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U15 Spine > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is Erythropoiesis

A

Erythropoiesis is the production of RBCs in the bone marrow.

  • It is dependent on the release of erythropoietin (EPO) from the kidneys
  • EPO is synthesised in the renal cortex by interstitial cells in the peritubilar capillary bed
  • Stimuli for EPO release include:
    • Hypoxaemia (decreased arterial PO2), severe anaemia, leftward shift on O2 dissociation curve, high altitude, and decreased 02 saturation (Sa02; CO poisoning, methemoglobinemia)
  • Increased 02 content suppresses EPO release (negative fedback; eg, polycythemia vera)
  • EPO is ectopically produced in renal cell carcinoma and hepatocellular carcinoma.
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2
Q

Haematopoiesis - where is this in foetal development

A
  • During foetal development, haematopoiesis is 1st established in the yolk sac mesencyme and later moves to the liver and spleen and then to the bony skeleton
  • From infancy to adulthood, there is progressive restriction of productive marrow to the xial skeleton and proximal ends of the long bones.
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3
Q

What are reticulocytes?

A
  • Reticulocytes are oyung RBCs containing RNA filaments in the cytoplasm
    • Newly released RBCs from the bone marrow
    • Peripheral blood markers of effective erythropoiesis in a perosn with anaemia
    • Effective rythropoiesus refers to an appropriate bone marrow response to anaemia
    • Correlates with an increase in the synthesis or release of reticulocytes from the bone marrow
  • Reticulocytes are easily identified in the peripheral blood with supravital stains. Supravotal stains detect te threadlike RNA filaments in the cytoplasm of immature RBCs
  • Reticulocyte becomes a mature RBC in 24hours. Maturaiton occurs with the help of splenic macrophages (MPs)
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4
Q

Describe a reticulocyte count and the normal.

A
  • Reticulocyte count is reported as a percentage (normal is 0.5%-1.5%)
  • A reticulocyte count is used to determine the number and/or percentage of retiuclocytes in the peripheral blood in order to evaluate disorders that affects RBCs such as anaema or bone marrow disorders. The purpose of the reticulocyte ocunt is to evaluate te bone marrow (BM) response to anaemia.
  • Using the percentage of reticulocyte count in anaemia alone gives a falsy increased percentage.
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5
Q

Reticulocyte index

A
  • A clinician must correct the percentage of reticulocytes for the degree of anaemia; called the reticulocyte index.
  • Reticulocyte index = (actual haematocrit/45) x reticulocyte count. 45 represents normal Hct
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6
Q

WHat does a reticulocyte index of <2% mean in anaemia

A
  • Reticulocyte index of <2% indicates that there is a poor BM response to the anaemia. This is ineffetive erythropoiesis
  • Examples of ineffective erythropoiesus are: Untreated irod deficiency, anaemia of chronic disease, folic acid deficiency and aplastic anaemia.
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7
Q

Types of anaemiaes

A
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8
Q

Extramedullary haematopoiesis (EMH)

A
  • Extramedullar haematopoiesis (EMH) = refers to RBC, WBC and platelet production that occurs outside the confines of BM.
  • COmmon sites for EMH are the liver and spleen
  • Causes:
    • Intrinsic BM disease (myelofibrosis..BM replaced by fibrous tissue)
    • Accelerated erythropoiesus (eg, severe haemolysis in sickle cell disease):
      • Eerythroud hyperplasia expands BM cavity
      • A radiograph of the skull shows a “hair-on-end” appearance caused by expansion of the BM in the skull bones by RBC progenitors.
  • EMH produces hepatosplenomegaly (enlargement of liver and spleen).
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9
Q

Locations of active marrow growth in foetus and adult

A
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10
Q

What is a Complete Blood Cell Count and Other studies

A
  1. Haemoglobin (Hb), Hct, RBC count
  2. RBC indices, RBC distribution width (RDW)
  3. WBC count with a differential count and platelet count
  4. Evaluation of the peripheral blood morphology

