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AT CHEMPATH > ChemPath: Hypoglycaemia > Flashcards

ChemPath: Hypoglycaemia Flashcards

1
Q

Outline the first step in the management of hypoglycaemia patients in the following states:

  1. Alert and orientated
  2. Drowsy/confused but swallow intact
  3. Unconscious or concerned about swallow
A
  1. Alert and orientated
    • Oral carbohydrates (short acting first (juice/sweets) then long-acting (complex caarbs e.g. sandwich))
  2. Drowsy/confused but swallow intact
    • Buccal glucose (e.g. glucogel)
  3. Unconscious or concerned about swallow
    • IV 100 mL 20% glucose
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2
Q

What should be considered if a hypoglycaemic patient is deteriorating or does not appear to be responding to the first step in their management?

A

IM/SC 1 mg glucagon

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3
Q

What is the benefit of giving glucose sublingually?

A

Bypasses hepatic first-pass metabolism

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4
Q

How long is it likely to take for IM glucagon to cause an increase in blood glucose?

A

15-20 mins

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5
Q

Which group of patients may not respond to IM glucagon?

A
  • Starving
  • Anorexic
  • Hepatic failure
  • Glucagon mobilises glycogen stores but these patients will have poor liver glycogen stores
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6
Q

Describe the triad of features that is used to define hypoglycaemia.

A

Whipple’s triad
* Low glucose
* Symptoms - adrenergic or neuroglycopaenic
* Relief of symptoms by administration of glucose

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7
Q

List some symptoms of hypoglycaemia.

A
  • Adrenergic: tremors, palpitations, sweating
  • Neuroglycopaenic: confusion, seizures coma
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8
Q

What is a consequence of recurrent episodes of hypoglycaemia?

A

Hypoglycaemia unawareness (loss of adrenergic symptoms with hypoglycaemia)

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9
Q

Describe the order in which physiological compensatory changes in response to hypoglycaemia take place.

A

Low glucose
* Suppression of insulin
* Release of glucagon
* SNS activation -> release of adrenaline
* Release of cortisol

^all of these tries to increase your glucose

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10
Q

How does the body obtain energy in low glucose/starving states

A

Reduced peripheral uptake of glucose
Increase glycogenolysis and gluconeogenesis
Increase lipolysis -> FFAs enter beta oxidation to create ATP -> ketone bodies produced

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11
Q

What investigation may need to be performed to demonstrate hypoglycaemia in an otherwise healthy person?

A

Prolonged fast

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12
Q

What is the gold standard for measuring blood glucose?

A

Venous glucose

NOTE: this is collected in a grey top container that has fluoride oxalate

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13
Q

Describe 3 methods of measuring blood glucose

A
  1. Venous glucose (gold standard)
  2. Capillary blood glucose
  3. Continuous glucose monitoring

2 & 3 are not precise at low levels (<2.2mmol/l)

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14
Q

List some causes of hypoglycaemia in diabetics.

A
  • Medications (inappropriate insulin, sulphonylureas)
  • Inadequate carbohydrate intake (missed meal)
  • Impaired awareness
  • Excessive alcohol
  • Strenous exercise
  • Co-existing conditions - end stage renal / liver cirrhosis (this alters drug clearance), Addison’s (compromises gluc counter-regulation)
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15
Q

List some diabetic medications that can causes hypoglycaemia.

A
  • Oral hypoglycaemics: sulphonylureas, meglitinides, GLP1 analogues
  • Insulin
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16
Q

List some non-diabetic medications that can cause hypoglycaemia.

A
  • Beta-blockers
  • Salicylates
  • Alcohol
17
Q

List some biochemical tests that may help differentiate between causes of hypoglycaemia.

A
  • Insulin levels (NOTE: exogenous insulin can interfere with assays)
  • C-peptide (marker of endogenous insulin production)
  • Drug screen (excluding sukphonylureasa needed for dx of insulinoma)
  • Autoantibodies
  • Cortisol/GH
  • Free fatty acids/ketone bodies
  • Lactate
  • IGF-2

NOTE: it is important to perform these tests at the time of the hypo (but try not to delay treatment)

18
Q

What would you expect the insulin and C-peptide levels to be in a hypoglycaemic patient who has anorexia nervosa but not diabetes?

A
  • Low insulin and low C-peptide
  • The patient is hypoglycaemic because of poor liver glycogen stores (not an issue with insulin) so their insulin response will be normal
19
Q

List some causes of Hypoinsulinaemic hypoglycaemia.

