This document discusses anemias caused by diminished red blood cell production. It covers various inherited and acquired causes, including nutritional deficiencies, bone marrow failure disorders, infiltrative bone marrow disorders, and decreased erythropoietin production. It focuses in depth on megaloblastic anemias caused by vitamin B12 and folate deficiencies, providing details on the mechanisms, morphology, and clinical features of pernicious anemia specifically.
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
Amyloidosis is a condition associated with a number of inherited and inflammatory disorders in which extracellular deposits of fibrillar proteins are responsible for tissue damange and functional compromise. (Robbins Basic Pathology, 9th Edition)
The following slideshow deals with the classification of Amyloidosis:
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
Amyloidosis is a condition associated with a number of inherited and inflammatory disorders in which extracellular deposits of fibrillar proteins are responsible for tissue damange and functional compromise. (Robbins Basic Pathology, 9th Edition)
The following slideshow deals with the classification of Amyloidosis:
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
This Presentation of Hemolytic Anemia try to cover important Hemato-pathological aspects of Red cell membrane disorders ( Hereditary Spherocytosis, others ) , Enzymopathies ( G6PD deficieny, others ) and Hemoglobinopathies ( Thallasemia, SCA) and their differentiation. References includes Robbins pathology, Wintrobes atlas and text, and others
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
Autoimmune hemolytic anemia (AIHA) is a type of normochromic normocytic anemia that is caused by autoantibodies that are produced in the patient against his/her own blood cells, particularly against RBCs. As a result hemolysis occurs leading to anemia.
Autoantibodies are produced secondary to autoimmune diseases, lymphoproliferative disorder (LPDs), certain infections or immunodeficiency syndromes.
In this presentation AIHA is under consideration on a broader scale, with only basic information and concepts.
causes of macrocytic anemia pathopysiology, sign and symptoms and the difference between macrocytic anemia megaloblastIc anemia. causes of hypersegmented neutrophils and its association between them. investigation and medical management plus pictures illustration.
This Presentation of Hemolytic Anemia try to cover important Hemato-pathological aspects of Red cell membrane disorders ( Hereditary Spherocytosis, others ) , Enzymopathies ( G6PD deficieny, others ) and Hemoglobinopathies ( Thallasemia, SCA) and their differentiation. References includes Robbins pathology, Wintrobes atlas and text, and others
Autoimmune hemolytic anemia (or autoimmune haemolytic anaemia; AIHA) occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration.
Autoimmune hemolytic anemia (AIHA) is a type of normochromic normocytic anemia that is caused by autoantibodies that are produced in the patient against his/her own blood cells, particularly against RBCs. As a result hemolysis occurs leading to anemia.
Autoantibodies are produced secondary to autoimmune diseases, lymphoproliferative disorder (LPDs), certain infections or immunodeficiency syndromes.
In this presentation AIHA is under consideration on a broader scale, with only basic information and concepts.
A condition in which the blood doesn't have enough healthy red blood cells.
Anaemia results from a lack of red blood cells or dysfunctional red blood cells in the body. This leads to reduced oxygen flow to the body's organs.
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
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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.
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
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
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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.
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This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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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.
2. Causes of inadequate production of red cells
• Nutritional deficiencies,
• That arise secondary to renal failure and chronic
inflammation.
• Disorders that lead to generalized bone marrow failure,
such as aplastic anemia, primary hematopoietic
neoplasms
• Infiltrative disorders that lead to marrow replacement
(such as metastatic cancer and disseminated
granulomatous disease).
