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FLASHCARDS from MEDED lectures COPY > cancer and bleeding conditions > Flashcards

cancer and bleeding conditions Flashcards

1
Q

Describe the lineage of tree of blood stem cells

A

blood stem cell

-> Myeloid stem cells

GIves rise to:

  • Myeloblast - granulocytes -(eosinophil, basophil and neutrophil)
  • platelets
  • red blood cells
  • > Lymphoid stem cells

give rise to :

  • Lymphoblast- B lymphocyte - plasma cells
  • t Lymphocytes
  • NK cells
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2
Q

what are the characteristics of acute onset leukaemias

  • ONSET?
  • Characteritisics?
  • CAUSE OF SYMPTOMS and SIGNS
  • SYMPTOMS and SIGNS
A
  • ONSET? rapid
  • Characteritisics? Immature cells (blasts) in the blood and bone marrow
  • CAUSE OF SYMPTOMS and SIGNS: bone marrow failure
  • SYMPTOMS and SIGNS:
    • Anaemia (↓ Hb): fatigue, pallor, breathlessness
    • Neutropenia (↓ neutrophils): recurrent infections
    • Thrombocytopenia (↓ platelets): bleeding and easy bruising
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3
Q

Acute myeloid leukaemia

  • Cause:
  • Risk factors:
  • Pathogenesis: where does the problem occur
  • Accumulation of what cell?
  • Diagnosis, pathology?
A
  • Cause: unknown
  • Risk factor: Down’s, irradiation, anti-cancer drugs, age (incidence ↑ with age)
  • Pathogenesis: Myeloblast does not differenciate into the granulocyte - NO basophil, eosinophil, neutrophil myeloblast cell
  • Diagnosis, pathology? Auer rods on blood film
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4
Q

What is a particularly aggressive sub type of acute myeloid leukaemia?

What gene causes it ?

What condition is it associated with?

A

Promyelocytic leukaemia

  • What gene causes it ? t(15;17)
  • What condition is it associated with? Associated with DIC
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5
Q

Acute lymphoblastic leukaemia

  • Cause:
  • Risk factors:
  • Pathogenesis: where does the problem occur
  • Accumulation of what cell?
  • Diagnosis, pathology?
  • Symptoms:
A
  • Cause: unknown
  • Risk factor: commonest childhood cancer (75% under 6 years old)
  • Pathogenesis: where does the problem occur? Uncontrolled proliferation of lymphoblasts (3/4 of WBC are B cells)
  • Diagnosis, Investigations pathology?
    • Bloods: ↑↑ WCC, ↓ Hb, ↓ plts
    • BM film: >20% lymphoblasts
  • Symptoms:
    • ​Bone marrow failure symptoms
    • organ infiltration (hepatosplenomegaly, enlarged lymph nodes, swollen testes)
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6
Q

What would a mass in the neck of child with ALL indicate,

what symptoms could it cause?

A

could be T cell ALL -

what symptoms could it cause? thymus enlarged symptoms: mediastinal compression -> stridor, wheeze, SVCO

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7
Q

chronic lymphoblastic leukaemia

Cause:

Risk factors:

Pathogenesis: where does the problem occur

Accumulation of what cell?

Diagnosis, pathology?

Symptoms:

A
  • Cause:
  • Risk factors:
  • Pathogenesis: where does the problem occur: lymphocytes unable to undergo apoptosis
  • Accumulation of what cell?Accumulation of mature incompetent lymphocytes
  • Diagnosis, pathology?
    • Bloods: ↑ lymphocytes, ↓ Hb, ↓ neutrophils, ↓ platelets
    • Blood film: smear/smudge cells (lymphocytes very fragile)
  • Symptoms
    • ​Asymptomatic in 50%
    • Symptoms of BM failure: recurrent infections (including herpes zoster), sx of anaemia, easy bruising/bleeding
    • O/E: enlarged non-tender lymphadenopathy, hepatosplenomegaly
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8
Q

What other condition can chronic lymphocytic be associated with?

What is the name of this condition?

A
  • associated with autoimmune thrombocytopenia + anaemia
  • Evan’s syndrome
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9
Q

into what more aggressive condition can chronic lymphocytic leukaemia develop into?

