This document summarizes key aspects of hematology, including hemostasis, platelet function, coagulation pathways, and classifications of anemia. It describes the vascular response to injury, roles of platelets and von Willebrand factor in adhesion and aggregation. The extrinsic and intrinsic coagulation pathways and anticoagulant systems are outlined. Approaches to evaluating anemia include classification by cell size and distinguishing iron deficiency anemia from anemia of chronic disease based on laboratory findings. Common causes and treatments are summarized for different types of anemia.
Platelet and coagulation post graduate lecture Monkez M Yousif
This lecture is prepared for postgraduate students in Internal medicine. It presents a physiologic and basic background of the process of homeostasis followed by a practical approach to diagnosis and brief information of different causes of bleeding disorders
Anticoagulation in patients with liver cirrhosis copyM Soliman
Presentation on Anticoagulation in patients with liver cirrhosis
including normal physiology of hemostasis, the role of the liver in hemostasis, effect of liver cirrhosis in hemostatic system and indication and use of anticoagulant in portal vein thrombosis & DVT
The aim of this work is to illustrate a difficult diagnostic in vitamin B12 deficiency because of using of multivitamin preparations to a patient with unknown etiology of anemia. History Patient: a 70 year old engineer, following 8 years vegetable – dietary, was admitted to the county hospital, in neurology department, with diagnostic of poli-radiculonevrites, received in ward the treatment with milgama (containing 250 micro-gram multivitamin). After a lipotimia status the patient was transferred to cardiology department. Laboratory examinations showed in peripheral blood: Hb = 6 3 g/dl; Ht = 18.8%; RBC= 290.000/mm³; PLT. = 214000/mm³; WBC = 5300/³mm; Ret. = 3, 7%; Erythrocytes indices = normal values; ESR = 38 mm/h, moderate increase and serum iron decreased, 36 microgram/dl value. On blood smear in optic microscopy was registered: Band = 5% (with nucleus in ring!!!), differential count being normally with aspect flags on Coulter HMX Analyzer with 22 parameters: neutrophilia, lymphopenia, anemia. To microscopic examination of slide from bone morrow, have occurred the hyperplasic series of erythrocytes ~ 45%, deficiency of erythropoiesis, poly-cromathopil and acidophil erythroblasts with megaloblastic character, large metamielocytes and giant band forms. Macrocytes and ovalocytes where also presented. Biopsy results from gastric mucosa showed lesions of chronic gastritis, non-atrophic epithelium. Conclusions: Megaloblastosis appears in some time with vitamin B12 deficiently in bone morrow but no in peripheral blood because of administration of multivitamin drugs, deleting haematological shape of megaloblastic anemia.
Platelet and coagulation post graduate lecture Monkez M Yousif
This lecture is prepared for postgraduate students in Internal medicine. It presents a physiologic and basic background of the process of homeostasis followed by a practical approach to diagnosis and brief information of different causes of bleeding disorders
Anticoagulation in patients with liver cirrhosis copyM Soliman
Presentation on Anticoagulation in patients with liver cirrhosis
including normal physiology of hemostasis, the role of the liver in hemostasis, effect of liver cirrhosis in hemostatic system and indication and use of anticoagulant in portal vein thrombosis & DVT
The aim of this work is to illustrate a difficult diagnostic in vitamin B12 deficiency because of using of multivitamin preparations to a patient with unknown etiology of anemia. History Patient: a 70 year old engineer, following 8 years vegetable – dietary, was admitted to the county hospital, in neurology department, with diagnostic of poli-radiculonevrites, received in ward the treatment with milgama (containing 250 micro-gram multivitamin). After a lipotimia status the patient was transferred to cardiology department. Laboratory examinations showed in peripheral blood: Hb = 6 3 g/dl; Ht = 18.8%; RBC= 290.000/mm³; PLT. = 214000/mm³; WBC = 5300/³mm; Ret. = 3, 7%; Erythrocytes indices = normal values; ESR = 38 mm/h, moderate increase and serum iron decreased, 36 microgram/dl value. On blood smear in optic microscopy was registered: Band = 5% (with nucleus in ring!!!), differential count being normally with aspect flags on Coulter HMX Analyzer with 22 parameters: neutrophilia, lymphopenia, anemia. To microscopic examination of slide from bone morrow, have occurred the hyperplasic series of erythrocytes ~ 45%, deficiency of erythropoiesis, poly-cromathopil and acidophil erythroblasts with megaloblastic character, large metamielocytes and giant band forms. Macrocytes and ovalocytes where also presented. Biopsy results from gastric mucosa showed lesions of chronic gastritis, non-atrophic epithelium. Conclusions: Megaloblastosis appears in some time with vitamin B12 deficiently in bone morrow but no in peripheral blood because of administration of multivitamin drugs, deleting haematological shape of megaloblastic anemia.
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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!
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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7. Von Willebrand Factor
● Quantitative (types 1 and 3) and qualitative
(types 2A, 2B, 2M, and 2N) abnormalities of
vWF result in vWD.
● The 2 main functions of vWF are
– 1) to mediate platelet adhesion and aggregation
and
– 2) to act as a carrier protein for factor VIII,
protecting it from proteolytic inactivation
8. Disorders of Platelet Adhesion
Von Willebrand disease
Autosomal dominant
Spontaneous bleeding from mucous membranes, prolonged
bleeding from wounds, and menorrhagia in young females.
Bleeding may be exacerbated by aspirin or NSAID use
Hemarthrosis is uncommon.
