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YEAR 3 - SEMESTER 1 > CASE 5 - LEUKAEMIA > Flashcards

CASE 5 - LEUKAEMIA Flashcards

1
Q

Human Papillomavirus (HPV) infection is required for cervical cancer to develop. Which types of HPV are responsible for the majority of HPV cases?

A

HPV 16 / 18

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2
Q

What other types of cancer can HPV 16 / 18 cause?

A

Anal cancer

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3
Q

Outline the HPV-related pathophysiology of cervical cancer development

A
  1. Infection with HPV
  2. Integration of HPV into host genome
  3. Cell transforms –> cervical dysplasia (aided by other RFs such as smoking)
  4. MOST infections are cleared by the immune system
  5. In some women, the infection progresses into high-grade cervical intraepithelial neoplasia (CIN3) and CERVICAL CANCER
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4
Q

Describe the 2 most common cervical cancer subtypes

A
  1. SQUAMOUS CELL CARCINOMA
    Originates from cells on the surface (ecto-cervix)
  2. ADENOCARCINOMA
    Originates from glands of the cervix (endo-cervix)
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5
Q

List 4 common symptoms of cervical cancer

A
  • Bleeding after intercourse
  • Bleeding in between menstrual periods
  • Abnormal vaginal discharge
  • Post-menopausal bleeding
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6
Q

Over __% of HPV infections clear up after 2 years, whilst up to __% of persistent oncogenic HPV infections progress into cancer

A

Over 80% of HPV infections clear up after 2 years, whilst up to 30% of persistent oncogenic HPV infections progress into cancer

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7
Q

4 factors that promote the development of cervical cancer

A
  • Smoking
  • Early age of first sexual intercourse (more to do with chronic or re-infections)
  • Multiple sexual partners
  • Immunosuppression
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8
Q

In which area of the cervix do most cervical cancers originate?

A

Transformation zone / squamocolumnar junction

This is where the squamous and columnar cells meet

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9
Q

How is the transformation zone (TZ) classified? Explain them. (3 types)

A

TYPE I - TZ fully visible and ecto-cervical

TYPE II - TZ fully visible, but partially in the endocervical canal (most common during reproductive years)

TYPE III - TZ not fully visible and is in the endocervical canal (most common in post-menopausal women)

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10
Q

The number of women diagnosed with cervical cancer has dropped by __% since cervical cancer screening began in 1991 (1991-2005).

A

The number of women diagnosed with cervical cancer has dropped by 4.5% since cervical cancer screening began in 1991 (1991-2005).

This is an impressive decrease, not seen in any other screening program!

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11
Q

Name the prophylactic vaccine for HPV 16, 18, 6, and 11.

What percentage of cervical cancers does it protect against?

A

Gardasil

Also v effective!

Protects against 77% of cervical cancers

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12
Q

Name the new vaccine that now protects against 93% of cervical cancers

A

Gardasil 9

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13
Q

A new cervical screening program was implemented in 2018 (5-yearly HPV testing w/liquid-based cytology). Describe the process involved.

A

5-yearly screening from women aged 25-69 years.

  1. Uses a primary HPV test (smear taken and tested for HPV infection).
  2. It undergoes cytological examination ONLY if HPV infection is found (if not, the woman continues with 5-yearly screening).
  3. HPV 16/18: refer for colposcopy
  4. HPV NOT 16/18: repeat screening in 1 year
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14
Q

What is colposcopy and why is it used in women with a positive HPV 16/18 test?

A

Colposcopy is the examination of the cervix with a magnifying instrument.

It is used to further evaluate abnormal cervical screening tests.

Acetic acid applied –> infected cells stain white and can be visualised

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15
Q

Why do abnormal cells stain white (acetowhite changes)?

A

Reflects higher protein content due to increased cellular protein and DNA content during HPV infection

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16
Q

How is cervical cancer diagnosed? Describe the 2 approaches/types of investigations.

