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HD4 > Heme > Flashcards

Heme Flashcards

0
Q

Microcytic anemias

A

1 Fe deficiency

  1. anemia of chronic disease
  2. Thalassemia
    Also: Hemoglobinopathy, lead poisoning, sideroblastic anemia
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1
Q

Anemia signs and symptoms

A

= reduced RBC mass
Signs: low # RBCs, low hemoglobin (Hb), low hematocrit (Hct)
Sxs: fatigue, angina, poor mentation

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2
Q

Etiologies of Iron-deficient anemia

A
  • Nutritional: esp. kids, pregnant women, vegetarians
  • Bleeding: GI bleed *increased risk cancer!
  • Malabsorption:
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3
Q

Blood donation requirements

A

“healthy and well” to avoid risks assoc. w/ blood loss and transfusion

  • no Temp
  • weight > 110
  • Hemoglobin > 12.5 (#1 cause for deferral)
  • skin inspection (check for signs of IV drug use)
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4
Q

Infectious diseases tested for in donated blood

A
  1. HIV 1 & 2
  2. HBV, HCV
  3. HTLV 1 & 2
  4. Syphilis
  5. WNV
  6. trypanosoma cruzi (Chagas)
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5
Q

Leukoreduced pRBCs

A

pRBC w/ WBCs removed
=> decrease risk of:
- febrile non-hemolytic transfusion rxns
- CMV & EBV transmission, etc.

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6
Q

Irradiated pRBCs

A

inactivate lymphocytes in donated blood

=> reduce risk of graft vs. host disease

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7
Q

RBC transfusion indication and thresholds

A

Indication: to increase oxygen carrying capacity (decreased bc low RBC mass)
Thresholds: Hb = 7 or 8 mg/dl or less
(if stable, hospitalized. 8 if w/ heart disease)

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8
Q

platelet storage requirements

A

20-24 C (room temp) w/ continuous agitation, for up to 5 days
* released for use on day 2, (but results from culture available day 5)

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9
Q

platelet transfusion indications:

A

TRANSFUSE if: <50K/L

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10
Q

Indications for plasma transfusion

A

DIC, TTP, rapid warfarin effect reversal, massive bleeding, coagulation deficiency (congenital)
Use to get INR down to 1.8 (target INR depends some on starting INR)

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11
Q

“Release Reaction” in hemostasis

A

= release of proteins from endothelium that recruit & activate MORE platelets,
initiated by activated platelets on endothelium.
(ie: thromboxanes, adenosine diphosphate)

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12
Q

von Willebrand factor

A

molecule involved in clotting, released under stress.
-> participates in & strengthens binding between platelets and endothelium (by binding GPIb & GPIIb to subendothelial matrix)
AND stabilizes Factor VIII

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13
Q

Prothrombinase complex

A

= the (final) common pathway

  1. Factor Xa
  2. Factor Va (cofactor)
  3. Ca2+
  4. Phospholipase (= surface for complex formation)
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14
Q

2 ways to activate Factor X (for coagulation)

A
  1. VIIa and TF
    (* TF drives normal hemostasis)
  2. VIIIa and IXa (no IX in hemophilia)
    *note: VII turns on IX!
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15
Q

Contact-activation system

A

NOT very important in vivo, but helpful for PTT test

  1. Factor XII (common hereditary def, no bleeding problem)
  2. HMW kininogen (no bleed problem)
  3. Prekallikrein (no bleed problem)
  4. Factor XI: activates IX –> X… (mild bleeding problem)
16
Q

Thrombin time measures:

b) what prolongs TT?

A

Fibrinogen –> Fibrin –> Clot
(mediated by thrombin)
Long if:
a) low or faulty fibrinogen
b) thrombin inhibitor (ie: w/ Heparin) or auto-Ab
c) steric inhibition (too much Ig (w/ mult. myeloma) or fibrinogen)

17
Q

PT measures?

b) what prolongs PT?

