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Heme and Lymph > Final Study Guide > Flashcards

Final Study Guide Flashcards

1
Q

Erythropoietin (EPO)

A
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2
Q

What are common causes of Microcytosis (low MCV)?

A

Iron deficiency
decreased globin chains
decreased heme

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3
Q

Macrocytosis (high MCV)

A

An increased MCV (>100 fL) is typically attributed to asynchronous maturation of nuclear chromatin, although other causes may also be present.

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4
Q

Whar is a common cause of macrocytosis (high MCV)?

A

megaloblastic anemia

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5
Q

Megaloblastic maturation can be due to:

A

Vitamin B12 deficiency
Folate deficiency
Copper deficiency
Drugs that interfere with DNA synthesis

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6
Q

Reticulocytosis

A

Reticulocytes are larger than mature RBCs, and reticulocytosiswill increase the MCV

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7
Q

Reticulocytosis may be increased in?

A

Hemolytic anemias (acute or chronic)
*
Recovery from bleeding
*
Replacement of iron or other nutrient in deficiency anemia
*
Recovery from bone marrow suppression such as binge drinking alcohol

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8
Q

Which state does glutamate switch with valine?

A

at condon 6 of the beta chain producing a sticky patch

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9
Q

What do hemoglobin crystals do to RBCs?

A

distort the RBC’s into a curvilinear ‘sickle’ shape

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10
Q

Treatment of sickle cell disease

A

*Vaccines, especially pneumococcal, haemophilus, meningococcal, hepatitis B
*prophylactic penicillin from diagnosis at least through puberty

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11
Q

What are the two categories of beta-thalassemia?

A

*B0mutation associated with absent B-globin synthesis
*B+mutation associated with reducedB-globin synthesis

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12
Q

What are the results of beta thal

A

Visible in the skull
crewcut sign
chipmunk facies

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13
Q

What causes an enlaregement of the liver and spleen in anemia?

A

red cell destruction
extramedullary hematopoiesis
iron overload later in the course of disease

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14
Q

What causes and expansion of bone in anemia?

A

-marrow hyperplasia
-characteristic facial appearance
+large cheekbones, protuberant maxilla, depressed nasal bridge

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15
Q

What are the clinical signs of iron deficiency anemia?

A

pallor –skin, conjunctiva, mucous membranes

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16
Q

What are the lab signs of iron deficiency anemia?

A

Decreased Hg, Ferritin, serum iron; increased TIBC

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17
Q

What is the morphology of deficiency anemia?

A

peripheral smear
bone marrow

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18
Q

What is the peripheral smear morphology of deficiency anemia?

A

microcytic and hypochromic red cells with increased poikilocytosis

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19
Q

What is the bone marrow morphology of deficiency anemia?

A

decreased to absent storage iron

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20
Q

What physiological states show an increased demand duing iron deficiency anemia?

A

pregnancy and childhood

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21
Q

What causes of blood loss show an increased demand duing iron deficiency anemia?

A

inflammatory bowel disease
peptic ulcer disease
GI malignancies
Blood donation

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22
Q

In microcytosis what is the range of RBCs in fL?

A

<80

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23
Q

What is the size of normal RBCs?

A

~7.5-8um

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24
Q

What is hyperchromaplasia?

A

normal RBC’s have a zone of central pallor measuring ~1/3 of cell diameter due to decreasing Hb content of cell

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25
Q

What is the level of reticulocyte count for the level of anemia?

A

low (decreased RPI)

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26
Q

What happens when oral iron therapy is instituted

A

reticulocyte count increases

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27
Q

What is megaloblastic anemia?

A

Asynchronous nuclear maturation (megaloblastosis), in which the rate of cell division is reduced relative to cytoplasmic expansion (most common) resulting in large, structurally abnormal, immature red blood cells

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28
Q

Megaloblastic maturation can be due to:

A

vitamin b12
folate deficiency (except in pregnancy)
copper deficincy (rare)

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29
Q

Vitamin B12 deficiency

A

malabsorption
poor dietary intake
surgical

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30
Q

folate deficiency

A

poor dietary intake
increased demand (pregnancy)
malabsorption
antifolate drugs

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31
Q

Describe the serum ferritin concentration during iron deficiency anemia

A

low

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32
Q

Describe the serum ferritin concentration during anemia of chronic disease

A

increased

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33
Q

Describe the percentage of reticulocytes in the blood serum during iron deficiency anemia

A

high

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34
Q

Describe the percentage of reticulocytes in the blood serum during during anemia of chronic disease?

A

low

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35
Q

What is the cascade to megaloblastic anemia?

