The primary function of platelets is their role in hemostasis. Briefly, under normal physiological conditions, platelets will adhere to and begin to spread over the surface of subendothelial cells exposed by damage to the vascular endothelium.(1) Adhesion is dependent on the platelet membrane glycoprotein lb complex. The von Willebrand factor (vWF) is required for both adhesion and spreading.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Platelets have many functions, including phagocytosis of viruses, latex, immune complexes and iron; maintenance of vascular integrity
by filling gaps that form in the endothelium and by directly supporting endothelial cells; synthesis and release of vWF in humans and some animal species, and fibronectin;
participating in surface adhesion andactivation processess (Caen and Rosa, 1995; Clemetson, 1995; Nurden, 1995);
production and release of potent smooth muscle and endothelial cell proliferating factor( s); and retraction of clots, a process that stabilizes the initial hemostatic plug and activates clot lysis.
Hemostasis is the mechanism that leads to cessation of bleeding from a blood vessel. It is a process that involves multiple interlinked steps. This cascade culminates into the formation of a “plug” that closes up the damaged site of the blood vessel controlling the bleeding.
Disseminated Intravascular coagulation is a very common and life endangering pathological condition due to consumptive coagulopathy.
This is a very serious disease and prompt diagnosis may help in early initiation of treatment.
A detailed description of various stages in blood coagulation, clotting factors involved, the role of calcium, vitamin K, thrombin, phospholipids in blood coagulation, various tests for blood clotting, the significance of bleeding disorders in the treatment of periodontal disease and management.
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
More Related Content
Similar to platelets :its role in normal and diseases.pdf
Hemostasis is the mechanism that leads to cessation of bleeding from a blood vessel. It is a process that involves multiple interlinked steps. This cascade culminates into the formation of a “plug” that closes up the damaged site of the blood vessel controlling the bleeding.
Disseminated Intravascular coagulation is a very common and life endangering pathological condition due to consumptive coagulopathy.
This is a very serious disease and prompt diagnosis may help in early initiation of treatment.
A detailed description of various stages in blood coagulation, clotting factors involved, the role of calcium, vitamin K, thrombin, phospholipids in blood coagulation, various tests for blood clotting, the significance of bleeding disorders in the treatment of periodontal disease and management.
Coagulation: In medicine, the clotting of blood. The process by which the blood clots to form solid masses, or clots.
More than 30 types of cells and substances in blood affect clotting. The process is initiated by blood platelets. Platelets produce a substance that combines with calcium ions in the blood to form thromboplastin, which in turn converts the protein prothrombin into thrombin in a complex series of reactions. Thrombin, a proteolytic enzyme, converts fibrinogen, a protein substance, into fibrin, an insoluble protein that forms an intricate network of minute threadlike structures called fibrils and causes the blood plasma to gel. The blood cells and plasma are enmeshed in the network of fibrils to form the clot.
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Many evidences that CSCs also play a central role in the pathogenesis and progression of carcinomas of the head and neck (HNSCC), including OSCC,have been found.
Early tissue culture studies showed that only a subpopulation of OSCC cells can form expanding tumor colonies, suggesting that human OSCC may contain some form of stem cells and it was subsequently shown that only a small subpopulation of the cells in OSCC corresponds to tumor-initiating cells.
These finding are in accordance with CSCs concept (17,34) that the tumor mass is a mixture of (a) CSCs dividing themselves to feed the tumor's growth, b) transient amplifying cells that divide themselves a few times before maturing into (c) differentiated tumor cells that do not contribute to tumor growth (4).
The isolation of CSCs from oral cancers has mainly been performed with the CD44 marker that was initially used to isolate breast cancer CSCs.
Clinical Description
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia representing a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features [Golan et al 2000]. Most individuals are diagnosed because they have classic features. CCD spectrum disorder affects most prominently those bones derived from intramembranous ossification, such as the cranium and the clavicles, although bones formed through endochondral ossification can also be affected. Cooper et al [2001] recorded the natural history of 90 probands and 56 first- and second-degree relatives; findings highlight the clinical variability of this condition within affected members of the same family who harbor the same pathogenic variant. Roberts et al [2013] reviewed their experience with more than 100 affected individuals in South Africa.
