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pathophysiology > lecture 11: Hematopoetic and lymphatic systems > Flashcards

lecture 11: Hematopoetic and lymphatic systems Flashcards

1
Q

blood transports substances to tissues via…

A

circulatory system

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2
Q

components of blood:

A

-PLASMA (fluid component of blood)
-OXYGEN, NUTRIENTS, HORMONES, LEUKOCYTES, RBCs, PLATELETS, Abs, CLOTTING FACTORS
- ALBUMIN (oncotic pressure), Ab (immunity)
- CO2 and other WASTE of cell metabolism to excretory organs of body

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3
Q

volume of blood

A

5-6L, varies according to size of individual

  • almost half of blood consists of cellular elements suspended in plasma (viscous fluid)
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4
Q

cellular elements of blood

A

RBC
- oxygen/ CO2 exchange (hemoglobin)

LEUKOCYTES (WBC)
- immune functions

PLATELETS
- hemostasis

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5
Q

leukocytes: neutrophils

A

most numerous, first line (vital)
- 60-70% of total circulating WBC
- PHAGOCYTIC
- inflammatory reactions (predominant)

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6
Q

leukocytes: monocytes

A

phagocytic macrophages
- 3-5%
- increased in certain chronic infections
- circulate to sites of inflammation
- transition to MACROPHAGES (APC)
- infection/ tissue repair

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7
Q

leukocytes: eosinophils

A

allergy, parasitic infections
- increased in allergic reactions
- increased in animal-parasite infections
- LOW amounts

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8
Q

leukocytes: lymphocytes

A

adaptive immunity
- 15-20%
- next most COMMON (B/T cells)
- predominant leukocytes in children
- small amount in circulation
- most in LN, SPEEN, LYMPHOID TISSUES
- traffic through lymphatic system
- CELL-MEDIATED and HUMORAL defence reactions

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9
Q

leukocytes: basophils

A

parasitic infections
- increased in allergic reactions
- increased in animal-parasite infections
- LOW amounts

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10
Q

stem cells

A

precursor cells in BONE MARROW that DIFFERENTIATE to form red cells, white cells, and platelets

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11
Q

RBCs (hemoglobin)

A
  • transport of oxygen
  • BICONCAVE disc (large sa:volume ratio) - allows squeezing through capillaries
  • MOST numerous cells in blood
  • survive 4 months (120 days)
  • ERYTHROBLAST: precursor cell in bone marrow
  • HEMOGLOBIN: oxygen-carrying protein formed by the developing red cell
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12
Q

leukocytes

A
  • LESS numerous
  • different types
  • survive hours to years
  • GRANULOCYES/ POLYMORPHPNUCLEARGRANULOCYTES (PMN - eosinophils, basophils, neutrophils)
  • some produced in bone marrow but mainly found in LN and SPLEEN
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13
Q

platelets

A

essential for BLOOD COAGULATION
- SMALLER than leukocytes
- no nucleus - bits of the cytoplasm of megakaryocytes (largest PRECURSOR cells in bone marrow - platelets come from mega…)
- SHORT SURVIVAL: 10 days

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14
Q

hematopoiesis

A

formation and development of blood cells
- bone marrow replenishes blood cells (due to damage/ age)

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15
Q

substances necessary for hematopoiesis

A

vitamin B12 + folic acid (need for DNA synthesis)
iron
protein, lipid production

*decreased RBC production if any of these are lacking
*regulated by OXYGEN content in blood (stimulates epo release from kidneys)

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16
Q

maturation of RBCs

A
  1. proerythroblasts in bone marrow mature (3 days) in to reticulocytes (earliest RBC) in blood (1 day)
  2. reticulocytes (large, DNA/RNA present) leave bone marrow and DIFFERENTIATE into RBC in circulation
  3. high reticulocyte count indicates the body is creating a lot of RBC
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17
Q

Erythropoietin (epo)

A

STIMULATES RBC PRODUCTION
released from KIDNEYS (regulates according to OXYGEN content in arterial blood)

*RBC derive energy from enzymatic breakdown of glucose (anaerobic glycolysis)
*no nucleus, so enzymes can’t be replaced
*activity gradually declines over 4 months (RBCs die)