A

gastric atrophy > reduced intrinsic factor secretion > Failure of absorption of B12 > deficiency of B12 > megaloblastic anemia

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36
Q

What is aplastic Anemia (AA)?

A

pancytopenia in association with bone marrow hypoplasia/aplasia (<30% cellularity), most often due to immune injury to multipotent hematopoietic stem cells

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37
Q

In bone marrow aplasia, what is the normal and aplastic percentages?

A

Normal: Birth 100%, Ped 70-90%, Adult 40-60%
Aplastic: <30%

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38
Q

What is extravascular hemolysis?

A

red cells are removed from circulation by reticuloendothelial system (mostly spleen and liver) and broken down

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39
Q

What are the principle clinical features of extravascular hemolysis?

A

anemia
splenomegaly
jaundice

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40
Q

In regard to the lab findings in hemolytic anemias, what are the features of incresed RBC breakdown?

A

*Increased serum bilirubin
*Increased urine urobilinogen, hemoglobinuria
*Decreased serum haptoglobin due to chelation of free hemoglobin (occurs in intravascular hemolysis and may also occur with extravascular hemolysis due to escape of hemoglobin from phagocytes)

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41
Q

In regard to the lab findings in hemolytic anemias, what are peripheral blood abnormalities?

A

schistocytes - INTRAvascular hemolysis, especially microangiopathic
spherocytes - EXTRAvascular hemolysis, especially in splenic clearance

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42
Q

What are some hemoglobin defects due to intrinsic RBC defects?

A

Sickle cell anemia
HbC disease

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43
Q

In the diagnosis of immune hemolytic anemia, what does the Direct Coombs test do?

A

detect antibodies and/or complement bound to patient’s red cells

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44
Q

In the diagnosis of immune hemolytic anemia, what does the indirect Coombs test do?

A

detects antibodies in patient’s serum

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45
Q

What are the 3 main clinical features of acute hemolytic transfusion reactions?

A

hemolytic shock phase
oliguric phase
diuretic phase

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46
Q

What two phase of the main clinical features of acute hemolytic transfusion reactions are involved in kidney disease?

A

oliguric and diuretic

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47
Q

What is Von Willebrand Disease?

A

a bleeding disorder caused by a deficiency of the von Willebrand factor

Must have less than 30% of von Willebrand Factor levels for a diagnosis.

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48
Q

What is Type I of Von Willebrands?

A

Partial decrease of von Willebrand Factor autosomal dominant disease

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49
Q

What is Type II of Von Willebrands?

A

Several qualitative defects in von Willebrand Factor autosomal dominant disease

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50
Q

What is Type III of Von Willebrands?

A

Complete deficiency of von Willebrand Factor autosomal recessive and most severe form

51
Q

What is hemostasis

A

defined as the process of clot formation

52
Q

What is the first stage of hemostasis?

A

involves the creation of a platelet plug consequent from disruption of the vascular endothelium from injuries due to diabetes, hypertension, smoking as well as vascular wall tear. Following damage to the vascular wall, the Von Willebrand factor (VWF) is released by the endothelial cells and megakaryocytes, which mediates platelet adhesion to the damaged vascular surface, and aggregation of platelets.

53
Q

What is the second stage of hemostasis?

A

propagation of clots by activation of various proenzymes to their active form

54
Q

What is the third stage of hemostasis?

A

termination of clot formation and the antithrombin control mechanism which are designed to prevent and mediate the extent of clot formation, thereby preventing processes that can lead tothrombosis, vascular inflammation, and tissue damage

55
Q

What is the fourth stage of hemostasis?

A

Removal of the clot by fibrinolysis is the last stage in clot formation. This stage ensures the removal of organized clots by plasmin as well as wound healing and tissue remodeling.

56
Q

What is the initial maneuver to control post operative bleeding?

A

pressureby placing a moist folded gauze directly over the socket

57
Q

Is it normal for an extraction site to ooze for up to 24 hours after the extraction process?

A

yes

58
Q

What in a tea bag acts as a vasocontrictor for continuous bleeding?

A

tannic acid

59
Q

What are things that may dislodge a clot?

A

forceful spitting, smoking, sucking through a straw

60
Q

What are additional ways to control bleeding?

A

suture

61
Q

Why does a suture do?

A

Primary closure of wound margins
Provide a physical barrier to hold the clot

62
Q

What are the 2 types of sutures?

A

resorbable and non-resorbable

63
Q

What is gelfoam?

A

Sterile sponge intended for application to bleeding surfaces as a hemostatic. Absorbed completely, with little tissue reaction in two to five days

64
Q

What is surgicel?

