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Adv Pathophysiology > Chapter 23: Disorders of the Hematologic System > Flashcards

Chapter 23: Disorders of the Hematologic System Flashcards

1
Q

Hypercoagulability

A

exagerrated hemostasis
thrombocytosis (>1,000,000)
predispose to thrombosis

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2
Q

Arterial Thrombi

A

associated with turbulent blood flow = atherosclerotic plaque, hyperlipidemia, smoking, DM
treat with antiplatelet aggregates (ASA)

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3
Q

Venous Thrombi

A

associated with stasis of blood flow = immobility, sickle cell, elevated estrogen, malignancy, obesity
treat with anticoagulants

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4
Q

Primary (Essential) Thrombocytosis

A

disorder of stem cells

results in dysfunctional platelets

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5
Q

Secondary (Reactive) Thrombocytosis

A

condition that stimulates thrombopoietin

tissue damage, cancer, chronic inflammatory disorders

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6
Q

Antiphospholipid Syndrome

A

autoantibodies (IgG) against anticoagulant phospholipids = inc coag activity
recurrent venous and arterial thrombosis
recurrent fetal loss
thrombocytopenia

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7
Q

Thrombocytopenia

A

platelet count <150,000

commonly causes leukemia, splenomegaly (sequestration), and autoimmune responses

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8
Q

_____ bleeding seen in platelet disorders

A

Superficial

petechia, purpua, ecchymosis, gingival bleeding, epistaxis

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9
Q

Drug-Induced Thrombocytopenia

A

antigen-anitbody response that results in plt destruction

Treat by D/C drug and plt count increases

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10
Q

Heparin-Induced Thrombocytopenia (HIT)

A

person develops antibodies to plt Factor 4 = activates platelets = thrombosis
can occur with increased levels of serotonin
Stop heparin and give direct thrombin inhibitor

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11
Q

Immune Thrombocytopenia Purpura (ITP)

A

autoimmune cell d/o = T-cell dysfunction
plt antibody formation and excess destruction of plts
platelets do not aggregate = bleeding

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12
Q

Clinical Manifestations of ITP

A 
ecchymosis
bleeding from gums
epistaxis
melena
splenomegaly (spleen is site for plt destruction)
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13
Q

Treatment for ITP

A

if no symptoms = no treatment
can give steroids (suppress immune response)
infuse plts
IV gamma globulin (slows rate of plt destruction, temp fix)

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14
Q

Thrombotic Thrombocytopenia Purpura (TTP)

A

Deficiency of enzyme Adam T513 that degrades vWF
more thrombosis than bleeding
EMERGENCY = wide spread occlusions
thrombocytopenia + hemolytic anemia + neuro abnormalities

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15
Q

Clinical Manifestations of TTP

A 
purpura
petechia
vaginal bleeding
neuro symptoms - altered LOC, seizures
jaundice (inc bilirubin)
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16
Q

Treatment for TTP (emergent)

A

Plasmapheresis
FFP
Give missing enzyme

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17
Q

von Willbrand Disease

A

deficiency or defect in von Willebrand Factor (vWF)
affects both primary and secondary hemostasis
lacking plt function, not plts

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18
Q

DDAVP (synthetic vasopressin)

A

treatment for von Willebrand Disease

stimulates endothelial cells to release vWF

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19
Q

Hemophilia A

A

Deficiency or defect of Factor VIII
affects BOTH intrinsic and extrinsic pathways
see increase in both PTT and PT

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20
Q

Clinical Manifestations of Hemophilia A

A

deep, systemic bleeding
soft tissues, GI tract, joints
joint bleeding can be seen in children when they start walking

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21
Q

Hemophilia B

A

Deficiency of Factor IX

involved in intrinsic pathway = PTT will be elevated

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22
Q

Factors II, VII, IX, X, prothrombin, and protein C require ______ to convert to their active form

A

Vitamin K

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23
Q

Disseminated Intravascular Coagulopathy (DIC)

