Metabolic Flashcards
Typically, why are ketones not present in those with type II diabetes (in acute setting)?
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
Discuss signs and symptoms of DKA
- 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
Electrolyte findings in DKA
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
Discuss the mechanisms behind hypercalcaemia of malignancy
- Paraneoplastic syndrome - tumour secretion of PTH related peptide (e.g. SCC, renal and ovarian)
- Non PTHr - calcitriol (vitamin D) mediated hypercalcaemia assocaited with lymphomas (this is also seen in granulomatous diseases such as active sarcoidosis or TB)
- Osteolytic hypercalcaemia
How can gentamicin cause acute renal failure
acute interstitial nephritis
Where is most sodium reabsorbed in the nephron ?
Proximal convoluted tubule
Via what mechanism is sodium reabsorbed in the DCT and collecting ducts?
Aldosterone mediated
secretion of potassium and absorption of sodium (ion exchanger)
From when and how often is diabetic eye disease screened for in the NHS?
from 12 - annually
Metabolic abnormalities associated with severe vomiting
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)
Why are patients with nephrotic syndrome at higher risk of VTE?
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.
Explain the physiology behind hyperchloraemic acidosis
- 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
What happens to serum calcium and phosphate when PTH is increased (e.g. in primary hyperparathyroidism)
Calcium increases Phosphate decreases (as PTH acts on kidney to increase calcium reabsorption and excrete phosphate)
Causes of hyperkalaemia
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
Define Nephrotic syndrome
- Proteinuria > 3g
- Hypoalbuminaemia <25 g/l
- Oedema
- Hyperlipidaemia
Describe the pathophysiology of minimal change glomerulonephritis
Nephrotic syndrome caused by podocyte fusion