Factors that affect normal range of Hb, Hct, RBC are age, sex and pregnancy

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11
Q

Anaemia on a FBC

A
  • Anaemia = decrease in Hb, Hct or rbc concentration from any cause
  • Sa02 and Pa02 (partial pressure of arterial PO2) are normal. o2 exchange in the lungs is normal; therefore, the Pa02 and Sa02 are normal
  • 02 content is decreased in anaemia: 02 contnt = (Hb g/dl x1.34) x Sa02 + Pa02 x0.002. If Hb decrease the O2 content must also be decreased
  • Mechanisms include:
    • Decreased production of RBCs (hypo-proliferative)
    • Increased destruction of RBCs (hemolysis)
    • Acute blood loss (haemorrhage)
  • Anaemia is a sign of underlying disease rather than specific diagnosis
  • General clinical findings:
    • Fatige, dyspnoea with exertion, inability to concentrate and dizziness
    • Pulmonary valve flow murmur caused by decreased blood viscosity. Indicates severe anaemia (<5 g/dl)
    • Pallor of the skin, conjuctivae and palmar creases. Incates severe is <5g/dl
    • High output cardiac faulure. Caused by decreased blodo viscosiy in severe anaemia (<5 g/dl)
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12
Q

RBC indices

A
  1. Mean corpuscular volume - average volume of RBCs.
    • Microcytic anaemia MCV<80 um^3
    • Normocytic 80-100
    • Macrocytic MCV >100
  2. Mean corpuscular Hb concentration (MCHC) - avergae Hb conc in RBCs
    • Decreased - decreased RBC synthesis of Hb (eg, iron def anaemia) and the central area of palor in a RBC is greater than normal because there is less Hb in the cell, called hypochromasia.
    • Increased- presence of spherical RBCs which is in hereditary spherocytosis (HS). Mature RBCs are biconcave disks. Spherocytes lack the central area of pallor that is present in mature RBC which is hyperchromasia.
  3. RDW - variation in size of peripheral blood RBCs
    • Variation in size - anisocytosis. RDW only signfiicant if increased.
    • RDW increased- if RBCs not unfiromly same size eg microcytic and normocytic mix
    • Most useful in distinguishing iron deficiency (increased RDW- ue to normocytic and microcytici) from other causes of microcyctic anaemia (RBcs usually mor eunifrom and rdw normal eg in anaemia of chronic disease and mil thalassemia.
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13
Q

Iron metabolism

A
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14
Q

Characteristics of mature RBCs

A
  1. Biconcave disk - enhances gas exchange and alongside flexible cytoskelton allows RBC to deform readily so they can squeeze through cpaillaries. Electrolyte and water content and lipud composition of cell membrane affects shape
  2. Lack mitochondria - so no citric acid cycle, B-oxidation of fatty acids or ketone body synthesis
  3. Mature RBCs lack nucleus - cant synthesis DNA/RNA
  4. Use anaerobic glycolysis as primary source of ATP - lactic acid is end porduct of anaerobic metabolism which is converted by liver into glucose (gluconeogenesis) and then glucose used by RBCs to synthesise ATP
  5. RBCs use pentose phosphate pathway - synthesised glutathione (gsh) which is an antioxidant that converts hydrogen peroxide to water and neutralises acetaminophen free radicals. Hyrogen peroxide alsoproduce of oxidative metabolus in every living cell so this pathway must be functional to prevent destruction of RBCs by hydrogen peroxide.
  6. Mature rBCs use the methaemoglobin (etHb) reductase pathway: Heme iron in methemoglobin is oxidised Fe3+ so cant bind 02. Methmoglobin reductae system converts oxdised iron back to its ferrous state so it can bind o2.
  7. Mature RBcs use Luebering-Rapoport pathway: this synthesis 2,3 biphosphoglycerate (2,3-BPG), which is required for rightward shifting of oxygen dissociation curve (ODC), leading to release of 02 to tissue
  8. Mature RBCs lack human leukocyte antigens (HLAs) on their membranes
  9. Fate of senescent RBCs: normal RBC life span is 100 to 120days in peripheral blood. Senescent RBCs are phagocytosed in the cords of Billroth by splenic MPs. Heme degredation by the splenic MPs producs unconjugated bilirubin (UCB). Most of the UCB that is normally present in blood derives from destruction of senescent RBCs.
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15
Q

