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CMS > Blood > Flashcards

Blood Flashcards

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Introductory Sommelier Exam (CMS) flashcards
1
Q

The correct name for RBCs =
The correct name for WBCs =

A

RBCs= Erythrocytes
WBCs = leukocytes

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2
Q

Lifespan of an erythrocyte is __

A

120 days

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3
Q

All blood cells are derived from:

A

Haematopoietic stem cell

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4
Q

Myeloid stem cells matures into:

A

Erythrocytes, platelets, eosinophil, neutrophils, basophils

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5
Q

What is leukaemia

A

Cancer of the haematopoietic stem cell in bone marrow

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6
Q

What are the 4 classifications of leukaemia (in chronology of when they present)

A

Acute Lymphoblastic
Chronic Lymphoblastic
Chronic Myeloid
Acute Myeloid

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7
Q

Outline acute lymphoblastic leukaemia

A
  • acute proliferation of a single type of lymphocyte (usually beta)
  • causes replacement of other cells in bone marrow
  • most common cancer in children (peaks ~2-4 yrs age)
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8
Q

Outline Chronic lymphoblastic leukaemia

A

chronic proliferation of lymphocytes (usually B)
Richter’s transformation = can transform into high-grade lymphoma

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9
Q

what are ‘smudge cells’ and what do they suggest?

A

during preparation of blood film, the fragile WBC rupture to leave a smudge on the film
Chronic lymphoblastic leukaemia

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10
Q

Outline Chronic Myeloid Leukaemia

A

3 phases:
Chronic (~5 years durations, often asympto)
Accelerated (abnormal blast cells)
Blast (even high proportions of blast cells, often fatal)

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11
Q

Outline Acute Myeloid leukaemia

A

Most common leukaemia in adults
Blood films will show Auer Rods (rods in the cytoplasm)

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12
Q

Define pancytopenia

A

(pan = many, cyt = cell, penia = lack of)
A lack of all 3 cellular blood components,
Anaemia, Leukopenia, thrombocytopenia

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13
Q

What are oral manifestations of leukaemia

A
  • New/rapidly changing gingival hyperplasia +/- bleeding, ulceration, petechial haemorrhages (pinprick red/brown macules on hard palate)
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14
Q

How is leukaemia diagnosed

A

Bone marrow biopsy
FBC (full blood count)
CT, MRI, PET

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15
Q

Define lymphoma

A

Umbrella term encompassing a range of cancers derived from lymphocytes

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16
Q

What is the difference between lymphoma and leukaemia?

A

Leukaemia = develops in bone marrow
Lymphoma = develops in lymph nodes

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17
Q

What outlines Hodgkin’s lymphoma?

A
  • Prescence of Reed-sternberg cells (multinucleated cells in lymph nodes)
  • preferentially in cervical lymph nodes
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18
Q

Risk Factors for Hodgkin’s lymphoma

A
  • Family history
  • HIV/AIDs
  • EBV (Epstein-Barr Virus)
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19
Q

Tx for Hodgkin’s lymphoma

A

Radiotherapy as often well localised

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20
Q

What differentiates Hodgkin’s vs non-Hodgkin’s lymphoma?

A

Presence (Hodgkins) or absence (non-hodgkins, (85% of lymphomas) of Reed-Sternberg cells

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21
Q

Clinical presentation of Non-Hodgkin’s lymphoma:

A
  • Cervical lymphadenopathy
  • fever
  • night sweats
  • Cancer red flags (unexplained weight loss, loss of appetite, fatigue)
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22
Q

Tx of non-Hodgkin’s lymphoma

A

depends of grade of disease
combo of local radiotherapy and chemo (Rituximab)

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23
Q

Define Myeloma

A

Blood cancer arising from plasma cells (B lymphocytes that produce specific antibodies)
Same thing as multiple myeloma (it’ll always occur in more than one location)

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24
Q

Aetiology of Myeloma

A

DNA is damaged during development of plasma cells, causing abnormal replication, all producing the same antibody

25
Q

Problems associated with myeloma

A

normally issues come from the build-up of the excessive antibody (paraprotein)
- deposition into organs can cause kidney failure

26
Q

What are the key CRAB features of Myeloma?

A

C - calcium (hypercalcaemia)
R - Renal failure
A - anaemia
B - bone disease

27
Q

Dental impacts of myeloma

A

Hyperviscocity of blood - spontaneous bleeding
impaired renal function
MRONJ from medications

28
Q

What can happen after a bone marrow transplant?

A

Graft vs Host Disease

29
Q

Effects of leukaemia/myeloma on pt:

A
  • infections from lack of WBCs (longer lasting, more severe)
  • bleeding and bruising in skin from thrombocytopenia
  • medications
  • side effects of chemo
30
Q

Define Anaemia

A

reduction of haemoglobin in the blood

31
Q

what are the normal ranges of haemoglobin?

