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Clinical Medicine > Hematology > Flashcards

Hematology Flashcards

1
Q

What is the composition of plasma?

A

Water (92%)
Nutrients such as glucose, proteins, fats, and electrolytes
Contains albumin and other transport proteins, immunoglobulins, clotting factors, and enzymes
Contains small amounts of dissolved CO2 and oxygen (not bound to hemoglobin)

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2
Q

What is plasma serum?

A

Plasma minus the clotting factors; specimen is not antio-coagulated

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3
Q

What are acute phase reactants?

A

defined as proteins that change their serum concentration by >25% in response to inflammatory cytokines (IL-1, IL-6, TNFα)

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4
Q

What system are the acute phase reactants a part of?

A

Innate immune system

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5
Q

What can APRs play a role in mediating?

A

Fever, leukocytosis, thrombocytosis, increased cortisol, decreased thyroxine, and decreased serum ion

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6
Q

Positive APRs

A 
C reactive protein
Fibrinogen (ESR)
complement
globulin
D-dimer
prothrombin
factor VIII
vW factor
ferritin		
hepcidin
ceruloplasmin
haptoglobin
alpha-1 antitrypsin
platelets
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7
Q

Negative APRs

A 
albumin                
pre-albumin         
transferrin
antithrombin
transcortin 
retinol-binding protein
transthyretin
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8
Q

What lab test is used as a marker for inflammation in the body?

A

ESR

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9
Q

White blood cells include?

A

Granulocytes, Monocytes, and Lymphocytes

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10
Q

What are the three granulocytes?

A

Neutrophils, eosinophils, and basophils

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11
Q

What are platelets derived from?

A

Megakaryocytes

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12
Q

What are band cells?

A

Immediate precursor to the mature granuloctyes

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13
Q

What is the main component of RBCs?

A

Hemoglobin

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14
Q

4 pyrrole rings equals what?

A

1 protoporphyrin complex

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15
Q

1 protoporphyrin complex + 1 atom of reduced iron equals what?

A

1 heme unit

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16
Q

4 heme units + 4 globulin polypeptides (1 heme unit per globulin polypeptide) equal what?

A

1 molecule of hemoglobin

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17
Q

After separating from the iron ion, the cleaved protoporphyrin complex gives rise to what?

A

bilirubin

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18
Q

What is a CBC?

A

Complete Blood Count- automated reading in the lab that gives numbers and percentages of cells, quantifies RBC size, shape and color among other indices

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19
Q

What is the most abundant blood cell type?

A

RBC

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20
Q

Where are microcytic cells seen?

A

Iron deficiency and thalassemia

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21
Q

Macrocytic cells are seen when?

A 
BAD Hemoglobin Level
B12 and folic acid deficiency
Alcoholism
Down syndrome
Hypothyroidism
Liver disease
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22
Q

What is RDW?

A

Red cell distribution of width. If the number is high, it suggests a divergent population of red cells of different sizes

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23
Q

What is anisocytosis?

A

RBCs of different sizes

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24
Q

If you have pure macrocytosis what will your MVC and RDW values be?

A

Elevated MVC, Normal RDW

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25
Q

Iron deficiency anemia, what will your MVC and RDW values be?

A

Low MVC, Normal RDW

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26
Q

Mixed macroctyosis and microctyosis, what will your MVC and RDW values be?

A

Normal MCV, Elevated RDW

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27
Q

Hemolytic anemia with reticulocytes, what will your MVC and RDW values be?

A

Elevated MCV, Elevated RDW

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28
Q

Ovalocytes and elliptocytes characterize some inherited red cell abnormalities, what disease are these seen in?

A

hereditary elliptocytosis

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29
Q

Spheroctyes are seen in what diseases?

A

hereditary spherocytosis and autoimmune hemolytic anemia.

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30
Q

Schistoctyes are found when?

A

point to destruction within the vascular spaces. these are seen in hemolytic anemia, thrombotic thrombocytopenic purpura (TTP), disseminated intravascular coagulation (DIC), or a prosthetic heart valve.

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31
Q

Tear drop cells are found where?

A

in extramedullary hematopoiesis (EMH)

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32
Q

extramedullary hematopoiesis (EMH) comes into play when?

A

bone marrow failure.

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33
Q

EMH occurs in what conditions?

