Lipid disorders + Calcium , magnesium and phosphate Flashcards by Roma Bannon

What is the difference between a sensitive and a specific test

A sensitive test picks up all individuals with disease

A specific test is only positive in disease

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What are the 3 regulating mechanisms for calcium

Parathyroid hormone
Vit D
Renal function

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How do you adjust calcium for a fall in albumin

Increase calcium by 0.02mmol for every 1g drop in albumin below 40g/L

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How do you take an accurate Calcium blood sample

Fasting and with no tourniquet

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Describe the effects of parathyroid hormone on calcium

Low calcium causes release of PTH

PTH increases renal absorption of calcium and increases renal excretion of phosphate
PTH increases bone resorption by stimulating osteoclast activity and increases the calcium released in bones
PTH increases intestinal calcium absorption and amount of Vit D synthesis

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Describe how vitamin D is metabolised

UV light converts cholesterol to Vit D3
Vit D3 converted to 25OHD3 in the liver
The kidney then converts this to its active form 1, 25 D3

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What are the causes of hypercalcaemia

Excess PTH
Excess vit d (given or sarcoid)
Excess Ca intake
Drugs- thiazides
Malignant disease
Endocrine disease (Thyrotoxicosis, addisons)
Familial hypocalciuric hypercalcaemia - not enough calcium excreted in urine

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What are the symptoms of hypercalcaemia

Bones Stones Groans and Moans 
Bone pain 
Renal calculi 
Abdo pain 
Psychi moans 
Peptic ulcer 
Fatigue/ Malaise 
Polydipsia/ polyuria 
Signs of underlying disease

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What investigations need to be conducted in hypercalcaemia

-serum phosphate (low)
-Renal function
-parathyroid hormone
-Alkaline phosphatase (underlying bone malignancy)
-Vit D
CXR (sarcoid/ tumour)
-Urine calcium

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What is the management of hypercalcaemia

Rehydrate- normal saline 4L-6L over 24 hrs
Monitor urine output and replace fluids in excess of losses
Give loop diuretic- furosemide- promote Ca excretion
Monitor K
Give bisphosphates in malignancy - help bind calcium and stop it being released from bone
Hydrocortisone in sarcoid or myeloma

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What are the 3 main causes of hypocalcaemia and what investigations would you carry out

Renal failure ( due to increased phosphate)
Hypoparathyroidism
Vitamin D deficiency

Also bisphosphate drugs

Investigations
-u&e -Phosphate -Magnesium -PTH -Vit D

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Discuss the various features of hypocalcaemia

Neuromuscular irritability
Tetany
Positive Chovstek’s sign - tap facial nerve and spasm of muscle
Positive Trousseaus sign- BP cuff on and inflate above systolic pressure for 3 mins- wrist flexion and finger extension
Prolonged QT interval on ECG

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What is the management of moderate and severe hypocalcaemia

Moderate- Oral calcium and vit D

Severe- IV calcium gluconate

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What are the 2 main causes of hypophosphataemia

Decreased intake

2. Decreased absorption- due to malabsorption or vit d deficiency

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What are the 3 events that make phosphate shift into cells

RIG

Respiratory alkalosis
Insulin
Glucose and amino acids

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What can cause increased excretion of phosphate in the urine

Hyperparathyroidism- excess PTH

- Renal Tubular defects- too much PO43- in the urine

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What are the clinical features of hypophosphataemia and who is likely to have it

Asymptomatic
Rhabdomyosis- lack of PO43- in energy production so skeletal muscle breakdown
Cardiomyopathy
Resp failure
Erythrocyte (O2 carrying capacity) and leucocyte dysfunction (phagocytosis)

It is associated with alcohol abuse and alcohol withdrawal and those who are being fed through iv eneteral act
Refeeding syndrome causes abrupt insulin production for the first time in a while - shifts phosphate into cells

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What are the treatments for hypophosphataemia

-Milk
-Oral supplementation
-IV - dipotassium hydrogen phosphatase every 12 hrs
12mmol in saline or dextrose over 12 hrs
administered once in any 24 hr period

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What causes hyperphosphataemia

Renal failure

- Conditions of cell breakdown- tumour lysis or rhabdomylosis

What causes hypomagnesaemia

Poor intake/malabsorption
Increased losses- kidney/ GIT
Malabsorption
Diarrhoea
Fistula
Refeeding syndrome
Alcoholism/ withdrawl
Loop diuretics

Anything that will increase fluid loss in LOH will lower magnesium

What are the clinical features and Treatment for hypomagnesaemia

Clinical features the same as hypocalcaemia

-Treatment= oral/ IV magnesium 30mmol 1st 24hrs then 20mmol per 24 hrs

What are the 3 main causes of an elevated ALP

Physiological - growth- childhood and pregnancy
Bone- healing fractures, bone mets, paget’s, hyperparathyroidism
Hepatic- obstructive jaundice, liver disease

