Blood Dyscrasias Flashcards

1
Q

What are the functions of WBC?

A
  • Neutrophil are active in non-specific phagocytosis (non-specific defence)
  • Lymphocyte - T and B cells involved with specific/acquired immunity
  • Eosinophils play a role in allergic reactions and control of helminthes (parasites)
  • Monocyte are important in non specific pahgocytosis, migrate into the tissues to become marcophages
  • Basophils release histamine and heparin
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2
Q

Define Leucytosis

A
  • WBCC < 11x10^9/L
  • Protective response to physiological stresses such as infection, inflammation, drugs, surgery and pregnancy
  • High number of WBCs cause fever
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3
Q

Define Leukopaenia

A
  • WBCC > 4x10^9/L
  • Life threatening
  • Can be caused by radiation, chemotherapy, anaphylactic shock, auto-immune diseases, thrush in patients with immunosupression
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4
Q

Define Leukaemias

A

Replacement of bone marrow by neoplastic white cell precursors, abnormal WBCs in blood

Classified as

  • Acute - immature cells predominate and divide rapidly (fatal if untreated, prognosis is better - targeting with chemotherapy)
  • Chronic - predominance of more mature cells which divide slowly (difficult to treat)
  • Lymphocytic
  • Non-Lymphocytic
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5
Q

What are the causes of leukaemia?

A
  • Hereditary factors - fragile chromosomes
  • Chromosomes abnormalities e.g. down’s syndrome
  • Haematological disease
  • Viruses
  • Chemical Carcinogens
  • Radiation
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6
Q

How do you manage leukemia?

A
  • Big ICE and G-CSF chemotherapy
  • Etoposide - mitotic poison
  • Idarubicin
  • Cytrarabine
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7
Q

Define Neutropoenia

A
  • Decrease in absolute neutrophil count

Effects
- Risk of life threatening infection, and ulceration of mouth and GIT, diarrhoea, and skin infections

Treatments

  • Isolation to reduce further infections
  • Oral care to minimise thrush
  • G-CSF to stimulate BM
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8
Q

Define Hodgkin’s Lymphoma

A
  • Cancer from WBC called lymphocytes
  • Swollen but painless lymph nodes
  • Presence of giant Reed-Sternberg cells
  • Good prognosis compared to Non-Hodgkins
  • Well managed by radiation or chemotherapy
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9
Q

Define Non-Hodgkins Lymphona

A
  • Massive cervical lymphadenopathy
  • Weakened immune system
  • Different subtypes depending on rate of growth of malignant cells
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10
Q

Define Multiple Myeloma

A
  • Malignancy involving plasma cells in BM
  • 2nd most common blood cancer after Non-Hodgkins Lymphoma
  • Oncogene on chromosome 14, higher risk to petrol industry and metal workers
  • High number of plasma cells cause increased pressure on bones creating holes and high blood Ca2+
  • Blood becomes very viscous due to high concentration of antibodies and Ca2+ which can cause renal damages
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11
Q

RBC Structure

A
  • maximise Hb content

- faciliates diffusion of gases

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12
Q

How does the body handle old RBCs

A
  • removed by marcophages in spleen and liver
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13
Q

Define Anaemia

A
  • Blood is deficient in quality or quantity of Hb
  • leads to hypoxia as RBC cannot transport sufficient O2

Causes

  • impaired RBC production (bone marrow defect)
  • blood loss
  • RBC destruction e.g. malaria
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14
Q

What the clinical manifestation of anaemia?

A
  • Fatigue - insufficient O2
  • Cold - reduced peripheral circulation
  • Pallor of mucous membranes, conjuctiva and skin
  • Tachycardia
  • Palpitations
  • Dyspnoea
  • Dizziness
  • Jaundice
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15
Q

How does the body respond to Anaemia?

