This document discusses various types of anemia. It defines anemia as a condition with fewer than normal red blood cells or hemoglobin. The types discussed include iron deficiency anemia, thalassemia, anemia of chronic disease, sideroblastic anemia, and hemolytic anemia. For each type, the document outlines causes, pathophysiology, clinical presentation, laboratory findings, and management. Key points like ringed sideroblasts, ineffective erythropoiesis, and hereditary spherocytosis are explained. Treatment involves addressing the underlying cause, iron supplementation, blood transfusions, or splenectomy in some cases.
Information about megaloblastic anemia and it's etiology and its classification.
Vitmain b12 deficiencies
Folic acid deficiencies
Signs and symptoms of megaloblastic anemia
Neural tube defects
Information about megaloblastic anemia and it's etiology and its classification.
Vitmain b12 deficiencies
Folic acid deficiencies
Signs and symptoms of megaloblastic anemia
Neural tube defects
p
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1-Differentiate between the different causes of anemia
2. Discuss the investigations that may clarify the diagnosis
3. Recognize the predisposing factors and consequences of iron deficiency anemia and discuss how to manage it
4. Discuss the hereditary basis and clinical features of sickle cell anemia and thalassemia .
prepared by med_students0
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!
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
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.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
- 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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S 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
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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.
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2. What is anemia?
any condition in which the number of red cells, the amount of hemoglobin
or the volume of packed red blood cells per unit volume is less than
normal.
a pathophysiological condition in which the body cannot meet its
demands for oxygen
4. Erythrocyte Indices:
Hemoglobin (Hgb)
Hematocrit (Hct)
Mean Corpuscular Volume (MCV)
Mean Corpuscular Hemoglobin (MCH)
Mean Corpuscular Hemoglobin Concentration (MCHC)
Red Cell Distribution Width (RDW)
[Packed Cell Volume (PCV)]
5. RBC “rule of 3’s”:
For normal erythrocytes:
hemoglobin (g/dL) 3 x RBC count (millions)
hematocrit (%) 3 x hemoblogin (g/dL) 3%
Failure to obey this “rule of 3’s” suggests an
abnormality in erythrocytes (sickle cells, etc)
6. classification of anemia by color:
1. hypochromic (decreased color)
• increased central pallor
2. normochromic (normal color)
• central pallor ~1/3 of the RBC diameter
3. hyperchromic (increased color)
(~spherocytosis)
• loss of central pallor
8. When to say anemia?
M: Hb <13.5 Hct <41
F: Hb <12 Hct <36
9. classification by volume:
I. microcytic anemia (MCV <80)
1. iron deficiency anemia
2. thalassemia syndromes
3. anemia of chronic disease
4. sideroblastic anemia
II. normocytic anemia (MCV 80-100)
1. anemia of blood loss
2. hemolytic anemia
III. macrocytic anemia (MCV >100)
1. megaloblastic anemia
10. 1-Iron Deficiency Anemia
Iron: absorbed in duodenum
When iron loss exceeds its intake for a long time, iron storage decreases and
insufficient amount of iron is available for hemoglobin production
Iron deficiency anemia develops in sequence of stages:
1. Iron Depletion
2. Iron Deficient Erythropoiesis
3. Iron Deficiency Anemia
11. Iron Deficiency Anemia cont.
This occurs when
1- iron losses or
2- iron malabsorption
3- physiological requirements exceed absorption.
Daily requirement is 10 mg.
12. Iron Deficiency Anemia cont.
Blood loss
The most common explanation in men and postmenopausal women is
gastrointestinal blood loss, (malignancy, gastritis, peptic ulceration,
inflammatory bowel disease).
In women of child-bearing age, menstrual blood loss, pregnancy and
breastfeeding contribute to iron deficiency.
13. Iron Deficiency Anemia cont.
Malabsorption
Gastric acid is required to release iron from food and helps to keep iron in the soluble
ferrous state.
Causes:
1. Achlorhydria in the elderly.
2. Drugs such as proton pump inhibitors.
3. Previous gastric surgery.
4. Coeliac disease.
Physiological demands
Iron requirement increased in infancy, puberty and pregnancy.
14.
15. Clinically:
Clinical:
- general fatigue
- SOB
- spoon nails (koilonychia)
- smooth, sore tongue
- epithelial atrophy
- cheilosis; scaling and fissures at the corners of the mouth
- pica (eating unusual things [e.g., dirt])
26. Treatment:
Transfusion is not necessary and oral iron replacement is appropriate.
