White Blood Cell and Lymphatic Disorders Flashcards

1. Illustrate the haematopoietic system 2. Knowledge of WBCs and their functions 3. Knowledge of signs and symptoms of WBC disorders 4. Knowledge of indices used to analyse WBC disorders 5. Interpret basic haematological data for WBC disorders 6. Elucidate dental aspects of WBC disorders

1
Q

Name the three types of granulocytes

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils, mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the morphology of neutrophils

A

Lobed nucleus

Granulocytes in cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where are neutrophils located

A

Mostly circulating; few in tissues except in inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the function of neutrophils

A

Phagocytose and digest engulfed material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the morphology of eosinophils

A

Non-segmented/bilobed nucleus

Large eosinophilic granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are eosinophils located

A

Few in tissues except in inflammation or allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the function of eosinophils

A

Participate in inflammatory reaction and immunity to parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the morphology of basophils

A

Lobed nucleus

Large basophilic granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where are basophils located

A

They are circulating as mast cells in most tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the function of basophils

A

Release histamine and inflammatory-causing chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name the three types of mononuclear phagocytes

A
  1. Monocytes
  2. Macrophages
  3. Dendritic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the morphology of monocytes and macrophages

A

Single nucleus

Abundant in cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where are monocytes located

A

In circulation where they differentiate into macrophages or dendritic cells once they reach tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the function of monocytes

A

Phagocytose and digest engulfed materials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Where are macrophages located

A

In all tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the function of macrophages

A

Phagocytose and digest materials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the morphology of dendritic cells

A

They are branched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where are dendritic cells located

A

Initially in all tissues, but migrate to the lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the function of dendritic cells

A

To gather antigens from tissues and present it to lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the morphology of lymphocytes

A

Single nucleus

Little cytoplasm before differentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are lymphocytes located

A

In lymphoid organs and in circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the function of lymphocytes

A

Participate in adaptive immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What WBC disorder involves increased production of WBCs

A

Leucocytosis (WBC > 11 bil/L)

Increased production due to reactive leucocytosis or drugs (prednisolone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What WBC disorder involves decreased production of WBCs

A

Leucopenia (WBC < 4 bil/L)

Secondary to aplastic anaemia
Cyclic neutropenia (rare autosomal dominant condition)
Chemotherapy; radiation; HIV drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is leukaemia

A

The malignant proliferation of WBCs due to;

genetics, radiation, chemotherapy, viruses, myelodysplastic syndromes (not enough healthy blood cells causing blood cancer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the classifications used for leukaemia

A
  1. Cell of origin : Lymphoid or Myeloid

2. Cell maturity : Immature (acute) or Mature (chronic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Define ALL

A

Acute lymphoblastic leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Define AML

A

Acute myeloblastic leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define CLL

A

Chronic lymphocytic leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Define CML

A

Chronic myeloid leukaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the common symptoms of leukaemia

A
  • fevers, frequent infections, night sweats, fatigue
  • easy bleeding, general CNS symptoms an GI symptoms
  • shortness of breath, painful lymph nodes
  • blurred vision, poor gait, bone + joint pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the characteristics of Acute Leukaemia

A
  1. Rapid accumulation of dysfunctional immature cells in blood and bone marrow
  2. Reduction in normal functions of RBCs/WBCs/platelets
  3. Short history of feeling unwell; neutropenic fever, bleeding and increased blasts in blood film
  4. Rashes, lumps, gingival enlargement, testiscular swelling, inter cranial pressure (meninges)
33
Q

What is ALL

A

Most common childhood leukaemia with peak incidence at ages 2-4

  • prognosis is worse in adults
  • clinically indistinguishable from AML
  • myeloperoxidase; auer rod marker
34
Q

What is AML

A

Most common adult acute leukaemia

  • poor prognosis in adults and children
  • gingival swelling in 20-30% of patients
  • nuclear stained TdT marker (DNA polymerase found in lymphoblasts/myeloblasts)
35
Q

What are the characteristics of Chronic Leukaemia

A
  1. Progresses slowly so allows more mature cell production from bone marrow
  2. Often asymptomatic so found accidentally
  3. Both forms are more common in adults
  4. Blood film: increased circulating mature lymphocytes/myeloid cells
36
Q

What is CLL

A

It is more common in men
Rare in asians
Mostly B-cell neoplasm
Splenomegaly + lymphadenopathy is common in CLL

37
Q

What is CML

A

Most patients are over 40

Associated with Philadelphia chromosome in 90% of cases (were part of chromosome 9 translocates to chromosome 22)