Classic CCD. The most prominent clinical findings in individuals with classic CCD are listed in Suggestive Findings and include: abnormally large, wide-open fontanelles at birth that may remain open throughout life; clavicular hypoplasia resulting in narrow, sloping shoulders that can be opposed at the midline; and abnormal dentition
Further medical problems identified in individuals with CCD spectrum disorder include short stature, skeletal/orthopedic findings, dental complications, ENT complications, endocrine findings, and mild developmental delay.
Molecular Pathogenesis
RUNX2 encodes runt-related transcription factor 2 (RUNX2), a transcription factor involved in osteoblast differentiation and skeletal morphogenesis. RUNX2 is essential for osteoblast differentiation during intramembranous ossification as well as chondrocyte maturation during endochondral ossification [Zheng et al 2005]. RUNX2 contains an N-terminal stretch of consecutive polyglutamine and polyalanine repeats known as the Q/A domain, a runt domain, and a C-terminal proline/serine/threonine-rich (PST) activation domain. The runt domain is a 128-amino-acid polypeptide motif originally described in the Drosophila runt gene that has the unique ability to independently mediate DNA binding and protein heterodimerization [Zhou et al 1999].
The majority of RUNX2 pathogenic variants in individuals with classic CCD affect the runt domain and most are predicted to abolish DNA binding [Lee et al 1997, Mundlos et al 1997, Otto et al 2002]. Pathogenic missense variants cluster at arginine 225 (p.Arg225) of RUNX2, a critical residue for RUNX2 function. In vitro studies have shown that pathogenic missense variants at p.Arg225 interfere with nuclear accumulation of RUNX2.
Hypomorphic RUNX2 alleles with partial loss of protein function, c.90dupC and c.598A>G, are associated with mild CCD, isolated dental anomalies, and significant intrafamilial variability.
Mechanism of disease causation. Loss of function
RUNX2-sp
Cleidocranial dysplasia (CCD) spectrum disorder is a skeletal dysplasia representing a clinical continuum ranging from classic CCD (triad of delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and dental abnormalities), to mild CCD, to isolated dental anomalies without other skeletal features [Golan et al 2000]. Most individuals are diagnosed because they have classic features. CCD spectrum disorder affects most prominently those bones derived from intramembranous ossification, such as the cranium and the clavicles, although bones formed through endochondral ossification can also be affected. Cooper et al [2001] recorded the natural history of 90 probands and 56 first- and second-degree relatives; findings highlight the clinical variability of this condition within affected members of the same family who harbor the same pathogenic variant. Roberts et al [2013] reviewed their experience with more than 100 affected individuals in South Africa.
Wound healing is a highly dynamic process and involves complex interactions of extracellular matrix molecules, soluble mediators, various resident cells, and infiltrating leukocyte subtypes.
The immediate goal in repair is to achieve tissue integrity and homeostasis
PV is caused by autoantibodies that target cadherins, specifically desmogleins, though there may be some role for desmocollin; thus, this is a type 2 hypersensitivity reaction.[24][25] Acantholysis, or the loss of keratinocyte–keratinocyte adhesion, is interrupted by circulating IgG autoantibodies to intercellular adhesion molecules.[26][27] Acantholysis is seen as a result of the autoantibodies destroying the intracellular connections, leading to bullae that can easily rupture (known clinically as the Nikolsky sign).
A “super-compensation hypothesis” recently submitted by Sinha et al. proposes that additional factors may also play a role in PV.[28] Multiple mechanisms for antibody-induced acantholysis have been suggested, including the induction of signal transduction and the inhibition of adhesive molecule function through steric hindrance, which can trigger cell separation.[29] The pathogenesis of PV has been described in more detail by Hammers et al.[30]
In patients with PV, autoantibodies against desmoglein 1 (Dsg 1) and desmoglein 3 (Dsg 3) is the purported cause.[31] Desmogleins are transmembrane glycoproteins that are an integral part of desmosomes which, in part, are required for cell–cell adhesion via interaction with intermediate filaments. The most common targets of desmoglein for IgG antibodies are the extracellular cadherin domains, which can result in the loss of desmosome-adhesive properties. These signaling pathways trigger endocytosis, depletion, and direct inhibition of Dsg 3 interactions.[32] It is generally believed that the amino portion of the cadherin proteins is most implicated in the pathogenesis of acantholysis leading to PV.[33]
Many animal models have shown that enzymatic inactivation of Dsg 1 and gene deletion of Dsg 3 results in pathology similar to PV.[34][35] This phenomenon was observed to be dose-dependent and suggests that reducing the circulating levels of IgG against Dsg 1 and Dsg 3 can improve patient outcomes.[36] In patients with primarily cutaneous disease, Dsg 1 likely plays a role more superficially, whereas Dsg 3 is more likely to be found in deeper cutaneous structures and mucous membranes.[37][38] The implication is that Dsg 3 can compensate for the absence of Dsg 1 in mucosal structures (thus demonstrating PV in cutaneous lesions only). In contrast, Dsg 1 without Dsg 3 is insufficient to manage mucous membranes or cutaneous lesions alone, implying that Dsg 1 is in lower proportion in mucous membranes.