Ferrous sulphate 200 mg 3 times daily is adequate.
It should be continued for 3–6 months to replete iron stores.
Many patients suffer gastrointestinal side-effects with ferrous sulphate,
including dyspepsia and altered bowel habit.
27. Treatment cont.:
When this occurs, reduction in dose to 200 mg twice daily or a switch to
ferrous gluconate 300 mg twice daily
The haemoglobin should rise by around 10 g/L every 7–10 days and a
reticulocyte response will be evident within a week.
Patients with malabsorption or chronic gut disease may need parenteral
iron therapy.
28. 2-Thalassemia Syndromes:
~heterogeneous hemolytic disorders characterized by
quantitative abnormalities of hemoglobin synthesis
• genetic defect in globin production
• selective depression or absence of a- or b- chain of hemoglobin
• broad spectrum of presentation
• predominantly seen in persons of Mediterranean, African and
Asian ancestry
29. Thalasemia types:
α-thalassemia : α-chain deficiency due to gene deletion
β-thalassemia : β-chain deficiency due to point mutation
(Cooley’s anemia)
30. Thalasemia cont.:
Two (2) pathological mechanisms to contribute to develop
anemia
1. inadequate Hgb formation low MCHC,
hypochromasia
2. relative excess of unaffected Hgb chain
aggregation and precipitation of excess chain
damage to the cell membrane
loss of K+ and impaired DNA synthesis
apoptosis of RBCs in BM
(“ineffective erythropoiesis”)
32. B-thalassemia :
Beta thalassemia syndromes are a group of hereditary
disorders characterized by a genetic deficiency in the
synthesis of beta-globin chains. In the homozygous
state, beta thalassemia (ie, thalassemia major) causes
severe, transfusion-dependent anemia. In the
heterozygous state, the beta thalassemia trait (ie,
thalassemia minor) causes mild to moderate microcytic
anemia
33. B-thalassemia cont.:
Mutations in globin genes cause thalassemias.
Beta thalassemia affects 1 or both of the beta-globin
genes.
These mutations, by causing impaired synthesis of the
beta-globin protein component of Hb, result in anemia.
β+ → some β chain production
β0 → no β chain production
34. B-thalassemia cont.:
The most common type of thalassaemia.
Most prevalent in the (Mediterranean area).
Heterozygotes have thalassaemia minor, a condition in which there
is usually mild anaemia and little or no clinical disability.
Homozygotes have thalassaemia major, either are unable to
synthesise haemoglobin b or, at best, produce very little; after the
first 4–6 months of life, they develop profound hypochromic
anaemia.
35. Thalasemia major:
• homozygous β+/β+ or β0/β0
• severe anemia at 6 to 9 months of age requiring
blood transfusion
• death at early age, if not transfused
• severe erythrophagocytosis and extramedullary
hematopoiesis
hepatosplenomegaly
36. Thalasemia major cont.:
• marked red marrow expansion “Crew-Cut” sign
• hemosiderosis
• heart disease 2º to hemochromatosis is the major
cause of death in older patients
40. Thalasemia minor:
• much more common than Thalassemia major
• heterozygous b+/b or b0/b
• peripheral smear: hypochromia, microcytosis,
basophilic stippling, target cells
usually asymptomatic or mild anemia (microcytic
anemia)
41. A-thalassemia:
The alpha thalassemia (α-thalassemia) syndromes are a
group of hereditary anemias of varying clinical severity.
They are characterized by reduced or absent
production of 1 or more of the globin chains of which
human hemoglobin is composed
42. A-thalassemia cont.:
There are two alpha gene loci on chromosome 16 and therefore each
individual carries four alpha gene alleles.
If one is deleted, there is no clinical effect.
If two are deleted, there may be a mild hypochromic anaemia.
If three are deleted, the patient has haemoglobin H disease.
If all four are deleted, the baby is stillborn (hydrops fetalis).
43. Work up:
Check for iron deficiency anemia: serum iron/ TIBC/ serum ferritin.
Blood film: may show target cells, microcytosis, hypochromia, and
anisopoikilocytosis
hemoglobin electrophoresis.
