hypoglycaemia Flashcards

(37 cards)

1
Q

how would you manage acute hypoglycaemia in an alert and orientated patient ?

A
  1. Oral Carbohydrates:
    - Rapid acting; juice / sweets
    - Longer acting; sandwich

If Deteriorating: consider IM /SC 1mg Glucagon

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2
Q

how would you manage acute hypoglycaemia in a drowsy/confused patient ?

A

If swallow is intact;

  1. Buccal glucose
    - Hypostop / glucogel
    - > Consider IV access

Poor swallow OR unconscious;

  1. IV Access
    - 50 ml, 50 % glucose mini-jet
    - 100ml, 20% glucose

Deteriorating / refractory /insulin induced /difficult IV access: consider IM /SC 1mg Glucagon

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3
Q

patient has just had iv treatment for hypoglycaemia, they develop pain, redness, warmth and lump near the venous access site. whats happened?

A

extravasation of IV glucose: irritant, phlebitis

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4
Q

what 2 things should you remember about giving glucagon?

A
  1. mobilises glycogen stores so takes 15-20 mins to work

2. Danger of rebound hypoglycaemia, as will cause insulin release

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5
Q

What level of glucose defines hypoglycaemia?

A

numerous but generally less than 4

neonates is when it drops < 2.5 mmol/L (K meeran)

Neonate < 2 (according to NICU)

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6
Q

list some symptoms you may see in hypoglycaemia?

A

Adrenergic

  • tremor
  • sweating
  • palpitations
  • hunger

Neuro-glyco-paenic:

  • somnolence
  • confusion
  • seizures, coma
  • Incoordination

None

  • hypoglycaemic unawareness (lack of adrenergic symptoms during hypoglycaemia)
  • If a patient experiences recurrent hypoglycaemic episodes
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7
Q

what is the order of physiological change following the detection of hypoglycaemia?

A

○ Suppression of insulin
○ Release of glucagon
○ Release of adrenaline
○Release of acth, cortisol, gh

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8
Q

which hormones are involved in glucose counter-regulation?

A

The action of insulin is counterregulated by glucagon, adrenaline, noradrenaline, cortisol, and growth hormone.

These counterregulatory hormones constitute a principal defense against hypoglycemia, and levels are expected to rise as the glucose falls.

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9
Q

describe the events in glucose counter regulation

A

Low glucose -> A + B

A. Insulin suppressed + Glucagon increased:

- Reduce peripheral uptake of glucose
- Increase glycogenolysis
- Increase gluconeogenesis
- Increase lipolysis

Subsequently -> inc Glucose + FFA:
FFA -> beta oxidation -> ATP (energy) + ketones

B. low neuronal glucose sensed in hypothalamus

  • Sympathetic Activation - catecholamines
  • ACTH, cortisol and GH production
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10
Q

how does the hormone profile change in exercise-induced reduction in blood glucose ?

A

glucagon willl not be released as part of counter regulation, only;

adrenaline, noradrenaline, cortisol, and growth hormone.

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11
Q

how can you measure blood glucose ?

what is the gold standard?
which source of blood?
caveats?

A
Lab Glucose:
Grey top (flouride oxalate)
Venous sample
2 mls blood
Gold std to make the diagnosis
Delay in results
Blood glucose meter
-Point-of-care device
-Instant result
- Capillary blood
But…
- Poor precision at low glucose levels
- Often poorly maintained
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12
Q

aetiology of hypoglycaemia in non-diabetic?

A
Fasting or reactive?
Paediatric vs. adult
Critically unwell
Organ failure
Hyperinsulinism
Post gastric-bypass
Drugs
Extreme weight loss
Factitious
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13
Q

aetiology of hypoglycaemia in a diabetic patient?

A
Diabetic Medications
Inadequate CHO intake / missed meal
Impaired awareness - due to to autonomic neuropathy
Excessive alcohol
Strenuous exercise

Co-existing autoimmune conditions - eg Addison’s- polyglandular autoimmune syndrome

Co-existing renal / liver failure alters drug clearance, and reduced doses needed.

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14
Q

which meds are associated with hypoglycaemia and why?

A

Oral Hypoglycaemic
Sulphonylureas e.g. glicazide
GLP-1 agents

Insulin
Rapid acting with meals: inadequate meal
Long-acting : hypo’s at night or in between meals

Other drugs
B-blockers, salicylates, alcohol ( inhibits lipolysis)

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15
Q

A very good HbA1c level in a diabetic, may be due to ?

A

reccurent hypos

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16
Q

impaired awareness of hypos may be due to __ ?

A

autonomic neuropathy

17
Q

how does continuous glucose monitoring work?

A

This device is applied to the abdominal wall with a small cannula that sits in the interstitial space in the subcutaneous fat

• The sensor does NOT accurately read blood sugar when it drops below 2.2 mmol/L
18
Q

How can we differentiate the cause of hypoglycaemia?

A

history, exam

take blood during hypos then;
biochemical tests; c-peptide, ketones, FFAs

19
Q

what is c peptide?

utility?

