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HLS Pathology

Hematopoeitic and Lymphatic System Pathology

What is anemia? Reduction of total RBC MASS below normal amount Reduction of oxygen carrying capacity of the blood
Which diagnostic tests are used in the cases of RBC diseases? Hemoglobin concentration (g/dL) Hematocrit (ratio of packed RBCs to total blood volume)
What are the general causes of anemia? 1) Increased destruction (hemolytic anemia) 2) Diminished Erythropoiesis 3) Blood loss
What are the causes of hemolytic anemia? Extrinsic factors (infection, antibody, mechanical) Intrinsic RBC abnormalities: 1) Hereditary (membrane, enzyme, Hg abnormalities) 2) Acquired (Paroxysmal nocturnal hematuria)
What are the causes of diminished Erythropoiesis? 1) Iron deficiency anemia 2) Megaloblastic anemia 3) Aplastic anemia 4) Pure red cell aplasia 5) Myelophthisic anemia 6) Myelodysplastic syndrome
How can anemia be classified according to morphology? 1) Hypochromic microcytic anemia 2) Normochromic normocytic anemia 3) Macrocytic anemia 4) Shape
Causes of Hypochromic microcytic anemia: 1) Iron deficiency 2) Thalassemia 3) Anemia of chronic disease 4) Sideroblastic anemia
Causes of Normochromic normocytic anemia: 1) Anemia of chronic disease 2) some hemolytic anemias
Causes of Macrocytic anemia: 1) Megaloblastic anemia 2) Myelodysplastic syndrome 3) Hypothyroidism
How is anisopoikelocytosis measured? by RBCs distribution width (RDW)
Hypochromic microcytic anemia usually reflects Impaired Hg synthesis
Macrocytic anemia reflects Stem cell disease and maturation
What are the clinical features of anemia? 1) Dizziness 2) Fatigue 3) Pallor 4) Headache 5) Hypotension 6) Tachycardia 7) Tachypnea 8) Hemolytic anemia: jaundice, splenomegaly, bone and joint pain, growth retardation
What occurs in anemia of acute blood loss? RBCs are rapidly lost outside circulatory system and the body responds by shifting fluid from interstitial to intravascular space Anemia worsens by dilution Erythropoietin secretion is stimulated, activating BM erythropoiesis
The symptoms of anemia of acute blood loss are related to: Decreased intravascular volume Might lead to cardiovascular shock and death
How does a blood sample from anemia of acute blood loss appear? 1) Mature RBCs as well as Reticulocytes appear in blood after 5 days 2) Anemia is normochromic normocytic (may become hypochromic microcytic), with reticulocytosis 3) Leukocytosis
When does anemia of acute blood loss occur? When the rate of RBC loss exceeds regeneration
RBCs age is around 120 days
Aged RBCs are engulfed by: Macrophages in the spleen, liver and BM
In hemolytic anemia, there is; 1) Abnormal and premature destruction of RBCs 2) Accumulation of Hg degradation products 3) Retention of iron 4) High erythropoietin, LDH, Retic count 5) Secondary increased erythropoiesis
In Extravascular hemolysis, there is: Increased phagocytic activity
In Intravascular hemolysis, there is: Hemolysis inside of blood vessels
Characteristics of extravascular hemolysis: 1) RBCs are less deformable 2) Abnormal RBC movement in splenic sinusoids 3) Attracts histiocytes to engulf abnormal RBCs 4) Hg is converted to bilirubin in histiocytes 5) Free Hg in serum binds Haptoglobin
The triad of extravascular HA is: 1) Anemia 2) Splenomegaly 3) Jaundice
Characteristics of intravascular HA: 1) Less common, severe 2) Caused by mechanical damage, complement fixation, microbes, toxins 3) Lots of free Hg, haptoglobin cleared 4) Free Hg in serum oxidized to met-Hg - hypoxia 5) Excess free Hg and met-Hg are excreted in urine (Hg-uria)
What condition may occir in intravasular HA? Renal Hemosiderosis
What is the etiology of Hereditary spherocytosis? Frameshift mutation in a gene that encodes structural proteins(the vertical ones) inside RBC membrane These proteins are : spectrin (alpha or beta unit may be affected) ,ankyrin , band 4.2 and band 3
Mode of inheritance of Hereditary spherocytosis? Autosomal dominant
Prevalence of Hereditary spherocytosis in: Northern Europe
