CHAPTER 1 - HEMOSTASIS PART 3 Flashcards
1
Q
Severe bleeding from loss of blood from a damaged blood vessel.
A
hemorrhage
2
Q
- hemorrhage Types:
A
a. Localized
b. Generalized
c. Congenital
d. Von Willebrand Disorder
e. Vitamin K Deficiency
3
Q
bleeding from a single location
A
Localized
4
Q
bleeding from multiple sites; often spontaneous, sometimes recurring
A
Generalized
5
Q
Ex. Dengue (low platelet)
A
Generalized
6
Q
- Mucocutaneous aka
A
Systemic haemorrhage
7
Q
Mucocutaneous includes:
A
Petechiae
Purpura
Ecchymoses
8
Q
: pinpoint hemorrhage
A
Petechiae
9
Q
: purple lesions
A
Purpura
10
Q
: bruises greater than 1 cm
A
Ecchymoses
11
Q
all are due to trauma
A
Mucocutaneous
12
Q
failure in primary hemostasis (blood vessels and platelets)
A
Mucocutaneous
13
Q
failure in the secondary hemostasis entire body
A
Anatomic
14
Q
lack in 1 Cf may lead to clotting problems over the entire body
A
Anatomic
15
Q
since birth
A
с. Congenital
16
Q
due to qualitative disorders of blood cell and
blood vessels
A
с. Congenital
17
Q
very vital in forming coagulation factor
A
e. Vitamin K Deficiency
18
Q
Factor II, VII, IX, X will not be produced if this is absent
A
e. Vitamin K Deficiency
19
Q
VASCULAR DISORDERS
A
20
Q
- Hereditary Hemorrhagic Telangiectasia aka
A
“Osler-Weber-Rendu” Disease
21
Q
- Hereditary Hemorrhagic Telangiectasia
-Cause:
A
Genetic mutations in the genes
22
Q
-Autosomal dominant inheritance
A
- Hereditary Hemorrhagic Telangiectasia
23
Q
- Hereditary Hemorrhagic Telangiectasia
-Characterized by:
A
thin walled, disorganized, and dilated BV with discontinuous endothelium= red pinpoint lesions.
24
Q
- Hereditary Hemorrhagic Telangiectasia
-Laboratory tests:
A
Bleeding time, platelet function test, CFT and CT are all NORMAL
25
2. Congenital Hemangiomata (Kasabach-Meritt Syndrome)
-Cause:
Protruding tumors composed of blood vessels that swells and bleed.
26
-Indicative of diffuse DIC
2. Congenital Hemangiomata (Kasabach-Meritt Syndrome)
27
3. Other Vasculopathies and their pathophysiology
A. Multiple Myeloma
B. Systemic Amyloidosis
C. Moyamoya Disease
28
: Light chain immunoglobulin crystalline deposits in the BV
A. Multiple Myeloma
29
: Amyloid protein with light chain Ig deposits in the BV
B. Systemic Amyloidosis
30
: Blockage of arteries at the base of the brain
C. Moyamoya Disease
31
: Fragile arterioles
D. Cerebral small Disease
32
: inflamed blood vessels.
VASCULITIS
33
VASCULITIS
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
2. Cryoglobulinemia
34
-Seen in SLE and Wegener's Granulomatosis.
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
35
- associated with cryoglobulin immune deposits.
2. Cryoglobulinemia
36
- seen in Waldenstrom's primary macroglobulinemia
2. Cryoglobulinemia
37
- PIt count is normal, plt adhesiveness is abnormal, FVIll is low.
2. Cryoglobulinemia
38
3. Hypergammaglobulinemic Purpura
- characterized by
polyclonal hypergammaglobulinemia
39
3. Hypergammaglobulinemic Purpura- seen in
Sjorgen's syndrome and SLE, even in Hepatitis C
40
- Triggers of purpura attack :
1. Prolonged walking and standing
2. alcohol consumption
3. tight-fitting clothes
41
- otherwise known as
"Purpura rheumatica/anaphylactoid purpura”
42
-occurs in children between 4-11 years old.
4. Henoch-Schonlein Purpura
43
-characterized by reddish purple spots that looks like bruises.
