Final Study Guide Flashcards
1
Q
Erythropoietin (EPO)
A
2
Q
What are common causes of Microcytosis (low MCV)?
A
Iron deficiency
decreased globin chains
decreased heme
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.
4
Q
Whar is a common cause of macrocytosis (high MCV)?
A
megaloblastic anemia
5
Q
Megaloblastic maturation can be due to:
A
Vitamin B12 deficiency
Folate deficiency
Copper deficiency
Drugs that interfere with DNA synthesis
6
Q
Reticulocytosis
A
Reticulocytes are larger than mature RBCs, and reticulocytosiswill increase the MCV
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
8
Q
Which state does glutamate switch with valine?
A
at condon 6 of the beta chain producing a sticky patch
9
Q
What do hemoglobin crystals do to RBCs?
A
distort the RBC’s into a curvilinear ‘sickle’ shape
10
Q
Treatment of sickle cell disease
A
*Vaccines, especially pneumococcal, haemophilus, meningococcal, hepatitis B
*prophylactic penicillin from diagnosis at least through puberty
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
12
Q
What are the results of beta thal
A
Visible in the skull
crewcut sign
chipmunk facies
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
14
Q
What causes and expansion of bone in anemia?
A
-marrow hyperplasia
-characteristic facial appearance
+large cheekbones, protuberant maxilla, depressed nasal bridge
15
Q
What are the clinical signs of iron deficiency anemia?
A
pallor –skin, conjunctiva, mucous membranes
16
Q
What are the lab signs of iron deficiency anemia?
A
Decreased Hg, Ferritin, serum iron; increased TIBC
17
Q
What is the morphology of deficiency anemia?
A
peripheral smear
bone marrow
18
Q
What is the peripheral smear morphology of deficiency anemia?
A
microcytic and hypochromic red cells with increased poikilocytosis
19
Q
What is the bone marrow morphology of deficiency anemia?
A
decreased to absent storage iron
20
Q
What physiological states show an increased demand duing iron deficiency anemia?
A
pregnancy and childhood
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
22
Q
In microcytosis what is the range of RBCs in fL?
A
<80
23
Q
What is the size of normal RBCs?
A
~7.5-8um
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
25
What is the level of reticulocyte count for the level of anemia?
low (decreased RPI)
26
What happens when oral iron therapy is instituted
reticulocyte count increases
27
What is megaloblastic anemia?
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
28
Megaloblastic maturation can be due to:
vitamin b12
folate deficiency (except in pregnancy)
copper deficincy (rare)
29
Vitamin B12 deficiency
malabsorption
poor dietary intake
surgical
30
folate deficiency
poor dietary intake
increased demand (pregnancy)
malabsorption
antifolate drugs
31
Describe the serum ferritin concentration during iron deficiency anemia
low
32
Describe the serum ferritin concentration during anemia of chronic disease
increased
33
Describe the percentage of reticulocytes in the blood serum during iron deficiency anemia
high
34
Describe the percentage of reticulocytes in the blood serum during during anemia of chronic disease?
low
35
What is the cascade to megaloblastic anemia?
gastric atrophy > reduced intrinsic factor secretion > Failure of absorption of B12 > deficiency of B12 > megaloblastic anemia
36
What is aplastic Anemia (AA)?
pancytopenia in association with bone marrow hypoplasia/aplasia (<30% cellularity), most often due to immune injury to multipotent hematopoietic stem cells
37
In bone marrow aplasia, what is the normal and aplastic percentages?
Normal: Birth 100%, Ped 70-90%, Adult 40-60%
Aplastic: <30%
38
What is extravascular hemolysis?
red cells are removed from circulation by reticuloendothelial system (mostly spleen and liver) and broken down
39
What are the principle clinical features of extravascular hemolysis?
anemia
splenomegaly
jaundice
40
In regard to the lab findings in hemolytic anemias, what are the features of incresed RBC breakdown?
*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)
41
In regard to the lab findings in hemolytic anemias, what are peripheral blood abnormalities?
schistocytes - INTRAvascular hemolysis, especially microangiopathic
spherocytes - EXTRAvascular hemolysis, especially in splenic clearance
42
What are some hemoglobin defects due to intrinsic RBC defects?