A

Males = 13.5 g/dL
Females = 11.5g/dL

32
Q

What is MCV (Mean Corpuscular volume)

A

describes size of erythrocytes, measures mean cellular volume

33
Q

Give 2 examples of what causes Macrocytic anaemia

A

Macrocytic - large RBCs
-B12 deficiency anaemia
- Folate deficiency anaemia

34
Q

Give an example of what causes microcytic anaemia

A

Iron-deficient anaemia (usually due to diet, chronic blood loss)

35
Q

Key causes of anaemia:

A
  • reduced production (chronic inflammation, leukaemia, marrow failure)
  • increased loss of RBCs (bleeding, haemorrhoids, trauma, peptic ulcer)
  • increased demand (pregnancy, malignancy)
36
Q

Signs and symptoms of anaemia:

A
  • pale conjunctiva
  • depapillation of tongue (smooth)
  • common oral ulcerations
37
Q

Tx of anaemia:

A

Treat the cause =
Folate deficiency - folate tablets
iron deficiency - iron tablets
B12 deficiency - B12 intramuscular injections

38
Q

Dental relevance of anaemia

A
  • lots of dental presentations
  • Reduced O2 carrying capacity (sedation/GA risk)
  • more prone to candidiasis
39
Q

What is thalassemia, and what are the two types?

A

Hereditary condition (autosomal recessive) affecting the globin protein chains of haemoglobin, RBCs break down more easily
2 types: Alpha is affects the alpha chains, Beta if affects the Beta chains

40
Q

What are some presentations of thalassemia?

A

Splenomegaly - spleen swells to collect all destroyed RBCs + act as seive

41
Q

Dental Relevance of thalassemia:

A
  • Chronic anaemia
  • Cirrhosis
  • iron deposition in all glands (inc. salivary) = xerostomia
  • GA and sedation risk from <O2 carrying
42
Q

Aetiology of Sickle Cell Anaemia

A

Mutation in the HBB (Beta-Haemoglobin Gene)
Autosomal Recessive - causes sickle shaped RBCs and Haemolytic anaemia (anaemia from excess haemolysis)

43
Q

Outline what happens during a sickling crisis:

A

Umbrella term for acute conditions:
- Painful > sickle shape clogs capillaries, causing distal ischaemia
- Sequestration > sickle cells pool in liver, spleen
- Aplastic > Bone marrow just gives up producing RBCs

44
Q

Outline the steps involved in Haemostasis:

A
  • Vascular spasm
  • platelet plug
  • blood coagulation
  • growth of fibrous tissue
45
Q

What is the intrinsic pathway of haemostasis?

A

exposure of sub-endothelium collagen in vessel wall

46
Q

What causes the extrinsic pathway of haemostasis?

A

cells releasing Tissue Factor after damage, foreign body

47
Q

What pathways does Warfarin Act on?

A

2, 7, 9 ,10

48
Q

Which pathways does Apixaban, Rivaroxaban and Edoxaban act on?

A

Activation of factor X -> Xa

49
Q

Outline clot breakdown

A

Thrombin catalyses plasminogen to plasmin, which causes fibrinolysis

50
Q

Describe the action of aspirin

A

Irreversibly binds to platelets, inactivates COX enzymes required for thromboxane (kickstarts platelet aggregation, inflammation)

51
Q

Describe action of clopidogrel

A

Binds to P2Y12 receptor, irreversibly presents ADP mediated aggreagation
Takes a long time to wear off
irreversible antiplatelet

52
Q

Frequency of platelet turnover

A

~ every 10 days

53
Q

Do you stop clopidogrel or aspirin for dental surgery?

A

No. (they bind irreversibly, stopping it the day before is going to do nothing anyway)

54
Q

Never give aspirin to ____

A

Children: link to Reye’s syndrome (high morbidity, multi-organ swelling)

55
Q

How is the INR calculated

A

Prothrombin time of pt / prothrombin time of a control group
prothrombin relates to factor 7 activity

56
Q

What is the half-life of warfarin?

A

around 48 hours

57
Q

Why do you not stop warfarin for dental care?

A

if you do, pts are at an increased risk of severe thromboembolic event (there’s a reason they’re on it in the first place)

58
Q

What can cause dangerous interactions with warfarin?

A

Antifungals, antibiotics, grapefruit juice, NSAIDs
Metronidazole, Erythromycin
Carbamazepine (decreases INR)

59
Q

What is tranexamic acid used for?

A

prevents blood clot from being broken down, promotes clotting in surgery in secondary/tertiary care centres (expensive)

CMS (15 decks)

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