Red blood cells pathology. (Subject 10)

Содержание

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Lecture Plan Blood volume changes Anemia classifications Clinical features and specific signs of anemias Erythrocytosis (Polycytemia)

Lecture Plan

Blood volume changes
Anemia classifications
Clinical features and specific signs of anemias
Erythrocytosis

(Polycytemia)
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Hypervolemia transfusion of blood large doses; during intensive physical work Vaquez'

Hypervolemia

transfusion of blood large doses; during intensive physical work

Vaquez' disease

, hypoxia

diseases of kidneys; disturbances of water-electrolyte balance

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Hypovolemia dehydration (diarrhoea, vomiting, abundant sweating, burns, overheating), shock in the

Hypovolemia

dehydration (diarrhoea, vomiting, abundant sweating, burns, overheating), shock

in the second

stage of acute blood loss; severe anemias

immediately after acute blood loss

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Anemia Anemia is a lack of red blood cells and/or hemoglobin. This results in a hypoxia

Anemia

Anemia is a lack of red blood cells and/or hemoglobin. This

results in a hypoxia
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Anemia classifications Pathogenic classification. Posthemorrhagic (acute or chronic). Haemolytic - acute

Anemia classifications

Pathogenic classification.
Posthemorrhagic (acute or chronic).
Haemolytic - acute and chronic.

Chronic haemolytic anaemias can be inherited and acquired.
Anemias caused by disturbances of hemopoiesis:
deficiency of iron, proteins; vitamin В12, folic acid;
hypoplastic and aplastic anaemias;
metaplastic anaemia;
disregulatory anemia.
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Anemia classifications Classification due to haemoglobin content in RBC. Normally haemoglobin

Anemia classifications

Classification due to haemoglobin content in RBC.
Normally haemoglobin content

in erythrocyte is 0,8—1,05. This index is named color index (CI).
hyperchromic – CI > 1,05 ( В12 and pholate-deficiency)
hypochromic – CI < 0,8 (iron deficiency)
normochromic – CI is normal (inherited haemolytic anaemias)
Classification based on the degree of regeneration.
Normally reticulocytes constitute 0.5 to 1.5% of the RBC.
regenerative - normal reticulocytes count (most of anemias)
hyporegenerative - reticulocytes <0.5 (chronic posthemorrhagic)
non-regenerative anemia - reticulocytes are absent (bone marrow aplasia)
hyperregenerative - reticulocytes >1,5 (inherited hemolytic anemias)
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Anemia classifications Classification based on the on the type of RBC

Anemia classifications

Classification based on the on the type of RBC maturation.


erythroblastic anemias
megaloblastic anemias (B12 vitamin, folic acid deficiency)
Classification based on the on the size of RBC.
The size of RBC refers to mean corpuscular volume (MCV).
microcytic anemia - MCV is under 80 (iron deficiency)
normocytic - MCV (80-100) acute posthemorrhagic
macrocytic – MCV is over 100 (B12 vitamin, folic acid deficiency)
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Clinical features of anemia olygocythemic normovolemia (in most anemias); hypovolemia (acute

Clinical features of anemia

olygocythemic normovolemia (in most anemias);
hypovolemia (acute posthemorrhagic

anaemia, pernicious anaemia);
paleness of skin and visible mucous membranes;
decreased ability to work;
CNS: the lowering of mental ability to work, the decline of memory, insomnia, fatigueability, dizziness, noise in ears, head aches, attacks of faintness;
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Clinical features of anemia Decreased function of endocrine organs (especially thyroid

Clinical features of anemia

Decreased function of endocrine organs (especially thyroid gland);
GIT:

anorexia, flatulence, nausea, constipation and weight loss may also occur.
Heart and lungs: tachycardia, systolic murmur, dyspnoe in exertion. In eldery people heart failure can develop.
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Specific signs of anemias Posthemorrhagic anaemia – signs of blood loss

Specific signs of anemias

Posthemorrhagic anaemia – signs of blood loss from

different organs;
Iron deficiency - perversion of taste, trophic disorders of skin, often gastric achylia;
Chronic anaemia with marked hypoxia -drumstick fingers with spoon-shaped nails;
Haemolytic anaemia – jaundice.
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Regenerative forms of RBC Bone marrow Peripheral blood Normal state Increased demands

Regenerative forms of RBC

Bone marrow

Peripheral blood

Normal state

Increased demands

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Degenerative forms of RBC Poikilocytosis – abnormal variation in shape target

Degenerative forms of RBC

Poikilocytosis – abnormal variation in shape

target cell

sickle cell

Anisocytosis

– abnormal variation in size
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Degenerative forms of RBC Abnormalities in Hb content – coloring hypochromic