Pathogenesis of Hereditary spherocytosis: Loss of structural protein(s) --> weak cell membrane, any minor physical trauma can cause cell membrane loss with time membrane, no longer biconcave, they become spherical --> Histiocytes identify spherocytes and take them out --> EXTRAvascular HA
What is the morphology of RBCs in Hereditary spherocytosis? Low Mean Cell Volume (MCV) Normal Hb (MHC) High MCHC Reticulocytosis Small, hypochromatic cells Howell-Jolly bodies
Treatment for hereditary spherocytosis by: Splenectomy
MCHC = Ratio of MCH/MCV
How do we test for Hereditary spherocytosis? Osmotic Fragility Test Early lysis of RBCs in osmotic fragility test indicates they’re spherocytes
The clinical course of this disease depends on: Severity of the mutation
Signs and symptoms are those of extravascular hemolytic anemia including Anemia Jaundice Splenomegaly
What are the two main functions of G6PD? 1) Glycolysis 2) Conversion of NADP to NADPH (Imp. for Neutralizing free radicals)
Etiology of G6PD deficiency: This disease is inherited Mode of inheritance is X-linked recessive *Mostly males affected, females occasionally and mildly affected
Prevalence of G6PD deficiency in which region? The Middle East and Africa
Normal G6PD is called G6PD –B
In G6PD-A : The enzyme is deficient;quantity is low Symptoms are mild
In G6PD-M: The enzyme is present in normal quantity but it’s not functioning (poor quality) Symptoms here are more severe
Pathogenesis of G6PD deficiency: This disease affects the RBCs the most since they are non nucleated-->They have to adapt to live with the limited amount of enzymes they’re released with --> RBCs that lyse due to G6PD deficiency are the older ones
Degree of deficiency : RBCs have extra reserve due to their long life-span G6PD deficiency lytic symptoms appear when G6PD is below 20% of normal amount Symptoms vary (mild-moderate-severe) according to the degree of deficiency
Increase of H2O2 due to any cause alters The normal configuration of globin chains in Hb , these chains become more condensed and the cell in that region will be harder than normal
These condensations in are visualized by a special stain, which is? Crystal violet or supravital stain
These condensation in G6PD deficiency appear as bodies known as: Heinz Bodies Altered condensed globin chains secondary to G6PD deficiency
What is characteristic about RBCs in G6PD defiency? They look bitten into, because Heinz bodies ONLY are phagocytosed by histiocytes
Why does crisis occur sometimes in G6PD deficiency? 1) Drugs (sulfonamides, malaria, vitamin K, large doses of aspirin)- Metabolism of some drugs leads to production of free radicals 2) Infections (Myeloperoxidase from neutrophils increases free radicals) 3) Fava beans - increase O2
Symptoms take how long to appear in G6PD deficiency: 1-2 days
How severe is G6PD deficiency? Usually it’s severe as it’s INTRAvascular hemolysis Heinz bodies can break cell membrane and cause cell lysis . Hypoxia and met-hemoglobinemia which leads to bone pain , red urine
How is Diagnosis of G6PD done? Enzyme assay is done to check for its quality and quantity . NADPH is measured, if G6PD is deficient or abnormal, NADPH won’t be produced
How long should we wait until after the onset of G6PD deficiency crisis to diagnose it? Around a month, or at least until the patient is stable
What does Paroxysmal Nocturnal Hematuria mean? Paroxysmal --> sudden onset Nocturnal -->at night Hematuria --> blood in urine
Is Paroxysmal Nocturnal Hematuria acquired or inherited? Acquired
All intrinsic causes are hereditary except in Paroxysmal nocturnal hematuria , which is acquired intrinsic hemolytic disease
Etiology of Paroxysmal Nocturnal Hematuria: A mutation in the gene phosphatidylinositol glycan group A (PIG-A)
Pathogenesis of Paroxysmal Nocturnal Hematuria: PIG-A encodes cell membrane protein which is glycosylphosphatidylinositol (GPI), an anchoring protein CD55 and CD 59 are no longer anchored by GPI These proteins function normally to antagonize the complement system - cells are perforated
The disease becomes active only if the mutated stem cell becomes predominant
