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Patho > Hematology (exam 4) > Flashcards

Hematology (exam 4) Flashcards

1
Q

What are the chief functions of blood?

A

Delivery of substances needed for cellular metabolism
Removal of wastes
Defense against microorganisms and injury
Maintenance of acid-base balance (buffer system= bicarb_

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2
Q

What makes up the composition of blood?

How much of the blood does each make up?

A 
Plasma (~55%)
Formed elements (Cells= RBC, WBC, platelets, ~45%)
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3
Q

What makes up the blood plasma?

How much of the blood plasma does each make up?

A

Water (~90%)

Solutes (organic and inorganic/ proteins and electrolytes, ~10%)

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4
Q

What are the plasma proteins?
What do they do?
Which is the most abundant?
Where are they made?

A

Albumin: most abundant, carriers of calcium, control the plasma oncotic pressure (pull fluid into capillaries), ~58%
Globulins: carrier proteins and immunoglobins (antibodies), ~38%
Clotting factors: mainly fibrinogen, ~4%
All made in the liver except the immunoglobins

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5
Q

What are the formed elements (cells)?

Which is the most abundant?

A

Erythrocytes: red blood cells, most abundant
Leukocytes: white blood cells, least abundant
Thrombocytes: platelets, middle amount

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6
Q

What are erythrocytes?
What do they do?
What characteristics do they have?
How long do they live?

A

Red blood cells, floating packets of hemoglobin
Most abundant cell in the body
Biconcavity and reversible deformity (moldable, high surface area)
120 day life cycle

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7
Q

What are leukocytes?
What do they do?
What types are there?

A

White blood cells
Defend the body against infection and remove debris
Granulocytes (basophils, eosinophils, neutrophils)
Agranulocytes (T & B cells, natural killers, monos/ macros

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8
Q

What do basophils do?

A

Induce inflammation= histamine
Basophils in blood
Mast cells in tissues

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9
Q

What do eosinophils do?

A

Regulate inflammation= histaminase

Immmune fighting in parasitic infections

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10
Q

What do neutrophils do?

A

1st responders

Phagocytes in early inflammation

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11
Q

What do monos/ macros do?

A

Make up the mononuclear phagocyte system (MPS)

Ingest and digest (destroy) microorganisms and foreign material

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12
Q

What are the lymphocytes?

A

T & B cells

Natural killer cells

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13
Q

What characteristics do T & B cells have?

A

Specific

Memory

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14
Q

What do natural killer cells attack?

A

Viral and cancer cells

non-specific

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15
Q

What are thrombocytes?
What is their shape?
What do they do?
What regulates them?

A

Platelets
Disk-shaped cytoplasmic fragments
Essential for blood coagulation and control of bleeding
Regulated by thrombopoietin (TPO): released by liver, stimulate platelet production after blood loss, trauma

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16
Q

What is the spleen?

What does the spleen do?

A

Largest secondary lymphoid organ
Filters the blood
Masses of lymphoid tissue containing macros, T & B cells
Phagocytosis of old, damage, dead blood cells
Blood storage

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17
Q

What are lymph nodes?
What systems are they a part of?
What do they do?
How many vessels in? out? why?

A

Lymphoid organ
Part of the immune and hematologic systems
Facilitates maturation of lymphocytes
Transports lymphatic fluid back into circulation
Cleanses the lymphatic fluid of microbes and foreign particles
Multiple vessels in, 1-2 out to ensure filtration

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18
Q

What is the MPS?
What makes it up?
Where does it work?

A

Mononuclear Phagocyte System
Mons/ macros
Ingest and destroy microbes and foreign material
Mostly the liver and spleen

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19
Q

What is hematopoiesis?
How many stages are there?
What are the types?

A

The process of blood cell production in the bone marrow (myeloid tissue), red produce blood cells, yellow= fat
2 stages: mitosis, maturation and differentiation
Erythropoiesis, Leukopoeisis, Thrombopoeisis

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20
Q

What is erythropoiesis?
What is the stimuli for it?
How does it work?

A

Making red blood cells (floating packets of hemoglobin)
Stimulated by hypoxia which stimulates EPO
Erythroblasts have a nuclei and go through steps that gradually increase the amount of hemoglobin and decrease the nucleus size to form erythrocytes
Erythropoietin (EPO) is produced and secreted by the liver to stimulate maturation of RBCs

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21
Q

Where is erythropoietin produced?

