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Hematologic Disorders > Anemias and Coagulation > Flashcards

Anemias and Coagulation Flashcards

1
Q

Where does the common coagulation cascade begin?

A

Factor X activation

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2
Q

What does PT measure?

A

Extrinsic + common pathway

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3
Q

What does PTT measure?

A

Intrinsic + common pathway

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4
Q

Where does the intrinsic pathway begin?

A

Factor XII

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5
Q

Where does the extrinsic pathway begin?

A

Factor VII activation by tissular factor

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6
Q

Heparin function in coagulation

A

Inhibit Xa

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7
Q

Primary hemostasis disorders are caused by _______ dysfunction

A

Platelet

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8
Q

Secondary hemostasis disorders are caused by ________ dysfunction

A

Coagulation

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9
Q

Primary hemostasis disorders manifestations

A

Mucous membrane bleeding
- Epistaxis
- Bleeding gums
- GI bleeding

Cutaneous:
- Petechiae
- Purpura
- Ecchymoses
- Easy bruising

  • Menorrhagia
  • Prolonged bleeding, but it STOPS
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10
Q

Secondary hemostasis disorders manifestations

A

Deep tissue bleeding
- Hemarthrosis
- Hematomas

Large, palpable ecchymoses
>80% male

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11
Q

Splenomegaly’s effect on platelets

A

Platelet sequestration of 90%

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12
Q

Mechanisms of failure of platelet production

A

Selective megakaryocytic depletion by drug or virus

Bone marrow failure

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13
Q

Mechanisms of increased platelet consumption (6)

A
  • ITP
  • TTP
  • UHS
  • Infections (HIV, protozoa, H.pylori, malaria)
  • Post-transfusion (10 days)
  • Drug-induced (heparin)
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14
Q

Glanzmann’s disease

A

Primary aggregation of platelet failure because of IIb/IIIA deficiency

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15
Q

Bernard-Soulier sx

A

Large platelets without GPIb and defective adhesion

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16
Q

Half-life of platelets

A

7 days

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17
Q

Anti-platelet drugs

A

Aspirin
Clopidogrel
Dipyridamole

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18
Q

Platelet and coagulation disorders that cause microangiopathic hemolytic anemia

A

DIC
TTP

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19
Q

Hemophilia A

A

Factor VIII deficiency
- Joints and soft tissue bleeding
- Painful hemarthroses and muscle hematomas
- Pressure = necrosis
- Pseudotumors

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20
Q

Abnormal test in Hemophilia A

A

PTT
Factor VIII clotting assay

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21
Q

Hemophilia B

A

Factor IX deficiency
Abnormal PTT

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22
Q

Von Willebrand Disease

A
  • Decreased platelet ADHESION
  • Premature VIII destruction
  • Type 1 is partial deficiency, most common
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23
Q

Abnormal tests in Von Willebrand’s disease

A
  • Elevated PTT
  • PFA-100
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24
Q

Vitamin K deficiency affected factors

A

II
VII
IX
X
Proteins C and S

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25
Q

Abnormal tests in vitamin K deficiency

A

Prolonged PT and PTT

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26
Q

Abnormal tests in DIC (4)

A
  • Decreased platelets
  • Decreased fibrinogen
  • Increased PT
  • Increased D-dimers
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27
Q

DIC mechanisms

A

Increased thrombin activity
+ plasmin = fibrinogen and factor depletion

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28
Q

MCV normal values

A

80-100 fL

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29
Q

Hb normal values

A

13.5 - 17.5 g/dL male
12-16 g/dL female

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30
Q

MCH normal values

A

25.4 - 34.6 pg/cell

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31
Q

Reticulocyte count normal value (%)

A

0.5 - 1.5%

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32
Q

Hematocrit normal values

A

41 - 53% males
36 - 46% females

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33
Q

Iron deficiency anemia iron values

A

Decreased:
- Serum iron
- Ferritin

Increased:
- Iron-binding capacity TIBC

34
Q

Normal iron values (serum, ferritin, binding capacity)

A

Serum iron: 10 - 30 mmol/L
Serum ferritin: 40 - 340 mg/L ; 14 - 150 mg/L
Iron-binding capacity: 40 - 70 mmol/L