How do CD55 and CD59 inactivate the complement system ? By inhibiting C3-convertase that’s necessary for activation of the complement system
Diagnosis of Paroxysmal Nocturnal Hematuria is done by: The flow cytometry test
How is the flow cytometry test done? 1) Viable blood cells are taken 2) Antibodies against CD55 and CD59 are added 3) Shadows of antibody-protein reactions can be seen
Clinical features of Paroxysmal Nocturnal Hematuria: ¼ cases (25%) have acute symptoms Severe pain at night Blood in urine In chronic cases,symptoms are mild but persistent Anemia, neutropenia and thrombocytopenia Low platelets and thrmobosis- Imp
How can thrombosis be present if platelets are low? Because when platelets lyse , their contents are released . These contents include proteins that promote thrombus formation such as Thromboxane A2
In 10% of PNH cases, stem cells acquire more mutations and progress into Neoplasm
The Complement system is activated efficiently in what cases? Acidosis (which increases during infection)
Thalessemia is also known as: Mediterranean anemia
Is Thalessemia acquired or inherited? Inherited
Etiology of Thalessemia: Autosomal recessive Deficiency in Hb A Alpha thalessemia --> deletion mutation Beta thalessemia--> point mutation
There is a prevalence of thalessemia in which regions? Mediterranean Region , Middle East, Tropical Africa , India and South-East Asia
2 genes encode beta globin chain while 4 genes encode alpha globin chain Which type of thalessemia is milder? Alpha or beta? Alpha More genes encode the chain
What are the molecular classifications of B-Thalessemia? 1) Beta thalassemia minor 2) Beta thalassemia intermedia 3) Beta thalassemia major
In B-thalessemia minor, there is loss of: 1 gene -Asymptomatic
In B-thalessemia major, there is loss of: Both genes
In B-thalessemia intermedia, there is loss of: Possibly 1 or two genes, but with less severe mutations, so the function is not greatly impaired
What are the molecular classifications of alpha thalassemia? 1) 1 gene lost --> silent carrier 2) 2 genes lost --> alpha thalessemia minor 3) 3 genes lost --> Hemoglobin H disease (Hb Barts) 4) 4 genes(all genes) lost --> alpha thalassemia major
Why don't we see alpha thalessemia major in patients? Patients die in utero because NO Hb can be formed
Symptoms of thalassemia in symptomatic cases appear after the age of six months because During the first 6 months, the infant depends mostly on HbF
Pathogenesis of Thalessemia: Hypochromic Microcytic anemia due to Hb deficiency- hypoxia Beta-thalessemia - Increased HbA2 and F,excess alpha binds delta and gamma instead Hemolysis due to excess globin chain accumulation in RBCs Int +extravascular HA Ineffective erythopoeisis
How we can diagnose beta thalassemia? By Hb electrophoresis
How is Hb electrophoresis done? Different globin chains have different electrical charges Hg is separated on gel and an electrical current is applied Each type of Hb migrates a specific distance and hence can be recognized
Excess unpaired alpha chains form solid masses called: Hemichromes
Persistent increase in erythropoietin causes many symptoms and complications, which are? 1) Hepcidin inhibition 2) Melanocyte proliferation 3) Hemosiderosis 4) Extra medullary hematopoiesis 5) Normoblast proliferation 6) Abnormal bone growth due to hypoxia
Why is inhibition of Hepcidin harmful? Hepcidin is an important hormone in iron metabolim which normally prevents absorption of iron in GIT Increased absorption of iron in GIT --> patients will have secondary hemisderosis
What is Hemosiderosis? Masses of iron diffuse and accumulate into cells where they are not usually found
Why do we have high RBC count in thalassemia? This is secondary to increased erythropoietin stimulation
Reactive bone formation and high normoblast count in thalessemia leads to what appearance? A crew cut appearance Small spikes on the skull
Increased stimulation of erythropoeitin leads to what? Hepatomegaly Splenomegaly
Heart failure is common to secondary thalassemia major. Why? 1) Anemia 2) Transfusion of blood causes increase in the volume of blood 3) Hemisiderosis
