1) Bleeding disorders can involve vascular, platelet, or coagulation disorders and cause symptoms like bruising, bleeding, and prolonged bleeding from minor cuts.
2) Important bleeding disorders discussed include hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), von Willebrand disease (a disorder of the von Willebrand clotting factor), and fibrinogen deficiency.
3) These disorders are diagnosed through tests of bleeding time and clotting factor levels and activity. Treatment involves replacing the missing clotting factor through products like cryoprecipitate, desmopressin, or clotting factor concentrates.
Bleeding disorders Causes, Types, and DiagnosisDr Medical
https://userupload.net/v3l4i8jsk7wq
Factor II, V, VII, X, or XII deficiencies are bleeding disorders related to blood clotting problems or abnormal bleeding problems. Von Willebrand's disease isthe most common inherited bleeding disorder. It develops when the blood lacks von Willebrand factor, which helps the blood to clot.
This would give an idea of the various bleeding disorders, associated clotting factors and more specifically management in the dental office of the patients with bleeding disorders
Bleeding disorders Causes, Types, and DiagnosisDr Medical
https://userupload.net/v3l4i8jsk7wq
Factor II, V, VII, X, or XII deficiencies are bleeding disorders related to blood clotting problems or abnormal bleeding problems. Von Willebrand's disease isthe most common inherited bleeding disorder. It develops when the blood lacks von Willebrand factor, which helps the blood to clot.
This would give an idea of the various bleeding disorders, associated clotting factors and more specifically management in the dental office of the patients with bleeding disorders
Investigation of bleeding disorder || bleeding disorderparveen singh
this is a topic on investigation of bleeding disorder.
This may result from:
1 Vascular disorders
a] Thrombocytopenia
2Platelet Disorder
b] Defective platelet function
3Defective coagulation
4Defective Fibrinolysis
it is due to
-Inherited bleeding disorders
-Acquired bleeding disorders
investigation include:
first line test {basic test daily done in coagulation lab}
second line test {some important test done whenever all first line investigation test are normal }
Main Credit Goes To__-----___--- nitin dudeja {senior}
INTRODUCTION
• Blood must be maintained in a fluid state in order to function as a transport system, but must be able to solidify to form a clot following vascular injury.
• Successful haemostasis is achieved by complex interactions between vascular endothelium, platelets, coagulation factors etc.
HAEMOSTASIS
• The term haemostasis is derived from the Greek word haem= blood and stasis=halt.
• Process of stoppage of bleeding after blood vessels are punctured , cut , or otherwise damaged.
• It is a complex natural physiological response.
• Bleeding disorders are due to altered ability of blood vessels, platelets , and coagulation factors to maintain haemostasis.
• Steps of natural haemostasis:
• Pre-injury conditions-> Early haemostatic response-> Fibrin clot formation-> Limiting clot formation-> Fibrinolysis
Demands for Haemophilia tratment centres to fullfull universal health access...SEJOJO PHAAROE
Haemophilia ia a rare disease that affect 1: 10 000 people. Demands for services, medication and access to cheap effective clotting factors is a human right for people living with haemophilia. A haemophilia registry is a demand from the Government at large .. Essential drug list should also contain haemophilia medication.
we need to be contacted for more information
www.thinktankent.com
Investigation of bleeding disorder || bleeding disorderparveen singh
this is a topic on investigation of bleeding disorder.
This may result from:
1 Vascular disorders
a] Thrombocytopenia
2Platelet Disorder
b] Defective platelet function
3Defective coagulation
4Defective Fibrinolysis
it is due to
-Inherited bleeding disorders
-Acquired bleeding disorders
investigation include:
first line test {basic test daily done in coagulation lab}
second line test {some important test done whenever all first line investigation test are normal }
Main Credit Goes To__-----___--- nitin dudeja {senior}
INTRODUCTION
• Blood must be maintained in a fluid state in order to function as a transport system, but must be able to solidify to form a clot following vascular injury.
• Successful haemostasis is achieved by complex interactions between vascular endothelium, platelets, coagulation factors etc.
HAEMOSTASIS
• The term haemostasis is derived from the Greek word haem= blood and stasis=halt.
• Process of stoppage of bleeding after blood vessels are punctured , cut , or otherwise damaged.
• It is a complex natural physiological response.
• Bleeding disorders are due to altered ability of blood vessels, platelets , and coagulation factors to maintain haemostasis.
• Steps of natural haemostasis:
• Pre-injury conditions-> Early haemostatic response-> Fibrin clot formation-> Limiting clot formation-> Fibrinolysis
Demands for Haemophilia tratment centres to fullfull universal health access...SEJOJO PHAAROE
Haemophilia ia a rare disease that affect 1: 10 000 people. Demands for services, medication and access to cheap effective clotting factors is a human right for people living with haemophilia. A haemophilia registry is a demand from the Government at large .. Essential drug list should also contain haemophilia medication.
we need to be contacted for more information
www.thinktankent.com
Hemophilia is a rare disorder in which your blood doesn't clot normally because it lacks sufficient blood-clotting proteins (clotting factors). If you have hemophilia, you may bleed for a longer time after an injury than you would if your blood clotted normally. Small cuts usually aren't much of a problem.