A

Peritubular cells of the kidney

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22
Q

What is hemoglobin?

What are its subunits?

A

Oxygen-carrying protein of the erythrocyte

2 alpha, 2 beta (protein subunits) containing an iron heme which binds to oxygen, causing red color

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23
Q

What are the nutritional requirements for hemoglobin?

A

Proteins/ amino acids
Vitamins: B12 and folic acid for the lifespan of the RBC
Iron: to build heme, carry oxygen
Folate (folic acid)

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24
Q

What is the destruction of erythrocytes called?
What destroys them?
Where are they destroyed
How are they destroyed?

A

Senescent
Macros of the MPS destroy them
Destroyed primarily in spleen, liver if spleen doesn’t work
Globins are broken down to amino acids
Porphyrins are broken down to bilirubin which is secreted as bile or the yellow pigment in urine

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25
Q

What is leukopoeisis?
What do the cells arise from?
Where does maturation occur?

A

Producing white blood cells (leukocytes)
Arise from stem cells in the bone marrow
Granulocytes (basos, eos, neutros) mature in bone marrow
Agranulocytes (T & B cells) must exit blood and be activated to mature
Agranulocytes (monos) are activated when they leave the blood to macros

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26
Q

What is thrombopoeisis?
How does it work?
What regulates levels?
What is the lifespan?

A

Producing platelets
Endomitosis is the process where a megakaryocyte undergoes nuclear phase of cell division but the cell does not divide
DNA continues doubling, expanding the cell
Cell explodes into cytoplasmic fragments (platelets)
Maintained by thrombopoietin (TPO)
Lifespan is 10 days

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27
Q

What is hemostasis?

What does it require?

A

To arrest or stop bleeding

Requires: platelets, clotting factors, blood flow, endothelial cells, fibrinolysis (break apart and dissolve a clot

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28
Q

What are the steps of hemostasis?

A

Vascular spasm/ vasoconstriction: spasms in response to injury, induce vasoconstriction
Platelet plug formation: expose colagen so steps start= activation, adhesion, activation, aggregation, secretion
Coagulation/ formation of the fibrin clot: classical pathway of coagulation

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29
Q

What is the vascular spasm/ vasoconstriction phase of hemostasis?

A

1st step
Spasms in response to injury, induce vasoconstriction
Cause endothelial damage and colagen exposure

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30
Q

What is the platelet plug formation phase of hemostasis

A

expose colagen so:
Activation: due to calcium
Adhesion: of platelets due to the von Willebrand factor (vWF)
Activation: due to calcium, chemotaxis for more platelets
Aggregation: of platelets to form a temporary clot
Secretion: of calcium, histamine, seratonin, epinephrine, factors that increase or quicken coagulation

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31
Q

What are the 4 most important players in the Classical Pathway of Coagulation?

A

Prothrombin
Thrombin
Fibrinogen
Fibrin

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32
Q

What is the Classical Pathway of Coagulation

A

Xa
Prothrombin——> Thrombin
Fibrinogen—————-> Fibrin
(the thing above arrow induces the next thing)

33
Q

What is the extrinsic pathway of the classical pathway of coagulation?
What stimulates is?

A

Activated when tissue factor (TF) is released by damaged endothelial cells
From trauma/ damage to vessel from outside
Can stimulate the intrinsic pathway and usually does
TF
VII——->VIIa
X——->Xa
Prothrombin——-> Thrombin
Fibrinogen—————> Fibrin
(what is over the arrow is induces the next thing)

34
Q

What is the intrinsic pathway of the classical pathway of coagulation?
What stimulates it?

A

Activated when factor XII contacts subendothelial substances (collagen) ecposed by vascular injury
Damage from inside (inflammation, HTN, athero)
exposed collagen
XII—————————–>XIIa
XI——->XIa
IX—–>IXa
VIII——->VIIIa
X——–>Xa
Prothrombin—->Thrombin
Fibrinogen———-> Fibrin
(what is above the arrow induces the next thing)

35
Q

What is clot retraction?

A

Fibrin strands shorten and become denser to pull wounds/ tissue together to facillitate repair

36
Q

What are the causes of thrombosis? Virchow’s Triad?