Lab studies: Type 1 - a mild to moderate reduction in vWF
antigen (vWF:Ag) and activity
Type 3 - vWF is absent.
Healthy people with blood group O have vWF levels that are 25%
to 30% lower than in people with blood groups A, B or AB; thus,
they may receive a misdiagnosis of vWD. Therefore, ABO typing
should be part of the initial testing.
Normal platelet count, Normal PT,
Prolonged PTT, Prolonged bleeding time
9. Diagnostic: Abnormal platelet response to ristocetin
Normalizes after addition of normal plasma
Treatment: Desmopressin (ADH Analog)
Intravenous infusion of 0.3 mcg/kg body weight releases vWF
from its storage sites; levels should be measured 60 minutes after infusion.
Side effects include facial flushing, headache, mild decrease in blood pressure,
mild tachycardia, and hyponatremia. Repeated doses at intervals shorter than 24
hours may result in a decrease or loss of response (tachyphylaxis) and syndrome
of inappropriate antidiuresis (SIAD), leading to hyponatremia and seizures.
Type 3 vWF: purified plasma-derived vWF concentrates are the therapy of
choice
10.
Bernard-Soulier syndrome
Autosomal recessive
Lack of GpIb receptor.
Labs: Prolonged Bleeding Time, Thrombocytopenia
Abnormal ristocetin cofactor assay
Not correctable with normal plasma infusion
11. Platelet Aggregation
ADP and Thromboxane A2
Insertion of glycoprotein IIb/IIIa (GpIIb/GpIIIa)
receptors on the platelet surface.
Platelets bind to each other by binding to
fibrinogen using GPIIb-IIIa
12. Disorders of Platelet Aggregation
Uremia or Renal Failure
Accumulation of toxic products
Inhibition of platelet phospholipids
Prolonged Bleeding Time
Treatment: Dialysis & Desmopressin acetate
Glanzmann disease
Autosomal recessive
Gp IIb/IIIa receptor deficiency
Prolonged BT
13. Coagulation Cascade
Two Pathways
Extrinsic Pathway – Defect in PT
Intrinsic Pathway – Defect in PTT (25 to 40
seconds)
Activation of Factor II to IIa and Fibrinogen to Fibrin
Extrinsic Pathway
Trauma to the endothelium
Tissue Factor (factor III) and tissue phospholipids.
TF-FVII complex
Co-factors: Vitamin K, Calcium
14.
15.
Intrinsic Pathway
Activation of Factor XII
Collagen
Key Points:
Vitamin K dependent factors: II, VII, IX, X, Protein C
& S
All Vitamin K dependent factors require Calcium
Clinical: Neonates require Vitamin K
Constant activation of the coagulation system leads
to deficiency in I, II, V and VIII. (sepsis, DIC)
16. Anticoagulant System
Regulate clot formation
Two systems
Protein C & S
Vit. K dependent
Protein C activated by thrombomodulin.
Inactivates Factors Va, VIIIa
Protein S – cofactor for activated Protein C
Antithrombin
Serine protease inhibitor
Inhibits Factors Iia, VIIa, Ixa, Xa, Xia, Xiia
Heparin*
18. Lab Report of CBC
Hb – Concentration of Hb in the blood
Hct – Percentage Value of volume of RBCs in
the blood
MCV - average RBC volume; normal range is
80 to 100 fL
RDW - measure of the variation in width of
RBCs
MCHC – average concentration of Hb in RBCs.
Reticulocyte count - decreased RBC
production or decreased survival of RBCs
Corrected reticulocyte count = (measured
Hct/45) × reticulocyte count.
19. Approach to Anemia
Determine whether patient is anemic by looking
at the Hb.
Classify the anemia as microcytic, normocytic,
or macrocytic by looking at the MCV.
Determine whether the bone marrow is
compensating appropriately by looking at the
reticulocyte count (use correction formulas if
necessary).
23. Microcytic Anemia
Acquired – Iron Deficiency Anemia
Functional Iron – Hemoglobin, myoglobin,
Catalase and Cytochrome
Ferritin
Hemosiderin
Ferroportin
inhibited by hepcidin
Retention of Iron inside cells
Transferrin
TIBC – 300microgm/L
Saturation – 33%
24.
Iron Deficiency Anemia
Dietary deficiency - elderly populations,
children,poor, pregnant women
Decreased absorption
Generalized malabsorption
Post-gastrectomy
Chronic Blood loss
25. Stages of IDA
Decreased storage iron leading to Decreased
serum ferritin.
Decreased circulating iron.
Formation of microcytic/hypochromic anemia.
26. Pathophysiology of IDA
Clinical signs of IDA include the following:
Pallor, fatigue, shortness of breath
Glossitis—inflammation of the tongue
Koilonychia—concave or spoon-shaped nails
Pica—obsessive craving for nonnutritional
materials (e.g., ice, dirt)
Plummer Vinson Syndrome
27.
28.
29. Laboratory
Increased RDW
Hb, Hct, and MCV are decreased
Serum iron and Ferritin levels will be decreased
Iron saturation will be decreased
TIBC will be increased
Increased free erythrocyte protoporphyrin
(FEP)
31. Anemia of Chronic Disease
Iron being trapped in bone marrow
macrophages
Most common anemia in hospitalized patients
Chronic illness leads to continued released of
cytokines (Il-6)
IL-6 signals the liver to release Hepcidin
Increased retention of iron in cells