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18
Q

WBC production

A

regulated by INTERLEUKIN LEVELS/ RESPONSE TO INFECTION
- complex

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19
Q

Thrombopoietin (TPO)

A

STIMULATES PLATELET PRODUCTION

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20
Q

red bone marrow contains stem cells that can become…

A

RBC
WBC (lymphocytes (B/T), neutrophils, eosinophils, basophils, monocytes, neurophils)
platelets

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21
Q

hemoglobin

A

96% of RBC content (no organelles/ nucleus)

TETRAMER composed of 4 SUBUNITS, each one consisting of heme and globin
- 4 subunits AGGREGATE to form Hb tetramer

  • most common in adults 96-98% - HbA (2-alpha, 2-beta s.u.)
  • rest is HgF (2-alpha-2-gamma), HgA2 (2alpha-2detla)
    (most COMMON subunit = HbA)

*changes as you age, after birth they are produced more in bone marrow (airbreathing/ placental)
*low level in adults

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22
Q

hemoglobin: heme

A

PORPHYRIN RING that contains IRON atom

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23
Q

hemoglobin: globin

A

LARGEST part of hemoglobin
forms different CHAINS (alpha, beta, gamma, delta, epsilon)

globin chains: produced by RIBOSOMES
- joined to heme to form a hemoglobin unit (a and B)

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24
Q

hemoglobin: porphyrin ring

A

produced by mitochondria, iron inserted to form heme

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25
Q

hemoglobin: reticulocyte

A

YOUNG red cell WITHOUT NUCLEUS but retains some organelles (identified by special strains)
- once they exit bone marrow, in 24-48h they mature and survive in circulation for 4 MONTHS (RBC)

Hg in these RBCs

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26
Q

RBC life cycle

A
  • worn out RBC are removed by SPLEEN
  • Hb regraded and excreted as BILE
  • conjugated to GLUCURONIC ACID (soluble)

PORPHYRIN RING: not salvaged
GLOBIN CHAINS: break down and used to make other proteins
IRON: extracted and SAVED to make new Hb (we don’t get rid of iron unless we bleed)

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27
Q

how is RBC production regulated?

A

by OXYGEN content in ARTERIAL BLOOD
- reduced oxygen stimulates EPO to make RBCs
- reduced oxygen tension does NOT ACT DIRECTLY on bone marrow… it’s mediated by the kidney which produces EPO which then makes RBCs from the bone marrow

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28
Q

oxygen transport by hemoglobin

A

MUST BE IN FERROUS FORM (Fe2+) to enter reversible combination with oxygen
- if not in ferrous form, it won’t bind to oxygen and deliver oxygen properly

high partial pressure from oxygen in lungs: promotes binding
low partial pressure from oxygen in tissues: promotes release

methemoglobin iron (Fe3+) not in ferrous state so it can’t bind oxygen!!
- inherited disorder or response to toxic agents (trace amounts present spontaneously)
- several drugs/ chemicals can oxidize Hb to methemoglobin
- tx: oxygen therapy, ascorbic acid (reduced oxidation), methylene blue (reverses), transfusion

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29
Q

oxygen transport by hemoglobin: carboxyhemoglobin

A

binds CO with high affinity (200x stronger than oxygen), blocks oxygen binding, products of incomplete combustion

tx: hyperbaric oxygen therapy (pure oxygen 2-3x atm. pressure) - push oxygen into RBCs

CO BOUND TO HG IS STRONGER THAN O TO HG

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30
Q

iron metabolism

A

iron reserves: stored in LIVER, BONE MARROW, SPLEEN
- no mechanism for iron elimination in body (other than blood loss)

DUODENAL cells produce HEPCIDIN to block iron uptake by duodenal cells which interferes with transport
- hepcidin levels are decreased/ increased in response to iron stores
(hepcidin regulated iron uptake so we only abosorb it when we need it)

*dietary iron
*iron combines with protein (apoferratin) in duodenal mucosa to form ferratin
*iron transported in blood by trasnferrin (here it could be stored for later use)
*or its carried to marrow by transferrin and used to MAKE HEMOGLOBIN
*Hg broken down when red cells wear out –> iron recycled and reused when RBC dies (ferratin)

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31
Q

hemochromatosis (hereditary/ acquired)