A

hemoglobinopathies, myeloproliferative disorders, or bone marrow infiltration by tumors

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34
Q

EMH occurs in what parts of the body?

A

spleen, liver, and occasionally the lymph nodes. less common organs; pleura, lungs, gastrointestinal tract, breast, skin, kidneys, and adrenal glands

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35
Q

EMH is part of what system of the body?

A

Reticular endothelial system

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36
Q

Macrocytic anemia will be shown in patients with what kind of deficiency?

A

Vitamin B12

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37
Q

Schistocytes are seen in what time of anemia?

A

Microangipathic hemolytic anemia

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38
Q

In hereditary spheroctyosis, there is a lack of what protein?

A

spectrin

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39
Q

What kind of protein is spectrin?

A

a key RBC cytoskeletal membrane protein

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40
Q

What test can be given in the lab to prove hereditary spherocytosis?

A

increased osmotic fragility

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41
Q

What do rouleaux RBCs look like?

A

stacked together long chains

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42
Q

When are rouleaux seen?

A

with increased serum proteins, fibrinogen and globulin. this is the mechanism for the erthrocyte sedimentation rate

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43
Q

what is the erthrocyte sedimentation rate for?

A

increases specifically with inflammation and increased “Acute phase” serum proteins

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44
Q

what are reticulocytes?

A

normal, immature form of the RBC. they develop and mature in the bone marrow and then circulate for about a day in the blood stream before fully maturing into RBCS

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45
Q

instead of a cell nucleus, what do reticulocytes have?

A

residual ribosomal RNA in their cytoplasm

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46
Q

what are howell jolly bodies?

A

rbc inclusion. inclusions of nuclear chromatin (DNA) remnants

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47
Q

what is basophillic stippling?

A

small dots at the periphery of red cells. the dots represent ribosomes

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48
Q

in what conditions is basophillic stippling seen?

A

lead and heavy metal poisoning, thalassemias, and alcohol abuse

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49
Q

what are heinz bodies and when are they seen?

A

denatured hemoglobin seen in G6PD deficiency

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50
Q

when are nucleated RBC seen?

A

bone marrow stress

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51
Q

what is one white blood cell inclusion?

A

dohle bodies

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52
Q

what are dohle bodies?

A

light, blue-gray oval, basophillic inclusions located in the peripheral cytoplasm of neutrophils

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53
Q

what are dohle bodies remnants of?

A

rough endoplasmic reticulum

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54
Q

when you see a high amount of poikilocytes, anisocytes and rbc inclusions, what does this usually mean?

A

spleen is not present

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55
Q

how many lobes in a neutrophil?

A

3-4 lobes

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56
Q

how many lobes in a eosinophil?

A

bilobed

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57
Q

how many lobes in a basophil?

A

3 lobed but difficult to see

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58
Q

what is the most abundant type of granulocyte?

A

neutrophils

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59
Q

more than 4 lobes of a neutrophil means they are what?

A

hyper segmented

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60
Q

what is the least plentiful blood cell type

A

leukocytes (WBCs)

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61
Q

how do neutrophils defend the body and when?

A

defend by phagoctyosis and enzymatic lysis. during infection

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62
Q

when do eisonophils defend the body and how?

A

react in allergic reactions and parasitic infection. defend by phagoctyosis and enzymatic lysis

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63
Q

what do basophils produce?

A

histamine, heparin, and IL-4

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64
Q

how do basophils defend?

A

release of chemical mediators

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65
Q

what do monocytes become?

A

macrophages

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66
Q

what are lymphocytes responsible for?

A

antibody production, cell mediated immunity, innate immunity

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67
Q

when are immature neutrophils seen?

A

during bone marrow stress. more neutrophils are produced as seen with infection, pregnancy, recovery from bone marrow suppression, and or hemotolgic malignancies

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68
Q

how many lobes in a band cell

A

uni-lobar

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69
Q

5 or more lobes of a neutrophil?

A

hyper segmented

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70
Q

when are hypersegmented neutrophils seen?

A

in megaloblastic processes (b12, folate deficiency)

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71
Q

a very high WBC count (>50,000) that is not leukemia, is what?

A

leukomoid reaction

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72
Q

when do you see an increased number of eosinophils?

