Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Symptoms Midterm > Platelets > Flashcards

Platelets Flashcards

1
Q

What are the major components of plats

A

Plasma membrane with lots proteins invaginated canalicular system

microtubles

Granles: alpha and dense are key

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

How do plats get around the blood and in what state?

A

Inactive state

  1. Adhesion to vessel endothelium till find a break in vessel
  2. Secreation of granules
  3. Aggretation to each other
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What tethers Platelts to collagen once plateltes stick to tear in vessel?

A

Platelet–GPIb–vWF–Collagen

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

What happens when a platelet gets activated?

A

undergoes biochemical and physical changes

You see plates squeeze all granules to center

then podocyte processes reach out to surroundings

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

What are inside our Dense or Delta plat granules?

A

ADP, ATP, Seratonin (key for vasoconstriction) and Calcuim

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

What is inside the Alpha granules

A

Fibrinogen, factor V

Thrombosponsin

*****PDGE, PF4 and TG-B which are all key in atherosclerotis pathogenesis (how clotting contributes to this disease)

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

There are receptors on the surface of platelets that once activated will induce activity of phospholipase A inside the platet… what does this result in?

A

PL-A cleaves phospholipids to arachadonic acid

this is the key precursor to prostaglandins and thromboxanes

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

Arachadoinc Acid —-> PGG2 and PGH2

A

via Cyclooxygenase (inhibted by aspirin and COX inhibitors)

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

PGG2 and PGH2—> TXA2 and TXAb

A

Via thromboxane synthase

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

What is the role of thromboxanse and where do they come from

A

from AA inside plats

fnx to make membranes fuse and dump contnets out of cell

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

What two paths does PGG2 or PGH2

A

thromboxane synthase—> to TxB2 = platelet stimulation

OR
Prostacyclin synthast –> PGI2 = Plate INHIBTION

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

How to platelets adhere to one another?

A

Plat–GPIIIa/GPIIb —–FIBRINOGEN—-GPIIIa/GPIIb—–Plat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is characteristic of Quantitative platelet disorders?

A

Decreased Platelet count

Prolongued bleeding time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is characteristic of Qualitative Plat disorders?

A

Normal plat cound

Prolounged bleed time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

von-Willebrands disease is what type of disorder?

A

Cofactor abnormality of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ehlers Danlos, Scury and Pseudoxanthoma elastiucm are all expamples of

A

Substrate abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do we see in von Willebrand Disease

(whats missing, what test confirms it, what happens to bleed time)

A

Decreased vWF acitivty and antigen

Abnormal Ristocetin aggregation

Prolongued beelding time

18
Q

What do we see in Bernar Soulie syndrome (insufficiency of GPIb)

A

normal vWF activity

Abnormal Ristocetin aggregation

Prolonged bleed time

19
Q

What do we see when there are collagen abnormalities

A

normal vWF activity and antigen

Normal Ristocetin aggregation

Prolongued bleed time

20
Q

phospholipase, cyclooxygenase and thromboxane synthase disorders are all what types of defects?

A

Defects of secreation: Prostaglandin defects

21
Q

If a platet is missing granules, what type of defect is this?

A

storage pool defect

22
Q

Membrane changes like Glanzmanns thrombasthenia and Peniccillin/carbenicillin are what type of defects

A

defects of aggregation

23
Q

What are two types of defects seen with Increased Destruction of platelets?

A

Increased utlization: DIC, TTP and abnormal valves

Immunological destruciton: Idiopathic TTP, Lupus, Drugs

24
Q

4 yo girl comes to the office with purpura on her trunk and legs. She has prominent bleeding from an IV site. She has a viral infection last week and has no prior hx of bleeding

A

Acute ITP; often proceeded by viral syndrome

25
Q

How is chronic ITP differnt from acute ITP

A

chronic: bleeding is less prominent and often discovered incidentally. Plats are usually low and pt has long hx of bruising
3: 1 (F:M)

26
Q

What are some different characteristics of ITP antibodies

A

Platelet specific, restricted heterogeneity, Antigenic heterogeneity (GPIb, GPIIb) and site of produciton (spleen or BM)

27
Q

What do we need to make a dx of ITP

A
  1. Evidence for immune thrombocytolysis
    - thrombocytopenia—Normal or incresase megakaryocytes—antiplat antibody
  2. Absence of other causes of thrombocytopenia (like lupus or DIC)
  3. Absence of splenomegaly
28
Q

What do we tx those dx with ITP with?

