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Hematology 2 Lec > CHAPTER 1 - HEMOSTASIS PART 3 > Flashcards

CHAPTER 1 - HEMOSTASIS PART 3 Flashcards

1
Q

Severe bleeding from loss of blood from a damaged blood vessel.

A

hemorrhage

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2
Q
  • hemorrhage Types:
A

a. Localized
b. Generalized
c. Congenital
d. Von Willebrand Disorder
e. Vitamin K Deficiency

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3
Q

bleeding from a single location

A

Localized

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4
Q

bleeding from multiple sites; often spontaneous, sometimes recurring

A

Generalized

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5
Q

Ex. Dengue (low platelet)

A

Generalized

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6
Q
  1. Mucocutaneous aka
A

Systemic haemorrhage

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7
Q

Mucocutaneous includes:

A

Petechiae
Purpura
Ecchymoses

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8
Q

: pinpoint hemorrhage

A

Petechiae

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9
Q

: purple lesions

A

Purpura

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10
Q

: bruises greater than 1 cm

A

Ecchymoses

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11
Q

all are due to trauma

A

Mucocutaneous

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12
Q

failure in primary hemostasis (blood vessels and platelets)

A

Mucocutaneous

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13
Q

failure in the secondary hemostasis entire body

A

Anatomic

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14
Q

lack in 1 Cf may lead to clotting problems over the entire body

A

Anatomic

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15
Q

since birth

A

с. Congenital

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16
Q

due to qualitative disorders of blood cell and
blood vessels

A

с. Congenital

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17
Q

very vital in forming coagulation factor

A

e. Vitamin K Deficiency

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18
Q

Factor II, VII, IX, X will not be produced if this is absent

A

e. Vitamin K Deficiency

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19
Q

VASCULAR DISORDERS

A
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20
Q
  1. Hereditary Hemorrhagic Telangiectasia aka
A

“Osler-Weber-Rendu” Disease

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21
Q
  1. Hereditary Hemorrhagic Telangiectasia

-Cause:

A

Genetic mutations in the genes

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22
Q

-Autosomal dominant inheritance

A
  1. Hereditary Hemorrhagic Telangiectasia
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23
Q
  1. Hereditary Hemorrhagic Telangiectasia
    -Characterized by:
A

thin walled, disorganized, and dilated BV with discontinuous endothelium= red pinpoint lesions.

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24
Q
  1. Hereditary Hemorrhagic Telangiectasia
    -Laboratory tests:
A

Bleeding time, platelet function test, CFT and CT are all NORMAL

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25
Q
  1. Congenital Hemangiomata (Kasabach-Meritt Syndrome)
    -Cause:
A

Protruding tumors composed of blood vessels that swells and bleed.

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26
Q

-Indicative of diffuse DIC

A
  1. Congenital Hemangiomata (Kasabach-Meritt Syndrome)
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27
Q
  1. Other Vasculopathies and their pathophysiology
A

A. Multiple Myeloma
B. Systemic Amyloidosis
C. Moyamoya Disease

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28
Q

: Light chain immunoglobulin crystalline deposits in the BV

A

A. Multiple Myeloma

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29
Q

: Amyloid protein with light chain Ig deposits in the BV

A

B. Systemic Amyloidosis

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30
Q

: Blockage of arteries at the base of the brain

A

C. Moyamoya Disease

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31
Q

: Fragile arterioles

A

D. Cerebral small Disease

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32
Q

: inflamed blood vessels.

A

VASCULITIS

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33
Q

VASCULITIS

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
  2. Cryoglobulinemia
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34
Q

-Seen in SLE and Wegener’s Granulomatosis.

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
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35
Q
  • associated with cryoglobulin immune deposits.
A
  1. Cryoglobulinemia
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36
Q
  • seen in Waldenstrom’s primary macroglobulinemia
A
  1. Cryoglobulinemia
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37
Q
  • PIt count is normal, plt adhesiveness is abnormal, FVIll is low.
A
  1. Cryoglobulinemia
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38
Q
  1. Hypergammaglobulinemic Purpura
    - characterized by
A

polyclonal hypergammaglobulinemia

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39
Q
  1. Hypergammaglobulinemic Purpura- seen in
A

Sjorgen’s syndrome and SLE, even in Hepatitis C

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40
Q
  • Triggers of purpura attack :
A
  1. Prolonged walking and standing
  2. alcohol consumption
  3. tight-fitting clothes
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41
Q
  • otherwise known as
A

“Purpura rheumatica/anaphylactoid purpura”

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42
Q

-occurs in children between 4-11 years old.

