Haematological Flashcards
What is the main difference between Hodgkin and non-Hodgkin Lymphoma
HL occurs in the Reed-Sternberg cells, whereas NHL occurs in either B or T cell Lymphocytes
How is Iron maintained in the body
Controlled by absorption in the intestines and is related to cell iron content and overall rate of erythropoiesis
- Low iron stores or High erythropoiesis leads to rapid transport from intestinal wall to plasma
- High iron stores or Low erythropoiesis leads to passive crossing of intestinal membrane where its temporarily stored as Ferretin.
- Either utilised within the body or excreted in the faeces via mucosal sloughing
What Identify 6 types of anaemia
Sickle cell anemia Haemolytic anaemia Aplastic anaemia Vitamin deficient anaemia Iron-deficiency anaemia Anaemia of chronic disease
Describe Iron deficient anaemia
- Caused by inadequate iron intake or absorption, or increased requirements or losses
- Cells appear small and pale, and low in numbers
- Most frequent and common amongst females r/t menstruation and pregnancy
Describe Pernicious anaemia
- Megablastic type of anaemia caused by lack of intrinsic factor needed for Vitamin B12 transport
- Defective cells die early l/t insufficient numbers
Describe Folate deficient anaemia
Folate is required for DNA synthesis in developing Erythrocytes.
It is normally absorbed in upper small intestine and stored in the liver. This type of anaemia is common in alcoholics, malnourished or those with liver disease
Describe Aplastic anaemia
Failure of bone marrow to produce RBCs
- Chemicals
- Drugs
- Autoimmune
- Radiation
- Infection
Describe anaemia of chronic disease (Renal anaemia)
Impaired ability of the kidneys to detect hypoxia and product Erythropoietin, resulting in too few RBCs
Describe Sickle Cell anaemia
A hereditary disorder where haemoglobin links during time of Hypoxia which leads to a rigid “sickle” shape.
Classic anaemia S+S’s plus painful swelling of joints, hands and feet
Sickle cell crisis = extreme pain r/t pooling of blood in the liver and spleen, as well as, the back flow of blood and can occur in more than one location at once
Describe Haemolytic anaemia
Rupture or Haemolysis of RBCs due to an acquired congenital condition
Occurs when a the placenta with a Rh +ve Fetus detaches and enters the bloodstream of a Rh -ve mother, resulting in the production of antibodies.
If mother is given IgG antibody treatment within 72 hours it can prevent the formation of Rh antibodies
What is the Pathological mechanism of Anaemia
Anaemia may arise as a result of states whereby substances for Erythrocyte production and function are absent or defective. Such as, Iron, Folate, Vitamin B12, and intrinsic and genetic factors. Anaemia can also result from excessive Erythrocyte loss as in haemorrhage, where RBC stores are depleted quicker than can be replaced, or genetic predispositions leading to the loss of RBCs via haemolysis
What is Relative Polycythaemia
Haemoconcentration related to dehydration
What is Absolute Polycythaemia
Actual excessive RBC ratioin, can be divided in 2 categories
1- Primary: Excessive production despite low Erythropoietin
2- Secondary: Physiological response to Hypoxia, thus increased Erythropoietin levels
= COPD, High Altitudes, CHF
What is Thrombocytopaenia
Low platelet count
Low production or high consumption, radiation, Heparin
= acquired congenital conditions, Cancer, Cancer treatment, Medications
What is Heparin-Induced Thrombocytopaenia
Immune-mediated ADR to Heparin administration where IgG antibodies attach to platelet receptors causing aggregation
What is Haemophillia
An X - Chromosomal - Linked genetic abnormality
What is Haemophillia A and Haemophillia B
Haemophillia A - Von Willebrand disease, impaired factor 8
Haemophillia B - impaired factor 9
What is impaired haemostasis
Inability to promote coagulation and develop a stable fibrin clot
Associated with liver dysfunction and Vitamin K deficiency