A 
NAACP.
N- neoplastic
A- asthma
A- allergic reactions
C- collagen vascular disease (rheumatologic)
P- parasites
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73
Q

what is basophilia?

A

increase of basophils in a persons blood

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74
Q

when is basophillia seen?

A

basophilic leukocytosis; associated with leukemia
(chronic myelongenous leukemia)
hypersensitivty
inflammatory reactions
hypothyroidism
infects with; TB, some viruses, Helminthic (parasitic) infections

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75
Q

what do B cells do

A

scan the intracellular environment for foreign invaders
directly kill virally or bacterially infected cells
naturally eradicate cancer cells
activate and help other immune cells including other lymphocytes that either chaperone, ingest, or make antibodies against foreign invaders
can remember a foreign invader they encountered decades ago

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76
Q

natural killer cells

A

cells kill tumor cells and virally infected cells. scan the surface. allows them to hunt down and destroy cells that are infected or that have become cancerous.

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77
Q

atypical lymphocytes

A

larger than normal. large nucleoli. more cytoplasm.

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78
Q

when are atypical lymphocytes seen

A

infectious mononucleosis or leukemia

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79
Q

monocytes

A

largest cell in the blood. produced in the bone marrow and stored in the spleen.

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80
Q

what do monocytes become when they travel to the site of infection and enter tissues?

A

macrophages

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81
Q

what do monocytes do?

A

perform phagocytosis, antigen presentation, and cytokine production to kill microbes

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82
Q

what are platelets?

A

anuclear cells derived from megakaryocytes

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83
Q

second most plentiful type of blood cell

A

platelets

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84
Q

what type of substances do platelets release for wound healing?

A

vasoactive compounds (vasoconstrictors) and platelet chemotactic agents (cytokines)

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85
Q

antigens a and b are what kind of antigens

A

carbohydrate

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86
Q

2nd most important consideration in transfusion medicine

A

D (Rh) antigen

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87
Q

when should RhoGAM be given:

A
  • after delivery of an Rh positive baby
  • routine prevention of Ph immunization at 26 to 28 weeks
  • maternal or fetal bleeding during pregnancy from certain conditions
  • actual or threatened pregnancy loss at any stage
  • ectopic pregnancy
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88
Q

blood components

A

PRBCs, platelets, and fresh-frozen plasma

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89
Q

risks of transfusion:

A
  • transfusion reaction
  • GVDG (graph vs. host disease: WBCs and antibodies in the donors blood attack the recipient)
  • fluid overload (give furosemide)
  • infection (Hep B, C, HIV, etc.)
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90
Q

Immature cell types

A

bone marrow problem

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91
Q

smudge cells

A

CLL. WBC in the process of death = apoptosis

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92
Q

what do blast cells usually show?

A

great physiological stress or tumor cells

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93
Q

when are smudge cells indicated?

A

in the presence of lymphocytic leukemia

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94
Q

definition of a blast cell

A

very immature cells with larger nuceli that contain nucleoli. indicative of acute lymphocytic leukemia

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95
Q

Low hb/hct indicative of:

A

anemia

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96
Q

anemia: Red cell loss

A 
GI bleeding
menorrhagia
excess phlebotomy
blood donation
(high retic count)
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97
Q

anemia: inadequate production

A 
(low retic count)
absence of stimulus to produce: 
- low erythropoietin level in CVD
- hypothyroidism
- androgen deficiency
lack of/abnormal raw materials:
- folic acid
- vitamin b12
- Fe
- hemoglobinopathy
intrinsic bone marrow problem:
- myelofibrosis
- malignancy
- aplastic anemia
- poisons, drugs
- radiation
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98
Q

normal lifespan of RBC

A

110-120 days (4 months)

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99
Q

symptoms of anemia:

A

dyspnea at rest, fatigue, lethargy, confusion, CHF, angina, MI, and arrhythmia, and depend on both MAGNITUDE and the RATE OF DEVELOPMENT

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100
Q

in acute bleeding, what is the main problem?

A

hypovolemia

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101
Q

normal adult blood volume

A

~5L

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102
Q

blood volume according to age:

A

adult female: 65mL/kg
adult male: 70mL/kg
children: 80mL/kg
neonates: 100mL/kg

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103
Q

when does shock happen and what are the symptoms?

