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Blood Disorders Flashcards

1
Q

Thrombocytopenia

A

Plts < 150K

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2
Q

Function of VWF

A

Act as a bridge to bind collagen and platelets after vascular injury occurs, so that primary hemostasis can occur.

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3
Q

Life Span of plts

A

9-10 days

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4
Q

What nutritional deficiency can lead to thrombocytopenia

A

B12 deficiency

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5
Q

Symptoms of thrombocytopenia

A
  • Easy bruising
  • Petechiae
  • Decreased Plt count
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6
Q

Patient at risk for life threatening hemorrhage when platelets are less than____

A

10K

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7
Q

Types of thrombocytopenia

A
  • HITT
  • Idiopathic thrombocytopenic purpura
  • Post-transfusion purpura
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8
Q

Cause of HITT

A

Patients have antibodies against PF4/Heparin Complex

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9
Q

Pathophysiology of HITT

A
  • plts are destroyed by spleen
  • Plts activated and consumed
  • Plt chains leading to thrombus
  • Endothelial cell damage—> increased r/f thrombosis
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10
Q

Clinical symptoms of HITT

A

Thrombosis: DVT, PE

NOT bleeding

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11
Q

Diagnosis of HITT

A

Immunoassays to detect antibodies of PF4/heparin complexes

-BLE US, even in the absence of clinical evidence of LE DVT

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12
Q

Idiopathic Thrombocytopenic Purpura (Autoimmune)

A
  • Decreased platelet count in the absence of identifiable cause.
  • Normal Bone marrow, body made antibodies against plts
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13
Q

Pathogenesis of ITP

A

plts have antibodies to specific platelet membrane proteins

-Increased peripheral platelet destruction

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14
Q

Causes of ITP

A

Acute: Infection, spont. resolution within 2 months
Chronic: No cause, lasts >6mo.

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15
Q

Complications of ITP

A

Hemorrhage/ICH

  • -> mortality rate, children 1%, Adults 5%
  • ->Spont. Remission in 80% of children, remission rare in adults
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16
Q

Treatment of ITP

A
  • Corticosteroids
  • IV Ig
  • Plt. transfusion
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17
Q

Post-Transfusion purpura

A

Thrombocytopenia 3-12 days after transfusion in a patient who has had previous transfusions or is pregnant

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18
Q

Pathophys of PTP

A
  • Strong female predominance
  • plts <10k
  • Plts develop antibodies to HPA-1, GP IIb/IIIa
  • Antibody mediated destruction of both donor platelets as well as patients own plts.
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19
Q

Qualitative PLT disorders

A

VWD

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20
Q

VWD

A

Lack of, or abnormal circulating VWF

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21
Q

Where is VWF synthesized and stored

A
  • vascular endothelium (stored secretory granules)

- Bone marrow megakaryocytic (stored in plt. granules)

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22
Q

Factors that release VWF

A
  • Stress drugs- DDAVP

- Following platelet aggregation

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23
Q

Categories of VWD

A
  • Type 1
  • Type 2
  • Type 3
  • Aquired
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24
Q

