Endocrine - Type 1 and 2 Diabetes Mellitus and DKA (CP1)

What causes T1DM?

Autoimmune destruction of pancreatic B-cells which produce insulin.

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At what age can T1DM present? When is it most common?

Presents in childhood/adolescence but might appear at any age.

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What are the clinical presentations of T1DM?

Polyuria (high sugar = high wee); polydipsia (due to fluid loss); weight loss (breakdown of fat/water loss); and DKA.

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What is T2DM? Briefly, causes?

Insulin resistance: associated with age, obesity, genetic factors and other environmental ones. Eventually B-cells may decompensate and produce less insulin.

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What are some of the secondary causes of T2DM?

Pancreatitis; Endocrine (Cushing's, acromegaly etc); Congenital disease; Drug-induced (thiazide diuretics for example)

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What are some of the micro- and macro-vascular complications of DM?

Microvascular: diabetic retinopathy; nephropathy; neuropathy Macrovascular: stroke; hypertension; peripheral vascular disease - e.g. of the foot; erectile dysfunction

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At what HbA1c level is diabetes diagnosed? (>__ mmol/mol and __%)

HbA1c of over 48 mmol/mol (6.5%)

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Name 5 populations or groups in which you cannot use HbA1c.

- <18 years old. - Acutely unwell. - Taking medication which will increase blood sugar. - CKD (chronic kidney disease) - HIV

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If you can't use Hb1Ac - you could diagnose diabetes with a fasting plasma glucose level of > ___ mmol/L

> 7 mmol / L

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True of false: black and asian populations of children are less at risk of T2DM than Caucasians.

False: black and asian populations are at greater risk.

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When given a 75g glucose load - normal results will have a fasting glucose of <_ mmol/L and a level after 2hrs of <_._ mmol/L.

When given a 75g glucose load - normal results will have a fasting glucose of <7 mmol/L and a level after 2hrs of <7.8 mmol/L.

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Someone has an impaired glucose tolerance (not DM yet) if after 75g glucose load they have fasting level of <_mmol/L but their level after 2hrs is >_._ and less than __mmol/L

Someone has an impaired glucose tolerance (not DM yet) if after 75g glucose load they have fasting level of <7mmol/L but their level after 2hrs is >7.8 but less than 11mmol/L

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Someone has DM if after 75g glucose load their fasting level is >_mmol/L and their level after 2hrs 0s >__ mmol/L

Someone has DM if after 75g glucose load their fasting level is >7 mmol/L and their level after 2hrs 0s >11 mmol/L

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Describe how you would differentiate between T1DM and T2DM in a presenting patient.

T1 often = before puberty + T2 = often starts older. T1 = polydipsia, polyuria, weight loss, ketosis, (DKA). T2 = gradual symptom onset, fatigue/lack of energy, visual blurring usually first complaints.

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What is DKA? Is it associated with Type 1 or Type 2 DM?

DKA is a potentially-life threatening metabolic complication almost always associated with Type 1 DM.

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Explain why rapid lipolysis and osmotic diuresis occurs in DKA.

In the absence of insulin hepatic glucose production increases, however peripheral uptake of glucose decreases. The lack of insulin means tissues are starved of glucose and rapid lipolysis occurs in these tissues.

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Explain why someone with DKA may have metabolic acidosis. Explain what tests are used where it may be detected.

Lipolysis releases Free Fatty Acids which are converted into fatty acetyl CoA in liver cells. These are converted to ketone bodies which can be used for energy but cause acidosis. These ketones can be detected with breath and urine tests.

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What are the signs and symptoms of DKA (and why do these happen?)

Dehydration + polyuria + thirst (osmotic diuresis); nausea + vomiting (acidosis); Kussmaul breathing; confusion; exhaustion (prostration)

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Renal perfusion decreases in DKA - this leads to the impaired excretion of what? and the increased secretion of what?

There is impaired excretion of ketones and H+ (acidosis) and increased excretion of sodium and potassium (hypokalaemia)

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What happens to K+ levels in a DKA patient?

A lot of K+ is lost due to osmotic diuresis. K+ blood levels may stay the same or increase (pseudo-hyperkalaemia) because of the lack of insulin (normally causes K+ to be taken into cells). There is a risk of severe hypokalaemia after treatment.

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What is the normal level of potassium in the body?

3.5-5.0 mmol/L (so <3.5 mmol/L = hypokalaemia)

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What is the most serious outcome of severe hypokalaemia which might happen with someone suffering from DKA?

It can cause abnormal heart rhythms - often slow - which can lead to cardiac arrest.

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The collection of ketone bodies can cause metabolic acidosis. What compensation might occur? What other symptom might acidosis cause which leads to further electrolyte loss?

Metabolic acidosis may be compensated by the respiratory system - i.e. hyperventilation. Acidosis can cause vomiting - which leads to further electrolyte loss.

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What is Kussmaul breathing and why does it sometimes occur with DKA?

Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis of DKA (also kidney failure)

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There are 3 steps to confirming a diagnosis of DKA: 1. blood glucose > ???? or previous history of ?????

Blood glucose of >11mmol/L or PH of diabetes

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Step 2 in diagnosing DKA: capillary ketones >_ mmol/L or ketones >_ in the urine

Capillary ketones = >3mmol/L or ketones in urine = >2mmol/L

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Step 3 in diagnosing DKA: venous pH = <7.__ (or venous _________ of <15mmol/L)

Venous pH = <7.35 (i.e. acidosis) or venous bicarbonate <15mmol/L (again showing that acidosis - remember bicarbonate is what increases pH in body)

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What blood investigations would you do in DKA and why?

U&Es which includes urea, creatinine, Na+ and K+ (urea and creatinie measures kidney function + electrolytes are important in DKA). Blood glucose (obvious), venous blood gas (looks at pH)

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Which colour blood bottle is used for U&Es and which is used for glucose?

Gold for U&Es (lots of the biochemistry tests are in gold tube) and Grey for glucose

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The severity of DKA is decided by pH. What are the pH values for mild, moderate, and severe DKA?

Normal pH = 7.35-7.45. Mild DKA = >7.3. Moderate = 7.1-7.3. Severe = <7.1

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When interpreting blood gas values for a metabolic acidosis caused by DKA. What would you expect to see with pH, HCO3- (bicarbonate) and pCO2 values?

pH = decreased (<7.35) - acidosis. HCO3- = decreased - this is the metabolic part. pCO2 levels may be normal or decreased (if there's respiratory compensation)

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What condition which results in hyperosmolarity (not DKA) is much more common in T2DM?

Hyperosmolar hyperglycaemic State

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Briefly explain the pathophysiology of HHS.

An insulin deficiency means that blood glucose levels increase to a high amount. This draws more water and osmotic molecules into the blood. High serum osmolarity = incr. urination (osmotic diuresis) = depletes volume+ increases glucose conc more

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Why do ketones not form in HHS?

The presence even of the small amount of insulin prevents fat breakdown (by hormone-sensitive lipase) to ketones.

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What kind of person would HHS normally present in?

Typically in elderly people - particularly in those with undiagnosed diabetes - because even a small amount of insulin will prevent this!

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What kind of lifestyle factors and medications might cause HHS?

Consumption of glucose-rich fluids (i.e. lucozade?) or thiazide diuretics, steroids and B-blockers

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Endocrine - Type 1 and 2 Diabetes Mellitus and DKA (CP1)

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