Vitamin B12 deficiency can result in megaloblastic anemia characterized by large, immature red blood cells. It is most commonly caused by pernicious anemia where autoimmune destruction of gastric parietal cells leads to lack of intrinsic factor needed for vitamin B12 absorption. Clinical features include anemia, jaundice, and neurological problems. Diagnosis is based on morphological changes in blood and bone marrow showing megaloblasts, low vitamin B12 levels, and a positive Schilling test demonstrating impaired absorption. Treatment involves lifelong vitamin B12 injections or high dose oral supplementation.
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.
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.
B12 metabolism..................................... and role of various proteins in b12 metabolism..... necessity of supplementation..........................................
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.
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
2. Introduction ..
Characterized by defective synthesis of
deoxyribonucleic acid (DNA) in all proliferating cells
Most commonly result from lack of folic acid or
vitamin B12
4. Normal Vitamin B12 Metabolism
Vitamin B12 is composed of
A corrin nucleus which has 4 pyrrole rings bound to
a central cobalt atom
A 5,6 dimethylbenzimidazole group which is
attached to the corrin ring and to the central cobalt
atom
Important cobalamins that are distinguished
according to the ligand attached to the central
cobalt atom are : cyanocobalamin,
hydroxocobalmin, adenosylcobalamin and
methylcobalamin
5. Sources
Liver, dairy products and seafish are major
sources
Although bacteria in the large intestine synthesize
vitamin B12 it cannot be absorbed from this site
Minimum amount required for an adult is 1 to 4 µg
per day
6. Absorption of Vitamin B12
2 mechanism
Active (75%) – requires the presence of intrinsic
factor ( a glycoprotein produced by gastric mucosa)
Passive – absorption occurs by diffusion and works
when pharmacological doses of vitamin B12 are
ingested
8. Transport of Vitamin B12
Following absorption by the ileal mucosal cells,
vitamin B12 is carried in the plasma by various
transporting proteins:
Transcobalamin I
Transcobalamin II
Transcobalamin III
9. Transcobalamin I (TC I) is an alpha-globulin
produced by granulocytes. It functions as a
circulating reserve store of B12. TC I carries mostly
methylcobalamin.
Transcobalamin II (TC II) is a beta-globulin formed
in the liver and is the dominant carrier of B12
immediately after absorption. It is the main agent
for rapid transport of B12 to the body cells.
Transcobalamin III (TC III) is an alpha-globulin.
TC III may act as a defence mechanism by
depriving pathogens of B12 at sites of infection
10. Storage sites
Total amount of vitamin in body is 2-5 mg (
adequate for 3 years )
Major site : liver
Excreted through the bile and shedding of
intestinal epithelial cells
Most of the excreted vitamin B12 is again
absorbed in the intestine (enterohepatic
circulation)
11. Functions of Vitamin B12
Synthesis of methionine from homocysteine
Conversion of methyl malonyl CoA to succinyl
CoA
12. FH4
FH2Methylene FH4
Methyl FH4Intestinal cell
Dietary folates
Dihidrofolate
Redutase
MethionineHomocysteine
Thymidylate Synthase
DNA Synthesis
dTMPdUMP
Role of Vitamin B12 and Folate in DNA synthesis
VitB12 (Methylcobalamin)
14. PERIPHERAL BLOOD FINDINGS
1. Hemoglobin – decreased
2. Hematocrit – decreased
3. RBC count – decreased/normal
4. MCV - >100fl ( normal 82-98fl)
5. MCH –increased
6. MCHC – NORMAL
7. Reticulocytopenia.
8. Total WBC count – normal / low
9. Platelet count – normal/ low
10. Pancytopenia, especially if anaemia is severe.
15. PERIPHERAL SMEAR
RBC:
- Macro ovalocytes (macrocytic normochromic)
[ macrocytosis is the earliest sign in Vit B12 deficiency
and can be detected even before the onset of anaemia
]
- In severe anaemia in addition to macrocytosis,
marked anisopoikilocytosis, basophilic stippling, howell
jolly bodies, Cabot’s rings may be found
16. Late or intermediate erythroblast with fine, open
nuclear chromatin (megaloblast) may be seen in
peripheral blood in severe anaemia
19. PERIPHERAL SMEAR
WBC
Normal count or reduced count
Hypersegmented neutrophils is one of the earliest sign of
megaloblastic haematopoiesis and can be detected even
in the absence of anaemia (when more than 5% of
neutrophils show ≥ 5 lobes; 1% neutrophils with ≥ 6 lobes)
PLATELETS:
Normal or decreased (severe anaemia)
Giant platelet can occur
20.
