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Path - Chem Path > Therapeutic Drug Monitoring, Calcium, Enzymes and Cardiac Markers > Flashcards

Therapeutic Drug Monitoring, Calcium, Enzymes and Cardiac Markers Flashcards

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1
Q

Phenytoin

  • used to treat?
  • signs of toxicity?
A
  • Seizures

- Ataxia and nystagmus

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2
Q

Phenytoin

  • interactions and cautions?
  • treatment?
A
  • At high levels liver becomes saturated -> surge in blood levels
  • Omit/ reduce dose
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3
Q

Digoxin

  • used to treat?
  • signs of toxicity?
A
  • Arrythmias

- Arrythmias, heart block, confusion, xanthophsia (seeing yellow)

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4
Q

Digoxin

  • Interactions and cautions?
  • Treatment?
A
  • Levels increased with hypokalaemia. Reduce dose in renal failure and in elderly
  • Digibind AKA Digoxin immune Fab
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5
Q

Lithium

  • used to treat?
  • Signs of toxicity?
A
  • Mood disorders eg bipolar

- Tremor (early), lethargy, fits, arrhythmia, renal failure

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6
Q

Lithium

  • Interactions and cautions?
  • Treatment?
A
  • Excretion impaired by hyponatreamia, decreased renal function and diuretics
  • Renal failure may need heamodialysis
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7
Q

Gentamicin

  • Used to treat?
  • Signs of toxicity?
A
  • Infection

- Tinnitus, deafness, nystagmus, renal failure

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8
Q

Gentamicin

  • Interactions and cautions?
  • Treatment?
A
  • Mostly use single daily dosing. Monitor peak and trough level before next dose
  • Omit/ Reduce dose
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9
Q

Theophyline

  • Used to treat?
  • Signs of toxicity?
A
  • COPD, Asthma - Bronchodilator

- Arrythmias, anxiety, tremor convulsions

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10
Q

Theophyline

  • Interactions and cautions?
  • Treatment?
A
  • Variation in 1/2 life; e.g. 4hr for smokers, 8hrs for non smokers, 30hrs in liver disease. Level increased by erythromycin, cimetidine and phenytoin
  • Omit/ Reduce dose
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11
Q

Normal range for Calcium and body composition? (can’t think of the correct way of saying it)

A
  1. 2-2.6mmol/l
    - 45% isonised (free- biologically active form)
    - 50% bound to albumin, therefore affected by albumin level- use corrected calcium
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12
Q

What are the two main hormones involved in calcium metabolism?

A

PTH

1,25 (OH)2D - Calcitriol

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13
Q

PTH - Parathyroid Hormones - how does it have its effects?

A
  • Increases tubular 1alpha hydroxylation of vitamin D (25(OH)D) leading to increased intestinal absorption via calbindin
  • Mobilises calcium from bone
  • Increase renal calcium reabsorption
  • Increase renal phosphate excretion
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14
Q

1,25 (OH)2D - Calcitriol -how does it have its effects?

A
  • Increase calcium and phosphate absorption from the gut

- Bone remodelling

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15
Q

Disorders of Calcium Balance

  • Primary Hyperparathyroidism
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Increase in PTH (80% parathyroid adenoma)
  • Ca = HIGH
  • PO4 = LOW
  • PTH = HIGH/NORM
  • Alk Phos = HIGH/NORM
  • Vit D = NORM
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16
Q

Disorders of Calcium Balance

  • Secondary Hyperparathyroidism
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Renal Osteodystrophy
  • Ca = LOW/NORM
  • PO4 = HIGH
  • PTH = HIGH
  • Alk Phos = HIGH
  • Vit D = NORM
17
Q

Disorders of Calcium Balance

  • Tertiary Hyperparathyroidism
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Autonomous PTH secretion post renal transplant
  • Ca = HIGH
  • PO4 = LOW
  • PTH = HIGH
  • Alk Phos = HIGH/NORM
  • Vit D = NORM
18
Q

Disorders of Calcium Balance

  • Hypoparathyroidism
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Low levels of PTH. Primary = DeGeorge Syndrome. Secondary = Post Thyroid Surgery
  • Ca = LOW
  • PO4 = HIGH
  • PTH = LOW
  • Alk Phos = LOW/NORM
  • Vit D = NORM
19
Q

Disorders of Calcium Balance

  • Rickets/ Osteomalacia
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Vitamin D deficiency
  • Ca = LOW
  • PO4 = LOW
  • PTH = HIGH
  • Alk Phos = HIGH
  • Vit D = LOW
20
Q

Disorders of Calcium Balance

  • Paget’s Disease
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Re-modelling of bone
  • Ca = NORM
  • PO4 = NORM
  • PTH = NORM
  • Alk Phos = HIGH
  • Vit D = NORM
21
Q

Disorders of Calcium Balance

  • Osteoporosis
    • primary defect?
    • Ca, PO4, PTH, Alk Phos, Vit D levels?
A
  • Bone loss
  • Ca = NORM
  • PO4 = NORM
  • PTH = NORM
  • Alk Phos = NORM
  • Vit D = NORM
22
Q

Causes of Hypercalcaemia with High Albumin?