A

CHRONICALLY ABSORB TOO MUCH IRON (high ferritin)
- genetic disease as autosomal recessive

due to:
- iron overload or blood disorders w lots of RBC destruction (sickle cell)

causes:
- organ damage, scarring, permanent derrangement of organ fxn

manifestations: can take years to develop
- tan to brown skin
- DM
- cirrhosis (liver damage)
- heart failure
- blood test (evaluated serum iron/ ferritin)

treatment: periodically remove blood (phlembotomy) until iron stores are depleted, iron chelation tx to remove iron

32
Q

anemia (and its 2 causes)

A

REDUCTION IN RBC OR SUBNORMAL LEVELS OF Hb

  1. inadequate production of RBCs
    - insufficient raw materials
    - inability to deliver RBCs to circulation (BM damage/ destruction (aplastic anemia) - and WBCs are lost, replacement of marrow by foreign cells (cancer)
  2. excessive loss of RBCs
33
Q

anemia: inadequate production of RBCs

A

insufficient raw materials
- iron deficiency
- vitamin B12 deficiency
- folic acid deficiency

inability to deliver RBCs
- BM destruction/ damage (aplastic anemia)
- replacement of marrow (cancer)

34
Q

anemia: excessive loss of RBCs

A
  • external blood loss (hemorrhage)
  • shortened survival of RBC in circulation (sickle cell, thalassemia)
  • defective RBCs: hereditary anemia
  • accelerated destuction: of cells from anti-RBC Ab or mechanical trauma to RBCs
35
Q

anemia: morphologic classification

A

based on RBC appearance (size and colour) suggests the etiology of anemia

36
Q

anemia: morphologic classification - NORMOCYTIC ANEMIA

A

normal size and appearance (but lysis still)

37
Q

anemia: morphologic classification - MACROCYTIC ANEMIA

A

cells LARGER than normal impaired
- FOLIC ACID DEFICIENCY
- VITAMIN B12 DEFICIENCY

38
Q

anemia: morphologic classification - MICROCYTIC ANEMIA

A

SMALLER cells
- THALASSEMIA
- IRON DEFICIENCY

39
Q

anemia: morphologic classification -HYPOCHROMIC ANEMIA

A

REDUCED HEMOGLOBIN content (pale)

40
Q

anemia: morphologic classification - HYPOCHROMIC MICROCYTIC ANEMIA

A

SMALLER than normal and REDUCED HEMOGLOBIN content (pale)

41
Q

iron-deficiency anemia

A

HYPOCHROMIC MICROCYTIC (not enough iron)
- most common anemia

  • iron absorbed from DUODENUM (gut), transferred via transferrin, stored as ferritin

pathogenesis:
- you don’t eat enough of it
- you eat it but don’t absorb it
- you eat it but not enough to maintain stores
- infants during periods of rapid growth
- GI-chronic infection/ inflammation, cancers (increased IL-6 production increases HEPCIDIN production - blocks iron uptake)
- chronic bleeding (from GI tract or women periods)
- too frequent blood donations
- chronic disease (treat the chronic disease - CAUSE)

42
Q

iron-deficiency anemia: lab tests in blood and results!!

A

serum ferritin: LOW
serum iron: LOW (and low iron saturation)
serum iron-binding capacity: HIGH
- because iron isn’t absorbed so there’s none attached to heme

43
Q

iron-deficiency anemia: symptoms and treatment

A

tx:
primary: learn CAUSE
- direct tx towards cause rather than symptoms
- administer supplementary IRON if needed

symptoms:
- dizziness
- arrhythmia
- shortness of breath
- fatigue
- cold skin
- paleness
- chest pain
- headaches

44
Q

vitamin B12 and folic acid deficiency anemia

A

MACROCYTIC ANEMIA

VITAMIN B12: most B12 comes from animals (vegetarians at risk)
- for structure and integrity of NERVOUS system (deficiency–> neurologic disturbances)

FOLIC ACID: from leafy veg and animals
- relatively common, body has limited stores so depleted quickly in not replenished
- pathogenesis:
- inadequate diet (in alcoholics)
- poor absorption (chronic intestinal disease)
- pregnancy (increased demand for folic acid)
- chronic increased RBC production

45
Q

absence/ deficiency of vitamin B12 and folic acid

A

both vitamin B12 and folic acid are required for normal hematopoiesis and maturation of other cells

