This document summarizes hemostasis and evaluating bleeding patients. It describes the phases of hemostasis, clues from history and physical exam, laboratory evaluation, and treatment of common causes of coagulopathy. Key points include the phases of primary and secondary hemostasis, patterns of bleeding that suggest platelet or coagulation factor defects, tests of platelet function and coagulation factors, and treatment of liver disease, anticoagulation, DIC, von Willebrand disease, and hemophilia.
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
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
This seminar includes hemostasis,mechanism of blood clotting and associated blood dyscrasias commonly seen in children and their treatments with a note on antifibrinolytics
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
- 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
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
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
2. Phases of hemostasis
• Primary hemostasis
– platelet adhesion and aggregation
• platelet number and function
• von Willebrand factor
• Secondary hemostasis
– activation of the coagulation system
• extrinsic
• intrinsic
• common pathway
3. The bleeding patient
Clues from the history
• Life long history of bleeding
• Family history of bleeding
• History of liver disease
• History of hematologic disorder – ITP, leukemia
• Medication history – ASA, NSAIDS . . .
4. The bleeding patient
Clues from the physical exam
• Pattern of skin and mucosal bleeding seen in
defects of primary hemostasis - suggest
thrombocytopenia, platelet defect or vWD
• Pattern of muscle/deep bleeding suggesting
defect in secondary hemostasis - coagulopathy
• Stigmata of liver disease – arterial nevi,
splenomegaly, palmar erythema
• Pattern and clinical scenario of DIC
5. Clues from the physical exam
Primary hemostatic defects
PetechiaeBruising
6. Clues from the physical exam
Severe primary hemostatic defects
Mucosal bleeding = “wet” purpura
7. Clues from the physical exam
Secondary hemostatic defects
Hemophiliac joint bleed Deep muscle bleed
r/o compartment syndrome
10. Laboratory evaluation of the
bleeding patient
• Hemoglobin/hematocrit
– to assess effect of bleeding
• Platelet count
– bruising below 50K
– bleeding below 10-20K
• Platelet function – PFA-100
– Replaces “bleeding time”
• Basic tests of coagulation – PT, PTT
– Use these to guide specific factor testing
11. PFA-100 testing
Platelet Function Analyzer
Tests 1º hemostasis with
collagen-ADP and collagen-
epinephrine agonists
Very sensitive (90%) for
- vWD diagnosis
- platelet dysfunction
Useful in monitoring DDAVP
therapy
13. Common causes of coagulopathy
• Advanced liver disease – especially low factor VII
– liver makes all coagulation factors, except factor VIII
• Anticoagulants
– Warfarin inhibits factor II, VII, IX and X
– “new” oral anticoagulants – anti-Xa and anti
thrombin inhibitors
• DIC
• Von Willebrand disease
• Hemophilia
• Other inherited factor deficiencies – afibrinogenemia,
factor VII deficiency, etc.
• Coagulation inhibitors
14. Treating the common causes of
coagulopathy
• Advanced liver disease – especially low factor VII
Treat only with bleeding
• Disseminated intravascular coagulation (DIC)
– Treat cause
– Maintain circulation
– Transfuse platelets if platelets <50K and patient is
bleeding, aiming to maintain platelets 50-75K
– Transfuse cryoprecipitate to keep fibrinogen
>50mg/dL
Note: Plasma infusion not often needed as other
coagulation factors not as depleted as fibrinogen
15. Cryoprecipitate
• Contains only
– Fibrinogen
– VIII and vWD factor
– Factor XIII
• Cryoprecipitate packs
pooled from 5 donors
• Short shelf life after
thawing – 4 hours
16. Von Willebrand disease
• Autosomal dominant inherited condition
• Reduced or dysfunctional von Willebrand
factor affects:
– Platelet adhesion and aggregation
– Initiation of secondary hemostasis
– Transport of factor VIII
20. Classification of
von Willebrand’s Disease
Type 1 Quantitative deficiency of vWF 75-80%
Autosomal dominant
Type 2 Qualitative deficiency of vWF 15-20%
Autosomal dominant
Type 3 Absence of vWF 1:1,000,000
Autosomal recessive