35
Q

Anisocytosis

A

Size variation

36
Q

Poikilocytosis

A

Shape variation

37
Q

Iron form absorbed by enterocytes

A

Fe2+ = ferric

38
Q

Iron form in the bloodstream

A

Fe3+ = ferrous

39
Q

Platelet normal levels

A

150,000-450,000

40
Q

ITP effects

A

IgG remove platelets in 7-10 days or hours
Increase in megakaryocytes
GPIIb/IIIa or GPIb antibodies

Children post-vax or chicken pox or mono infection

41
Q

ITP treatment

A

Corticosteroids
IVIG
Immunosuppression
Rituximab
Splenectomy if <30,000

42
Q

TTP characteristics

A
  • Familial or acquired
  • Metalloprotease deficiency, breaks vWF multimers

Microvascular thrombosis = less platelets, hemolytic anemia, fever, renal, neuro, increase LDH, schistocytosis

43
Q

_____ (PT/PTT) is used as a vigilant for heparin

A

PTT

44
Q

When is PT abnormal?

Options: TTP, hemophilia A, hemophilia B, Von Willebrand disease, vit K deficiency, DIC

A
  • Vit K deficiency
  • DIC
45
Q

When is PTT abnormal

Options: TTP, hemophilia A, hemophilia B, Von Willebrand disease, vit K deficiency, DIC

A
  • Hemophilia A
  • Hemophilia B
  • Von Willebrand disease
  • Vit K deficiency
  • DIC
46
Q

In which diseases are MACROCYTES seen?

A

Liver disease
Alcoholism
Megaloblastic anemia (B12 or folate deficiency)

47
Q

In which diseases are TARGET CELLS seen?

A

Iron deficiency
Thalassemia
Liver disease
Hemoglobinopathies
Splenectomy

48
Q

In which diseases are STOMATOCYTES seen?

A

“Mouth cells”
Liver disease
Alcoholism
Hemolytic anemias

49
Q

In which diseases are PENCIL CELLS seen?

A

Iron defficiency

50
Q

In which diseases are ECHINOCYTES seen?

A

“Burr cells”
Liver disease
Splenectomy
Uremia
Pyruvate kinase deficiency

51
Q

In which diseases are SPHEROCYTES seen?

A

Hereditary
Autoimmmune hemolytic anemia
Septicemia
Blood transfusion reaction

52
Q

In which diseases are RBC FRAGMENTS seen?

A

DIC
Microangiopathy
HUS
TTP

53
Q

In which diseases are SCHISTOCYTES seen?

A

Microangiopathic hemolytic anemia
Mechanical damage

54
Q

In which diseases are DACROCYTES seen?

A

Myelofibrosis
Thalassemia
Splenomegaly

55
Q

In which diseases are SICKLE CELLS seen?

A

Sickle cell anemia
Hypoxia

56
Q

Hepcidin function

A

Inhibits Fe release from MQ and ECs

57
Q

Iron deficiency anemia clinical

A
  • Glossitis
  • Angular stomatitis
  • Koilonychia
  • Dysphagia
  • Pica
  • Irritable children
58
Q

Iron deficiency anemia causes (4)

A
  • Blood loss
  • Demand increase: infancy and adolescence, pregnancy, lactation, menstruation >80mL
  • Gluten enteropathy, gastrectomy, atrophic gastritis
  • Poor diet (rare)
59
Q

How long does it take to replenish iron storage?

A

At least 6 months
Increase 2 g/dl every 3 weeks

60
Q

Anemia of chronic disorders iron labs

A

Decreased:
- Iron
- Iron-binding capacity TIBC
- Reticulocytes

Increased:
- Ferritin

61
Q

RBC in anemia of chronic disorders

A

Normo normo

62
Q

Anemia of chronic disorders pathogenesis

A

More HEPCIDIN = less release of iron
- Ferroportin degradation
Or less RBC lifespan

NON PROGRESSIVE, relates to disease severity

63
Q

Sideroblastic anemia

A

Iron granules not randomly distributed, ringed

64
Q

Lead poisoning and anemia

A

Inhibition of heme and globin synthesis
Hypochromatic, hemolytic
Ring sideroblasts
Increased free protoporphin

65
Q

Anemias classified by size

A

Micro:
- Iron def.
- Thalassemia

Normo:
- Chronic disease
- Blood loss
- Hemolytic

Macro:
- Folate or B12 def.
- Liver disease

66
Q

Megaloblastic vs non megaloblastic anemia

A

Megaloblastic: defective DNA synthesis, hypersegmented neutrophils, B12/folate def.

