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Nursing Science 3 > WEEK 5 - Haematological Disorders > Flashcards

WEEK 5 - Haematological Disorders Flashcards

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1
Q

Blood is classified as?

A

A specialised connective tissue

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2
Q

What is the function of blood and what are its constituents?

A

Transports oxygen, food and wastes around the body to maintain homeostasis.

Made up of blood cells (45%) and plasma (55%)

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3
Q

What is plasma made up of?

A

90% water and 10% solutes (proteins)

Most abundant proteins are albumin, globulins (antibodies) and fibrinogen - made by the liver

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4
Q

What is the function of plasma proteins?

A

Functions in:

  • Transport
  • Maintenance of oncotic pressure (esp. albumin)
  • Immunity
  • Clotting
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5
Q

Name the three types of blood cells?

A
  • Erythrocytes (RBCs)
  • Leukocytes (WBCs)
  • Thrombocytes (platelets)
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6
Q

Are all blood cells true cells?

A

NOP

  • Mature RBCs = no nuclei
  • Platelets = cell fragments
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7
Q

Where do blood cells originate?

A

From bone marrow, renewed via division of stem cells in bone marrow

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8
Q

Where is bone marrow found (what kind of bones)?

A

In long bones, vertebrae, cranium and sternum

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9
Q

Primary role of RBCs?

A

Transport of O2 and CO2

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10
Q

What molecule in RBCs carry O2? How many O2 molecules can each one carry?

A

Haemoglobin

Each Hb has four Fe = each one carries one O2 = four O2 per Fe

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11
Q

What makes up the cytoskeleton of RBCs?

A

Spectrin

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12
Q

Rate of RBC production depends on?

A

EPO production via the kidneys (erythropoietin)

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13
Q

At the end of their life, how are RBCs broken down?

A

Via macrophages

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14
Q

What are the five types of WBCs?

Which are granulocytes and which are agranulocytes?

A

Granulocytes:

  1. Neutrophils
  2. Eosinophils
  3. Basophils

Agranuloctes:

  1. Lymphocyte
  2. Monocytes
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15
Q

What do neutrophils do?

A

They are phagocytes - first to respond to injury

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16
Q

What do lymphocytes do?

A

B and T cells - immunity cells
T = directly attack and kill foreign cells
B = make antibodies that go and do the killing

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17
Q

What do eosinophils do?

A

Form the immune system of the GIT, have a role against parasitic worms

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18
Q

What do basophils do?

A

Contain histamines, active in allergic and inflammatory responses

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19
Q

What is the difference between leukocytosis and leukopenia?

A

Leukocytosis = WBC count higher than normal, may be due to infection

Leukopenia = WBC count lower than normal, may be due to infection or bone marrow suppression

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20
Q

What is the difference between platelets and sticky platelets?

A

Sticky = name of platelets when they are forming a blood clot ONLY

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21
Q

What are the two roles of platelets?

A
  1. Haemostasis - formation of a platelet plug to stop bleeding after injury
  2. Coagulation - release of chemical mediators by platelets required for blood clotting
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22
Q

Number of platelets in blood depends on?

A

Thrombopoeitin produced by the liver and kidneys

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23
Q

Define and describe haemataopoiesis?

A

The process of blood cell formation
Blood cells are made from haematopoietic stem cells, which then differentiate to follow the myeloid (most blood cells) or lymphoid (NK cells or T/B lymphocytes) lines.

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24
Q

What are the four blood types and their present antigens?

A 
A = A antigens
B = B antigens
AB = A and B antigens
O = no antigens
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25
Q

What are the two principles of blood typing?

A
  1. Plasma does not contain antibodies against the antigens present on its own RBCs
  2. Plasma contains antibodies against A/B antigens if they are not present on its own RBCs
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26
Q

How does the Rhesus blood typing work?

A

Gives positive or negative blood.
Rhesus antigen present = +ve blood
No Rhesus antigens = -ve blood

Those with positive blood = can have both positive and negative blood

Those with negative blood = can ONLY have negative blood, exposure to positive blood = antibody production

27
Q

What happens if the wrong blood type is give in a blood transfusion?