https://userupload.net/szgab9mr3vdz
Epidemiology is the study of health and disease in populations and of how these states are influenced by biology, heredity, and physical and social environment, as well as personal behavior. Advances in research over recent years have led to a fundamental change in our understanding of the periodontal diseases. As recently as the mid-1960s, the prevailing model for the epidemiology of periodontal diseases included the following precepts: (1) all individuals were considered more or less equally susceptible to severe periodontitis; (2) gingivitis usually progressed to periodontitis with consequent loss of bone support and eventually loss of teeth; (3) susceptibility to periodontitis increased with age and was the main cause of tooth loss after age 35–55. Since the development of this paradigm, advances in the understanding of periodontal diseases have led this disease model to be reevaluated.
https://userupload.net/l2enk8kbflj8
Incidence, mortality, and survival are the primary measures for assessing the impact of cancer in population groups. Incidence is the frequency of new cancer cases during a defined period of time, generally expressed as the rate per 100,000 persons per year; the mortality rate is the frequency of cancer deaths per 100,000 persons per year. The observed survival rate is the proportion of persons with cancer who survive for a specified period of time after diagnosis, usually 5 years. This statistic is often presented as a relative survival rate, in which survival from cancer is corrected for the likelihood of dying from other causes.
Dentist patient relationship and quality careDr Medical
https://userupload.net/mo2f5z40rv8v
Although quality is a genuine concern for dentistry, nowadays more emphasis is placed on quality issues. As dentist-patient interaction is involved in many aspects of care and it is more crucial for dentistry when compared to many other professions, a good dentist-patient relationship is an integral element of quality care. This series of 'practice articles' examines various important dimensions of this interaction. The first and second papers examine the value of trust and communication, the third paper focuses on informed consent and the fourth paper evaluates the relatively broadened role of dentists in behavioural modification.
https://userupload.net/06gt5zcwvh90
Genetic counseling is the process of advising individuals and families affected by or at risk of genetic disorders to help them understand and adapt to the medical, psychological and familial implications of genetic contributions to disease.[1] The process integrates:
Interpretation of family and medical histories to assess the chance of disease occurrence or recurrence
Education about inheritance, testing, management, prevention, resources
Counseling to promote informed choices and adaptation to the risk or condition.
https://userupload.net/yk8shpcpwk19
Dentistry can do so much these days to improve a person’s health, appearance and self-confidence. From barely noticeable braces that straighten crooked smiles to dental implants that replace missing teeth, there is a state-of-the-art solution to virtually any dental problem. Of course, like anything that involves the time and resources of skilled professionals, highly technical and sophisticated dental treatment doesn’t come inexpensively; indeed, the phrase “you get what you pay for” probably applies doubly to dentistry. Also, the types of treatment mentioned above, as well as many others, are often considered elective and therefore may not be covered (or only partially covered) by dental insurance. This can be the case even when a given procedure offers proven health benefits.
https://userupload.net/8mky0eijld91
An understanding of the physiology of body fluids is essential when considering appropriate fluid resuscitation and fluid replacement therapy in critically-ill patients. In healthy humans, the body is composed of approximately 60% water, distributed between intracellular and an extracellular compartments. The extracellular compartment is divided into intravascular, interstitial and transcellular compartments. The movement of fluids between the intravascular and interstitial compartments, is classically described as being governed by Starling forces, leading to a small net efflux of fluid from the intravascular to the interstitial compartment. More recent evidence suggests that a model incorporating the effect of the endothelial glycoclayx layer, a web of glycoproteins and proteoglycans that are bound on the luminal side of the vascular endothelium, better explains the observed distribution of fluids. The movement of fluid to and from the intracellular compartment and the interstitial fluid compartment, is governed by the relative osmolarities of the two compartments. Body fluid status is governed by the difference between fluid inputs and outputs; fluid input is regulated by the thirst mechanism, with fluid outputs consisting of gastrointestinal, renal, and insensible losses. The regulation of intracellular fluid status is largely governed by the regulation of the interstitial fluid osmolarity, which is regulated by the secretion of antidiuretic hormone from the posterior pituitary gland. The regulation of extracellular volume status is regulated by a complex neuro-endocrine mechanism, designed to regulate sodium in the extracellular fluid.
https://userupload.net/s5uyonki1n7m
Pain is a somatic and emotional sensation which is unpleasant in nature and associated with actual or potential tissue damage. Physiologically, the function of pain is critical for survival and has a major evolutionary advantage. This is because behaviours which cause pain are often dangerous and harmful, therefore they are generally not reinforced and are unlikely to be repeated.
https://userupload.net/3ppacneii1wj
Toxicologic Pathology (Second Edition), 2010
INTRODUCTION
The oral mucosa is, in many ways, similar to the skin in its architecture, function, and reaction patterns. This section only emphasizes those characteristics of the oral mucosa that influence or result in a distinct group of pathologic entities.
Because of its location at the entrance of the digestive and respiratory tracts and its proximity to the teeth, the oral mucosa is subjected to numerous natural and man-made xenobiotics. The peculiar architecture and absorption characteristics of the oral mucosa, especially in areas of extreme thinness, coupled with the rich microorganism flora of the mouth, makes the oral mucosa a peculiar site deserving separate discussion.
https://userupload.net/6jbhjqr3gczd
Behavioural sciences explore the cognitive processes within organisms and the behavioural interactions between organisms in the natural world. It involves the systematic analysis and investigation of human and animal behavior through the study of the past, controlled and naturalistic observation of the present, and disciplined scientific experimentation and modeling. It attempts to accomplish legitimate, objective conclusions through rigorous formulations and observation.[1] Examples of behavioral sciences include psychology, psychobiology, anthropology, and cognitive science. Generally, behavior science deals primarily with human action and often seeks to generalize about human behavior as it relates to society
Antifluoridation lobby - Water fluoridation controversyDr Medical
https://userupload.net/u5vppli3jy1y
The water fluoridation controversy arises from political, moral, ethical, economic, and health considerations regarding the fluoridation of public water supplies.