The binding of antibodies to desmogleins has been confirmed by epitope mapping and is presumed to disrupt desmoglein binding by affecting steric hindrance.[39] Another theory for the pathophysiology of PV is the desmoglein nonassembly depletion hypothesis. This theory suggests that autoantibodies not only bind desmoglein but that they also bind each other, leading to crosslinking and the inability of desmosomes to maintain cell–cell adhesion.[40][41]
PV is caused by autoantibodies that target cadherins, specifically desmogleins, though there may be some role for desmocollin; thus, this is a type 2 hypersensitivity reaction.[24][25] Acantholysis, or the loss of keratinocyte–keratinocyte adhesion, is interrupted by circulating IgG autoantibodies to intercellular adhesion molecules.[26][27] Acantholysis is seen as a result of the autoantibodies destroying the intracellular connections, leading to bullae that can easily rupture (known clinically as the Nikolsky sign).
A “super-compensation hypothesis” recently submitted by Sinha et al. proposes that additional factors may also play a role in PV.[28] Multiple mechanisms for antibody-induced acantholysis have been suggested, including the induction of signal transduction and the inhibition of adhesive molecule function through steric hindrance, which can trigger cell separation.[29] The pathogenesis of PV has been described in more detail by Hammers et al.[30]
In patients with PV, autoantibodies against desmoglein 1 (Dsg 1) and desmoglein 3 (Dsg 3) is the purported cause.[31] Desmogleins are transmembrane glycoproteins that are an integral part of desmosomes which, in part, are required for cell–cell adhesion via interaction with intermediate filaments. The most common targets of desmoglein for IgG antibodies are the extracellular cadherin domains, which can result in the loss of desmosome-adhesive properties. These signaling pathways trigger endocytosis, depletion, and direct inhibition of Dsg 3 interactions.[32] It is generally believed that the amino portion of the cadherin proteins is most implicated in the pathogenesis of acantholysis leading to PV.[33]
Many animal models have shown that enzymatic inactivation of Dsg 1 and gene deletion of Dsg 3 results in pathology similar to PV.[34][35] This phenomenon was observed to be dose-dependent and suggests that reducing the circulating levels of IgG against Dsg 1 and Dsg 3 can improve patient outcomes.[36] In patients with primarily cutaneous disease, Dsg 1 likely plays a role more superficially, whereas Dsg 3 is more likely to be found in deeper cutaneous structures and mucous membranes.[37][38] The implication is that Dsg 3 can compensate for the absence of Dsg 1 in mucosal structures (thus demonstrating PV in cutaneous lesions only). In contrast, Dsg 1 without Dsg 3 is insufficient to manage mucous membranes or cutaneous lesions alone, implying that Dsg 1 is in lower proportion in mucous membranes.
The binding of antibodies to desmogleins has been confirmed by epitope mapping and is presumed to disrupt desmoglein binding by affecting steric hindrance.[39] Another theory for the pathophysiology of PV is the desmoglein nonassembly depletion hypothesis. This theory suggests that autoantibodies not only bind desmoglein but that they also bind each other, leading to crosslinking and the inability of desmosomes to maintain cell–cell adhesion.[40][41]
The primary function of platelets is their role in hemostasis. Briefly, under normal physiological conditions, platelets will adhere to and begin to spread over the surface of subendothelial cells exposed by damage to the vascular endothelium.(1) Adhesion is dependent on the platelet membrane glycoprotein lb complex. The von Willebrand factor (vWF) is required for both adhesion and spreading.
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Phagocytosis begins with adhesion of the phagocyte surface receptors to the pathogen, which then is internalized into vesicles called phagosomes.
Inside the phagocyte, the phagosome fuses to lysosomes, whose contents are released with consequent digestion and pathogen elimination.