A

Changes in blood vessel wall (endothelial damage)
Changes in blood flow (usually decrease or blockage)
Changes in blood composition (increase viscosity, dehydration–> blood thicker, overproduction

37
Q

What is fibrinolysis?
What activates it?
What are the end products?

A

Lysis of blood clots
Plasminogen and plasmin start actively degrading a clot
Products are D-dimers, little snippets, leftover waste

38
Q

What does -cytosis mean?

Pathologies?

A

Increase cell count
Erythrocytosis (polychthemia): increase RBC count
Leukocytosis: increase WBC count
Thrombocytosis: increase platelet count, could lead to hypercoaguability

39
Q

What does -cytopenia mean?

Pathologies?

A

Decrease cell count
Erythrocytopenia: decrease RBC count, anemia
Leukocytopenia: decrease WBC count, pathologic
Thrombocytopenia: decrease platelets, risk of hemorrhaging and bleeding out

40
Q

What is anemia?

What is used to classify anemias?

A

Low red blood cell count or functioning
size= cytic (macrocytic, normocytic, microcytic)
hemoglobin content= chromic (normochromic, hypochromic)

41
Q

What are the physiologic manifestations of anemia?

Symptoms of anemias?

A

Reduced oxygen-carrying capacity, leads to hypoxia

Fatigue, weakness, dyspnea, pallor

42
Q

What is koilonychia?

A

Spoon shape of nails
Bend of nail beds
Hypochromic anemias typically
Not enough oxygen causes it

43
Q

What Macrocytic- Normochromic anemias?

What are the types?

A 
Large size red blood cells, normal hemoglobin content
Megablastic anemia (pernicious anemias and folate deficiency anemias)
44
Q

What are pernicious anemias?
What is the cause?
How is it treated?
Distinct symptoms?

A

Macrocytic-Normochromic anemia
Caused by a lack of intrinsic factor, which is produced in the stomach and binds to B12 to be absorbed by the liver
Results in a deficiency in B12
Treated with B12 orally (if not intrinsic factor problem), B12 injections
Decreased neurologic functioning

45
Q

What are the folate deficiency anemia?
What is the cause?
How is it treated?

A

Macrocytic-Normochromic anemia
Caused from a folate deficiency in the diet
Treated with a daily dose of folate orally

46
Q

What are the microcytic-hypochromic anermias?

What are the types?

A

Small red blood cells, reduced hemoglobin content
Iron deficiency anemia
Sideroblastic anemia
Thalassemia

47
Q

What is an iron deficiency anemia?
What is the cause?
Distinct symptoms?

A 
Microcytic-hypochromic anemia
Most common type of anemia worldwide
Nutritional iron deficiency 
Spoon shaped nails (koilonychia)
Red, sore, painful tongue (strawberry tongue)
48
Q

What is sideroblastic anemia?

A

Microcytic-hypochromic anemia

Altered mitochondrial metabolism causing bad iron uptake, therfore dysfunctional hemoglobin synthesis

49
Q

What is thalassemia?

A

Microcytic-hypochromic anemia
Inherited anemia, genetic disorder
Autosomal recessive trait
Originated in the Mediterranean region

50
Q

What are normocytic-normochromic anemias?

What are the types?

A 
Normal size and hemoglobin content, not enough cells or not functioning right though
Aplastic anemia
Posthemorrhagic anemia
Hemolytic anemia
Sickle cell anemia
Anemia of chronic inflammation
51
Q

What is aplastic anemia?

Types?

A

Normocytic-normochromic anemia
Not making enough RBCs
Pancytopenia: all blood cells are decreased in number, bone marrow issue
Pure red cell aplasia: not enough RBCs

52
Q

What is posthemorrhagic anemia?

A

Normocytic-normochromic anemia

Caused by acute blood loss

53
Q

What is hemolytic anemia?

Types:

A

Normocytic-normochromic anemia
Accelerated destruction of RBCs (spleen or liver dysfunction)
Breaking open
Autoimmune hemolytic anemias: increase bilirubin in blood= JAUNDICE

54
Q

What is sickle cell anemia?

A 
Normocytic-normochromic anemia
Autosomal recessive disorder
RBC has a "sickle" shape
Most often in times of ypoxia
Bad gas exchange, sickle cells get stuck
55
Q

What is anemia of chronic inflammation?

