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Skin, Blood & Lymph Exam #2 > Fatigue > Flashcards

Flashcards in Fatigue Deck (21)
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1
Q

How do petechiae tend to look in thrombocytopenia?

How are purpura and bruises characterized?

A

“Pinpoint hemorrhages”

“Confluent petechiae”

2
Q

When is hemarthrosis most often seen?

A

Severe hemophilia

3
Q

What types of diseases do telangiectasias suggest?

A

CT disease or hereditary hemorrhagic telangiectasia

4
Q

If you must only order 1 exam in a workup for a patient with a CC of “fatigue”, what would it be?

A

Reticulocyte count

5
Q

What is the most common disorder associated with the following defects?

Proliferation/distribution of stem cells

Proliferation/distribution defects of erythroid progenitor cells

Disturbance of DNA synthesis

Disturbance of Hb synthesis

A

Proliferation/distribution of stem cells = aplastic anemia.

Proliferation/distribution defects of erythroid progenitor cells = CKD.

Disturbance of DNA synthesis = megaloblastic anemia (vit. B12, folate, meds, etc.).

Disturbance of Hb synthesis = iron deficiency, hemoglobinopathy.

6
Q

What symptoms are often present in a patient with iron deficient anemia?

What lab features suggest it?

A

Constitutional symptoms.

Decreased serum iron and ferritin (measure of total iron stores).
Increased TIBC (transferrin is less saturated with iron and increased capacity for iron transport exists).
7
Q

How is therapy approached in patient with anemia of chronic disease? (3)

What kind of anemia does it cause?

A
  • Iron supplementation is NOT recommended.
  • Supportive care is given only if the anemia is mild (Hb 10-12).
  • If the anemia is severe, transfusions can be helpful to keep Hb > 9.

Iron deficiency anemia.

8
Q

What is factitious anemia?

What is another name for it?

What kind of anemia does it cause?

A

Anemia due to autophlebotomy. Patients likely have underlying psychiatric problems; treatment of those problems results in resolution.

Lasthenie de Ferjol syndrome.

Iron deficiency anemia.

9
Q

What is march hemoglobinuria?

Which patients is it most common in?

What is the treatment?

What kind of anemia is it?

A

Anemia due to striking of feet on the ground repeatedly which leads to damage/lysis of RBCs in capillaries on the plantar surface of the feet.

Marathon runners, soldiers, etc.

Well-padded footwear and reassurance.

Mechanical/traumatic anemia.

10
Q

What patients may cause cardiac anemia?

How severe is the anemia? What kind of anemia is it?

A

Anemia due to severe aortic stenosis (valve gradient > 50 mmHg) and patients with prosthetic valves. This leads to ongoing lysis of RBCs.

Anemia is usually mild; mechanical/traumatic anemia.

11
Q

What kind of anemia is seen in G6PD (size, color)?

What histologic findings suggest it?

A

Normocytic, normochromic anemia.

Heinz bodies - seen early on.
“Bite cells” - RBCs have that have had denatured Hb removed in the spleen.

12
Q

How does Lead cause hemolysis?

A

It interferes with a cation pump on the RBCs which shortens its survival time. It slows the production of RBCs in the spleen.

13
Q

What is the most common cause of hemolytic anemia worldwide?

A

Malaria

14
Q

What is “blackwater fever”?

How is it treated?

A

It describes the severe hemolysis in malaria, which leads to the marked Hb and dark color seen in the urine.

Antimalarial agents and supportive care.

15
Q

What is the treatment for warm antibody hemolysis? (4)

A

Most patients are not in imminent danger.

  • transfusions can be helpful, but it can be tough with the cross-matching (watch for signs of hemolysis).
  • **steroids - mainstay of therapy and generally result in long-term remission.
  • immunosuppressives - some benefit (Cyclophosphamide and Azathioprine are most commonly used).
  • splenectomy - used in patients who require chronic steroid use.
16
Q

What is the presentation of a patient with polycythemia vera? (4)

A

Facial rubor.

Hyperviscosity symptoms: HA, diziness, vision chanes, heaviness of arms/legs.

Pruritis with hot shower/bath.

Splenomegaly

17
Q

What is the prognosis of a patient with polycythemia vera?

What is the usual COD in treated patients?

A

Without treatment - 50% mortality at 18 mo.

  • increased risk for DVT, PE, MI, etc.
  • linked to Budd-Chiari syndrome.

With treatment patients can live for years/decades.

COD is often progressive marrow fibrosis with pancytopenia (a.k.a. “spent phase” polycythemia).

18
Q

What are some secondary causes of an elevated RBC ct.? (5)

A

Hemoconcentration

Pulmonary disease (smokers erythrocytosis)

EPO-producing tumors (RCC, NE tumors)

Hemoglobinopathy with high affinity hemoglobin (holds onto O2 more avidly than normal Hb resulting in ischemia to tissues and increased RBC mass)

Living at high altitudes (hypoxia from decreased FiO2).

19
Q

What should be part of a workup in a patient with polycythemia vera? (5)

A

H/P exam.

Routine CBC and biochemical profile.

Exclude hemoconcentration: dehydration, BUN/creatinine.

Exclude abnormal EPO level: serum EPO level and US kidneys (optional).

Exclude abnormal lung function: (1) pulseox with ABG, (2) PFT with DLCO.

20
Q

What lab/molecular findings correctly identify polycythemia vera in 98% of cases? (2)

A

+ JAK2 mutation and normal EPO level.

21
Q

What is the treatment for a patient with polycythemia vera? (3)

A

Lowering RBC mass is essential to avoid hyperviscosity complications:

  • phlebotomy of 250-500 cc every 2 wks. as long as Hct. > 50%.
  • may use hydroxyurea 500-1500 mg/day.
  • may use alkylating agents (busulfan, chlorambucil, etc.), but it is discouraged due to risk of development of leukemia.