A

when supply cannot meet demand. symptoms; confusion, dyspnea, diaphoresis, frank hypotension leading to permanent organ damage and possibly death

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104
Q

CBC:

A

H/H and red cell indices: MCV, MCH, MCHC, and RDW

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105
Q

reticulocyte count:

A

should be high if marrow is intact and responsive; if low look for problems in the marrow that impact cell production

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106
Q

WBC:

A

If low, consider bone marrow suppression; if high, consider infection, chronic inflammation or malignancy. Check for hypersegmented PMN’s whenever RBCs are macrocytic and reduced in number.

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107
Q

platelets

A
  • If low, consider bone marrow suppression, hypersplenism, alcoholism, autoimmune states;
  • If high, consider iron deficiency, inflammation, infection, malignancy, stress
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108
Q

microcytic anemia:

A

MCV <80fL
iron deficiency, chronic blood loss, alpha or beta thalassemia minor, and anemia of chronic disease/inflammation; lead poisoning

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109
Q

macrocytic anemia

A

MCV >100fL
B12, folate deficiency, alcohol abuse, Down syndrome, hypothyroidism, liver disease; also drugs (hydroxyurea, AZT), myelodysplasia, leukemia, reticulocytosis

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110
Q

Normocytic anemia

A

Acute blood loss, early iron deficiency, anemia of chronic disease, bone marrow suppression, chronic renal insufficiency, hypothyroidism, aplastic anemia, sickle cell anemia

111
Q

iron deficiency anemia causes what most commonly

A

microcytic-hypochromic anemia

112
Q

usual suspects of iron deficiency anemia:

A

NSAID use, gastric ulcers, heavy menses, colon cancers, blood donation; low dietary intake in pregnant women and children

113
Q

an enzyme ______, on the brush border of the ________ and ________ reduces iron from ferric to ferrous making it more absorbable

A
  • ferric reductase

- duodenum and proximal jejunum

114
Q

most of the iron in the body is found where

A

hemoglobin

115
Q

where are smaller percentages of iron found?

A

ferritin and hemosiderin

116
Q

very small amount (3 mg) is present in the transport form which is?

A

attached to transferrin

117
Q

iron is transported bound to a molecule called

A

transferrin

118
Q

what measures transferrin levels

A

total iron-binding capacity (TIBC)

119
Q

what is the main storage form of iron?

A

ferritin

120
Q

labile form of iron storage

A

ferritin

121
Q

stable form of iron storage which consists of ferritin and cell debris

A

hemosiderin

122
Q

diagnostic test for iron deficiency

A

ferritin

123
Q

indirect marker of the total amount of iron stored in the body

A

plasma ferritin- diagnostic test for iron deficiency

124
Q

are platelets an acute phase reactant

A

yes

125
Q

treatments for iron deficiency

A
  • 325 mg ferrous sulfate po tid x 6 months w/ Vit C

- Ferrous gluconate 240/324 mg might be better tolerated

126
Q

lead interferes with the biosynthesis of what?

A

heme

127
Q

desire to eat non-nutritive things

A

pica

128
Q

ingestion of lead

A

plumbophagia

129
Q

compulsive consumption of ice

A

pagophagia

130
Q

most common form of adult anemia

A

anemia of chronic disease

131
Q

what are reduced during anemia of chronic disease

A

serum ion and transferrin saturation

132
Q

Cytokines released in inflammatory and infectious disorders induce excess synthesis of what?

A

hepcidin

133
Q

what is the primary intrinsic regulator of anemia of chronic disease

A

hepcidin

134
Q

hepcidin, through the down-regulation of what it inhibits transfer of stored intracellular iron back into plasma, thereby blocking reuse of iron by the marrow

A

ferroportin, a transfer protein

135
Q

levels of transferrin in fe def.

A

elevated

136
Q

levels of TIBC in fe def

A

elevated

137
Q

levels of ferritin in fe def

A

low

138
Q

levels of transferrin in anemia of chronic illness

A

low

139
Q

levels of TIBC in anemia of chronic illness

A

low

140
Q

levels of ferritin in anemia of chronic illness

A

increased

141
Q

structural abnormalities in the globin

A

hemoglobinopathies (qualitative)

142
Q

underproduction of normal globin subunits

A

thalassemias (quantitative)

143
Q

Caused by a genetic defect that results in abnormal structure of one of the globin chains of the hemoglobin molecule

A

hemoglobintopathy

144
Q

what kind of traits are hemoglobinopathies inherited as

A

autosomal co-dominant traits

145
Q

sickle cell disease is what?