3. DECREASED RED CELL PRODUCTION
Inherited genetic defects
Defects leading to stem cell depletion Fanconi anemia, telomerase defects
Defects affecting erythroblast maturation Thalassemia syndromes
Nutritional deficiencies
Deficiencies affecting DNA synthesis B12 and folate deficiencies
Deficiencies affecting hemoglobin
synthesis
Iron deficiency anemia
Erythropoietin deficiency Renal failure, anemia of chronic disease
Immune-mediated injury of progenitors Aplastic anemia, pure red cell aplasia
Inflammation-mediated iron sequestration Anemia of chronic disease
Primary hematopoietic neoplasms Acute leukemia, myelodysplasia,
myeloproliferative disorders ( Chapter 13 )
Space-occupying marrow lesions Metastatic neoplasms, granulomatous disease
Infections of red cell progenitors Parvovirus B19 infection
Unknown mechanisms Endocrine disorders, hepatocellular liver
disease
7. Megaloblastic Anemias
• Megaloblastic anemias are a heterogeneous group of
disorders that share common morphologic characteristics.
• Erythrocytes are larger
• Neutrophils can be hyper segmented
• Megakaryocytes are abnormal
11. UNRESPONSIVE TO VITAMIN B12 OR FOLIC ACID
THERAPY
• Metabolic inhibitors of DNA synthesis and/or
folate metabolism (e.g., methotrexate)
12. Biochemical Functions of Vitamin B12
• Only two reactions in humans are known to require vitamin B12.
• In one, methylcobalamin serves as an essential cofactor in the
conversion of homocysteine to methionine by methionine synthase.
• In the process, methylcobalamin yields a methyl group that is
recovered from N5-methyltetrahydrofolic acid (N5-methyl FH4), the
principal form of folic acid in plasma.
• The other known reaction that depends on vitamin B12 is the
isomerization of methylmalonyl coenzyme A to succinyl coenzyme A,
which requires adenosylcobalamin as a prosthetic group on the
enzyme methylmalonyl–coenzyme A mutase
13.
14. Hypothesis on neuronal damage in B12 deficiency
• A deficiency of vitamin B12 leads to increased plasma and urine levels of
methylmalonic acid.
• Interruption of this reaction and the consequent buildup of
methylmalonate and propionate (a precursor) could lead to the formation
and incorporation of abnormal fatty acids into neuronal lipids.
• It has been suggested that this biochemical abnormality predisposes to
myelin breakdown and thereby produces the neurologic complications of
vitamin B12 deficiency.
• However, rare individuals with hereditary deficiencies of methylmalonyl–
coenzyme A mutase, while having complications related to methylmalonyl
acidemia, do not suffer from the neurologic abnormalities seen in vitamin
B12 deficiency, casting doubt on this explanation.
15. ‘Folate Trapping’
• Fundamental cause of the impaired DNA synthesis in vitamin B12
deficiency is due to reduced availability of FH4.
• which is “trapped” as N5-methyl FH4.
• The FH4 deficit may be further exacerbated by an “internal” folate
deficiency caused by a failure to synthesize metabolically active
polyglutamylated forms.
• This stems from the requirement for vitamin B12 in the synthesis of
methionine, which contributes a carbon group needed in the metabolic
reactions that create folate polyglutamates
• Whatever the mechanism, lack of folate is the proximate cause of anemia
in vitamin B12 deficiency, since the anemia improves with administration
of folic acid.
16.
17.
18.
19.
20.
21. Morphology – peripheral smear
• The presence of red cells that are macrocytic and oval
(macro-ovalocytes) is highly characteristic.
• They are larger than normal and contain ample
hemoglobin, most macrocytes lack the central pallor of
normal red cells and even appear “hyperchromic,” but
the MCHC is not elevated.
• There is marked variation in the size (anisocytosis) and
shape (poikilocytosis) of red cells.
• The reticulocyte count is low.
• Nucleated red cell progenitors occasionally appear in
the circulating blood when anemia is severe.
• Neutrophils are also larger than normal
(macropolymorphonuclear) and hypersegmented,
having five or more nuclear lobules instead of the
normal three to four
22.
23.
24. Morphology – Bone marrow
• The marrow is markedly hypercellular as a result of
increased hematopoietic precursors, which often completely
replace the fatty marrow.
• Megaloblastic changes are detected at all stages of erythroid
development.
• The most primitive cells (promegaloblasts) are large, with a
deeply basophilic cytoplasm, prominent nucleoli, and a
distinctive, fine nuclear chromatin pattern.