What is osteoporosis and what would its blood picture look like

low bone density

Ca, PO4 ALP and vit d all normal
ALP elevated if there is a fracture

What is osteomalacia and what would its blood picture look like

Defective bone mineralisation - ADULT RICKETS think vit D deficiency

Low calcium and phosphate and Vit D
High ALP

What is pages disease and what would the blood picture look like

Abnormal bone remodelling due to an elevated ALP | -Increased ALP with normal Calcium and phosphate

What would the blood profile look ;like in bone metastases

Calcium and ALP elevated

What would the blood profile for primary hyperparathroidism look like

High calcium with low or normal phosphate

What are the two components measured in a lipid profile

Cholesterol and Triglycerides

What is the role of cholesterol

Hormone production- oestrogen, testosterone and cortisol Cell membranes Vit D synthesis Bile acid synthesis

What are the different types of lipoproteins and their roles

1. Chylomicrons- transport fat (triglycerides mainly) through the gut after they've been absorbed from diet 2. VLDL- carries endogenous triglycerides- TG from liver to other tissues 3. IDL- Formed from HDL and LDL 4. LDL- Main carrier of cholesterol- bad- atheroma 5. HDL- Clears cholesterol from circulation (non hepatic tissues to the liver) good

What are the functions of apolipoproteins

- Transport lipids (hydrophobic) - Co-factor for enzymes of lipid metabolism - Receptor binding- allow lipids to be taken up into liver and muscle cells - Allow transfer of cholesterol fractions

What are the main types of alipoprotein and what do they transport

Alipoprotein A- 2 types A 1 and A 11- found in liver and GIT- removes HDL and VDLmainly Alipoprotein B- 2 types B-48 and B-100- 48 in GIT, 100 Liver , removes LDL Alipoprotein E- in triglyceride rich fractions- found in liver and macrophages

Discuss the 3 main ways to transport lipids

1. Exogenous (dietary) transport- across gut and moved to liver by chylomicrons, stored in liver or can go directly to cells needing it- muscle or fat 2. Endogenous (hepatic) transport- from liver to peripheral circulation- VLDL help liver export stored triglycerides and move them to tissues, some remaining factors go back to liver for more processing 3. Reverse Cholesterol transport-from tissue back to liver for removal from circulation Via HDL- advantageous as this prevents atheroma

What components does a lipoprotein measurement look at

Lp (a) ApoA 1 ApoB Type of Apo E

What is the NICE guidance on primary prevention of dyslipidaemia

- Identify at risk 40-84 yr olds | - Take lipid profile

How do you calculate LDL cholesterol

Total cholesterol - HDL - (Triglycerides/ 2.2) in mol/L If triglycerides are high equation is invalid

What causes increases and decreases LDL in secondary dyslipidaemia

``` Increases - bad Hypothyroidism Nephrotic syndrome- protein loss from kidneys compensated for by extra lipoprotein synth Drugs- cyclosporin Cholestasis Anorexia nervosa ``` Decreases severe Liver disease Malabsorption and malnutrition

What causes increased and decreased high density lipoproteins in secondary dyslipidaemia

``` Decreases - bad Smoking Obesity malnutrition Anabolic steroids T2DM ``` Increases- good Exercise Moderate alcohol Oestrogen

What increases VLDL in dyslipidaemia

``` Obesity T2DM Hepatits Alcohol misuse Kidney disease HIV protease inhibitors Retinoic acid ```

What are the two major types of primary dyslipidaemia

Type 2- Familial hypercholesterolaemia and familial combined hyperlipidaemia both increase LDL- shows tendon xanthomas Type 3- Familial dysbetalipoprotinaemia (increased TGs) shows palmar xanthomas

What are the three types of dyslipdaemias

Hypercholesterolaemia Hypertrigluceridaemia Mixed dyslipiademia

What is the pathology behind familial hyperchlesterolaemia

Autosomal dominant genetic condition Tendon Xanthoma, corneal arcus, xanthelasma Problem with Apo B so it doesn't bind to LDL receptor or a problem with the LDL receptor causes increased levels of cholesterol in the circulation

What is type 3 dyslipidaemia or dysbetalipoprotinaemia

Abnormal Apo E receptors (mainly apo E 3) - Not screened for as only 20% individuals with show dyslipidaemia - Increased VLDL

What is the treatment for dislipidaemia

Levels above 7.5 mol/l total cholesterol or 4.9 LDL - Assess Q risk - Lifestyle interventions Primary prevention- 20mg atorvastatin Secondary prevention- 80 mg atorvastatin Aim for 40% reduction in non- HDL cholesterol

What factors are considered in a Qrisk score

``` Gender Smoking Diabetes Fam history Medication Cholesterol and HDL ratio ```

What are the two risk factors associated with hypertriglyceridaemia

Pancreatitis and CVS

What will a metabolic syndrome do to triglycerides and HDL

- Decrease HDL and increased triglycerides | - Cause HTN , insulin resistance and visceral obesity