Public health authorities throughout the world find a medical consensus that fluoride therapy at appropriate levels is a safe and effective means to prevent dental caries,[1] whether by fluoridation of the public water supply or topical application strategies.[2][3] Proponents of water fluoridation see it as a question of public health policy and equate the issue to vaccination and food fortification, claiming significant benefits to dental health and minimal risks
https://userupload.net/21or432od2kp
It is recommended that pacifiers and other types of artificial nipples be avoided for at least the first 3-4 weeks. I’d personally suggest that most breastfed babies – if they get a pacifier at all – would be better off without a pacifier until mom’s milk supply is well established (6-8 weeks, usually) and the 6 week growth spurt is over. That way you’ve established a good milk supply and don’t lose any much-needed breast stimulation to a pacifier.
https://userupload.net/5x4jgtw5sqs2
Behaviour modelling is frequently used to modify children's behaviour. The psychological techniques of encouragement-reprobation are an integral part of the behaviour shaping. Three hundred clinically healthy children were recruited in this study. They were aged 54-96 months and allocated to three groups according to the specific technique used: group 1 in which we applied the "live patients model" technique, in group 2 the "encouragement-reprobation" techniques was applied and group 3 was a control group. The patient's behaviour was assessed using L. Venham's Cooperative Behavioral Scale. A behavioral improvement was noticed in the experimental groups after applying the techniques for behaviour modification. The comparison shows a statistically significant difference between the two experimental groups and the control one and absence of a significant difference between the influenced groups. The study shows that there is a stable for behaviour
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
https://userupload.net/69zxggv1yww1
The mouth and teeth play an important role in social interactions around the world. The way people deal with their teeth and mouth, however, is determined culturally. When oral healthcare projects are being carried out in developing countries, differing cultural worldviews can cause misunderstandings between oral healthcare providers and their patients. The oral healthcare volunteer often has to try to understand the local assumptions about teeth and oral hygiene first, before he or she can bring about a change of behaviour, increase therapy compliance and make the oral healthcare project sustainable. Anthropology can be helpful in this respect. In 2014, in a pilot project commissioned by the Dutch Dental Care Foundation, in which oral healthcare was provided in combination with anthropological research, an oral healthcare project in Kwale (Kenia) was evaluated. The study identified 6 primary themes that indicate the most important factors influencing the oral health of school children in Kwale. Research into the local culture by oral healthcare providers would appear to be an important prerequisite to meaningful work in developing countries.
https://userupload.net/ucq2c1km5pb7
Preventive dentistry aims to stop the progression of dental caries by promoting daily habits and clinical therapies that either promote the remineralization of the tooth surface or prevent the formation of the oral biofilm responsible for lowering the oral pH levels in an attempt to prevent cavity formation.
Here is an overall glance on some recent concepts/advances in preventive dentistry with a detail note on pit and fissure sealants
Anomalies of the first and second branchial archesDr Medical
https://userupload.net/8n9v7tg9jkl1
Anomalies of the branchial arches are the second most common congenital lesions of the head and neck in children [1]. They may present as cysts, sinus tracts, fistulae or cartilaginous remnants and present with typical clinical and radiological patterns dependent on which arch is involved. The course of a particular branchial anomaly is caudal to the structures derived from the corresponding arch and dorsal to the structures that develop from the following arch. Branchial anomalies are further typed into cysts, sinuses, and fistulas.
Ankyloglossia a congenital oral anomaly Dr Medical
https://userupload.net/h9ig9byum706
Ankyloglossia, also known as tongue-tie, is a congenital oral anomaly that may decrease mobility of the tongue tip and is caused by an unusually short, thick lingual frenulum, a membrane connecting the underside of the tongue to the floor of the mouth. Ankyloglossia or tongue-tie is the result of a short, tight, lingual frenulum causing difficulty in speech articulation due to limitation in tongue movement. Ankyloglossia is a congenital condition in which a neonate is born with an abnormally short, thickened, or tight lingual frenulum that restricts mobility of the tongue. Ankyloglossia may be associated with other craniofacial abnormalities, but is also often an isolated anomaly.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
4. History
• In the Talmud, 2nd
century AD
•A 12th century Arab physician named Albucasis
•In the U.S., the transmission of hemophilia from mothers
to sons was first described in the early 1800s.
•In 1803, a Philadelphia physician named Dr. John Conrad
Otto wrote an account of "a hemorrhagic disposition
existing in certain families."
• The word "Hemophilia" first appeared in a description of a
bleeding disorder condition at the University of Zurich in
1828.
5. CLICK HERE TO DOWNLOAD
THIS PPT
https://userupload.net/wxvqfbo7ywqu
7. Finding the Cause
In the 20th century doctors looked for the cause of
excessive bleeding. Until then, they had believed
that the blood vessels of hemophiliacs were simply
more fragile.