• As these cells differentiate and begin to accumulate
hemoglobin, the nucleus retains its finely distributed
chromatin and fails to develop the clumped pyknotic
chromatin typical of normoblasts.
• The anemia is further exacerbated by a mild degree of red
cell hemolysis of uncertain etiology.
25.
26.
27.
28.
29. nuclear-to-cytoplasmic asynchrony and Ineffective
erythropoiesis
• While nuclear maturation is delayed, cytoplasmic maturation
and hemoglobin accumulation proceed at a normal pace,
leading to nuclear-to-cytoplasmic asynchrony.
• Because DNA synthesis is impaired in all proliferating cells,
granulocytic precursors also display dysmaturation in the
form of giant metamyelocytes and band forms.
• Megakaryocytes, too, can be abnormally large and have
bizarre, multilobate nuclei.
• The marrow hyperplasia is a response to increased levels of
growth factors, such as erythropoietin.
• However, the derangement in DNA synthesis causes most
precursors to undergo apoptosis in the marrow (an example of
ineffective hematopoiesis) and leads to pancytopenia.
31. Vitamin B12 absorption
• Absorption of vitamin B12 requires intrinsic factor, which is secreted by the
parietal cells of the fundic mucosa.
• Vitamin B12 is freed from binding proteins in food through the action of pepsin
in the stomach and binds to salivary proteins called cobalophilins, or R-binders.
• In the duodenum, bound vitamin B12 is released by the action of pancreatic
proteases. It then associates with intrinsic factor.
• This complex is transported to the ileum, where it is endocytosed by ileal
enterocytes that express intrinsic factor receptors on their surfaces.
• Within ileal cells, vitamin B12 associates with a major carrier protein,
transcobalamin II, and is secreted into the plasma.
• Transcobalamin II delivers vitamin B12 to the liver and other cells of the body,
including rapidly proliferating cells in the bone marrow and the gastrointestinal
tract.
• In addition to this major pathway, there is also an alternative uptake mechanism
that is not dependent on intrinsic factor or an intact terminal ileum.
• Up to 1% of a large oral dose can be absorbed by this pathway, making it
feasible to treat pernicious anemia with high doses of oral vitamin B12.
32.
33. Anemias of Vitamin B12 Deficiency: Pernicious Anemia
• Pernicious anemia is a specific form of megaloblastic
anemia caused by autoimmune gastritis and an attendant
failure of intrinsic factor production, which leads to vitamin
B12 deficiency.
• Histologically, there is a chronic atrophic gastritis marked
by a loss of parietal cells, a prominent infiltrate of
lymphocytes and plasma cells, and
• Megaloblastic changes in mucosal cells similar to those
found in erythroid precursors are present.
34. Auto antibodies in pernicious anemia
• Three types of autoantibodies are present in many, but not all,
patients.
• About 75% of patients have a type I antibody that blocks the
binding of vitamin B12 to intrinsic factor.
• Type I antibodies are found in both plasma and gastric juice.
• Type II antibodies prevent binding of the intrinsic factor–vitamin
B12 complex to its ileal receptor.
• These antibodies are also found in a large proportion of patients
with pernicious anemia.
• Type III antibodies, present in 85% to 90% of patients, recognize
the α and β subunits of the gastric proton pump, which is normally
localized to the microvilli of the canalicular system of the gastric
parietal cell.
35. Role of CD4+ T cells in pernicious anemia
• Autoreactive T-cell response initiates gastric mucosal injury and
triggers the formation of autoantibodies, which cause epithelial
injury.
• When the mass of intrinsic factor–secreting cells falls below a
threshold (and reserves of stored vitamin B12 are depleted),
anemia develops.
• The common association of pernicious anemia with other
autoimmune disorders, particularly autoimmune thyroiditis and
adrenalitis, is also consistent with an underlying immune basis.
• The tendency to develop multiple autoimmune disorders,
including pernicious anemia, is linked to specific sequence
variants of NALP1,an innate immune receptor is located on
chromosome 17p13.