A
  1. corticosteroids (see 70% respond w/ high relapse rate)
  2. Splenectomy (50% response and low relapse, remove source of antiB prodcution)
  3. Immunosuppresive agents
29
Q

18 yo girl, bilateral rash on ankles for 3 days, petichae and has progressively increased

feels fine, no recent illness on birth control, active and in high school

LMP: 3 weeks ago w/ moderate bleeds for 5 days changed out every 6 hrs

neg for lymphadenopathy, normal vitals

normal coagulation times and CBC below

– WBC =7.0 (normal 4-10) with normal differential

– Hemoglobin = 11.9 (normal 11.2-15.4)

– Platelet count = 6 (normal 150-350)

next step?

A

Peripheral blood smear

30
Q

Get peripheral blood smear for girl with petichae and CBC of

– WBC =7.0 (normal 4-10) with normal differential

– Hemoglobin = 11.9 (normal 11.2-15.4)

– Platelet count = 6 (normal 150-350)

What are some differentials you should include in workup

A

IMmune thrombocytopenia: autoimmune syndormes, drugs, infections

DIC: unlikley bc no prolongued bleeds

TTP: no hemotonizing, so prbly not

Hematologic malignancy: not likley bc nothing going on with WBC and no lymphadenopathy

31
Q

Your pt is dx with ITP, what do you treat her with

A

prednisone and IVIg

32
Q

Pt has hx of ITP managed for 10 yrs with prednisone and IVIg.

Decreased tolerance to running (marathon runner) and gtes tired. Uses aspirin 4-5x week for ankle pain and ibuprofen for mentral pain prn.

Vegetarian but eats fish and has increased menorrhagia over past two months

PE: slight tachy, thin conjunctival pallor, no rash but bruising.

– WBC = 5.2 (normal 4-10) with normal differential

– Hemoglobin = 8.1 (normal 11.2- 15.4)

– Platelet count = 216 (normal 150- 350)

– MCV = 70 (normal 80-100)

Normal coag times

A

Microcytic hemochromatic

Iron deficiency anemia

33
Q

What studies could you use to confirm a dx of iron deficency anemia?

A

– Ferritin

– Iron (transferrin) saturation

– Total iron binding capacity

– Reticulocyte count

34
Q

MCV Decreased

RDW: incresed

Iron sat% Decreased

Ferritin: Decreased

BM irone: Decreased

A

Fe defiency anemia

35
Q

MCV: low or normal

RDW: normal

IRon Sat%: Decreased/normal

Ferritin: Increased/normal

BM Iron: increased

A

Anemia of Chronic Disease

36
Q

MCV: decreased

RDW: increased/normal

IRon Sat%: increased

Ferritin: BIG increase

BM Iron: Big increase

A

Thalassemias

37
Q

MCV: decreased

RDW: increased

IRon Sat%: increased/normal

Ferritin: increase

BM Iron: increase

A

Sideroblastic anemia

38
Q

Further evaluation of the patient’s bleeding includes:

– Von Willebrand’s antigen = 90% (nml 60-130)

– Von Willebrand’s activity = 110% (nml 60-130)

– Factor VIII activity =95% (nml 65-140)

– Von Willebrand multimers = normal distribution

– Thrombin time = 13 seconds (nml 12-14 sec)

– Platelet function assay- prolongation on collagen/epinephrine cartridge >300 sec (nml <180); normal on collagen/ADP cartridge

what caused this?

A

d. decreased platelet aggregation due to reduce formation of thromboxane A2 : from aspirin use

39
Q

Mechanism of aspirin

A

Decreaes plat aggregatiob via COX-1 inhibiton

see decreased thromboxane formation which is responsible for platelet aggregation via mediation of GPIIB/IIIA

40
Q

cause mucocutaneous bleeding including petechiae and mucosal bleeding (epistaxis, gingival bleeding, menorrhagia)

A

Defects of primary hemostasis (formation of platelet plug)

41
Q

Disorders that affect primary hemostasis include

A

qualitative and quantitative platelet defects, vW disease, and disorders of the endothelium

42
Q

is a diagnosis of exclusion, requiring lab testing to evaluate for other causes of bleeding

A

ITP

Symptoms Midterm (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions