HAEM Flashcards

1
Q

What is required for RBC production?

A

Iron + B12 + Folate + Erythropoietin (hormone)

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2
Q

What are some symptoms of Low O2 levels?

A

Tiredness/fatigue
Pallor
Tacchy
Dizzy/faint

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3
Q

What are some causes of MICROCYTIC Anaemia?

A

-Fe Deficient
-Chronic Inflam Disease
-Thalassemia

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4
Q

What is THALASSEMIA?

A

Blood disorder which effects production of Hb.

Alpha + Beta

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5
Q

What is the difference between ALPHA + BETA Thalassemia?

A

ALPHA = Mutation in gene for alpha-chain of Hb (4 genes responsible)

BETA = Mutation in gene for beta-chain of Hb (2 genes responsible) -> Elevated levels of HbA2 (delta) bc compensation for low HbA (beta)

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6
Q

What are some cause for NORMOCYTIC Anaemia?

A

HIGH Retic - Blood loss/Haemolytic

LOW Retic - Dec production = Bone marrow disease + CKD

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7
Q

What are some cause of MACROCYTIC Anaemia?

A

MEGABLASTIC = B12 + Folate deficient (can be drug induced)

Non-MEGABLASTIC = Alcohol + Liver disease + HYPOTHYROIDISM

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8
Q

Why is it important to rule out B12 Deficiency before Folate?

A

B12 deficiency = unnoticed neurological effects

If only addressing Folate –> Supplementation = fix anaemic symptoms but NOT Address NEURO effect!!!

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9
Q

What is TIBC?

A

‘Total Iron Binding Capacity’

  • Max amount of Fe that can be bound by proteins (MAINLY TRANSFERRIN)
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10
Q

What does TIBC indicate?

A

When Fe levels are low –> body produce more transferrin to capture more Fe –> Increase in transferrin = Increase in TIBC

**If TIBC levels are LOW = Iron overload + chronic diseases/infections/inflammation + malnutrition

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11
Q

What are the typical COMPONENTS of Fe studies?

A
  • Serum Iron
  • TIBC
  • Transferrin saturation
  • Serum Ferritin
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12
Q

What is Polycythaemia Rubra Vera?

A
  • Overproduction of RBC
  • 95% association w a JAK2 mutation

DIAGNOSE =
-High RBC + Hb + MCV
-Low EPO (Suggests there is something genetic making inc RBC)

TREATMENT = Regular RBC removal

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13
Q

What is Essential Thrombocytosis/Thrombocytopenia?

A
  • Excessive platelet production

SIGNS =
- Thrombotic events - frequent blood clots
- Headaches

TREATMENT = Aspirin

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14
Q

What is Primary Myelofibrosis?

A
  • Scarring of bone marrow due to PROLIFERATIVE bone marrow fibroblasts

DIAGNOSE =
Blood film -> tear drop cells

TREATMENT =
Bone Marrow Transplant OR Stem cell

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15
Q

What is CHRONIC MYELOID LEUKEMIA?

A

-Abnormal WBC production –> Abnormal myeloblast production
-SLOW PROGRESSION

CAUSE = Philadelphia Chrmosome –> Translocation of Chromo 9 +22

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16
Q

What is ACUTE CHRONIC LEUKEMIA?

A

-Overproduction of Myeloblasts –> Bone marrow crowding –> Decrease in differentiation (WBC + RBC + Platelets)

CAUSE =
-Myeloproliferative disorders
-Mutations

SYMTOMS =
- Anaemia
- Thrombocytopenia - easy bruising
- Neutropenia –> Recurrent infections
- Enlarged lymph nodes
- Splenomegaly –> fullness feeling

17
Q

What is MULTIPLE MYELOMA?

A
  • Uncontrolled proliferation of plasma cells producing monoclonal Igs

SIGNS =
- Hypercalcaemia + Renal failure + Anaemia

18
Q

Which factors are involved with the Extrinsic Pathway?

A

Factor 7
Tissue Factor (Factor 3)

19
Q

Which factors are involved with the Intrinsic Pathway?

A

Factor 12 + 11 + 9 + 8

20
Q

Which factors are involved with the Common Pathway?

A

Factor 10 + 5 + 2 + 1 + 13

21
Q

Which factors require Vitamin K?

A

Factor 2 + 7 + 9 + 10

22
Q

Which factors are NOT made in the liver?

A

Factor 3 (tissue factor) + 8

23
Q

Which factors require Calcium?

A

Factor 1 + 2 + 7 + 8 + 10 + 11

24
Q

Which factors does HEPARIN antagonise?

A

Factor 2 + 10

-Good with pregnancy

25
Q

Which factors does WARFARIN antagonise

A

*** Vit K blocker –> 2,7,9,10

26
Q

What is the process of breaking down a CLOT?

A

Plasminogen –> Plasmin (tPA + uPA = activates this)

Fibrin –> Fragments + D-dimers (Plasmin causes this)

27
Q

What are some DRUGS to effect fibrinolytic process?

A

1 = PRO-FIBRINOLYSIS = Alteplase (synthetic tPA)

2 = ANTI-FIBRINOLYSIS = Tranexamic Acid (inhibit Plasmin)

28
Q

What can D-dimer levels indicate?

A

Increased levels of D-dimer = increases clot formation + breakdown

High levels = DVT + PE + Recent CVS (MI + Stroke)

29
Q

Outline the process of Primary Haemostasis?

A

1- Injury to endothelium thus exposing it (collagen + tissue factor exposed)

2- Platelet Adhesion –> Activation (Von Wille = attach to collagen)

3- Vasoconstriction
3- Throm A2 + ADP being released

4- Platelet aggregation –> Fibronogen binding to platelet

30
Q

What does CLOPIDOGREL do?

A

ANTI-PLATELET
- Inhibit ADP

**PPIs decrease effect

31
Q

What does ASPIRIN do?

A

ANTI-PLATELET
- COX inhibit –> Decrease production of Throm A2

***Cannot take w Warfarin!!!

32
Q

What doe ABCIXMIAB and TIROFIBAN do?

A

ANTI-PLATELET
- Stop fibrinogen binding to platelets