A

Mixture of antigens (agglutinogens) and antibodies (agglutinins) = agglutination reaction

Reaction severity depends on the individual and the amount of blood given

28
Q

What is anaemia and what causes it?

A

Blood disorder in which there is either a decreased number of RBCs or decreased Hb in RBCs

Caused by:

  • Impaired RBC production
  • Severe blood loss
  • Increased or premature RBC destruction
29
Q

Anaemia is classified by?

A

RBC size and Hb content

  • ‘-cytic’ refers to cell size
  • ‘-chromic’ refers to Hb content
30
Q

What are some of the clinical manifestations of anaemia?

A
  • Hypoxia
  • Diluted blood = increased HR, preload and SV = increased CO
  • Increased RR, dyspnoea
  • Palpitations, tachycardia, angina
  • Dizziness, fatigue
  • Yellowed, pale skin
  • Thinning, greying of hair
  • Numbness and weakness due to myelination disruption
  • GI disturbances leading to weight loss
31
Q

What is megaloblastic anaemia?

A
  • Larger than normal RBCs and smaller nuclei = macrocytic-normochromic anaemia
  • Due to defective DNA synthesis as a result of lack of Vit B12 or folate
32
Q

What is the most common type of megaloblastic anaemia?

A

Pernicious anaemia, occurs in those 60+, vague, unspecific symptoms

33
Q

What is the pathophysiology of pernicious anaemia?

A 
Genetic disorder (congenital)/gastric mucosal atrophy (autoimmune)/loss of parietal cells
Leads to lack of intrinsic factor (transporter for Vit B12)
Leads to Vit B12 deficiency
Leads to pernicious anaemia

Lack of B12 may also be due to lack of intake in diet

34
Q

Evaluation for pernicious anaemia?

A
  • Serology = presence of parietal cell ABs, decrease in B12, IF
  • Bone marrow aspirate
  • Schilling test (admin of radioactive B12 to determine excretion)
  • Gastric biopsy

All to determine if anaemia caused by lack of IF or B12

35
Q

Treatment of pernicious anaemia? What happens if it is left untreated?

A
  • B12 replacement via injection or oral dose
  • Lifelong supplementation needed if autoimmune

PA left untreated is FATAL - leads to cardiac failure

36
Q

What is iron deficiency anaemia?

A

Most common type of anaemia - due to a lack of iron

Abnormally small RBCs with low Hb content = microcytic-hypochromic anaemia

37
Q

What causes iron deficiency anaemia?

A
  • Blood loss (ulcers and cancer)
  • Poor nutritional intake or absorption (most common)
  • Increased iron requirements during youth
38
Q

How to treat iron deficiency anaemia?

A
  • Treat underlying cause = reversible

- Admin of oral or parenteral iron replacement

39
Q

What is aplastic anaemia? What is it caused by?

A

Anaemia as a result of a dysfunctional bone marrow

Caused by pancytopenia (failure of bone marrow stem cells), usually autoimmune disease, affects all blood cell types

40
Q

Treatment for aplastic anaemia?

What happens if it is not treated?

A
  • Immunosuppressants
  • Steroids
  • Bone marrow transplant

If left untreated will progress to death

41
Q

What is haemolytic anaemia?

A

Premature or accelerated destruction of own blood cells

May be due to genetics (autoimmune) or secondary to other diseases

42
Q

What is leukaemia?

A

Malignant disorder of the blood in which there is uncontrolled proliferation of WBCs that disrupts normal bone marrow function and function of the body

43
Q

How is leukaemia classified?

A

Based on cell origin (myeloid/lymphoid) and maturity of cells (acute-immature/chronic-mature)

44
Q

What are the four types of leukaemia?

