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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
Q

Extrinsic Causes of DIC

A

release of extensive tissue factor

OB complications, trauma, burns, sepsis, cancers

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26
Q

Erythroblastosis Fetalis

A

hemolytic disease that occurs in Rh positive newborns of Rh negative mothers

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27
Q

Hydrops Fetalis

A

mother’s immune system causes baby’s RBCs to break down = anemia
see splenomegaly and hepatomegaly

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28
Q

Kernicterus

A

abnormally high levels of unconjugated bilirubin (toxic)

results in severe brain damage or death

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29
Q

Hemodilution

A

caused by movement of fluid into the intravascular space in hypovolemic conditions

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30
Q

Iron Deficiency Anemia

A

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
Q

Iron is absorbed in _____

A

the duodenum of the small intestines

32
Q

Populations that lose more and require more iron consumption

A

pregnant females, menstruating females, and children and adolescents

33
Q

Total Iron Binding Capacity (TIBC)

A

not usually able to be measured

elevated/measurable in IDA because it is not bound to iron

34
Q

____ enhances the absorption of iron

A

Vitamin C

35
Q

Clinical Manifestations of Iron Deficiency Anemia

A 
fatigue, pallor
palpitations/tachycardia, angina
dyspnea
cheilosis
smooth tongue
pica
koilonychia
36
Q

Poikilocytosis

A

abnormally shaped cells

37
Q

Anisocytosis

A

different sized cells

38
Q

Vitamin B12

A

essential for DNA synthesis and RBC maturation
absorbed in the ileum
only derived from animal products

39
Q

Parietal gastric cells

A

secrete hydrochloric acid and intrinsic factor

40
Q

Need _____ to extract Vitamin B12 from fod

A

hydrochloric acid

41
Q

Need ____ to absorb Vitamin B12

A

intrinsic factor

42
Q

Achlorhydria

A

very little hydrochloric acid

seen in pernicious anemia

43
Q

Pernicious Anemia

A

autoimmune process where anitbodes react to parietal gastric cells = breaks up the IF-B12 complex

44
Q

Vitamin B12 Deficiency Anemia

A

Decreased intake of vitamin B12 (alcoholism, vegans)

Malabsorption (gastric bypass, ileal resection, IBS)

45
Q

Risk Factors for Pernicious Anemia

A 
long term use of PPIs & H2RAs
celiac disease
gastrectomy or gastric bypass
ileitis
vegetarians/vegans
46
Q

Clinical Manifestations of Pernicious Anemia

A 
paresthesia, lack of coordiantion
palpitations/tachycardia, angina
can lead to HF
N/V/anorexia, wgt loss
gingival bleeding, glossitis, jaundice
47
Q

Glossitis

A

smooth, beefy red tongue

48
Q

Schillings Test

A

most definitive test for pernicious anemia

49
Q

Folic Acid

A

essential for formation and maturation of RBCs and synthesis of DNA

50
Q

Folic Acid Deficiency Anemia

A

increased in alcoholism, tumors, and certain medications

51
Q

Clinical Manifestations of Folic Acid Deficiency

A

same as B12 with more severe GI symptoms

no neuro symptoms

52
Q

Aplastic Anemia

A

primary condition of bone marrow stem cells - unable to produce mature cells
see pancytopenia = pallor, fatigue, weakness

53
Q

Sickle Cell Anemia

A

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
Q

HbS becomes sickle-shaped with…

A

deoxygenation or low O2 tension
stress, physical exertion, cold, infection, dehydration
hypoxia, acidosis

55
Q

Acute Chest Syndrome

A

vaso-occlusive crisis that is the leading cause of death in sickle cell anemia

56
Q

Thalassemia

A

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
Q

Alpha Thalassemia

A

gene deletion that results in defective alpha chain synthesis
most common among Asians

58
Q

Hydrops Fetalis Syndrome

A

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
Q

Beta Thalassemia

A

defect in the beta chain synthesis = excess alpha chains are denatured in Heinz bodies

60
Q

Manifestations of Beta Thalassemia

A

growth retardation
bone marrow expansion = chipmunk facies
splenomegaly and hepatomegaly

61
Q

Heinz bodies

A

denatured alpha chains that impair DNA synthesis and damage RBC membranes

62
Q

_____ is a major complication of beta thalassemia

A

iron overload

63
Q

Inherited Enzyme Defect G6PD

A

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
Q

Oxidative Drugs

A

aspirin, sulfonamides, nitrofurantoin, dapsone, quinidine

65
Q

Hematocrit greater than ____ can lead to hypoxia

A

> 60%

66
Q

Primary Absolute Polycythemia (Polycythemia Vera)

A

pathologic - occurs irrespective of body’s needs
increase in RBCs, Hgb, Hct, WBCs, platelets
treat with periodic phlebotomy

67
Q

Complications of Polycythemia Vera

A

increased blood viscosity
Thromboembolism
Hemorrhage

68
Q

Secondary Absolute Polycythemia

A

physiologic increase in erythropoietin level
frequently a compensatory response to hypoxia
seen in high altitudes, chronic heart or lung dx, smoking

69
Q

Infectious Mononucleosis

A

caused by Epstein Barr virus
“kissing disease”
leukocytosis (EBV attaches to B cells)

70
Q

Clinical Manifestations of Mono

A

prodromal period precedes occurence
fever
pharyngitis (palatal petechia)
lymphadenopathy

71
Q

Complications of Mono

A

Hepatitis

Splenomegaly (concern for rupture)

72
Q

Monospot

A

detects EBV antibodies

can have false negative if done too early

73
Q

Serologic tests for Mono

A

detects rise in IgG and IgE - occurs early

Adv Pathophysiology (22 decks)

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