4. Henoch-Schonlein Purpura
44
VASCULAR OBSTRUCTION
1. Thrombus
2. Emboli
3. Other Occlusions
45
1. Thrombus COMPONENT
-Blood clot
46
2. Emboli COMPONENT
-Septic emboli
-Thromboemboli
47
3. Other Occlusions
a. Immunoglobulins
b. Plasma Proteins
c. Fibrin
d. Red blood cells
e. Platelets
f. Fats
48
1. Thrombus DISEASE CAUSED
-DIC
49
2. Emboli DISEASE CAUSED
-Endocarditis
-Atrial Fibrilation
3. Other Occlusions:
50
a. Immunoglobulins
-Waldenstrom's Primary Macroglobulinemia
51
b. Plasma Proteins
-Cryoglobulinemia
52
c. Fibrin
-Cryofibrinogenemia
53
d. Red blood cells
-Polycythemia
54
e. Platelets
-Thrombocytosis
55
-Fat emboli syndrome
f. Fats
56
-group of rare connective tissue disorders caused by collagen synthesis or processing abnormalities.
1. Ehlers-Danlos Syndrome
57
-excessive bruising and bleeding (greatest in EDS type
1. Ehlers-Danlos Syndrome Type 4
58
-prone to arterial aneurysms and dissection, significant bleeding from spontaneous rupture of medium sized abdominal arteries and intestinal rupture.
1. Ehlers-Danlos Syndrome
59
1. Ehlers-Danlos Syndrome screening test:
Skin biopsy
60
1. Ehlers-Danlos Syndrome result:
1) No hemostatic abnormality (normal plt, CF, and bleeding time) but with bleeding
2) Abnormal bone extension
61
2. Pseudoxanthoma Elasticum
-also known as
"Groenblad Strandberg Syndrome”
62
-inherited connective tissue disorder resulting from calcification and mineralization of elastic fibers.
2. Pseudoxanthoma Elasticum
63
-autosomal recessive inheritance
2. Pseudoxanthoma Elasticum
64
2. Pseudoxanthoma Elasticum -autosomal recessive inheritance (gene involved ?)
ABC-C6 gene
65
-development of narrowing arteries (arteriosclerosis) or "claudication"
2. Pseudoxanthoma Elasticum
66
narrowing arteries (?) or
arteriosclerosis
67
characterized by cramping and pain during exercise because of decreased blood flow to the arms and legs.
claudication
68
- Characterized by absence of Vitamin C
3. Scurvy
69
-Weakened collagen strands as a result of abnormal triple helical structure.
3. Scurvy
70
3. Scurvy -Predisposes patients to
capillary fragility, delayed wound healing, petechiae and purpura, oral, urinary and digestive bleeding.
71
promotes activation of procollagen to collagen
Vitamin C
72
4. Senile Purpura
-otherwise known as
"Solar purpura”
73
-commonly found on hands and forearms without any known preceding trauma
4. Senile Purpura
74
-thin skin as a result of loss of subcutaneous fat and changes in both amount and quality of
4. Senile Purpura
75
4. Senile Purpura-Hemostasis tests are
NORMAL
76
5. Purpura associated with Infections
(?) caused by microbial agents associated with (?) producing petechiae.
-direct endothelial cell damage
acute febrile illness
77
5. Purpura associated with Infections
-Bacterial toxins produce deendothelization induced by an
endotoxin
78
5. Purpura associated with Infections-commonly known diseases:
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
79
- causes by varicella zoster virus
6. Acquired purpura Fulminans
80
- caused by any gram negative bacteria
7. Acute infectious purpura fulminans
81
-can be a result of
contact dermatitis, steroid use, drug reactions or allergies
82
6. Purpura related to miscellaneous causes
-some may be observed in
Kaposi sarcoma and vascular tumors.