A

BIOPSY:

  1. LOOP EXCISION: thin, electrical wire used to obtain cervical tissue (also called large loop excision of the transformation zone, LLETZ)
  2. CONE BIOPSY / CONIZATION: cone-shaped sample of the uterine cervix is removed. Allows evaluation of deeper layers.
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17
Q

How does treatment differ for early-stage vs. advanced cervical cancers?

A

EARLY STAGE: operable

ADVANCED: combined chemo and radiotherapy

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18
Q

What type of surgery is usually performed for cervical cancer?

A

Extent of surgery depends on stage of disease

Usually, it is a Radical Hysterectomy (removal of uterus & tissue next to the cervix. NOT the ovaries and tubes, as cervical cancer doesn’t spread here)

Pelvis lymph nodes also removed to ensure cancer hasn’t spread

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19
Q

What does cervical cancer chemo and radiotherapy entail?

A

EBRT + Brachytherapy

Chemotherapy given during radiotherapy as a sensitiser to make the cancer cells more susceptible to X-rays

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20
Q

Do HPV vaccines negate cervical screening?

A

NO: vaccines do not protect against ALL forms of cervical cancer, therefore screening is still necessary.

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21
Q

What is leukaemia?

A

Cancers that develop in the bone marrow

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22
Q

Neutrophilia indicates what type of leukaemia?

A

Myeloid

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23
Q

Lymphocytosis indicates what type of leukaemia?

A

Lymphoid

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24
Q

List the 4 main types of leukaemia in ascending order according to the age groups they most commonly manifest in

A
  1. Acute lymphoblastic leukaemia (ALL): most common in children 2-5 years
  2. Chronic myeloid leukaemia (CML): most common in adults ~50-60 years old
  3. Acute myeloid leukaemia (AML): ~65 years old
  4. Chronic lymphocytic leukaemia (CLL): ~70 years old, but not uncommon in younger populations (30-39). Incidence increases with age.

(memory tip: LATERAL/LYMPHOID at the bookends, MEDIAL/MYELOID in the middle, ACAC order)

https://www.youtube.com/watch?v=Cf15SKTg2Us

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25
Q

What are haematopoietic stem cells, and where do they originate?

A

HSCs are stem cells that give rise to other blood cells.

They originate in the bone marrow.

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26
Q

Name the 2 lineages that haematopoietic stem cells can differentiate along

A

Myeloid

Lymphoid

(look up picture)

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27
Q

What is flow cytometry used for?

A

Detecting physical characteristics and chemical properties of a cell.

Useful when trying to tell blood cells apart, as the appearance is not always indicative.

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28
Q

Name 3 causes of leukocytosis

A
  • Viral infections (e.g. EBV, HIV)
  • Drug hypersensitivity
  • Medical stress (e.g. MI, trauma, status epilepticus)
  • Lymhpoid leukaemias
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29
Q

Name 3 causes of fatigue

A
  • Iron-deficiency anaemia
  • Diabetes mellitus
  • Hypothyroidism
  • Depression
  • CHF
  • Sleep apnoea
  • Multiple sclerosis
  • Fibromyalgia (associated w/ muscle pain)
  • Drugs (prescription and recreational)
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30
Q

What is the difference in fatigue reporting when it comes to patients with underlying medical conditions vs. psychological conditions?

A

Patients with underlying medical conditions often associate fatigue with activities they are unable to complete.

By contrast, patients with fatigue that is related to psychological conditions, medication toxicity, or substance use may be tired all the time; their fatigue is not necessarily related to exertion, and it does not improve with rest.

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31
Q

Name 3 causes of splenomegaly

A
  • Leukaemias (infiltration by neoplastic cells)
  • Liver disease, e.g. cirrhosis (causes the spleen to become engorged with blood)
  • Vascular obstruction (reduced blood flow caused by obstruction –> increased pressure)
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32
Q

What types of cells are affected by acute and chronic leukaemias?

A

ACUTE LEUKAEMIAS: occur in immature, nonfunctional white blood cells, and proliferate rapidly

CHRONIC LEUKAEMIAS: occur in mature cells, and build up gradually

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33
Q

Acute leukaemias impair normal haematopoiesis and lead to pancytopenia. How does this manifest clinically?