A

autosomal recessive disease that leads to hemolytic anemia

146
Q

sickle cell mutation

A

HbS

147
Q

when do sickle cell symptoms begin

A

when HbF production ends

148
Q

what creates painful crises lasting hours to days exacerbated by dehydration, acidosis, hypoxemia

A

vascular occlusions

149
Q

salmonella osteomyelitis

A

if you get some salmonella in your GI tract you may not get sick but if it ends up in your bones and you have sickle cell- you are more likely to get infected and get sick. These only happens when you auto splenectomies your spleen.

150
Q

what kind of cells will you see in a sickle cell disease smear?

A

normochromic RBC’s, nucleated RBC, sickle cells, Howell-Jolly Bodies, Retic count increased, increased bilirubin

151
Q

short term sickle cell treatment

A

pain control, IVF in acute crisis (medically lowering the hematocrit and making the blood more viscous), oxygen

152
Q

long term sickle cell treatment

A 
transfusion
red cell exchange aphaeresis
hydroxyurea (promotes HbF production)
PCN prophylaxis- prophylax with penicillin
pneumoccal vaccination
folate supplementation
avodiance of smoking
iron chelators
153
Q

thalassemias

A

hereditary microcytic aenmia; unresponsive to Fe

154
Q

Alpha-Thalassemia in what type of ancestry

A

asian

155
Q

Beta-Thalassemia in what type of ancestry

A

mediterranean

156
Q

Due to a deletion or mutation in one or more of the four alpha globin gene copies.

A

Alpha thalassemia

157
Q

microcytic, hypochromic anemia with low MCV.

A

Alpha Thalassemia Trait

158
Q

what can HbH disease cause?

A

moderate to severe anemia and splenomegaly

159
Q

Hydrops fetalis (fetal congestive heart failure) = Bart’s Anemia

A

barts anemia

160
Q

hydrops fetalis

A

congestive heart failure (fetal) swollen appearance of the patient.

161
Q

what is beta thalassemia caused by?

A

polymorphic mutations in one or both of 2 beta globin (HB ß) genes

162
Q

Beta Thalassemia Trait (Thalassemia Minor)

A

one normal gene and one with a mutation; hypochromic, microcytic; unresponsive to iron

163
Q

Beta Thalassemia Intermedia

A

two abnormal genes but still producing beta globin unit variety(ies) with some functionality; the severity of the anemia and health problems experienced depend on the mutations

164
Q

Beta Thalassemia major (Cooley’s anemia)

A

two (very) abnormal genes; no beta globin produced; no Hgb A

165
Q

when does cooleys anemia appear

A

in an infant after 3 months of age after loss of Hgb F; life threatening anemia

166
Q

atypical, abnormal nucleated erythroblasts with granules of iron accumulated in perinuclear mitochondria

A

sideroblasts

167
Q

Sideroblastic Anemia

A

The body has iron available but cannot incorporate it into hemoglobin = ineffective erythropoiesis

168
Q

causes of sideroblastic anemia

A 
B6 (pyridoxine) deficiency 
Hereditary; isoniazid 
INH use
Lead Poisoning 
Zinc Poisoning
169
Q

Mnemonic for Microcytic Anemia

A 
T- thalassemia
A- anemia of chronic disease/inflammation
I- iron deficiency
L- lead poisoning
S- sideroblastic anemia
170
Q

bound in the duodenum to intrinsic factor, which is produced by gastric parietal cells of the stomach. The complex is then absorbed in the terminal ileum (receptors that can bind to the intrinsic complex B12) and stored in the liver

A

vitamin b12

171
Q

inadequate b12 levels are due to what?

A

dietary deficiency or deficient absorption

172
Q

deficient b12 absorption is found in what?

