Wednesday [17/08/22]

Question 1

Reference range for sodium [1]

Answer 1

135-145

Question 2

reference range for potassium [1]

Answer 2

3.5-5

Question 3

causes of hyponatraemia [7]

Answer 3

diuretics: thiazides, loop diuretics
SIADH
diarrhoea, vomiting, sweating
IV dextrose, psychogenic polydipsia
secondary hyperaldosteronism: heart failure, liver cirrhosis
burns
Addison's disease
diuretic stage of renal failure
hypothyroidism

Question 4

Causes of hypernatraemia [4]

Answer 4

dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline

Question 5

Common causes of hyponatraemia [2]

Answer 5

Common
Thiaizide diuretics
Selective serotonin reuptake inhibitors

Question 6

Less common causes of hyponatraemia [4]

Answer 6

Infrequent
Loop diuretics: side-effects
Lung cancer

Rare
Sulfonylureas: side-effects
Malaria (Falciparum)
Addison's disease
Legionella pneumonia
Psittacosis
Acute intermittent porphyria
Carbamazepine

Question 7

What are the pathways of coagulation? [3]

Answer 7

1. Extrinsic
2. Intrinsic
3. Common pathways
   All work together to form a blood clot

Question 8

How do the extrinsic and intrinsic pathways work basically? [2]

Answer 8

The extrinsic and intrinsic coagulation pathways both lead into the final common pathway by independently activating factor X

Question 9

Which factor does the extrinsic pathway work on? [1]

Answer 9

The extrinsic pathway involves initiation by factor III (i.e., tissue factor) and its interaction with factor VII.

Question 10

Which factors does the intrinsic pathway work on? [1]

Answer 10

Whereas, factors XII, XI, IX, and VIII are utilized in the intrinsic pathway.

Question 11

Which factors does the common pathway work on? [1]

Answer 11

Then, the common pathway uses factors X, V, II, I, and XIII.

Question 12

When does the extrinsic pathway get activated? [2]

Answer 12

The extrinsic pathway begins when there is injury to the endothelial tissue (i.e., skin tissue), exposing tissue factor (factor III) to the blood. Tissue factor then becomes bound with calcium and factor VIIa to activate factor X. Factor VII is present in the blood and requires vitamin K to be activated.

Question 13

When does the intrinsic pathway get activated? [2]

Answer 13

Meanwhile, the intrinsic pathway begins when factor XII or the Hageman factor is exposed to collagen, kallikrein, and high molecular weight kininogen (HMWK) and is subsequently activated. Factor XIIa activates factor XI into XIa. With a calcium ion, factor XIa activates factor IX. Then, factor IXa, factor VIIIa, and calcium form a complex to activate factor X. Factor VIII is found in the blood and is often activated by thrombin (factor IIa).

Question 14

What happens at the common pathway? [2]

Answer 14

The common pathway may result after the activation of factor X at the end of either pathway. The common pathway begins when factor Xa, Va, and calcium bind together, forming a prothrombinase complex. The prothrombinase complex then activates prothrombin (factor II) into thrombin (factor IIa). Next, thrombin cleaves fibrinogen (factor I) into fibrin (factor Ia). Afterwards, thrombin cleaves the stabilizing factor (factor XIII) into XIIIa. Factor XIIIa binds with calcium to then create fibrin crosslinks to stabilize the clot. Thrombin has several functions, including activating platelets (cell fragments involved in clot formation) and activating factors V, VIII, and IX.

Question 15

When is fibrin produced during the coagulation cascade? [2]

Answer 15

Fibrin (factor Ia) is a long, thin protein with branches produced at the end of the coagulation cascade when fibrinogen (factor I) is converted to fibrin, which stabilizes the blood clot.

Question 16

What is the main goal of coagulation? [2]

Answer 16

The main goal of coagulation is to form a stable blood clot to stop bleeding and allow time for the tissue to be repaired.

Question 17

Go through some common coagulation disorders [4]

Answer 17

Coagulation disorders are disorders which affect the coagulation cascade and can either cause excessive or inadequate clotting. Coagulation disorders usually involve a deficiency in at least one clotting factor, and the most common disorders include von Willebrand disease, hemophilia, and vitamin k deficiency.

Von Willebrand disease is the most common bleeding disorder and is characterized by a deficiency in von Willebrand factor due to an autosomal dominant genetic mutation. The von Willebrand factor is mostly involved in primary hemostasis where it helps platelets stick together. The factor also plays a role in secondary hemostasis by helping stabilize factor VIII.