A
  • Anaemia (dec. RBCs)
  • Clotting disorders (dec. thrombocytes)
  • Increased susceptibility to infection (dec. functional WBCs / leukopenia)
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34
Q

RFs for Acute lymphoid leukaemia

A
  • Prior bone marrow damage (e.g. alkylating chemotherapy, ionizing radiation)
  • HTLV
  • Genetic disorders, e.g. Downs syndrome

In most cases, there are no identifiable causes or RFs

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35
Q

RFs for Acute myeloid leukaemia

A
  • Pre-existing haematopoietic disorder
  • Environmental exposures (e.g. alkylating chemotherapy, ionizing radiation, benzene exposure)
  • Genetic disorders, e.g. Downs syndrome

In most cases, there are no identifiable causes or RFs

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36
Q

Describe the clinical features of acute leukaemias in general

A
  1. Anaemia: pallor, fatigue, etc.
  2. Thrombocytopenia: epistaxis, bleeding gums
  3. Immature leukocytes: Frequent infections
  4. Leukaemic infiltration: hepatosplenomegaly
  5. Bone pain & tenderness: marrow expansion due to infiltration of subperiosteum

Abrupt: most patients present within 3 months of onset

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37
Q

Name 5 clinical features of acute LYMPHOID leukaemia (ALL)

A
  • Fever
  • Night sweats
  • Painless lymphadenopathy
  • Airway obstruction due to thymic infiltration
  • Meningeal leukaemia (neck stiffness, headache, visual field changes)
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38
Q

2 clinical features that are more characteristic of acute MYELOID leukaemia (AML)

A
  • Leukaemia cutis

- Gingival hyperplasia

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39
Q

Fever and lymphadenopathy are rare in ___, but can be common first signs in ___.

A

Fever and lymphadenopathy are rare in AML, but can be common first signs in ALL.

ALL = Lymphadenopathy, fever.

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40
Q

Most clinical manifestations of acute leukaemias are caused by what pathophysiological mechanism?

A

Bone marrow failure due to suppression of the growth of normal haematopoietic stem cells

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41
Q

CNS symptoms (e.g. headache, vomiting, nerve palsies) are more common in which types of acute leukaemia? And what age group?

A

More common in ALL

More common in children

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42
Q

How are acute leukaemias diagnosed?

A

Peripheral blood smear (PBS)

Confirmatory diagnosis can be carried out using bone marrow aspiration and biopsy

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43
Q

What would you expect to see on a CBE of someone with acute leukaemia?

A
  • Anaemia
  • Thrombocytopenia
  • Raised WBCs / leukocytosis (but this is not a reliable indicator as WBC can be low, elevated, or normal in leukaemia)
44
Q

What would you expect to see in the peripheral blood smear (PBS) of someone with ALL?

A

Raised lymphoblasts (immature WBCs)

45
Q

What would you expect to see in the peripheral blood smear (PBS) of someone with AML?

A

Raised myeloblasts

Some subtypes have Auer rods

46
Q

Diagnostic feature in bone marrow biopsy of someone with ALL vs. AML?

A

ALL: >20% lymphoblasts in bone marrow
AML: >20% myeloblasts in bone marrow

47
Q

Which type of leukaemia is associated with the Philadelphia chromosome?

A

CML / Chronic myeloid leukaemia

48
Q

What is the Philadelphia chromosome?

A

A translocation between chromosomes 9 and 22 which results in an abnormal chromosome 22 (Philadelphia chromosome)

BCR-ABL1 fusion gene (BCR from 22, ABL1 from 9)

49
Q

Name the 3 phases of chronic myeloid leukaemia and their characterising features (CAB)

A
  1. CHRONIC: can persist for up to 10 years and is often subclinical
  2. ACCELERATED: splenomegaly, anaemia, infections, fever (SAIF)
  3. BLAST CRISIS: terminal, symptoms resemble acute leukaemia, rapid progression of bone marrow failure –> bone pain
50
Q

Why do recurrent infections occur during the early stages of AML but not CML?

A

The granulocytes are still functional in the early stages of CML

51
Q

Which type of leukaemia causes the most severe leukocytosis?