Sickle cell anemia
HbC disease
43
In the diagnosis of immune hemolytic anemia, what does the Direct Coombs test do?
detect antibodies and/or complement bound to patient's red cells
44
In the diagnosis of immune hemolytic anemia, what does the indirect Coombs test do?
detects antibodies in patient's serum
45
What are the 3 main clinical features of acute hemolytic transfusion reactions?
hemolytic shock phase
oliguric phase
diuretic phase
46
What two phase of the main clinical features of acute hemolytic transfusion reactions are involved in kidney disease?
oliguric and diuretic
47
What is Von Willebrand Disease?
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.
48
What is Type I of Von Willebrands?
Partial decrease of von Willebrand Factor autosomal dominant disease
49
What is Type II of Von Willebrands?
Several qualitative defects in von Willebrand Factor autosomal dominant disease
50
What is Type III of Von Willebrands?
Complete deficiency of von Willebrand Factor autosomal recessive and most severe form
51
What is hemostasis
defined as the process of clot formation
52
What is the first stage of hemostasis?
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
What is the second stage of hemostasis?
propagation of clots by activation of various proenzymes to their active form
54
What is the third stage of hemostasis?
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
What is the fourth stage of hemostasis?
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
What is the initial maneuver to control post operative bleeding?
pressureby placing a moist folded gauze directly over the socket
57
Is it normal for an extraction site to ooze for up to 24 hours after the extraction process?
yes
58
What in a tea bag acts as a vasocontrictor for continuous bleeding?
tannic acid
59
What are things that may dislodge a clot?
forceful spitting, smoking, sucking through a straw
60
What are additional ways to control bleeding?
suture
61
Why does a suture do?
Primary closure of wound margins
Provide a physical barrier to hold the clot
62
What are the 2 types of sutures?
resorbable and non-resorbable
63
What is gelfoam?
Sterile sponge intended for application to bleeding surfaces as a hemostatic. Absorbed completely, with little tissue reaction in two to five days
64
What is surgicel?
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
What is bone wax?
*Used to stop osseous bleeding by creating a physical barrier.
*It is combined with paraffin, softening agents, and beeswax.
*Non-absorbable.
66
What are the main indications for anticoagulation?
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
What is anticoagulation therapy?
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
What are some types of anticoagulants?
Unfractionated Heparin (UFH)
Low Molecular Weight Heparin (LMWH)
Vitamin K Dependent Antagonists (VKA)
Direct Thrombin Inhibitors
Direct Factor 10a Inhibitors
69
What are the bleeding risks of anticoagulation?
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
What are the age related risks of anticoagulation?
Age
Underlying medical conditions
Recent Surgery
Coagulopathy
71
If a patient is on coumadin (warfarin) what is the INR supposed to be?
4.0 or lower 48 hours prior to procedure
72
What are the categories of bleeding risks?
Low/very low
moderate
high
73
What is a high risk surgery?
any with neuraxial anesthesia (spinal or epidural)
74
What is a moderate risk surgery?
hernia, breast, othopedic
involving an incision or cutting bone
75
What is a low/very low risk surgery?
1-2 teeth dental extraction
root canal
cataract surgery
76
What are some hereditary bleeding disorders?
Hemophilia A
Hemophilia B
Hemophilia C
Von Willebrand Disease
Hereditary Hemorrhagic Telangiectasia (HHT)
Specific Clotting Factor Deficiencies
77
What is HEMOPHILIA B?
Hemophilia B is an inherited disease caused by insufficient production of Factor IX
78
What is Hemophilia C?
Hemophilia C is an inherited disease caused by insufficient production of Factor XI
79
Cryoprecipitate (thawing fresh frozen plasma) contains
Factor VIII and von Willebrand’s Factor
80
Aminocaproic Acid (Amicar)
is an inhibitor of fibrinolysis to promote clotting
81
Desmopressin (DDAVP)
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
Fresh Frozen Plasma: Contains all coagulation factors except
platelets
83
Treatment of Von Willebrand's Disease
*
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
Where does the production of platelets begin?
stem cells (hemocytoblast)
85
What are the ultrastructures?
