HEME 3

Question 1

Immune Thrombocytopenia (ITP) is an autoimmune destruction of platelets, often following a viral illness. It presents with petechiae, mucosal bleeds, or sudden onset bleeds.

What is the classic lab finding?

How do you DX?

What is the management/TRX?

What is prognosis?

Answer 1

LABS = Isolated plt < 100,000 (No other abnormalities)

DX= of exclusion

TRX= 
IF asymptomatic or mild symptom (petechiae/bruising) 
           - Observation 
IF Mucosal bleed or internal bleeding 
           - IVIG or STEROIDS 

PROGNOSIS:
- 50% will have spontaneous remission in years.

Question 2

What is the difference between Type I Heparin induced Thrombocytopenia and Type II HIT?

Answer 2

TYPE I HIT:

• NON autoimmune
• Transient decrease in platelets that occurs within 2 days of Heparin. No clinical significance
• Can continue Heparin

TYPE II HIT:

• Autoimmune
• Occurs 5-10 day after Heparin start.
• Platelets decrease by at least 50%
• Arterial and Venous Thrombosis

Question 3

What is the pathophysiology behind TYPE II HIT?

How do you DX TYPE II HIT?

Answer 3

Abs form against Platelet Factor 4 (PF4), causing complex with Heparin –> Deposition causes thrombosis.

DX = Serotonin Release Assay (GOLD STANDARD) or Heparin PF4 ab ELIZA.

Question 4

You suspect HIT and DC Heparin…What next?

Answer 4

Immediately start another form of AC

Preferably Direct Thrombin Inhibitor:

• Agatraban
• Bivalirudin

Question 5

Once a patient develops HIT, can they get any form of Heparin in the future?

Answer 5

NO

Should be listed as Allergy

Question 6

The primary SE of Anthocycline (DOXORUBICIN, DAUNORUBICIN) Chemotherapy, which is often used in Leukemia, is what?

What test si best to monitor for this SE while on this chemotherapy?

Answer 6

CARDIOTOXICITY (DILATED CARDIOMYOPATHY, DECREASED EF)

RADIONUCLEOTIDE VENTRICULOGRAPHY (not Echo, bc more accurate)

Question 7

What is a Pancoast Tumor?

What is the clinical presentation?

Answer 7

Tumor of the superior pulmonary sulcus, generally non-small cell lung cancer

PRESENTATION:
1. Shoulder pain (most common)

2. Horners syndrome
   - Ipsilateral Meiosis
   - Ipsilateral Ptosis
   - Ipsilateral anhydrosis
3. C8-T2 nerve impingement - weakness and paresthesia of hands.
4. Enlarged supraclavicular lymph nodes.
5. Weight loss.

Question 8

What is the most common inherited hyper-coagulable disease?

What is the pathophysiology?

Answer 8

Factor V Leiden

Mutation in Factor V gene, such that protein C can no longer be inactivated by Factor V –> get unregulated prothrombin activation –> Increased clots.

Question 9

What are the two calcium pattern of Malignant Pulmonary nodules?

What are he three calcium pattern so Benign Pulmonary Nodules?

Answer 9

MALIGNANT:

• Eccentric
• stippled or punctate

BENIGN:

• concentric/laminated
• popcorn
• diffuse/homogenous

Question 10

In iron def anemia, how long after Iron supplementation is started would you expect to see Hct/Hbg start to increase?

Answer 10

3-4 weeks

by 1-2 weeks you start seeing increase Reticulocytes

Question 11

In children a Hbg < 11 and low MCV should be presumptively treated as?

Answer 11

Iron deficiency Anemia with Empirical Iron supplementation.

Question 12

What are three protective factors against Colorectal Cancer?

Answer 12

PROTECTIVE FACTORS:

• High fiber diet
• Regular NSAID use
• Regular exercise

Question 13

Sickle cell Aplastic Crisis is characterized by a sudden cessation of production of erythropoiesis…

What virus is implicated?

What do the LABS show?

Why is it that you rarely see Aplastic Crisis in adulthood?

TRX?

Answer 13

Parvo B19.

Lab:

• Decreased Hbg/Hct
• Preserved Plt and WBC (bc Parvo preferentially attack RBC cell lines)
• Decreased Reticulocytes.

You develop immunity against Parvo B19 in childhood after exposure.

TRX = blood transfusion until RBC recovers

Question 14

How is Aplastic Anemia differ from Aplastic Crisis?

Answer 14

Aplastic Crisis – seen in SS, with only decreased RBC.

Aplastic Anemia – is due to many causes (mainly ideopathic, but also radiation, viral infections, insecticides), and causes depression of ALL cell lines…so you get thrombocytopenia, anemia and leukopenia.

Question 15

Alpha Thalassemia is due to a defect in making Alpha-Globing chin in Hbg synthesis. There are 4 genes that control Alpha global…

How does clinical presentation change depending on how many genes are deleted? What is the trx?

Answer 15

1 gene deletion:
–> No anemia

2 gene deletion: “alpha thalassemia minor”
–> Mild anemia, no trx required.

3 gene deletion: “alpha thalassemia major”

• -> severe anemia
• -> Body compensates and makes HgH (4 beta)
• -> TRX= blood transfusions

4 gene deletion: “hyprops fetalis”