A 
crohns disease
short bowel syndrome
cystic fibrosis
bacterial overgrowth syndrome
pernicious anemia
173
Q

type of b12 deficiency caused by lack of intrinsic factor

A

pernicious anemia

174
Q

what causes the lack of intrinsic factor

A
  • atrophic gastritis- achlorhydria: destruction of gastric parietal cells
  • anti- intrinsic factor antibodies
  • gastric bypass
  • gastrectomy
175
Q

water without chloride. your stomach doesn’t make enough stomach acid

A

Achlorhydria

176
Q

most important system to absorb B12

A

intrinsic factor

177
Q

more sensitive method of screening for B12deficiency is measurement? why?

A

serum methylmalonic acid and homocysteinem levels. because they are increased early in b12 deficiency

178
Q

what else is elevated in B12 deficiency

A

MMA and homocysteine

179
Q

what is elevated in both b12 and folate deficiency

A

homocysteine

180
Q

what are hypersegmented PMNs

A

white cell changes

181
Q

if you give both a homocysteine test and MMA and only MMA is high, what is the deficiency?

A

folic acid problem

182
Q

if you give both a homocysteine test and MMA and both are high, what is the deficiency?

A

B12 deficiency

183
Q

neurologic problems

A

b12 deficiency

184
Q

important to the formation of fetus brain

A

folic acid deficiency

185
Q

Paresthesias- numbness or tingling

A

b12 deficiency

186
Q

Big cells in the bone marrow

A

megaloblastic anemia

187
Q

Big cells that get into the blood stream

A

macrocytic

188
Q

causes of folate deficiency anemia

A

poor intake, pregnancy, ETOH, MTX

189
Q

hypersegmented PMNs

A

folate deficiency anemia

190
Q

what kind of cells can you see in folate deficiency anemia

A

howell-jolly bodies

191
Q

where are megaloblasts found?

A

RBC precursors found in the bone marrow

192
Q

where are macroctyes found?

A

in the peripheral blood stream

193
Q

megaloblastic-macrocytosis can be caused by?

A

Folate and B12 deficiency

194
Q

Intrinsic hemolytic anemia

A

hemoglobinopathies, some thalassemias, spherocytosis (osmotic fragility test), elliptocytosis, paroxysmal nocturnal hemoglobinuria, sickle cell disease; G6PD deficiency

195
Q

Extrinsic hemolytic anemia

A

autoimmune, drug induced, HUS (hemolytic uremic syndrome), DIC (disseminated intravascular coagulopathy), metallic heart valves, infection, burns, hypotonic hemodilution

196
Q

signs of hemolytic anemia

A

decreased haptoglobin

197
Q

inclusions of denatured hemoglobin in the RBC found in G6PD deficiency

A

heinz bodies

198
Q

bone marrow disorder where excessive RBC’s are produced (polycythemia rubra vera)

A

polycythemia

199
Q

due to chronic hypoxemia (COPD), living at high altitudes

A

polycythemia

200
Q

what can polycythemia lead to?

A

hyper viscosity

201
Q

Normal MMA with elevated homocysteine suggests anemia secondary to?

A

pure folate deficiency

202
Q

Low serum iron, elevated TIBC suggest?

A

iron deficiency

203
Q

control of blood loss

A

hemostasis

204
Q

first step in all wound healing

A

hemostasis

205
Q

what does hemostasis do?

A

limits blood loss by precisely regulated interactions between components of the blood vessel wall, platelets, and plasma proteins

206
Q

which natural set of anticoagulants keep hemostasis in check?

A

plasmin system and proteins C, S, and Z

207
Q

what can unregulated activation of hemostasis cause?

A

thrombosis and embolism

208
Q

what are the 3 major steps in hemostasis?

A
  1. vasoconstriction
  2. temporary blockage of break in the wall of a blood vessel by a platelet plug vis platelet adhesion
  3. formation of a fibrin clot
209
Q

what happens during vasoconstriction during hemostasis?

A

the blood vessel will automatically contract to stop blood loss. Nervous system tells muscular wall to contract in order to slow the bleeding.

210
Q

what happens during temporary blockage of a break in the wall of a blood vessel?

A

Platelets will start getting sticky and they will aggregate and adhere to one another to make a platelet plug. They don’t stay here for long but they are fast.

211
Q

what happens during formation of a fibrin clot?

A

Fibrin is a plasma protein and a final step in the activation of a clotting cascade. There are 13-14 clotting factors. Fibrin is like a fiber that criss crosses and form a mesh in every direction. First it is loose then the clot matures and the mesh tightens and it forms a solid plug.

