Karl Kingston Flashcards

1
Q

How much calcium is in blood

A

10mg/dL

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2
Q

What are the forms of calcium in blood, what % do they account for, what is their concentration
3

A

Protein bound- 41%
1mmol/L

Ionised- 50%
1.2mmol/L

Complexed- 9%
0.2mmol/L

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3
Q

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

A

1000mg /day
350mg/day
250mg/day
9000mg/day

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4
Q

How much calcium is deposited into and absorbed from bone each day

A

500mg/day

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5
Q

What is normal blood calcium concentration

A

1.2mmol/L

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6
Q

What happens when blood calcium level rises

5

A

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

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7
Q

What happens when blood calcium falls

4

A

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

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8
Q

What is the flow of vitamin D into and within the body

A

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

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9
Q

What is the action of vitamin D in the gut

In bone

In parathyroid gland

A

Stimulates transepithelial transport of calcium and phosphate into duodenum

Stimulates differentiation of osteoclasts which mobilise calcium

Inhibits transcription of PTH

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10
Q

What age does skeletal mass peak

A

30 years

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11
Q

What is the interaction between osteoblasts, osteoclasts and osteoprotegrin

A

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

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12
Q

What is hypocalcemia

What is hypercalcemia

What is hyperparathyroidism

What is hypoparathyroidism

A

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

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13
Q

Define heamostasis

Define thrombosis

Define coagulation

Define fibrinolysis

A

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

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14
Q

What are the phases of haemostasis

5

A
Vascular phase
Platelet plug
Clot formation 
Clot retraction 
Fibrinolysis
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15
Q

What happens during vascular phase of haemostasis

A

Vasoconstriction of vascular smooth muscle to limit blood loss and reduce blood flow

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16
Q

How is the platelet plug formed

A

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

17
Q

How does aspirin prevent platelet plug formation

A

Inhibits enzyme that makes thromboxane a2

18
Q

What is the intrinsic pathway of clot formation

A

Blood exposed to sub endothelial surfaces
Prekallikrien converted to kallikrien
Cascade reaction activates factor 9
Factor 8a is the cofactor for factor 9a

19
Q

What is the extrinsic pathway of clot formation

A

Tissue factor is released during injury from smooth muscle sup endothelial cells
Thrombin activates factor 7
TF acts as cofactor for 7a

20
Q

What is the common pathway of clot formation

A

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

21
Q

What happens during fibrinolysis

A

Plasminogen in clot converted to plasmin by tissue plasminogen activator and urokinase
Plasmin breaks down fibrin in clot to fibrin degradation products
Clot liquifies

22
Q

What is the interaction of warfarin and vitamin K

A

Warfarin is a competitive antagonist of vitamin K so k can’t be used to form clotting factors thus increasing INR

23
Q

What are the symptoms of haemophilia
3

What is the treatment of haemophilia
2

A

Frequent severe bleeding
Bleeding in joints
Intracranial bleeding

Replacement protein factors
Gene therapy

24
Q

What happens in people with haemophilia A

What is the genetics of haemophilia A

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

25
Q

What happens in haemophilia B

What is it’s genetics

A

Defected factor 9 compromises cascade reaction in intrinsic pathway

X linked recessive

26
Q

What % account for haemophilia A and B

A

80% A

20% B

27
Q

What happens in Von willebrands disease

What is the genetics

What is it’s prevalance

A

Lack of vWf compromises platelet adhesion to collagen leading to excessive bruising and bleeding gums

Autosomal dominant

1-2% of population