A

Urea high = Dehydration

Urea normal = Cuffed (left the tourniquet on too long when taking blood)

23
Q

Causes of Hypercalcaemia with Low/Norm Albumin and Low phosphate?

A

Primary or Tertiary hyperparathyroidism - confirm with ++ PTH

24
Q

Causes of Hypercalcaemia with Low/Norm Albumin and High phosphate?

A
  • High ALP (increased bone turnover) - Bone metastasis, Thyrotoxicosis, Sarcoidosis (increased 1alpha OH)
  • Normal ALP - Myeloma, Excess Vit D, Sarcoid, Milk alkali syndrome ( + high HCO3)
25
Q

Symptoms of Hypercalcaemia?

A 
Stones (renal)
Bones (pain)
Groans (psych)
Moans (abdo pain)
Polyuria
Muscle Weakness
26
Q

Treatment for Hypercalcaemia?

A

Correct dehydration
Bisphosphonates
Correct cause e.g. chemo for cancer

27
Q

Causes of hypocalcaemia with High Phosphate?

A

Chronic Kidney Disease
Hypoparathyroidism (inc post thyroid surgery)
Pseudohypoparathyroidism
Hypomagnesaemia

28
Q

Causes of hypocalcaemia with Norm/Low Phosphate?

A

Osteomalacia
Acute pancreatitis
Over hydration
Respiratory alkalosis (low ionised/active Ca)

29
Q

Symptoms of Hypocalcaemia?

A

Perioral paraesthesia
carpopedal spasm
neuromuscular excitability
(Trousseau’s and Chvostek’s sign)

30
Q

Treatment for Hypocalcaemia?

A

Mild - Give calcium
Chronic Kidney Disease - Alfacalcidol
Severe - 10% calcium gluconate IV

31
Q

Risk Factors for Renal Stones

A

Dehydration , abnormal urine pH (e.g. meat intake, renal tubular acidosis), increased excretion of stone constituents, urine infection (treat infection), anatomical abnormalities

32
Q

Renal Stones - Calcium Stones

  • due to?
  • preventative management?
A

most patients are normocalcaemic
Results from
-Hyperoxaluria - Increased intake, absorption etc
-Hyercalciuria - increased intake, renal leak
Preventative management - avoid dehydration, reduce oxalate intake, maintain Ca intake, thiazides -> hypocalciuric, citrate (alkalinise urine)

33
Q

Investigations for recurrent Renal Stones

A
  • Serum - Cr, Bicarbonate, Ca, Phosphate, Urate, PTH (if hypercalcaemic)
  • Stone analysis
  • Spot urine
34
Q

6 different stone compositions, Frequency and X ray appearance

A
  • Calcium mixed - 45% - Radio-opaque
  • Calcium oxalate - 35% - Radio-opaque
  • Calcium phosphate - 1% - Radio-opaque
  • Tripple phosphate “Struvite” - 10% - Radio-opaque “staghorn calculi” (branching calcific densities overlying the renal outline
  • Uric acid - 5% - Radiolucent
  • Cysteine - 1-2% - Radiolucent
35
Q

Amylase levels in pancreatitis?

A

High serum levels in acute pancreatitis - usually >10x upper limit of normal (normal serum amylase test - 40-140U/L

36
Q

Creatine Kinase is a marker of? Raised levels due to?

A

CK is a Marker of muscle damage (CK-MM = Skeletal muscle, CK-MB (1&2) = cardiac muscle)

  • raised levels due to
    • Physiological - Afro-Caribbean (5x upper limit of normal)
    • Pathological - Duchenne Muscular Dystrophy (>10x Upper limit of normal), MI (>10xULN), Statin related myopathy, Rhabdomyolysis
37
Q

Alkaline Phosphatase - Causes of raised levels?

A

Present in high concentrations in liver, bone, intestine and placenta
-causes of raised ALP :-
-Physiological - Preganacy (third trimester), Childhood (during growth spurt)
- Pathological
->5xULN = Bone (Pagets, osteomalacia), Liver (Cholestasis, Cirrhosis)
-

38
Q

Troponin (NOT an enzyme) - Biomarker for?

A

Myocardial injury biomarker

Measure at 6 hours and then at 12 hours post onset of chest pain, remains elevated for 3-10 days

39
Q

Diagnostic Criteria for Acute MI

A

1) Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) with at least one of the following…
- ischemic symptoms
- pathological Q waves on the ECG
- ECG changes indicative of schema
- Coronary artery intervention
2) Pathological findings of an acute MI

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