A

• Richter’s syndrome

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10
Q

chronic myloid leukaemia

Cause:

Risk factors:

Pathogenesis: where does the problem occur

Accumulation of what cell?

Diagnosis, pathology?

Symptoms:

A
  • Cause:

Philadelphia chromosome in >80% of those with CML

t(9,22) forming BCR-ABL gene which encodes a constitutively active TK receptor à continuous cell proliferation

  • Risk factors:
  • Pathogenesis: where does the problem occur: Uncontrolled proliferation of granulocyte precursors in BM but slower progression than AML
  • Accumulation of what cell?Ugranulocyte precursors
  • Diagnosis, pathology?
    • Bloods: ↑↑ WCC (often >100 x109)
    • Cytogenetics: look for Philadelphia chromosome t(9;22)
  • Symptom
    • ​Up to 50% are asymptomatic
    • Hypermetabolic symptoms: weight loss, malaise, sweating
    • Symptoms of BM failure: lethargy, dyspnea, easy bruising/epistaxis (overcrowding)
    • Hyperviscosity symptoms: visual disturbance, headaches, thrombotic event (high RBC)
    • Gout
    • MASSIVE splenomegaly in 90% (not in acute because not enough time)
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11
Q

What can Chronic myeloid leukaemia develop into?

A

•Can transform into accelerated phase (10-19% blasts) or into acute leukaemia phase (>20% blasts)

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12
Q

What are the main points to remember for each condition?

AML:

ALL:

CML:

CLL:

A

AML: Auer rods

ALL: children <6 years

CML: Philadelphia chromosome t(9;22), BCR-ABL gene

CLL: smear/smudge cells

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13
Q

Hodgkin lymphoma

Cause:

Risk factors:

Pathogenesis: where does the problem occur

Accumulation of what cell?

Diagnosis, pathology, Investigation?

Presentation:

A
  • Cause: 50% of cases associated with EBV infection
  • Risk factors: Bimodal age distribution peaks in 20-30 and >50y
  • Pathogenesis: where does the problem occur? Malignant proliferation of lymphocytes, accumulate in LNs -> lymphadenopathy
  • Accumulation of what cell? lymphocytes
  • Diagnosis, pathology, Investigation?
    • Lymph node biopsy under microscopy = Reed Sternberg cells
    • Ann Arbour staging
  • Presentation:
    • ​Painless enlarging mass (most often in neck, occasionally axilla or groin)
    • more painful after alcohol ingestion
    • B symptoms: fevers >38, night sweats, weight loss (>10% in last 6 months)
    • O/E: non tender firm rubbery lymphadenopathy, splenomegaly +/- hepatomegaly
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14
Q

What cell is this?

A

reed steinberg cell

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15
Q

non- Hodgkin lymphoma

Cause:

Risk factors:

Pathogenesis: where does the problem occur

Accumulation of what cell?

Diagnosis, pathology, Investigation?

Presentation:

A
  • Cause: Associated with EBV, HIV, SLE, Sjogren’s
  • Risk factors: ↑ with age
  • Pathogenesis: where does the problem occur?
    • Malignancy of lymphoid cells originating in LNs without Reed Sternberg cells
    • 85% are B cell
    • 15% are T cell or NK cell
  • Diagnosis, pathology, Investigation? Lymph node biopsy –> Ann arbour staging
  • Presentation:
    • ​Painless enlarging mass in neck, axilla or groin
    • Systemic symptoms (less common than in HL): weight loss, night sweats, fever
    • Organ involvement (more common than in HL): skin rashes, headache hepatosplenomegaly, sore throat, cough
    • Signs of BM failure: anaemia, neutropenia, thrombocytopenia
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16
Q

what is an important subtype of Non- Hodgekin Lymphoma?

IN what demographic most prevelant:

Presentation

What would you be able to see under a microscope

A
  • what is an important subtype of Non- Hodgekin Lymphoma? BURKITT’s Lymphoma
  • In what demographic most prevelant: •African child
  • Presentation: Large LN in the jaw (fast-growing)
  • What would you be able to see under a microscope: starry sky appearance
17
Q

What is this condition?

What does it look like under the microscope?