1925
Although it is probably the most common hereditary
bleeding disorder (affecting approximately 1% to 2%
of the population), von Willebrand disease was not
recognized until 1925.
8. 1937,
Patek and Taylor, two doctors at Harvard,
They called it "anti-hemophilic globulin."
1944
Pavlosky, a doctor from Buenos Aires,
Argentina, did a lab test which showed that
blood from one hemophilic patient could
correct the clotting problem in a second and
vice-versa.
9. Identifying Clotting Factors
In the 1960s the clotting factors were identified
and named.
An article in Nature in 1964
In the 1950s and early 1960s, hemophilia and
other bleeding problems were treated with whole
blood or fresh plasma. Unfortunately, there
wasn't enough of the factor VIII or IX proteins in
these blood products to stop serious internal
bleeding.
Then, in the 1960s, cryoprecipitate was
discovered by Dr. Judith Pool
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11. Then, later in the 1960s and early 1970s,
concentrates containing factor VIII and IX
began to be available. (freeze-dried
powdered concentrates)
blood products carried blood-borne viruses
like hepatitis C and HIV.
In the 1990s, modern treatment, using safer
factor concentrates, has again improved the
outlook
12. Recent progress includes:
• New clotting factor products and drugs such as desmopressin
acetate also known as DDAVP,
• New, synthetic (not derived from plasma) clotting products
that take advantage of recombinant technologies
• Better screening methods to detect and remove viruses and
other agents from factor concentrates and blood products
• Improved surgical options
• Advanced genetic testing methods
• Medically supervised home-infusion therapy
• Prophylactic treatment
14. Platelets-origin
Life span : 7-14 days
Site of destruction: Spleen
Normal count : 1.5 - 4.5 lacks / cc
Increase in count : Thrombocytosis
Decrease in count : Thrombocytopenia
Decrease in platelet count below 40,000is associated with hemorrhagic disorders.
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16. a. Physiological Variations :
Seasonal - Count is more during winter season.
Pregnancy - Count decrease
Exercise, excitement, injection of adrenaline, high altitude
- Increased count.
b. Pathological Variations :
Increased platelet count seen after splenectomy idiopathic.
Decreased platelet count is seen in
Viral infection
Aplastic anaemia
Idiopathic
17. HEMOSTASIS
Primary Hemostasis
Blood vessel contraction
Platelet Plug Formation
Secondary Hemostasis
Activation of Clotting Cascade
Deposition & Stabilization of Fibrin
Tertiary Hemostasis
Dissolution of Fibrin Clot
Dependent on Plasminogen Activation
29. Henoch-Schonlein purpura
20y Male, fever, painful symmetric polyarthritis for a day. During the next two days,
edema and palpable purpura developed.
30. Disorders of coagulation
Hemophilia A(Factor VIII Deficiency)
What Is It?
The incidence of hemophilia A is one in 10,000
live male births. About 17,000 Americans have
hemophilia.
31. Inheritance Pattern
Hemophilia A is caused
by an inherited sex-
linked recessive trait with
the defective gene
located on the X
chromosome.
32.
33. Genetic counseling may be
advised for carriers.
Female carriers can be identified by testing.
A woman is definitely a hemophilia carrier if she is:
• the biological daughter of a man with hemophilia;
• the biological mother of more than one son with hemophilia;
• the biological mother of one hemophilic son who has at least
one other blood relative with hemophilia.
A woman may or may not be a hemophilia carrier if she is:
• the biological mother of one son with hemophilia;
• the sister of a male with hemophilia;
• an aunt, cousin or niece of an affected male related through
maternal ties;
• the biological grandmother of one grandson with hemophilia.
34. Symptoms & Diagnosis
Bruising
Spontaneous bleeding
Bleeding into joints and associated pain and
swelling
Gastrointestinal tract and urinary tract hemorrhage
Blood in the urine or stool
Prolonged bleeding from cuts, tooth extraction, and
surgery
People whose clotting activity is 5 percent of normal
may have only mild hemophilia.
35.
36. Treatments
In the past, mild hemophilia A was typically
treated with infusion of cryoprecipitate or
desmopressin acetate (DDAVP),
. Today, experts recommend desmopressin
injection or Stimate nasal spray.
cryoprecipitate
37. Depending on the severity of the disease, DDAVP
or factor VIII concentrate -prior to dental extractions
and surgery to prevent bleeding.
Immunization with hepatitis B vaccine.
Gene therapy and fetal tissue implant techniques
People who have hemophilia should also avoid
certain drugs that can aggravate bleeding problems:
Aspirin
Heparin
Warfarin
Certain analgesics such as nonsteroidal anti-
inflammatory drugs
38. MASAC made recommendations for treatment of
hemophilia in November of 1999.
They include:
1. Factor VIII products for patients who are HIV
seronegative, including Recombinant factor VIII,
2. Immunoaffinity purified factor VIII concentrates
3. Cryoprecipitate is not recommended because of the
risk of HIV and hepatitis infection.
4. Mild hemophilia A should be treated with
desmopressin, in a DDAVP injection or Stimate
nasal spray.
40. Hemophilia B
(Factor IX Deficiency)
. Hemophilia B ("Christmas disease" )
Is a deficiency in clotting factor IX.
Hemophilia A is seven times more common
than hemophilia B.
The incidence of hemophilia B is one in
34,500 men.