  • abnormal RBC maturation or MEGALOBLASTIC ERYTHROPOEISIS with formation of large cells (MEGALOBLASTS)
  • mature RBCs are LARGER than normal and macrocytes; corresponding anemia is called MACROCYTIC ANEMIA
  • abnormal development of WBC precursors and megakaryocytes result in:
    -LEUKOPENIA (low WBC)
    -THROMBOCYTOPENIA (low platelets)
46
Q

pernicious anemia

A

MACROCYTIC ANEMIA

lack of intrinsic factor that you need in order to absorb vitamin B12 (decreased B12 absorption)
- vitamin B12 in food combines with intrinsic factor (in stomach lining)
- vitamin B12: intrinsic factor complex absorbed in ileum

causes: (gastric/ stomach issues)
- gastric mucosal atrophy (lack of secretion of acid and digestive enzymes - aging)
- auto Ab against mucosal cells
- surgery to remove secretion of stomach (ulcer, gastric bypass, gastric cancer resection)
- chronic intestinal diseases (chrons, IBS)
- genetic

tx: increased oral dose (B12 SUPPLEMENTS) or intramuscular injections

47
Q

conditions that depress bone marrow function

A

(suppression) ANEMIA OF CHRONIC DISEASE
- can infect RBCs and precursors
- resolves when infection resolved

(damage) APLASTIC ANEMIA (BM damaged or destroyed)
- both RBC and WBC affected/ depleted
- marrow injured by radiation
- anticancer drugs/ chemicals or other drugs
- auto antibodies
- idiopathic causes

*suppression of bone marrow prescursors also effect WBC and PLATELETS (PANCYTOPENIA) - anemia, leukopenia, thrombocytopenia

(infiltration) MARROW INFILTRATED BY TUMOR/ REPLACED BY FIBROUS TISSUE

48
Q

bone marrow suppression, damage or infiltration treatment

A

depends on CAUSE

supportive symptomatic: RBC and platelet transfusions

autoimmune: immunosuppressive drugs

aplastic anemia (cord blood, bone marrow, peripheral stem cells): hematopoietic stem cell transplant in highly selected cases

no specific treatment in most cases

49
Q

accelerated blood destruction

A
  • from INTRINSIC defect in RBC STRUCTURE
  • from EXTRINSIC condition that SHORTENS CIRCULATING LIFE of RBC

*RBC lasts 4 months
- defects in RBC or damage will have them TARGETED FOR DESTRUCTION IN SPLEEN prematurely

*can be autoimmune
(increased breakdown of RBCs –> jaundice)

50
Q

hereditary hemolytic anemias

A

hereditary hemolytic anemias: genetic abnormality prevents normal survival of RBCs (they get destructed)

  1. abnormal shape
    - hereditary spherocytosis
  2. abnormal hemoglobin
    - hemoglobin S (sickle cell)
    - hemoglobin C
    both in people of African descent
  3. defective hemoglobin synthesis
    - thalassemia - globin mutations (alpha/ beta), synthesis is defective
    - south east asia, greek and italian ancestry
51
Q

hereditary spherocytosis

A

RBCs circular/ ball shape
- mutation defect in CYTOSKELETON protein - failure to form a bi-concave disc

results in:
- smaller SA: size
- fragile, less flexible/ deformable
- increased destruction by spleen
- mild/ moderate anemia

tx: transfusion, B12/ folic acid, splenectomy (remove spleen) so it can’t destroy it

*also seen in autoimmune hemolytic anemias

52
Q

thalassemia

A

defective synthesis of alpha or beta Hg

ALPHA: 4 genes
- 1 (no change), 2 (trait with mild disease), 3 (severe disease), 4 (incompatible with life - hydrops fetalis)
- lack of alpha and excess beta chains form UNSTABLE BETA TETRAMERS (defective oxygen exchange), stiff/ malformed RBC
- MICROCYTIC HEMOLYTIC ANEMIA (may require repeated transfusions) - iron overload risk, BMT

BETA: 2 genes
- heterozygous-mild/ asymptomatic, homo-severe
- overproduction of alpha chains precipitates RBC and SHORTENS SURVIVAL (chronic anemia)
- HYPOCHROMIC, MICROCYTIC ANEMIA