A

cleavage product of PRO insulin

C-peptide levels are a good marker of beta-cell function

Also good to help differentiate the cause of hypoglycaemia

20
Q

name some of the pharmacodynamics of insulin vs c-peptide?

A

Insulin:
Half-life, 4-6 minutes
Hepatic clearance
Exogenous insulin may interfere

C-peptide:
Half-life, ~ 30 minutes
Renal Clearance

21
Q

Hypoglycaemia due to excess injected insulin would result in what c-peptide level?

A

LOW c-peptide

because it comes from pro-insulin not insulin/ ready formed insulin

22
Q

patient presents with hypoglycaemia. what do the following results mean;

a. Low insulin, low C-peptide
b. High insulin, high C-peptide
c. High insulin, low C-peptide

which is the appropriate response to a hypo?

A

a. Hypoinsulinaemic hypoglycaemia
- appropriate response to a hypo
- not t1dm/dka as they would have hyperglycaemia

b. Hyperinsulinaemic hypoglycaemia - excess endogenous insulin production is causing the hypo
c. Exogenous insulin - injection

23
Q

What is 3-hydroxybutyrate?

A

a ketone body

aka beta-hydroxybutyrate

24
Q

What does the absence of ketones signify

(glucose 1.9, ketones negative)?

A

Fatty acid oxidation defect

25
list some explainable and then pathological causes of neonatal hypoglycaemia
``` Explainable Maternal gestational diabetes Premature, co-morbidities, IUGR, SGA Inadequate glycogen and fat stores Should improve with feeding ``` Pathological Inborn metabolic defects eg: - Fatty acid oxidation defect
26
what is going on in the following picture and name some possible causes? Neonatal hypoglycaemia with suppressed insulin + C-peptide. FFA raised, but low ketones
suppressed insulin + C-peptide and rasied FFA is the appropriate response to hypoglycaemia BUT there must be an error of metabolism of FFAs BECAUSE ketones must be raised as well ``` causes; Inherited metabolic disorders: FAOD : no ketones produced GSD type 1 ( gluconeogenetic disorder) Medium chain acyl coA dehydrogenase def. Carnitine disorders ``` fatty acid oxidation defect Glycogen Storage Disease
27
name 3 ketone bodies?
Betahydroxybutyrate/ acetoacetate / acetone
28
list some causes of the following presentation in a neonate: persistent hypoglycaemia <2.5 (despite correction) FFA normal/low ketone normal/low
hyperinsulinism (think logically: suppression of insulin normally leads to inc fatty acid production. so normal/low ffa must mean insulin is not suppressed) hypopituitarism
29
list some causes of the following presentation in a neonate: persistent hypoglycaemia <2.5 (despite correction) FFA raised Ketone raised
Hepatomegaly: haemochromatosis gsd 1,3,6 fructose 1,6 phosphatase defi ``` No hepatomegaly: GSD type 0 hereditary fructose intolerance septicaemia GH, corticosteroid deficiency and more ```
30
list some causes of innapropriately high insulin levels?
Islet cell tumours – insulinoma Drugs; insulin, sulphonylurea Islet cell hyperplasia: Infant of a diabetic mother Beckwith Weidemann syndrome Nesidioblastosis
31
how would you screen for Sulphonylurea abuse?
Sulphonylurea drug screen – urine or serum
32
what is the physiology of normal insulin secretion?
Glucose crosses the membrane and enters glycolysis via glucokinase Glycolysis will produce ATP The rise in ATP leads to closure of the ATP-sensitive K+ channel The closure of this channel leads to membrane depolarisation, calcium influx and insulin exocytosis NOTE: there are a lot of genetic mutations that affect this channe
33
A Negative screen of what is required for diagnosing insulinoma? why?
sulphonylurea Sulphonylureas bind to the ATP-sensitive K+ channel and makes it close, independently of ATP So, you get insulin release even when there is no ATP around - this is why sulphonylureas can cause hypoglycaemia
34
charactersie and give the epidemiology of insulinomas. hwo are they treated?
Usually small solitary adenoma 10% malignant 8% associated with MEN1 Treatment: resection
35
whats is the diagnosis and reason behind: Hypoglycaemia persists – glucose infusion Insulin and C-peptide undetectable Free fatty acids – undetectable Ketones negative
Non-islet cell tumour hypoglycaemia the secretion of big IGF-2 Big IGF-2 binds to IGF-1 receptors and insulin receptors This behaves like insulin so your own endogenous insulin production is switched off and FFA production is suppressed
36
list some genetic causes of hypoglycaemia with high insulin and c peptide
Glucokinase activating mutation ``` Congenital hyperinsulinism: KCNJ11 /ABCC8 GLUD-1 HNF4A HADH ```
37
list causes for reactive/post-prandial hypoglycaemia?
``` Hypoglycaemia following food intake Can occur post-gastric bypass Hereditary fructose intolerance Early diabetes In insulin sensitive individuals after exercise or large meal ```