WBC count and differential in FBC

A
  • A 100- cell differential count divides leukocytes by percentage (eg, neutrophils, lymphocytes) and further subdivides neutrophils into segmented and band neutrophils
  • Multiplication of the percentage and the total WBC count gives the absoloute number of a particular leukocyte. Eg: lymphocytes 30%, total WBC count 10,000/mm^3; absoloute lymphocyte count is 0.3x10000=3000 cells/mm^3
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16
Q

Platelet count in FBC

A
  1. Platelets lack a nucleus (anucleate)
  2. Derived from cytoplasmic budding of megakaryocytes in BM
  3. Unlike mature RBCs, they have HLAs on their membranes
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17
Q

Relative frequencies of anaemia

A
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18
Q

Iron studies

A
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19
Q

Serum iron in a FBC

A
  • Iron bound to transferrin in the circulating blood - Transferrin is ysnthesised by the liver and binds iron for transport in the bloodstream
  • Serum iron shoidl be normally abotu 100ug/dl
  • Iron shown coming in tot MPs (macrophages) in in Figure A is from the degredrion of senescent MPs not transferrin. The amoutn of iron coming into the MP is equal to the amount of iron leaving MP to bidn with transferrin
  • Decreased serum iron = iron deficieny adn ACD
  • Increased serum iron occurs in overload diseases such as sideroblastic anaemias and hemochromatosis.
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20
Q

Serum total iron-binding cabaity (TIBC)

A
  • Correlaes with th econcerntration of transferrin, the binding protein of iron:
    • Height of column in figure A correlates with serum transferrin and TIBC
    • Normal TIBC is about 300ug/Dl
  • Relationship of transferrin synthesis with ferritin stores in MP
    • Inverse relationshiop between transferrin synthesis and ferritin stores in MP
    • Decreased ferritin stores -> increased liver synthesis of transferrin. Increases in transferrin and TIBC is present in iron deficiency
    • Increased ferritin tores -> decrease liver synthesis of transferrin. Decreased in transferrin and tIBC occur in ACD and iron overload disease
  • Primayr function of transferrin comes from BM MPs and from the duodenum, the primary site for iron absorption.
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21
Q

Iorn saturation signficiance

A
  • Refers to the percentage of bindings sites on transferrin that are ocucpied by iron.
    • iron saturation % = serum iron / TIBC x100
    • In the figure, the normal percentage of saturation is 100/300 x 100 or 33%
  • Decreased iron saturation uis present in iron deficiency and ACD
  • Increased iron saturation is present in iron overloaf diseases.
22
Q

Haemogloin and haemoglogbinopathies basic

A
23
Q

Hb Electrophoresis

A
  • Used to detect hemoglinopathies which include:
    • Abnormlaities in globin chain structure (eg sickle cell disease)
    • Abnormalities in globin chain synthesis (eg, thalassemia)
  • Types of norml Hb in adults that are detected by Hb electrophoriesis include:
    • Hba - 2ALPHA 2b globin chains (97% in adults)
    • HbA2 - which has 2A/2 delta globin chains (2% adults)
    • HbF - 2a/2y globin chains (1% adults)
  • Examples of a few abnormal Hb detected by electrophoresis are: Sickle Hb, Hb, H, Hb bart
24
Q
A

Types of anaemias on electrophoresis

25
Q

Microcytic anaemias

A

Types:

  • Iron deficiency (most common)
  • ACD
  • Thalassemia (thal a and B)
  • Sideroblastic anaemias (least common)

Patho:

  • all microcytic anaemias hve a defect in Hb synthesis: Hb= heme + globin chains
  • Defects in heme synthesis (ie iron + protoporphyrin) include: iron deficienct, ACD and sideroblastic anaemia
  • Defects in globin chain synthesis (a or B) are a- B- thalassemia
26
Q