A
  1. Henoch-Schonlein Purpura
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43
Q

-characterized by reddish purple spots that looks like bruises.

A
  1. Henoch-Schonlein Purpura
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44
Q

VASCULAR OBSTRUCTION

A
  1. Thrombus
  2. Emboli
  3. Other Occlusions
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45
Q
  1. Thrombus COMPONENT
A

-Blood clot

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46
Q
  1. Emboli COMPONENT
A

-Septic emboli
-Thromboemboli

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47
Q
  1. Other Occlusions
A

a. Immunoglobulins
b. Plasma Proteins
c. Fibrin
d. Red blood cells
e. Platelets
f. Fats

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48
Q
  1. Thrombus DISEASE CAUSED
A

-DIC

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49
Q
  1. Emboli DISEASE CAUSED
A

-Endocarditis
-Atrial Fibrilation
3. Other Occlusions:

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50
Q

a. Immunoglobulins

A

-Waldenstrom’s Primary Macroglobulinemia

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51
Q

b. Plasma Proteins

A

-Cryoglobulinemia

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52
Q

c. Fibrin

A

-Cryofibrinogenemia

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53
Q

d. Red blood cells

A

-Polycythemia

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54
Q

e. Platelets

A

-Thrombocytosis

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55
Q

-Fat emboli syndrome

A

f. Fats

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56
Q

-group of rare connective tissue disorders caused by collagen synthesis or processing abnormalities.

A
  1. Ehlers-Danlos Syndrome
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57
Q

-excessive bruising and bleeding (greatest in EDS type

A
  1. Ehlers-Danlos Syndrome Type 4
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58
Q

-prone to arterial aneurysms and dissection, significant bleeding from spontaneous rupture of medium sized abdominal arteries and intestinal rupture.

A
  1. Ehlers-Danlos Syndrome
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59
Q
  1. Ehlers-Danlos Syndrome screening test:
A

Skin biopsy

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60
Q
  1. Ehlers-Danlos Syndrome result:
A

1) No hemostatic abnormality (normal plt, CF, and bleeding time) but with bleeding
2) Abnormal bone extension

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61
Q
  1. Pseudoxanthoma Elasticum
    -also known as
A

“Groenblad Strandberg Syndrome”

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62
Q

-inherited connective tissue disorder resulting from calcification and mineralization of elastic fibers.

A
  1. Pseudoxanthoma Elasticum
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63
Q

-autosomal recessive inheritance

A
  1. Pseudoxanthoma Elasticum
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64
Q
  1. Pseudoxanthoma Elasticum -autosomal recessive inheritance (gene involved ?)
A

ABC-C6 gene

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65
Q

-development of narrowing arteries (arteriosclerosis) or “claudication”

A
  1. Pseudoxanthoma Elasticum
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66
Q

narrowing arteries (?) or

A

arteriosclerosis

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67
Q

characterized by cramping and pain during exercise because of decreased blood flow to the arms and legs.

A

claudication

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68
Q
  • Characterized by absence of Vitamin C
A
  1. Scurvy
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69
Q

-Weakened collagen strands as a result of abnormal triple helical structure.

A
  1. Scurvy
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70
Q
  1. Scurvy -Predisposes patients to
A

capillary fragility, delayed wound healing, petechiae and purpura, oral, urinary and digestive bleeding.

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71
Q

promotes activation of procollagen to collagen

A

Vitamin C

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72
Q
  1. Senile Purpura
    -otherwise known as
A

“Solar purpura”

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73
Q

-commonly found on hands and forearms without any known preceding trauma

A
  1. Senile Purpura
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74
Q

-thin skin as a result of loss of subcutaneous fat and changes in both amount and quality of

A
  1. Senile Purpura
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75
Q
  1. Senile Purpura-Hemostasis tests are
A

NORMAL

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76
Q
  1. Purpura associated with Infections

(?) caused by microbial agents associated with (?) producing petechiae.