41. Inheritance Pattern
Hemophilia B is caused
by an inherited sex-
linked recessive trait
with the defective gene
located on the X
chromosome. Females
are carriers of this trait.
42. Genetic counseling may be advised for carriers. Female carriers can be
identified by testing.
A woman is definitely a hemophilia carrier if she is:
the biological daughter of a man with hemophilia;
the biological mother of more than one son with hemophilia; • the
biological mother of one son with hemophilia and has at least one
other
blood relative with hemophilia.
A woman may or may not be a hemophilia carrier if she is:
the biological mother of one son with hemophilia;
the sister of a male with hemophilia;
an aunt, cousin or niece of an affected male related through maternal
ties;
the biological grandmother of one grandson with hemophilia.
43. Symptoms include:
nosebleeds
bruising
spontaneous bleeding
bleeding into joints and associated pain and
swelling
gastrointestinal tract and urinary tract hemorrhage
blood in the urine or stool
prolonged bleeding from cuts, tooth extraction and
surgery
prolonged bleeding following circumcision
People whose clotting activity is 5% of normal may
have only mild hemophilia.
44. DIAGNOSIS:
A doctor may suspect hemophilia in a child
whose bleeding is unusual.
A laboratory analysis of blood samples
Determine the severity by testing the activity
of factor IX.
45. Treatments
• Infusing the missing clotting factor.
• To prevent a bleeding crisis- taught to administer
factor IX concentrates at home at the first signs of
bleeding.
• Factor IX concentrate may be given prior to dental
extractions and surgery to prevent bleeding.
• Milder forms of hemophilia need to have dental or
other surgery, the drug desmopressin acetate
(DDAVP) may be given to improve clotting temporarily
so that transfusions can be avoided.
46. MASAC made recommendations for treatment of
hemophilia B in
November of 1999. They include
• Recombinant factor IX products for patients who are HIV
seronegative,
• Patients who are HIV-seropositive should also be treated
with high purity products such as immunoaffinity purified
and recombinant factor VIII products.
• For patients with inhibitors to factors VIII and IX, there is
Recombinant Factor VIIa (NovoSeven). Produced by baby
hamster kidney cells, no human albumin or other proteins
are used in its production, reducing virus risk.
There is also Porcine factor VIII (Hyate C) and activated
prothrombin complex concentrates
47. Complications
• Chronic joint deformities,
• Intracerebral hemorrhage
may also occur.
• Thrombosis may occur
following use of factor IX
concentrate.
48. Von Willebrand Disease
What Is It?
von Willebrand disease is a hereditary
deficiency or abnormality of the von
Willebrand factor in the blood, a protein that
affects platelet function
49.
50. Researchers have identified many variations of the
disease, but most fall into the following classifications
• Type I: This is the most common and mildest form of von
Willebrand disease. Levels of von Willebrand factor are
lower than normal, and levels of factor VIII may also be
reduced.
• Type II: In these people, the von Willebrand factor itself
has an abnormality. Depending on the abnormality, they
may be classified as having Type IIa or Type IIb.
In Type IIa, the level of von Willebrand factor is
reduced, as is the ability of platelets to clump together.
In Type IIb, although the factor itself is defective, the
ability of platelets to clump together is actually increased.
51. Type III: This is severe von Willebrand
disease. These people may have a total
absence of von Willebrand factor, and factor
VIII levels are often less than 10%.
Pseudo (or platelet-type) von Willebrand
disease: This disorder resembles Type IIb von
Willebrand disease, but the defects appears to
be in the platelets, rather than the von
Willebrand factor.
52. Inheritance Pattern
Like hemophilia, the disease is passed down through the
genes. occurs in men and women equally.
Types I and II are usually inherited in what is known as a
"dominant" pattern.
Type III von Willebrand disease, however, is usually
inherited in a "recessive" pattern.
53. Symptoms and Diagnosis
A parent with a history of bleeding problems.
Typically, a child bruises easily or has bleeds
excessively after a skin cut, tooth extraction,
tonsillectomy or other surgery.
A woman may have increased menstrual
bleeding. Bleeding may worsen at times.
On the other hand, hormonal changes, stress,
pregnancy, inflammation and infections may
stimulate the body to increase production of the
von Willebrand factor and temporarily improve
clot formation.
54. Diagnostic signs can include:
normal platelet count
prolonged bleeding time
reduced von Willebrand factor level
reduced platelet adhesion may occur
reduced or increased platelet aggregation
(platelet aggregation test)
ristocetin cofactor is reduced
55. MASAC made recommendations for treatment
of von Willebrand disease in November of
1999. They include:
• Stimate, desmopressin acetate.
(DDAVP),nasal spray or injection
• Viral-inactivated factor VIII preparations rich in
von Willebrand factor, such as Alphanate,
Humate-P and Koate DVI, are
recommended.
• Cryoprecipitate is not recommended except in
life-threatening emergencies because of the
risk of HIV and hepatitis infection.
56. Complications
After any kind of surgery, hemorrhaging may occur.
The condition is worsened by the use of aspirin and
other nonsteroidal anti-inflammatory drugs.
Women may have heavy menstrual periods as well
as risks during pregnancy and childbirth. .
57. Factor I Deficiency (Afibrinogenemia)
What Is It?
Fibrinogen, also known as factor I, is needed
for most types of platelet aggregation. It's the
last step in the clotting process—the "glue"
that holds the clot together.
