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HYMS PPT > Metabolic > Flashcards

Metabolic Flashcards

1
Q

What is the immediate management of AKI?

A
  • IV fluid therapy
  • Withdrawal of nephrotoxins
  • Withholding of hypotensive agents and diuretics
  • Withhold atorvastatin
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2
Q

What is spirolactone’s mechanism of action?

A

Aldosterone antagonist in distal renal tubules

Increasing NaCl and water excretion while conserving K+ and H+ ions; may have effect on arteriolar smooth muscle as well

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3
Q

What are the indications for use of spirolactone?

A
  • Systolic heart failure
  • Resistant hypertension
  • Temporary treatment of Conn’s syndrome
  • Liver failure (oedema)
  • Management of oedema associated with excessive aldosterone excretion/ congestive heart failure.
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4
Q

What are the cardiovascular and neurological side-effects of Spirolactone?

A

CV: vasculitis
CNS: ataxia, confusion, lethargy

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5
Q

What are the dermatological side effects of Spirolactone?

A
  • DRESS syndrome
  • Erythematous maculopapular rash
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Urticaria
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6
Q

What are the GI side effects of Spirolactone?

A
  • Abdo cramps
  • Diarrhoea
  • Gastritis
  • GI haemorrhage
  • GI ulcer
  • Nausea
  • Vomiting
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7
Q

What are the renal side effects of Spirolactone?

A
  • Increased blood urea nitrogen
  • Renal failure
  • Renal insufficiency
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8
Q

What is Furosemide’s mechanism of action?

A

Inhibits reabsorption of Na+ and Cl- in the ascending loop of Henle and distal renal tubule -> increased water, Na+, Cl-, Mg2+ and Ca2+ excretion

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9
Q

What are the indications for use of loop diuretics?

A
  • Management of oedema associated with heart failure and hepatic/ renal disease
  • Acute pulmonary oedema
  • Resistant hypertension
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10
Q

What are the the indications for Ramipril’s use?

A
  • Hypertension
  • Symptomatic heart failure
  • Prophylaxis after MI
  • Prevention of CV events in patients with atherosclerotic CVD, diabetes and at least one additional risk factor
  • Nephropathy
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11
Q

What are the most common side effects of Ramipril?

A
  • Increased cough (7-12%)
  • Hypotension (11%)
  • Hyperkalaemia (1-10%)
  • Headache
  • Dizziness
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12
Q

What is the difference between pharmacokinetics and pharmacodynamics?

A

Pharmacokinetics - what the body does to the drug

Pharmacodynamics - what the drug does to the body

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13
Q

What are pharmacodynamic drug-drug interactions?

A

Interacting drugs have additive effects (increasing overall effect) or opposing effects (decreased overall effect/ cancelled out)

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14
Q

What are pharmacokinetic drug-drug interactions?

A

One drug changes the systemic concentration of another drug (can reflect amount at site of action or period of time for which the whole concentration exists there)

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15
Q

What are examples of pharmacodynamic drug interactions of ACE inhibitors?

A

BP lowering with diuretics/ other antihypertensives = hypotension
Increase in plasma K+ with potassium sparing diuretics/ ARBs = hyperkalaemia

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16
Q

How are NSAIDs thought to contribute to the development of AKI?

A

Directly inducing different forms of kidney injury

NSAID induced attenuation of (PG mediated) renal vasodilation

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17
Q

How could you measure GFR?

A

Measure urine clearance of an ideal filtration marker (gold standard = inulin)

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18
Q

Why is inulin the gold standard exogenous filtration marker?

A
  • Physiologically inert
  • Not secreted, reabsorbed, synthesised or metabolised by the kidney
  • Amount of inulin filtered at glomerulus matches the amount excreted in urine
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19
Q

Why is inulin not a commonly used method for estimation of GFR?

A
  • Expensive
  • Limited
  • Difficult to assay
  • Requires continuous IV infusion, multiple blood samples and bladder catheterisation
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20
Q

What are the most common methods used to estimate GFR?

A
  • Creatinine clearance
  • Estimation equations:
    Cockcroft-Gault
    MDRD
    CKD-EPI
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21
Q

Why is CrCl from Cockcroft and Gault more accurate than an eGFR from a BCP?

A

It uses weight to add further information (may overestimate)

Allows creatinine clearance to be estimated from serum creatinine (only good in patients with stable values)

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22
Q

Why is it important to know a patient’s eGFR/ CrCl?

A
  • To safely prescribe drugs that could affect/ be affected by renal function
  • Good to monitor changes in renal function
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23
Q

How could you make eGFR more accurate?

A

Adjust it to the patient’s actual body weight

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24
Q

When would you use absolute eGFR / Cockcroft & Gault’s CrCl when prescribing drugs?

A
  • Patients at the extreme of body mass
  • Any Hx of renal disease
  • Prescribing certain drugs
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25
Q

What effect will renal impairment have on the half life of a drug that is cleared by the kidney?