Degenerative forms of RBC

Abnormalities in Hb content – coloring

hypochromic

normochromic

RBC containing

different pathological inclusions

Howell-Jolly bodies

Kebot rings

Heinz bodies

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Anemia of blood loss The main reasons of blood loss: blood

Anemia of blood loss

The main reasons of blood loss:
blood vessels or

heart walls safety loss (incision, rupture, tumor growth, aneurysm)
increased vessels permeability (radiation sickness, leukemia, sepsis, vitamin C deficiency)
decreased blood coagulation (coagulation factors deficiency).
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Acute posthemorrhagic anemia 1st stage – heart rate and blood vessel

Acute posthemorrhagic anemia

1st stage – heart rate and blood vessel tonus

are increased, centralization of bloodflow, normocytic hypovolemia. First hours after blood loss.
2nd stage (hydremic) – increased tissue fluids outflow to blood stream, olygocytemic normovolaemia (or hypovolaemia). 1-5 day after blood loss.
3rd stage – activation of erythropoiesis and liver function, high reticulocyte count . 6 – 10 day after acute blood loss .
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Principles of blood loss therapy Etiologic treatment: the increasing of blood

Principles of blood loss therapy

Etiologic treatment: the increasing of blood coagulation,

the reconstruction of vessel or heart walls.
Pathogenic treatment: the transfusion of blood, native or synthetic plasma (the normalizing of blood volume), the infusion of proteins and ions.
Symptomatic therapy: normalization of respiration, heart work, liver and kidneys function.
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Chronic posthemorrhagic anaemia RBC number and Hb content is decreased Hypochromic

Chronic posthemorrhagic anaemia

RBC number and Hb content is decreased
Hypochromic (colour

index is 0,6-0,4)
This anaemia is hyporegenerative.
Degenerative forms: hypochromic erythrocytes, poikilocytosis, anisocytosis with microcytes
WBC - leukopenia, neutropenia and relative lymphocytosis
Bone marrow: process of RBCs saturation with haemoglobin is violated, the decrease of erythroblasts maturation
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Chronic posthemorrhagic anaemia Regeneratory stage: Hb, RBC, colour index are lower

Chronic posthemorrhagic anaemia

Regeneratory stage: Hb, RBC, colour index are lower that

normal. Its duration depends on the intensity of blood loss and regenerative ability of the bone marrow.
Hyporegenerative stage: Hb and RBC lower than in 1st stage. Colour index < 0,5. Microcytes prevail. The level of serum iron is low.
Non-regenerative stage (marrow exhaustion): Reticulocytes are absent.
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Hemolytic Anemias Types of hemolysis Extravascular (common) – occurs in phagocytic

Hemolytic Anemias

Types of hemolysis
Extravascular (common) – occurs in phagocytic cells of

the spleen, liver, and bone marrow.
Intravascular (rare) – RBC undergo lysis in the circulation and release their content into plasma. Hemoglobinemia, hemoglobinuria.
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Hemolytic Anemias Classification Acute Chronic Acquired Inherited immune mechanical injury toxic effects RES hyperactivity

Hemolytic Anemias Classification

Acute

Chronic

Acquired

Inherited

immune
mechanical injury
toxic effects
RES hyperactivity

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Acquired hemolytic anemias Immune abnormalities due to antibodies production: against own

Acquired hemolytic anemias

Immune abnormalities due to antibodies production:
against own undamaged

RBC (autoimmune hemolytic anemia);
against RBC which membrane structure was changed as a result of drugs taking (sulfonamides, penicilline);
when antibodies are acquired by blood transfusions, pregnancies and hemolytic disease of the newborns (isoimmune haemolytic anemia).
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Acquired hemolytic anemias Mechanical injury of RBC due to abnormalities of

Acquired hemolytic anemias

Mechanical injury of RBC due to abnormalities of microcirculation.


during high physical activity – prolonged marchers, joggers. March hemoglobinuria.
patients with prosthetic cardiac valves or artificial grafts.

schistocytes
Microangiopathic hemolytic anemia

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Acquired hemolytic anemias Direct toxic effect Infectious agents toxic effect (α-

Acquired hemolytic anemias

Direct toxic effect
Infectious agents toxic effect (α- or

β-hemolytic streptococci, meningococci)
Invasion of infectious agent and destruction of the RBC by the organism (Plasmodium malaria).
Non-infectious agents – copper , lead, snakes and spiders venoms, extensive burns.
Increased reticuloendothelial activity
Splenomegaly (enlargement of spleen).
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Hereditary hemolytic anemias Pathology of RBC membrane Hereditary spherocytosis autosomal dominant

