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Pathophysiology > Hematology > Flashcards

Hematology Flashcards

1
Q

blood

A

plasma/water = 55%
formed elements = 45%
* Chief Function: delivery of substances needed for cellular metabolism, removal of waste, defense against microorganisms and injury, maintenance of acid-base balance
- body contains 6 liters

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2
Q

plasma

A
  • fluid component of blood - 90% water, 10% solutes

- contains proteins and electrolytes

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3
Q

plasma proteins

A
  • All made in liver*
  • albumin: most abundant, carriers and control plasma oncotic pressure. carry calcium. pull fluid into capillaries
  • globulins: carrier proteins and immunoglobins (antibodies). hemoglobin, thyroglobulins
  • Clotting factors: mainly fibrinogen
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4
Q

cells (formed elements)

A

erythrocytes - red blood cells
leukocytes - white blood cells
thrombocytes - platelets

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5
Q

erythrocytes (RBCs)

A
  • carry hemoglobin, deliver o2 to tissues
  • most abundant cell in the body
  • 120 day life cycle (3-4 months)
  • bioconcavity = lots of surface area, moldable shape (squeeze through liver, blood vessels smoothly)
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6
Q

leukocytes (WBCs)

A
  • defend the body against infection and remove debris
  • Granulocytes: baso (induce inflame) , eso (regulate inflame with histamine), neutros (phagocytosis). inflammatory and immune functions.
  • agranulocytes: monos/macros, lymphocytes T, B and NK
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7
Q

Thrombocytes (platelets)

A
  • cell fragments
  • disk-shaped cytoplasmic fragments
  • essential for blood coagulation and control of bleeding
  • thrombopoietin - main regulator of platelets
  • released by liver and stimulate production of platelets
  • after trauma, internal hemmhorage
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8
Q

Spleen

A
  • filters blood
  • largest secondary lymphoid organ
  • contains t and B cells (macrophages)
  • phagocytosis of old, damaged, and dead blood cells
  • blood storage (released during trauma)
  • “lymph node” to cardio system
  • mono = infected spleen
  • if spleen ruptures – bad blood explodes throughout the body
  • if you don’t; have a spleen – lymph nodes, liver help out
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9
Q

lymph nodes

A
  • part of the immune system and hematologic systems
  • facilitates maturation of lymphocytes - T and B and Macros are in lymph organs to kill bad cells
  • transports lyphatic fluid back to circulation
    cleanses lyphatic fluid or microorganisms and foreign particles
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10
Q

Mononuclear Phagocyte System (MPS)

A
  • consists of monocytes in blood and mature macrophages in tissues
  • ingest and destroy microorganisms and foreign material
  • MPS is mostly liver and spleen
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11
Q

Hematopoiesis

A
  • process of blood cell production
  • erythrocytes = rbc formation
  • two stages: mitosis and maturation/differentiation

Bone Marrow: myeloid tissue. red and yellow bone marrow when born, adults have active bone marrow in pelvic, vertebrae, cranium, ribs, humorous, femur

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12
Q

Erythropoiesis

A
  • erythrocytes derived from erythroblasts (normoblasts)
  • maturation stimulated by erythropoietin EPO kidneys
  • quantity of hemoglobin increases and the nucleus decreases in size “packet of hemoglobin”
  • number of cirrculatiing RBCs in healthy people remain constant
  • ## hypoxia - stimulates the production and release of erythropoetin - increases production of RBCs
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13
Q

Hemoglobin

A
  • oxygen carrying protein of the erythrocyte
  • RBCs have 4 heme groups (300-400 hemoblobins)
  • ## heme contains iron, brinds to o2 = red
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14
Q

Hemoglobin Synthesis

A
  • proteins and amino acids are needed
  • B12 and folate = lifespan of RBCs
  • iron and copper are needed to make RBCs
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15
Q

destruction of aged RBCs

A
  • aged red cells (senescent) are destroyed by macrophages of the MPS
  • primarily destroyed in the spleen
  • liver takes over if the spleen isn’t functioning correctly
  • globin chains are broken down into amino acids
  • porphyrin is reduced to bilirubin, transported to the liver, and secreted in the bile
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16
Q

leukopoesis

A
  • leukocytes arise from stem cells in bone marrow
  • granulocytes mature in bone marrow
  • agranulocytes are released into the bloodstream before they fully mature
  • activated when they leave the blood stream and are put to work
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17
Q

thrombopoesis

A
  • endomitosis - platelet formation
  • megakaryocyte undergoes nuclear phase of cell division but fails to undergo division and explodes – releases platelets
  • only activated or “turned on” when needed. turn sticky when needed, not always
  • thrombopoetin regulates platelets leves
  • platelets circulate for 10 days before losing their functional capacity - then removed by spleen/liver
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18
Q

