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Phase 2A extra > Extra Haematology > Flashcards

Extra Haematology Flashcards

1
Q

ARTERIAL THROMBOSIS

A

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2
Q

Why do you get rest pain in calves that is classically nocturnal in arterial thrombosis?

A

When you are lying down you have removed the resistance to gravity and there is reduced CO2 so the blood flow isn’t even helped by gravity so leads to Acute limb ischemia

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3
Q

Describe the pathophysiology of arterial thrombus

A

1) Occurs as a result of an atheroma that forms in areas of turbulent blood flow such as the bifurcation of arteries
2) Platelets adhere to the damaged vascular endothelium and aggregate in response to ADP and Thromboxane A2
3) Plaque ruptures and leads to exposure of blood containing factor VIIa to tissue factor within plaque which may trigger blood coagulation and lead to thrombus formation
4) This can lead to complete occlusion of the vessel or embolisation that produces distal obstruction.

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4
Q

DVT

A

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5
Q

Where are some unusual places for venous thrombosis to occur?

A

Venous thrombosis may also occur in the upper extremities or in more unusual sites, such as the portal, mesenteric, ovarian, and retinal veins, as well as the veins and venous sinuses of the brain.

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6
Q

Name some provoked causes of DVT

A
  • Surgery
  • long haul flights
  • leg fracture
  • oral contraceptive pill
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7
Q

Pathogenesis of DVT

A
  • All factors lead to one element of Virchow’s triad.
  • Venous stasis, Hypercoagulabity, Vascular injury.
  • Venous thrombosis tends to occur in areas with decreased or mechanically altered blood flow such as the pockets adjacent to valves in the deep veins of the leg
  • While valves help to promote blood flow through the venous circulation, they are also potential locations for venous stasis and hypoxia
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8
Q

Name some genetic causes of DVT

A

These genes increase the chance of thrombus formation or lead to an antithrombin or protein C/S deficiency

1) Factor V Leiden (Factor 5 suffering)
2) PT20210A

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9
Q

Name 3 acquired causes of DVT

A

1) Anti-phospholipid syndrome
2) Lupus anticoagulant
3) Hyperhomocystaemia

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10
Q

How can you differentiate DVT from Cellulitis?

A

Duplex scan

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11
Q

How does DIPRYMIDOLE work?

A

Inhibits the phosphodiesterase-mediated breakdown of cyclic AMP which prevents platelet activation.

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12
Q

How does tissue plasminogen activator work?

A

Generates plasmin which degrades the fibrin clot.

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13
Q

What is plasma D-dimer?

A

Type of fibrinogen degradation product that is released into the circulation when a clot begins to dissolve.

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14
Q

G6PD deficiency pathophysiology

A
  • G6PD protects cells against oxidative damage from compounds like hydrogen peroxide
  • If there is a deficiency for this enzyme there is a REDUCED RBC LIFESPAN due to oxidant damage.
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15
Q

Name 5 drugs that can cause acute drug-induced haemolysis

A

1) Asprin
2) Antimalarials: primaquine, quinine, chloroquine
3) Antibacterials
4) Dapsone
5) Quinidine

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16
Q

LEUKAEMIAS

A

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17
Q

What is leukaemia?

A

Cancer of the white blood cells. Essentially leukaemia is the presence of rapidly proliferating immature blast blood cells in the bone marrow that are non-functional and defective. These can be the pre-cursors of RBC’s, platelets or white cells.

18
Q

What are the problems of leukaemia?

A

1) The leukaemia cells are dividing rapidly but they serve no function so this is WASTING ENERGY making useless cells and thus there is LESS ENERGY AVAILABLE to make useful functional cells.
2) The rapid replication of these cells means that take up a lot of space within the bone marrow meaning there are LESS SPACE AND FOOD for other cells to grow.
3) Because of this the bone marrow cannot make as many functional cells»>less functioning cells in blood&raquo_space;»symptoms of leukaemia.
4) When there is no more space in the bone marrow the leukaemia cella will be present in the blood too.

19
Q

Is leukaemia an age-specific disease?

A

They can occur at any age and the type of leukaemia varies with age. ALL seen in children, CLL seen in elderly.

