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Flashcards in Bloody hell more questions? Deck (52):
1

Haemoglobin
- Low
- High
~primary vs secondary

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

2

MCV
- Micro
- Normo
- Macro

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

3

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

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

4

What does the RDW mean? What does anisocytosis mean?
Examples of disease causing high RDW

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

5

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

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

6

What is low platelets called?
What causes low platelets?

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

7

What is a high WCC called?
What are some causes?

Leukocytosis
- Infection
- Malignancy = ALL, lymphoma

8

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

Leukopenia
- no production = bone marrow failure (drugs, malignancy, fibrosis)
- destruction = viral (HIV)

9

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

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

10

What is high neutrophils called? What are some causes?

Neutrophillia / left shift
- bacterial infection
- CML
- trauma/stress

11

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

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

12

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

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

13

Megaloblastic anaemia - what does it mean?
Causes

Large nucleus
Folate and B12 deficiency

14

What does Poikilocytosis mean?

Different shapes of red blood cells

15

Macrocytes - oral vs round causes
Hypersegmented neutrophils - causes?

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

16

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

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

17

Rouleaux cells causes?
Spherocytes causes?

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

18

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?

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

19

Polycythaemia rubra vera
- Mutation

JAX 2 mutation

20

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

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

21

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

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

22

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

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

23

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?

Lumbar lymph nodes
Germ cell cancer (95%)
Cryptorchidism

24

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

25

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

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

26

Where is most of the iron from the diet absorbed?

Duodenum

27

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

Falls
Shifts to the right

28

What conditions can cause folate deficiency?

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

29

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?

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

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?

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

31

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?

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

32

Where is the thymus located?
What is it’s role?

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

What does thalassaemia mean?
What is the significance physiologically?
How many forms of beta and alpha thalasaemia are there?
How is a diagnosed confirmed (following FBE)?

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
Haemoglobin electrophoresis + beta-thalassaemia has elevated HbF

34

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

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

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

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

What is the pathophysiology behind type I hypersensitivity reactions?

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

What is the pathophysiology behind type II hypersensitivity reactions?

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

What is the pathophysiology behind type III hypersensitivity reactions?

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

What is the pathophysiology behind type IV hypersensitivity reactions?

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

What is the role of prostaglandins F2-alpha?
What are the precursors of these prostaglandins?

Bronchoconstriction and uterine contraction
Essential fatty acids

41

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

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

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?

IgG, IgA and IgM
placenta = IgG
primary = IgM
secondary = IgG
complement = IgM

43

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?

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

44

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

Fever
Rh alloimmunisation

45

What is amyloid?
What is amyloidosis?

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

46

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

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

What does ANCA stand for?
What is the pathogenesis in ANCA diseases?

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

What vitamin increase absorption of oral iron?

Vitamin C

49

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

Severe malaria
Strep. Pneumonia

50

What is haptoglobin’s role in the body?
When will it be decrease?

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

51

What are the 2 Coombs tests and what do they screen for?
Which one is used in pregnancy?

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

Pathophysiology of Factor V Leiden disease

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