Type 1 VWD

A
  • partial deficiency, lvls low but function normally
  • 75% of symptomatic pts with VWD
  • Mild-Mod bleeding
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25
Type 2 VWD
Abnormal (mutations) VWF, multiple subtypes - levels normal or slightly decreased, function abnormally - 25% of cases - Moderate bleeding
26
Type 3 VWD
- Total deficiency/ F8 also very low - Severe bleeding - Rare - Small % develop post transfusion of plasma products
27
Acquired VWD
- Autoimmune (SLE, cancer) - Shear-induced proteolysis - increased binding of VWF
28
Treatment of Type 1 VWD
- DDAVP- stimulates release from endothelial cells - Diminished effects with repeated doses - VWF concentrate if Tx >3 days
29
Tx of T2 VWD
will respond to DDAVP, but still fxns abnormally | -Type 2A and 2M VWD responds to DDAVP
30
Tx T3 VWD
- DDAVP not useful | - VWF concentrate
31
What conditions should DDAVP be used in caution in?
Brain, ocular and coronary surgeries. VWF concentrates should be used in these settings
32
DDAVP + Excess fluid =
hyponatremia
33
VWF concentrates
Humate-P Alphanate SD/HT Off label- Koate DVI
34
When should Cryo be used in VWF?
In life-threatening situations when no VWF concentrate is available
35
Why should cryo be avoided in VWD?
It is not virally inactive
36
Quantitative WBC D/Os
Leukocytosis | Leukopenia
37
Qualitative WBC D/Os
Chronic Granulematous disease Leukocyte adhesion deficiency Specific granule deficiency syndrome
38
Neutrophil maturation
2 weeks from "scratch" - Proliferation 6-7 Days - Maturation 6-7 Days - Intravascular-12 hours - Tissues- 12 hours
39
Neutrophilia
Abnormally high ANC (>7700/ml) | -Increased Bands
40
Causes of neutrophilia
- Acute shift from marginating to circulating | - chronic stimulation
41
What is the most common cause of neutrophilia?
Bacterial infection
42
Eosinophilia
increased count - parasitic infection - bronchoallergic reaction - skin rash * * if >5% can lead to cardiomyopathy
43
Monocytosis
Increased monocyte count - Occurs late during acute infections - with chronic infections (TB, endocarditis)
44
Lymphocytosis
Increased lymphocyte count - acute/chronic viral infections - chronic lymphocytic leukemia
45
Leukopenia
WBC <4000 - Increased destruction, decreased production - Radiation/chemo
46
When are WBC lowest after induction of chemo?
7-14 days
47
When is monocytopenia seen?
- glucocorticoid therapy - Hairy cell leukemia - Aplastic anemia
48
When is lymphopenia seen?
- aging | - HIV, AIDS
49
Neutropenia
ANC <1500
50
ANC 500-1000
increased r/f infection from exposure
51
ANC <500
r/f opportunistic infection
52
ANC <200
inflammatory response nonexistent
53
ANC in african americans
decreased normal counts (1000-1200)
54
Causes of Neutropenia
- Intrinsic-decrease in myeloid cells | - acquired-decreased production , increased destruction
55
Cyclic neutropenia
- 21 day cycle - autosomal dominant - fever/mouth ulcers - Tx GCSF (granulocyte- colony stimulating factor) - Usually improves after puberty
56
Leukemia
Neoplastic D/O-Uncontrollable production of undifferentiated immature blood cells - Myeloid - Lymphocytic - acute - chronic
57
Acute Leukemia
abrupt onset, high proportion of immature cells
58
Chronic leukemia
increased mature cells, insidious onset | -Cells able to function normally
59
Acute Lymphoblastic leukemia
lymphocytes
60
Acute Myeloid leukemia
Granulocytes
61
Chronic Lymphocytic leukemia
B. Cells
62
Chronic Myelocytic Leukemia
Granulocytes
63
Pathophysiology of Leukemia
- expanding mass of cells infiltrate bone marrow- cells become aplastic - cells infiltrate spleen, liver, meninges
64
What does the use of nutrients by rapidly proliferating leukemia cells cause?
metabolic starvation of normal tissues
65
Signs and symptoms of leukemia
- infection unresponsive to Tx or excessive bleeding - mult. infections - anemia - bone pain - fever - enlarge lymph nodes
66
What happens when WBC >100,000
circulatory sludging and increased blood viscosity | -VTE prophylaxis necessary
67
Sickle Cell Anemia
Caused by a single amino acid substitution (glutamine-->valine) in B-glubulin chain -HbS
68
Triggers for sickling in SCD
Hypoxia, hypothermia, Acidosis, hypovolemia, infection, emotional stress
69
Clinical manifestations of SCD
- Vaso-occlusive crisis - Anemia- functional - Aplastic crisis - Pulm. HTN - Splenic sequestration - Acute Chest - CNS involvement
70
Tx of SCD
Hydroxylurea in children - Transfusion r/t anemia (acute chest/pregnancy, stoke, pre-op) - BMT (can cure)
71
Hydroxylurea
increases levels of fetal hemoglobin, which retards sickling
72
Aplastic Anemia
Bone Marrow Failure - Congenital (20%) - Acquired (80%)
73
Aplastic anemia pathophysiology
- neutropenia - thrombocytopenia - anemia
74
TX for aplastic anemia
- Transfusions - Immunosuppressive Drugs - BMT
75
Anesthesia considerations with Aplastic Anemia
- ABX - Spinal/epidural contraindicated - Nitrous oxide can cause bone marrow suppression - need good pulmonary toilet after
76
Granulocytes
Neutrophils Basophils Eosinophils
77
Agranulocytes
- Lymphocytes | - Monocytes
78
Polycythemia
^Hb in blood.
79
Causes of Polycythemia
1- Intrinsic factors r/t RBC precursors 2-Functional hypoxia 3-Benign epo-secreting lesions
80
Anemia of chronic disease
Usually a response to EPO, lack of or inadequate response to. -Disregulation of iron homeostasis

Physiology Test 2 content (9 decks)

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