38
Q

What are the clinical features and oral manifestations of leukaemia

A
  1. Decreased RBCs - fatigue, pallor, hard to perform tasks
  2. Decreased platelets - mucosal bleeding, petechiae, easy bleeding and bruising
  3. Decreased WBCs - increased infection risk, poor wound healing
  4. Increased immature, abnormal, dysfunctional WBCs infiltrating organs - enlargement of gingival, lymph nodes, spleen and liver
39
Q

Management of leukaemia

A
  1. Adjunct supportive therapy
    - if anaemic give blood transfusion
    - if bleeding problems give platelet transfusion
    - if increased infection risk give granulocyte colony stimulating factor transfusion (stimulate bone marrow to make WBCs)
  2. Specific treatments
    - chemotherapy
    - radiotherapy
    - targeted therapy
    - bone marrow (stem cell) transplantation (matching donor and immunosuppressants needed)
40
Q

What is a lymphoma

A

A solid tumour (Hodgkin’s/Non-Hodgkin’s = most)

41
Q

Why do lymphomas occur

A

Due to malignant proliferation of lymphocytes within extranodal sites

42
Q

What are the signs of a lymphoma

A
  • painful lymph node
  • non-specific symptoms; fever, chills, weight loss, sweats, lack of energy, pruritus
  • swollen cervical lymph nodes and occasional mouth swellings
43
Q

What causes Hodgkin’s lymphoma

A

B-cell dysfunction therefore accumulation of abnormal B-cells

44
Q

What are the risk factors for Hodgkin’s lymphoma

A
  1. Male
  2. Bimodal age distribution; early 20s and >70
  3. Immunocompromised
  4. Positive family history
  5. History of infectious mononucleosis
45
Q

Describe the clinical presentation of Hodgkin’s lymphoma

A
  • progressive painless enlargement of lymph nodes (neck)
  • this pressurises neighbouring ducts
  • tiredness/weakness/fatigue
  • fever, anorexia, weight loss, flu-like symptoms
  • jaundice (when spread to liver), shortness of breath (when spread to lungs), bone pain
  • pruritis
46
Q

How is Hodgkin’s lymphoma testes for

A

Paplation/visually and then lymph node biopsy which show Reed-Sternberg cells (owl-like)

FBC, radiographs, CT, MRI, PET scans

47
Q

Stage I lymphoma (description and treatment given)

A

Single lymph node is involved/ single extra lymphatic

Radiotherapy

48
Q

Stage II lymphoma (description and treatment given)

A

2 or more lymph nodes on the same side of diaphragm; may have localised extralymphatics

Radiotherapy

49
Q

Stage III lymphoma (description and treatment given)

A

Lymph nodes on both sides of diaphragm; may include spleen/ localised

Radiotherapy/ Quadruple therapy (combined chemotherapy)

50
Q

Stage IV lymphoma (description and treatment given)

A

Diffuse extra lymphatic disease (liver, bone marrow, lung, skin)

Bone marrow transplant

51
Q

Dental presentation of lymphomas (rarely affects mouth)

A

Cannot distinguish Hodgkins/Non-Hodgkin’s lymphoma

  • oral infections
  • mucositis/ oral ulceration by cytotoxic drug
  • hypo salivation
  • anaemia, bleeding tendancies
  • impaired resperitary function

LA regional blocks cannot be used if bleeding tendencies so give GA in hospital

52
Q

What is Non-Hodgkin’s lymphoma

A
  1. B/T cell associated
  2. More common than HL and has a poorer prognosis and occurs at any age
  3. Can be aggressive (high grade) or non-aggressive (low)
  4. Greater presentation for EN sites (GIT, CNS)
  5. Usually multi-focal
  6. Dental aspects; Waldeyer’s ring (tonsils) is more common that in HL
53
Q

What is Burkitt’s lymphoma

A

Highly aggressive NHL associated with EBV

- starry sky pattern Burkitt cells with lipid droplets

54
Q

Endemic Burkitt’s lymphoma

A
  • African children and young adults
  • Boys
  • Jaw swellings and abdominoviscero involvement (pain and nausea)
55
Q

Sporadic Burkitt’s lymphoma

A
  • Western world
  • Males
  • Greater incidence in HIV/AIDS
56
Q

What are the causes of multiple myeloma

A

Proliferation of malignant plasma cells; overabundance of monoclonal paraproteins (M-proteins) produced by defective immunoglobulins

Malignant plasma cells release osteoclast-activating factors which cause bone resorption and pain

This had genetic links

57
Q

What are the risk factors for multiple myeloma

A
  1. > 60
  2. Males
  3. African
  4. Immunosuppression
  5. Radiation exposure
  6. Strong family history
58
Q