Morphology of RBCs in Thalessemia: 1) Hypochromic and microcytic 2) Target cells --> red dot in middle of RBCs 3) Basophilic stippling: blue small dots all over the cell 4) Nucleated RBCs 5) Supravital stain -> Golf Ball shaped cells
Etiology of Sickle Cell Anemia: A mutation in Beta chain of the glutamate; when one of the codons(6th AA) is mutant it will give rise to Valine instead of Glutamate Valine is hydrophobic while glutamate is hydrophilic, so it changes the physical characteristics of the beta chain
Mode of inheritance of Sickle Cell Anemia: Autosomal recessive
Prevalence of Sickle cell anemia in: Common in Middle East, South Arabia, in Africa, and India
What is the sickle cell trait? Heterozygous mutant sickle cell gene We have a normal one and the other is abnormal, the normal one masks the abnormal one therefore the patient is asymptomatic These carriers have 50% hemoglobin S, and 50% hemoglobin A
In Homozygous mutant genes, how much HbS and HbA is present? 90% hemoglobin S and no HbA
Sickle cell anemia patients are historically known to be resistant to: Malaria infection
Pathogenesis of Sickle Cell anemia: Hemoglobin S is hydrophobic, it doesn’t like the cytosol polymerizes and gets condensed longitudinally in a needle shape Tear in cell membrane- intravascular HA Abnormal shape enguled by spleen- extravascular HA Hypoxia - Increased Erythropoeitin
Increased erythropoeitin results in: Hepcidin inibition Hemosiderosis Hepatosplenomegaly but later they have absent spleen (autosplenomegaly) Crewcut appearance like in thalessemia
Certain conditions cause this polymerization (sickling) like: 1) Hypoxia 2) Dehydration 3) Acidosis
Medical treatment of Sickle Cell anemia: We can manage it through a decrease in symptoms to prevent complications Blood transfusion Increasing fetal hemoglobin and hbA2 Possibly, bone marrow transplantation
Clinical complications of Sickle Cell anemia: 1) Vaso-occlusive crisis 2) Aplastic crisis 3) Sequestration crisis 4) Autospleenectomy 5) Pariapism 6) Skin ulcers
What happens in the case of vaso-occlusive crisis? RBCs stick to each other because of their shape, leading to thrombosis Patients may have MI in adolescence of MI
What happens in the case of Aplastic crisis? It means that there is no hematopoiesis, its secondary to either bone marrow infarction or infection by parvovirus B19
What happens in sequestration crisis? The spleen is hyper functioning leading to increased engulfment of all blood cells; RBCs and WBCs The spleen becomes massively enlarged, it will be full of blood causing hypovolemic shock
What happens to cause autospleenectomy? The spleen is enlarged because of all the RBCs, but these RBC wills destroy the spleen because of repetitive spleen infarction leading to fibrosis and at the end it will disappear
Pariapism is caused by: Persistent erection of the penis in men, its secondary to thrombosis in the veins of the penis, if the circulation stops during erection, the patient will have persistent priapism
Skin ulcers are caused by: are Circulation is slower in the lower limb, so it's more prone to thrombosis leading to skin ulcers
What methods can we use to view sickle cells? Blood film Hemoglobin electrophoresis You can see pronormoblast which is the earliest stage in the erythroid line! Para particles are seen in aplastic crisis secondary to parvovirus infection
Etiology of Autoimmune Hemolytic anemias: Secondary to synthesis of abnormal immunoglobulins that target normal cell membrane proteins on the RBCs
Diagnosis of Autoimmune Hemolytic anemias: Done by Coomb's test
What is Coomb's test? We give a serum that has antibodies that target the antibodies on the RBCs surface, if the disease is present, they will combine and cause the RBCs to come close to each other causing what’s known as “agglutination" -turbidity
Types of autoimmune hemolytic anemia: 1) The warm type 2) The cold type
The Warm Type is named so, because: it occurs in the body's core
Auto-antibodies of interest in the warm type are: IgG and IgA
