Haematology Flashcards
1
Q
What are the Cellular Components of blood?
A
Erythrocytes (RBC)
Leucocytes (WBC)
Platelets (Thrombocytes)
2
Q
Blood Constituents -
55% ________
A
Plasma
Leucocytes and Platelets
Erythrocytes
3
Q
What is Haematocrit?
A
The percentage of erythrocytes as proportion of the total blood volume.
(Adult female - 37-47%)
(Adult male - 40-54%)
4
Q
Erythrocytes (Red Blood Cells (RBC) ) contain millions of molecules of _______________.
A
Haemoglobin (Hb)
5
Q
Erythrocytes life-span is ______ days.
Old erythrocytes are destroyed by ________ in liver and spleen.
A
120.
Macrophages.
6
Q
Iron from recycled Hb is used to form new RBC.
True or False?
A
True!
7
Q
What is Erythropoiesis?
A
Production of Erythrocytes.
8
Q
Explain the cycle of Erythropoiesis.
A
- Too few RBC leads to hypoxia.
- Hypoxia detected by kidney.
- Kidney secretes hormone erythropoietin (EPO).
- EPO stimulates red bone marrow to produce RBCs.
9
Q
Specific dietary needs are required for Erythropoiesis.
These include……..
A
Iron - Production of Hb.
Vitamin B12 - Production of DNA.
Folic Acid (Folate) - Production of DNA.
10
Q
A decrease in Hb in blood (below normal for age and sex), resulting in hypoxia and hypoxaemia is known as ______________.
A
Anaemia.
Can be due to: Decreased production of RBC, increased destruction of RBC or increased loss of RBC.
11
Q
Hypoxia secondary to anaemia causes compensatory mechanisms in the _____________ system and the _________ system.
A
Cardiovascular system - vasodilation, causes increased HR and SV to compensate, can lead to heart failure.
Respiratory system - increased respiratory rate and depth, Dyspnoea.
12
Q
Typical symptoms of Anaemia include:
A
Fatigue, Dyspnoea on exertion. Coldness. Pallor. Dizziness. Lips, skin, conjunctivae, nail beds may appear pale. Poor wound healing. Abdominal pain, nausea, vomiting.
(If mild anaemia, symptoms only occur upon exertion).
13
Q
In Anaemia diagnosis, what do blood tests measure?
A
Mean cell volume (MCV), size of RBC. Mean cell Hb (MCH), Hb content (can be indicated by colour of RBCs). Total Hb (g/L). Haematocrit. Reticulocyte count (immature cell).
14
Q
What is Plasma made up of?
A
Plasma is 90% water, plasma proteins, globulins (Antibodies), clotting factors, electrolytes.
15
Q
There are many different types of Anaemia.
List the types of Anaemia that occur from Decreased RBC production:
A
Iron deficiency anaemia
Folate deficiency anaemia
Pernicious anaemia
16
Q
What type of Anaemia occurs from Increased RBC destruction or loss.
A
Post haemorrhagic anaemia.
17
Q
The most common type of Anaemia is ___________.
What are the causes?
A
Iron deficiency anaemia.
Causes:
Inadequate iron intake (vegan etc.)
Inadequate iron absorption (coeliac).
Increased iron requirement (growth, pregnancy).
Excessive iron loss (bleeding, chemotherapy).
18
Q
RBC characteristics in Iron deficiency anaemia are:
Microcytic &
Hypochromic.
What do these terms mean?
A
Microcytic - cells too small.
Hypochromic - cells too pale (not enough iron).
19
Q
How is Iron deficiency anaemia managed?
A
Treat cause of blood loss.
Assess body iron status (fingerprint test).
Iron supplements, oral or parenteral (injection).
20
Q
Folate deficiency anaemia occurs due to inadequate folate intake or increased requirements.
The RBC characteristics are:
Macrocytic &
Normochromic.
What do these terms mean?
A
Macrocytic - cells too large (don’t fit in tiny vessels).
Normochromic - Normal colour.
21
Q
Who is at risk of Folate deficiency anaemia?
A
Alcoholics. Pregnant, lactating females. Malabsorption sufferers. People who don't eat veges. Some medications.
22
Q
Folate deficiency anaemia should be treated with oral supplements.
What can occur during pregnancy if folate intake is inadequate?
A
Birth defects.
23
Q
What is Pernicious anaemia?
A
Anaemia caused by insufficient intrinsic factor in the stomach. (Inability to absorb vitamin B12 from small intestine).
