UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
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Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Slideshow is from the University of Michigan Medical
School's M2 Hematology / Oncology sequence
View additional course materials on Open.Michigan: openmi.ch/med-M2Hematology
Thrombotic Microangiopathies and AntiPhospholipid SyndromeRichard McCrory
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This was a Nephrology seminar from last year on Thrombotic Microangiopathies, and I covered a small piece on Antiphospholipid Syndrome at the end. I hope it's informative!
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Slideshow is from the University of Michigan Medical
School's M2 Hematology / Oncology sequence
View additional course materials on Open.Michigan: openmi.ch/med-M2Hematology
Thrombotic Microangiopathies and AntiPhospholipid SyndromeRichard McCrory
Â
This was a Nephrology seminar from last year on Thrombotic Microangiopathies, and I covered a small piece on Antiphospholipid Syndrome at the end. I hope it's informative!
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Thrombocytopenia is most frequently encountered Hematological problem in hospitalized patients. The most common causes and differential diagnosis of In-patient and Outpatient presentations of Thrombocytopenia is discussed here. Useful for Internal Medicine Boards . Archer Internal Medicine Board review lectures will be released soon.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Blood banking and transfusion medicine i&iiAbdulKaderSouid
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UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
UAEU - CMHS - Hematology-Oncology Course - MMH 302 - HONC 320. Education material for medical students - It cover basic principles of hematology and oncology, including CAR-T and gene editing. It can be used for study and review. It illustrates main principles of hematology and oncology.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
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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 Departmentâs official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Prix Galien International 2024 Forum ProgramLevi Shapiro
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June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMENâS HEALTH: FERTILITY PRESERVATION
- WHATâS NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
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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.
New Drug Discovery and Development .....NEHA GUPTA
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The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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- 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
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years â 64.8%, 20 years â 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP â 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 N0âN12, 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 N0âN12 (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.
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, Ganongâs 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
4. Patient
âą A 12-year-old boy has anemia and thrombocytopenia.
â âHemoglobin, âreticulocyte count, âRBC fragments (schistocytes), and
hemoglobinuria â intravascular hemolysis.
âą His thrombocytopenia responded to plasma transfusion.
âą He then had recurrent seizures.
49/26/2018
Black arrows point to RBC fragments, red arrow points to a
large platelet, and blue arrow to a spherocyte.
8. von Willebrand factor-cleaving protease (VWFCP) deficiency â TTP
âą Autosomal recessive disease
âą Intravascular (microangiopathic) hemolysis
âą Consumptive thrombocytopenia
âą The pathologic process is reversed by plasma infusion
âą Seizure disorder
3) Factor VIII delivery
1) Platelet adhesion to collagen
2) Platelet-platelet spreading and aggregation
Collagen
vWF
GPIb-ïĄ
Platelet
GPIIb/IIIa
vWF
Fibrinogen
Platelet
Factor VIII
-S-S-
-S-S-
Results of his work-up:
âą von Willebrand factor-cleaving protease (VWFCP) activity <5% (normal, â„67%)
âą VWF antigen and activity are normal.
âą VWF Multimer Analysis = âmolecular weight multimers
9. âą Von Willebrand factor (VWF) is a multimeric plasma glycoprotein that mediates
platelet adhesion and aggregation.
âą ADAMTS13 is a protease that cleaves VWF in circulating blood and thereby
limits platelet aggregation.
Familial Thrombotic Thrombocytopenic Purpura =
von Willebrand Factor-Cleaving Protease Deficiency =
ADAMTS13 Deficiency
âą His ADAMTS13 gene sequencing shows homozygous splice site mutation,
c.2234+2T>C in ADAMTS13.
âą ADAMTS13: âA Disintegrin-like and metalloproteinase with thrombospondin
type 1 motif, member 13â.
âą ADAMTS13 gene is located at: 9q34.2. MIM#604134
(http://omim.org/entry/604134)
10. âą In patients with TTP, abnormally large VWF multimers in
the plasma cause excessive intravascular platelet
aggregation.