212
Q

In the normal state, the endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule called?

A

thrombomodulin

213
Q

what does thrombomodulin do?

A

inhibits thrombin (clotting factor IIa)

214
Q

When endothelial injury occurs, the endothelial cells slow secretion of thrombomodulin and increase secretion of what?

A

von Willebrand factor

215
Q

what does von Willebrand factor initiate?

A

platelet adhesion

216
Q

Factor II

A

prothrombin

217
Q

Activated factor II

A

thrombin

218
Q

primary hemostasis

A

platelet plug

219
Q

secondary hemostasis

A

plasma coagulation system that results in fibrin mesh formation—starts within 20 sec of injury. Makes a better clot. Step 3.

220
Q

Thrombocytosis (aka thrombocythemia)

A

too many platelets. excessive clotting or bleeding.

221
Q

Thrombocytopenia

A

Not enough platelets- can only result in bleeding

222
Q

Von Willebrand’s disease

A

(defective adhesion; not really the platelets’ fault)
you have some sort of defect adhesion of the platelets but the platelets are too many or too few, its that the factor is not there or doing its job so it doesn’t make the platelets sticky like it should. The lack of or abnormality of the Von Willebrand adhesion.

223
Q

Tiny, microscopic bleeding capillaries that form spots. Enough in the skin take a lot of the surface of the skin. Can form little purple spots known as purpura. Purpura can form bigger patches known as ecchymosis- black and blue

A

Petechiae, some purpura

224
Q

bleeding time and platelet count

A

Abnormal platelet count or the bleeding test will have an abnormality. Not great tests available for platelet function but for the count we do.

225
Q

Local measures generally suffice to control bleeding

A

Putting pressure on the bleed

226
Q

Thrombocytosis

A

Platelet count above 500k/microliter. 100,000-450,000 is normal count.

227
Q

what can cause thrombocytosis/thrombocypenia?

A

Can be caused by an acute reactive process (an APR: recent surgery, bacterial infection, iron deficiency, or trauma) or a bone marrow disorder which is a malignancy known as essential thrombocythemia)- cancer on platelets or megakaryocytes

228
Q

treatment for thrombocytosis/thrombocypenia

A
  • Treat underlying cause if possible (is it an acute phase reactant?)
  • Antiplatelet medications, unless there is bleeding (next slide)
  • Platelet-pheresis might be needed. Blood is removed from the pt. platelets are removed then blood is given back to the patient.
  • hydroxyurea or anagrelide to lower platelet count in high-risk patients two drugs used to lower platelet count
229
Q

irreversibly blocks the aggregation of platelets by interfering with the production of. Thromboxane (causes vasoconstriction) (prostaglandin- involved in fever, vasomotor tone)

A

aspirin

230
Q

P2Y12 inhibitors (ADP receptor blockade)

A

block platelet aggregation

231
Q

Thrombocytopenia

A
  • decreased bone marrow production
  • increased splenic sequestration: spleen isn’t allowing them to go into circulation
  • accelerated destruction of platelets (ITP, TTP): increased destruction
232
Q

Idiopathic Thrombocytopenic Purpura (acute)

A

immune mediated ITP is mostly seen in children with sudden onset of severe thrombocytopenia following recovery from a viral illness.

233
Q

Idiopathic Thrombocytopenic Purpura (chronic)

A

mostly seen in adults. the antibodies never go away and keep attacking your platelets

234
Q

Thrombotic Thrombocytopenic Purpura (TTP)

A

Initiated by vessel wall injury initiating an exaggerated clotting cascade leading to a tetrad of thrombocytopenia, hemolysis (red cells), renal failure, and CNS signs (central nervous system problems- mild to severe) such as fluctuations in levels of consciousness, confusion, and seizures

235
Q

The only major clotting factor not made by the liver.

A

Von Willebrand Factor

236
Q

what does the von willebrand factor bind to and protect?

A

inactive factor VIII from spontaneous degradation

237
Q

what is responsible for the uncoupling of factor VIII from vWF

A

thrombin

238
Q

what makes platelets sticky?

A

Free vWF

239
Q

shearing stress

A

when the blood is rapidly flowing

240
Q

treatment for von willebrands disease?