24
Q
In Pernicious anaemia, RBC characteristics are:
Macrocytic &
Normochromic.
What do these terms mean?
A
Macrocytic - cells too large (can’t fit through tiny vessels).
Normochromic - normal colour.
25
What are the clinical features of Pernicious anaemia?
Typical symptoms of anaemia.
Usually severe on presentation (develops over many years).
Neurological abnormalities may develop;
Numbness, tingling, difficulty walking, confusion, depression.
26
Who is at risk of Pernicious anaemia?
What are the treatments?
Vegan/vegetarian children.
Elderly (gastric atrophy).
Gastritis sufferers.
Treatment could be high oral doses or injections of vitamin B12.
27
What is Acute Posthaemorrhagic anaemia?
How is it treated?
Rapid loss of large blood volume from trauma or surgery.
Treatment is blood transfusion.
28
What is Chronic Posthaemorrhagic anaemia?
What is the treatment?
Slower blood loss. It can cause Iron Deficiency anaemia due to excess menstruated flow or GI bleeding (ulcers, aspirin).
Treatment should be supplemental Iron.
29
What is Polycythaemia?
Excess RBC production, results in increased blood viscosity. (Eg. EPO administration).
Can also occur through dehydration.
30
What is Secondary Polycythaemia?
A physiological response to prolonged Hypoxia.
It occurs in:
Individuals with COPD or Heart failure.
Individuals living at high altitude.
Smokers with increased blood levels of carbon monoxide.
31
Erythrocytes have surface antigens. Surface antigens are cells that ______ _____.
Belong 'to us'.
| Antigens determine major blood groups.
32
You can only receive blood from a donor which has antigens that __________! (Or no antigens)
You already have
33
```
ABO blood groups are based on two Antigens; A and B.
AB - A & B
B - B only
A - A only
O - ??
```
What is O?
Neither A nor B.
34
Type AB have both antigens. They can receive _______ types: universal recipient.
Type O have neither antigen. They can donate to ___ types: universal donor.
All
| All
35
Rh(D) blood groups are based on Rh(D) antigens (Rhesus factor).
Rh(D)+ has ___________.
Rh(D) - has ___________.
D antigen.
| No D antigen.
36
Blood groups B and A can receive their own blood groups in a transfusion, and they can also receive group O in a transfusion.
Why?
Because O group blood contains neither A or B antigens and is a universal donor.
(You can only receive blood from a donor who has the SAME antigens as you, or no antigens)
37
Transfusion of mismatched blood causes agglutination of RBCs (clump together) (NOT blood coagulation!).
What are the dangers of this?
Small blood vessels can get blocked.
Haemolysis (break down) occurs.
Release of Hb causes kidney damage.
May be fatal.
38
Leucocytes form our immune system and protect us from..........,
Bacteria, viruses, parasites, toxins and tumour cells.
39
What are the 5 different types of Leucocytes, and their roles?
Neutrophils- phagocytosis of bacteria, debris. Present in large numbers during bacterial infection.
Eosinophils - release enzymes that digest parasitic worms.
Basophils - produce histamine, vasodilator, attract other WBCs. (Mast cells produce heparin - anticoagulant).
Monocytes including Macrophages - phagocytosis in specific tissues.
Lymphocytes - B & T lymphocytes: for specific immunity; Natural Killer cells: destroy tumour cells and viruses.
40
What is Leukaemia?
Uncontrolled production of malignant Leucocytes.
Insufficient production of other blood cells due to 'overcrowding' of bone marrow.
Cause - unknown
(Leucocytosis - increased number of Leucocytes, but are abnormal, don't function properly).
41
What are the clinical features of Leukaemia?
Repeated infections.
Tiredness, dizziness, shortness of breath, pale complexion.
Bleeding or Bruising.
42
Leukaemia patients may develop secondary Anaemia or thrombocytopenia.
Why?
Because so many WBC are being produced, the bone marrow is 'overcrowded' and there is not enough room for RBC or platelet production.
43
What methods may be used for Leukaemia diagnosis?
Blood test (for immature cells).
Bone marrow biopsy (spinal tap).
Lumbar puncture (looking for metastasis in CSF).
Chest x-Ray.
44
What treatment is available for Leukaemia?
```
Chemotherapy
Bone Marrow or stem cell transplant (taken from patient prior to chemo or from a family member).
Radiotherapy
Steroid therapy
Treat anaemia and thrombocytopenia
Treat infection.
```
45
Acute Lymphoblastic Leukaemia is rare but is the most common _____ _______.