A
  • Fasting/starvation
  • Strenous exercise
  • Critical illness
  • Endocrine deficiencies (adrenal failure, hypopituitarism)
  • Liver failure
  • Anorexia nervosa
  • Drugs: Beta blockers, sulphonylureas

NOTE: this is a normal response to hypoglycaemia

20
Q

What does hypoglycaemia with a high insulin and low C-peptide suggest?

A

Exogenous insulin use

21
Q

Name 3 ketone bodies.

A
  • 3-hydroxybutyrate
  • Acetone
  • Acetoacetate
22
Q

List some physiologically explicable causes of neonatal hypoglycaemia.

A
  • Prematurity
  • IUGR
  • Inadequate glycogen/fat stores

NOTE: this should improve with feeding

23
Q

What is a pathological cause of neonatal hypoglycaemia?

A

Inborn errors of metabolism

24
Q

List some causes of neonatal hypoglycaemia with high FFAs and low ketones.

A
  • Fatty acid oxidation defects
  • MCAD deficiency
  • Carnitine disorders
  • HMG-CoA lyase deficiency
  • GSD type 1
25
Q

List some causes of inappropriately high insulin levels.

A
  • Islet cell tumours (eg. insulinoma)
  • Drugs (e.g sulphonylureas)
  • Post-prandial/reactive (post gastic bypass dumping)
  • Autoimmune insulin syndrome

In neonates specifically:
* Islet cell hyperplasia
* Infant with diabetic mother
* Beckwith-Wiedemann syndrome (overgrowth disorder)
* Nesidioblastosis (excessive function of beta cells with abnormal microscopic appearance)
* Congenital hyperinsulin (KCNJ11/ABCC8)

(all will have high c-peptide)

26
Q

State two causes of Hyperinsulinaemic hypoglycaemia with a high C-peptide.

A
  • Insulinoma
  • Sulphonylurea abuse
27
Q

What test could help differentiate between insulinoma and sulphonylureas?

A

Urine or serum sulphonylureas

28
Q

Describe the mechanism by which beta cells release insulin in response to blood glucose.

A
  • Glucose crosses the membrane of beta cells and enters glycolysis via glucokinase
  • Glycolysis produces ATP
  • The rise in ATP leads to the closure of ATP-sensitive K+ channels
  • This leads to membrane depolarisation, calcium influx and insulin exocytosis
29
Q

Describe the mechanism of action of sulphonylureas.

A

They bind to the ATP-sensitive K+ channel making it close independently of ATP -> membrane depolarisation, calcium influx -> insulin exocytosis

30
Q

State two causes of Hyperinsulinaemic hypoglycaemia with a low C-peptide.

A
  • Factitious result
  • Oral hypoglycaemic usage (not sulphonylureas)
31
Q

What can cause the following: low glucose, low insulin, low C-peptide, low FFAs and low ketones?

A
  • This suggests that something is pretending to be insulin
  • This is non-islet cell hypoglycaemia caused by secretion of big IGF-2
  • Big IGF-2 binds to IGF-1 receptors and insulin receptors
  • It behaves like insulin, so it causes hypoglycaemia and suppresses insulin and FFA/ketone production
  • It is a paraneoplastic syndrome usually caused by mesenchymal tumours (e.g. mesothelioma, fibroblastoma) and epithelial tumours (carcinoma)
32
Q

Describe an autoimmune cause of hypoglycaemia.

A
  • Autoimmune insulin syndrome - antibodies are directed towards insulin so sudden dissociation of the antibodies can precipitate hypoglycaemia (could be caused by drugs e.g. hydralazine, procainamide)
33
Q

List some genetic causes of hypoglycaemia.

A
  • Glucokinase activating mutation
  • Congenital hyperinsulinism (KCNJ11 /ABCC8, GLUD-1, HNF4A, HADH)
34
Q

What is reactive hypoglycaemia?

A
  • Hypoglycaemia following food intake (post-prandial)
  • Can occur after gastric bypass (dumping in SI causing big increase of insulin)
  • May be suggestive of early diabetes
  • May occur in insulin-sensitive individuals after exercise or large meals
  • May be due to hereditary fructose intolerance
35
Q

What level of glucose is considered hypoglycaemic

A

Depends on context

Generally <4mmol/l
- In diabetes: <3.5mmol/l
- In paeds: <2.5mmol/l (hypoglyc common in children)

36
Q

What is c-peptide & what is its half life?

A

Cleavage product of proinsulin, secreted in equimolar amounts to insulin

Hence is a marker of endogenous insulin and good beta cell function

Half life = 30 mins

37
Q

What tumours are responsible for paraneoplastic secretion of big IGF-2?

A

Mesenchymal: mesothelioma, fibroblastoma
Epithelial tumours: carcinoma

AT CHEMPATH (24 decks)

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