A

-direct endothelial cell damage

acute febrile illness

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77
Q
  1. Purpura associated with Infections

-Bacterial toxins produce deendothelization induced by an

A

endotoxin

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78
Q
  1. Purpura associated with Infections-commonly known diseases:
A
  1. Rickettsial disease
  2. Brazilian purpura fever
  3. Rat bite fever
  4. Vibrio vulnificus infection
  5. Strongyloides
  6. Acquired purpura Fulminans
  7. Acute infectious purpura fulminans
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79
Q
  • causes by varicella zoster virus
A
  1. Acquired purpura Fulminans
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80
Q
  • caused by any gram negative bacteria
A
  1. Acute infectious purpura fulminans
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81
Q

-can be a result of

A

contact dermatitis, steroid use, drug reactions or allergies

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82
Q
  1. Purpura related to miscellaneous causes
    -some may be observed in
A

Kaposi sarcoma and vascular tumors.

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83
Q

occurs in women during menstrual period

A

Purpura simplex

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84
Q

Purpura simplex also known as

A

“factitious or self-imposed purpura”

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85
Q

Purpura simplex Types:

A

a. Anaphylactoid purpura
b. Henoch’s
c. Schonlein’s

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86
Q

Promotes vasoconstriction

A

CONSTRICTOR

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87
Q

Dilates the blood vessels; widens the lumen; reestablishes blood flow

A

DILATOR

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88
Q

CONSTRICTOR

A

ENDOTHELIN-I

ANGIOTENSIN-I

PROSTAGLANDIN

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89
Q

DILATOR

A

PROSTACYCLIN

NITRIC OXIDE

ENDOTHELIUM DERIVED RELAXING FACTOR (EDFR)

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90
Q

: blood vessel disorders

A

VASCULAR DISORDER

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91
Q

very vital in forming coagulation factor

A

Vitamin K

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92
Q

will not be produced if Vitamin K is absent

A

Factor II, VII, IX, X

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93
Q
  • Genetic disorder
A
  1. Hereditary Hemorrhagic Telangiectasia
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94
Q
  • Autosomal dominant: needs at least 2 dominant genes from the parents to manifest (Ex. AA cannot manifest the disease since it is recessive)
A
  1. Hereditary Hemorrhagic Telangiectasia
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95
Q
  • cause: reduced amount of functional protein in the tissue lining of the bv
A
  1. Hereditary Hemorrhagic Telangiectasia
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96
Q
  • endothelium lacks protein due to the genetic mutation in the following genes:
A
  1. ENG gene (TYPE 1 HHT)
  2. ACVRL gene (TYPE 2 HHT)
  3. SMAD 4 (JUVENILLE TYPE)
  4. Unknown (TYPE III HHT)
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97
Q

– growing but not maturing to that kind of disease or not progressive)

A
  1. SMAD 4 (JUVENILLE TYPE)
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98
Q

When these genes mutate in the body, it causes proteins to not form in the endothelium

A
  1. Hereditary Hemorrhagic Telangiectasia
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99
Q

protein contributes to the integrity of the blood vessels

A
  1. Hereditary Hemorrhagic Telangiectasia
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100
Q

one of the most important proteins: tissue factor, collagen

A
  1. Hereditary Hemorrhagic Telangiectasia
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101
Q

characterized by thin-walled, disorganized and dilated blood vessels (due to absence of protein in the endothelium)

A
  1. Hereditary Hemorrhagic Telangiectasia
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102
Q

Laboratory findings: Bleeding time, platelet function tests, Capillary Fragility test and coagulation tests are all normal

A
  1. Hereditary Hemorrhagic Telangiectasia
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103
Q

(no problem on platelet, coagulation factor, but bleeding is due to the problem in the endothelial lining)

A
  1. Hereditary Hemorrhagic Telangiectasia
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104
Q

Small widened blood vessels (like ruptured/varicose veins)

A

telangiectasias?

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105
Q

Exhibit petechiae formation in the mouth

A

telangiectasias?

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106
Q

Epistaxis (prolonged bleeding due to endothelium)

A

telangiectasias?

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107
Q

Disorders associated with tumors composed of many entangled blood vessels.