21.
22. BONE MARROW
Markedly hypercellular
Myeloid : erythroid ratio decreased or reversed.
(Normally, there are three myeloid precursors
for each erythroid precursor resulting in a 3:1
ratio, known as the M:E (myeloid to erythroid)
ratio)
Erythropoiesis : MEGALOBLASTIC
23. MEGALOBLAST
1. Cell and nuclear size and amount of cytoplasm
(deeply basophilic royal blue) are increased
2. Nuclear chromatin is sieve like or stippled
(open)
3. Nuclear cytoplasmic asynchrony/dissociation
4. Abnormally large precursor (promegaloblast
and early megaloblast) are increased in BM –
Maturation arrest
5. Abnormal mitoses (increased)
24.
25.
26. Granulocytic series also display megaloblastic
changes
Most prominent change – giant metamyelocyte with
horseshoe shaped nuclei and finer nuclear chromatin,
and in band forms
Megakaryocytes are often large with multiple nuclear
lobes and paucity of cytoplasmic granules
27.
28. BIOCHEMICAL FINDINGS
Increase in serum unconjugated bilirubin-
because of ineffective erythropoiesis
Increase is LDH
Normal serum iron and ferritin
29. Causes of Vit B12 deficiency
Insufficient dietary intake (very rare)
Strict vegetarians
Deficient absorption
Pernicious anaemia
Total or partial gastrectomy
Prolonged use of PPI or H2 blockers
Diseases of small intestine
Fish tapeworm infestation
30. PERNICIOUS ANEMIA
Thomas Addison (1849)
Disease of elderly – 5th to 8th decades (median
age at diagnosis – 60 years)
Genetic predisposition
Tendency to form antibodies against multiple self
antigens
31. PATHOGENESIS
Immunologically mediated, autoimmune
destruction of gastric mucosa
CHRONIC ATROPHIC GASTRITIS – marked loss
of parietal cells
Three types of antibodies:
a) Type I antibody- 75% - blocks vitamin B12 and IF
binding
b) Type II antibody – prevents binding of IF-B12
complex with ileal receptors
c) Type III antibody – 85-90% patients – against
specific structures in the parietal cell
32. Pathological changes are infiltration by mononuclear
cells in submucosa and lamina propria of fundus and
body of the stomach, progressive loss of parietal and
chief cells, and their replacement by intestinal type
mucous cells
33. Associated with other autoimmune disorders
like Hashimoto’s, Graves’, vitiligo, diabetics
mellitus, primary hyperparathyroidism,
Addison’s and Myasthenia gravis
Patients with pernicious anaemia have
increase risk of gastric cancer
34. DIAGNOSTIC FEATURES
1. Moderate to severe megaloblastic anemia
2. Leucopenia with hypersegmented neutrophils
3. Mild to moderate thrombocytopenia
4. Mild jaundice due to ineffective erythropoiesis and
peripheral hemolysis
5. Neurologic changes
6. Low levels of serum B12
35. 7. Elevated levels of homocysteine
8. Striking reticulocytosis after parenteral
administration of vitamin B12
9. Serum antibodies to intrinsic factor (specific)
and anti parietal cell antibodies in serum
10. Abnormal Schilling test, pentagastrin-fast
achlorhydria
36. GASTRECTOMY
Total gastrectomy :
Secondary to Vit B12 deficiency as it removes the
site of synthesis of intrinsic factor
Prophylactic vitamin B12 after surgery
Partial gastrectomy
Regular follow up after surgery for early detection of
deficiency
37. DISEASES OF SMALL INTESTINE
Tuberculosis, whipple’s disease, blind loop syndrome or
resection of small intestine may interfere with absorption
that occurs in the terminal ileum
Blind loop syndrome –
stasis of small intestine contents (diverticulum / stricture)
may predispose to bacterial colonization and proliferation
Utilization of most of the ingested Vit B12 by bacteria may
lead to reduced or non avail of Vit for absorption
38. INFESTATION BY FISH
TAPEWORM
Diphyllobothrium latum (inadequately cooked fish)
Vitamin deficiency by competing with the host for
vitamin in food
Diagnosis made by demonstration of ova in stool
39. CLINICAL FEATURES
Anaemia, mild jaundice and sometimes
neurological involvement
Neurological involvement in the form of
Peripheral neuropathy
Subacute combined degeneration of spinal cord
Cerebral changes (personality changes, dementia &
psychosis)
Patients can present with only neurological
abnormalities without megaloblastic anaemia
40. LABORATORY FEATURES
1. Morpholgical changes of megaloblastic anaemia in
PS and BM
2. Serum vitamin B12 assays
3. Methylmalonic acid (MMA) and homocysteine in
serum
4. Schilling test
5. Intrinsic factor antibodies in serum
41. 1. SERUM VITAMIN B12 ASSAYS
Various methods are available, e.g.