A
  • vWF/factor VIII concentrate
  • recombinantvon Willebrandfactor (r-vWF)
  • desmopressin, which raises vWF. Given for surgery, major trauma, or other active bleeding.
241
Q

primary site of synthesis of most of the clotting factors as well as the proteins involved in the fibrinolytic (keeps coagulation factor in check) system.

A

liver

242
Q

body’s natural system
of anticoagulation that serves as a constant servo-
mechanism offsetting the coagulation cascade

A

The fibrinolytic system

243
Q

liver pro-coagulation factors?

A

vitamin K-dependent: II (prothrombin), VII, IX, X (2,7,9,10)

non-vitamin K-dependent: I (fibrinogen), V, XIII (1, 5, 13) basically all the other ones

244
Q

liver anti-coagulation factors?

A

vitamin K-dependent:
proteins C, S, Z: made by the liver that interfere with the clotting cascade (not enough Vitamin-K)
non-vitamin K-dependent:
antithrombin-III and plasminogen

245
Q

not synthesized by the liver and not vitamin K dependent

A

von willebrand factor (pro-coagulant)- vascular endothelial cells
thrombomodulin (anti-coagulant)
tPA (tissue plasminogen activator)- subendothelial tissue

246
Q

important cofactor along many points in the coagulation cascade

A

Calcium (factor IV)

247
Q

what are vitamin K dependent factors?

A

factors II, VII, IX, X, protein S, protein C, and protein Z

248
Q

what do you see in coagulation factor disorders?

A

large palpable ecchymoses and large, spreading, deep soft tissue hematomas

249
Q

what makes the fibrin clot tighten up?

A

factor XII

250
Q

Prothrombin time (PT)

A

Tests extrinsic pathway and final common pathway

251
Q

Activated Partial Thromboplastin time (aPTT)

A

Tests intrinsic pathway and final common pathway.

252
Q

Thrombin time

A

tests for quantitative (fibrinogen deficiency) or qualitative (dysfunctional fibrinogen) defect. Thrombin is added to the patient’s plasma in the lab. Time till clot formation begins is noted. Measure of how long it takes for fibrinogen to make a cross link clot. Measures from after Fibrinogen (factor I) and down to where the clot is formed

253
Q

What is the most common inherited plasma coagulopathy?

A

Factor VIII Deficiency: Hemophilia A

254
Q

what does factor VIII deficiency cause?

A

hemophilia A

255
Q

what is a common cellular coagulopathy?

A

Van B Disease

256
Q

what does factor IX deficiency cause?

A

hemophilia B

257
Q

second most common inherited plasma coagulopathy

A

hemophilia B

258
Q

what is factor XI deficiency?

A

autosomal recessive. less severe form of hemophilia.

259
Q

body’s natural system of anti-coagulation that keeps coagulation in check

A

plasmin system

260
Q

what is plasmin?

A

proteolytic enzyme that lyses fibrin clots

261
Q

what does protein S do?

A

activates protein C with the help of thrombomodulin

262
Q

what does protein C do?

A

inactivates factors Va and Vllla

263
Q

what does protein Z do?

A

inactivates Xa

264
Q

what does antithrombin do?

A

inactivates thrombin (IIa) and Xa

265
Q

what does thrombodulin do?

A

converts thrombin (IIa) into an anti-coagulant; helps protein S activate protein C

266
Q

what does tissue factor pathway inhibitor (TFPI) do?

A

inactivates VIIa

267
Q

what does warfarin do?

A

blocks the activity of Vitamin K

268
Q

what is used to monitor the anticoagulant effects of warfarin?

A

Prothrombin time

269
Q

naturally occurring mixture of varied chain lengths of glycosaminoglycans (GAGs) derived from porcine intestine

A

heparin

270
Q

what does heparin activate?

A

antithrombin

271
Q

what does antithrombin inactivate?

A

factor Xa and also inactivates activated thrombin

272
Q

Warfarin messes with?

A

Vitamin K (2,7,9,10)- if you get a drug that messes with Vitamin K, it messes with everything Vitamin K is needed for. Messes with both coagulant factors and anti.

273
Q

what does heparin bind to?

A

platelet factor 4 (PF4) which triggers the formation of anti-heparin antibodies

Clinical Medicine (1 decks)

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