Changes in the oxidase’s gene system components present in phagolysosome membrane lead to disability in respiratory burst and generation of reactive oxygen species (ROS).
Tooth development proceeds with reciprocal inductive interactions between stomadeum ectoderm and underlying ectomesenchymal cells in a strictly controlled temporal and spatial order.
Well studied at the molecular biologic level, over 300 genes and 100 growth and differentiation factors are implicated in the control of cellular differentiation and crosstalk in dental development that result in structures containing combination of mineralized tissues (enamel, dentine, cementum), soft connective tissues (dental pulp, periodontal ligament), blood vessels, nerves and lymphatics.
Tooth development proceeds with reciprocal inductive interactions between stomadeum ectoderm and underlying ectomesenchymal cells in a strictly controlled temporal and spatial order.
Well studied at the molecular biologic level, over 300 genes and 100 growth and differentiation factors are implicated in the control of cellular differentiation and crosstalk in dental development that result in structures containing combination of mineralized tissues (enamel, dentine, cementum), soft connective tissues (dental pulp, periodontal ligament), blood vessels, nerves and lymphatics
Diagnostic polymerase chain reaction (PCR) is an extremely powerful, rapid method for diagnosis of microbial infections and genetic diseases, as well as for detecting microorganisms in environmental and food samples.
However, the usefulness of diagnostic PCR is limited, in part, by the presence of inhibitory substances in complex biological samples, which reduce or even block the amplification capacity of PCR in comparison with pure solutions of nucleic acids .
In general, diagnostic PCR may be divided into four steps: (1) sampling, (2) sample preparation, (3) nucleic acid amplification, and (4) detection of PCR products
Diagnostic polymerase chain reaction (PCR) is an extremely powerful, rapid method for diagnosis of microbial infections and genetic diseases, as well as for detecting microorganisms in environmental and food samples.
However, the usefulness of diagnostic PCR is limited, in part, by the presence of inhibitory substances in complex biological samples, which reduce or even block the amplification capacity of PCR in comparison with pure solutions of nucleic acids .
In general, diagnostic PCR may be divided into four steps: (1) sampling, (2) sample preparation, (3) nucleic acid amplification, and (4) detection of PCR products
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
The etiology of a disease refers to the causative trigger(s), whereas pathogenesis refers to the mechanism(s) by which the disease progresses.
In other words, while the microbial biofilm developing on the tooth surface constitutes a necessary etiological factor, its mere presence is insufficient for the initiation of the disease.
Further risk factors, such as host genetics, lifestyle, stress, and systemic conditions, that dictate the immunopathogenesis are crucial for the transition from a healthy to a diseased state.
Nano-composite scaffolds based on electrospun nanofibers have gained great attention due to their ability to emulate natural extracellular matrix (ECM) that affects cell survival, attachment and reorganization.
Promoted protein absorption, cellular reactions, activation of specific gene expression and intracellular signaling, and high surface area to volume ratio are also important properties of nanofibrous scaffolds.
Moreover, several bioactive components, such as bioceramics and functional polymers can be easily blended into nanofibrous matrixes to regulate the physical-chemical-biological properties and regeneration abilities.
Simultaneously, functional growth factors, proteins and drugs are also incorporated to regulate cellular reactions and even modify the local inflammatory microenvironment, which benefit periodontal regeneration and functional restoration
Nano-composite scaffolds based on electrospun nanofibers have gained great attention due to their ability to emulate natural extracellular matrix (ECM) that affects cell survival, attachment and reorganization.
Promoted protein absorption, cellular reactions, activation of specific gene expression and intracellular signaling, and high surface area to volume ratio are also important properties of nanofibrous scaffolds.
Moreover, several bioactive components, such as bioceramics and functional polymers can be easily blended into nanofibrous matrixes to regulate the physical-chemical-biological properties and regeneration abilities.
Simultaneously, functional growth factors, proteins and drugs are also incorporated to regulate cellular reactions and even modify the local inflammatory microenvironment, which benefit periodontal regeneration and functional restoration
Immunologically mediated mucocutaneous diseases constitute a large group of oral mucosal disorders and are triggered by cellular or humoral responses directed against epithelial or connective tissues in a chronic, recurrent pattern.
The treatment of these disorders should be directed not only toward relief from symptoms but also toward treating the underlying immune dysregulation, preventing recurrences, and preserving organ integrity and function
Immunologically mediated mucocutaneous diseases constitute a large group of oral mucosal disorders and are triggered by cellular or humoral responses directed against epithelial or connective tissues in a chronic, recurrent pattern.
