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Haem - pathology > PT 1 > Flashcards

PT 1 Flashcards

1
Q
  1. Q. What shifts Hb to left (increased affinity for oxygen), right (reduced affinity for oxygen)?
A

A. Right shift = reduced oxyhemoglobin saturation: increased temp, increased 2-3DPG, increased H+ i.e. at exercise etc

B. Left shift = increased saturation: decreased temp, decreased 2-3DPG, decreased H+ (increased pH), CO

C. 92% -when graph begins to plummet around 60% (resp failure)
D. Saturation O2 40mmHg = 75%, 20mmHg = 25%,

60mmHg = 92%

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2
Q
  1. Q. When are eosinophils raised in pathology? Describe their appearance
A

Raised in allergy, parasitic infections, lymphoma

Bi-lobed, 5% of circulating white cells

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3
Q
  1. Q. When are basophils raised in pathology?
A

Hypersensitivity reactions, raised in most chronic inflammatory conditions

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4
Q

Hypersensitivity reactions, raised in most chronic inflammatory conditions

A

Raised in viral infection, inflammation, lymphocytic leukaemia
Depleted in HIV, chemotherapy etc

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5
Q
  1. Q. What are deficiency is haemophilia A and B?
A

Coagulation factors A = 8 and B = 9

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6
Q
  1. Q. Where are coagulation factors synthesized?
A

All in liver except factor 4 which is calcium

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7
Q
  1. Q. Which clotting factors depend on vitamin K?
A

2,7, 9, 10 (malabsorption, inflammatory bowel disease, cystic fibrosis, liver disease, diet - leafy greens?) → anaemia, bleeding, brusing, heavy menstrual cycles

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8
Q
  1. Q. What chromosome is associated with leukaemia? Which?
A

Philadelphia chromosome - 95% of chronic myeloid leukaemia (CML), some ALL acute lymphoblastic leukaemia - translocated mutation of 9 and 22, this results in accelerated tyrosine kinase activity - which is an oncogene

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9
Q
  1. Q. What are the most common leukaemias? Who do they affect? What is the prognosis?
A

A. Chronic lymphocytic leukaemia (CLL): mature B cell accumulation - the most common leukaemia in adults, associated with enlarged rubbery non-tender nodes, lymphocytosis seen on blood film AE: elderly, trisomies, pneumonia

B. Chronic myeloid leukaemia (CML) – basophil, neutrophil, eosinophil mutations, affects middle aged and the elderly - palliative care

C. Acute lymphoblastic leukaemia (ALL) – lymphoblast mutations, most common paediatric malignancy (esp 3-7 yrs), rarer in adults, acute presentation: bone marrow failure, organ infiltration - good prognosis (AE radiation, downs syndrome), CNS

D. Acute myeloid leukaemia (AML):clonal expansion of myeloblasts in BM, blood and other tissues, typically older adults - GUM BLEEDING

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10
Q
  1. Q. What is seen in Ix of CLL? - 30% no tx
A

A. FBC: lymphocytosis
B. BM aspirate - lymphocytes
C. Blood film - SMUDGE/SMEAR CELLS
D. Most common leukaemia - often asympatomatic

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11
Q
  1. Q. What is seen in Ix of AML?
A

A. Blood film - auer rods
B. BM aspirate - blast cells
C. Immunophenotyping
D. (Sx - GUMBLEEDING)

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12
Q
  1. Q. How are leukaemias investigated?
A

A. FBC - low Hb, plts, MCV high, RBC/neutrophils/monocyes

B. Blood film (AML = auer rods, CLL = smudge/smear cells)

C. Bone marrow aspirate and trephine biopsy - increasing blasts

Genetics - Philadelphia chromosome in CML

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13
Q
  1. Q. Describe the basics of leukaemia treatment
A

Induction – this aims to remove 99% of leukaemic cells and restore previous bone marrow function
Consolidation – Lower intensity treatment aimed at removing that 1%
Maintenance – Background therapy taken for 2-3 years to maintain remission
(ALSO CNS Prophylaxis)

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14
Q
  1. Q. How is CML treated?
A

Treat with Imatinib - a tyrosine kinase inhibitor - the enzyme that is created by the philidelphia chromosome - stem cell transplanation is the only curative therapy