A

What is this condition? Burkitt’s Lymphoma

What does it look like under the microscope? starry sky appearance

18
Q

Multiple myeloma

Cause:

Risk factors:

Pathogenesis: where does the problem occur

Accumulation of what cell?

Diagnosis, pathology?

Symptoms:

A
  • Cause:unknown – possible viral trigger
  • Risk factors:
    • ionizing radiation, HIV, agricultural work, occupational chemical exposure e.g. benzene, herbicides
    • >70 years. Afrocarribeans > Caucasians > Asians
  • Pathogenesis: where does the problem occur? proliferation of plasma cells + production of a monoclonal immunoglobulin (usually IgG or IgA)
  • Diagnosis, pathology?
    • Serum/urine electrophoresis: Bence Jones proteins
    • Bloods: ↑ ESR, ↑CRP, ↑ urea/Cr, ↑ Ca, ALP normal
    • Blood film: rouleax formation
    • Serum MONOCLONAL protein >30g/L
    • BM aspirate = ↑ plasma cells (>10%)
  • Symptoms:
    • ↑ Ca -> tired, thirsty, polyuria, nausea, constipation
    • _Renal impairmen_t -> Ig and its fragments (light chains) deposit in the kidney – present in 20% at diagnosis (associated with worse prognosis)
    • Anaemia (+ neutropenia, thrombocytopenia) due to marrow infiltration by plasma cells. Also get recurrent bacterial infections due to low levels of other Ig
    • Bone pain/lesions: increased osteoclast activation due to myeloma cell signaling ->back/rib pain
19
Q

What is MGUS?

What could it develop into?

What the symptoms?

A

What is MGUS? Monoglonal gammopathy of unknown significance

What could it develop into? •1% acquire additional mutations -> Multiple Myeloma

What the symptoms?•Absent CRAB features​

20
Q

What is genetic inheritance pattern of Haemophilia?

A

X-linked recessive inheritance -> typically affects boys

21
Q

What are the different types of haemophilia?

Which is more common?

A
  • What are the different types of haemophilia?

Haemophilia A = deficient factor 8 (more common)

Haemophilia B = deficient factor 9

  • Which is more common? Haemophilia A = deficient factor 8 (more common)
22
Q

Girl with what condition can get more easily haemophilia?

A

Turner syndrome

23
Q

haemophilia

Cause:

Risk factors:

Pathogenesis: where does the problem occur

Accumulation of what cell?

Diagnosis, pathology, Investigation?

Presentation:

A
  • Cause :
    • Haemophilia A = deficient factor 8 (more common)
    • Haemophilia B = deficient factor 9
  • Risk factors: FH (but 30% have no FH)
  • Diagnosis, pathology, Investigation? prolonged APTT (intrinsic pathway); factor assay confirms diagnosis
  • Presentation:
    • ​Usually presents early in life or after surgery/trauma
    • Haemarthrosis after minimal trauma -> swollen painful joints
    • Haematomas -> painful bleeding into muscles (increased pressure can lead to compartment syndrome or nerve palsies)
    • Excessive bruising or bleeding
    • Haematuria
  • O/E – as a result of deep bleeding
    • Multiple bruises, muscle haematomas
    • Joint deformity from haemarthrosis
    • Signs of IDA e.g. pallor
  • Female carriers are usually asymptomatic but may have low enough levels to cause excess bleeding after trauma
24
Q

Von Willebrand disease

Cause and types :

Diagnosis, pathology, Investigation?

Presentation:

A
  • Cause:
    • ​Type 1: reduced levels of normal vWF ( AUTOSOMAL DOMINANT )
    • Type 2: defective vWF ( AUTOSOMAL DOMINANT)
    • Type 3: complete lack of vWF and highly reduced factor 8 (Autosomal recessive)
  • Diagnosis, pathology, Investigation?
  • •↑ APTT, ↑ bleeding time, ↓ vWF levels, N plts, normal PT, (↓ factor 8)
  • Presentation: - plts can still attach to subendothelium directly without vWF via GP1a
    • ​More superficial bleeding compared to haemophilias
    • Bruising, epistaxis, menorrhagia
    • Increased gum bleeding post tooth extraction
    • Prolonged bleeding from minor wounds
    • HOWEVER type 3 ->bleeding into joints and soft tissues
25
Q

What is the vWF factor involved in?

