Karl Kingston Flashcards
How much calcium is in blood
10mg/dL
What are the forms of calcium in blood, what % do they account for, what is their concentration
3
Protein bound- 41%
1mmol/L
Ionised- 50%
1.2mmol/L
Complexed- 9%
0.2mmol/L
What is the average calcium intake a day
How much calcium is absorbed a day from gut
How much calcium is secreted into duct per day
How much calcium is lost in feces per day
1000mg /day
350mg/day
250mg/day
9000mg/day
How much calcium is deposited into and absorbed from bone each day
500mg/day
What is normal blood calcium concentration
1.2mmol/L
What happens when blood calcium level rises
5
Blood calcium rises above 2.25mmol/L
Thyroid gland releases calciforin
Calciforin surpresses reabsorbtion of calcium in bone
Calciforin increases excretion of calcium from kidneys in urine
Calciforin decreases conversion of 25 hydroxyl D3 to 1.25 hydroxyl D3 in kidneys
What happens when blood calcium falls
4
Parathyroid secretes parathyroid hormone
PTH stimulates bone resorbtion
PTH stimulates renal reabsorbtion of calcium
PTH stimulates conversion of 25 hydroxyl D3 to 1.25 hydroxyl D3 which promotes calcium absorption in intestine
What is the flow of vitamin D into and within the body
Vitamin D synthesised in skin from sunlight and passed to liver
Vitamin D from diet absorbed in intestine and passed to liver
In liver D3 converted to 25 hydroxyl D3 and passed to kidneys
In kidneys PTH received from parathyroid and 25 hydroxyl D3 converted to 1.25 hydroxyl D3
1.25 hydroxyl D3
1.25 hydroxyl D3 increases bone resorbtion and travels to intestine
What is the action of vitamin D in the gut
In bone
In parathyroid gland
Stimulates transepithelial transport of calcium and phosphate into duodenum
Stimulates differentiation of osteoclasts which mobilise calcium
Inhibits transcription of PTH
What age does skeletal mass peak
30 years
What is the interaction between osteoblasts, osteoclasts and osteoprotegrin
Osteoblasts release osteoprotegrin
OPG binds to RANKL receptors on osteoblasts to prevent it binding to RANK on osteoclasts
RANK on osteoclasts complementary to RANKL on osteoblasts
What is hypocalcemia
What is hypercalcemia
What is hyperparathyroidism
What is hypoparathyroidism
Low calcium in blood
High calcium in blood
High PTH in blood leading to bone weakness through loss of calcium
Low PTH leading to lack of calcium causing muscle spasm
Define heamostasis
Define thrombosis
Define coagulation
Define fibrinolysis
Stopping of bleeding
Formation of blood clot within circulatory system
Process of blood forming solid clot
The enzymatic breakdown of fibrin in blood clots turning them to liquid
What are the phases of haemostasis
5
Vascular phase Platelet plug Clot formation Clot retraction Fibrinolysis
What happens during vascular phase of haemostasis
Vasoconstriction of vascular smooth muscle to limit blood loss and reduce blood flow
How is the platelet plug formed
Collagen of ECM exposed
Von willebrand factor adheres to collagen and attracts platelets
Platelets bond to VWF and each other
Platelets release ADP, thromboxane a2, thrombin and serotonin to attract more platelets and assist vasoconstriction
How does aspirin prevent platelet plug formation
Inhibits enzyme that makes thromboxane a2
What is the intrinsic pathway of clot formation
Blood exposed to sub endothelial surfaces
Prekallikrien converted to kallikrien
Cascade reaction activates factor 9
Factor 8a is the cofactor for factor 9a
What is the extrinsic pathway of clot formation
Tissue factor is released during injury from smooth muscle sup endothelial cells
Thrombin activates factor 7
TF acts as cofactor for 7a
What is the common pathway of clot formation
Factor 9a with cofactor 8a from intrinsic pathway or factor 7a with tissue factor cofactor from extrinsic pathway activates factor 10 into 10a
10a with 5a converts prothrombin to thrombin
Thrombin converts fibrinogen to fibrin forming clot
What happens during fibrinolysis
Plasminogen in clot converted to plasmin by tissue plasminogen activator and urokinase
Plasmin breaks down fibrin in clot to fibrin degradation products
Clot liquifies
What is the interaction of warfarin and vitamin K
Warfarin is a competitive antagonist of vitamin K so k can’t be used to form clotting factors thus increasing INR
What are the symptoms of haemophilia
3
What is the treatment of haemophilia
2
Frequent severe bleeding
Bleeding in joints
Intracranial bleeding
Replacement protein factors
Gene therapy
What happens in people with haemophilia A
What is the genetics of haemophilia A
Lack of factor 8 leads to failure of intrinsic pathway as factor 8 needed as a cofactor for 9a to activate factor 10 in final pathway
Recessive X linked disease mostly found in males of a family
What happens in haemophilia B
What is it’s genetics
Defected factor 9 compromises cascade reaction in intrinsic pathway
X linked recessive
What % account for haemophilia A and B
80% A
20% B
What happens in Von willebrands disease
What is the genetics
What is it’s prevalance
Lack of vWf compromises platelet adhesion to collagen leading to excessive bruising and bleeding gums
Autosomal dominant
1-2% of population