Hereditary hemolytic anemias

Pathology of RBC membrane
Hereditary spherocytosis
autosomal dominant disease


defects in erythrocyte membrane proteins (spectrin, ankyrin) synthesis
abnormally shaped red cells (which are typically older) are destroyed by the spleen

Spherocytes
(small, without central pallor zone)

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Hereditary hemolytic anemias Pathology of RBC enzymes Glucose-6-phosphate dehydrogenase deficiency. X-linked

Hereditary hemolytic anemias

Pathology of RBC enzymes
Glucose-6-phosphate dehydrogenase deficiency.
X-linked recessive
G6PD

is necessary for glutathione synthesis, which is an antioxidant, destroying peroxides.
Oxidative stress is possible in severe infection, some medicines (sulfonamides, primaquine (an antimalarial), glibenclamide) and certain foods.
Oxidation and precipitation of Hb within RBC (Heinz bodies) occur in G6PD deficiency.
Favism – hemolytic anemia as a result of broad beans consumption
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Hereditary hemolytic anemias Pathology of haemoglobin Sickle cell disease is a

Hereditary hemolytic anemias

Pathology of haemoglobin
Sickle cell disease is a qualitative

disorder of Hb (abnormal Hb is synthesized)
Thalassemia is a quantitative disorder (abnormal quantity of Hb chains)
Normally RBC contain Hb A which consist of 2 alfa and 2 beta chains (α2β2)
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Sickle cells disease substitution of valine for glutamic acid in HbA

Sickle cells disease

substitution of valine for glutamic acid in HbA turns

it to HbS
HbS is polymerized and RBC turn sickle cells in during deoxygenation
RBC become stuck in blood vessels
This causes ischemia and infarction.
The consequences of infarction are determined by their location.

Sickle cells

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Thalassemia classification α thalassemia, the production of α globin is deficient

Thalassemia classification

α thalassemia, the production of α globin is deficient
β thalassemia

the production of β globin is defective.
The heterozygous form manifests as thalassemia minor - asymptomatic or mildly symptomatic.
The homozygous form – thalassemia major – severe hemolytic anemia.
Beta thalassemia major is also known as Cooley's Anemia.
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Thalassemia deficiency in the production of one globin chains type lead

Thalassemia

deficiency in the production of one globin chains type lead

to excess production of other globin chains.
Excessive globin chains are precipitated within the RBC (target-type RBC).
Enlargement of liver and spleen, excess of tissue iron stores.

target cells

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Anemias caused by disturbances of haemopoiesis Iron deficiency reasons: chronic blood

Anemias caused by disturbances of haemopoiesis

Iron deficiency reasons:
chronic blood losses

due to - excessive menstruations, other bleedings;
increased iron requirements (pregnancy, lactation, spurts of growth in infancy, childhood and adolescence);
inadequate dietary intake;
insufficient absorption (achlorhydria, partial or total gastrectomy, intestinal malabsorbtion).
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Anemias caused by disturbances of haemopoiesis nails (koilonychia or spoon-shaped nails),

Anemias caused by disturbances of haemopoiesis

nails (koilonychia or spoon-shaped nails),


tongue (atrophic glossitis)
mouth (angular stomatitis).
low colour index and RBC number.
low blood serum iron
treatment with iron medicines.

Microcytes poikylocytes

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Anemias caused by disturbances of haemopoiesis Syderoblastic anemia (refractory to iron)

Anemias caused by disturbances of haemopoiesis

Syderoblastic anemia (refractory to iron)
defect enzymes

that include iron to hemoglobin.
inherited
acquired (lead intoxication).
Level of plasma iron is high.
Bone marrow: erythroblasts with increased iron content are observed (syderoblasts).
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Anemias caused by disturbances of haemopoiesis Megaloblastic anaemia deficiency of vitamin

Anemias caused by disturbances of haemopoiesis

Megaloblastic anaemia
deficiency of vitamin B12

and folic acid.
impaired DNA synthesis and abnormalities in haemopoiesis.
cells synthesize much more RNA than normal and much less DNA.
megaloblastic type of erythropoiesis
leucopenia and thrombocytopenia
megalocytes average life of 40 days.
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Megaloblastic anemia The reasons of B12 deficiency: inadequate dietary intake (strict