A

Increased half-life-> takes longer to reach steady state

More likely to be toxic dose

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26
Q

How might you alter the prescription of a drug that’s excreted through the kidney in a patient with significant renal impairment

A
  • Give smaller dose initially and then titrate it up to a therapeutic level
  • Give loading dose if needed to reach steady state quickly (lower at more frequent intervals in impairment)
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27
Q

What is the most frequently prescribed oral treatment for iron deficiency anaemia?

A
  • Ferrous sulfate
  • Ferrous fumarate
  • Ferrous gluconate
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28
Q

What is the most frequently prescribed parenteral treatment for iron deficiency anaemia?

A
  • Parenteral iron
  • Iron dextran
  • Iron sucrose
  • Ferric carboxymaltose
  • Iron isomaltoside 1000
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29
Q

What is the difference between the iron taken from omnivorous and herbivorous diets?

A

Omnivorous - iron absorbed from meat in the ferrous form of haem (Fe2+)
Herbivorous - non-haem iron is in the ferric state (Fe3+)

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30
Q

What are important adverse effects of iron?

A
  • GI disturbances

- Oral iron turns stools black -> may obscure view in endoscopy

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31
Q

What dose of iron should be prescribed in iron deficiency anaemia and why?

A

100-200mg of elemental iron

To correct the anaemia and replace the depleted stores

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32
Q

How long should iron be given in iron deficiency anaemia?

A

3-4 weeks after Hb concentration is stable

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33
Q

What other measures could be considered in iron deficiency anaemia for a patient who experiences heavy periods?

A
  • Combined contraceptive pill
  • Endometrial ablation
  • Hormonal therapy
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34
Q

Why is folic acid used in pregnancy?

A

Reduced risk of neural tube defects

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35
Q

What dose of folic acid would be appropriate for pregnant women?

A

Women with a previous child with neural tube defects/ taking anticonvulsants associated with neural tube defects should take 5mg

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36
Q

What is the recommended duration of folic acid treatment in pregnant women?

A

From conception until the 12th week of pregnancy (end of organogenesis)

37
Q

What drug is offered to BPH patients?

A

Tamsulosin

38
Q

How does Tamsulosin work?

A

Alpha blocker

Causes smooth muscle dialtion

39
Q

What drugs are given in urinary obstruction linked to the bladder?

A

Finasteride (5-alpha reductase inhibitor)

40
Q

What is anastrozole?

A

Aromatase inhibitor

41
Q

What is tamoxifen?

A

Selective oestrogen receptor modulator

Inhibits breast cancer cell growth by antagonising the oestrogen receptor

42
Q

What is tamoxifen indicated for?

A
  • Adjuvant treatment of premenopausal women with breast cancer
  • Postmenopausal women who are not candidates for an aromatase inhibitor
43
Q

What is the initial drug treatment for adults with type 2 diabetes?

A

Standard-release metformin

44
Q

What do you need to consider before prescribing metformin?

A

Renal function - increased risk of lactic acidosis

  • Review metformin dose if eGFR is <45ml/min/1.73m2
  • Stop it if eGFR is <30
  • Use with caution if the patient is at risk of sudden deterioration in kidney function
45
Q

How would you introduce metformin?

A

Gradually increase the dose over several weeks to minimise risks of GI side effects

46
Q

What are the common side effects of metformin?

A

Abdo pain, anorexia, diarrhoea, nausea & vomiting, taste disturbance

47
Q

If metformin does not control HbA1c levels, what should the next steps in treatment be?

A

Dual therapy of metformin with either:

  • DPP-4 inhibitor
  • Pioglitazone
  • Sulfonylurea
48
Q

What are the main side effects of sulfonylureas?

A

Hypoglycaemia (usually indicates excessive dosage)

49
Q

What drugs are available for triple therapy of diabetes?

A
  • Metformin + DPP-4 inhibitor + sulfonylurea
  • Metformin + pioglitazone + sulfonylurea
  • Insulin-based treatment
50
Q

What features are necessary for you to diagnose a DKA?

A
  • Ketonaemia > 3.0mmol/ L
  • Blood glucose > 11.0mmol/L
  • Bicarbonate <15.0mmol/L OR venous pH <7.3
51
Q

What is the immediate management for DKA?

A
  • ABCDE
  • IV Fluids - 0.9% NaCl 500mL over 15 mins
    T= 0 at time IV fluids are started
  • Fixed rate intravenous insulin infusion after starting IV fluids
52
Q

What is important to communicate to the patient with respect to monitoring?

A
  • Hourly blood glucose
  • Hourly ketone measurement
  • At least 2 hourly serum potassium & bicarbonate for the first 6 hours
  • Clinical & biochemical assessment of the patient
53
Q

How does intravenous insulin work?

A
  • Reduction in blood glucose

- Suppression of lipolysis to resolve ketonaemia

54
Q

How is insulin produced for the management of diabetes?

A

Genetic engineering: implant insulin gene in bacteria grown in vats, then remove insulin

55
Q

What are examples of short acting human insulins?

A

Humulin S

Actrapid

56
Q

What are examples of ultra-short acting human insulins?