53
Q

sickle cell

A

Hemoglobin S (beta Hgb point mutation) - single point mutation in b (HbS instead of HbA)

  • where malaria is (deoxygenated conditions)
  • HgbS forms rigid fibers causing SICKLING, reversible
  • constant sickling wears out cells and sickle cells are targeted by SPLEEN
  • cells are STICKY and form blockages in blood vessels
  • (sickle cell trait) heterozygous, asymptomatic
  • (sickle cell disease) homozygous, chronic health problems
  • VASO-OCCLUSIVE CRISIS (severe abdominal pain (lung - ASC, kidney, liver spleen infarction)
  • chronic bone (occlusion in bone marrow) - joint pain - with anemia
  • SPLENIC SEQUESTRATION CRISIS

tx: RBC transfusion, hydroxy urea, BMT, pain control
- gene therapy trials promising - point mutation betaH

54
Q

acquired hemolytic anemia

A

NORMAL red cells that are unable to survive in a HOSTILE ENVIRONMENT
- attacked and destroyed by ANTIBODIES
- destruction of red cells by mechanical TRAUMA

pass through enlarged spleen (splenomegaly) causes damage - liver cirrhosis

  • damaged by contact with some part of artificial heart valve

clotting disorders: DIC, TTP - clots form in small blood vessels damaging RBC

55
Q

diagnostic evaluation of anemia

A
  • history and physical
  • iron, ferritin, iron binding capacity, RBC size (MCV)/ variability (MCHC), hemoglobin levels
  • complete blood count (CBC) to assess degree of anemia, leukopenia (low WBC), and thrombocytopenia (low platelet)
  • blood smear to determine if normocytic, macrocytic, or hypochromic microcytic
  • reticulocyte count (early RBC) to assess rate of PRODUCTION of new RBCs
  • lab tests to determine iron, B12, folic acid levels
  • bone marrow study to study characteristic abnormalities in marrow cells
  • evaluation of blood loss from the gastrointestinal tract to localize the site of bleeding
56
Q

polycythemia

A

too many RBCs!!!

primary (polycythemia vera) - rare
- diffuse marrow hyperplasia (making too much of all bone marrow cells)
- OVERPRODUCTION of WBCs, RBCs, and platelets
-evolve to granulocytic leukemia
tx: drugs to suppress marrow function (hydroxy urea)

secondary - common
- in response to something
- reduced arterial oxygen –> COMPENSATORY INCREASE IN RBCs
- increased epo production
- emphysema, pulmonary fibrosis, congenital heart disease, malignancy, increased erythropoietin produced renal tumor, splenectomy/ liver disease, chronic infection/ inflammation
tx: periodic removal of excess blood (TREAT CAUSE)

*complications:
- CLOT FORMATION due to increased blood VISCOSITY and PLATELET count

57
Q

lymphatic system

A

primary function: immunologic defence against foreign material via cell-mediated and humoral defence

  • return of lost circulatory volume to vascular system

structure:
LN - bean-shaped, mass of lymphocytes supported by meshwork of reticular fibers with phagocytic cells
- as lymph flows through nodes, phagocytic cells filter out and destroy microorganisms and foreign matter
- clustered where lymph channels are located

58
Q

lymphoid tissue

A

in thymus, tonsils, adenoids, lymphoid aggregates in intestinal mucose, respiratory tract, bone marrow

59
Q

thymus

A

overlies base of heart, LARGE during infancy and childhood, UNDERGOES ATROPHY in adolescence
- essential in prenatal development of lymphoid system and in formation of body’s immunologic defense mechanisms (T cell development/ selection)

60
Q

spleen

A

FILTERS BLOOD
- compact mass of LYMPHOCYTES and network of sinusoids (capillaries with wide lumens)
- macrophages (phagocytosis)
- for ANTIBODY formation - pathogen elimination and phagocytosis of senescent red cells
- detection and removal of pathogens in blood
- immune cells can exit the lymphatic system but not enter the spleen

61
Q

splenectomy

A

reasons:
- traumatic injury (to prevent fatal hemmorhage)
- blood diseases: excessive destruction of blood cells in spleen (hereditary hemolytic anemia)
- prevent chronic splenomegaly (enlarged spleen)
- cancer (leukemia/ lymphoma)

effects:
- less-efficient elimination of bacteria (especially blood borne)
- impaired production of Ab!!!
- predisposed systemic infections
- risk of steptococcus pneumoniae, haemophilys influenzae, meningococcus infections
- risk of increased platelet/ RBC (due to inefficient clearance/ removal) - PROCOAGULATORY (increased risk of clots)

