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Biochemistry > Lipid disorders + Calcium , magnesium and phosphate > Flashcards

Lipid disorders + Calcium , magnesium and phosphate Flashcards

1
Q

What is the difference between a sensitive and a specific test

A

A sensitive test picks up all individuals with disease

A specific test is only positive in disease

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2
Q

What are the 3 regulating mechanisms for calcium

A

Parathyroid hormone
Vit D
Renal function

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3
Q

How do you adjust calcium for a fall in albumin

A

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

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4
Q

How do you take an accurate Calcium blood sample

A

Fasting and with no tourniquet

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5
Q

Describe the effects of parathyroid hormone on calcium

A

Low calcium causes release of PTH

  1. PTH increases renal absorption of calcium and increases renal excretion of phosphate
  2. PTH increases bone resorption by stimulating osteoclast activity and increases the calcium released in bones
  3. PTH increases intestinal calcium absorption and amount of Vit D synthesis
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6
Q

Describe how vitamin D is metabolised

A

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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7
Q

What are the causes of hypercalcaemia

A
  1. Excess PTH
  2. Excess vit d (given or sarcoid)
  3. Excess Ca intake
  4. Drugs- thiazides
  5. Malignant disease
  6. Endocrine disease (Thyrotoxicosis, addisons)
  7. Familial hypocalciuric hypercalcaemia - not enough calcium excreted in urine
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8
Q

What are the symptoms of hypercalcaemia

A 
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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9
Q

What investigations need to be conducted in hypercalcaemia

A

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

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10
Q

What is the management of hypercalcaemia

A
  1. Rehydrate- normal saline 4L-6L over 24 hrs
  2. Monitor urine output and replace fluids in excess of losses
  3. Give loop diuretic- furosemide- promote Ca excretion
  4. Monitor K
  5. Give bisphosphates in malignancy - help bind calcium and stop it being released from bone
  6. Hydrocortisone in sarcoid or myeloma
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11
Q

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

A
  1. Renal failure ( due to increased phosphate)
  2. Hypoparathyroidism
  3. Vitamin D deficiency

Also bisphosphate drugs

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

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12
Q

Discuss the various features of hypocalcaemia

A
  • 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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13
Q

What is the management of moderate and severe hypocalcaemia

A

Moderate- Oral calcium and vit D

Severe- IV calcium gluconate

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14
Q

What are the 2 main causes of hypophosphataemia

A
  1. Decreased intake

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

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15
Q

What are the 3 events that make phosphate shift into cells

A

RIG

  • Respiratory alkalosis
  • Insulin
  • Glucose and amino acids
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16
Q

What can cause increased excretion of phosphate in the urine

A
  • Hyperparathyroidism- excess PTH

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

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17
Q

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

A
  • 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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18
Q

What are the treatments for hypophosphataemia

A

-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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19
Q

What causes hyperphosphataemia

A
  • Renal failure

- Conditions of cell breakdown- tumour lysis or rhabdomylosis

20
Q

What causes hypomagnesaemia

A
  • 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

21
Q

What are the clinical features and Treatment for hypomagnesaemia

A

Clinical features the same as hypocalcaemia

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

22
Q

What are the 3 main causes of an elevated ALP

A
  1. Physiological - growth- childhood and pregnancy
  2. Bone- healing fractures, bone mets, paget’s, hyperparathyroidism
  3. Hepatic- obstructive jaundice, liver disease
23
Q

What is osteoporosis and what would its blood picture look like

A

low bone density

  • Ca, PO4 ALP and vit d all normal
  • ALP elevated if there is a fracture
24
Q

What is osteomalacia and what would its blood picture look like

A

Defective bone mineralisation - ADULT RICKETS think vit D deficiency

  • Low calcium and phosphate and Vit D
  • High ALP
25
Q

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

A

Abnormal bone remodelling due to an elevated ALP

-Increased ALP with normal Calcium and phosphate

26
Q

What would the blood profile look ;like in bone metastases

A

Calcium and ALP elevated

27
Q

What would the blood profile for primary hyperparathroidism look like

A

High calcium with low or normal phosphate

28
Q

What are the two components measured in a lipid profile

A

Cholesterol and Triglycerides

29
Q

What is the role of cholesterol

A

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

30
Q

What are the different types of lipoproteins and their roles

A
  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
31
Q

What are the functions of apolipoproteins

A
  • 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
32
Q

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

A

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

33
Q

Discuss the 3 main ways to transport lipids

A
  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
34
Q

What components does a lipoprotein measurement look at

A

Lp (a)
ApoA 1
ApoB
Type of Apo E

35
Q

What is the NICE guidance on primary prevention of dyslipidaemia

A
  • Identify at risk 40-84 yr olds

- Take lipid profile

36
Q

How do you calculate LDL cholesterol

A

Total cholesterol - HDL - (Triglycerides/ 2.2) in mol/L

If triglycerides are high equation is invalid

37
Q

What causes increases and decreases LDL in secondary dyslipidaemia

A 
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

38
Q

What causes increased and decreased high density lipoproteins in secondary dyslipidaemia

A 
Decreases - bad 
Smoking 
Obesity
malnutrition 
Anabolic steroids 
T2DM

Increases- good
Exercise
Moderate alcohol
Oestrogen

39
Q

What increases VLDL in dyslipidaemia

A 
Obesity 
T2DM 
Hepatits 
Alcohol misuse 
Kidney disease 
HIV protease inhibitors 
Retinoic acid
40
Q

What are the two major types of primary dyslipidaemia

A

Type 2- Familial hypercholesterolaemia and familial combined hyperlipidaemia both increase LDL- shows tendon xanthomas

Type 3- Familial dysbetalipoprotinaemia (increased TGs) shows palmar xanthomas

41
Q

What are the three types of dyslipdaemias

A

Hypercholesterolaemia
Hypertrigluceridaemia
Mixed dyslipiademia

42
Q

What is the pathology behind familial hyperchlesterolaemia

A

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

43
Q

What is type 3 dyslipidaemia or dysbetalipoprotinaemia

A

Abnormal Apo E receptors (mainly apo E 3)

  • Not screened for as only 20% individuals with show dyslipidaemia
  • Increased VLDL
44
Q

What is the treatment for dislipidaemia

A

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

45
Q

What factors are considered in a Qrisk score

A 
Gender 
Smoking 
Diabetes 
Fam history 
Medication 
Cholesterol and HDL ratio
46
Q

What are the two risk factors associated with hypertriglyceridaemia

A

Pancreatitis and CVS

47
Q

What will a metabolic syndrome do to triglycerides and HDL

A
  • Decrease HDL and increased triglycerides

- Cause HTN , insulin resistance and visceral obesity

Biochemistry (8 decks)

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