The treatment of these disorders should be directed not only toward relief from symptoms but also toward treating the underlying immune dysregulation, preventing recurrences, and preserving organ integrity and function
More from Romissaa ali Esmail/ faculty of dentistry/Al-Azhar university (20)
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!
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.
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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platelets :its role in normal and diseases.pdf
1.
2. Platelets
Disorders
• By
• Romissaa Aly Esmail
• Assistant lecturer of Oral
Medicine, Periodontology,
Diagnosis and Dental
Radiology (Al-Azhar
University)
3. Current nomenclature categorizes platelet disorders based on
normal, increased, or decreased platelet counts; normal or
abnormal platelet function; and whether the diseases are
inherited or acquired.
Platelets are a key component in the hemostatic system.
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9. Figure 111–2. Origin and
development of megakaryocytes.
The pluripotential stem cell
produces a progenitor committed to
megakaryocyte differentiation
(colony-forming unit–
megakaryocyte [CFU-MK]), which
can undergo mitosis.
Eventually the CFU-MK stops
mitosis and enters endomitosis.
During endomitosis, neither
cytoplasm nor nucleus divides, but
DNA replication proceeds and gives
rise to immature polyploid
progenitors, which then enlarge and
mature into morphologically
identifiable, mature
megakaryocytes that shed platelets.
This figure does not necessarily
imply that endomitosis and platelet
formation are
sequential but they can occur
simultaneously. Meg-CFC,
megakaryocyte colony-forming
cells.
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39. NORMAL PLATELET FUNCTION :
THE PRIMARY FUNCTION OF PLATELETS IS THEIR
ROLE IN HEMOSTASIS. BRIEFLY, UNDER NORMAL
PHYSIOLOGICAL CONDITIONS, PLATELETS WILL
ADHERE TO AND BEGIN TO SPREAD OVER THE
SURFACE OF SUBENDOTHELIAL CELLS EXPOSED BY
DAMAGE TO THE VASCULAR ENDOTHELIUM.(1)
ADHESION IS DEPENDENT ON THE PLATELET
MEMBRANE GLYCOPROTEIN LB COMPLEX. THE VON
WILLEBRAND FACTOR (VWF) IS REQUIRED FOR BOTH
ADHESION AND SPREADING.
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43. Figure 112–1. Platelet adhesion,
activation, aggregation, and
platelet-leukocyte interactions.
A. Endothelial cells limit platelet
deposition because they separate
platelets from the adhesive proteins
in the subendothelial area, produce
two inhibitors of platelet function
(nitric oxide [NO] and prostacyclin
[PGI2]), and contain a potent
enzyme (CD39) that can digest
adenosine diphosphate (ADP)
released from platelets.
Platelet adhesion is initiated by loss
of endothelial cells (or, in the case of
an atherosclerotic lesion, rupture or
erosion of the plaque), which
exposes adhesive glycoproteins such
as collagen and von Willebrand
factor (VWF) in the subendothelium.
In addition, VWF and perhaps other
adhesive glycoproteins in plasma
deposit in the damaged area, in part
by binding to collagen.
Platelets adhere to the
subendothelium via receptors that
bind to the adhesive glycoproteins.
Glycoprotein (GP) Ib binding to VWF
plays a prominent role, but integrin
α2β1 (GPIa/IIa) and GPVI binding to
collagen and other platelet
receptors probably also play a role.
After platelets adhere, they undergo an activation process
that leads to a conformational change in integrin αIIbβ3
receptors involving headpiece extension and leg
separation resulting in their ability to bind with high-
affinity select multivalent adhesive proteins, most
prominently fibrinogen and VWF, including the VWF that
binds to collagen in the subendothelial area.
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48. The spreading phenomenon
involves a platelet shape change
from discoid to spheroid, with the
extension of pseudopodia. (2)
During this time, the platelets will
also begin to release the contents
of their dense and alpha granules
including adenosine diphosphate
(ADP), serotonin, vWF, and
fibrinogen.
49. The subsequent interaction of the aggregated platelet mass and coagulation
factors leads to the formation of a stable hemostatic plug.
Aggregation, unlike adhesion, requires fibrinogen binding to the platelet
membrane glycoprotein Ilb/IIIa complex.3
The combined effects of platelet shape change and release prepare the initial
layer of adherent platelets for interaction with circulating inactivated
platelets and the start of platelet aggregation.
