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RBC Disorders > RBC Disorders > Flashcards

RBC Disorders Flashcards

1
Q

In primary hemostasis, what are the 2 products that activate platelets & what 2 products inhibit platelets?

A

Platelet activators: 1) Thromboxane A2, 2) ADP

Platelet inhibitors: 1) NO, 2) PG

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2
Q

What is the function of platelet activators?

A

They help to activate the platelets so they are 1) more sticky, 2) release more vWF, serotonin (which attracts more plt) Ca2+, ADP, TXA2

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3
Q

What is the compound that links all of the platelets together?

A

Fibrinogen

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4
Q

What are the various steps in primary hemostasis?

A

Adhesion of vWF & plt

Activation of plt

Aggregation of plt

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5
Q

What is secondary hemostasis? What is the goal of secondary hemostasis?

A

Clotting cascade

Involves intrinsic & extrinsic pathway & common pathway

Intrinsic requires Factor XII to bump into the platelet plug

Extrinsic activated when endothelium is damaged & releases tissue factor (III)

Goal is to produce fibrin mesh

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6
Q

What does factor XIII do?

A

Cross links the fibrin mesh

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7
Q

What are the 3 roles of thrombin (clotting factor II)?

A

1) activates Factor V, VIII, XI, XIII
2) activates platelets
3) cleaves fibrinogen-fibrin

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8
Q

Which clotting factor will degrade in the blood unless bound to vWF?

A

Factor VIII

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9
Q

What releases vWF?

A

Activated platelets AND endothelial cells

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10
Q

What is fibrinolysis?

A

Degradation of fibrin mesh

Plasminogen converted into plasmin via tPA

Plasmin cuts fibrin mesh

Endothelial cells secrete tPA when exposed to thrombin & Factor X

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11
Q

What is d-dimer?

A

Platelets are attached to a D subunit, when the clot is broken down - D subunit breaks apart from the platelet

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12
Q

What clotting factors are dependent on Vitamin K?

A

X, IX, VII, II (1972)

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13
Q

Why can’t those clotting facts become activated without Vitamin K?

What medication affects this pathway?

A

Vitamin K is cofactor needed for a series of conversion that leads to the activation of those clotting factors

Warfarin ~ affects epoxide reductase = responsible for converting Vitamin K into its co-factor from

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14
Q

What kind of bleeding do you get with disorders of primary hemostasis?

A

Mucocutaneous bleeding - epistaxis, gingival bleeding, menorrhagia, petechia, GI bleeding

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15
Q

What kind of bleeding do you get with secondary hemostasis?

A

Get more hemarthroses & hematomas

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16
Q

3 primary ways in which anemia can occur?

A

Blood loss
Increased destruction
Decreased production

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17
Q

Indications for RBC transfusion

A
  • symptomatic anemia
  • sickle cell crisis
  • acute blood loss >30% volume
  • Transfuse when Hb <70 for all patients except those who:
    — hemodynamically unstable ~ transfuse before
    — Stable CV or ACS ~ transfuse before
    — Acute orthopaedic or cardiac surgery ~ transfuse before
    — severe treatment related to thrombocytopenia
18
Q

Risks & complications with blood transfusions?

A
  • infection
  • allergic or immune transfusion reaction (acute transfusion reaction OR delayed)
  • volume overload
  • hyperkalemia ~ bc K+ release from RBCs during storage bc some get damaged
  • iron overload
19
Q

What is the differential for microcytic anemia?

A

IRON LAST

  • iron deficiency anemia
  • Lead poisoning
  • Anemia of chronic disease?
  • Sideroblastic anemia
  • Thalassemia
20
Q

What are signs of iron deficiency?

What are symptoms of iron deficiency anemia?

A

Pallor
Brittle hair
Glossitis
Cheilosis ~ corners of mouth become inflamed
Koilonychia ~ spoon nails ~ become concave

Symptoms

  • Pica
  • Fatigue
  • SOB
  • Palpitations
  • Pallor
  • Weakness
  • Dizziness
21
Q

What would you see on a peripheral smear for sickle cell anemia?

A
  • Sickled cells
  • Howell Jolly bodies ~ residual RBC nuclei remnants ~ usually removed by spleen but in SCD have asplenia
  • Target cells
22
Q

How does sickling of a RBC occur?

What brings on sickling?

What happens to RBC with repeated sickling?

A

When oxygenated it can carry it appropriately, but when deoxygenated, the Hb proteins stick together in the RBC & form that crescent shape

  • Acidosis, low flow vessels (Hb has lots of time to give away its oxygen), fevers
  • damages the membrane & promotes destruction of the RBC —> leads to anemia, increased Hb recycling & build up of UCB - signs of jaundice
23
Q

What is involved in a sickle cell crisis?

A

1) aplastic crisis
- Parvovirus B19
- virus infects RBC in BM ~ impairs cell division for a few days
- in N pts ~ drop in minor drop in Hb, in SC pt ~ severe drop in Hb
- self limiting

2) Splenic sequestration
- occurs in childhood
- blood pools in spleen & acute drop in Hb
- doesn’t really occur in adults bc of splenic infarction

3) vaso-occlusive crisis
- sickled RBC occlude vessels —> ischemia-reperfusion injury (heart ~ MI, spleen ~ splenic infarct, brain ~ CVA)

4) acute chest syndrome
- pulmonary micro vascular conclusions ~ common cause of death

24
Q

What is the differential for normocytic anemia with a low reticulocyte count?

A 
PANCYTOPENIA
L-leukaemia 
A-aplastic anemia
M-myelofibrosis
B- BM invasion/suppression

NON-PANCYTOPENIA
L- liver failure
A - anemia of chronic disease
R - renal failure

25
Q

What is myelofibrosis, how does it occur & what are clinical features? what would you find on BM aspiration & biopsy?