There are three types of hemophilia that are caused by genetic mutations in clotting factor genes and can be passed on from parent to child. Hemophilia A is a deficiency in factor VIII, hemophilia B is a deficiency in factor IX, and hemophilia C is a deficiency in factor XI. All types of hemophilia affect the intrinsic pathway.

A vitamin K deficiency may occur when a sufficient amount of vitamin K is not absorbed from foods or when not enough foods with vitamin K are consumed (e.g., leafy dark green vegetables like spinach). Vitamin K is a cofactor required to make factors II, VII, IX, and X functional. Therefore, vitamin K deficiency affects all three pathways.

Question 18

What are the most important facts to know about the coagulation cascade? [3]

Answer 18

The coagulation cascade refers to the series of steps that occur during the formation of a blood clot after injury by activating a cascade of proteins called clotting factors. There are three pathways: intrinsic, extrinsic, and common. The intrinsic pathway is activated by factors in the blood, while extrinsic is activated by tissue factor. Both pathways result in activation of factor X leading into the common pathway, which ends with converting fibrinogen into fibrin to form a stabilized blood clot. Coagulation disorders occur when there is a deficiency in a clotting factor involved, and the most common disorders are hemophilia and vitamin K deficiency.

Question 19

What does the word haematinics mean? [2]

Answer 19

Haematinics are the nutrients needed by the bone marrow to make blood cells in the process of haematopoiesis. Without adequate amounts of these nutrients, cytopenia(s) and related symptoms can develop. Excess amounts can also be pathological and can point to various underlying disease states.

Question 20

Vitamins involved in haematinics [7]

Answer 20

This guide to haematinics interpretation will focus on deficiencies of the most clinically relevant haematinics: vitamin B12 (cobalamin), vitamin B9 (folate), and iron.

Other haematinics not covered in this guide include:

Vitamin A
Vitamin B2 (riboflavin)
Vitamin B3 (nicotinic acid)
Vitamin B6
Vitamin C
Vitamin E
Copper
Cobalt

Question 21

IDA iron in blood results

Answer 21

ferritin = low or normal
transferrin/TIBC = high
transferrin saturations = low
STFR = high/normal

Question 22

acute=phase response iron studies

Answer 22

high ferritin

low transferrin/TIBC

Question 23

anaemia of chronic disease iron studies

Answer 23

normal ferritin, normal/low transferrin/TIBC, normal/low transferrin saturations, normal STFR

Question 24

Treatment of IDA [3]

Answer 24

Traditional dosing guidelines suggested aiming for 100-200mg of elemental iron a day however, more recent studies performed in iron deficient, non-pregnant women have shown that once-daily dosing of around 45-80mg elemental iron is more effective and avoids many of the gastrointestinal side effects. This amount of elemental iron roughly equates to one tablet of either ferrous fumarate 210mg or ferrous sulphate 200mg. A response in the haemoglobin count should be seen within a few weeks of starting therapy.

In certain scenarios, intravenous iron may be preferred. This includes patients with chronic kidney disease, inflammatory bowel disease, those intolerant of oral iron, those needing rapid replacement due to the degree of anaemia or certain pregnant patients. The safety profile has improved with more recent formulations but there is still a risk of anaphylactoid reactions and permanent skin staining.

Question 25

What should be co-prescribed with IDA? [2]

Answer 25

For most patients, oral iron is a safe, effective and cheap method of treating iron deficiency. Co-administration of vitamin C improves the absorption of oral iron.

Question 26

When can ferinject not be given? [1]

Answer 26

I think it is during an infection? As microbes can metabolise it

Question 27

Clinical features of B12 deficiency [3]

Answer 27

B12 deficiency often develops over years, with clinical features occurring insidiously.

Patients with B12 deficiency can present with features related to anaemia such as fatigue, shortness of breath, weakness, and reduced exercise tolerance as well as neuropsychological features (motor and sensory peripheral neuropathies, ataxia, retinopathy, optic atrophy, cognitive impairment etc.) and glossitis.

In severe deficiency, subacute degeneration of the spinal cord can develop.

Importantly, not all patients with clinical vitamin B12 deficiency will have anaemia or macrocytosis.

Therefore, if a patient presents with clinical features of B12 deficiency, is in an at-risk population (see below) or has been identified to have macrocytic anaemia, investigations of B12 stores should be undertaken.

Infants can also present with faltering growth, movement disorders or developmental delay.

Question 28

Causes of B12 deficiency [4]

Answer 28

Malabsorption: pernicious anaemia, Crohn’s, coeliac disease, gastric/bariatric surgery, atrophic gastritis
Dietary: vegetarians/vegans
Infection: H.pylori, giardia, tapeworm
Infants: congenital causes