50. • Activated platelets also
express P-selectin on their
surface, which leads to
recruitment of leukocytes
via interactions between
platelet P-selectin and P-
selectin glycoprotein
ligand-1 (PSGL-1)
expressed on the surface
of leukocytes.
51. Figure 112–1. B. Platelet aggregation occurs
when the multivalent adhesive
glycoproteins bind simultaneously to
integrin αIIbβ3 receptors on two different
platelets, resulting in receptor crosslinking.
Clustering of the receptors probably also
contributes to the stability of the aggregates
(not shown).
C. After platelets adhere and aggregate,
they help to initiate coagulation by binding
tissue factor-containing vesicles circulating
in the plasma, exposing negatively charged
phospholipids on their surface (not shown),
releasing platelet factor V (not shown), and
releasing procoagulant microparticles.
Activated platelets also express P-
selectin on their surface, which leads
to recruitment of leukocytes via
interactions between platelet P-
selectin and P-selectin glycoprotein
ligand-1 (PSGL-1) expressed on the
surface of leukocytes.
Other interactions between platelets
and leukocytes are detailed in Fig.
112–9.
Thrombus formation is a dynamic
cyclical process, with platelets
repeatedly adhering, aggregating,
and then breaking off and
embolizing downstream.
Platelet–leukocyte aggregates,
platelet aggregates, platelet
microparticles, thrombin,
thromboxane A2 (TXA2),
leukotrienes (LTs), and serotonin
probably all go downstream and
affect the microvasculature.
Ultimately, the vessel either
becomes fully occluded or loses its
thrombogenic reactivity; that is, it
becomes passivated
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54. Figure 113–27. Cascade model of coagulation. This model
shows successive activation of coagulation factors proceeding
from the top of the schematic to thrombin generation and fibrin
formation at the bottom of the schematic.
The intrinsic and extrinsic pathways are indicated.
HK, high-molecular-weight kininogen; PK, prekallikrein; TF, tissue
factor.
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56. Figure 112–17. Collagen
activation of platelets. The
platelet collagen receptor
GPVI is physically and
functionally coupled to the
immunoreceptor tyrosine-
based activation motif (ITAM)-
containing FcRγ-chain.
Upon collagen binding to
GPVI, GPVI dimerizes as a
result of oxidation of
intracytoplasmic
thiol groups (not shown)
and then tyrosine motifs
within the FcRγ-chain are
phosphorylated (P) by the
Src family kinase Fyn.
This action initiates a chain of events
that includes recruitment of the
tyrosine kinase Syk, which is
phosphorylated and activated by Fyn
and Lyn, and phosphorylation of
adaptor proteins LAP and SLP76.
A signaling cascade
activates Bruton tyrosine
kinase (BTK),
phospholipase C (PLC)-2,
protein kinase C (PKC),
and phosphoinositol 3′-
kinase (PI3K).
Ultimately integrins α2β1
and αIIbβ3 are converted
to a high-affinity
(“active”) state.
Activation of α2β1
promotes firm adhesion
to collagen and reinforces
intracellular signaling
pathways.
57. Figure 113–30. The role of immune cells: immunothrombosis. Endothelial cell activation by perturbation or infection causes
neutrophil adhesion and monocyte activation.
Induced tissue factor (TF) expression causes initial fibrin formation, while neutrophil activation by platelet interactions results in
depolymerization of the DNA that bursts out the neutrophil as a mesh-generating neutrophil extracellular trap (NET).
NETs may trap bacteria as innate immune defense, but also cause thrombosis by DNA-dependent factor XII activation and
histone-dependent platelet activation.
Furthermore, von Willebrand factor (VWF) may interact with DNA, which enhances platelet interaction with NETs.
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64. Diagnosis and Evaluation of Bleeding Disorders: Bleeding disorders in which
there are platelet abnormalities may exist as independent entities, in conjunction
with coagulation factor and/or vascular defects, or as secondary manifestations
of numerous other diseases. Careful examination of the patient's history, physical
condition, and laboratory results are all essential for proper diagnosis and
management.|
66. History and Clinical Symptoms: patient history about the nature and frequency of
any past bleeding episodes as well as familial information, current medications
(prescription and over-the-counter- preparations), and information regarding any
past and/or coexisting medical conditions.