Non: liver disease, hemolytic, cytotoxicity, etc.

67
Q

Labs in megaloblastic anemia

A

Decrease:
- Reticulocytes
- WBC

Increase:
- Unconjugated bilirrubin
- LDH

68
Q

Why is B12/cobalamine necessary?

A

It binds to cubilin or amnionless —> endocytosis of IF-B12 at ileum

Transcobalamins —> bone marrow

Aids in DNA synthesis

69
Q

Megaloblatic anemia clinical findings

A

Typical anemia symptoms +:
- Purpura
- Vitiligo
- Infertility
- Peripheral neuropathy
- Gastritis
- Depression, psychosis

70
Q

What is pernicious anemia?

A

Lack of B12
- Gastric atrophy
- Decreased IF
- Increased gastrin

71
Q

Folate deficiency causes

A
  • Malnutrition: chronic alcoholism
  • Malabsorption: enteropathy
  • Increased requirement: pregnancy, hemolytic anemia
  • Meds: anticonvulsants, barbiturates, sulfonamides, methotrexate, phenytoin, TMP
72
Q

Bone marrow in hemolytic anemia

A

Hyperplasic

73
Q

Lab findings in hemolytic anemia

A

Increased:
- Reticulocytes
- Serum bilirrubin
- Urine Urobilinogen
- LDH
- Cholesterol

NO serum haptoglobins

  • Hemoglobinemia
  • Hemoglobinuria
  • Hemosiderinuria
  • Methamalbuminemia
74
Q

Hereditary causes of hemolytic anemia (5)

A
  • Spherocytosis AD can’t pass through spleen
  • Elliptocytosis
  • G6P dehydrogenase def. XL = oxidative stress (asymptomatic, females with malaria resistance)
  • Glutathione def. = prickle cells, like G6P
  • Hemoglobin synthesis —> sickle cell anemia (b-globin)
75
Q

Acquired hemolytic anemia (5)

A
  • Autoimmune: keep warm to avoid
  • Alloimmune - ABO and Rh
  • Drug: penicillin, rifampicine, methyldopa
  • Others: fragmentation, march hemoglobinuria, infections, chemical, physical, secondary
  • Paroxysmal nocturnal hemoglobinura XL = less GPI
76
Q

Hemolytic anemia clinical manifestations (6)

A
  • Typical
  • Splenomegaly
  • Dark urine
  • Ankle ulcers
  • Aplastic crises - parvovirus
  • Pigment gallstones
77
Q

Sickle cell anemia crisis (4)

A
  • Vaso-occlusive: infection, acidosis, dehydration = bone infarcts with severe pain hands and feet, lung & spleen
  • Visceral: blood pooling/sequestration in chest, liver, spleen
  • Aplastic: parvovirus or folate def.
    Less reticulocytes
  • Hemolytic: increase in reticulocytes, painful
78
Q

Sickle cell clinical manifestations are typical for hemolytic anemias + ______ (7)

A
  • Lower leg ulcers = local ischemia
  • Pulmonary HTA
  • Tricuspid regurgitation
  • Retinopathy
  • Kidney papillary necrosis
  • Nocturnal enuresis
  • Osteomyelitis
79
Q

What type of hemoglobin do patients with sickle cell anemia have?

A

F

80
Q

Sickle cell anemia treatment (7)

A
  • Avoidance
  • Folic acid
  • Nutrition, vaccines, penicillin
  • Crisis: rest, warm, hydration, analgesia
  • Transfusions
  • Hydroxycarbamide increases HbF
  • Stem cell transplant

Hematologic Disorders (6 decks)

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