Granulomere and hyalomere
86
What are the 3 types of granulomeres?
alpha
delta
lambda
87
What are granulomeres?
the darker central region containing organelles and granules
88
what are hyalomeres?
A lighter staining peripheral zone containing a marginal bundle of cytoskeleton system of microtubules, actin, and myosin
Maintains the platelets' discoid shape
89
What are the major components of hemostasis?
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
What is the function of a platelet?
to quickly form a mechanical plug-in response to vascular injury
91
Platelet disorders can be a defect of what?
primary hemostasis
secondary hemostasis
92
what is primary hemostasis?
Platelet plug formation
93
what is secondary hemostasis?
coagulation cascade and regulation
94
What is in the clinical history of bleeding disorders?
single site
multiple site
coagulopathy
95
What are syndromes that can affect the vascular wall?
Marfan
Ehlers-Danlos
Osler-Weber-Rendu (HHT)
96
What is the main effect of marfan's syndrome on the vascular wall?
enlarged aorta
97
What is the main effect of Ehlers-Danlos syndrome on the vascular wall?
Blood vessels prone to rupture
98
What is the main effect of Osler-Weber-Rendu (HHT) on the vascular wall?
Dilated and fragile vessels ➔ more prone to bleeding
99
What is the patient management for conditions affecting the vascular wall?
Local anesthesia with vasoconstrictor
Avoid NSAIDs (inhibit TXA2 ➔ Inc bleeding risk)
100
How do platelets aggregate?
*Activated platelets release GP IIb/IIIa
*GP IIb/IIIa binds free-floating Fibrinogen
*Platelet plug formed and secured by fibrin
101
Von Willebrand Disease
*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
When does spontaneous bleeding occur in thrombocytopenia?
Spontaneous bleeding seen if platelet count is <20,000 platelets/uL
103
What is the platelet count for thrombocytopenia?
Platelet count < 150,000 platelets/uL
104
What is a normal platelet count?
150,000 to 450,000 platelets/uL
105
What are the different test for platelets?
Ivy Bleeding Test (BT)
Peripheral Blood Smear
Platelet Aggregation Test
Platelet Function Analyzer (PFA-100)
106
Is there a factor 6?
NO
107
Where are all factors (except 3, 4, 13) produced?
liver
108
Vitamin K depedent factors are
2, 7, 9, 10
109
What clotting factor does Von Willebrand's disease affect?
8
110
What clotting factor does hemophilia A affect?
8 is most common
111
What clotting factor does hemophilia B affect?
Christmas disease
factor 9
112
What clotting factor does hemophilia C affect?
Rosenthal syndrome Factor 11 deficiency
113
What are 2 drugs for anticoagulant therapy?
Warfarin (reduces vitamin K)
Heparin (blocks factor 2)
114
What are the 2 coagulation tests?
Activated Partial Thromboplastin Time (aPTT)
INR – calculated from Prothrombin Time (PT)
115
What is the normal Activated Partial Thromboplastin Time (aPTT)
21-35 seconds
116
What is the normal PT range?
11-15 seconds
117
What are some medications to Avoid While on Warfarin therapy?
NSAIDS
Metronidiazole & Erythromycin
Herbal supplements
Barbiturates and Steroids
118
Vitmain K does what to INR?
lowers it
119
When should the INR be taken for dental care?
within 2 days
120
What does an INR of 2-3 indicate?
*Considered therapeutic
*Minimal bleeding concerns during dental treatment
121
What does an INR of 3-3.5 indicate?
*Ensure adequate hemostasis techniques
*Simple, single tooth extractions are ok to proceed with
*Defer and refer anything more complex
122
What does an INR of >3.5 indicate?
REFER REFER REFER
123
What are some effects on the oral cavity from bleeding disorders?
*Gums bleed spontaneously
*Petechiae
*Ecchymoses
*Hemophilia associated hemarthrosis in the TMJ
