Health problems
o Radiation/Chemotherapy
o Age
o Enviromental factors
* Female
o Age
o Stress
o Poor diet
o Athletic training
o Over/underweight
o Tobacco
o ETOH
o STD’s
o Health problems
* Anovulation (10-20%)
* Anatomic defects of the female genital tract (30%)
* Abnormal spermatogenesis (40%)
* Unexplained (10%-20%)
Evaluation of the Infertile couple
* History and Physical exam
* Semen analysis
* Thyroid and prolactin evaluation
* Determination of ovulation
o Basal body temperature record
o Serum progesterone
o Ovarian reserve testing
* Hysterosalpingogram
Abnormalities of Spermatogenesis
Male Factor
Semen Analysis (SA)
* Obtained by masturbation
* Provides immediate information
o Quantity
o Quality
o Density of the sperm
* Abstain from coitus 2 to 3 days
* Collect all the ejaculate
* Analyze within 1 hour
* A normal semen analysis excludes male factor 90% of the time
* Morphology
* Motility
Normal Values for SA
Volume
Sperm Concentration
Motility
Viscosity
Morphology
pH
WBC
Causes for male infertility
Abnormal Semen Analysis
* Azospermia
* Oligospermia
* Abnormal volume
Evaluation of Abnormal SA
* Repeat semen analysis in 30 days
* Physical examination
o Testicular size
o Varicocele
* Laboratory tests
o Testosterone level
o FSH (spermatogenesis- Sertoli cells)
o LH (testosterone- Leydig cells)
* Referral to urology
Evaluation of Ovulation
Menstruation
* Ovulation occurs 13-14 times per year
* Menstrual cycles on average are Q 28 days with ovulation around day 14
* Luteal phase
* Progesterone causes
* Involution of the corpus luteum causes a fall in progesterone and the onset of menses
Menstrual Cycle
Ovulation
* A history of regular menstruation suggests regular ovulation
* The majority of ovulatory women experience
o fullness of the breasts
o decreased vaginal secretions
o abdominal bloating
* Absence of PMS symptoms may suggest anovulation
o mild peripheral edema
o slight weight gain
o depression
Diagnostic studies to confirm Ovulation
* Basal body temperature
o Inexpensive
o Accurate
* Endometrial biopsy
o Expensive
o Static information
* Serum progesterone
o After ovulation rises
o Can be measured
* Urinary ovulation-detection kits
o Measures changes in urinary LH
o Predicts ovulation but does not confirm it
Basal Body Temperature
* Excellent screening tool for ovulation
o Biphasic shift occurs in 90% of ovulating women
* Temperature
o drops at the time of menses
o rises two days after the lutenizing hormone (LH) surge
* Ovum released one day prior to the first rise
* Temperature elevation of more than 16 days suggests pregnancy
Serum Progesterone
* Progesterone starts rising with the LH surge
o drawn between day 21-24
* Mid-luteal phase
o >10 ng/ml suggests ovulation
Anovulation Symptoms Evaluation
* Irregular menstrual cycles
* Amenorrhea
* Hirsuitism
* Acne
* Galactorrhea
* Increased vaginal secretions
* Follicle stimulating hormone
* Lutenizing hormone
* Thyroid stimulating hormone
* Prolactin
* Androstenedione
* Total testosterone
* DHEAS
* Order the appropriate tests based on the clinical indications
Anatomic Disorders of the Female Genital Tract
Sperm transport, Fertilization, & Implantation
* The female genital tract is not just a conduit
o facilitates sperm transport
o cervical mucus traps the coagulated ejaculate
o the fallopian tube picks up the egg
* Fertilization must occur in the proximal portion of the tube
o the fertilized oocyte cleaves and forms a zygote
o enters the endometrial cavity at 3 to 5 days
* Implants into the secretory endometrium for growth and development
Acquired Disorders
* Acute salpingitis
* Intrauterine scarring
* Endometriosis, scarring from surgery, tumors of the uterus and ovary
* Trauma
Congenital Anatomic Abnormalities
Hysterosalpingogram
* An X-ray that evaluates the internal female genital tract
* Performed between the 7th and 11th day of the cycle
* Diagnostic accuracy of 70%
Hysterosalpingogram
* The endometrial cavity
* Fallopian tubes
* Dye should spill promptly
Unexplained infertility
Treatment of the Infertile Couple
Inadequate Spermatogenesis
Clomid
Superovulatory Medications
Anatomic Abnormalities
Assisted Reproductive Technologies (ART)
Emotional Impact
Conclusion
Test Question Case
Causes for Abnormal SA
* No sperm
o Klinefelter’s syndrome
o Sertoli only syndrome
o Ductal obstruction
o Hypogonadotropic-hypogonadism
* Few sperm
o Genetic disorder
o Endocrinopathies
o Varicocele
o Exogenous (e.g., Heat)
Abnormal Count
* Abnormal Morphology
o Varicocele
o Stress
o Infection (mumps)
* Abnormal Motility
o Immunologic factors
o Infection
o Defect in sperm structure
o Poor liquefaction
o Varicocele
* Abnormal Volume
o No ejaculate
+ Ductal obstruction
+ Retrograde ejaculation
+ Ejaculatory failure
+ Hypogonadism
o Low Volume
+ Obstruction of ducts
+ Absence of vas deferens
+ Absence of seminal vesicle
+ Partial retrograde ejaculation
+ Infection
Infertility.ppt