Ultrasonography of the liver, gallbladder, and spleen
Polymerase chain reaction (PCR) and restriction endonuclease
gene mapping and anti-L globin monoclonal antibodies.
44. Management of thelasemia:
Allogeneic haematopoietic stem cell transplantation (HSCT) from HLA-
compatible sibling.
Transfusion to maintain Hb > 10 g/dL.
Folic acid 5 mg daily.
Splenectomy; if there is splenomegaly causing mechanical problems or
there is excessive transfusion needs.
45. 3-anemia ofchronic disease:
A common type of anaemia, particularly in hospital populations.
It occurs in the setting of chronic infection, chronic inflammation or
neoplasia.
The anaemia is not related to bleeding, haemolysis or marrow infiltration.
It is mild, with haemoglobin in the range of 8,5–11,5 g/dL, and is usually
associated with a normal MCV (normocytic, normochromic).
The serum iron is low but iron stores are normal.
46. Anemia of chronic disease cont.:
Pathogenesis
Hepcidin production is induced by proinflammatory cytokines, especially
IL-6.
Hepcidin binds to ferroportin on the membrane of iron-exporting cells,
such as small intestinal enterocytes and macrophages, internalising the
ferroportin and thereby inhibiting the export of iron from these cells into the
blood.
The iron remains trapped inside the cells in the form of ferritin, levels of
which are therefore normal or high in the face of significant anaemia.
47. Anemia of chronic disease cont.:
Diagnosis
It is often difficult to distinguish ACD associated with a low MCV from iron
deficiency.
Examination of the marrow may ultimately be required to assess iron stores
directly
49. Anemia of chronic disease cont.:
Treatment: The preferred initial form of therapy for
anemia of chronic illness is treatment of the underlying
disease
Use of erythropoiesis-stimulating agents (ESAs)
and blood transfusion are reserved for severe and
symptomatic cases.
50. 4-sideroblastic anemia:
a heterogeneous group of disorders associated with
various defects in the porphyrin biosynthetic
pathway:
-porphyrn biosynthesis defects
-diminished heme synthesis
-increased cellular iron uptake
51. sideroblastic anemia cont.:
characterized by the association of anemia with
presence of ringed sideroblast (a normoblast containing
excessive deposits of iron within mitochondria) in bone
marrow
52. sideroblastic anemia cont.:
characterized by the association of anemia with
presence of ringed sideroblast (a normoblast containing
excessive deposits of iron within mitochondria) in bone
marrow
56. sideroblastic anemia cont.:
clinical: characterized by hypochromic, often microcytic, red
cells in the blood usually mixed with normochromic cells
hypochromic anemia
hyperferremia
increased transferrin saturation
58. sideroblastic anemia cont.:
Treatment:Treatment of sideroblastic anemia may include
1- removal of toxic agents;
2- administration of pyridoxine, thiamine, or folic acid;
3-transfusion (along with antidotes if iron overload develops from
transfusion);
4- other medical measures; or bone marrow or liver transplantation.
64. Hereditary spherocytosis:
Treatment:
1- Aplastic crises occasionally can cause the hemoglobin level to fall
because of ongoing destruction of spherocytes that is not balanced by
new red blood cell (RBC) production. RBC transfusions often are necessary
in these cases
2- Patients with HS are instructed to take supplementary folic acid for life in
order to prevent a megaloblastic crisis.