Hemostasis

A
  • to arrest or stop bleeding
  • after trauma, injury, loss of blood
  • requires: platelets, clotting factors, blood flow ad shear forces, endothelial cells, fibrinolysis

STEPS:

  1. vascular spasm/vasoconstriction: blood vessel injury, constricts to slow blood loss
  2. platelet plug formation: not permanent
  3. Coagulation/formation of fibrin clot: fibrin protein, hold everything in place on vessel wall.
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19
Q

Hemostasis: Platelet Plug Formation

A
  1. Activation: exposure to collagen and reacts with platelets
    - calcium is essential for platelet activation
  2. adhesion: productes platelet plug stickiness
    - von Hillebrand factor - stickiness activation
  3. activation (again): release chemotaxis to get more platelets and calcium
  4. aggregation: stick together, temporary plug
  5. Secretion: Granules release: seratonin, coagulation factors, calcium histamine
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20
Q

4 Players in classical pathway coagulation

A

thrombinogen, thrombin, fibrinogen, fibrin

* “ogen/pro” means not activated yet

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21
Q

VII vs VIIa

A

without a = in blood

with a = activated

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22
Q

coagulation cascade

A

extrinsic: activated when tissue factor (TF) (Tissue thromboplastin) is released by damaged endothelial cells
intrinsic: activated when factor XII contacts sub endothelial substances (collagen) exposed by vascular injury

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23
Q

extrinsic pathway

A
  • trauma, scape, pierce
  • TF - 7 - 10
  • can also activate intrinsic pathway

TF –> VII –> VIIa –> X –> classical pathway (thrombinogen/prothrombin - Xa -> thrombin –> fibrinogen –> fibrin

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24
Q

intrinsic pathway

A
  • damaged endothelium & exposed collagen
  • 12 - 11 - 9 - 8 - 10
  • atherosclerosis, inflammation, hypertension, infection

exposed collagen –> XII –> XIIa –> XI –> XIa –> IX –> IXa –> VIII –> VIIIa –> X –> Xa –> thrombin –> fibrinogen –> Fibrin

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25
Q

clot retraction

A
  • fibrin strands shorten, become denser and stronger to approximate the edges of the injured vessel and site of injury
  • platelets within clot and actin-like contractile proteins in platelets
  • pulls wound/tissues together to facilitate repair
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26
Q

virchow’s triad - causes of thrombosis

A

inadvertent clot formation

  1. changes in bood vessel wall - endothelial damage
  2. changes in blood flow - blockage, decreased blood flow, clot
  3. changes in blood composition: overproduction or RBCs, dehydration (thick blood), overproduction of clotting factors. increase in Vitamin K
27
Q

thrombosis

A

thrombotic disease: overproduction of clots

- plasma breaks down thrombosis

28
Q

fibrinolysis

A

lysis of blood clots

  • fibrinolytic system
  • plasminogen and plasmin - cuts plasma strands apart and left with fibrinodegredation products (indicator of clot breakdown, thombitic disease)
  • fibrin degradation products - D-dimers: measure of thrombosis
29
Q

cytosis

A
  • increased cell count, pathologic
  • erythrocytosis (polycythemia)
  • leukocytosis - infection
  • thrombocytosis - platelets, increased coagulation
30
Q

cytopenia (penia)

A
  • decreased cell count
  • erythrocytopenia - decreased RBCs, anemia
  • leukocytopenia - decreaed WBCs, immuno compromised
  • thrombocytopenia - decreased platelets, hemmhoraging, bleeding out
31
Q

anemia

A

physiolgic - reducted O2 carrying capability

  • classic symptoms: fatigue, weakness, dyspnea, pallor
  • low RBC function
  • Low RBC count
  • Cytic = size - macrocytic, microcytic, normocytic (good size)
  • Chromic = hemoglobin content - normochromic and hypochromic. no hyper chromic
32
Q

anisocytosis

A

red cells are present in various sizes

33
Q

poikilocytosis

A

red cells are preset in various shapes

34
Q

koilonychia

A

spooned nails

- result of hypo chromic anemia

35
Q

macrocytic-normochromic anemias

A
  • megaloblastic anemias
  • too big but normal amounts of hemoglobin
  • b12 and folate deficiency
  • affects RBC lifespan
  • defective DNA synthesis
36
Q

pernicious anemia

A
  • results in B12 deficiency (macrocytic normochomic)
  • lack of intrinsic factor from gastric parietal cells (required for b12 absorption, produced in stomach and absorbed in small intestine)
  • causes: can’t produce B12 or don’t eat enough
  • treatment: IM shots because if eaten the stomach can use it anyways or HIGH doses of oral B12
  • manifestations: neurologic, nerve demyelination, loss of appetite, abdominal pain, beefy red tongue, icterus, splenic enlargement
37
Q

