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Haem/Onco > Bloody hell more questions? > Flashcards

Bloody hell more questions? Flashcards

1
Q

Haemoglobin
- Low
- High
~primary vs secondary

A 
Low = anaemic 
Look at MCV 
High = polycythaemia 
- primary = polycythaemia rubra vera 
- secondary = dehydration, hypoxia (COPD, Smoking, obesity, altitude) or excess EPO (renal cell carcinoma)
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2
Q

MCV

  • Micro
  • Normo
  • Macro
A 
Micro
- iron deficiency 
- thalassemia 
- sideroblastic
Normo 
- ACD 
- acute bleed 
- haemolysis 
Macro 
- B12/folate deficiency 
- hypohyroidism 
- pregnancy 
- alcohol/liver disease 
- Myelodysplastic syndrome
- methotreaxate
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3
Q

What do high reticulocytes indicate? Examples
What do low reticulocytes indicate?
Examples

A

Bone marrow still working, trying to replace loss RBC, bleeding, haemolytic anaemia, haemolytic disease of the newborn

Bone marrow failure, low EPO (kidney disease), alcoholism, Fe deficiency

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4
Q

What does the RDW mean? What does anisocytosis mean?

Examples of disease causing high RDW

A

Red cell distribution width, the average variation in size of RBC.
RBC of unequal size.
Sickle cell beta thalassemia, Iron deficiency, myelodysplastic syndrome

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5
Q

What is high platelets called?

What causes high platelets? (Primary vs secondary/reactive)

A 
Thrombocytosis 
Primary 
- polycythaemia rubra vera 
Secondary 
- reactive = stress/Infection/Inflammation, haemorrhage, malignancy (essential thrombocytosis, CML), post-splenectomy/surgery
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6
Q

What is low platelets called?

What causes low platelets?

A

Thrombocytopenia
Production
- DRUGS! (ace-i, penicillins, cephalosporins)
- b12/folate deficiency
- Leukaemia
- viral illness
Destruction
- immune = drug-induced, ITP, rheumatological
- non-immune = DIC, splenomegaly, mechanical heart valves

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7
Q

What is a high WCC called?

What are some causes?

A

Leukocytosis

  • Infection
  • Malignancy = ALL, lymphoma
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8
Q

What is low WCC called?
What are some causes?
(Production vs destruction)

A

Leukopenia

  • no production = bone marrow failure (drugs, malignancy, fibrosis)
  • destruction = viral (HIV)
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9
Q

What is low neutrophils called?
What are some causes?
Treatment?

A 
Neurtropenia 
- splenomegaly 
- viral 
- drugs (chemo, steroids)
- malignancy 
Treatment = colony stimulating factors, prophylactic antibiotics
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10
Q

What is high neutrophils called? What are some causes?

A

Neutrophillia / left shift

  • bacterial infection
  • CML
  • trauma/stress
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11
Q

What is high lymphocytes called?
What are some causes?
What is low lymphocytes called?
What’s are some causes?

A 
Lymphocytosis 
- viral (EBV)
- ALL/leukaemia 
- CLL (most common adult haem disease)
Lymphopenia 
- steroids 
- autoimmune
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12
Q

What causes high eosinophils?
What causes high basophils?
Nucleated RBC causes?

A 
Eo = Allergy / atopy or Vasculitis 
Baso = Parasitic infections 
Nuc = Responding to bleed
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13
Q

Megaloblastic anaemia - what does it mean?

Causes

A

Large nucleus

Folate and B12 deficiency

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14
Q

What does Poikilocytosis mean?

A

Different shapes of red blood cells

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15
Q

Macrocytes - oral vs round causes

Hypersegmented neutrophils - causes?

A

Oval = megaloblastic b12/folate deficiency
Round = liver disease/alcohol/myelopdysplasia
B12 Deficiency & myelodysplasia

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16
Q

Target cells causes?
Types?
Tear drop cells - causes
Pencil cells?

A

Target = Thalassaemia,
Alpha and Beta
Myelofibrosis = squeezing out of RBC. Cause = Tumour metastasis
Pencil = iron deficiency

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17
Q

Rouleaux cells causes?

Spherocytes causes?

A 
Roul = Inflammation, Autoimmune and Plasma cell disorders
Sphero = Autoimmune Haemolytic Anaemia or hereditary spherocytosis
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18
Q

What is measured on iron studies?
What can go up in infection on iron studies and why?
What’s the difference between iron deficiency and anaemia of chronic disease on iron studies?