Etiology of the warm type of autoimmune hemolytic anemia: 50% of the cases are idiopathic The remaining 50% is usually due to drugs which are administered intravenously with large doses and the most common ones are antibiotics like cephalosporin and penicillin
Pathophysiology of the warm type of autoimmune hemolytic anemia: RBCs coated with Abs reach the spleen IgG has an fc fragment which attaches to the Histiocytes RBCs are identified - part of the cell membrane lost through pinching Ig Spherocytes reach spleen- destroyed EV HA-patients --> jaundice + splenomegaly
The Cold Type is named so, because: It affects the peripheral circulation commonly in organs like: nose, fingers, toes and heels
Auto-Antibody of interest in the cold type is: IgM
What are the 2 clinical setting for the cold type? 1) Acute 2) Chronic
How does the acute type appear? 1) The most well-known type is mycoplasma pneumonia which causes pneumonia 2) Influenza virus which causes a self-limited disease
How does the chronic type appear? most commonly seen in cases of lymphomas They can be functional and secrete huge amounts of immunoglobulins including IgM
Pathophysiology of the cold type Adherence of IgM to the RBCs Attract part of the complement RBCs in high temperatures IgM leaves RBCs and the complement stays there Reach the spleen, senses complement and takes them out spherocytes form, return, and are destroyed causing EV HA
What types of trauma can occur to the RBCs? 1) Physical trauma - from strenuous exercise - IV HA 2) Prosthetic valves - foreign bodies may be rejected 3) Microangiopathic diseases -thrombi
What do the different types of RBC trauma have in common? Broken RBCs referred to as schictocytes
What is hypersplenism? Increased function of the spleen Hypersplenism is not related to haemolytic disease as it can be associated with other diseases like Rheumatoid Arthritis
Pathophysiology of hypersplenism: Spleen increases in size Marked increase in function causing destruction to RBCs, WBCs, and platelets Patients will have pancytopenia in the peripheral blood in addition to anemia, leucopoenia, thrombocytopenia and a very large spleen
Felty’s syndrome is when Hypersplenism occurs with rheumatoid arthritis
Patholgies of Decreased bone marrow production: 1) Iron Deficiency anemia 2) Megaloblastic anemia 3) Drugs 4) Vitamin b12 deficiency 5) Dialysis, in chronic renal failure
What is the most common type of anemia? Iron Deficiency anemia
Causes of iron deficiency: 1) Lack of meat 2) Pregnancy 3) GI diseases and here the absorption of iron is decreased 4) Celiac disease 5) Chronic blood loss
Prevalence of iron deficiency anemia: Worldwide, specifically in developing countries
Pathogenesis of Iron deficiency anemia: Not enough Heme synthesis--> not enough Hb synthesis RBCs will look small and pale Not enough stores in the body it will block the bone marrow and become insensitive to erythropoietin even if it is present in high amounts
Morphology in Iron deficiency anemia: The cell membrane would become more rigid than normal so piokilocytosis RBCs are having a very pale central part and the central pallor is more than one third
on deficiency is a major cause of Thrombocytosis - increase in platelet count
Systemic symptoms associated with iron deficiency: 1) Hair loss 2) Thin and fragile nails (spoon-like nails) 3) Most common organ affected is the esophagus with abnormal peristalsis 4) Blue sclera 5) Neurologic diseases along with cognitive dysfunctions 6) Pica 7) Stressed leg syndrome
What is megaloblastic anemia? A deficiency in vitamin b.12 or folate or both of them
Vit.b12 is exclusively found in: Animal products like in red meat, milk, pigs, but not in vegetables
Causes of megaloblastic anemia: 1) Vegetarianism/Veganism 2) Pernicious anemia 3) GI disease 2+3 disrupt absorption 4) Drugs
What is pernicious anemia? An autoimmune disease in the stomach that causes destruction of the parietal cellswhich are responsible for the production of the intrinsic factor