âą These extremely adhesive VWF multimers arise due to a
deficiency of VWF-cleaving protease.
109/26/2018
Blood 1997;89:3097-3103
Familial Thrombotic Thrombocytopenic Purpura =
von Willebrand Factor-Cleaving Protease (VWFCP) Deficiency =
ADAMTS13 Deficiency
11. âą All studied six patients with familial TTP lacked vWFâcleaving protease
activity, but had no inhibitor.
âą Of studied 24 patients with non-familial TTP, an inhibitor (IgG) of vWFâ
cleaving protease was found in 20 of these patients.
âą All 10 patients with familial HUS had normal protease activity.
âą All 13 patients with non-familial HUS had normal or slightly protease
activity.
119/26/2018
NEJM 1998;339:1578-1584
Familial Thrombotic Thrombocytopenic Purpura =
von Willebrand Factor-Cleaving Protease (VWFCP) Deficiency =
ADAMTS13 Deficiency
12. âą Mutations in a member of the ADAMTS gene family cause thrombotic
thrombocytopenic purpura.
âą Proteolysis of VWF observed in normal plasma is decreased in TTP patients.
âą In four pedigrees of humans with congenital TTP, the responsible protease was mapped to
chromosome 9q34.
âą A predicted gene in the identified interval corresponded to a new member of the ADAMTS
family of zinc metalloproteinase genes (ADAMTS13).
âą Analysis of patients' genomic DNA identified 12 mutations in the ADAMTS13 gene,
accounting for 14 of the 15 disease alleles studied.
âą Deficiency of ADAMTS13 is the molecular mechanism responsible for TTP.
âą Physiologic proteolysis of VWF and other ADAMTS13 substrates is required for
normal vascular homeostasis.
129/26/2018
Familial Thrombotic Thrombocytopenic Purpura =
von Willebrand Factor-Cleaving Protease (VWFCP) Deficiency =
ADAMTS13 Deficiency
Nature 2001;413:488-94.
13. Familial Thrombotic Thrombocytopenic Purpura
von Willebrand Factor-Cleaving Protease (VWFCP) Deficiency
ADAMTS13 Deficiency
9/26/2018 13
Day Treatment
Hemoglobin
(g/L)
Platelet
count
(x109/L)
Hemoglobinuri
a
ADAMTS13
activity
-1 - 100 99 Small <5%
0 Plasma 10.9 118 Small 19
1 - 10.3 103 Small 31
6 - 11.8 203 Negative 12
8 - 11.9 264 Negative 18
10 - 11.8 188 Negative <10
17 - 11.6 114 Trace <10
20 - 11.0 33 Large <10
22 Plasma 10.7 22 Moderate 23
Plasma infusion every two weeks is recommended as the treatment
of choice.
14. A 17-year-old girl presents with pallor, bruising and seizure. Her examination shows significant
pallor and purpura. Her lymph nodes, liver, and spleen are normal.
Her WBC count is 8 x109/L (normal, 5 to 10), hemoglobin concentration 73 g/L (normal, 110 to
130), reticulocyte count 318 x109/L (normal, 35 to 100), and platelet count 65 x109/L (normal, 150
to 400). Blood smear shows numerous schistocytes with a markedly reduced number of platelets.
PT/INR, aPTT, TT, fibrinogen, and D-Dimer level are normal.
Her serum creatinine is normal. Her urinalysis is remarkable for 2 RBC per high power field
(normal, <5) and 3+ hemoglobin (normal, negative).
She received plasma infusion, which promptly improved her thrombocytopenia.
Which one of the following results on further investigation is correct?