58. Included under factor I deficiency are several
rare coagulation disorders known as
congenital fibrinogen defects. They include:
• afibrinogenemia
• hypofibrinogenemia
• dysfibrinogenemia
59. Inheritance Pattern
The disorder is not sex-linked
It affects both males and females with equal
frequency.
It is autosomal recessive.
60. Symptoms and Diagnosis
Few people who have any of these
disorders suffer symptoms, although some are
predisposed to form blood clots (thrombosis).
61. Treatments
-Many people with hypofibrinogenemia or
dysfibrinogenemia need no treatment.
-Those who require treatment may be given
cryoprecipitate or fresh frozen plasma.
The goal of treatment is to raise the patient's
fibrinogen level to 100 mg/dL for minor bleeding
and up to 200 mg/dL for surgery or severe
bleeding. (One unit of fresh frozen plasma has
about 450 mg of fibrinogen.)
62. Complications
-Risk of thrombosis.
-In women, menstrual bleeding can be a
severe problem and must be controlled
63. Factor II Deficiency(Prothrombin)
What Is It?
Prothrombin is a vitamin K-dependent
proenzyme that functions in coagulation.
1)a congenital version called
hypoprothrombinemia,
2)acquired version called
dysprothrombinemia.
64. congenital, factor II deficiency is extremely
rare.
Acquired factor II deficiency is more common.
It results from vitamin K deficiency, severe
liver disease and therapeutic use of
anticoagulant drugs.
65. Inheritance Pattern
A congenital factor II deficiency is a very rare
inherited disorder that results in deficient
blood clotting. The disorder is not sex-linked
as is hemophilia.
It affects both males and females with equal
frequency.
It is autosomal recessive,
66. Symptoms include:
• umbilical cord bleeding at birth
• nose bleeds
• abnormal menstrual bleeding
• abnormal bleeding after delivery
• bleeding after trauma
• bleeding after surgery
• easy bruising
Signs and Tests:
• prolonged prothrombin time
• prolonged partial thromboplastin time
• factor II assay showing decreased activity
• levels of prothrombin ranging from 2% to 50% of normal
67. Treatments
MASAC made recommendations for treatment of
factor II deficiency in November of 1999.
They include:
• Prothrombin complex concentrates (PCCs) can be
used, but these products vary considerably in the
amount of factors they contain.
• Fresh frozen plasma can be used as along as it is
processed to reduce the risk of viral infection.
68. Complications
Bleeding has to be
controlled in instances
of trauma or surgery, or
else bleeding into the
brain or skull can occur.
69. Factor V Deficiency (Para hemophilia)
What Is It?
Factor V deficiency is also known as Owren's
disease or parahemophilia.
This deficit was identified in Norway in 1943. Since
then about 150 cases have been reported, occurring
in both men and women. The exact frequency of this
rare disorder is unknown, but is estimated to be one
per 1 million
70. Inheritance Pattern
The disorder is not sex-linked as is hemophilia.
It affects both males and females with equal
frequency.
It is autosomal recessive,
Several families with combined deficiencies of factors
V and VIII have been reported.
71. Symptoms and Diagnosis
Symptoms include:
bleeding into the skin
excessive bruising with minor injuries
nose bleeds
bleeding of the gums
excessive menstrual bleeding
prolonged or excessive loss of blood with surgery or
trauma
Diagnosing the deficiency involves tests and signs such
as:
factor V assay showing decreased activity
slightly prolonged bleeding time (in some people)
prolonged partial thromboplastin time
prolonged prothrombin time
72. Treatments
-There are no commercially available
concentrates of factor V, so fresh plasma or
fresh frozen plasma infusions are used .
-The half-life of factor V is 24 hours.
-This is an inherited disorder; there is no known
prevention.
Complications
-Dangerous hemorrhaging can occur if bleeding
isn't controlled quickly.
- If platelets are used as a source of factor V,
antiplatelet antibodies can be induced.
73. Factor VII Deficiency (Proconvertin or
Stable Factor)
What Is It?
This extremely rare disorder can be inherited
or acquired by people who do not have
hemophilia who take Coumadin, a drug used
to inhibit blood clotting.
74. This disorder occurs in one in 500,000 males
and females.
Congenital factor VII deficiency should be
distinguished from acquired factor VII
deficiency, which may result from liver
disease, vitamin K deficiency or other
malabsorption conditions.
75. Inheritance Pattern
The disorder is not sex-linked as is hemophilia.
It affects both males and females with equal
frequency.
It is also autosomal recessive,
Those who have inherited a defective factor VII
gene from only one parent will usually have only
moderate levels of the factor but no symptoms.
76. Symptoms and Diagnosis
Symptoms include:
• bleeding of mucous membranes
• spontaneous nosebleeds
• excessive bruising
• prolonged menstrual bleeding
• bleeding into muscles
• bleeding into joints
Diagnosis is made by testing for factor VII in
the blood.
77. • Signs and tests include:
-prolonged prothrombin time
-- normal partial thromboplastin time
-- decreased factor VII assay
78. MASAC made recommendations for treatment of Factor VII
deficiency in November of 1999. They include:
• Recombinant factor VIIa (NovoSeven).
• Prothrombin complex concentrates (PCCs) can be
used, but these products vary considerably in the
amount of factors they contain.
• Fresh frozen plasma can be used as along as it is
processed to reduce the risk of viral infection.