A

a) factor VII (low, low VitK, warfarin)
b) factor X (“ “)
c) factor II (“ “)
- —
d) factor V *NOT affected by vit K!
* OR anything that makes TT long (but PT is less sensitive)

18
Q

PTT (aka: INR*) measures…

b) what prolongs PTT?

A

a) factor XII (def –> NO bleeding disorder)
b) factor XI (def, mild bleeding problem)
…and Prekallikrein or HMW heparin)
c) factor VIII *most common (Hemophilia A)
d) factor IX (Hemophilia B, warfarin, vitK def.)
e) low phospholipid (NO bleeding disorder, but may be SLE)
*OR anything that prolongs TT

19
Q

Primary vs. Secondary bleeding problems

A

Primary (platelets): prolonged initial bleed (takes LONG time to stop)
- petechiae, mucosal bleeding, excessive bruising
Secondary (factor def.): later re-bleeding (stops, but clot not stable)
- hemarthroses, eccymoses, soft tissue bleeds

20
Q

Causes of thrombocytopenia

A
  1. Decreased production: bone marrow failure/replacement, drugs, B12/folate def.
  2. Destruction/Consumption: ITP, HIT, drugs, DIC, TTP
  3. Hypersplenism
21
Q

ITP (Immune Thrombocytopenic Purpura)

A

1 cause of thrombocytopenia in otherwise healthy adult

*usually insidious, spontaneous.
Labs: platelets increased platelet clearance by spleen

22
Q

Causes of normocytic anemia

A
  1. Anemia of chronic disease
  2. Acute blood loss
  3. renal failure (low Epo)
  4. Endocrine disorders
  5. Insufficient HSCs/bone marrow malignancy (aplastic anemia, RBC aplasia, etc.)
23
Q

Pentad of TTP clinical presentation

A
  1. microangiopathic hemolytic anemia
  2. thrombocytopenia
  3. CNS Sxs (ie: confusion, headache, or stroke/TIA)
  4. renal insufficiency
  5. fever
24
Q

normal myeloid to lymphoid ratio (in bone marrow)

A

2-4 myeloid precursors to 1 lymphoid precursor

25
Q

Leukemia (broad definition)

A

clonal disorders of Hematopoietic Stem Cells

  • > suppress normal stem cells
  • > change # cells in bone marrow & circulating (RBCs, WBCs, platelets, etc.)
26
Q

Cut-off for emergency treatment of neutropenia

A

treat empirically with antibiotics bc high risk spontaneous infections

27
Q

When use HSC transplant

hematopoietic stem cell

A
  1. hematologic malignancy
  2. aplastic anemia
    Goals: WBC >10,000; platelets >50,000
28
Q

Times to recovery of normal cell counts after HSC transplant

A 
Neutrophils: 2-4 weeks
Immunoglobulins: 3-6 months
T cells: 6-12 months
* so need prophylactic antibiotics until cell counts return to normal
(and anti-fungals, anti-virals)
29
Q

Acute Graft vs. Host Disease w/ HSC transplant

A

“Rejection rxn” <100 days after transplant.
Sxs: blistering, diarrhea/nausea/vomitting, jaundice
donor T cells recognize and attack the host Ag
(initially triggered by some damage & inflammation in host initially @ transplant)

30
Q

Chronic Graft vs. Host Disease (GVHD)

A

“Rejection rxn” >100 days after transplant.
Sxs: hyperpigmentation (affecting entire thickness of skin!)
* serious disease prevented by rejection prophylaxis

31
Q

Meds used to prophylactically treat GVHD in transplant patients

A

cyclosporine, methotrexate, prednisone, ATG (anti-thymocyte globulin)

32
Q

Anti-tumor effect from donor immune cells

A
  1. T cells => “Graft vs. Tumor Effect”

2. NK cells (B type = more effective at killing leukemia cells!)

HD4 (6 decks)

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