A

Absorbable Hemostat (oxidized regenerated cellulose) used in surgical procedures to assist in the control of capillary, venous, and small arterial hemorrhage when ligation or other conventional methods of control are impractical or ineffective. Physical hemostatic agent that acts as a barrier to blood and then becomes a sticky mass that serves as an artificial coagulum.

65
Q

What is bone wax?

A

*Used to stop osseous bleeding by creating a physical barrier.
*It is combined with paraffin, softening agents, and beeswax.
*Non-absorbable.

66
Q

What are the main indications for anticoagulation?

A
  1. Atrial Fibrillation
  2. Venous Thromboembolism Treatment
  3. Heart Valve Replacement
  4. Acute Myocardial Infarction
  5. Left Ventricular Thrombus
  6. Left Ventricular Aneurysm
  7. Venous Thromboembolism Prophylaxis
  8. Treatment of Venous Thromboembolism in Cancer Patients
  9. Pregnancy
  10. Heparin-Induced Thrombocytopenia
67
Q

What is anticoagulation therapy?

A

Anticoagulants derive their effect by acting at different sites of the coagulation cascade. Some act directly by enzyme inhibition, while others indirectly, by binding to antithrombin or by preventing their synthesis from the liver (vitamin K dependent factors).

68
Q

What are some types of anticoagulants?

A

Unfractionated Heparin (UFH)
Low Molecular Weight Heparin (LMWH)
Vitamin K Dependent Antagonists (VKA)
Direct Thrombin Inhibitors
Direct Factor 10a Inhibitors

69
Q

What are the bleeding risks of anticoagulation?

A

Risk of significant bleeding is higher with Coumadin (Warfarin) than with DOACs

Dose of Anticoagulant

Concomitant use of other medications (antiplatelet agents) that independently increase the risk of bleeding

70
Q

What are the age related risks of anticoagulation?

A

Age
Underlying medical conditions
Recent Surgery
Coagulopathy

71
Q

If a patient is on coumadin (warfarin) what is the INR supposed to be?

A

4.0 or lower 48 hours prior to procedure

72
Q

What are the categories of bleeding risks?

A

Low/very low
moderate
high

73
Q

What is a high risk surgery?

A

any with neuraxial anesthesia (spinal or epidural)

74
Q

What is a moderate risk surgery?

A

hernia, breast, othopedic
involving an incision or cutting bone

75
Q

What is a low/very low risk surgery?

A

1-2 teeth dental extraction
root canal
cataract surgery

76
Q

What are some hereditary bleeding disorders?

A

Hemophilia A
Hemophilia B
Hemophilia C
Von Willebrand Disease
Hereditary Hemorrhagic Telangiectasia (HHT)
Specific Clotting Factor Deficiencies

77
Q

What is HEMOPHILIA B?

A

Hemophilia B is an inherited disease caused by insufficient production of Factor IX

78
Q

What is Hemophilia C?

A

Hemophilia C is an inherited disease caused by insufficient production of Factor XI

79
Q

Cryoprecipitate (thawing fresh frozen plasma) contains

A

Factor VIII and von Willebrand’s Factor

80
Q

Aminocaproic Acid (Amicar)

A

is an inhibitor of fibrinolysis to promote clotting

81
Q

Desmopressin (DDAVP)

A

is a synthetic form of the vasopressin hormone that causes the release of von Willebrand’s antigen from the platelets. The von Willebrand’s antigen is the protein that carries Factor VIII

82
Q

Fresh Frozen Plasma: Contains all coagulation factors except

A

platelets

83
Q

Treatment of Von Willebrand’s Disease

A

*
1. Desmopressin (DDAVP): Causes von Willebrand Factor release from endothelial cells. Can be given intranasally, subcutaneously, or by IV form.
**Can’t be used on von Willebrand Type III **
*
2. Von Willebrand Factor replacement: for Type III
*
3. Aminocaproic Acid (Amicar) is an inhibitor of fibrinolysis to promote clotting.
*
Administration: oral tablets and IV doses.
*
Treatment for von Willebrand’s Disease.
*
4. Tranexamic Acid: Helps stabilize the clot formation.

84
Q

Where does the production of platelets begin?

A

stem cells (hemocytoblast)

85
Q

What are the ultrastructures?

A

Granulomere and hyalomere

86
Q

What are the 3 types of granulomeres?

A

alpha
delta
lambda

87
Q

What are granulomeres?

A

the darker central region containing organelles and granules

88
Q

what are hyalomeres?