TREATMENTS
79. Complications
These can include hemorrhages, strokes or
other neurological problems related to central
nervous system bleeding.
• Fatal intracranial bleeding caused by birth
trauma has occurred.
• Menstrual bleeding may also be severe.
80. THROMBOCYTOPENIA
Definition
Thrombocytopenia is any disorder in which
there are not enough platelets. Platelets are
cells in the blood that help blood to clot. This
condition is sometimes associated with
abnormal bleeding.
81. Causes, incidence, and risk factors
Thrombocytopenia is often divided into three
major causes of low platelets:
1) Low production of platelets in the bone
marrow
2) Increased breakdown of platelets in the
bloodstream (called intravascular)
3) Increased breakdown of platelets in the
spleen or liver (called extravascular
82. 1)Disorders that involve low production in the
bone marrow include:
-Aplastic anemia
-Cancer in the bone marrow
-Infections in the bone marrow (rare)
-Drugs (very rare)
84. Symptoms
-Bruising
-Nose bleeds or bleeding in the mouth
` -Rash (pinpoint red spots)
-Other symptoms may be present as well,
depending on the cause of the condition. Mild
thrombocytopenia can occur without symptoms.
85. Signs and tests
-CBC shows low platelets
-Bone marrow aspiration or Biopsy may be
normal or may show low megakaryocytes
(platelet precursors) or an infiltrating disease.
-PTTclotting study is normal
-PTclotting study is normal
-Platelet associated antibodies may be present
86. Treatment
Treatment depends on the cause of the condition.
In some cases, a transfusion of platelets may be
required to stop or prevent bleeding.
Expectations (prognosis)
The outcome depends on the disorder causing the
low platelet counts.
Complications
- Hemorrhage
-Gastro intestinal blleding
-Bleeding in the brain (intracranial hemorrhage)
87. DISSEMINATED INTRAVASCULAR
COAGULATION
DIC is a syndrome arising as a complication of many
different serious and life-threatening illnesses.
1) Acute (overt) form it is a hemorrhagic disorder,
2) Chronic (nonovert) DIC, on the other hand, is more
subtle and involves thromboembolism accompanied by
evidence of activation of the coagulation system.
91. Clinical and laboratory findings in DIC
Acute DIC
Clinical findings
Multiple bleeding sites
Ecchymoses of skin, mucous membranes
Visceral hemorrhage
Ischemic tissue
92. Laboratory abnormalities
Coagulation abnormalities:
prolonged prothrombin time,
activated partial thromboplastin time,
thrombin time; decreased fibrinogen levels;
increased levels of FDP (eg, on testing for
FDP, D dimer)
Platelet count decreased as a rule but may be
falling from a higher level yet still be normal
Schistocytes on peripheral smear
93. Clinical and laboratory findings in DIC
Chronic DIC
Clinical findings
Signs of deep venous or arterial thrombosis or embolism
Superficial venous thrombosis, especially without varicose
veins
Multiple thrombotic sites at the same time
Serial thrombotic episodes
94. Laboratory abnormalities
Modestly increased prothrombin time in some patients
Shortened or lengthened partial thromboplastin time
Normal thrombin time in most patients
High, normal, or low fibrinogen level
High, normal, or low platelet count
Increased levels of FDP (eg, on testing for FDP, D dimer)
Evidence of molecular markers* (eg, thrombin-antithrombin
complexes, activation markers on platelet membranes,
prothrombin fragment F1+2)
95. Treatment options for DIC syndrome
. Treat the underlying disease
Avoid delay
Treat vigorously (eg, shock, sepsis, obstetrical problems)
Manage the DIC
Acute DIC
Without bleeding or evidence of ischemia
No treatment
With bleeding
Blood components as needed
Fresh frozen plasma
Cryoprecipitate
Platelet transfusions
With ischemia
Anticoagulants (see "with thromboembolism" below) after
bleeding risk is corrected with blood products
96. Chronic DIC
Without thromboembolism
No specific therapy needed but prophylactic drugs
(eg, low-dose heparin, low-molecular-weight heparin)
With thromboembolism
Heparin or low-molecular-weight heparin, trial of warfarin
sodium (Coumadin).
*Some patients respond to warfarin, others do not. Use of
low-molecular-weight heparin for prolonged periods has
potential hazards and is expensive but can be useful when
warfarin therapy fails despite good control (international
normalized ratio [INR], 2-3).
98. What causes ITP?
Who gets ITP?
How does ITP affect children?
How is ITP diagnosed?
How is ITP treated in children?
How does ITP affect adults?
How is ITP treated in adults?
99. What about ITP in pregnant women?
Diagnosing ITP during pregnancy can be difficult,
because platelet counts may be low for other reasons.
About 5% of women have mildly low platelet counts at
the end of a normal pregnancy. The cause of this is
unknown. The platelet count goes back to normal right
after delivery.
A baby born to a mother with ITP may have a low blood
platelet count a few days to a few weeks after birth.
These babies are usually kept in the hospital for several
days for observation (watching to make sure they are ok)
before they go can home.
100. Thrombotic thrombocytopenic purpura
What is thrombotic thrombocytopenic purpura?
Thrombotic thrombocytopenic purpura (TTP) is a rare
blood condition characterised by the formation of
small clots (thrombi) within the circulation, which
results in the consumption of platelets and thus a low
platelet count (thrombocytopenia).