A

Humalog

Novorapid

57
Q

Why are Humalog and Novorapid faster in clinical effect than Humulin S and Actrapid?

A

The former two have been altered in molecular structure.

They more easily separate into insulin dimers and monomers which speeds up absorption from the injection site.

58
Q

What are examples of NPH (isophane) intermediate acting insulins?

A

Insulatard

Humulin I

59
Q

What are examples of analogue long acting insulins?

A

Lantus

Levemir

60
Q

How are long acting analogue insulins different from isophane insulins?

A

Lantus has been genetically altered to make it more soluble in its cartridge (higher pH) than in the blood, slowing absorption.

Levemir has a fatty acid moiety sick to it, delaying absorption.

61
Q

What are biphasic insulins?

A

Mix of analogue ultra short acting insulin with an NPH/ isophane form of insulin

62
Q

What are biphasic insulins indicated for?

A
  • Used in adults with learning difficulties and T1DM

- Patients with poor compliance

63
Q

What does the number in ‘mix’/ biphasic insulins refer to?

A

Percentage of quick acting insulin in the mixture

64
Q

What does U100 mean in the context of insulins?

A

100 units of insulin per mL.

Most insulins are described as this.

65
Q

What are potential disadvantages of introducing insulin Degludec which comes as U100 and U200?

A

Could lead to dosing errors.

The manufacturer only supplied Degludec in pre-filled pens which reduces the risk of this error.

66
Q

What is the initial therapy for management of hyperthyroid symptoms?

A

Beta blocker - can be started once the diagnosis is made, irrespective of whether Graves’ is confirmed

67
Q

Besides direct beta receptor antagonism, how do beta blockers help with hypothyroidism?

A

Slowly decreasing T3 concentrations by inhibiting 5’-monodeiodinase (converter of T4 to T3)

68
Q

How long does it take to see the T3 reducing effect of beta blockers?

A

7-10 days

69
Q

What is carbimazole?

A

Thionamide

70
Q

How does carbimazole work?

A

Inhibits thyroid peroxidase and therefore thyroid hormone synthesis

71
Q

How long does it take to see the T4 and T3 lowering effect of carbimazole?

A

4-6 weeks

72
Q

How does propylthiouracil (PTU) work in hyperthyroidism?

A

Inhibits 5’ monodeiodinase that converts T4 to T3 in extra thyroidal tissue

73
Q

What is methimazole (MMI)?

A

An active metabolite of carbimazole

74
Q

What is the difference between MMI and PTU?

A

MMI’s better
Half-life of MMI = 4-6 hours
Half-life of PTU = 75 mins
Intrathyroidal MMI concentration remains high for up to 20 hours which is considerably longer than PTU.

75
Q

Why might PTU be the preferential thionamide in early pregnancy?

A

All the antithyroid drugs have been associated with teratogenic effects but they’re less common and less severe in PTU.

76
Q

Why isn’t PTU used as the first-line therapy in non-pregnant adults?

A

Severe hepatic reactions have been reported including patients requiring liver transplant and death

77
Q

How do you advise pregnant patients of potential PTU hepatic effects?

A

Teach them how to recognise signs of liver disorder

Discontinue drug if significant liver-enzyme abnormalities develop

78
Q

When commencing a patient on carbimazole, what do you warn them of?

A

Agranulocytosis - 0.1 - 0.5%, usually within first 2 months of treatment
Any sign of illness e.g. fever/ sore throat, discontinue drug and get WCC done.

79
Q

What are the two ways of treating thyrotoxicosis with carbimazole?

A

Titration therapy

Block and replace therapy

80
Q

Why do doctors generally pre-treat with carbimazole before giving radioiodine?

A

Small risk of inducing thyroid storm after radioiodine

Contraindications of radiotherapy:

  • Pregnancy
  • Significant thyroid eye disease
81
Q

What hormones would you use to replace anterior pituitary function?

A

Hydrocortisone
Growth hormone analogue
Levothyroxine
Testosterone/ Oestrogen

82
Q

How would you give glucocorticoid replacement therapy?

A

Hydrocortisone 15-30mg daily in 2-3 divided dose in the morning later in the day

83
Q

What are the risks of under over replacement with glucocorticoids

A 
Under = Addison's
Over = Cushing's
84
Q

Do you need to give fludrocortisone in a patient with secondary adrenal insufficiency?

A

Not usually because if the adrenal gland’s fine, aldosterone function is preserved

85
Q

How do you treat and monitor TSH deficiency?

A

T4 and T3

T4 shouldn’t be administered until adrenal function has been evaluated and found to be normal/ treated

86
Q

Why is it important to manage a patient with coexisting hypothyroidism and hypoadrenalism appropriately?

A

Treating the hypothyroidism alone may increase the clearance of the little cortisol that is produced -> makes Addison’s worse

87
Q

How do you measure treatment of FSH and LH deficiency?

A

Measurements of serum testosterone/ oestrogen

88
Q

Is it necessary to treat GH deficiency?

A

No but you could monitor levels via centripetal (abdominal) obesity

HYMS PPT (4 decks)

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