A

BM fibrosis leading to BM failure

Can be primary (genetic. ~ leads to fibroblasts laying down fibrin - fills BM & replaces hematopoietic stem cells) or secondary

CF: Sx ~ anemia: fatigue, palpitations, dizziness, pallor, cold extremities + bone pain + hepatosplenomegaly

BM aspiration - “dry tap”

BM biopsy - Fibrosis, thickening of trabeculae,

26
Q

What is the differential for normocytic anemia with a high reticulocyte count?

A 
HEMOLYTIC
- Hereditary
— G- G6PD
— T - thalassemia 
— S - spherocytosis
  • Acquired
    — D - disseminated intravascular coagulation
    — O - oxidative/drug related
    — I - infection (malaria)
    — T - TTP: thrombotic thrombocytopenic purpura
    — H - HUS: hemolytic uremic syndrome
    — H - HELLP: hemolytic anemia, elevated liver enzymes, low platelets
    — H - Hemolytic disease of the newborn

Post-hemorrhagic causes
- GU, GI, other

27
Q

How does maternal sensitization occur re: hemolytic disease of a newborn with ABO & Rh blood groups?

A
  • through delivery
  • through spontaneous/induce abortion
  • antenatal hemorrhage
28
Q

When is Rhogam given

A

Given to a Rh- mom at 28 weeks & second dose is within 72 hr of birth

29
Q

What are the complications associated with hemolytic disease of the newborn?

A

Kernicterus

Hyperbilirubinemia

Hydros fetalis —> edema over whole body (subq tissue, pleural/pericardial effusions, ascites ~ in all body cavities) bc related to severe anemia-induced hypoxemia

30
Q

What is the difference between a direct & indirect coomb’s test?

A

Direct Coomb’s Test

  • Diagnose the cause of hemolytic anemia
  • Detects the presence of antibodies attached to RBCs
  • Procedure: Pts RBCs get washed (free floating antibodies are removed), add IgG coomb’s agent & if the patient does have hemolytic anemia ~ IgG coomb’s agent will attach to antibodies already on RBCs —> POSITIVE TEST

INDIRECT COOMB’S TEST
- Only used for “pre-transfusion” testing
- Looking for antibodies in the recipient’s blood to donor’s RBCs
- Procedure:
— Recipient’s blood: separated the serum (has all antibodies) from the RBCs THEN mix the Donor’s RBCs with the Recipient’s serum PLUS Coomb’ reagent, if not a match = agglutination of RBCs & antibodies = POSITIVE TEST

31
Q

What would you see on antenatal testing for a patient with hemolytic disease of the newborn regarding coomb’s tests?

At birth is this different?

A

Indirect coomb’s test = positive bc antibodies to baby’s RBCs

Direct coomb’s test

32
Q

What is TTP?

What is the clinical presentation?

Smear show?

A

Thrombotic thrombocytopenic purpura —> genetic disorder where have reduced activity of ADAMTS13 -> increased amount vWF on endothelial surface of b.v —> plt to attach-aggregate-active —> small clots forming

Does 2 things: 1) use up all your plt - low plt, 2) clots forming all over body ~ contributing to a level of ischemic, 3) clots damage RBCs pass by & so you get hemolytic anemia, 4) bc using up all your plt you get mucocutaneous bleeding

CP: - classic pentad:
- Microangiopathic hemolytic anemia
- thrombocytopenia
- Renal insufficiency ~ AKI
- fever
- neurological dysfunction (HA, confusion, seizures, coma)
\++ mucocutaneous bleeding: epistasix, purpura/petechiae, gingival bleeding
\++dark urine

Smear ~ schistocytes

33
Q

When is a type & screen used vs a cross & match?

A

Type & screen —>used if you might need to give a transfusion

Cross & match —> used just before the transfusion (last step before transfusion)

34
Q

What is heparin induced thrombocytopenia?

A

Heparin binds to plt & in some people is immunogenic = tagged by IgG for destruction == low plts

PLUS heparin binding to plt activates platelet = clot formation = uses up all plt

Increased risk of bleeding ++ clot formation causing thrombotic events

35
Q

What are the clinical features of heparin induced thrombocytopenia?

A

Venous: DVT, PE, cerebral sinus thrombosis

Arterial: MI, CVA, organ ischemia

Heparin induced skin necrosis

36
Q

When should you suspect heparin induced thrombocytopenia?

How do we treat it?

A

If pt recently started heparin OR plt count has dropped within 1-2 weeks or 1 day (with previous heparin use)

D/C any form of heparin (UFH, LMWH), start on fondaparinux

2-3 mon if no thrombotic event

3-6 mon if thrombotic event

37
Q

What is hemolytic uremic syndrome?

A

Caused by shiga toxin (e coli) —> absorbed through intestines - damages cells here ~ hematochezia

Filtered by kidneys ~ damages tiny b.v here - AKI PLUS tiny clots form here - uses up plt (low plts) & MAHA bc of the clots causing damage to the RBCs

38
Q

What is the differential for polycythemia?

A

Primary —> polycythemia rubra Vera

Secondary —>

  • altitude
  • iatrogenic: anabolic steroids, testosterone use, EPO administration
  • relative: third space loss, plasma volume depletion
  • EPO secreting tumour
39
Q

What is polycythemia rubra Vera?

A

Genetic disorder where you have mutation in hematopoietic stem cells —> continuously dividing even in absence of EPO

Over time te stem cells die = myelofibrosis

40
Q

What complications can occur with polycythemia rubra Vera?

A

Increased cell volume leads to abnormal flow of blood ~ dysfunction of plt

Clotting + Bleeding disorders: DVT, PE, MI, Budd-Chiari syndrome, can even progress to AML

RBC Disorders (1 decks)

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