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
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108
Q

Tumor composed of blood vessels that commonly swell and bleed

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
109
Q

Formation of fibrin clots, platelet consumption and red cell destruction secondary to vascular obstruction occur at the site of tumor

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
110
Q

indicative of diffuse DIC (disseminated intravascular coagulation)

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
111
Q

Very lethal disorder

A

diffuse DIC (disseminated intravascular coagulation)

112
Q

Coagulation and fibrinolysis happens at the same time

A

diffuse DIC (disseminated intravascular coagulation)

113
Q

tumor protrudes from the skin surface

A

diffuse DIC (disseminated intravascular coagulation)

114
Q

affects infants/babies

A

diffuse DIC (disseminated intravascular coagulation)

115
Q

aka Hemangiomata with thrombocytopenia/Hemangioma thrombocytopenia syndrome

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
116
Q

swollen blood vessel will clot the blood inside while the platelets are being consumed resulting to thrombocytopenia

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
117
Q

congenital: dangerous when operating a baby but removing the tumor is possible to repair the bv

A
  1. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
118
Q
  1. Other Vasculopathies
A
119
Q

Light chain immunoglobulin crystalline deposits in the BV

A

Multiple Myeloma

120
Q

Production of abnormally large plasma cells that produces many light chains that deposits in the bv, causing fragile vessels

A

Multiple Myeloma

121
Q

Portion of the Ab is attacking the blood vessel

A

Multiple Myeloma

122
Q

Main problem: production of abnormal plasma cells

A

Multiple Myeloma

123
Q

Side effect: vasculopathy or deposition of light chain Ig in the bv

A

Multiple Myeloma

124
Q

Even minor trauma causes bleeding to the vessels

A

Multiple Myeloma

125
Q

Most specific type of vasculitis: Necrotizing vasculitis (cell damage and death) – w/o marker

A

Multiple Myeloma

126
Q

caused by light chain Ig deposition

A

Multiple Myeloma

127
Q

Amyloid protein with light chain Ig deposits in the BV

A

Systemic Amyloidosis

128
Q

Systemic Amyloidosis TYPES:

A
129
Q

AL-Amyloidosis

A

1o Systemic Amyloidosis

130
Q

amyloid + ligh chain Ig

A

1o Systemic Amyloidosis

131
Q

concerns the skin purpura and skin blisters without co-existing disease

A

1o Systemic Amyloidosis

132
Q

more on skin than organ involvement

A

1o Systemic Amyloidosis

133
Q

coexisting w/ infection or inflammation

A

2o Systemic Amyloidosis

134
Q

amyloid protein and light chain both deposits in the blood vessel

A

2o Systemic Amyloidosis

135
Q

no skin; more on organ involvement

A

2o Systemic Amyloidosis

136
Q

amyloidosis iseasily diagnosed using

A

congo red

137
Q

congo red (also stains smear - w/ high affinity to amyloid proteins - color is)

A

yellow bifringence

138
Q

Blockage of arteries at the base of the brain

A

Moyamoya Disease

139
Q

main artery in the brain delivers oxygen is blocked

A

Moyamoya Disease

140
Q

smaller arteries entangle w/ each other to compensate for oxygen

A

Moyamoya Disease

141
Q

entangled bv: “puff of smoke”

A

Moyamoya Disease

142
Q

cause of blockage: due to clot or emboli - may cause intracranial haemorrhage or brain infarcts

A

Moyamoya Disease

143
Q

Fragile arteries

A

Cerebral Small Disease

144
Q

arterioles are so fragile that they tend to burst

A

Cerebral Small Disease

145
Q

may suffer from recurrent stroke, mini stroke, cognitive impairment

A

Cerebral Small Disease

146
Q

cause: fragile arterioles

A

Cerebral Small Disease

147
Q

MRI (white portion): deprived of oxygen

A

Cerebral Small Disease

148
Q
  • inflamed blood vessels; complement system is activated
A

Vasculitis

149
Q

VASCULITIS

A
150
Q

neutrophil is dying since ANCA attacks the body’s own neutrophil

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
151
Q

Ig autoantibody

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
152
Q

attacks the cytoplasm or or the granule of the neutrophil

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
153
Q
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
    TYPES:
A

pANCA
cANCA:

154
Q

pANCA: - targets the

A

primary granule (myeloperoxidase)

155
Q

cANCA: - targets

A

proteinase 3 (enzyme found in the tertiary granule of the neutrophil) and cytoplasm