3-Splenectomy is the definitive treatment for HS
65. Ellipticosis:
-intrinsic defect in the membrane cytoskeleton
-genetic: autosomal dominant
-pathoetiology: impaired aggregation of spectrin
-anemia:90% of pt. are non-anemic
non-hypochromic elliptocytes >25%
(nl=<15%)
Sx: splenomegaly
67. G6DP
-Pathophysiology: decreased half life of G6PD
increased vulnerability to oxidative denaturation due to
limited generation of NADPH (older RBCs are preferentially
destroyed)
-Genetics:
high genetic heterogeneity
x-linked recessive ( full expression in male hemizygote)
68. G6DP
hemolysis after exposure to oxidant stress
- drugs: primaquine, chloroquine, sulfonamides, nitrofurantoins
- infections: viral hepatitis, pneumonia, typhoid fever
“favism” : hemolysis after ingestion of fava beans (Mediterranean
type)
69. G6DP
LABS:
Complete blood cell count (CBC) and reticulocyte count
Lactate dehydrogenase (LDH) level
Indirect and direct bilirubin level
Serum haptoglobin level
Urinalysis for hematuria
Urinary hemosiderin
Peripheral blood smear poikilocytes, some spherocytes
- Heinz bodies : precipitates of denatured hemoglobin material
- “bite cells”
71. G6PD
TREATMENT:
Most individuals with glucose-6-phosphate dehydrogenase (G6PD)
deficiency do not need treatment. However, they should be taught to
avoid drugs and chemical exposures that can cause oxidant stress
72. Sickle cell disease
prototype of hereditary hemoglobinopathies
structurally abnormal hemoglobin from a point
mutation
75. Sickle cell disease
Typical baseline abnormalities in the patient with SCD are as follows:
Hemoglobin level is 5-9 g/dL
Hematocrit is decreased to 17-29%
Total leukocyte count is elevated to 12,000-20,000 cells/mm 3 (12-20 X
109/L), with a predominance of neutrophils
Platelet count is increased
Erythrocyte sedimentation rate is low
Peripheral blood smears demonstrate target cells, elongated cells, and
characteristic sickle erythrocytes
Presence of RBCs containing nuclear remnants (Howell-Jolly bodies)
indicates that the patient is asplenic
78. Sickle cell disease
Traetment:The drugs used in treatment of sickle cell disease (SCD) include
antimetabolites, analgesics, antibiotics, and vaccines.
Management of vaso-occlusive crisis
Management of chronic pain syndromes
Management of chronic hemolytic anemia
Prevention and treatment of infections
Management of the complications and the various organ damage
syndromes associated with the disease
Prevention of stroke
Detection and treatment of pulmonary hypertension
79. Megaloblastic anemia
This results from a deficiency of vitamin B12 or folic acid, or from
disturbances in folic acid metabolism.
Folate is an important substrate of, and vitamin B12 a co-factor for, the
generation of the essential amino acid methionine from homocysteine.
Deficiency of either vitamin B12 or folate will therefore produce high
plasma levels of homocysteine and impaired DNA synthesis.
The end result is cells with arrested nuclear maturation but normal
cytoplasmic development: so-called nucleocytoplasmic asynchrony.
80. Megaloblastic anemia
Vitamin B12 deficiency, is associated with neurological disease in up to
40% of cases, although advanced neurological disease due to B12
deficiency is now uncommon in the developed world.
The main pathological finding is focal demyelination affecting the (spinal
cord, peripheral nerves, optic nerves and cerebrum).
The most common manifestations are sensory, with peripheral
paraesthesiae and ataxia of gait
83. Megaloblastic anemia
Vitamin B12
1 μg daily requirement.
The liver stores enough vitamin B12 for 3 years, so B12 deficiency takes years to
become manifest.
Measurements:
Normal > 210 ng/L
Intermediate 180–200 ng/L
Low < 180 ng/L
84. Megaloblastic anemia
Causes of deficiency:
1. Dietary deficiency.
2. Gastric pathology.
3. Pernicious anemia.
4. Small bowl pathology.
85. Megaloblastic anemia
Treatment of B12 deficiency:
Treat with hydroxycobalamin 1000 μg IM for 6 doses 2 or 3 days apart, followed
by maintenance therapy of 1000 μg every 3 months for life.
The reticulocyte count will peak by the 5th–10th day after starting replacement
therapy.
The haemoglobin will rise by 10 g/L every week until normalised.
A sensory neuropathy may take 6–12 months to correct.
Long-standing neurological damage may not improve
86. Megaloblastic anemia
Folic acid
The minimum daily intake of 50 μg.
Excess cooking destroys folates.
Total body stores of folate are small and deficiency can occur in a matter
of weeks.
88. Megaloblastic anemia
Pregnancy-induced folate deficiency is the most common cause of
megaloblastosis worldwide and is more likely in the context of twin
pregnancies, multiparity and hyperemesis gravidarum.
89. Megaloblastic
Treatment of folic acid deficiency:
Oral folic acid 5 mg daily for 3 weeks will treat (acute deficiency).
5 mg once weekly is adequate (maintenance therapy).
Prophylactic folic acid in pregnancy prevents megaloblastosis in women
at risk, and reduces the risk of fetal neural tube defects.
The use of folic acid alone in the presence of vitamin B12 deficiency may
result in worsening of neurological deficits.