folate deficiency anemia

A
  • dietary deficiency (macrocytic normochormic anemia)
  • no neuro manifestations
  • not dependent on any other factor
  • absorption of folate occurs in the small intestine
  • treatemnt = daily oral administration of folate
38
Q

microcytic-hypochromic anemias

A
  • small and not enough hemoglobin
  • red cells that are abnormally small and contain reduced amounts of hemoglobin
  • related to: disorders of iron metabolism, porphyrin and heme synthesis, global synthesis
39
Q

iron-deficiency anemia

A
  • most common anemia (microcytic-hypochromic)
  • nutritional iron deficiency
  • metabolic or functional deficiency
  • progression of iron deficiency causes: brittle, thin, coarsely ridge and spoon shaped nails, red/sore/painful tongue strawberry tongue
40
Q

sideroblastic anemia

A
  • bad mitochondrial functioning decreases hemoglobin
  • ineffective iron uptake and resulting in dysfunctional hemoglobin synthesis
  • diagnostic: ringed sideroblasts in bone marrow (erythroblasts that contain iron granules that have not been synthesized into hemoglobin)
41
Q

thalassemia

A
  • autosomal recessive trait, inherited anemia
  • genetic disorder that produces malformed hemoglobin chains
  • produce less hemoglobin and have low number of RBCs
  • mediterranea decent
  • everyone is a carrier but 25% actually show it
42
Q

normocytic-normochromic anemias

A
  • “right size, right amount just not enough of them”

- red cells that are relatively normal in size and hemoglobin content but insufficient in NUMBER

43
Q

aplastic anemia

A

low count of RBCs, either pancytopenia (all blood cells are low) or pure red cell aplasia (not making enough RBCs in bone marrow)
- bone marrow issue - radiation, chemo, leukemia

44
Q

posthemmorhagic anemia

A
  • acute blood loss
  • ## internal hemmohorage
45
Q

hemolytic anemia

A

overdestroyed RBCs

  • spleen or liver issue
  • accelerated desturction of red blood cells
  • apenomegaly = mono
  • autoimmune hemolytic anemias - pallor, increased bilirubin in blood, jaundice
46
Q

sickle cell anemia

A
  • autosomal recessive disorder that distorts hemoglobin proteins, genetic
  • decrease o2 carrying, get stuck in places
  • sickle during times of hypoxia
47
Q

anemia of chronic inflammation

A
  • mild to moderate anemia seen in: AIDS, RA, lupus, hepatitis, renal failure, malignancies
48
Q

polycythemia

A

overproduction of RBCs

  • relative polycythemia: result of dehydration, low blood volume increases hematology reading but really there is less of everything
  • absolute polycythemia - true overproduction of RBCs. abnormality of stem cells in bone marrow (polythemia vera) or increase in erythropoietin in response to hypoxia or inappropriate response to erythropoietin- secreting tumors
  • treatment: blood donation
49
Q

leukocytosis

A

too many WBCs

- normal physiologic response to stressors (infection)

50
Q

leukopenia

A

not normal and not beneficial

bone marrow issue, treatment and drugs cause immunosupression

51
Q

infectious mononucleosis

A 
infection of B cells by EBV
- acute, self-limiting infection of B cells transmitted by saliva through personal contact
- spleen enlarges
- epstein barr virus
-
52
Q

leukemia

A

cancers of excessive accumulation of leukemic cells in marrow

  • T, B and NK cells are precursors
  • acute leukemia: presence of undifferentiated or immature cells, blast cells
  • chronic leukemia: predominant cell is mature and does not function normally, tumor cells
53
Q

acute lympocytic leukemia ALL

A

most common in children

54
Q

chronic myelogenous leukemia CML

A

philadelphia chromosome

55
Q

chronic lymphocytic leukemia CLL

A

most common in adults

56
Q

Lymphadenopathy

A

swelling, inflammation of lymph node

57
Q

lymphoma

A

cancer of lymph system

  • hodkin - reed sternberg cells
  • nonhodkin - c neoplasms, t and nk cell neoplasms
58
Q

burkitt’s lymphoma

A

3rd word
arises from EBV or HIV
lesions of submandibular lymph nodes

59
Q

albumin

A

largest protein molecule in blood, oncotic pressure, carrier

60
Q

hypocalcemia

A

hypoabuminemia is most common cause. liver disease or failure

61
Q

thrombocytopenia

A

thrombocytopenia: platelet count < 150000
Thrombocythemia: platelet count > 400000

62
Q

alterations of coagulation

A
  • von Hillebrand factor deficiency
  • vitamin k deficient - vit k increase coagulation
  • liver disease: all plasma proteins are made in liver
  • hemophilia A: deficiency in factor VII
  • hemophelia B: deficiency in factor IX Christmas disease
63
Q

disseminated intravascular coagulation DIC

A

death is coming

  • highly fatal
  • clotting and hemorrhage simultanously occur and end up bleeding out

Pathophysiology (13 decks)

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