A

Normocytic-normochromic anemia

Mild to moderate anemia seen in: AIDS, RA, lupus erythematosus, hepatitis, renal failure, malignancies

56
Q

What is polycythemia?

Types?

A

To many red blood cells
Relative polycythemia
Absolute polycythemia

57
Q

What is relative polycythemia? Causes?

A

Result of dehydration

Fluid loss results in relative increases of RBC counts

58
Q

What is absolute polycythemia?

Causes?

A

Abnormality of stem cells in the bone marrow (increase in RBC production), Polycythemia vera (PV)
Increase in EPO in reponse to chronic hypoxia or inappropriate response to EPO-secreting tumores, can lead to increased coagulation
Treatment= blood donation

59
Q

What is leukocytosis?

Pathologic or Physiologic?

A

To many WBCs

Physiologic: normal protective response to stressors

60
Q

What is leukopenia?

Pathologic or Physiologic?

A

Low WBC count
Not normal, not beneficial
Pathologic: predisposes a patient to infections
Immunosuppressed patients

61
Q

What is infectious mononucleosis?

A

Infection of B lymphocytes
Transmitted by saliva
Commonly cause by Epstein-Barr virus (EBV), ~85% of cases
Symptom= speen enlargement (spleenomegaly)

62
Q

What is the most common anemia?

A

Iron deficiency anemia

63
Q

What is leukemia?
Types?
Precursors?

A

Cancers of excessive leukemic cells in the marrow
Types: Acute leukemia (undifferentiated or immature cells), Chronic leukemia (cells is mature, don’t function normally
Precursors: Lymphocytic (lymphoblastic)- precursor lymphocytes (T & B cells, NK cells), myelogenous (bone marrow)- precursor RBCs, platelets, granulocytes

64
Q

What are the 4 types of leukemias?

A

Acute lymphocytic leukemia (ALL): mostly kids
Acute myelogenous leukemia (AML)
Chronic myelogenous leukemia (CML): philadelphia chromosome translocation issue during mitosis or miosis
Chronic lymphocytic leukemia (CLL): mostly adults

65
Q

What is lymphadenopathy?
Types?
Indicative of?

A

Enlarged lymph nodes
Local lymphadenopathy: drainage of an inflammatory lesion located near the enlarged lymph nodes
Chronic lymphadenopathy: occurs in the presence of malignant or nonmalignant disease
Prolonged lymphadenopathy indicative of lymphomas

66
Q

What are lymphomas?

Types? Key characteristics?

A

Malignant transformation of lymphocytes (T & B cells into cancer cells)
Hodgkin lymphoma: Reed-Sternber (RS) cells (1 nuclei, owl like face)
Non-Hodgkin lymphomas: B-cell neoplasms, T & NK cell neoplasms

67
Q

What is Burkitt’s lymphomas?
Arise from?
Most common where?

A

Lymphomas that arise from EBV or HIV
Lesions of submandibular lymph nodes
South Africa, 3rd world areas

68
Q

What is the largest protein molecule in the blood?

A

Albumin

69
Q

What is the most common cause of hypocalcemia?

A

Hypoalbuminemia

From liver disease or failure

70
Q

What is thrombocytopenia?

A

Low platelet count

71
Q

What is thrombocythemia?

A

High platelet count

Increase clots

72
Q

What does a von Willebrand factor deficiency do?

A

Platelets can’t stick together

Decrease coagulation

73
Q

What does a vitamin K deficiency do?

A

Decrease coagulation

74
Q

What affect does liver disease have on coagulation?

A

Liver makes ALL plasma proteins so wide range of effects

75
Q

What is PTT?

What pathway does it affect?

A

Partial Thromboplastin Time

Measures Intrinsic pathway

76
Q

What is PT?

What pathway does it affect?

A

Prothrombin time

Measures Extrinsic pathway

77
Q

What is hemophilia A?

A

Intrinsic pathway issue
Deficiency in clotting factor VIII
Males affected more, genetic disorder (recessive X linked)

78
Q

What is hemophilia B?

A

Intrinsic pathway issue
Deficiency in clotting factor IX
Called Christmas disease
Males more affected, genetic disorder (recessive X linked)

79
Q

What is disseminated intravascular coagulation (DIC)?

A

Death is coming
Clotting and hemorrhage simultaneously
Most often from sepsis or trauma
Hemorrhage because you have used all your coagulating factors

Patho (17 decks)

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