A

widespread coagulation and bleeding = thrombo-hemorrhagic disorder

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24
Q

Intrinsic Causes of DIC

A

activation d/t severe endothelial damage

viruses/bacteria, hypoxia, acidosis, shock, hypo/hyperthermia

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25
Extrinsic Causes of DIC
release of extensive tissue factor | OB complications, trauma, burns, sepsis, cancers
26
Erythroblastosis Fetalis
hemolytic disease that occurs in Rh positive newborns of Rh negative mothers
27
Hydrops Fetalis
mother's immune system causes baby's RBCs to break down = anemia see splenomegaly and hepatomegaly
28
Kernicterus
abnormally high levels of unconjugated bilirubin (toxic) | results in severe brain damage or death
29
Hemodilution
caused by movement of fluid into the intravascular space in hypovolemic conditions
30
Iron Deficiency Anemia
microcytic, hypochromic anemia a deficiency in iron leads to dec Hgb synthesis = impairment of O2 delivery more RBCs are produce in response to low O2
31
Iron is absorbed in _____
the duodenum of the small intestines
32
Populations that lose more and require more iron consumption
pregnant females, menstruating females, and children and adolescents
33
Total Iron Binding Capacity (TIBC)
not usually able to be measured | elevated/measurable in IDA because it is not bound to iron
34
____ enhances the absorption of iron
Vitamin C
35
Clinical Manifestations of Iron Deficiency Anemia
``` fatigue, pallor palpitations/tachycardia, angina dyspnea cheilosis smooth tongue pica koilonychia ```
36
Poikilocytosis
abnormally shaped cells
37
Anisocytosis
different sized cells
38
Vitamin B12
essential for DNA synthesis and RBC maturation absorbed in the ileum only derived from animal products
39
Parietal gastric cells
secrete hydrochloric acid and intrinsic factor
40
Need _____ to extract Vitamin B12 from fod
hydrochloric acid
41
Need ____ to absorb Vitamin B12
intrinsic factor
42
Achlorhydria
very little hydrochloric acid | seen in pernicious anemia
43
Pernicious Anemia
autoimmune process where anitbodes react to parietal gastric cells = breaks up the IF-B12 complex
44
Vitamin B12 Deficiency Anemia
Decreased intake of vitamin B12 (alcoholism, vegans) | Malabsorption (gastric bypass, ileal resection, IBS)
45
Risk Factors for Pernicious Anemia
``` long term use of PPIs & H2RAs celiac disease gastrectomy or gastric bypass ileitis vegetarians/vegans ```
46
Clinical Manifestations of Pernicious Anemia
``` paresthesia, lack of coordiantion palpitations/tachycardia, angina can lead to HF N/V/anorexia, wgt loss gingival bleeding, glossitis, jaundice ```
47
Glossitis
smooth, beefy red tongue
48
Schillings Test
most definitive test for pernicious anemia
49
Folic Acid
essential for formation and maturation of RBCs and synthesis of DNA
50
Folic Acid Deficiency Anemia
increased in alcoholism, tumors, and certain medications
51
Clinical Manifestations of Folic Acid Deficiency
same as B12 with more severe GI symptoms | no neuro symptoms
52
Aplastic Anemia
primary condition of bone marrow stem cells - unable to produce mature cells see pancytopenia = pallor, fatigue, weakness
53
Sickle Cell Anemia
results from a point mutation in the beta chain of hemoglobin molecule (HbS) glutamic acid is replaced with valine affects black American after 6 months of age
54
HbS becomes sickle-shaped with...
deoxygenation or low O2 tension stress, physical exertion, cold, infection, dehydration hypoxia, acidosis
55
Acute Chest Syndrome
vaso-occlusive crisis that is the leading cause of death in sickle cell anemia
56
Thalassemia
group of inherited d/o of Hbg synthesis due to absent of defective synthesis of the alpha or beta chains of HbA the unaffected chain continues to synthesize, builds up in cell, and interferes with maturation/function
57
Alpha Thalassemia
gene deletion that results in defective alpha chain synthesis most common among Asians
58
Hydrops Fetalis Syndrome
most severe form of alpha thalassemia that occurs in infants (no alpha globin genes) Hb Bart is formed = high O2 affinity & does not release to tissues results in death in utero or shortly after
59
Beta Thalassemia
defect in the beta chain synthesis = excess alpha chains are denatured in Heinz bodies
60
Manifestations of Beta Thalassemia
growth retardation bone marrow expansion = chipmunk facies splenomegaly and hepatomegaly
61
Heinz bodies
denatured alpha chains that impair DNA synthesis and damage RBC membranes
62
_____ is a major complication of beta thalassemia
iron overload
63
Inherited Enzyme Defect G6PD
X-linked recessive d/o that makes RBCs and Hgb more vulnerable to oxidation (usually from medications) = inactive form of Hgb with low O2 affinity
64
Oxidative Drugs
aspirin, sulfonamides, nitrofurantoin, dapsone, quinidine
65
Hematocrit greater than ____ can lead to hypoxia
>60%
66
Primary Absolute Polycythemia (Polycythemia Vera)
pathologic - occurs irrespective of body's needs increase in RBCs, Hgb, Hct, WBCs, platelets treat with periodic phlebotomy
67
Complications of Polycythemia Vera
increased blood viscosity Thromboembolism Hemorrhage
68
Secondary Absolute Polycythemia
physiologic increase in erythropoietin level frequently a compensatory response to hypoxia seen in high altitudes, chronic heart or lung dx, smoking
69
Infectious Mononucleosis
caused by Epstein Barr virus "kissing disease" leukocytosis (EBV attaches to B cells)
70
Clinical Manifestations of Mono
prodromal period precedes occurence fever pharyngitis (palatal petechia) lymphadenopathy
71
Complications of Mono
Hepatitis | Splenomegaly (concern for rupture)
72
Monospot
detects EBV antibodies | can have false negative if done too early
73
Serologic tests for Mono
detects rise in IgG and IgE - occurs early

Adv Pathophysiology (22 decks)

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