What causes TTP?
101. DRUG-INDUCED IMMUNE
THROMBOCYTOPENIA
DRUG-INDUCED IMMUNE
THROMBOCYTOPENIA is a condition where
the use of certain drugs leads to the formation
of antibodies against platelets. These
antibodies can cause a low platelet count,
which make bleeding more likely. If these
antibodies are formed during pregnancy, they
may pass from the mother to the fetus.
102. Thrombocytopenia (nonimmune) drug-
induced; Nonimmune
thrombocytopenia - drug-induced
Drug-induced nonimmune thrombocytopenia
is a reduction in normally functioning platelets
that can be caused by certain drugs.
Platelets are important in forming blood clots.
Certain drugs may decrease the number of
platelets by damaging the bone marrow where
platelets are made. Decreased platelets may
cause easy bruising or abnormal bleeding.
103. PRIMARY THROMBOCYTHEMIA
Essential thrombocythemia; Essential
thrombocytosis
Primary thrombocythemia is a condition of
overproduction of platelets without a
recognizable cause.
104. Causes, incidence, and risk factors
Primary thrombocythemia is a slowly progressing
disorder caused by overgrowth of a type of cell that is
a precursor of blood cells. Although the platelets are
primarily affected, the red blood cells and white blood
cells are also involved
The formation of blood clots, called thrombosis, may
coincide with bleeding episodes.
It may even cause strokes in some people.
Risk factors are unknown.
The incidence is about 3 out of 100,000 people
105. Symptoms
Nosebleeds (epistaxis )
Bleeding from the gums
Bleeding from the gastrointestinal tract
Easy bruising
Prolonged bleeding from surgical procedures or tooth
extraction
Enlarged lymph nodes (rare)
Bloody stools
Headache
Numbness of hands or feet
Dizziness
Ulcers on fingers or toes
106. Signs and tests
Bone marrow aspiration.
CBC that shows elevated platelet count.
Uric acid level may be elevated.
Physical examination may show enlarged
spleen or liver
107. Treatment
If a patient is having life-threatening complications-
platelet pheresis.
Long-term decrease of the platelet count using
medications can reduce both bleeding and clotting
complications.
Most common medications include hydroxyurea,
interferon-alpha, or anagrelide. For patients with a known
clotting tendency, aspirin may help decrease clotting
episodes.
Some patients do not need any treatment.
108. Expectations (prognosis)
The outcome varies with reports ranging from
prolonged periods without complications in some
people, to fatalities from complications related to
hemorrhage and thrombosis in others.
Complications
Severe hemorrhage
Thrombotic episodes (stroke, heart attack, or blood
clots in extremities)
Acute leukemia or myelofibrosis can develop in some
patients
109. HYPERSPLENISM
Hypersplenism is increased activity of the
spleen caused by tumors, anemia, malaria,
tuberculosis, and various connective tissue
and inflammatory diseases.
An enlarged spleen is often accompanied by
a low level of one or more types of blood
cells. The enlarged spleen can cause
stomach pain on the left side, as well as
feeling full prematurely after eating
110. DENTAL EVALUATION
good thorough medical historygood thorough medical history
a physical examination
screening clinical lab tests
excessive bleeding following surgical procedure
Family HX
Personal HX
Medications
Past & Present Illness
Spontaneous Bleeding
111. REVIEW PATIENT’S MEDS
FIVE DRUGS THAT INTERFERE WITH
HEMOSTASIS
ASPIRIN
ANTICOAGULANTS
ANTIBIOTICS
ALCOHOL
ANTICANCER
113. DENTAL PATIENTS
LOW RISK
Patients with No Hx of Bleeding Disorders
Normal Laboratory Results
MODERATE RISK
Patients on Chronic Oral Anticoagulant
Therapy. PT is 1.5 - 2 Times Control Range
Patients on Chronic Aspirin Therapy
HIGH RISK
Patients with Known Bleeding Disorders
Patients without Known Bleeding Disorders Who Have
Abnormal Laboratory Results
115. MODERATE RISK
PATIENTS
Anticoagulants -
Consult Physician
Aspirin Therapy - BT,
Consult Physician
HIGH RISK PATIENTS
Close Coordination
with Physician
Hospitalization (Platelet
Transfusion) (Factor
Replacement)(Vit K
Therapy)(Dialysis
116. CONCLUSIONS
The history (medical /family history) is
extremely important in evaluating patients with
disorders of hemostasis.
Dental extractions are a very common major
stresses of the haemostatic mechanism, and a
prior history of excessive bleeding following an
extraction is important.
So, thorough understanding and knowledge
about bleeding disorders is very much needed
for dental professionals to minimize the
complications of many treatment procedures.
117. References
Davidson’s “principles and practice of medicine-19th
edition;-Hanslet, Chilvers, Boon, Colledge, Hunters.
Medical emergencies in the dental practice –malammed;
5th edition
Bailey and Love’s Short practice of surgery-23rd edition;
Russel, Williams, Bulstrode;
Complications in Oral and Maxillofacial surgery-1st edition;
Kaban, Pogrel, Perrot.
Concise Medical Physiology;-5th edition; Chaudhari
Systemic disease in dental treatment-1st edition;-
Michael.J.Tullman, Spencer.W.Redding.
Clinical hematology-7th edition;-Maxwell.M.Wintrobe.
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