Haematological Flashcards

1
Q

What is the main difference between Hodgkin and non-Hodgkin Lymphoma

A

HL occurs in the Reed-Sternberg cells, whereas NHL occurs in either B or T cell Lymphocytes

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2
Q

How is Iron maintained in the body

A

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
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3
Q

What Identify 6 types of anaemia

A
Sickle cell anemia
Haemolytic anaemia
Aplastic anaemia
Vitamin deficient anaemia
Iron-deficiency anaemia
Anaemia of chronic disease
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4
Q

Describe Iron deficient anaemia

A
  • 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
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5
Q

Describe Pernicious anaemia

A
  • Megablastic type of anaemia caused by lack of intrinsic factor needed for Vitamin B12 transport
  • Defective cells die early l/t insufficient numbers
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6
Q

Describe Folate deficient anaemia

A

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

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7
Q

Describe Aplastic anaemia

A

Failure of bone marrow to produce RBCs

  • Chemicals
  • Drugs
  • Autoimmune
  • Radiation
  • Infection
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8
Q

Describe anaemia of chronic disease (Renal anaemia)

A

Impaired ability of the kidneys to detect hypoxia and product Erythropoietin, resulting in too few RBCs

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9
Q

Describe Sickle Cell anaemia

A

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

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10
Q

Describe Haemolytic anaemia

A

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

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11
Q

What is the Pathological mechanism of Anaemia

A

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

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12
Q

What is Relative Polycythaemia

A

Haemoconcentration related to dehydration

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13
Q

What is Absolute Polycythaemia

A

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

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14
Q

What is Thrombocytopaenia

A

Low platelet count
Low production or high consumption, radiation, Heparin
= acquired congenital conditions, Cancer, Cancer treatment, Medications

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15
Q

What is Heparin-Induced Thrombocytopaenia

A

Immune-mediated ADR to Heparin administration where IgG antibodies attach to platelet receptors causing aggregation

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16
Q

What is Haemophillia

A

An X - Chromosomal - Linked genetic abnormality

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17
Q

What is Haemophillia A and Haemophillia B

A

Haemophillia A - Von Willebrand disease, impaired factor 8

Haemophillia B - impaired factor 9

18
Q

What is impaired haemostasis

A

Inability to promote coagulation and develop a stable fibrin clot

Associated with liver dysfunction and Vitamin K deficiency

19
Q

What is Virchow’s Triad

A

Describes three broad categories of factors that are thought to contribute to thrombosis

  • Endothelial damage
  • Hypercoagubility
  • Impaired blood flow
20
Q

What is Disseminated Intravascular Coagulation (DIC)

A

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
21
Q

What are the manifestations of DIC

A

Results of either bleeding or thrombosis
Oozing from venepuncture sites, arterial lines or surgical wounds
Ecchymosis or haematoma formation
Blue finger/toe syndrome

22
Q

What do thrombolytics do

A

Convert plasminogen in the blood to plasmin which dissolves fibrin clots

Examples: Alteplase, Reteplase, Tenecteplase

23
Q

What does Warfarin do

A

Interferes with Vitamin K - dependent clotting factors

24
Q

What does Heparin do

A

Combines with Anti-Thromin 3 which interferes with the normal clotting cascade to prevent clot formation

25
What does LMWH (Enoxpaparin) do
Increases action of anti-thrombin 3 on factor 10a, inactivation factor 10a and preventing clot formation
26
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
27
What is aPTT
Activated Prothrombin TIme Measures the overall activity of the intrinsic coagulation pathway ``` Normal = 26 - 39 seconds Therapeutic = 50 - 90 seconds ```
28
What is ASPIRIN
``` 4 action drug: Antipyretic Analgaesic Anti-Inflammatory Anti-Platelet ``` COX - 1 inhibitor Suppresses Thromboxane - lasts 8 - 12 days
29
What is CLOPIDOGREL
Irreversibly binds to P2Y - 12 platelet receptor Inhibit factor 2b / 3a complex
30
What are BETA - BLOCKERS
Anti-hypertensives ending in ~olol
31
How do BETA - BLOCKERS work
Blocks sympathetic function on the heart by blocking Beta - 1 receptors * reducing HR * reducing myocardial contraction
32
What are the side effects of BETA - BLOCKERS
``` Bradycardia Fatigue Hypotension Decreased labido Impotence Broncoconstrictioin ```
33
What are the contraindications of BETA - BLOCKERS
Obstructive lung disease PVD Prinzmetal Angina
34
What are ACE INHIBITORS
Anti-hypertensives ending in ~pril
35
How do ACE INHIBITORS WORK
Inhibit the Angiotensin converting enzyme Preventing AT2 and it's effects Reducing BP
36
What are side effects of ACE INHIBITORS
``` Dry cough Rash Nausea/Vomiting Diarrhoea Angioedema Headache ```
37
What are the contraindications for ACE INHIBITORS
``` Pregnancy Asthma Chronic cough Allergy Kidney disease (renal stenosis) ```
38
What are CALCIUM CHANNEL BLOCKERS
Treats HTN, Angina and Arrhythmias By selectively blocking receptors in the pacemaker node and smooth muscle Verapamil, Diltizem, etc
39
What is DESMOPRESSIN
a drug used in Haemophillia A (Von Willebrands) Increases factor 8 IVI/IMI ADRs- Dyspnoea, HTN, Tachycardia
40
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
41
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
42
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