What is Virchow’s Triad
Describes three broad categories of factors that are thought to contribute to thrombosis
- Endothelial damage
- Hypercoagubility
- Impaired blood flow
What is Disseminated Intravascular Coagulation (DIC)
Widespread activation of coagulation leading to the formation of fibrin clots in medium and small vessels
Related to major physiological event or trauma
- Exposure of tissue factor, natural anticoags dimished
- Paradoxical haemorrhage r/t consumption of platelets and clotting factors
- Fibrin clot -> hypo-perfusion -> further exacerbation
What are the manifestations of DIC
Results of either bleeding or thrombosis
Oozing from venepuncture sites, arterial lines or surgical wounds
Ecchymosis or haematoma formation
Blue finger/toe syndrome
What do thrombolytics do
Convert plasminogen in the blood to plasmin which dissolves fibrin clots
Examples: Alteplase, Reteplase, Tenecteplase
What does Warfarin do
Interferes with Vitamin K - dependent clotting factors
What does Heparin do
Combines with Anti-Thromin 3 which interferes with the normal clotting cascade to prevent clot formation
What does LMWH (Enoxpaparin) do
Increases action of anti-thrombin 3 on factor 10a, inactivation factor 10a and preventing clot formation
What is INR
International Normalised Ratio
Measures activity of the extrinsic coagulation pathway
Normal INR = 1.0 - 1.3
Therapeutic with Warfarin = 2.0 - 4.0
What is aPTT
Activated Prothrombin TIme
Measures the overall activity of the intrinsic coagulation pathway
Normal = 26 - 39 seconds Therapeutic = 50 - 90 seconds
What is ASPIRIN
4 action drug: Antipyretic Analgaesic Anti-Inflammatory Anti-Platelet
COX - 1 inhibitor
Suppresses Thromboxane
- lasts 8 - 12 days
What is CLOPIDOGREL
Irreversibly binds to P2Y - 12 platelet receptor
Inhibit factor 2b / 3a complex
What are BETA - BLOCKERS
Anti-hypertensives ending in ~olol
How do BETA - BLOCKERS work
Blocks sympathetic function on the heart by blocking Beta - 1 receptors
- reducing HR
- reducing myocardial contraction
What are the side effects of BETA - BLOCKERS
Bradycardia Fatigue Hypotension Decreased labido Impotence Broncoconstrictioin
What are the contraindications of BETA - BLOCKERS
Obstructive lung disease
PVD
Prinzmetal Angina
What are ACE INHIBITORS
Anti-hypertensives ending in ~pril
How do ACE INHIBITORS WORK
Inhibit the Angiotensin converting enzyme
Preventing AT2 and it’s effects
Reducing BP
What are side effects of ACE INHIBITORS
Dry cough Rash Nausea/Vomiting Diarrhoea Angioedema Headache
What are the contraindications for ACE INHIBITORS
Pregnancy Asthma Chronic cough Allergy Kidney disease (renal stenosis)
What are CALCIUM CHANNEL BLOCKERS
Treats HTN, Angina and Arrhythmias
By selectively blocking receptors in the pacemaker node and smooth muscle
Verapamil, Diltizem, etc
What is DESMOPRESSIN
a drug used in Haemophillia A (Von Willebrands)
Increases factor 8
IVI/IMI
ADRs- Dyspnoea, HTN, Tachycardia
Describe the difference between ‘Acute’ and ‘Chronic’ Leukaemia
Acute Leukaemia grow rapidly with a sudden onset. Symptoms appear within weeks and the cells involved are very immature “blastic cells”. The cells bear no resemblance in appearance or function of mature specialised cells
Chronic Leukaemia grow slowly with a longer, gradual onset. Symptoms appearing over years and involving less immature cells. The cells bear some resemblance of mature specialised cells in appearance and function
How does Leukaemia occur
Haematopoietic stem cells lose the ability to fully mature, resulting in uncontrolled proliferation of immature cells that crowds out the bone marrow
How can Leukaemia be classified
Acute Lymphoid Leukaemia - arising from the Lymphoid cells proliferating rapidly
Acute Myeloid Leukaemia - arising from the Myeloid cells proliferating rapidly
Chronic Lymphoid Leukaemia - arising from the Lymphoid cells proliferating slowly
Chronic Myeloid Leukaemia - arising from the Myeloid cells proliferating slowly