83
occurs in women during menstrual period
Purpura simplex
84
Purpura simplex also known as
"factitious or self-imposed purpura"
85
Purpura simplex Types:
a. Anaphylactoid purpura
b. Henoch's
c. Schonlein's
86
Promotes vasoconstriction
CONSTRICTOR
87
Dilates the blood vessels; widens the lumen; reestablishes blood flow
DILATOR
88
CONSTRICTOR
ENDOTHELIN-I
ANGIOTENSIN-I
PROSTAGLANDIN
89
DILATOR
PROSTACYCLIN
NITRIC OXIDE
ENDOTHELIUM DERIVED RELAXING FACTOR (EDFR)
90
: blood vessel disorders
VASCULAR DISORDER
91
very vital in forming coagulation factor
Vitamin K
92
will not be produced if Vitamin K is absent
Factor II, VII, IX, X
93
- Genetic disorder
1. Hereditary Hemorrhagic Telangiectasia
94
- Autosomal dominant: needs at least 2 dominant genes from the parents to manifest (Ex. AA cannot manifest the disease since it is recessive)
1. Hereditary Hemorrhagic Telangiectasia
95
- cause: reduced amount of functional protein in the tissue lining of the bv
1. Hereditary Hemorrhagic Telangiectasia
96
- endothelium lacks protein due to the genetic mutation in the following genes:
1. ENG gene (TYPE 1 HHT)
2. ACVRL gene (TYPE 2 HHT)
3. SMAD 4 (JUVENILLE TYPE)
4. Unknown (TYPE III HHT)
97
– growing but not maturing to that kind of disease or not progressive)
3. SMAD 4 (JUVENILLE TYPE)
98
When these genes mutate in the body, it causes proteins to not form in the endothelium
1. Hereditary Hemorrhagic Telangiectasia
99
protein contributes to the integrity of the blood vessels
1. Hereditary Hemorrhagic Telangiectasia
100
one of the most important proteins: tissue factor, collagen
1. Hereditary Hemorrhagic Telangiectasia
101
characterized by thin-walled, disorganized and dilated blood vessels (due to absence of protein in the endothelium)
1. Hereditary Hemorrhagic Telangiectasia
102
Laboratory findings: Bleeding time, platelet function tests, Capillary Fragility test and coagulation tests are all normal
1. Hereditary Hemorrhagic Telangiectasia
103
(no problem on platelet, coagulation factor, but bleeding is due to the problem in the endothelial lining)
1. Hereditary Hemorrhagic Telangiectasia
104
Small widened blood vessels (like ruptured/varicose veins)
telangiectasias?
105
Exhibit petechiae formation in the mouth
telangiectasias?
106
Epistaxis (prolonged bleeding due to endothelium)
telangiectasias?
107
Disorders associated with tumors composed of many entangled blood vessels.
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
108
Tumor composed of blood vessels that commonly swell and bleed
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
109
Formation of fibrin clots, platelet consumption and red cell destruction secondary to vascular obstruction occur at the site of tumor
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
110
indicative of diffuse DIC (disseminated intravascular coagulation)
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
111
Very lethal disorder
diffuse DIC (disseminated intravascular coagulation)
112
Coagulation and fibrinolysis happens at the same time
diffuse DIC (disseminated intravascular coagulation)
113
tumor protrudes from the skin surface
diffuse DIC (disseminated intravascular coagulation)
114
affects infants/babies
diffuse DIC (disseminated intravascular coagulation)
115
aka Hemangiomata with thrombocytopenia/Hemangioma thrombocytopenia syndrome
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
116
swollen blood vessel will clot the blood inside while the platelets are being consumed resulting to thrombocytopenia
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
117
congenital: dangerous when operating a baby but removing the tumor is possible to repair the bv
2. Congenital Hemangiomata (Kasabach-Merritt Syndrome)
118
3. Other Vasculopathies
119
Light chain immunoglobulin crystalline deposits in the BV
Multiple Myeloma
120
Production of abnormally large plasma cells that produces many light chains that deposits in the bv, causing fragile vessels
Multiple Myeloma
121
Portion of the Ab is attacking the blood vessel
Multiple Myeloma
122
Main problem: production of abnormal plasma cells
Multiple Myeloma
123
Side effect: vasculopathy or deposition of light chain Ig in the bv
Multiple Myeloma
124
Even minor trauma causes bleeding to the vessels