156
Q

WBC is found inside the bv

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
157
Q

marker of primary necrotizing vasculitis

A
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
158
Q
  1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA) - Seen in
A

Systemic Lupus Erythematosus and Wegener’s Granulomatosis

159
Q
  1. Cryoglobulinemia - seen in
A

Waldenstrom’s Primary Macroglobulinemi a

160
Q
  1. Hypergammaglob ulinemic Purpura – seen in
A

Sjorgen’s syndrome and SLE, even in Hepatitis C

161
Q
  1. HenochSchonlein Purpura - aka
A

IgA Vasculitis or Anaphylactic vasculitis

162
Q

associated with deposited cryoglobulin

A
  1. Cryoglobulinemia
163
Q

cryoglobulin : protein that precipitates in cold temperature

A
  1. Cryoglobulinemia
164
Q

precipitated protein looks like a soliinsoluble pack in a test tube

A
  1. Cryoglobulinemia
165
Q

hypothermic temp will allow cryoglobulin to precipitate, obstructing the blood vessel

A
  1. Cryoglobulinemia
166
Q

causes: infarcts, ischemia

A
  1. Cryoglobulinemia
167
Q

plt count is normal; plt adhesiveness is abnormal (ptl cannot adhere to a precipitated protein); FVIII is low and will just precipitate

A
  1. Cryoglobulinemia
168
Q

blood is hyperviscous

A
  1. Cryoglobulinemia
169
Q

with many petechiae and purpura

A
  1. Cryoglobulinemia
170
Q

characterized by polyclonal hypergammaglobulinemia

A
  1. Hypergammaglob ulinemic Purpura
171
Q

increased IgG

A
  1. Hypergammaglob ulinemic Purpura
172
Q

once triggered it may lead to purpura attack

A
  1. Hypergammaglob ulinemic Purpura
173
Q

can be very reactive – bv are prone to it

A
  1. Hypergammaglob ulinemic Purpura
174
Q

Triggers of purpura attack:

A
  1. Prolonged walking and standing
  2. alcohol consumption
  3. tight-fitting clothes
175
Q

otherwise known as “Purpura rheumatica/anaphylactoid purpura”

A
  1. HenochSchonlein Purpura
176
Q

IgA Vasculitis or Anaphylactic vasculitis

A
  1. HenochSchonlein Purpura
177
Q

Targets OF Anaphylactic vasculitis:

A

GIT, kidney, skin, lungs, CNS

178
Q

occurs in children between 4-11 years old.

A
  1. HenochSchonlein Purpura
179
Q

characterized by reddish purple spots that looks like bruises

A
  1. HenochSchonlein Purpura
180
Q

: causes abdominal haemorrhage (more common on the GIT)

A

Henoch

181
Q

: causes joint (wrist, ankle) cavities haemorrhage

A

Schoenlein

182
Q

Cause: IgA deposition causing vasculitis

A
  1. HenochSchonlein Purpura
183
Q

TYPES OF VASCULAR OBSTRUCTION

A
184
Q

Thrombus • Composition:

A

1) platelets
2) rbc,
3) fibrin

185
Q

• clot attached to many constituents

A

Thrombus

186
Q

• clot attached to many constituents that travels

A

Emboli

187
Q

• travels down to the blood vessel that block the blood flow

A

Emboli

188
Q

• does not particularly creates a clot but accumulates to be a block

A

Other Occlusions

189
Q

• may accumulate and cause obstruction

A

Other Occlusions

190
Q

may accumulate and deposit in the bv causing fragility

A

a. Immunoglobulins

191
Q

• may form a plaque causing an obstruction

A

a. Immunoglobulins

192
Q

• precipitates when exposed to low temp

A

b. Plasma Proteins

c. Fibrin

193
Q

• viscous blood when many

A

Red blood cells

194
Q

• hyperviscosity may harden the rbcs as cells not as clot

A

Red blood cells

195
Q

• may be occluded when many

A

Platelets

196
Q

• clot attached to a fat

A

Fats

197
Q

• abnormal blood clot is seen

A

DIC

198
Q

• DIC complications:

