T1 L17 - Acute complications of diabetes Flashcards

1
Q

what are the 3 things you should know by the end of this

A
  • Diabetic keto-acidosis
  • Hyperosmolar hyperglycaemic state
  • Hypoglycaemia
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2
Q

give a quick overview of diabetic keto-acidosis

4 marks

A

1 a)Unchecked gluconeogenesis- Hyperglycaemia

b)Osmotic diuresis- Dehydration

2 a)Unchecked ketogenesis - Ketosis

b)Dissociation of ketone bodies into hydrogen ion and anions - Anion-gap metabolic acidosis

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3
Q

what are the physiological effects of insulin deficiency on adipose tissue

(4marks)

A

Increased lipolysis and reduced esterification of fat​
-Insulin deficiency​
-Glucagon/adrenaline excess ​
Results in excess FFA and glycerol from breakdown triglycerides​

FFA substrate for hepatic synthesis of ketone bodies​

  • Acetoacetate/Hydroxybutyrate – strong organic acids​
  • (Acetone) ​
  • Rate of ketogenesis is linked to rate of gluconeogenesis​

Muscle and brain can utilise ketones as main energy substrate​

Ketoacidosis results when ketone body production exceeds rate of utilisation in peripheral tissues (brain and muscle) and renal clearance

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4
Q

quick overview of how you would manage diabetic ketoacidosis

A

Giving lots of glucose
insulin
fluid
electrolytes

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5
Q

Managing diabetic ketoacidosis

A

1)Acidosis managed by​

-Intracellular buffering - H+ / K+ exchange​
Potassium hydrogen ion pump​

-Respiratory compensation – hyperventilation​
H+ stimulates respiratory centres​
Breathe off CO2 (H+ + HCO3- H2O + CO2)​

-Renal excretion of H+ (slow response)​

2) Electrolyte disturbances – renal losses​
- Potassium depletion – maybe >250mmol​
- Sodium depletion -​
- dehydration​

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6
Q

clinical features of diabetic ketoacidosis

A

Mostly young

relative/absolute insulin deficiency

blood glucose<40mmol/l

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7
Q

precipitating factors for diabetic ketoacidosis

A
  • Infections – pneumonia, urinary tract, viral illnesses, gastroenteritis​
  • Error/ missed insulin administration​
  • Myocardial infarction​
  • Previously undiagnosed Type 1 diabetes​
  • Drugs: steroids​
  • Unidentified ​
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8
Q

what are the symptoms and signs of diabetic ketoacidosis

A

Symptoms​
Cause​
Signs​

1)Thirst and polyuria ​
Weakness and malaise​
Drowsiness, confusion​

Hyperglycaemia + dehydration​
Dry mouth, Sunken eyes​
Postural or supine hypotension​
Hypothermia & Coma​

2)Nausea and vomiting​
Abdominal pain​
Breathlessness​

Acidosis​

Facial flush​
Hyperventilation​
Smell of ketones on breath and ketonuria​

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9
Q

look at case

A

how was it?

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10
Q

what does HHS stand for

A

Hyperosmolar Hyperglycaemic State

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11
Q

what is the pathophysiology of HHS

A

Insulin so no lipolysis, but not enough to stop high glucose causing u to pee out glucose, so you become dehydrated ​

So much so that you require 20 plus litres of water in order to restore body electrolyte fluid balance ​

Usually in frail elderly ppl

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12
Q

what are the clinical features of HHS

A
Age​
Usually >40years​
Precipitating causes​
previously undiagnosed, steroids, diuretics, sugar​
Serum sodium​
Usually high​
Blood glucose​
Often >40mmol/l​
Serum bicarbonate/pH​
Normal / pH 7.4​
Serum ketones​
0​
Mortality​
30% (thromboses)​
Subsequent course​
Diet/tablet controlled​

usually those with T2 diabetes

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13
Q

look at case history for HHS

A

how did it go

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14
Q

Apart from giving fluid to correct dehydration in HHS what else can you do (in elderly fluids must be given slowly to correct )

A

Rehydrate & monitor fluid balance​
Iv fluids - saline with added potassium​
Consider urinary catheter​
Lower glucose (once glucose not improving with fluids)​
Intravenous insulin – fixed rate 0.05Unit/kg/hr​
Monitor electrolytes​
Potassium (and sodium)​
Prevent clots​
Treatment low molecular weight heparin​

Patients are often elderly and severely ill.​

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15
Q

what are the symptoms of Hypoglycaemia (hypo)​

A

tachycardia

sweating

dizzy

anxious

hungry

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16
Q

define the state of hypo

A

Hypoglycaemia is a biochemical term and exists when blood sugar < 4mmol/l but is often used to describe a clinical state. The clinical syndrome associated with hypoglycaemia develops as the nervous system becomes glucose deficient or ‘neuroglycopaenic’. It can be classified:​

17
Q

split the symptoms into autonomic (sympathomedullary activation )

&

Neuroglycopenic

A

-Autonomic – sympathomedullary activation​

Sweating, feeling hot​
Trembling or shakiness​
Anxiety​
palpitations​

-Neuroglycopenic​
Dizziness, light-headedness​
Tiredness​
Hunger, nausea​
Headache​
Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism​
Coma and convulsions, hemiplegia​
18
Q

what are the causes of hypoglycaemia

A

Insulin​
Inappropriately excessive doses​

Not eating, or insufficient carbohydrate​
Sulfonylureas​

19
Q

how does the body usually handle hypo

A

-Glucagon, adrenaline, cortisol and GH all have ‘anti-insulin effects’​
Glucagon stimulates glycogenolysis and gluconeogenesis and is probably primary response​
Adrenaline increases glycogenolysis​
GH and cortisol limit glucose disposal in peripheral tissues, but this effect takes several hours so of little benefit acutely​

-Sympathetic nerves may also directly activate hepatic glycogenolysis and stimulate glucagon secretion​

20
Q

how do you treat minor and major hypoglycaemic episodes

A
-Minor episodes​
20g carbohydrate as sugary drink, fruit juice, glucose tablets, glucose gels followed by something ‘starchy’ to eat​
Glucose gels​
​
-Hypoglycaemic coma​
im or iv Glucagon 1mg​
iv dextrose 25g  (150ml 10% glucose)​