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Physiology Test 2 content > Blood Disorders > Flashcards

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
Q

Type 2 VWD

A

Abnormal (mutations) VWF, multiple subtypes

  • levels normal or slightly decreased, function abnormally
  • 25% of cases
  • Moderate bleeding
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26
Q

Type 3 VWD

A
  • Total deficiency/ F8 also very low
  • Severe bleeding
  • Rare
  • Small % develop post transfusion of plasma products
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27
Q

Acquired VWD

A
  • Autoimmune (SLE, cancer)
  • Shear-induced proteolysis
  • increased binding of VWF
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28
Q

Treatment of Type 1 VWD

A
  • DDAVP- stimulates release from endothelial cells
  • Diminished effects with repeated doses
  • VWF concentrate if Tx >3 days
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29
Q

Tx of T2 VWD

A

will respond to DDAVP, but still fxns abnormally

-Type 2A and 2M VWD responds to DDAVP

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30
Q

Tx T3 VWD

A
  • DDAVP not useful

- VWF concentrate

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31
Q

What conditions should DDAVP be used in caution in?

A

Brain, ocular and coronary surgeries. VWF concentrates should be used in these settings

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32
Q

DDAVP + Excess fluid =

A

hyponatremia

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33
Q

VWF concentrates

A

Humate-P
Alphanate SD/HT
Off label- Koate DVI

34
Q

When should Cryo be used in VWF?

A

In life-threatening situations when no VWF concentrate is available

35
Q

Why should cryo be avoided in VWD?

A

It is not virally inactive

36
Q

Quantitative WBC D/Os

A

Leukocytosis

Leukopenia

37
Q

Qualitative WBC D/Os

A

Chronic Granulematous disease
Leukocyte adhesion deficiency
Specific granule deficiency syndrome

38
Q

Neutrophil maturation

A

2 weeks from “scratch”

  • Proliferation 6-7 Days
  • Maturation 6-7 Days
  • Intravascular-12 hours
  • Tissues- 12 hours
39
Q

Neutrophilia

A

Abnormally high ANC (>7700/ml)

-Increased Bands

40
Q

Causes of neutrophilia

A
  • Acute shift from marginating to circulating

- chronic stimulation

41
Q

What is the most common cause of neutrophilia?

A

Bacterial infection

42
Q

Eosinophilia

A

increased count

  • parasitic infection
  • bronchoallergic reaction
  • skin rash
    • if >5% can lead to cardiomyopathy
43
Q

Monocytosis

A

Increased monocyte count

  • Occurs late during acute infections
  • with chronic infections (TB, endocarditis)
44
Q

Lymphocytosis

A

Increased lymphocyte count

  • acute/chronic viral infections
  • chronic lymphocytic leukemia
45
Q

Leukopenia

A

WBC <4000

  • Increased destruction, decreased production
  • Radiation/chemo
46
Q

When are WBC lowest after induction of chemo?

A

7-14 days

47
Q

When is monocytopenia seen?

A
  • glucocorticoid therapy
  • Hairy cell leukemia
  • Aplastic anemia
48
Q

When is lymphopenia seen?

A
  • aging

- HIV, AIDS

49
Q

Neutropenia

A

ANC <1500

50
Q

ANC 500-1000

A

increased r/f infection from exposure

51
Q

ANC <500

A

r/f opportunistic infection

52
Q

ANC <200

A

inflammatory response nonexistent

53
Q

ANC in african americans

A

decreased normal counts (1000-1200)

54
Q

Causes of Neutropenia

A
  • Intrinsic-decrease in myeloid cells

- acquired-decreased production , increased destruction

55
Q

Cyclic neutropenia

A
  • 21 day cycle
  • autosomal dominant
  • fever/mouth ulcers
  • Tx GCSF (granulocyte- colony stimulating factor)
  • Usually improves after puberty
56
Q

Leukemia

A

Neoplastic D/O-Uncontrollable production of undifferentiated immature blood cells

  • Myeloid
  • Lymphocytic
  • acute
  • chronic
57
Q

Acute Leukemia

A

abrupt onset, high proportion of immature cells

58
Q

Chronic leukemia

A

increased mature cells, insidious onset

-Cells able to function normally

59
Q

Acute Lymphoblastic leukemia

A

lymphocytes

60
Q

Acute Myeloid leukemia

A

Granulocytes

61
Q

Chronic Lymphocytic leukemia

A

B. Cells

62
Q

Chronic Myelocytic Leukemia

A

Granulocytes

63
Q

Pathophysiology of Leukemia

A
  • expanding mass of cells infiltrate bone marrow- cells become aplastic
  • cells infiltrate spleen, liver, meninges
64
Q

What does the use of nutrients by rapidly proliferating leukemia cells cause?

A

metabolic starvation of normal tissues

65
Q

Signs and symptoms of leukemia

A
  • infection unresponsive to Tx or excessive bleeding
  • mult. infections
  • anemia
  • bone pain
  • fever
  • enlarge lymph nodes
66
Q

What happens when WBC >100,000

A

circulatory sludging and increased blood viscosity

-VTE prophylaxis necessary

67
Q

Sickle Cell Anemia

A

Caused by a single amino acid substitution (glutamine–>valine) in B-glubulin chain -HbS

68
Q

Triggers for sickling in SCD

A

Hypoxia, hypothermia, Acidosis, hypovolemia, infection, emotional stress

69
Q

Clinical manifestations of SCD

A
  • Vaso-occlusive crisis
  • Anemia- functional
  • Aplastic crisis
  • Pulm. HTN
  • Splenic sequestration
  • Acute Chest
  • CNS involvement
70
Q

Tx of SCD

A

Hydroxylurea in children

  • Transfusion r/t anemia (acute chest/pregnancy, stoke, pre-op)
  • BMT (can cure)
71
Q

Hydroxylurea

A

increases levels of fetal hemoglobin, which retards sickling

72
Q

Aplastic Anemia

A

Bone Marrow Failure

  • Congenital (20%)
  • Acquired (80%)
73
Q

Aplastic anemia pathophysiology

A
  • neutropenia
  • thrombocytopenia
  • anemia
74
Q

TX for aplastic anemia

A
  • Transfusions
  • Immunosuppressive Drugs
  • BMT
75
Q

Anesthesia considerations with Aplastic Anemia

A
  • ABX
  • Spinal/epidural contraindicated
  • Nitrous oxide can cause bone marrow suppression
  • need good pulmonary toilet after
76
Q

Granulocytes

A

Neutrophils
Basophils
Eosinophils

77
Q

Agranulocytes

A
  • Lymphocytes

- Monocytes

78
Q

Polycythemia

A

^Hb in blood.

79
Q

Causes of Polycythemia

A

1- Intrinsic factors r/t RBC precursors
2-Functional hypoxia
3-Benign epo-secreting lesions

80
Q

Anemia of chronic disease

A

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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