A

Iron, transferrin, transferrin saturation, ferritin
Ferritin, as it’s an acute phase reactant
Iron deficiency has increased transferrin levels and low ferritin levels, where as chronic disease has lowered transferrin and normal ferritin

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19
Q

Polycythaemia rubra vera

- Mutation

A

JAX 2 mutation

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20
Q

What is the incubation for Malaria?
How long should you take prophylactic antibiotics for?
What is the investigation of choice?

A

12 days
One week before leaving and one month after
Microscopy thick and thin smear

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21
Q

What disorders is Desmopressin (DDAVP) used for?
What are the effect of Desmopressin?
What is it used for?

A

von Willebrand disease, haemophilia A and platelet function defects
Stimulates cAMP-stimulated endothelial cells to secrete von Willebrand factor and factor VIII.
Used for acute bleeding episodes or to prevent bleeding in surgery

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22
Q

What does a positive Coomb’s test indicate?
What other test will confirm this?
What will the blood film show?

A

Rhesus disease
Serum anti-D
Polychromasia (due to blue staining from ++ retic’s) & nucleated cells (retic’s)

23
Q

Which lymph nodes does testicular cancer usually metastasise to first?
What is the most common type of testicular cancer?
What abnormality increases the risk of testicular cancer?

A

Lumbar lymph nodes
Germ cell cancer (95%)
Cryptorchidism

24
Q 
Haemophilia A - what coagulation factor needs to be administered as a prophylactic during and after surgery?
What is a MSK-related complication?
What about haemophilia B?
How are they inherited?
Which is more common?
A

A = VIII - Haemarthrosis causing chronic deformities.
B = IX
X-linked recessive
Haemophilia A

25
Q

In pernecious anaemia what is lacking?
What is its role?
Where is this produced?

A

Intrinsic factor
Absorption of B12
Produced in parietal cells of the stomach

26
Q

Where is most of the iron from the diet absorbed?

A

Duodenum

27
Q

When CO2 is released into the blood from tissue, the blood pH rises or falls?
What happens to the 02 dissociation curve?

A

Falls

Shifts to the right

28
Q

What conditions can cause folate deficiency?

A

Pregnancy
Decreased intake (alcohol abuse, vegan)
Gastric bypass surgery
Methotrexate, Sulfasalazine

29
Q

Are RBC nucleated or non-nucleated?
Do they produce ATP aerobically or anaerobically?
What shape is a RBC?
Why are all of these points physiologically important?

A

Non-nucleated
Anaerobic ATP production
Biconcave shaped disc
No nucleus allows greater internal space to transport 02 with
Anaerobic energy production ensures RBC’s don’t use up any of the 02 they transport
Shape = greater surface area

30
Q

Where does erythropoiesis primarily occur in the first 8wks of fetal development?
Where does it occur primarily in adults?
What 4 elements are needed in erythropoiesis?
What is the life cycle of a RBC?

A

Liver and yolk sac?
Red bone marrow
Fe3+, globin, vitamin B12 & erythropoietin (EPO)
~120d

31
Q

How is the rate of erythropoiesis measured?
What is the normal amount of this substance in the blood?
How long does it take for this substance to mature?

A

By the reticulocyte count
0.5-1.5%
1-2 days

32
Q

Where is the thymus located?

What is it’s role?

A

Located in the mediastinum between the sternum and the aorta
Role = maturation of pre-T-cells via positive selection from epithelial cell and thymus hormone production

33
Q

What does thalassaemia mean?
What is the significance physiologically?
How many forms of beta and alpha thalasaemia are there?

A

Spectrum of diseases characterised by reduced or absent production of alpha or beta globin chains
Abnormal RBC are destroyed by the spleen, causing anaemia + iron overload from increase turnover
Beta = 3
Alpha = 4

34
Q

What is a cystic hygroma?
How is it diagnosed?
What are the consequences/risks of this?

A

Congenital malformation resulting from lymph accumulation in the jugular lymphatic sacs
1st trimester Pre-natal U/S
Fetal aneuploidy (trisomy 21), structural heart malformations, miscarriage

35
Q

What are the hypersensitivity reactions?
Give an example of each
What is the most common?

A

Type I = IgE mediated (most common) -> anaphylactic
Type II = Cytotoxic antibody-dependent -> ABO incompatibility
Type III = Immune complex disease -> RA & glomerulonephritis
Type IV = T-cell mediated -> TB, contact hypersensitivity

36
Q

What is the pathophysiology behind type I hypersensitivity reactions?