21. Laboratory Diagnosis of
von Willebrand Disease
• General screening tests
– PFA – 100 (replaces bleeding time)
– Activated partial thromboplastin time
• Tests specific to vWD
– Factor VIII coagulant function
– vW factor antigen
– vW factor (Ristocetin co-factor) assay
– Ristocetin-induced platelet aggregation
– vW factor Multimer analysis
22. Type 2 vWD:
Qualitative Abnormalities in vWF
Type 2A Impaired secretion or increased proteolysis
Absence of large and intermediate
multimers
Type 2B Increased affinity for gpIb
Absence of large multimers
Type 2M Decreased platelet-dependent function
Normal multimer pattern
Type 2N Decreased affinity for factor VIII
Normal multimers
23. Patterns of multimers in von Willebrand disease
subtypes
•Largest Multimers
•Intermediate
•Multimers
•Small Multimers
•Normal •Type I •Type IIA •Type IIB •Type III
24. Treatment of
von Willebrand Disease
• DDAVP to release vWF from endothelial cells
and platelets
• Replacement of vWF with plasma-derived
products - Humate-P, Alphanate or Wilate
• Prevention of fibrinolysis – mucous
membrane bleeding only – e-amino caproic
acid (Amicar®
)
• General measures – estrogens, topical agents
25. DDAVP in
von Willebrand’s Disease
Releases stored DDAVP from endothelial cells
Increases vWF 2-3 fold – need therapeutic trial
Route Dose Time to Peak
Intravenous 0.3 µg/Kg 30 minutes
Intranasal 300 µg 60 minutes
• Side effects: flushing, headache, hyponatremia,
? myocardial infarction
• Modest tachyphylaxis
26. Hemophilia
Inherited deficiency or dysfunction of factor:
VIII Hemophilia A 85%
(Classic hemophilia)
IX Hemophilia B 15%
(Christmas disease)
27. Types of Hemophilia
# in # in
TYPE FACTOR INCIDENCE USA TEXAS
Hemophilia A VIII 1:7000 17,500 1100
(Classical
hemophilia)
Hemophilia B IX 1:30,000 4000 250
(Christmas
disease)
28. Signs and Symptoms of Hemophilia
• Hemarthroses – joint bleeding
• Muscle hemorrhage
• Soft tissue hematomas
• CNS bleeding
• Uncommon: epistaxis, other mucosal bleeding,
prolonged bleeding from cuts, petechiae
29. Hemophilia Genetics
• X-linked recessive inheritance
• Disease almost exclusively in males
• High rate of spontaneous mutation
– one third new cases have negative
family history
• Carrier testing & pre-natal diagnosis available
(RFLP)
30. Degrees of Severity of Hemophilia
Factor level Frequency and Severity Type
(Normal 50-150%) of bleeding of bleeding
Severe <1% 30-50 times per year Spontaneous
Moderate 1-5% 3-10 times per year Occ spontaneous,
usually post trauma
Mild 5-30% <1 per year Post-trauma or
surgery only
31. Signs and Symptoms of
Hemophilia
• Soft tissue hematomas
• Hemarthroses
• Muscle hemorrhage
• CNS bleeding
• Uncommon: epistaxis, other mucosal
bleeding, prolonged bleeding from cuts,
petechiae
38. Laboratory Diagnosis of Hemophilia
• aPTT Prolonged
• Prothrombin time - INR Normal
• (Bleeding time) Normal
• PFA-100 Normal
• Platelet count Normal
• von Willebrand factor Normal
• Factor VIII One or
the other
• Factor IX reduced•}
39. Treatment in hemophilia
• For mild hemophilia A – always consider
DDAVP – will raise factor level 2-3X
• Factor replacement in doses related to the
severity of the bleed or procedure
40. Hemophilia
Factor VIII and IX Concentrates
• Heat or solvent-detergent treated
– “intermediate” purity factors, e.g. Humate-P
• Purified with
– Monoclonal antibodies
– Chromatography
• Recombinant factors
• In 2014 – factors with longer T1/2
41. Major Emergencies in Hemophilia
• Intra-cranial hemorrhage
• Iliopsoas hemorrhage
• Bleeding around airway
• Uncontrolled external bleeding
42. Management “pearls” for
hemophiliacs in the ER
• Most patients are very knowledgeable about their
disease, its treatment with concentrate and which
veins are best for infusion
• Laboratory testing (PT/PTT, factor assays, CBC, etc.)
or x-rays (e.g, of joints) not routinely necessary
• Following trauma or when any serious illness is
suspected, treat with factor concentrates first and
then do laboratory tests and x-rays
43. The bleeding patient
• Don’t panic!
• Try to figure the cause from history and
physical examination
• Order laboratory tests before blood or other
products given
• Ask for help – there’s a lot of it around!