A

1) excessive clot formation or thrombosis
2) hemolysis
3) fibrinolysis

199
Q

•: infected clot/abscessed embolism

A

Septic emboli

200
Q

• a pure clot that travels

A

Thromboemboli

201
Q

• Thrombus that travels

A

Thromboemboli

202
Q

• may travel to endocardium leading to endocarditis

A

Endocarditis

203
Q

• messes the bv of the heart

A

Atrial Fibrilation

204
Q

• irregular rhythm of the heart

A

Atrial Fibrilation

205
Q

• dangerous when hypothermic

A

Cryoglobulinemia

Cryofibrinogenemia

206
Q

Group of rare connective tissue disorders caused by abnormalities in collagen synthesis

A

DISORDERS OF PERIVASCULAR TISSUES

Hereditary Connective Tissue Defects

207
Q

– absence of collagen leads to bleeding

A

Ehlers-Danlos Syndrome

Vitamin C Deficiency (Scurvy)

208
Q
  • excessive bruising and bleeding
A
  1. Ehlers-Danlos Syndrome
209
Q
  • greatest in TYPE 4 EHLERDANLOS/VASCULAR; (may be bone, skin, elastic tissues, blood vessels
A
  1. Ehlers-Danlos Syndrome
210
Q
  • prone to arterial aneurysms and dissection
A
  1. Ehlers-Danlos Syndrome
211
Q
  • problem in the skin also affects the surrounding tissues, hence affecting the entire vascular system
A
  1. Ehlers-Danlos Syndrome
212
Q
  • significant bleeding from spontaneous rupture of medium sized abdominal arteries and intestinal rupture
A
  1. Ehlers-Danlos Syndrome
213
Q
  • problem on quantitative or qualitative collagen production defect
A
  1. Ehlers-Danlos Syndrome
214
Q
  • collagen is imp in platelet activation affecting hemostasis and perivascular tissues
A
  1. Ehlers-Danlos Syndrome
215
Q
  1. Ehlers-Danlos Syndrome
    - Screening test:
A

Skin biopsy

216
Q
  • to examine elasticity (too stretchy is abnormal)
A

Skin biopsy

217
Q
  1. Ehlers-Danlos Syndrome
    - Result:
A

1) No hemostatic abnormality (normal plt, CF, and bleeding time) but with bleeding and
2) Abnormal bone extension - fragile skin affects subcutaneous tissue passing fragility to bv

218
Q
  • inherited connective tissue disorder resulting from calcification and mineralization of elastic fiber
A
  1. Pseudoxanthoma elasticum
219
Q
  • attached to zinc or copper
A
  1. Pseudoxanthoma elasticum
220
Q
  • autosomal recessive inheritance (abnormal 2 recessive genes)
A
  1. Pseudoxanthoma elasticum
221
Q
  • gene involved : [?] to produce [?] protein is a vehicle contributing to the release of [?] from the cell and not use it
A

ABC-C6 gene

MRP6

ATP

222
Q

is done outside the cell and used to form pyrophosphate from phosphate

A
  • ATP
223
Q

is a regulator of calcium (4th most abundant intracellular cation); brings the Ca inside the cell to prevent deposition in bv and skin and stop elastic fiber calcification

A
  • Pyrophosphate
224
Q
  • development of narrowing arteries (arteriosclerosis) or “claudication”, characterized by cramping and pain during exercise because of decreased blood flow to the arms and legs
A
  1. Pseudoxanthoma elasticum
225
Q

: fat emboli; artery blocked byb fat

A
  • Athros
226
Q

: narrowing of artery

A
  • Arterios
227
Q
  • Characterized by absence of Vitamin C
A
  1. Vitamin C Deficiency (Scurvy)
228
Q
  • promotes activation of procollagen (zymogen; inactivated) to collagen
A
  1. Vitamin C Deficiency (Scurvy)
229
Q
  • Weakened collagen strands as a result of abnormal triple helical structure.
A
  1. Vitamin C Deficiency (Scurvy)
230
Q
  1. Vitamin C Deficiency (Scurvy)
    - Predisposes patients to
A

1) capillary fragility, 2) delayed wound healing, 3) petechiae and 4) purpura, and 5) bleeding (oral, urinary and digestive)

231
Q

–predisposed to more thrombosis than bleeding (they are anemic; wound healing is slow; other processing of the body is delayed)