A

CML

52
Q

What is the lifespan of each of the following components of blood?
RBCs
Platelets
Granulocytes

A

RBCs: 120 days
Platelets: 5-10 days
Granulocytes: hours - days

53
Q

Immature haematopoietic cells reside in the ________ and only ______ cells are released to circulate in peripheral blood.

A

Immature haematopoietic cells reside in the marrow and only mature cells are released to circulate in peripheral blood.

54
Q

How does the role of bone marrow in haematopoiesis change as we age?

A

In infancy, all marrow is haematopoietic (along with other tissues)

In adults, 30-70% of marrow is fat.
Extramedullary tissues (liver, spleen, and nodal tissues) can revert to haematopoiesis in disease states
55
Q

Normal maturation of stem cells undergoes different states. Name them.

A
  1. Loss of self-renewal capacity
  2. Loss of proliferative potential
  3. Acquiring special functional characteristics
56
Q

What is a malignant clone and why is it clinically significant?

A

Malignant clone = the abnormal cell from which all leukaemic cells arise

It can be used for diagnosis and assessment of treatment response (the clone may share morphology, immunophenotype, cytogenetics, molecular abnormalities, etc.)

57
Q

Define Chronic Myeloid Leukaemia

A

A malignancy of haematopoietic stem cells with excessive proliferation of the myeloid lineage

58
Q

What are the WHO criteria for CML stages? What is it based on?

A

Based on the blast (immature precursors) count in peripheral blood and bone marrow:

<10% = Chronic
10 - 19% = Accelerated
>20% = Blast crisis

59
Q

Describe the pathophysiology behind CML

A

Reciprocal translocation of the proto-oncogene ABL from chromosome 9 to chromosome 22, creating the BCR-ABL fusion gene.

Chromosome 22 (the Philadelphia chromosome) is now smaller.

BCR-ABL gene codes for BCR-ABL PROTEIN, a tyrosine kinase –> increased enzyme activity –> inhibits physiologic apoptosis w/ increased mitotic rate

60
Q

What does low LAP (leukocyte alkaline phosphatase) indicate, and which type of leukaemia is it characteristic of?

A

Low LAP is associated with an increased number of immature white blood cells

Distinctively associated w/CML

61
Q

List the clinical features associated with each of the following pathophysiological processes seen in CML:

  1. INCREASED WHITE CELLS
  2. CYTOPENIA
  3. OTHER
A
  1. INCREASED WHITE CELLS:
    - Bone pain
    - Hyperviscosity
    - Infiltration of other organs (liver, spleen)
    - Gout / hyperuricaemia due to increased turnover of abnormal cells –> inc. uric acid production (rarer)
  2. CYTOPENIA
    - Anaemia
    - Thrombocytopenia
    - Infection
  3. OTHER
    - Constitutional features
    - DIC (disseminated intravascular coagulation)
62
Q

Describe 3 principles of cytotoxic chemotherapy

A
  1. Malignant cells have a higher replication rate than their normal counterparts: we use agents that interfere with the cell cycle or DNA synthesis. Therapeutic window is the gap between the proliferation rate of the tumour and the normal cell.
  2. Most tumours will relapse: use combinations of drugs with different mechanisms of action
  3. Aim to give doses that enable safe recovery of normal haematopoiesis whilst still killing malignant cells: this is why chemo is given in doses (is safer, but can’t wait too long otherwise tumour will relapse)
63
Q

Why are normal cells with higher rates of proliferation more susceptible to side effects from chemotherapy?

A

The therapeutic window for cytotoxic chemotherapy is the gap between the proliferation rate of the tumour and the normal cell.

Faster proliferation mimics tumour properties and makes them a target

64
Q

What is the major cause of death during intensive chemotherapy?

A

Opportunistic infection

65
Q

In a patient with CLL, describe what might be seen on the following investigations:

  • CBC
  • PBS
  • Bone marrow biopsy
A

CBC: lymphocytosis (early, low risk), granulocytopenia (decreased production of granulocytes), low RBCs, low platelets

PBS: Crushed Little Lymphocytes (CLL) - Gumprecht shadows

BONE MARROW BIOPSY: >30% lymphocytes (small & mature), low myeloid progenitor cells

66
Q

What is the typical demographic of patients diagnosed with CLL?