A
  • Redistribution of blood to tissues that have a high O2 need
  • removal of more O2 by tissues
  • Increased HR or SV
  • Increased production of RBCs
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16
Q

Classification of Anaemias (Based on Morphology)

A

Hypochromic microcytic

  • small, pale RBC, normal or low RBC count
  • Iron deficiency
  • Thalassaemia (diseases relating to Hb)
  • Chronic disease

Normochromic normocytic

  • cells normal in size but low RBCC
  • blood loss
  • haemolytic anaemia

Normochromic macrocytic anaemia

  • large RBC, low RBCC, no central pallor
  • megaloblastic anaemia - folate of B12 deficiency
  • Aplastic anaemia
17
Q

Define Polycythaemia

A

Too many RBCs - increased synthesis in overactive bone marrow

  • problems include circulatory problems relating to increased viscosity and volume: elevated BP, CCF, venous pooling, thrombus formation and PO
18
Q

How is anaemia classified?

A

size of cell

19
Q

common clinical manifestations of anaemia?

A
  • yellow eyes
  • pale and cold skin
  • SOB
  • muscular weakness
  • changed stool colour
  • fatigue, dizziness and fainting
  • low blood pressure
  • rapid HR, chest pain, HA
  • spleen enlargement
20
Q

Mechanisms that triggers disseminated intravascular coagulation?

A
  • release of tissue factor into circulation

- widespread injury to endothelial cells

21
Q

Signs and Symptoms of Disseminated intravascular coagulation

A
  • formation of blood blots throughout the body followed by bleeding once all coagulation factors have been used
  • SOB
  • Chest pain
  • DVT
  • headaches, speech changes, signs of stroke
  • blood in urine and stools
  • low bp
22
Q

Define the term fever

A
  • 36-37 temperature due to the increase in hypothalamic set point
  • Pyrogens stimulate the release of prostaglandin (PGE2) which causes the hypothalamus to elicity body reponses that raise T
  • used to combat infections
  • increases mobility of leukocytes
  • increased proliferation of T cells
23
Q

What is lymphadenopathy?

A
  • disease of lymph nodes
  • lymph nodes swollen/enlarged
  • enlarged lymph nodes are commonly associated with infectious and malignant disease
24
Q

Define acute lymphoblastic leukaemia

A
  • a lymphoid progenitor cell becomes genetically altered by carcinogens which then undergoes uncontrolled proliferation and cell population expansion
  • spread to thymus gland, spleen, lymph nodes, testes and CNS (nausea, vomiting, seizures), joint pain (infiltration of malignant lymphoblasts)
25
Q

Signs and symptoms of Acute lymphoblastic leukaemia

A
  • ## anaemia (paleness and fatigue), neutropenia (fever secondary to infection), thrombocytopaenia (higher tendencies to bleed and bruise)
26
Q

Causes and risks factors of leukaemia

A
  • remain relatively unknown

- congential chromosomal abnormalities e.g. down’s syndrome, turner syndrome

27
Q

Why do enlarged lymph nodes occur?

A
  • lymph nodes infiltration with lymphoblasts
  • cells rapidly divide causing lymph node to swell
  • swelling may be observed in auxiliary, cervical and inguinal
28
Q

What do enlarged spleen occur?

A
  • spleen filters abnormal blood cells and removes them from circulation
  • spleen enlarges as it is infiltrated by malignant leukaemia cells
29
Q

Meningococcal meningitis signs

A

stiff neck, photosensitivity, severe headache, purpura

30
Q

Septicemia signs

A

tachycardia (fluid shift to systemic infection) and hypotension

31
Q

Why is low renal output a sign of septic shock?

A

Body compensates for low blood volume by retaining fluid thus decreasing urine output

32
Q

infection organisms associated with meningococcal

A

Neisseria Meningitidis

33
Q

Difference between meningitis and meningococcal septicaemia

A

Meningitis occurs as the result of bacteria entering the bloodstream and infecting the meninges resulting in inflammation which increases intracranial pressure leading to coma, seizures and death

Septiceamia occurs which blood enters the bloodstream, dividing rapidly leading to a systemic inflammatory reaction

both usually occur in tandem