Iron Metabolism

A
  1. Types iron: Reduced Fe2+ (ferrous heme iron in meat) and Oxidised Fe3+ (ferric nonheme iron in plants).
  2. Iron distribution:Funcitonal iron is present in Hb, enzymes, mypglobin. Amout 2500mg men and 2000mg women. Primarily stored as ferritin and hemosiderin in BM MPs. Amount of stored iron in men is about 1000mg and 400mg in women (decreased because of menses) . Total iron stores in men is about 3500 and owmen 2400
  3. Iron absorption and Reg:
    • Gastric acid frees elemental iron from heme (FE2+) and non heme produces (Fe3+). Explains why achlohydria (absence stomahc acid) decreases availability of iron for absorption
    • Iron form plants is in a nonheme or oxidised form (ferric, Fe3+). Nonheme (ferric) iron cant be absorbed in duodenum. It is converted by cytochrome B in duodenual mucosa into reduced iron (Fe2+) which can be reabsorbed. Reduced iron is absorbed by divalent metal transporter 1 (DMT1) into the mucosal cell of the duodenum.
    • Iorn form meat is in a heme or reduced form (F2+). ferrous form of iron is directly absorbed in duodenum by heme carrier protein 1.
    • Absorbed iron is stored as mucosal ferritin or it enters ferroportin 1 port and is immediately convverted by hephaestin or ceruloplasmin to ferric iron (fe3+) so that it can bind to transferrin in the blood which transports the iron todeveloping erythroi precursors in he marrow.
    • Iron absorption is regulation:
      • Abroption of iron dependent on total iron stores in body (reflected by amoutn of iron boudn to transferrin)
      • Transferrin with iron binds to transferrin receptors in immature precursor cells of normal enterocytes, which serve as iron sensors in the duodenum
      • HFE gene (hemochromatosis gene) protein product in the sesnory cells acting with the transferrin receptor causes differentiation of these cells into mature enterocytes that absrob iron.
27
Q

Iron absorption schematic

A
28
Q

When might the percentage of iron absorbed from the diet increase (eg, decreased hepcidin)?

A
  • Normal menstrual cycle
  • Pregnany and lactation
  • Any anaemia regardless of type
29
Q

Epidemiology of iron def anaemia

A
  • Most common overall anaemia in US
  • Most commo nutritional deficiency worldwide
  • Greatest prevalence in:
    • Toddlers 1-2years (caused by inaequate intake of iron)
    • Females 12-49 (caused by menstrual loss of iron)
30
Q

Iron deficiency anaemia - patho

A
  • Caused by insufficient iron for the normal synthesis of Hb
  • Decreased synthesis of heme (iron + protoporphyrin) which leas to decreased synthesis of Hb
31
Q

Clinical and lab findings of iron def anaemia

A

Chronic iron deficiency associated with:

  • Esophageal web (Pulmmer-Vinson syndrome), produces dysphagia
  • Achlorhydria (absence of HCL in stomach)
  • Glossitis and angula cheilosis (inflammation of the tongue and corner of the mouth)
  • Pallor the the conjuctivae and palmar skin creases
  • Spoon nails (koilonychia) and craving (pia) for ice

Lab findings: Mainly Decrease Hb, decrease iron and decrease ferritin (this can be high tho from inflamma as acute phase protein).

  • Decreased MCV, decreased serum iron and iron saturation, decreased serum ferritin, increased TIBC and RDW, microcytic and normocytic cells with increased centrla area of pallor, increased serum level of free erythrocyte protoporphyrun (FEP- ess iron to combine with protoporphyrin to form heme).
  • Thrombocytosis (increased platelet count): common in chornic irond ef. Reactive phenomenon that increases the blodo viscosity and prevent high output heart failure
  • Normla WBC count unles sother disorders present (eosinophilia occurs in hookwork infestations).