A

Second response to an allergen.
First response produces IgE antibodies that bind to surface of mast cells and basophils.
Allergen then attaches to IgE antibodies -> release of histamine, prostaglandins and leukotrienes -> vasodilation + capillary hyper-permeability + smooth muscle contraction in airways and mucus production

37
Q

What is the pathophysiology behind type II hypersensitivity reactions?

A

IgG or IgM antibodies directed against antigens on a persons blood cells (RBC’s, lymphocytes or platelets) or tissue cells
This leads to activation of complement and membrane attack complexes causing lysis of the cells

38
Q

What is the pathophysiology behind type III hypersensitivity reactions?

A

Antigens, antibodies (IgG or IgM) and complement
Immune complexes small enough to escape phagocytosis become trapped in the basement membrane under the endothelium of blood vessels
Activation of complement and inflammation pathways

39
Q

What is the pathophysiology behind type IV hypersensitivity reactions?

A

Appear 12-72hrs after exposure to an allergen
Antigen presenting cells migrate to lymph nodes and activate/proliferate T-cells
T-cells return toi site of allergen and active macrophages and tumor necrosis factor causing inflammation response

40
Q

What is the role of prostaglandins F2-alpha?

What are the precursors of these prostaglandins?

A

Bronchoconstriction and uterine contraction

Essential fatty acids

41
Q

What is the effect of 2,3-DPG on oxygen binding?
What conditions cause a rise in this?
What conditions lower this?

A

Lowers oxygens affinity for haemoglobin, shifting the O2 dissociation curve to the right
Hypoxaemia, chronic lung disease, anaemia, and congestive heart failure.
Septic shock and hypophosphataemia

42
Q

What are the top 3 circulating antibodys in blood?
Which one can cross the placental barrier?
Which one is produced in the primary immune response?
Which one is produced in the secondary immune response?
Which one activates the complement pathway?

A 
IgG, IgA and IgM
placenta = IgG
primary = IgM
secondary = IgG
complement = IgM
43
Q

Do T-cells or B-cells produce antibodies?
What is the role of mast cells?
What is the role of dendritic cells?
What is the role goblet cells?

A

B-cells
Mast = release of histamine/inflammatory mediators
Dendritic = antigen presentation
Goblet = mucus production

44
Q

What is the most common reactIon to a blood transfusion?
Which is the most likely complication of platelet transfusion when contamination occurs
with erythrocytes?

A

Fever

Rh alloimmunisation

45
Q

What is amyloid?

What is amyloidosis?

A 
amyloid = family of insoluble glycoproteins
Amyloidosis = infiltrative deposits of degradation-resistant amyloid protein causing bulk effect or vascular occlusion
46
Q

DVT in pregnancy;
Why is it more common?
More common in left or right leg?
Where in the leg does it more commonly occur?

A

Pregnancy prepares the mother for the risk of haemorrhage associated with delivery by increasing procoagulant tendency through rises in factors VIII, IX and X
Left leg
Iliac and femoral vein

47
Q

What does ANCA stand for?

What is the pathogenesis in ANCA diseases?

A

Anti-neutrophil cytoplasm antibodies
Pathogenesis = release of toxic substances from neutrophils causing damage to blood vessel walls and neutrophil migration causing inflammation in surrounding tissues

48
Q

What vitamin increase absorption of oral iron?

A

Vitamin C

49
Q

Asplenic patients are at increased risk of what overseas infectious disease?
What is the most common organism causing post-splenectomy infection?

A

Severe malaria

Strep. Pneumonia

50
Q

What is haptoglobin’s role in the body?

When will it be decrease?

A

Protein present in blood which binds to and removes free haemoglobin from blood.
Decrease = haemolytic anaemia

51
Q

What are the 2 Coombs tests and what do they screen for?

Which one is used in pregnancy?

A 
Direct = tests for an immune reaction attacking a persons own RBCs. Screen for autoimmune haemolytic anaemia 
Indirect = tests for an immune reaction against another persons RBCs. Screen before blood transfusion and in PREGNANCY
52
Q

Pathophysiology of Factor V Leiden disease

A

Factor V activates clot formation. The disease prevents the breakdown of Factor V by resistance to the protein C enzyme.

53
Q

Thalassaemia - How is a diagnosed confirmed (following FBE)?

What needs to occur before this?

A

Haemoglobin electrophoresis + beta-thalassaemia has elevated HbF
Need to have full iron stores before diagnoses can be made

Haem/Onco (2 decks)

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