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15
Q
  1. Q. What are the different stages of CML? What symptoms are seen?
A

A. Chronic phase (often lasts for years, asymptomatic), then accelerated phase (symptoms and splenomegaly occur), then blast formation (with features of acute leukaemia)

b. Vague symptoms: weight loss, night sweats, tiredness, bleeding, abnormal discomfort

C. Raised WCC across the board except lymphocytes

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16
Q
  1. Q. What is a possible cause of Hogkin’s lymphoma? What cells are seen? Who is affected?
A

EBV, Reed-steinberg cells, typically seen in younger people e.g. 20-40 yrs (alcohol related pain)

17
Q
  1. Q. How is Hodgkin’s lymphoma treated? Classified?
A

Treatment is chemotherapy, classified with Ann Arbor system PET scan (according to lymph nodes affected: single lymph node, 2+ on same side of diaphragm, both sides of diaphragm, diffuse involvement)

18
Q
  1. Q. How is multiple myeloma investigated? What would be seen?
A

A. Serum electrophoresis - monoclonal band

B. Marrow biopsy - increased plasma cells

C. End-organ damage (renal, anaemia) - CRAB

D. B-lytic lesions - bone - full skeletal survey - CT/MRI - pepper pot skull on MRI

E. Bence-Jones protein in the urine

19
Q
  1. Q. What emergencies are seen in haematology?
A

A. Spinal cord compression – 5% of all myeloma patients

B. SVC obstruction – might see this in lymphoma

C. Neutropenic sepsis – dangerous - leukaemia/chemotherapy side effects

D. Tumour lysis syndrome – typically at the start of chemotherapy

E. Hypercalcaemia – typically due to lytic lesions

20
Q
  1. Q. What Sx are seen in anaemia?
A

Symptoms: fatigue, breathlessness, reduced exercise tolerance + headache, faintness, angina, intermittent claudication, palpitations

Signs: pallor, tachycardia + systolic flow murmur, cardiac failure, pale mucus membranes and palmar creases - nail deformities and palmar creases

21
Q
  1. Q What is normal MCV?
A

75-95 fL
A. Microcytic < 76fl - reduced Hb production

B. Normocytic 75-95fl

C. Macrocytic > 95fl - due to reduced synthesis of RBC: B12, alcohol, liver disease, thyroid disease

22
Q
  1. Q. Name 3 causes of microcytic anaemia
A

A. Iron deficiency: bleeding, increased demand (pregnancy), malabsorption (small bowel disease - coeliac’s, crohn’s, gastrectomy), reduced intake - dietary rare. (Most common cause world wide is HOOKWORM - causes GI blood loss)

B. Thalassaemia - AR, decreased Hb, alpha/beta

C. Sickle cell anaemia

D. Anaemia of chronic disease: chronic inflammation, infection, malignancy (TB, crohn’s, SLE, RA

23
Q
  1. Q. What signs and symptoms are seen in iron deficiency anaemia?
A

Symptoms: tired, malaise, SOB, decreased exercise tolerance, angina etc

Signs: koilonychia (spoon shaped nails), brittle hair and nails, angular stomatitis (muscle ulcers) and glossitis (smooth due to loss of filiform, glazed tongue, painful)

24
Q
  1. Q. What test indicates Hb storage? Transport?
A

Ferritin - storage

Transferrin - transport

25
Q
  1. Q. What treatments affect folate/B12? What anaemia may this cause?
A

Methotrexate and trimethoprim - folate deficiency can cause macrocytic anaemia

26
Q
  1. Q. What are elliptocyes?
A

(or ovalocytes), enlongated Hb cells. Seen in iron deficiency anaemia and thalassemia.

Polikocytosis = abnormal shape

Anisocytosis - unequal size

27
Q
  1. Q. What signs are seen in iron deficiency anaemia? What foods are rich in iron?
A

A. Koilonychia - spoon shaped nails

B. Agular chelitis - ulcers at corners of mouth

C. Iron rich foods: dark green veg, meat, apricots, prunes, raisins, iron-fortified bread

D. Se: constipation, block poo, diarrhoea, nausea, heartburn

E. May lead to weakness due to subacute degeneration of the cord

28
Q
  1. Tx for iron deficiency
A

Iron replacement e.g. ferrous sulphate for 3/12

Haem - pathology (5 decks)

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