RBC REMOVAL IS TAKEN OVER BY LIVER (SECONDARY SPLEEN) - 30% of people

tx: vaccines, abx prophylaxis

62
Q

lymphatic system diseases: infectious mononucleosis

A

caused by EBV (EBV-Bcell 90%) or CMV (Tcell/ macrophages 5-7%)
- fever, sore throat, fatigue
- CD8 and Ab destroy most infected B cells
- enlarged and tender LN
- disease is self-limiting

risks:
- avoid body contact (avoid splenic ruptutre)
- compomised immune system - unrestrained B cell proliferation by give rise to B cell lymphoma

63
Q

lymphatic system diseases: enlarged LN

A
  • from local or systemic infection
  • from metastatic tumor in node
  • early manifestation of leukemia or malignant lymphoma
64
Q

lymphatic system diseases: spread of tissue neoplasms

A
  • metastatic tumors: breast, lung, colon, other sites
  • nodes first affected lie in immediate drainage area of tumor
  • tumour spreads to more distant LN through lymphatic channels
65
Q

lymphatic system diseases: malignant lymphoma

A
  • hodgkin lymphoma
  • nonhodgkin lymphoma

lymphocytic leukemia: from lymphoid precursor cells; ACUTE (primitive forms) or CHRONIC (mature cells)

66
Q

leukemia

A
  • cancer (neoplasm) of hematopoietic tissue
  • leukemic cells infiltrate the bone marrow and lymphoid tissues, spill over into the bloodstream and infiltrate throughout various organs of body
  • mature (chronic) or primitive (acute) cells
  • OVERPRODUCTION OF WBCs
67
Q

aleukemic leukemia

A

cancer cells are only in bone marrow
(# in peripheral blood is normal or decreased)

68
Q

myelodysplasia (preleukemia)

A

DISTURBED GROWTH AND MATURATION OF MARROW CELLS
anemia: reduced erythrocytes
leukopenia: reduced WBC
thrombocytopenia: reduced platelets

  • not all pts develop leukemia
    “myelodysplastic syndrome”
  • more severe disturbance in bone marrow = more likely that leukemia will occur
69
Q

leukemia classification

A

cell type:
- granulocytic, lymphocytic (lymphoid), monocytic (myeloid)

maturity
- acute
- ALL (children), CML, CLL, AML(adults)
- chronic (mature)

5 year survival rates
- CLL = highest –> CML –> ALL –> AML = worst

70
Q

leukemia clinical features

A

caused by impairment of bone marrow function

leukemic cells CROWD OUT normal cells causing:
- ANEMIA
- THROMBOCYTOPENIA causing bleeding
- INFECTIONS due to less WBC

71
Q

infiltration of organs by leukemic cells causes:

A
  1. splenomegaly (enlarged spleen)
  2. hepatomegaly (enlarged liver)
  3. lymphadenopathy (enlarged lymph nodes)
  4. bone pain (expansion of cells in bone marrow)

chronic leukemia: slow, can be outlived (CLL) - NOT AS BAD
acute leukemia: fast, difficult to control - BAD IN KIDS

72
Q

myeloma:

A

cancer of PLASMA CELLS (overproduction of Ab and increased viscosity/ renal failure

73
Q

lymphoma:

A

cancerous cells form solid tumors in LN
- disease of lymphocytes: most B, some T cells
- remain in LN (spleen, liver, thymus)
- disrupts immune function

hodgkin
- young
- starts in single LN and spreads
- detected as single or group of enlarged LN
- better prognosis
REED-STEINBERG CELLS (large atypical B cells) that act as nucleus of tumor and secrete cytokines to attract other tumor cells

non-hodgkin
- older
- variable appearence and progression
- not detected until widespread dissemination

74
Q

treatment of leukemia and lymphoma

A
  • destruction of malignant cells by chemo or radiation to produce remission
  • surgical removal
  • stem cell therapy (BMT, peripheral, cord blood)
  • self or nonself
  • donor
75
Q
A

pathophysiology (10 decks)

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