36. GI tract lesions in pernicious anemia
• The stomach typically shows diffuse chronic gastritis.
• The most characteristic alteration is atrophy of the fundic glands, affecting
both chief cells and parietal cells, the latter being virtually absent.
• The glandular lining epithelium is replaced by mucus-secreting goblet cells
that resemble those lining the large intestine, a form of metaplasia referred to
as intestinalization.
• Some of the cells as well as their nuclei may increase to double the normal
size, a form of “megaloblastic” change exactly analogous to that seen in the
marrow.
• With time, the tongue may become shiny, glazed, and “beefy” (atrophic
glossitis).
37. CNS lesions in pernicious anemia
• Central nervous system lesions are found in about three
fourths of all cases of florid pernicious anemia but can also
be seen in the absence of overt hematologic findings.
• The principal alterations involve the spinal cord, where there
is demyelination of the dorsal and lateral tracts, sometimes
followed by loss of axons.
• These changes give rise to spastic paraparesis, sensory
ataxia, and severe paresthesias in the lower limbs.
• Less frequently, degenerative changes occur in the ganglia
of the posterior roots and in peripheral nerves.
38.
39.
40.
41.
42.
43.
44. Diagnosis
(1) a moderate to severe megaloblastic anemia,
(2) leukopenia with hypersegmented granulocytes,
(3) low serum vitamin B12, and
(4) elevated levels of homocysteine and methylmalonic acid in the
serum.
The diagnosis is confirmed by a striking increase in reticulocytes and
an improvement in hematocrit levels beginning about 5 days after
parenteral administration of vitamin B12.
Serum antibodies to intrinsic factor are highly specific for pernicious
anemia. Their presence attests to the cause rather than the presence
or absence of vitamin B12 deficiency.
45.
46.
47. Long term effects of pernicious anemia
• Pernicious anemia is insidious in onset, so the anemia is
often quite severe by the time the affected person seeks
medical attention.
• Persons with atrophic and metaplastic changes in the gastric
mucosa associated with pernicious anemia are at increased
risk of developing gastric carcinoma.
• Serum homocysteine levels are raised in individuals with
vitamin B12 deficiency.
• Elevated homocysteine levels are a risk factor for
atherosclerosis and thrombosis, and vitamin B12 deficiency
may increase the incidence of vascular disease.
48. Prognosis in pernicious anemia
• The gastric atrophy and metaplastic changes are due to
autoimmunity and not vitamin B12 deficiency; hence,
parenteral administration of vitamin B12 corrects the
megaloblastic changes in the marrow and the epithelial cells
of the alimentary tract, but gastric atrophy and achlorhydria
persist.
• With parenteral or high-dose oral vitamin B12, the anemia
can be cured and the peripheral neurologic changes reversed
or at least halted in their progression, but the changes in the
gastric mucosa and the risk of carcinoma are unaffected.
49. Fe Deficiency Anemia
• Due to increased loss or decreased
ingestion, almost always, in USA,
nowadays, increased loss is the reason
• Microcytic (low MCV), Hypochromic
(low MCHC)
• THE ONLY WAY WE CAN LOSE IRON IS BY
LOSING BLOOD, because FE is recycled!
53. 2 BEST lab tests:
•Serum Ferritin
•Prussian blue hemosiderin
stain of marrow (also
called an “iron” stain)
54.
55. Anemia of Chronic Disease*
•CHRONIC INFECTIONS
•CHRONIC IMMUNE
DISORDERS
•NEOPLASMS
•LIVER, KIDNEY failure
* Please remember these patients may very very much
look like iron deficiency anemia, BUT, they have
ABUNDANT STAINABLE HEMOSIDERIN in the marrow!
56. APLASTIC ANEMIAS
• ALMOST ALWAYS involve platelet and
WBC suppression as well
• Some are idiopathic, but MOST are
related to drugs, radiation
• FANCONI’s ANEMIA is the only one that
is inherited, and NOT acquired
• Act at STEM CELL level, except for “pure”
red cell aplasia