A
  1. Senile Purpura
232
Q
  • common in elders
A
  1. Senile Purpura
233
Q
  • commonly found on hands and forearms without any known preceding trauma
A
  1. Senile Purpura
234
Q
  • thin skin as a result of loss of subcutaneous fat and changes in both amount and quality of collagen (quality of collagen decreases when aging)
A
  1. Senile Purpura
235
Q
  • Hemostasis tests are normal
A
  1. Senile Purpura
236
Q

• Direct endothelial cell damage caused by microbial agents associated with febrile illness producing petechiae

A
  1. Pupura associated with infections
237
Q

• commonly known diseases:

A
  1. Rickettsial disease
  2. Brazilian purpura fever
  3. Rat bite fever
  4. Vibrio vulnificus infection
  5. Strongyloides
238
Q
  • causes by varicella zoster virus
A
  1. Acquired purpura Fulminans
239
Q
  • caused by any gram negative bacteria
A
  1. Acute infectious purpura fulminans
240
Q

• bacterial toxins produce deendothelization induced by

A

endotoxin

241
Q

• can be a result of contact dermatitis, steroid use, drug reactions or allergies

A
  1. Purpura related to miscellaneous causes
242
Q

• some may be observed in Kaposi sarcoma and vascular tumors.

A
  1. Purpura related to miscellaneous causes
243
Q

occurs in women during menstrual period.

A

Purpura simplex

244
Q

Purpura simplex

• Also known as “factious or self-imposed purpura”

A
245
Q

Purpura related to miscellaneous causes Types:

A

a. Anaphylactoid purpura
b. Henoch’s
c. Schonlein’s

246
Q

• Sex-linked

A

Ehlers-Danlos Syndrome

247
Q

Caused by a defect in peptidase enzyme that converts procollagen to collagen

A

Ehlers-Danlos Syndrome

248
Q

• Characterized by hyperextensive joints and hyperplastic skin

A

Ehlers-Danlos Syndrome

249
Q

• Laboratory findings: Normal Coagulation test and platelet function studies

A

Ehlers-Danlos Syndrome

250
Q

Autosomal recessive

A

Pseudoxanthoma elasticum

251
Q

Characterized by calcified and structurally abnormal elastic fibers

A

Pseudoxanthoma elasticum

252
Q

for the formation of the intact structure of the vascular basement membrane

A

vitamin C

253
Q

• Characterized by gingival bleeding

A

Vitamin C Deficiency (Scurvy)

254
Q

hemorrhage into subcutaneous tissues and muscles

A

Vitamin C Deficiency (Scurvy)

255
Q

Large hemorrhagic areas may develop just below the eyes

A

Vitamin C Deficiency (Scurvy)

256
Q

splinter-like hemorrhage may also appear in the fingernail beds

A

Vitamin C Deficiency (Scurvy)

257
Q

splinter-like hemorrhage may also appear in the fingernail beds

A

Vitamin C Deficiency (Scurvy)

258
Q

Laboratory findings: CFT= usually positive

A

Vitamin C Deficiency (Scurvy)

259
Q

Related with normal aging process

A

Senile Purpura

260
Q

• Laboratory findings: CFT= positive; Bleeding time= normal or only slightly prolonged

A

Senile Purpura

261
Q

• Deposition of glycosylated proteins leading to thickening of capillary basement membrane affecting often the capillaries of the renal glomeruli and retina

A

Diabetes Mellitus

262
Q

• Excessive amyloid deposit in small vessels

A

Amyloidosis

263
Q

Autoimmune Vascular Purpura types

A

a. Drug Induced Purpura

b. Allergic purpura/Anaphylactoid purpura

264
Q

• associated with certain foods and drugs, cold temperature, insect bites and vaccinations.

A

b. Allergic purpura/Anaphylactoid purpura

265
Q

• Henoch’s Purpura = associated with

A

abdominal pain secondary to GIT hemorrhaging

266
Q

• Schonlein’s Purpura = associated with

A

joint, especially in the knees, ankles and wrists

267
Q

• Common drugs that induce purpura: sulfonamides & iodides quinine, procaine, penicillin, aspirin, sedatives, coumarin

A

Drug Induced Purpura

268
Q

• May be due to development of antibodies to vessel wall components, development of immune complexes, and changes in vessel wall permeability.

A

Drug Induced Purpura

269
Q

• Associated with bacterial; viral, Rickettsial and protozoal infections.

A

Infectious Purpura

Hematology 2 Lec (29 decks)

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