(microcytic- iron def, macrocytic (B12, folate def…)

32
Q

Anaemia of chronic disease (ACD) - what is it and epidemiology

A

Anaemia of chronic disease (ACD)

ACD is a disorder of iron homeostasis promoted by liver synthesis of hepcidin in response to inflammation

a. Most common anaemia in hospitalized patients
b. Second most common anaemia after iron deficiency anaemia
c. Occurs in approximately 10% of men and women ages 65 to 85 years
d. Occurs in >20% of adults older than 85 years
e. Common causes include:
(1) chronic inflammation (rheumatoid arthritis (RA), tuberculosis (TB), Crohn disease)
(2) alcoholism (ACD is the most common anaemia in alcoholism)
(3) malignancy (ACD is the most common anaemia in malignancy)

33
Q

Patho of anaemia of chronic disease

A
  • 1) Decreased heme synthesis
    2) Decreased renal production and/or impaired response to EPO
    3) Increased liver synthesis and release of hepcidin
    4) Hepcidin prevents the release of iron from enterocytes and MPs in the BM and

other sites (This keeps iron away from pathogens (iron blockade), which use it for

reproduction)

34
Q

Lab findings of anaemia of chronic disease

A

a. normal to decreased MCV.
1) In some cases, ACD presents as a normocytic anaemia.
2) More likely to present as a microcytic anaemia in the setting of severe active

inflammatory conditions such as rheumatoid arthritis (RA) and Crohn disease

b. decreased serum iron, TIBC, and percent iron saturation.
c. increased serum ferritin.
d. increased serum FEP level (Because there is less iron available to combine with protoporphyrin to form heme e. Hb rarely <9 g/dL.
f. increased BM iron in MPs.

35
Q

How is iron absorption regulated

A

▪ Iron absorption is regulatedL

(1) Absorption of iron is dependent on total iron stores in the body, which are reflected

by the amount of iron bound to transferrin.

(2) Transferrin with iron binds to transferrin receptors in immature precursor cells of

normal enterocytes, which serve as iron sensors in the duodenum.

(3) HFE gene (hemochromatosis gene) protein product in the sensor cells acting with the

transferrin receptor causes differentiation of these cells into mature enterocytes that

absorb iron

36
Q

How is iron from meat absrobed

A

▪ Iron from meat and meat products is in a heme or reduced form (ferrous, Fe2+).

• Ferrous form of iron is directly absorbed in the duodenum by heme carrier protein 1.

▪ Absorbed iron is stored as mucosal ferritin or it enters the ferroportin 1 port and is immediately converted by hephaestin or ceruloplasmin to ferric iron (Fe3+) so that it can bind to transferrin in the blood.

• Transferrin transports iron to developing erythroid precursors in the marrow.

37
Q

WHich is assoicated with intrinsic defect in RBC membrane

(a) Autoimmune haemolytic anaemia
(b) Hereditary spherocytosis
(c) Microangiopathic haemolytic anaemia
(d) Thermal injury causing anaemia

A

B. Hereditary spherocytosis

‘this inherited disorder is caused by intrinsic defects in the red cell membrane that render red cells spheroid, less deformable, and vulnerable le to splenic sequestration and destruction’ Other disorders with intrinsic defect in red cell mem-brane are hereditary elliptocytosis and abetalipoproteinemia.

38
Q

. Which of the following is not a stem cell of the bone marrow?

(a) Lymphoblast
(b) Myeloblast
(c) Myoblast
(d) Normoblast

A

Myoblast

Bone marrow cells include

  • Hematopoietic stem cells include lymphoblast, myeloblast and normoblast.
  • Marrow stromal cell/multipotent stem cells (MSC) including myoblast, osteoblasts, chondrocytes, adipocytes and endothelial cell precursors. Myoblast is an example of MSC giving rise to muscle cells or myocytes.
39
Q
  1. Which of the following surface glycoproteins is most often expressed in human hematopoietic stem cell?
    (a) CD 22
    (b) CD 40
    (c) CD 15
    (d) CD 34
A

D. CD 34

CD34 is expressed on pluripotent hematopoietic stem cells and progenitor cells of many lineages

40
Q
  1. Reticulocytosis is seen in all except:
    (a) P.N.H.
    (b) Haemolysis
    (c) Nutritional anaemia
    (d) Dyserythropoietic syndrome
A

C. nutritional anaemia

Reticulocytes are nonnucleated spherical cells bigger than normal RBCs and are polychromatic (having a blue colour) due to the presence of free ribosomes and RNA.