The classic clinical symptoms that suggest a platelet disorder include hemorrhages
that are superficial (as opposed to the deep bleeding more commonly associated
with coagulation factor defects), petechial hemorrhages, and bleedings that stop
after the application of pressure and do not spontaneously restart several hours or
days later.
67. Laboratory Evaluation :The screening
tools most readily available for the
evaluation of platelet function are the
platelet count, bleeding time, and
observation of clot retraction.
More rigorous testing, such as aggregation
studies, determination of platelet factor 3
(PF 3) levels, and methods for the
detection of antiplatelet antibodies,
should be carried out when indicated by
preliminary test results and/or the patient
history and clinical symptoms .(4-5)
68. The normal range for platelet counts in healthy adults is 150
to 440xl03L. Bleeding time tests evaluate the function of
platelets and are also influenced by the availability of vWF.
When performed properly, prolongation of the template
bleeding time in the presence of adequate numbers of
platelets indicates defective platelet function. (8)
71. Thrombocytopenia is characterized primarily by an abnormally low
platelet count.
This category includes a wide variety of both congenital and acquired
platelet disorders that can be further subdivided based on the causative
mechanism—decreased or defective production, abnormal
sequestration, enhanced destruction, or excessive loss of platelets. (10)
75. Enhanced Destruction
:Thrombocytopenia due to the
enhanced destruction of platelets
occurs in a variety of
circumstances.
Many of these conditions have a
suspected or confirmed
underlying immune mechanism,.
Nonimmunological mechanisms
include platelet consumption
disorders and situations in which
there is direct destruction of
platelets by physical forces or toxic
substances
76.
77. The initial event occurring in DIC is activation of the coagulation mechanism
with possible formation of circulating thrombi that may cause obstruction
of the microcirculation of organs.
The predominant consumption disorder present is disseminated
intravascular coagulation (DIC),.
Consumption Disorders: Thrombocytopenia due to platelet consumption
may occur in association with numerous conditions, including sepsis,
neoplasms, massive hemolysis.
80. Thrombotic thrombocytopenic
purpura : (TTP) is a disorder of
unknown etiology that is
characterized by thrombocytopenia,
renal failure, hemolytic anemia,
shistocytes on blood smear, and
neurological abnormalities.
81. DIRECT DESTRUCTION :
THROMBOCYTOPENIA DUE TO
DESTRUCTION OF PLATELETS BY PHYSICAL
FORCES IN EXTENSIVE BURNS. MORE
COMMONLY, DIRECT DESTRUCTION OF
PLATELETS IS THE RESULT OF CIRCULATING
SUBSTANCES THAT ACT AS PLATELET TOXINS.
RISTOCETIN, PROTAMINE SULFATE, AND
HEPARIN ARE CAPABLE OF CAUSING
THROMBOCYTOPENIA BY THIS TYPE OF
MECHANISM.17-18. VENOM OR VIRAL
TOXINS MAY DIRECTLY DESTROY PLATELETS.
82. Immune-Related Mechanisms :
Antiplatelet antibodies are associated with premature platelet destruction in
several different clinically defined thrombocytopenias. Patients with
idiopathic (immune) thrombocytopenic purpura (ITP).
83. Platelet antibodies
commonly are
produced in patients
receiving multiple
platelet transfusions.
Some patients may
fail to increase their
platelet count
following
transfusions because
the transfused
platelets are
destroyed by the
antibodies.
Such patients are said to
be "refractory" to random
donor platelet transfusions
and need to have immune-
compatible platelet donors
selected via HLA
compatibility testing or a
platelet cross match assay.
84. Neonatal isoimmune thrombocytopenia occurs in
newborns whose mothers produce an antiplatelet antibody
in response to a fetal antigen inherited from the father and
absent in the mother, analogous to erythroblastosis
fetalis.20
Similarly, mothers with ITP may also produce an antibody
that may cross the placenta and produce thrombocytopenia
in the neonate. (21)
85. Abnormal Sequestration :
Under normal physiological
conditions, approximately one
third of the body's total platelet
mass is sequestered within the
spleen.
A transient thrombocytopenia
may be seen in association with
hypothermic conditions as a
result of increased platelet
sequestration, but this is usually
clinically insignificant.
Hypersplenism can lead to an
increase sequestration of all
blood cell lines, although the
resulting thrombocytopenia is
rarely severe
86.
87.