Folate deficiency is a deficiency which can be caused by: Nutritional reasons when the individual is not eating enough green leaves and vegetables
How do drugs cause megaloblastic anemia? Inhibit the absorption or utilization -at the cellular level- of folate and vit.B12 anti-epilepsy drugs, OCP oral contraceptive pills Methotrexate inhibits DNA replication of folate at the cellular level
What are more causes of folate deficiency? 1) B12 deficiency 2) Dialysis, in chronic renal failure
Morphology of cells in megaloblastic anemia: Large normoblasts We have extra segments, 6 or more segments Megakaryocytes, also appear larger and more lobulated Large cells and slightly oval
Symptoms of megaloblastic anemia: No vit.B12--->No enough myelin--->nerves will be injure--->a patient will have neurologic symptoms
Which deficiency causes neurologic symptoms? B12, not folate
What is Anemia of chronic Diseases? Any chronic diseases especially chronic infections can cause anemia (like Tuberculosis), cancer, and rheumatologic diseases
What is the most common type of anemia in hospitalized patients? Anemia of chronic disease
Pathogenesis of anemia of chronic disease: chronic inflammation---> high levels of IL-6--->activated Hepcidin--->blocks transfer of iron from their stores to the normoblasts---> even if you have large amounts of iron, the cells cannot utilize it--->relative deficiency of iron
Morphology of anemia of chronic disease: Initially, normochromic normocytic anemia, but with time, it becomes hypochromic microcytic We check Hemosiderin in the bone marrow, it's very high because it's not utilized Serum ferritin is high in contrast to iron deficiency
Treatment of anemia of chronic disease: Treat the underlying cause meaning that you cannot treat anemia if you don't treat the real reason behind it
What is aplastic anemia? It’s a total bone marrow failure, where it cannot produce ANY cells, and most commonly it's idiopathic or caused by autoimmune disease
Which type of drug can cause aplastic anemia? Chloramphenicol
Prevalence of aplastic anemia is: common in children and young adults
What is Fanconi anemia? Aplastic anemia that is congenital
Pathogenesis of aplastic anemia: T-cells (abnormally functioning) destroy stem bone cells
Morphology of aplastic anemia: Normochromic normocytic anemia Pancytopenia
Diagnosis of aplastic anemia by: Conducting a bone marrow biopsy and we notice the predominance of fat over the hematopoietic cells
What is Myelopthisic anemia? Physical destruction of the bone marrow by any mechanism, most commonly cancer Cancer causes replacement and destruction of the hematopoietic cells
Causes of Myelopthisic anemia: Malignancy,especially Leukemia Myeloma Plasma cell lymphoma Granuloma: a large amount of histiocytes that transform into multi-nucleated giant cells and form masses destroying the bone marrow
Hypothyroidism causes which type of anemia: Microcytic anemia
How does anemia occur as a result of Hypothyroidism? Thyroxin is essential for cell metabolism anywhere in the body, If we have no Thyroxin, RBCs and hematopoietic cells will not mature normally
How does chronic renal failure cause anemia? In early stages, no erythropoietin--->no production of the RBCs from the bone marrow--->and morphologically, they appear normochromic normocytic
When chronic renal failure advances: we reach "uremia" which is basically accumulation of large amounts of toxic uric acid. Now this uric acid will change RBCs' morphology so we'll have circumferential spikes, we call them ecchinocytes
How does chronic liver disease cause anemia? no liver, no clotting factor, they bleed, anemia of blood loss--- also, vitamin b12 is stored in the liver---no liver, no vit.b12 is stored, deficiency in vitamin b12, megaloblastic anemia
Regarding the defective lipid synthesis >RBCs will have longer projections we call it acanthocytes
What is myelodysplastic syndrome? It is acquired, neoplastic, it's a bone marrow failure but neoplastic Can potentially progress into leukemia Can be normochrmoic normocytic or macrocytic anemia
Created by: Ulaisl



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