microbiological methods using
Lactobacillus leichmannii or radio-isotope
techniques (RIA) using 57CoB12, coated
charcoal and IF.
42. RADIO-ISOTOPE DILUTION ASSAY:
A known amount of radioactive (hot) B12 is
diluted with the non-radioactive (cold) B12
in the test serum, released from serum
proteins by heat or chemical means.
A measured volume of the hot and cold
mixture is bound to intrinsic factor (IF)
which is added in an amount insufficient
to bind all the hot B12. The bound B12 is
separated from the free and its
radioactivity counted.
43. The count is inversely proportional to the
B12 concentration in the test serum.
The higher the serum B12 the greater will
be the dilution of the radioactive B12 and
thus less radioactivity attached to the IF.
By comparison with standards of known
B12 content, the B12 content of the test
serum can be calculated.
44. In Vitamin B12 deficiency ,
Serum Vitamin B12 and red cell folate are depressed
Serum folate is normal or increased ( accumulation of
5-methyl tetrahydrofolate ) [folate trap]
45. 2. Methylmalonic acid (MMA) and
homocysteine in serum
Recent reports of S.methylmalonic acid and
S.homocysteine are more sensitive for detection of
Vitamin B12 than estimation of Vitamin B12
Raised early in tissue deficiency even before
appearance of hematological changes
46. 3. SCHILLING TEST
For evaluation of absorption of vitamin B12 in the
GIT
Performed in 2 parts – part 1 and part 2
Part 1 :
0.5 to 1 µg of radiolabelled vitamin B12 is given
orally
After 2 hrs IM dose (1000 µg) of unlabelled vitamin
B12 is given [ saturates binding sites of TC I and TC
II and displaces any bound radiolabelled vitamin B12
(thus permitting urinary excretion of absorbed
radiolabelled vitamin B12 )
47. Radioactivity is measured in subsequently
collected 24 hr urine sample and expressed as a
% of total oral dose
In normal persons, > 7% of the oral dose of
vitamin B12 is excreted in urine
If excretion is less than normal it indicates impaired
absorption, which may be due to either lack of IF or
small intestinal malabsorption
Part 2 performed if part 1 of test is abnormal
48. Part 2 : patient is orally administered
radiolabelled vitamin B12 along with IF while
remainder of test is carried out out as in part 1
Excretion becomes normal – lack of IF
Excretion remains below normal – defective
absorption in small intestine
49. 4. INTRINSIC FACTOR ANTIBODIES IN
SERUM
Detection of anti-IF antibodies in serum is diagnostic
of pernicious anemia
50. MANAGEMENT OF B12 DEFICIENCY
When B12 deficiency is suspected a trial of B12 is
essential. Failure of response can only be
determined after careful follow-up over a period of
several months, particularly if the patient is non-
anaemic.
Standard therapy for all cases of B12 deficiency is
by regular intramuscular injections of B12, usually
in the form of hydroxycobalamin. In patients with
inadequate dietary intake supplements may be
given by mouth. Underlying conditions should be
51. After initiation of therapy, reticulocyte count begins to
increase around 3rd day – peak by 6th or 7th day –
gradually returns to normal by end of 3rd week
Hematocrit steadily rises and normalises in about 1-
2 months
Blood transfusion is indicated in severely anaemic
symptomatic patients or in patients with CCF
52. NOTE:
Both B12 and folate are given to patients if
B12 deficiency has not been excluded.
This is to prevent neurological damage, e.g.
subacute combined degeneration of the
spinal cord.