Outline the pathogenesis of multiple myeloma

A

Malignant plasma cells overwhelm the bone marrow and so 3 cell types are damaged as it causes…

  1. Over production of BJ (Bence Jones) protein
  2. Decrease in immunoglobulins
  3. Increased osteoclastic activity

This overwhelm bone marrow

59
Q

What does the over production of BJ proteins in multiple myeloma cause

A
  1. Hyperviscocity
  2. Amyloidosis
  3. Renal failure
  4. M proteins show up as spikes in electrophoresis
60
Q

What does the decrease in immunoglobulins cause in multiple myeloma

A

Impaired humoral immunity and increased infection

M proteins show up as a spike in electrophoresis

61
Q

What does the increased osteoclastic activity in multiple myeloma cause

A

Multiple punched out lesions affecting large bones e.g. skull

Hyper calcaemia

Pathalogical bone fractures

62
Q

What does the overwhelmed bone marrow in multiple myeloma lead to

A
  1. Leucopenia
  2. Anaemia
  3. Thrombocytopenia
63
Q

What are the other clinical features of multiple myeloma

A
  • Blood hyperviscosity - thrombosis risk
  • Weakness
  • Visual disturbance
  • Bleeding/bruising - petechiae/ecchymosis
  • Infection risk
  • Osteoporosis
  • Amyloidosis (tongue) = abnormal protein infiltration
64
Q

How is multiple myeloma tested for

A
  • FBC, renal function (urea, electrolytes, creatine)
  • Bone profile (serum Ca2+ levels)
  • Serum protein electrophoresis (M protein spike)
  • Urine BJ protein
  • Bone marrow aspiration (total bone survey shows punched out lesions)
  • Radiography of affected bone (CT/MRIs)
  • Total body bone survey
65
Q

What is the dental relevance of multiple myeloma

A
  1. Dental treatment his complicated by anaemia, infections and hemorrhagic tendencies
  2. Jaw osteolytic lesions can involving post. mandible
  3. Root resorption, loosening teeth and pathological fractures
  4. Oral complications of chemo and radiotherapy
  5. Risk of MRONJ
  6. Rare complications include
    - gingival bleeding
    - oral petechiae
    - cranial nerve palsies
    - herpes simplex and zoster infections
66
Q

What dental treatment should be done pre-chemo

A

Removal of unstable teeth
Treat caries, OH, diet tips
Chlorhexidine prophylaxis

67
Q

What dental treatment should be done during induction

A

Prevenetative OH

Antivirals (acyclovir) and anti-fungal (nystatin/flucondzole) prophylaxis

68
Q

What dental treatment should be done during remission

A

Continued oral health preventative care

69
Q

What dental treatment should be done long term

A

Continued oral health preventative care and monitoring of orofacial and dental development

70
Q

What causes reactive leucocytosis

A

Disease, infections, inflammation, neoplastic conditions

It is the elevated count of WBCs

71
Q

Clinical presentation of acute leukaemia

A
  • short history of feeling unwell
  • present with neutropenia (susceptible to infections)
  • fever, bleeding tendencies, bruising, anaemia
  • organ infiltration can occur: skin, gums, testes, meninges
  • leucocytosis = circulating blasts and cytopenias
72
Q

Clinical presentation of chronic leukaemia

A
  • incidental finding
  • long term history of non-specific symptoms
  • splenomegaly
  • lymphadenopathy
  • leucocytosis = circulating mature lymphocytes/myeloid cells
73
Q

Risk factors for NHL

A
  1. Increasing age
  2. Immunosuppression
  3. EBV, H.pylori infections
  4. Exposure to benzene, herbicides, pesticides
  5. Strong family history of NHL
74
Q

Immunodeficiency related Burkitt’s lymphoma

A

Increased in HIV/AIDS

Oran transplants

75
Q

What is the classic tetrad of clinical features for multiple myeloma

A
  1. Calcium elevation (hypercalcaemia)
  2. Renal failure
  3. Anaemia
  4. Bone pain (especially spinal, pathological fractures)
76
Q

Outline treatment options for multiple myeloma

A
  • Chemotherapy + steroids to increase chemo effectiveness
  • Immunomodulatory drugs to inhibit growth and survival of myeloma cells
  • Bone marrow transplant
77
Q

How are the symptoms and complications of multiple myeloma treated

A

Analgesics, blood transfusion, dialysis, bisphosphonates helps with fractures, radiotherapy, surgery

78
Q

What is the prognosis for multiple myeloma

A

Variable; median survival is 3 years