20
Q

Describe the aetiology of Leukaemias

A

1) Radiation (x-rays)
2) Chemicals and dyes (benzene)
3) Genetic (Ph chromosome, trisomy 21)
4) Viruses (retrovirus type 1)

21
Q

What is lymphadenopathy?

A

Enlargement of the lymph nodes

22
Q

What are reticulocytes?

A

Immature blood cells

23
Q

ANAEMIA

A

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24
Q

What controls the process of erythropoiesis? What nutrients are needed for it?

A

Erythropoietin = key hormone
Other hormones= testosterone, thyroid hormone
Nutrients= Iron, folate, B12

25
Q

What are the causes of Microcytic Anaemia?

TAILS

A 
T – Thalassaemia
A – Anaemia of chronic disease
I – Iron deficiency anaemia
L – Lead poisoning
S – Sideroblastic anaemia
26
Q

What are the causes of normocytic anaemia?

3A’s 2H’s

A 
A – Acute blood loss
A – Anaemia of Chronic Disease
A – Aplastic Anaemia
H – Haemolytic Anaemia
H – Hypothyroidism
27
Q

What is the cause of macrocytic megaloblastic anaemia?

A

Megaloblastic anaemia is the result of impaired DNA synthesis preventing the cell from dividing normally. Rather than dividing it keeps growing into a larger, abnormal cell. This is caused by a vitamin deficiency.
Megaloblastic anaemia is caused by:
B12 deficiency
Folate deficiency

28
Q

What is the cause of macrocytic normoblastic anaemia?

A

Normoblastic macrocytic anaemia is caused by:
Alcohol
Reticulocytosis (usually from haemolytic anaemia or blood loss)
Hypothyroidism
Liver disease
Drugs such as azathioprine

29
Q

Causes of iron deficiency

A
  1. Decreased iron intake: strict vegan diet, cereal-based diet, chronic undernutrition
  2. Decreased iron absorption: hypochlorhydria(gastritis, PPI as iron absorbed here ), bowel disease(Celiac Disease, IBD, Whipple’s Disease), surgical resection of bowel
  3. Increased demand: pregnancy, lactation, growth spurt
  4. Increased iron loss: Chronic GI bleeding(cancer, ulcers, NSAIDs, hookworms), menorrhagia, bleeding disorders
30
Q

Pathophysiology of iron-deficient anaemia

A

Iron is required for haemoglobin synthesis
If there is inadequate iron, there is less iron to form the heme component
Less iron= less heme= less hemoglobin= ANEMIA

31
Q

How does iron travel around in the body?

A

Iron travels around the blood as ferric ions (Fe3+) bound to a carrier protein called transferrin.

32
Q

What is the Total iron-binding capacity (TIBC Total iron-binding capacity (TIBC

A

Total iron-binding capacity (TIBC) basically means the total space on the transferrin molecules for the iron to bind. Therefore, total iron-binding capacity is directly related to the amount of transferrin in the blood.

33
Q

Transferrin Saturation =

A

Transferrin Saturation = Serum Iron / Total Iron Binding Capacity

34
Q

Ferritin

A
  • Ferritin is the form that iron takes when it is deposited and stored in cells. Extra ferritin is released from cells in inflammation, such as with infection or cancer.
  • If ferritin in the blood is low it is highly suggestive of iron deficiency.
  • If ferritin is high then this is difficult to interpret and is likely to be related to inflammation rather than iron overload.
35
Q

Serum iron

A

Serum iron varies significantly throughout the day with higher levels in the morning and after eating iron-containing meals. On its own serum iron is not a very useful measure.

36
Q

What two things can increase the values of all of these results giving the impression of iron overload?

A

Supplementation with iron

Acute liver damage (lots of iron is stored in the liver)

37
Q

Pathophysiology of anaemia of chronic disease

A 
Inflammation🡪 Increase in cytokines and Hepcidin
Hepcidin:
Inhibits intestinal iron absorption 
Inhibits iron release from iron stores
Inhibits EPO sensitivity
Reduces erythrocyte life span
Net effect= Anemia!

Phase 2A extra (7 decks)

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