A

A lighter staining peripheral zone containing a marginal bundle of cytoskeleton system of microtubules, actin, and myosin

Maintains the platelets’ discoid shape

89
Q

What are the major components of hemostasis?

A
  1. Vascular injury
  2. platelet activation from collagen
  3. platelet plug (primary hemostasis)
  4. Fribrinogen to fibrin promotes secondary hemostasis and the formation of a blood clot
  5. plasmin promotes fibrinolysis and clot degradation
90
Q

What is the function of a platelet?

A

to quickly form a mechanical plug-in response to vascular injury

91
Q

Platelet disorders can be a defect of what?

A

primary hemostasis
secondary hemostasis

92
Q

what is primary hemostasis?

A

Platelet plug formation

93
Q

what is secondary hemostasis?

A

coagulation cascade and regulation

94
Q

What is in the clinical history of bleeding disorders?

A

single site
multiple site
coagulopathy

95
Q

What are syndromes that can affect the vascular wall?

A

Marfan
Ehlers-Danlos
Osler-Weber-Rendu (HHT)

96
Q

What is the main effect of marfan’s syndrome on the vascular wall?

A

enlarged aorta

97
Q

What is the main effect of Ehlers-Danlos syndrome on the vascular wall?

A

Blood vessels prone to rupture

98
Q

What is the main effect of Osler-Weber-Rendu (HHT) on the vascular wall?

A

Dilated and fragile vessels ➔ more prone to bleeding

99
Q

What is the patient management for conditions affecting the vascular wall?

A

Local anesthesia with vasoconstrictor
Avoid NSAIDs (inhibit TXA2 ➔ Inc bleeding risk)

100
Q

How do platelets aggregate?

A

*Activated platelets release GP IIb/IIIa
*GP IIb/IIIa binds free-floating Fibrinogen
*Platelet plug formed and secured by fibrin

101
Q

Von Willebrand Disease

A

*Deficiency in vWF (aids in platelet adhesion and carries coagulation factor VIII)
*The most common congenital bleeding disorder
*Platelets cannot adhere to the vessel wall!

102
Q

When does spontaneous bleeding occur in thrombocytopenia?

A

Spontaneous bleeding seen if platelet count is <20,000 platelets/uL

103
Q

What is the platelet count for thrombocytopenia?

A

Platelet count < 150,000 platelets/uL

104
Q

What is a normal platelet count?

A

150,000 to 450,000 platelets/uL

105
Q

What are the different test for platelets?

A

Ivy Bleeding Test (BT)
Peripheral Blood Smear
Platelet Aggregation Test
Platelet Function Analyzer (PFA-100)

106
Q

Is there a factor 6?

A

NO

107
Q

Where are all factors (except 3, 4, 13) produced?

A

liver

108
Q

Vitamin K depedent factors are

A

2, 7, 9, 10

109
Q

What clotting factor does Von Willebrand’s disease affect?

A

8

110
Q

What clotting factor does hemophilia A affect?

A

8 is most common

111
Q

What clotting factor does hemophilia B affect?

A

Christmas disease
factor 9

112
Q

What clotting factor does hemophilia C affect?

A

Rosenthal syndrome Factor 11 deficiency

113
Q

What are 2 drugs for anticoagulant therapy?

A

Warfarin (reduces vitamin K)
Heparin (blocks factor 2)

114
Q

What are the 2 coagulation tests?

A

Activated Partial Thromboplastin Time (aPTT)

INR – calculated from Prothrombin Time (PT)

115
Q

What is the normal Activated Partial Thromboplastin Time (aPTT)

A

21-35 seconds

116
Q

What is the normal PT range?

A

11-15 seconds

117
Q

What are some medications to Avoid While on Warfarin therapy?

A

NSAIDS
Metronidiazole & Erythromycin
Herbal supplements
Barbiturates and Steroids

118
Q

Vitmain K does what to INR?

A

lowers it

119
Q

When should the INR be taken for dental care?

A

within 2 days

120
Q

What does an INR of 2-3 indicate?

A

*Considered therapeutic
*Minimal bleeding concerns during dental treatment

121
Q

What does an INR of 3-3.5 indicate?

A

*Ensure adequate hemostasis techniques
*Simple, single tooth extractions are ok to proceed with
*Defer and refer anything more complex

122
Q

What does an INR of >3.5 indicate?

A

REFER REFER REFER

123
Q

What are some effects on the oral cavity from bleeding disorders?

A

*Gums bleed spontaneously
*Petechiae
*Ecchymoses
*Hemophilia associated hemarthrosis in the TMJ

Heme and Lymph (4 decks)

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