Metabolic Flashcards

1
Q

Typically, why are ketones not present in those with type II diabetes (in acute setting)?

A

Insulin (present in those with type II) inhibits lipolysis in the adipocytes therefore ketones are generally not present
Although insulin resistance prohibits glucose uptake, the effects of insulin on lipolysis are not inhibited

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2
Q

Discuss signs and symptoms of DKA

A
  • Known diabetes of features of diabetes
  • Nausea and vomiting
  • Abdominal pain
  • Dehydration (high levels of glucose in the blood causes fluid to move out of the cells)
  • Hyperventilation - kussmal
  • Reduced consciousness
  • Ketone breath
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3
Q

Electrolyte findings in DKA

A

Hyponatraemia because of the osmotic shift of water, plasma sodium concentrations fall, sodium is also lost via diuresis
Hyperkalaemia is common due to extracellular shift shift of potassium caused by insulin insufficiency

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4
Q

Discuss the mechanisms behind hypercalcaemia of malignancy

A
  1. Paraneoplastic syndrome - tumour secretion of PTH related peptide (e.g. SCC, renal and ovarian)
  2. Non PTHr - calcitriol (vitamin D) mediated hypercalcaemia assocaited with lymphomas (this is also seen in granulomatous diseases such as active sarcoidosis or TB)
  3. Osteolytic hypercalcaemia
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5
Q

How can gentamicin cause acute renal failure

A

acute interstitial nephritis

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6
Q

Where is most sodium reabsorbed in the nephron ?

A

Proximal convoluted tubule

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7
Q

Via what mechanism is sodium reabsorbed in the DCT and collecting ducts?

A

Aldosterone mediated

secretion of potassium and absorption of sodium (ion exchanger)

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8
Q

From when and how often is diabetic eye disease screened for in the NHS?

A

from 12 - annually

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9
Q

Metabolic abnormalities associated with severe vomiting

A

Metabolic alkalosis
Hyponatraemia, hypokalaemia and hypochloraemia - The kidneys compensate for these losses by retaining sodium in the collecting ducts at the expense of hydrogen ions (hydrogen ions are also lost from the GI tract)

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10
Q

Why are patients with nephrotic syndrome at higher risk of VTE?

A

Patients with nephrotic syndrome are at a higher risk of VTE due to the loss of anti-thrombin III in urine. Anti-thrombin III inhibits antagonises the action of thrombin and therefore loss of anti-thrombin results in unopposed thrombin activity creating a pro-coagulant state and therefore prophylactic LMWH is recommended.

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11
Q

Explain the physiology behind hyperchloraemic acidosis

A
  • Normal anion gap acidosis
  • Loss of Bicarbonate ions results in CL- ion retention to compensate
  • reduced bicarbonate ions to buffer H+ leads to acidosis
  • Bicarbonate is lost in diarrhoea and renal tubular acidosis
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12
Q

What happens to serum calcium and phosphate when PTH is increased (e.g. in primary hyperparathyroidism)

A
Calcium increases 
Phosphate decreases (as PTH acts on kidney to increase calcium reabsorption and excrete phosphate)
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13
Q

Causes of hyperkalaemia

A
Causes of hyperkalaemia:
acute kidney injury
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
metabolic acidosis
Addison's disease
rhabdomyolysis
massive blood transfusion
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14
Q

Define Nephrotic syndrome

A
  • Proteinuria > 3g
  • Hypoalbuminaemia <25 g/l
  • Oedema
  • Hyperlipidaemia
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15
Q

Describe the pathophysiology of minimal change glomerulonephritis

A

Nephrotic syndrome caused by podocyte fusion

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16
Q

Discuss fluid restriction in dialysis patients

A
  • Fluid restriction
  • Those who pass urine may be able to drink more
  • Those anuric should be restricted to fluids matching their insensible fluid loss (roughly 750ml)