88. Excessive Loss:
Thrombocytopenia due to the excessive loss of platelets
may occur as the result of extensive hemorrhage or
extracorporeal perfusion..(22)
In both of these situations the bone marrow is unable to
produce platelets quickly enough to compensate for the
acute reduction in the level of circulating platelets.
96. Primary thrombocytosis:
Examination of peripheral blood
smears show a broad range in
platelet size and shape, including
giant platelets and large
aggregates.
Patients with primary
thrombocytosis may experience
thrombotic and/or bleeding
complications.
Hemorrhagic complications are
more common and may result
from defects in platelet function,
consumption of coagulation
factors, and/or the ulceration of
infarcts
97. Secondary Thrombocytosis: The most common conditions that can
result in secondary thrombocytosis are listed in Table III.
The mechanisms that influence the overproduction of platelets
include overcompensation for previously decreased platelet levels,
presence of a platelet-stimulating factor in the plasma associated
with an increased sedimentation rate anemia, iron deficiency.24
98. While secondary thrombocytosis is
generally an asymptomatic
condition, some patients may
experience thrombotic
complications due to spontaneous
platelet clumping or increased
platelet coagulant activity.
Unlike primary thrombocytosis,
abnormal bleeding problems are
rare with secondary thrombocytosis
99. Hemorrhagic
manifestations : skin
manifestations: bruising,
subcutaneous hematomas,
ecchymoses, and epistaxis
or gum bleeding. Petechiae
are never seen.
01
A history of gastrointestinal
blood loss (melena and/or
hematemesis) or biological
evidence in favor of chronic
occult blood loss may be
evidenced at diagnosis.
02
Secondary bleeding,
eventually life-threatening
can also occur after trauma
or surgery
03
100.
101.
102. Qualitative Platelet Disorders:
Congenital and acquired
Congenital platelet defects in which
there are qualitative abnormalities
classified based on platelet function
that is abnormal—adhesion,
aggregation, or secretion.
The most widely used tool for the
diagnosis and/or differentiation of
these disorders is the study of
platelet aggregation patterns
103.
104. Defects of Adhesion
Bernard-Soulier syndrome, also referred to as the giant platelet
syndrome.
The mode of inheritance of this disorder is autosomal recessive,
and the hemorrhagic manifestations may be very severe.
Bernard-Soulier platelets have reduced levels of membrane
glycoprotein lb (GP lb), which is involved in the binding of vWF
and adhesion.25
105. Defects of Primary
Aggregation: Glanzmann's
thrombasthenia is an autosomal
recessive disorder characterized by
defective platelet aggregation.
This disorder is quite rare and the
bleeding manifestations vary
greatly among patients with
seemingly similar degrees of
platelet abnormalities..
106. Defects of Secretion:
two groups—those in which the
platelets contain decreased levels of a
secretable substance, or storage pool
deficiencies (SPDs), and those which
have defects in the physical process of
secretion itself, or primary secretory
defects.
Bleeding episodes
in these patients
are usually minor.
107. Acquired Qualitative Defects:
Idiopathic Thrombocytopeni Purpura: The increased destruction of platelets that
occurs in idiopathic thrombocytopenia purpura (ITP) is often the result of antiplatelet
antibodies.
Platelet functional abnormalities, including aggregation defects and reduced levels of
platelet factor 3 (PF 3), have also been reported in patients with ITP. 28
The biochemical basis of these defects and their influence on hemorrhagic
complications have not yet been clearly established.
108. Drug-Induced Disorders:
A variety of drugs have been observed to influence
platelet function through a number of different
mechanisms. Aspirin ingestion directly affects
platelet function by irreversibly inhibiting
cyclooxygenase, a key enzyme in the production of
thromboxane A2, and laboratory tests reveal an
aggregation pattern similar to that observed with
SPDs.
Penicillin, in high doses, has also
been shown to impair platelet
aggregation.29 Dextran and other
plasma expanders appear to
interfere with both adhesion and PF
3 activity.
109.
110.
111.
112.
113.
114. Giant platelet syndrome (Bernard-Soulier syndrome):
in which the platelets lack the ability to stick adequately to
injured blood vessel walls and as a result of this problem there is
abnormal bleeding.
The giant platelet syndrome usually presents in the newborn period,
infancy, or early childhood with bruises, nose bleeds (epistaxis),
and/or gum (gingival) bleeding. Later problems can occur with
anything which can induce bleeding such
as menstruation, trauma, surgery, or stomach ulcers.