Childhood cancer (0-14 years).
Progresses quickly, fatal if not treated adequately.
46
Uncontrolled proliferation of malignant lymphocytes is known as......
Lymphoma
47
Hodgkins Lymphoma makes up ____% of Lymphomas.
30
48
B cell, T cell and natural killer cell Lymphomas were previously known as _____ _______.
Non-Hodgkins Lymphoma
49
Causes of Lymphoma include:
Genetic mutations.
Age over 50.
Weakened immune system.
50
Lymphoma usually starts with _____ _____ _____.
Other symptoms include:
Enlarged Lymph nodes.
Recurrent fevers.
Lack of energy.
Night sweats.
Unintentional weight loss.
51
B & T cell Lymphomas- abnormal lymphocytes collect in lymph nodes:
____% are B cell lymphomas.
____% are T cell lymphomas.
80
| 20.
52
What treatment is available for Lymphoma?
Chemotherapy.
Radiotherapy.
Stem cell transplant.
(May not require treatment if slow growing. Lymphoma is often cured).
53
______ is suppressed in Lymphoma.
p53 gene
54
What are the 3 steps in Platelet Plug formation?
Platelet Adhesion - Platelets adhere to subendothelial collagen (vonWillebrand's factor is needed).
Activated Platelets Release - ADP: attracts platelets, Serotonin: causes vasoconstriction, Thromboxane A2: causes vasoconstriction and attracts platelets.
Platelet Aggregation - platelets coextensive with other platelets.
55
What is Coagulation?
Formation of a fibrin clot (strands/mesh).
Inactive clotting factors (in blood) become activated.
56
Coagulation cascade includes ______ and ________ pathways.
________ is essential!!
Intrinsic (blood)
Extrinsic (tissue)
Calcium!!!
57
What occurs at the final common pathway in coagulation?
Factor X becomes activated to Factor Xa.
Prothrombin is converted to Thrombin.
Fibrinogen is converted to a cross-linked fibrin mesh.
58
What is Fibrinolysis?
Break down of a clot.
Plasminogen Activator is released - converts plasminogen to plasmin - plasmin dissolves cross-linked fibrin threads.
59
What is Heparin and why is it used?
Anticoagulant
(Inactivates clotting factors, Inactivates thrombin).
Used to prevent and treat thrombosis.
Treat acute coronary syndromes.
Use IV prior to invasive surgery.
60
Heparin is a medication but our body also produces this.
| True or False?
True!
61
What is Warfarin and why is it used?
Anticoagulant.
(Inhibits production of vitamin k dependant clotting factors, takes several days to take effect).
Uses include treating Deep Vein Thrombosis, reduces the risk of stroke after atrial fibrillation.
62
Heparin and Warfarin are both anticoagulants. Which one is more likely to be used long-term?
Warfarin.
63
What is the role of Thrombolytics?
Break down fibrin.
Eg. Tissue plasminogen activator (tPA) streptokinase (Streptase).
Used to treat acute MI, unstable Angina.
64
Name an Antiplatelet drug. What does it do and what is it used for?
Aspirin.
Inhibits platelet aggregation and the production of COX enzyme.
It's used in acute MI and unstable Angina. It prevents thrombotic events in cardiovascular patients.
65
Anticoagulants such as Trisodium citrate can be used for prevention of coagulation in blood sample tubes.
Why can't these type of drugs be used in the body?
Because these drugs bind calcium. If this occurs in the body, no calcium will be available for neurotransmission.
66
Venous Thromboembolism (VTE) consists of........
```
Deep Vein Thrombosis (DVT) and
Pulmonary Embolism (PE).
```
67
What is Deep Vein Thrombosis (DVT)?
What are the causes?
Blood clot in deep vein (usually in lower limbs).
Caused by slow or turbulent blood flow eg. Prolonged bed rest, MI.
Damage to endothelium of blood vessel eg. Hypertension, surgery.
Excessive coagulation eg. Inherited factors.
68
According to Virchow's Triad, what are the 3 factors that contribute to DVT?
Abnormalities of blood vessel wall.
Abnormalities of blood flow.
Abnormalities of blood constituents.
69
What are the common pre-disposing causes of DVT?
Immobility.
Pregnancy and childbirth.
Oestrogen therapy.
Intravenous cannulae (vessel injury).
70
What are the clinical features of DVT?
Localised symptoms of redness, heat, tenderness, swelling and pain (usually in the lower limbs).
71
Name some ways to manage DVT.