A. Complement dysregulation (hemolytic uremic syndrome)
B. Mutation in ADAMTS13 gene (thrombotic thrombocytopenic purpura)
C. Low von Willebrand factor (VWD)
D. Positive direct antiglobulin test for IgG (autoimmune hemolytic anemia)
E. Missing CD59 on the surface of blood cells (paroxysmal nocturnal hemoglobinuria)
14
15. Which one of the following diagnoses is correct?
A. Macrophage activation syndrome (MAS)
B. Hemolytic uremic syndrome (HUS)
C. Thrombotic thrombocytopenic purpura (TTP)
D. Hemophagocytic lymphohistocytosis (HLH)
E. Disseminated intravascular coagulopathy (DIC)
15
A 17-year-old girl presents with pallor, bruising and seizure. Her examination shows significant
pallor and purpura. Her lymph nodes, liver, and spleen are normal.
Her WBC count is 8 x109/L (normal, 5 to 10), hemoglobin concentration 73 g/L (normal, 110 to
130), reticulocyte count 318 x109/L (normal, 35 to 100), and platelet count 65 x109/L (normal, 150
to 400). Blood smear shows numerous schistocytes with a markedly reduced number of platelets.
PT/INR, aPTT, TT, fibrinogen, and D-Dimer level are normal.
Her serum creatinine is normal. Her urinalysis is remarkable for 2 RBC per high power field
(normal, <5) and 3+ hemoglobin (normal, negative).
She received a fresh frozen plasma infusion, which promptly improved her thrombocytopenia.
16. Which one of the following treatments is correct?
A. Eculizumab (for HUS and PNH)
B. Packed red cell transfusion (for AHA)
C. Platelet transfusion (for bone marrow failure syndromes)
D. Plasma exchange (for TTP and HUS)
E. Immunoglobulin transfusion (for ITP)
16
A 17-year-old girl presents with pallor, bruising and seizure. Her examination shows significant
pallor and purpura. Her lymph nodes, liver, and spleen are normal.
Her WBC count is 8 x109/L (normal, 5 to 10), hemoglobin concentration 73 g/L (normal, 110 to
130), reticulocyte count 318 x109/L (normal, 35 to 100), and platelet count 65 x109/L (normal, 150
to 400). Blood smear shows numerous schistocytes with a markedly reduced number of platelets.
PT/INR, aPTT, TT, fibrinogen, and D-Dimer level are normal.
Her serum creatinine is normal. Her urinalysis is remarkable for 2 RBC per high power field
(normal, <5) and 3+ hemoglobin (normal, negative).
She received plasma infusion, which promptly improved her thrombocytopenia.
17. Which one of the following managements is correct?
A. Stool studies for Escherichia coli serotype O157:H7
B. Monitor hemoglobin concentration, platelet count, and serum creatinine
C. Platelet transfusion
D. Packed red blood cell transfusion
E. Plasma exchange
17
A 17-year-old girl presents to the emergency department with pallor, fatigue and abnormal
bruises. Her examination shows significant pallor, mild jaundice, and ecchymosis mostly in her
extremities. Her lymph nodes, liver, and spleen are normal.
Her WBC count is 8 x109/L (normal, 5 to 10), hemoglobin concentration 73 g/L (normal, 110 to
130), reticulocyte count 318 x109/L (normal, 35 to 100), and platelet count 65 x109/L (normal, 150
to 400). Blood smear shows schistocytes with decreased number of platelets. PT/INR, aPTT, TT,
fibrinogen, and D-Dimer level are normal.
Her serum creatinine is normal. Her urinalysis is remarkable for 2 RBC per high power field
(normal, <5) and 3+ hemoglobin (normal, negative).
18. Required Reading
âą George JN. Clinical practice. Thrombotic thrombocytopenic
purpura. N Engl J Med 2006;354:1927.
âą George JN. How I treat patients with thrombotic
thrombocytopenic purpura: 2010. Blood 2010;116:4060.
âą Levy GG, Nichols WC, Lian EC, et al. Mutations in a member of
the ADAMTS gene family cause thrombotic thrombocytopenic
purpura. Nature 2001;413:488.
9/26/2018 18