A

70-72 years
Male
Caucasian

67
Q

How does the typical rate of CLL progression inform treatment?

A

CLL is a low-grade malignancy that usually progresses slowly. Treatment is often unnecessary and unlikely to prolong survival.

Medical therapy is often palliative.

68
Q

What is the only curative option for CLL? Who is it typically used in?

A

Allogenic stem cell transplantation

Refractory CLL or recurrence in fit young people

69
Q

What is the treatment regime of CLL in symptomatic patients over 65-70 years?

A

Chemotherapy (chlorambucil)
If CD20 positive: rituximab (a MAB)

Note: treatment is based on the stage, symptoms, age, and comorbidities.

70
Q

Describe 5 clinical manifestations of CLL

A
  1. B symptoms: fever, fatigue, weight loss, night sweats
  2. Painless lymphadenopathy (more common in lymphoid leukaemia)
  3. Repeated infections
  4. Signs of anemia and thrombocytopenia
  5. Dermatological symptoms (e.g. leukaemia cutis)

NOTE THAT IT IS USUALLY ASYMPTOMATIC AND THAT SIGNS OF ANAEMIA AND THROMBOCYTOPENIA INDICATE ADVANCED DISEASE

71
Q

Outline the pathophysiology behind CLL and how it causes clinical features such as anaemia, chronic infections, and lymphadenopathy

A

Mutations in haematopoietic stem cells –> increased proliferation of leukaemic B cells –> impaired maturation and differentiation in the bone marrow.

This causes:
- Suppression of normal blood cell proliferation (manifests in anaemia, thrombocytopenia, immunosuppression)

  • Infiltration of the lymph nodes and spleen
72
Q

What is the difference between a prescribed relative and a substitute decision-maker?

A

PRESCRIBED RELATIVE: an adult with a close, continuing relationship with the patient who can make decisions about consent. E.g. a person legally married to the patient, an adult domestic partner, an adult related by blood or marriage.

SUBSTITUTE DECISION-MAKER: appointed within the patient’s advanced care directive. This person is able to make decisions on your behalf when you can no longer make those decisions yourself.

73
Q

What is tumour lysis syndrome?

A

Tumour cell lysis, causing release of intracellular contents

Can be spontaneous or result from treatment

IT IS AN ONCOLOGIC EMERGENCY

74
Q

The following lab findings can be seen in tumour lysis syndrome:

  1. Hyperuricaemia
  2. Hyperphosphatemia
  3. Hypocalcemia
  4. Hyperkalemia

Outline the pathophysiology behind these findings

A
  1. Hyperuricaemia: breakdown of purine nucleic acids to hypoxanthine then xanthine and finally uric acid (via xanthine oxidase)
  2. Hyperphosphatemia: phosphate concentration is much higher in malignant cells –> breakdown of these cells leads to hyperphosphatemia
  3. Hypocalcemia: caused by high phosphate levels. The phosphate binds to calcium, lowering calcium stores.
  4. Hyperkalemia: just bc the cells break lol

Think of “PUKE calcium” to remember the electrolytes affected in tumor lysis syndrome: Phosphorus, Uric acid, and potassium (K+) are Elevated; Calcium is decreased.

75
Q

Describe the underlying pathophysiology for each of the following manifestations of tumour lysis syndrome

  1. Acute kidney injury (flank pain, dysuria, oliguria)
  2. Arrhythmia
  3. Numbness, tingling, muscle spasms, seizure
  4. Nausea, vomiting, diarrhoea
A
  1. Acute kidney injury (flank pain, dysuria, oliguria): caused by uric acid deposition and crystallisation in the nephrons
  2. Arrhythmia: hypocalcemia and hyperkalemia
  3. Numbness, tingling, muscle spasms, seizure: hypocalcemia
  4. Nausea, vomiting, diarrhoea: hyperkalemia
76
Q

Name 2 risk factors for development of tumour lysis syndrome

A
  • Large tumour burden

- Rapidly-dividing tumours (e.g. acute leukaemias)

77
Q

When does tumour lysis syndrome typically occur?