A
  1. ALL - Acute lymphoblastic leukaemia (common in children)
  2. CLL - Chronic lymphocytic leukaemia (common in older population)
  3. AML - Acute myeloid leukaemia (common in adults)
  4. CML - Chronic myelocytic leukaemia
45
Q

What is ALL characterised by and what is the cause?

A

Characterised by the presence of malignant lymphoblasts in bone marrow or blood

Exact cause is unknown, may be due to radiation or toxins

46
Q

Describe the pathophysiology of ALL?

A

Lymphoblasts accumulate in bone marrow and precent normal blood cell production
Leukaemic cells are released into blood to accumulate in blood, spleen, liver, lymph nodes

Worse prognosis associated with presence of Philadelphia chromosome - translocation of genes across chromosomes leads to increased TKR activity = uncontrolled cancer cell proliferation

47
Q

Clinical manifestations of ALL?

A
  • Bone marrow suppression - fever, fatigue, bleeding and bruising
  • GI disturbance - weight loss and muscle wasting
  • Hepatomegaly, splenomegaly
  • Pts present with cold like symptoms
48
Q

Diagnosis of ALL?

A
  • Blood tests = anaemia, high WBC count

- Bone marrow aspirate

49
Q

Treatment of ALL?

A
  • Chemo
  • Stem cell transplantation - from bone marrow of donor
  • Supportive therapy - blood transfusions, nutritional support, immune system support
50
Q

Describe the pathophysiology of CLL?

A

Malignant transformation and accumulation of B lymphocytes in organs and bone marrow
B cells are defective and cannot mature into effector cells, live longer than healthy B cells

Usually occurs in adults over 60

51
Q

Diagnosis of CLL?

A

Lab analyses of blood and bone marrow

52
Q

Treatment of CLL?

A

No cure

Treated with chemo - chlorambucil - and monoclonal antibodies (immunotherapy)
Transplant is not an option for older patients

53
Q

Cause of multiple myeloma (MM)?

A

Unknown - may be due to genetics, radiation or chronic stimulation of the immune system

54
Q

Pathophysiology of MM?

A

Defective immunoglobulin is produced - infiltrates organs
Myeloma cells migrate to bone marrow, increase osteoclast activity = lesions in bones
Leads to brittle bones and can lead to kidney failure

55
Q

Clinical manifestations of MM?

A

Pain
Infections and anaemia
Renal failure

56
Q

Diagnosis of MM?

A

Radiography
Blood and bone marrow analysis
Urine tests

57
Q

Treatment of MM?

A

Chemo (thalidomide and dex)
Bortezomib - proteosome inhibitor (chemo)
Stem cell transplant - may be autologous

NOT CURATIVE, only 3-5 year survival

58
Q

What is the difference between ALL and lymphoma?

A

ALL - immature cells of the bone marrow are affected

Lymphoma - mature lymphoblasts are affected

59
Q

What is lymphoma?

A

Malignant B and T cell tumours that form in:

  • Primary lymphoid tissue (thymus)
  • Secondary lymphoid tissue (lymph nodes, spleen, tonsils)
60
Q

What are the two major types of lymphoma?

A

Hodgkin’s lymphoma and non-Hodgkin’s lymphoma

61
Q

Pathophysiology of Hodgkin’s lymphoma?

A
  • Trigger of malignant proliferation is unclear
  • Cytokines released by Reed-Sternberg cells = inflammatory damage
  • Usually starts in a single lymph node = progression to formational of masses at different body sites and organs
62
Q

Clinical manifestations of Hodgkin’s lymphoma?

A
  • Painless swelling or mass in the neck or chest
  • Enlargement of cervical, axillary, inguinal lymph nodes
  • Fever/sweating
  • Weight loss, fatigue
63
Q

Diagnosis of Hodgkin’s lymphoma?

A
  • CXR
  • Biopsy
  • Lymphangiography
  • Staging via Cotswold staging classification system (1-4)
64
Q

Treatment of Hodgkin’s lymphoma?

A
  • Chemo
  • Radiotherapy
  • Stem cell transplant

Nursing Science 3 (21 decks)

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