QUANTITATIVE Flashcards

1
Q

Aspirin and NSAIDs - Aspirin

A

acetylate the cyclooxygenase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

add one compound to the enzyme making it non functional

A

acetylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cyclooxygenase enzyme secretes

A

Thromboxane and Prostaglandin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CoX 2 inhibitor

A

Naproxen and Ibuprofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ticlopidine and Clopidogrel

A

Antiplatelet medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

prevent blood clots inside the blood vessel by preventing plt aggregation

A

Antiplatelet medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

prevent blood clots inside the blood vessel by preventing plt aggregation

A

Antiplatelet medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

administered to enhance fibrinolysis

A

Dextran

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

SIGNIFICANT PLT COUNT AND INTERPRETATION

A

Significant plt levels (plt count and clinical manifestation) ● <100,000/ul - abnormally low
● 30,000-50,000/ul- bleeding possible
● <30,000- spontaneous bleeding
● <5,000/ul- severe spontaneous bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Thrombocytopenia

A

possible bleeding anytime for the patient
● Decreased in circulating platelet
● Less than 100,000/uL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Thrombocytosis

A

significant with other manifestations
● Hall Mark for myeloproliferative diseases
● Increase in circulating plt
● More than 450,000/uL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

THROMBOCYTOPENIA

A
  1. Decrease production
  2. Blood transfusion
  3. Increased destruction/consumption
  4. Splenic sequestration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • Large platelet, dohle like bodies (20 um)
  • Mutation in MYH9 gene: encodes for the myosin heavy chain: which affects plt activation
A

MAY HEGGLIN ANOMALY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • Large platelet, dohle like bodies (20 um)
  • Mutation in MYH9 gene: encodes for the myosin heavy chain: which affects plt activation
A

MAY HEGGLIN ANOMALY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • Absence/ hypoplasia in radial bones
A

TAR SYNDROME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • Bone and visceral organ abnormalities
  • pancytopenia
  • Neonates
A

FANCONI ANEMIA

17
Q
  • Small platelets
  • Absence of megakaryocytes
    (chlorthiazide, tolbutamide)
  • directly affect the fetal BM megakaryocyte
  • 72 hours of birth : mothers pregnancy or baby’s delivery was exposed to TORCH infection
  • TORCH- Toxoplasma Rubella CMV HIV-HERPES
  • There is a case that the megakaryocyte is absent
A

NEONATAL THROMBOCYTOPENIA

18
Q

Low plt

19
Q
  • Dense granules
  • Small plt
A

WISKOTT ALDRICH

20
Q

for HIV treatment

A

Zidovudine

21
Q

treatment for thrombocytosis:

A

Anagrelide

22
Q

long term consumption of ethanol will be subjected to thrombocytopenia.

23
Q

restoring plts due to chemotherapy to stimulate BM to reproduce more megakaryocyte.

A

Recombinant IL2

24
Q

Donor

A

lost of platelet containing blood product

25
Recipient
May have alloantibodies directed against the antigens of blood products
26
TTP- thrombotic thrombocytopenic purpura
Deficiency disintegrate + ADAMTS 13- gene that produces enzyme that controls vWF (uncontrolled very large)
27
Disease TRIAD: MHA thrombocytopenia and neurologic abnormality Moschowitz syndrome
TTP- thrombotic thrombocytopenic purpura
28
DIC- Disseminated intravascular coagulation
Plt are trapped in fibrin clotsbecause of simultaneous coagulation
29
DIC- Disseminated intravascular coagulation
Acute onset with plt consumption, Factor V,VIII and fibrinogen reduced level Life threatening
30
-vWF involvement
HUS- Hemolytic uremic syndrome
31
- No apparent cause - Presence of anti-platelet AB (IgG) - Anti-plt antibodies destroys GpIIbIIIa - Remove to the circulation by the reticuloendothelial cells
ITP - idiopathic thrombocytopenic purpura renamed to immune TP
32
HIT- Heparin Induced thrombocytopenia
- Develops IgG antibody specific for heparin plt factor 4 complex - Due to unfractioned heparin administration - Heparin helps plt factor IV for aggregation
33
Acute: 1-3 weeks infection from mumps, chicken pox, measles (viral infection) Ag binds to AB = immune complex- plt GpIIBIIIa abrupt onset, usually on children.
Characterized by bruising, petechiae and epistaxis
34
Chronic: any age onset
Characterized by: menorrhagia, epistaxis and bruising
35
Splenic sequestration
- ⅓ of plt sequestered on spleen
36
true thrombocytosis - Has unregulated plt production and has variable size - More than 450,000/uL - Hallmark of myeloproliferative disorders : polycythemia Vera, chronic myelofibrosis. (Can exceed 1M/uL or go as High as 2M/uL - Essential thrombocythemia
Primary thrombocytosis
37
true thrombocytosis - Has unregulated plt production and has variable size - More than 450,000/uL - Hallmark of myeloproliferative disorders : polycythemia Vera, chronic myelofibrosis. (Can exceed 1M/uL or go as High as 2M/uL - Essential thrombocythemia
Primary thrombocytosis
38
Compensate the loss plt due to trauma - Does not exceed 800,000/uL - Secondary to inflammation and trauma (childbirth, splenectomy,IDA) - Betterment of body - Normal plt morphology - Variable sizes - Plt function normally because they could respond to normal stimuli or regulatory stimuli.
Secondary/ Reactive thrombocytosis