Anticoagulant therapy eg. Heparin.
Graduated compression stockings.
Intermittent pneumatic compression.
Early ambulation (up as quickly as possible!)
72
What are the 3 tests to evaluate haemostasis?
Coagulation tests.
Platelet count and platelet function.
D-dimer tests.
(Blood disorders)
73
What is measured in Coagulation tests?
```
Prothrombin time (PT). Assesses extrinsic pathway, Used to calculate INR (International normalised ratio) which is clotting time for patient compared to normal.
Activated partial thromboplastin time (aPTT) - assesses intrinsic pathway.
Thrombin Time - assesses final common pathway ( measuring conversion time of fibrinogen into fibrin).
```
74
What happens in a Platelet count and function test?
Measure number of platelets with full blood count. (Platelet function can also be tested).
75
What is a D-dimer test?
D-dimer is a degradation product of cross-linked fibrin. Levels can be measured. Elevated levels indicates recent or ongoing Fibrinolysis.
76
There are 3 different types of skin haemorrhages (from bleeding disorders) that are different in size.
What are they called?
Petechiae (1-2mm)
Purpura (1cm)
Ecchymoses (large patches).
77
Besides skin haemorrhages, what are other clinical features of bleeding disorders?
Bleeding gums.
Epistaxis (nose bleed).
Bleeding in joints or muscles.
Menorrhagia (excessive menstrual bleeding), GI bleeding, prolonged bleeding following surgery or tooth extraction.
78
What is von Willebrand Disease?
It's the most common bleeding disorder, hereditary.
| Occurs when there is insufficient functional von Willebrand factor (which is needed for normal platelet function).
79
What are the clinical features of von Willebrand disease?
Bleeding tendency mild to severe.
Spontaneous bleeding in mouth or nose.
Prolonged bleeding following trauma or surgery.
80
Diagnostic blood testing for von Willebrand disease will show........
Platelet function is decreased.
| Extended time for some coagulation tests.
81
What treatment is available for von Willebrand disease?
Desmopressin - Increases release of vWF (von Willebrand factor).
If mild, only needed with surgical procedures.
If severe, plasma transfusions.
82
Haemophilia A is............,
The most common form, and has a deficiency of clotting factor VIII.
83
Haemophilia B is..........
Deficiency of clotting factor IX.
84
Haemophilia is an hereditary disease which only affects males. However females can be carriers.
True or false?
True!
85
What are the clinical features of Haemophilia?
Mild - Bleeds usually only with trauma and surgery.
Severe - spontaneous bleeds, excessive bleeds into tissues and joints, causing loss of function and pain.
86
What will diagnostic blood tests show in haemophilia?
Platelet count normal.
| Extended time for some coagulation tests.
87
Ways to manage Haemophilia include........
Reduce risk of haemorrhage - lifestyle choices, avoiding aspirin.
Clotting Factor drugs- if mild, only treat during surgical procedures.
If severe, plasma transfusions.
88
What is Thrombocytopenia and how is it caused?
Low platelet count.
decreased production in platelets, or increased destruction or consumption of platelets.
Causes include, chemotherapy, viral infections such as HIV, heparin-induced thrombocytopenia
89
What is Heparin-induced Thrombocytopenia?
Heparin is used during surgery, but some patients have a reaction to Heparin.
It involves the immune system, antibodies go to platelets, which causes platelet aggregation and thrombosis.
May trigger MI, DVT or PE.
Limits available platelet numbers.
90
Treatment for Thrombocytosis includes....
Stop use of Heparin.
Use various other anticoagulant medications eg. Warfarin.
If severe, transfusion of platelets may be used.
91
What is Disseminated Intravascular Coagulation (DIC)?
A complex systemic disorder which is life threatening.
Usually associated with other major clinical conditions.. Obstetric emergencies etc.
92
What happens in Disseminated Intravascular Coagulation?
Excessive coagulation.
Severe bleeding.
Resulting in capillary damage, organ dysfunction.
93
What are the clinical features of Disseminated Intravascular Coagulation?
If acute, bleeding, continual oozing, Petechiae, purpura, ecchymoses, redness, heat and pain in lower limbs.
If chronic, organ damage/failure, gangrene of fingers/toes.
94
Treatment for Disseminated Intravascular coagulation includes:
Treat the underlying cause.
Stabilise patient.
Control bleeds.
Transfusion only if life threatening.
95
Use of Heparin is controversial in Disseminated Intravascular Coagulation.
Why?
It can help clots but exacerbate bleeding.