A

After initiating cytotoxic therapies in patients with haematologic malignancies

78
Q

What does prophylaxis against TLS involve?

A
  1. Vigorous IV hydration
  2. Allopurinol (xanthine oxidase inhibitor) 2-3 days before initiating treatment and for 10-14 days afterward
  3. Frequent monitoring of electrolytes and aggressive correction of abnormalities
79
Q

How is TLS diagnosed? Name the definition used.

A

Cairo-Bishop definition:

  1. LABORATORY TLS: 2 or more metabolic abnormalities, or a 25% change from baseline.
    Look at a table.
  2. CLINICAL TLS: presence of lab findings + one or more of the clinical features (AKI-related rise in creatinine, arrhythmia, seizures)
80
Q

What is the mainstay of TLS prophylaxis and treatment?

A

Hydration

81
Q

Name 4 investigations that would be ordered for TLS and what results you would expect to see

A
  1. Basic metabolic panel (creatinine, K+, calcium, phosphate)
  2. CBC: possible elevation of WBC count
  3. Urinalysis: uric acid crystals
  4. ECG: arrhythmia
82
Q

Leukaemia chemotherapy side effects affect which 3 organs?

A
  • GUT (mucositis)
  • BONE MARROW (increased infection risk due to decrease in normal as well as abnormal WBCs)
  • BRUISING (decreased platelets)
83
Q

How might the side effects of chemo be averted?

A

Colony-stimulating drugs?????

84
Q

Why is lymphadenopathy less common in myeloid leukaemias?

A

.

85
Q

How does the peripheral blood smear differ between CML and CLL?

A

CML: leukocytosis with midstage progenitor cells and mature cells

CLL: lymphocytosis with a high percentage of small, mature lymphocytes.

86
Q

Why is there a high percentage of small, mature lymphocytes in CLL?

A

One of the characteristics of the neoplastic lymphocytes is their increased lifespan, which allows them to accumulate.

87
Q

What is the Rai staging system? (Not as common in Australia)

A

It is used to assess prognosis in patients with CLL. Symptom-based:

Stage 0: asymptomatic or isolated lymphocytosis

Stage I: +lymphadenopathy

Stage II: lymphadenopathy + hepatomegaly or splenomegaly

Stage III: lymphadenopathy + hepatomegaly or splenomegaly + anaemia

Stage IV: lymphadenopathy + hepatomegaly or splenomegaly + anaemia + thrombocytopenia

88
Q

Describe the appearance of myeloblasts

A

Large cells with a high nuclear-to-cytoplasm ratio

89
Q

What is the Binet system?

A

Often used by Australian doctors to stage CLL.

Stage A - Low
<3 enlarged lymph nodes, NO anaemia or thrombocytopenia

Stage B - Intermediate
>3 enlarged lymph nodes, NO anaemia or thrombocytopenia

Stage C - High
Presence of anaemia and/or thrombocytopenia

90
Q

Why are corticosteroids used as an adjunct to chemotherapy?

A
  1. To treat chemotherapy-related nausea and vomiting
  2. To treat the cancer itself
  3. Immunosuppression (e.g. after bone marrow transplant)
91
Q

In which type of leukaemia are tyrosine kinase inhibitors used? Why?

A

CML - selectively inhibits BCR-ABL tyrosine kinase
(Philadelphia translocation present in~90% of CML patients).

E.g. imatinib

92
Q

Outline the treatment regime for ALL and AML

A
  1. Aggressive chemotherapy (most children achieve complete remission with chemotherapy)
  2. Radiation or targeted therapies may be indicated depending on the type and stage of disease
93
Q

Outline the 4 steps of chemotherapy

A
  1. Induction (4-6 weeks): high-dose with aim of massively reducing tumour cell count.
  2. Re-induction (4-6 weeks): high-dose with aim of massively reducing tumour cell count. Only performed if primary induction isn’t effective.
  3. Consolidation (months): commenced after remission. Goal is to destroy the remaining tumour cells.
  4. Maintenance (up to 2 years): maintain remission.
94
Q

Name 3 supportive therapies for leukaemia.