A

factor 8 stabilisation

26
Q

Disseminated intravascular coagulation

Cause:

Pathogenesis: where does the problem occur

Diagnosis, pathology, Investigation?

Presentation:

A
  • Cause: Emergency, can be life-threatening
    • Occurs in sepsis (esp children with meningococcal septicaemia), trauma, obstetric complications, malignancy
  • Pathogenesis: where does the problem occur? systemic activation of coagulation -> invascualr deposition of fibrin -(thrombosis of smlal and midsize vessels with organ failure) & depletion of platelets and coagulation factors (Bleeding)
  • Diagnosis, pathology, Investigation?
    • FBC (↓ plts, ↓ Hb)
    • Clotting (↓ fibrinogen, ↑ PT/APTT, ↑ fibrin degradation products)
    • Peripheral blood film: schistocytes (MAHA) (fibrin strand deposition in vasculation is like cheese wires laid down in microvasculature –> RBCs driven across strands under pressure and get fragmented )
  • Presentation:
    • ​Patient is severely unwell with Sx of underlying disease + evidence of bleeding:
    • Signs of underlying aetiology: fever, shock (hypotension, tachycardia), oliguria i.e. sepsis!!
    • Acute DIC: petechiae, purpura, ecchymoses, epistaxis, mucosal bleeding, hemorrhage, respiratory distress
    • Chronic DIC: signs of deep venous or arterial thrombosis or embolism
27
Q

A 5 year old boy of Indian ethnic origin presented with lymphadenopathy and a mediastinal mass on CXR.

  • WBC: 180 x 109/L
  • Hb: 93 g/L
  • Plts: 43 x 109/L
  • Blood film shows blast cells

What is the most likely cause of the mediastinal mass?

a) Thymoma
b) Acute myeloid leukaemia
c) Acute lymphoblastic leukaemia
d) Haemorrhage into the mediastinum
e) Pneumonia with leukaemoid reaction

A

a) Thymoma
b) Acute myeloid leukaemia

c)Acute lymphoblastic leukaemia

d) Haemorrhage into the mediastinum
e) Pneumonia with leukaemoid reaction

28
Q

An 83 year old man with no abnormal physical findings is found to have a high white cell count and high lymphocyte count on a blood test.

A blood film is requested and it is found to have smear cells.

What is the most likely diagnosis?

a) Acute lymphoblastic leukaemia
b) Chronic lymphocytic leukaemia
c) HIV infection
d) Infectious mononucleosis
e) Whooping cough

A

a)Acute lymphoblastic leukaemia

b)Chronic lymphocytic leukaemia

c) HIV infection
d) Infectious mononucleosis
e) Whooping cough

29
Q

A 1 year old boy presented to A&E department with a swollen right elbow following minor trauma. On examination and radiology there was no evidence of bony injury. He was sent home.

3 days later he was brought back with increased pain and swelling. Joint aspiration yielded haemorrhagic fluid.

A coagulation screen was performed which showed a normal PT and a prolonged APTT of 96 seconds (NR 24-35s). The prolonged APTT was corrected by mixing the infant’s plasma with normal plasma.

What is the most likely diagnosis?

a) Disseminated intravascular coagulation
b) Von Willebrand’s disease
c) Haemophilia
d) Autoimmune thrombocytopenia
e) Fracture of the elbow

A

a) Disseminated intravascular coagulation
b) Von Willebrand’s disease

c)Haemophilia

d) Autoimmune thrombocytopenia
e) Fracture of the elbow

30
Q

A 16 year old boy presents to his GP complaining of nosebleeds and bleeding after brushing his teeth. He is unsure of how long it has been going on for but decided to seek advice after having to continually excuse himself from lessons. On examination you notice he has some skin bruises. A blood test shows a prolonged bleeding time and APTT. Platelet count and PT are normal.

What is the most likely diagnosis?

a) Von Willebrand disease
b) Liver disease
c) Disseminated intravascular coagulation
d) Congenital afribrinogenaemia
e) Haemophilia

A

a)Von Willebrand disease

b) Liver disease
c) Disseminated intravascular coagulation
d) Congenital afribrinogenaemia
e) Haemophilia

FLASHCARDS from MEDED lectures COPY (35 decks)

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