Advanced Editing (pics)

Question 1

What are the 4 steps of primary hemostasis? Give details.

Answer 1

(Formation of a weak platelet plug to form a blood clot in response to injury of vessel)

1. Vasoconstriction (to dec blood flow)

2. Platelet adhesion (GP1b receptor on platelets binds to von Willebrand factor (vWF) on endothelial cells of vessel wall)

3. Platelet degranulation (platelets release ADP, which is essential for them to express Gp2a/3b receptors, and TXA2, which is made by platelet COX and promotes platelet aggregation)

4. Platelet aggregation (platelets come together and form a weak plug by Gp2a/3b receptors and fibrinogen linker molecules)

Question 2

Where does the von Willebrand factor come from in endothelial cells (2 places)?

Answer 2

1. Alpha-granules of platelets themselves
2. Weibel-Palade bodies of endothelial cells

Question 3

What 2 factors do Webber-Palade bodies in endothelial cells give rise to?

Answer 3

1. Von Willebrand factor (vWF)
2. P-selectin

Question 4

What are the 2 quantitative primary hemostasis disorders?

Answer 4

Quantitative primary hemostasis disorders (not enough platelets):

1. Immune Thrombocytopenia Purpura (ITP)

2. Microangiopathic Hemolytic Anemia

Qualitative primary hemostasis disorders (poor quality platelets):

1. Bernard-Soulier syndrome
2. Glanzmann Thrombasthenia
3. Aspirin
4. Uremia

Question 5

What’s the difference between petechiae, purpura, and ecchymoses?

Answer 5

Petechiae (1-2mm) < purpura (>3mm) < ecchymoses (>1cm)

Petechiae are smallest, Pupura in the middle, ecchymoses is largest. All are redness.

These are all signs of primary hemostasis disorders (clotting problem due to not enough platelets or poor quality platelets). Note that petechiae are a sign of thrombocytopenia (not enough platelets) and is not seen in qualitative (poor quality platelets).

Question 6

What are these?

Question 7

The coagulation cascade generates _______, which converts _______ to—> _______ to form a cross-linked clot (stabilize the weak platelet plug).

Answer 7

The coagulation cascade generates thrombin, which converts fibrinogen to—> fibrin to form a cross-linked clot (stabilize the weak platelet plug).

Question 8

Elevated PT time means what? Elevated PTT time means what?

Answer 8

Prolonged PT—> problem with clotting factor in extrinsic pathway of coagulation cascade (factor 7) or common factor (2, 5, 10, fibrinogen).

Prolonged PTT—> problem with clotting factor in intrinsic pathway of coagulation cascade (factors 12, 11, 9, or 8) or common factor (2, 5. 10, fibrinogen).

*If it’s a problem with the extrinsic pathway, you’ll see just prolonged PT. If it’s a problem with the intrinsic pathway, you’ll see just prolonged PTT. If it’s a problem with a common factor, you’ll see prolonged PT and PTT.

Question 9

What is Hemophilia A?

Answer 9

A secondary hemostasis (coagulation cascade) disorder. X-linked recessive (more common in boys) deficiency of factor 8 (in the intrinsic pathway). Presents with deep tissue bleeding.

Question 10

What is Hemophilia B aka Christmas Disease?

Answer 10

Deficiency of factor 9 of the intrinsic pathway of the coagulation cascade (presents like Hemophilia A, which is a deficiency of factor 8 of the intrinsic pathway, patients get deep tissue bleeding).

Question 11

Vitamin K deficiency disrupts function of which coagulation factors?

Answer 11

Question 12

Vitamin K helps activate which factors in the coagulation cascade?

Answer 12

Factors 2, 7, 9, 10, protein C, and protein S

(note: proteins C and S inhabit factors 5 and 7)

Question 13

A patient has disfunction of coagulation factors 2, 7, 9, 10, protein C & S. What is the most likely diagnosis?

Answer 13

Vitamin K deficiency

Answer 14

(DIC= pathologic activation of the coagulation cascade)

These 5 disease processes can lead to DIC bc they all involve pro-coagulants that activate the coagulation cascade.

1. Obstetric complications (tissue thromboplastin in amniotic fluid—> activates coagulation)

2. Sepsis (endotoxins from the bacteria and cytokines—> cause endothelial cells to make tissue factor—> promotes coagulation)

3. Adenocarcinoma (Mucin activates coagulation)

4. Acute Promyelocytic Leukemia (primary granules activate coagulation)

5. Rattlesnake bite (venom activates coagulation)

Question 15

What is DIC (Disseminated Intravascular Coagulation)?

Question 16

What is fibrinolysis?

Answer 16

Resolving/ removing the clot/ thrombus after the damaged vessel heals.

Question 17

What enzyme converts plasminogen to plasmin to resolve clots (fibrinolysis)?

Answer 17

TPA (tissue plasminogen activator)

Question 18

What fungi is this?

Answer 18

Candida (pseudohyphae)

Question 19

What Fungi is this?

Answer 19

Mucormycosis (from Mucor or Rhizopus species *rare)- right angle branching hyphae (non-septate hyphae that branch at 90 degree angles)

*remember, this is the fungi that DKA and immunocomprimised patients are prone to from spore inhalation, enters cribiform plate and rapidly invades blood vessels—> causes necrosis/ black face and gets into brain—> rapidly fatal (“mu car auto shop” in Sketchy)

Question 20

What fungi is this?

Answer 20

Blastomycoses (broad based budding)

(*remember the cannon balls in Sketchy)

Question 21

What fungi is this?

Answer 21

Coccidiodes Immitis (“valley fever”)

capsule with circles in it (spherule of endospores)

Question 22

What fungi is this?

Answer 22

Histoplasma

Ovoid bodies (macrophages filled with many yeasts)

Question 23

What is the replication process of Hep B?

Answer 23

Double stranded DNA—> (+) RNA aka mRNA—> circular, partially double stranded DNA (by reverse transcriptase)