Multiple Myeloma
125
Most specific type of vasculitis: Necrotizing vasculitis (cell damage and death) – w/o marker
Multiple Myeloma
126
caused by light chain Ig deposition
Multiple Myeloma
127
Amyloid protein with light chain Ig deposits in the BV
Systemic Amyloidosis
128
Systemic Amyloidosis TYPES:
129
AL-Amyloidosis
1o Systemic Amyloidosis
130
amyloid + ligh chain Ig
1o Systemic Amyloidosis
131
concerns the skin purpura and skin blisters without co-existing disease
1o Systemic Amyloidosis
132
more on skin than organ involvement
1o Systemic Amyloidosis
133
coexisting w/ infection or inflammation
2o Systemic Amyloidosis
134
amyloid protein and light chain both deposits in the blood vessel
2o Systemic Amyloidosis
135
no skin; more on organ involvement
2o Systemic Amyloidosis
136
amyloidosis iseasily diagnosed using
congo red
137
congo red (also stains smear - w/ high affinity to amyloid proteins - color is)
yellow bifringence
138
Blockage of arteries at the base of the brain
Moyamoya Disease
139
main artery in the brain delivers oxygen is blocked
Moyamoya Disease
140
smaller arteries entangle w/ each other to compensate for oxygen
Moyamoya Disease
141
entangled bv: “puff of smoke”
Moyamoya Disease
142
cause of blockage: due to clot or emboli - may cause intracranial haemorrhage or brain infarcts
Moyamoya Disease
143
Fragile arteries
Cerebral Small Disease
144
arterioles are so fragile that they tend to burst
Cerebral Small Disease
145
may suffer from recurrent stroke, mini stroke, cognitive impairment
Cerebral Small Disease
146
cause: fragile arterioles
Cerebral Small Disease
147
MRI (white portion): deprived of oxygen
Cerebral Small Disease
148
- inflamed blood vessels; complement system is activated
Vasculitis
149
VASCULITIS
150
neutrophil is dying since ANCA attacks the body’s own neutrophil
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
151
Ig autoantibody
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
152
attacks the cytoplasm or or the granule of the neutrophil
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
153
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
TYPES:
pANCA
cANCA:
154
pANCA: - targets the
primary granule (myeloperoxidase)
155
cANCA: - targets
proteinase 3 (enzyme found in the tertiary granule of the neutrophil) and cytoplasm
156
WBC is found inside the bv
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
157
marker of primary necrotizing vasculitis
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA)
158
1. Antineutrophilic Cytoplasmic Antibody Positive (ANCA) - Seen in
Systemic Lupus Erythematosus and Wegener's Granulomatosis
159
2. Cryoglobulinemia - seen in
Waldenstrom's Primary Macroglobulinemi a
160
3. Hypergammaglob ulinemic Purpura – seen in
Sjorgen's syndrome and SLE, even in Hepatitis C
161
4. HenochSchonlein Purpura - aka
IgA Vasculitis or Anaphylactic vasculitis
162
associated with deposited cryoglobulin
2. Cryoglobulinemia
163
cryoglobulin : protein that precipitates in cold temperature
2. Cryoglobulinemia
164
precipitated protein looks like a soliinsoluble pack in a test tube
2. Cryoglobulinemia
165
hypothermic temp will allow cryoglobulin to precipitate, obstructing the blood vessel
2. Cryoglobulinemia
166
causes: infarcts, ischemia
2. Cryoglobulinemia
167
plt count is normal; plt adhesiveness is abnormal (ptl cannot adhere to a precipitated protein); FVIII is low and will just precipitate
2. Cryoglobulinemia
168
blood is hyperviscous
2. Cryoglobulinemia
169
with many petechiae and purpura
2. Cryoglobulinemia
170
characterized by polyclonal hypergammaglobulinemia
3. Hypergammaglob ulinemic Purpura
171
increased IgG
3. Hypergammaglob ulinemic Purpura
172
once triggered it may lead to purpura attack
3. Hypergammaglob ulinemic Purpura
173
can be very reactive – bv are prone to it
3. Hypergammaglob ulinemic Purpura
174
Triggers of purpura attack:
1. Prolonged walking and standing
2. alcohol consumption
3. tight-fitting clothes
175
otherwise known as "Purpura rheumatica/anaphylactoid purpura”
4. HenochSchonlein Purpura
176
IgA Vasculitis or Anaphylactic vasculitis
4. HenochSchonlein Purpura
177
Targets OF Anaphylactic vasculitis:
GIT, kidney, skin, lungs, CNS
178
occurs in children between 4-11 years old.
4. HenochSchonlein Purpura
179
characterized by reddish purple spots that looks like bruises
4. HenochSchonlein Purpura
180
: causes abdominal haemorrhage (more common on the GIT)
Henoch
181
: causes joint (wrist, ankle) cavities haemorrhage
Schoenlein
182
Cause: IgA deposition causing vasculitis
4. HenochSchonlein Purpura
183
TYPES OF VASCULAR OBSTRUCTION
184
Thrombus • Composition:
1) platelets
2) rbc,
3) fibrin
185
• clot attached to many constituents
Thrombus
186
• clot attached to many constituents that travels
Emboli
187
• travels down to the blood vessel that block the blood flow
Emboli
188
• does not particularly creates a clot but accumulates to be a block
Other Occlusions
189
• may accumulate and cause obstruction
Other Occlusions
190
may accumulate and deposit in the bv causing fragility
a. Immunoglobulins
191
• may form a plaque causing an obstruction
a. Immunoglobulins
192
• precipitates when exposed to low temp
b. Plasma Proteins
c. Fibrin
193
• viscous blood when many
Red blood cells
194
• hyperviscosity may harden the rbcs as cells not as clot
Red blood cells
195
• may be occluded when many
Platelets
196
• clot attached to a fat
Fats
197
• abnormal blood clot is seen
DIC
198
• DIC complications:
1) excessive clot formation or thrombosis
2) hemolysis
3) fibrinolysis
199
•: infected clot/abscessed embolism
Septic emboli
200
• a pure clot that travels
Thromboemboli
201
• Thrombus that travels
Thromboemboli
202
• may travel to endocardium leading to endocarditis
Endocarditis
203
• messes the bv of the heart
Atrial Fibrilation
204
• irregular rhythm of the heart
Atrial Fibrilation
205
• dangerous when hypothermic
Cryoglobulinemia
Cryofibrinogenemia
206
Group of rare connective tissue disorders caused by abnormalities in collagen synthesis
DISORDERS OF PERIVASCULAR TISSUES
Hereditary Connective Tissue Defects
207
– absence of collagen leads to bleeding
Ehlers-Danlos Syndrome
Vitamin C Deficiency (Scurvy)
208
- excessive bruising and bleeding
1. Ehlers-Danlos Syndrome
209
- greatest in TYPE 4 EHLERDANLOS/VASCULAR; (may be bone, skin, elastic tissues, blood vessels
1. Ehlers-Danlos Syndrome
210
- prone to arterial aneurysms and dissection
1. Ehlers-Danlos Syndrome
211
- problem in the skin also affects the surrounding tissues, hence affecting the entire vascular system
1. Ehlers-Danlos Syndrome
212
- significant bleeding from spontaneous rupture of medium sized abdominal arteries and intestinal rupture
1. Ehlers-Danlos Syndrome
213
- problem on quantitative or qualitative collagen production defect
1. Ehlers-Danlos Syndrome
214
- collagen is imp in platelet activation affecting hemostasis and perivascular tissues
1. Ehlers-Danlos Syndrome
215
1. Ehlers-Danlos Syndrome
- Screening test:
Skin biopsy
216
- to examine elasticity (too stretchy is abnormal)
Skin biopsy
217
1. Ehlers-Danlos Syndrome
- Result:
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
- inherited connective tissue disorder resulting from calcification and mineralization of elastic fiber
2. Pseudoxanthoma elasticum
219
- attached to zinc or copper
2. Pseudoxanthoma elasticum
220
- autosomal recessive inheritance (abnormal 2 recessive genes)
2. Pseudoxanthoma elasticum
221
- gene involved : [?] to produce [?] protein is a vehicle contributing to the release of [?] from the cell and not use it
ABC-C6 gene
MRP6
ATP
222
is done outside the cell and used to form pyrophosphate from phosphate
- ATP
223
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
- Pyrophosphate
224
- development of narrowing arteries (arteriosclerosis) or "claudication", characterized by cramping and pain during exercise because of decreased blood flow to the arms and legs
2. Pseudoxanthoma elasticum
225
: fat emboli; artery blocked byb fat
- Athros
226
: narrowing of artery
- Arterios
227
- Characterized by absence of Vitamin C
3. Vitamin C Deficiency (Scurvy)
228
- promotes activation of procollagen (zymogen; inactivated) to collagen
3. Vitamin C Deficiency (Scurvy)
229
- Weakened collagen strands as a result of abnormal triple helical structure.
3. Vitamin C Deficiency (Scurvy)
230
3. Vitamin C Deficiency (Scurvy)
- Predisposes patients to
1) capillary fragility, 2) delayed wound healing, 3) petechiae and 4) purpura, and 5) bleeding (oral, urinary and digestive)
231
–predisposed to more thrombosis than bleeding (they are anemic; wound healing is slow; other processing of the body is delayed)
4. Senile Purpura
232
- common in elders
4. Senile Purpura
233
- commonly found on hands and forearms without any known preceding trauma
4. Senile Purpura
234
- 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)
4. Senile Purpura
235
- Hemostasis tests are normal
4. Senile Purpura
236
• Direct endothelial cell damage caused by microbial agents associated with febrile illness producing petechiae
5. Pupura associated with infections
237
• commonly known diseases:
1. Rickettsial disease
2. Brazilian purpura fever
3. Rat bite fever
4. Vibrio vulnificus infection
5. Strongyloides
238
- causes by varicella zoster virus
6. Acquired purpura Fulminans
239
- caused by any gram negative bacteria
7. Acute infectious purpura fulminans
240
• bacterial toxins produce deendothelization induced by
endotoxin
241
• can be a result of contact dermatitis, steroid use, drug reactions or allergies
6. Purpura related to miscellaneous causes
242
• some may be observed in Kaposi sarcoma and vascular tumors.
6. Purpura related to miscellaneous causes
243
occurs in women during menstrual period.
Purpura simplex
244
Purpura simplex
• Also known as "factious or self-imposed purpura"
245
Purpura related to miscellaneous causes Types:
a. Anaphylactoid purpura
b. Henoch's
c. Schonlein's
246
• Sex-linked
Ehlers-Danlos Syndrome
247
Caused by a defect in peptidase enzyme that converts procollagen to collagen
Ehlers-Danlos Syndrome
248
• Characterized by hyperextensive joints and hyperplastic skin
Ehlers-Danlos Syndrome
249
• Laboratory findings: Normal Coagulation test and platelet function studies
Ehlers-Danlos Syndrome
250
Autosomal recessive
Pseudoxanthoma elasticum
251
Characterized by calcified and structurally abnormal elastic fibers
Pseudoxanthoma elasticum
252
for the formation of the intact structure of the vascular basement membrane
vitamin C
253
• Characterized by gingival bleeding
Vitamin C Deficiency (Scurvy)
254
hemorrhage into subcutaneous tissues and muscles
Vitamin C Deficiency (Scurvy)
255
Large hemorrhagic areas may develop just below the eyes
Vitamin C Deficiency (Scurvy)
256
splinter-like hemorrhage may also appear in the fingernail beds
Vitamin C Deficiency (Scurvy)
257
splinter-like hemorrhage may also appear in the fingernail beds
Vitamin C Deficiency (Scurvy)
258
Laboratory findings: CFT= usually positive
Vitamin C Deficiency (Scurvy)
259
Related with normal aging process
Senile Purpura
260
• Laboratory findings: CFT= positive; Bleeding time= normal or only slightly prolonged
Senile Purpura
261
• Deposition of glycosylated proteins leading to thickening of capillary basement membrane affecting often the capillaries of the renal glomeruli and retina
Diabetes Mellitus
262
• Excessive amyloid deposit in small vessels
Amyloidosis
263
Autoimmune Vascular Purpura types
a. Drug Induced Purpura
b. Allergic purpura/Anaphylactoid purpura
264
• associated with certain foods and drugs, cold temperature, insect bites and vaccinations.
b. Allergic purpura/Anaphylactoid purpura
265
• Henoch's Purpura = associated with
abdominal pain secondary to GIT hemorrhaging
266
• Schonlein's Purpura = associated with
joint, especially in the knees, ankles and wrists
267
• Common drugs that induce purpura: sulfonamides & iodides quinine, procaine, penicillin, aspirin, sedatives, coumarin
Drug Induced Purpura
268
• May be due to development of antibodies to vessel wall components, development of immune complexes, and changes in vessel wall permeability.
Drug Induced Purpura
269
• Associated with bacterial; viral, Rickettsial and protozoal infections.
Infectious Purpura