A
  1. Infection prevention (surveillance to detect sources of infection in oropharynx and skin, paying attention to personal hygiene, avoiding crowds, etc.)
  2. Managing side effects: antiemetics, enteral and parenteral nutritional support, transfusion for severe cytopenia
  3. Prevention of TLS: allopurinol, fluid
95
Q

Outline the treatment regime for CML

A
  1. Tyrosine kinase inhibitors (e.g. imatinib) - lifelong treatment
  2. Allogenic stem cell transplantation (only considered in a small group)
96
Q

List 3 short-term and 3 long-term side effects of prolonged corticosteroid use

A

SHORT-TERM: infection, sodium and water retention, oedema

LONG-TERM: osteoporosis, weight gain, skin atrophy, menstrual irregularity, Cushing’s syndrome

97
Q

What is the pathophysiology behind leukaemia-induced bone pain?

A

Uncontrolled proliferation of leukaemic cells → bone marrow expansion → irritation of sympathetic nerve fibres supplying the periosteum → bone pain

98
Q

What is the pathophysiology behind epistaxis (Nosebleeds) caused by leukaemia?

A

Uncontrolled proliferation of leukaemic cells → suppression of maturation and differentiation of other haematopoietic cells → decreased platelet production –> thrombocytopenia –> decreased clotting ability –> frequent nosebleeds

99
Q

morphology of cancerous cells

A

.

100
Q

Name 4 criteria from Wilson and Jungner’s principles of screening

A
  1. The condition should be an important health problem
  2. There should be an accepted treatment for patients with the recognised disease
  3. Facilities for diagnosis and treatment should be available
  4. There should be a suitable test or examination
  5. The test should be acceptable to the population
  6. The natural history of the disease, from latent to declared disease, should be adequately understood
  7. There should be an agreed policy on whom to treat as patients

…etc look up the rest

101
Q

How does cancer induce a hypercoagulable state?

A

Some of the genetic changes that cause cancer increase the activation of clotting factors.

Many chemotherapy drugs also induce activation of clotting factors.

102
Q

What is the difference between metaplasia and dysplasia?

What is their relationship to one another?

A

METAPLASIA = replacement of one differentiated cell type with another mature differentiated cell type that is not normally present in that tissue.

DYSPLASIA = presence of abnormal cells within a tissue or organ.

Persistent metaplasia can be a precursor to dysplasia.

103
Q

Which of the following viruses is NOT thought to be a significant predisposing factor for the development of the tumour with which it is paired below?

A. Hepatitis B virus and hepatocellular carcinoma
B. Epstein- Bar Virus and Burkitt’s lymphoma
C. Human papilloma virus and endometrial cancer
D. Hepatitis C virus and hepatocellular carcinoma
E. Human T-lymphotropic virus and adult T-cell leukaemia

A

C - HPV causes cervical cancer

104
Q

What is febrile neutropenia?

How long after commencing chemotherapy does it occur?

A

Febrile neutropenia = fever (>38 degrees) + neutropenia (ANC <500 cells/mL OR expected to decrease to this level in the next 48 hours)

Usually starts 5-10 days after chemotherapy

105
Q

Why is febrile neutropenia an emergency?

A

A decrease in a patient’s absolute neutrophil count (ANC) can lead to potentially life-threatening infections.

106
Q

What is the empirical antibiotic regime for febrile neutropenia?

Which investigations are performed before empirical antibiotics are administered?

A 
EMPIRICAL ANTIBIOTIC REGIME: broad-spectrum
- Piperacillin + tazobactam 
OR
Cefepime 
OR
Ceftazidime

Investigations: blood, urine, and line cultures

107
Q

If high fevers persist for >5 days during febrile neutropenia, what additional treatment should be considered?

A

Empirical antifungals

YEAR 3 - SEMESTER 1 (15 decks)

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