Megaloblastic anemia

The reasons of B12 deficiency:
inadequate dietary intake (strict vegetarians)
inadequate production

of intrinsic factor (pernicious anemia, congenital lack)
malabsorption (disorders in absorption)
The reasons of folate deficiency:
inadequate dietary intake (teenagers, infants, old age, alcoholics)
malabsorption (coeliac disease, partial gastrectomy)
excess demand (pregnancy, lactation, infancy, malignant tumors).
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Vitamin B12 metabolism transport by transcobalamin haemopoiesis combines with intrinsic factor

Vitamin B12 metabolism

transport by transcobalamin

haemopoiesis

combines with intrinsic factor

absorption

myelination of nervous

fibers

regeneration of GIT epithelium

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Megaloblastic anemia hyperchromic, macrocytic, hyporegenerative hypersegmented neutrophil RBC with Howell Jolly bodies Megalocyte

Megaloblastic anemia

hyperchromic, macrocytic, hyporegenerative

hypersegmented neutrophil

RBC with Howell Jolly bodies

Megalocyte

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Megaloblastic anemia Specific clinical features of megaloblastic anemia: glossitis (inflammation of

Megaloblastic anemia

Specific clinical features of megaloblastic anemia:
glossitis (inflammation of the

tongue; smooth, beefy, red tongue),
mild jaundice,
symptoms of malabsorption,
weight loss and anorexia.
neurological signs - numbness or tingling of the extremities and an ataxic gait (only B12 deficiency)
Pernicious anemia (Addyson anemia) develops due to autoantibodies against intrinsic factor or parietal cells which produce intrinsic factor.
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Anemias caused by disturbances of haemopoiesis Hypoplastic and aplastic anaemias etiology:

Anemias caused by disturbances of haemopoiesis

Hypoplastic and aplastic anaemias etiology:
medicines with

myelotoxic effect (amidopyrine, sulfanilamides, cytostatic chemicals, antibiotics);
autoimmune reactions in bone marrow;
chemical substances: benzol, petrol, mercury ;
radiant energy;
different infections: sepsis, flu.
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Anemias caused by disturbances of haemopoiesis The picture of blood –

Anemias caused by disturbances of haemopoiesis

The picture of blood – pancytopenia

– decrease of all blood cells. Regenerative forms of blood cells are absent.

normal marrow

aplastic anemia

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Anemias caused by disturbances of haemopoiesis Metaplastic anaemias etiology: leukemic metaplasia

Anemias caused by disturbances of haemopoiesis

Metaplastic anaemias etiology:
leukemic metaplasia of bone

marrow (it consists of leukemic cells only);
cancer metastases in bones,
diffuse osteosclerosis with obliteration of marrow cavity.
Blood picture is the same as at hypoplastic anaemias.
Disregulatory anemia – lack of erythropoietin synthesis (kidney’s diseases).
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Erythrocytosis (Polycytemia) RBC count: more than 4,7*1012//L in women and more

Erythrocytosis (Polycytemia)

RBC count: more than 4,7*1012//L in women and more than

5,0*1012//L in men.

Erythrocytosis

Primary

Secondary

Polycytemia
vera

Relative

Absolute

Congenital

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Vaquez’ disease (Polycythemia vera) Tumor induced hyperplasia of bone marrow Normal blood smear Polycytemia vera

Vaquez’ disease (Polycythemia vera)

Tumor induced hyperplasia of bone marrow

Normal blood

smear

Polycytemia vera

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Vaquez’ disease (Polycythemia vera) Blood count: increased number of RBC, reticulocytes,

Vaquez’ disease (Polycythemia vera)

Blood count:
increased number of RBC, reticulocytes, WBC

and platelets.
Blood volume – polycytemic hypervolemia, hematocrit is increased > 52%.
Hb content is increased too up to 180-200 g/L. P
Increase of blood viscosity.
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Vaquez’ disease (Polycythemia vera) Clinical signs arterial hypertension ; plethora with

Vaquez’ disease (Polycythemia vera)

Clinical signs
arterial hypertension ;
plethora with congested mucous membranes

conjunctiva and retinal veins;
CNS disturbances (headache, dizziness, visual disturbances, paresthesias, strokelike symptoms)
cardiovascular symptoms (myocardial ischemia, vessels thrombosis);
enlargement of spleen and liver;
frequent bleedings.
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Secondary absolute erythrocytosis due to increased erythropoietin production General hypoxia: Chronic

Secondary absolute erythrocytosis

due to increased erythropoietin production
General hypoxia:
Chronic lung diseases;
Carbon

monoxide poisoning;
Smoker's erythrocytosis;
The local inhabitants of high-altitude territories.
Local renal hypoxia
renal artery stenosis,
final stages of renal diseases.
Tumors
hepatocellular carcinoma, renal cell cancer
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