41
Q
  1. Which of these are seen on Romanowsky stain?
    (a) Reticulocytes
    (b) Basophilic stippling
    (c) Heinz bodies
    (d) Howell-Jolly bodies
    (e) Cabot ring
A

Ans. (b) Basophilic stippling; (d) Howell-Jolly bodies; (e) Cabot ring

Romanowsky dyes are used for staining blood films. They are made up of combination of acid and basic dyes. The nucleus and neutrophilic granules are basophilic and stains blue. Haemoglobin is acidophilic and stains red.

  • Various modifications available are Leishman’s stain, Wright’s stain, Giemsa and Jenner’s stain.
  • Basophilic stippling, Howell-Jolly body and Cabot rings are seen by Romanowsky stain.
  • Basophilic stippling: These are small blue or black granules in red cells seen in megaloblastic anaemia, heavy metal poisonings, etc.
  • Howell-Jolly Body: These are remnants of the nucleus seen as small, round dark blue particles near the periphery of the cells; found in post-splenectomy, asplenia and severe haemolytic anaemia.
42
Q
  1. Which of the following surface glycoproteins is most often expressed in human hematopoietic stem cell?
    (a) CD22
    (b) CD40
    (c) CD15
    (d) CD34
A

CD34

43
Q
  1. Inappropriate erythropoietin level is found in all except:
    (a) Renal cell carcinoma
    (b) Lung disease
    (c) High altitude
    (d) Benign liver tumour
A

D. Benign liver tumour

44
Q

Size of RBC measured by

  1. The size of the red blood cells is measured by:
    (a) MCV
    (b) MCHC
    (c) ESR
    (d) MCH
A

a. mcv

45
Q
  1. Anaemia which is associated with pancytopenia is:
    (a) Haemolytic
    (b) Megaloblastic
    (c) Iron deficiency
    (d) All
A

c. Megaloblastic

Pancytopenia occurs when you have a combination of three different blood disorders:

46
Q
  1. Haematuria with dysmorphic RBCs are seen in:
    (a) Acute glomerulonephritis
    (b) Renal TB
    (c) Renal calculi
    (d) Chronic renal failure
A

(a) Acute glomerulonephritis

47
Q
  1. MCHC is increased in:
    (a) Iron deficiency anaemia
    (b) Spherocytosis
    (c) Thalassemia
    (d) All
A

Ans. (b) Spherocytosis

48
Q
  1. In polycythemia vera, all are raised except:
    (a) Haematocrit
    (b) Platelet count
    (c) RBCs
    (d) Erythropoietin
A

Ans. (d) Erythropoietin

Polycythemia vera - type of blood cancer. It causes your bone marrow to make too many red blood cells. These excess cells thicken your blood, slowing its flow, which may cause serious problems, such as blood clots. Polycythemia vera is rare.

49
Q
  1. Which of these does not indicate megaloblastic anaemia?
    (a) Increased reticulocyte count
    (b) Raised Bilirubin
    (c) Mild splenomegaly
    (d) Nucleated RBC
A

Ans. (a) Increased reticulocyte count

‘The reticulocyte count is low’.

Please be clear of the concept friends that the reticulocyte count is increased when the megaloblastic anaemia is being treated with vitamin B12 and folate supplementation i.e. after the initiation of the treatment in these patients.

• Nucleated red cell progenitors occasionally appear in the circulating blood when anaemia is severe.

50
Q
  1. The anaemia associated with leukaemia is:
    (a) Iron deficiency
    (b) Megaloblastic type
    (c) Myelophthisic type
    (d) None of the above
A

Ans. (c) Myelophthisic type

Myelophthisic anaemia describes a form of marrow failure in which space-occupying lesions replace normal marrow elements. The commonest cause is metastatic cancer, most often carcinomas arising in the breast, lung, and prostate

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