Endocrine Flashcards

1
Q

Define diabetes

A

a group of metabolic diseases characterised by hyperglycaemia due to problems with insulin secretion and/or the action of insulin on the cell
An increase in glucose levels results in an increase in insulin production, and vice versa when glucose levels decrease

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2
Q

What are the different types of diabetes?

A

Type 1: genetic, inability to produce insulin
Type 2: developed insulin resistance, requires supplementary insulin
Induced: onset, acute due to management eg. drugs
Gestational: acute, during pregnancy

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3
Q

Define hyperglycaemia

A

Lack of insulin means glucose accumulates in the blood, resulting in fluid shifting from the cells to the intracellular space. renal threshold is exceeded resulting in glucose being passed in the urine

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4
Q

Define fluid shift

A

Fluid shift causes cells to become dehydrated which stimulates the thirst response (polydipsia), Results in increased blood volume causing a diuresis (polyuria)
Fluid shifting and diuresis results in large losses of electrolytes (K+ and Na+)

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5
Q

Define alternative sources of glucose

A

As glucose cannot enter cells, cells are ‘starved’ simulating a feeling of hunger (polyphagia)
Body looks for alternate source of glucose which exacerbates hyperglycaemia: breakdown of glycogen to glucose in liver, and
breakdown of fats to glucose

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6
Q

Define how acidosis develops

A

Ketones are a by-product of breaking down fats to glucose
Ketones accumulate in the blood resulting in acidosis
Acidosis contributes to electrolyte imbalance by decreasing K+

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7
Q

What is the pathophysiology of diabetes?

A

glucose accumulates in blood -> hyperglycaemia -> fluid shifts out of cells -> increased fluid volume stimulates polyuria -> large losses of electrolytes -> cells seek alternate sources of glucose by breaking down glycogen and fats -> ketones are a by-product of breaking downs fats to glucose -? ketones accumulate in the blood -> blood becomes acidic -> electrolytes further decreased

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8
Q

Outline Diabetic Ketoacidosis (DKA)

A

a life threatening complication of diabetes. Usually associated with Type 1 diabetics. Onset of DKA is rapid and can be severe within hours
DKA results in acidosis, dehydration, and electrolyte imbalances. it is diagnosed when three states are present:
Hyperglycaemia, ketosis, acidosis

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9
Q

What are the most common causes of DKA?

A

imbalance in insulin and glucose
stress (physical and psychological)
infection
AMI

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10
Q

What investigations are done to determine DKA?

A

BGL, blood ketones, venous blood gas, pathology

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11
Q

What are the clinical manifestations of DKA

A

polyuria, polyphagia, polydipsia
abdominal pain
nausea and vomiting
acetone breath (sweet, fruity smell)
deep, rapid respirations (Kussmaul respirations)
tachycardia
hypotension
dry mucous membranes
altered conscious state (confusion and drowsiness)
coma

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12
Q

Outline Hyperglycaemic Hyperosmolar Syndrome (HHS)

A

Occurs when blood glucose levels remain high for an extended period of time. Onset is in days to weeks compared to DKA. critical differences include less severe insulin deficiency, less severe fluid loss, and none/limited ketone production

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13
Q

What are common causes of HHS?

A

infection, stroke, AMI and some medications such as diuretics and steroids

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14
Q

What are the investigatory methods for HHS?

A

BGL, blood ketones, pathology

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15
Q

What are the clinical manifestations of HHS?

A

the same as DKA except:
they are more dehydrated
have developed renal failure
may not require insulin therapy (type 2 diabetics are producing some insulin)
normal to slightly elevate ketones (some insulin means that fats are not broken down for fuel)
severe electrolyte imbalances

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16
Q

What is insulin’s relation to diabetes?

A

due to a relative or absolute lack of insulin
insulin required for glucose to enter cells -> without insulin glucose cant enter cells -> glucose accumulates in the blood = hyperglycaemia

17
Q

What is the effect of hyperglycaemia on metabolism?

A

the blood becomes hyperosmolar -> water in the cells is drawn into the ECF -> thirst is triggered as cells becomes dehydrated -> intravascular volume increases -> diuresis -> polyuria -> cells ‘hungry’, increasing general appetite -> further hyperglycaemia -> continuing diuresis and polyuria -> excess glucose reabsorbed in kidneys -> glucose excreted in urine -> sodium and potassium diluted by fluid shifting -> hypokalaemia -> potassium drawn out of cells into intravascular -> excess potassium excreted in urine

18
Q

What is the link between diabetes and ketones?

A

Cells that are starved fro glucose will breakdown fats and protein into glucose -> by-product of fat breakdown is ketones -> ketones acculumate in the blood -> blood becomes acidic (ketoacidosis)

19
Q

what are the key aspects of DKA/HHS?

A

Hyperglycaemic
Acidotic
Hypokalaemic and electrolyte imbalances
Dehydrated

20
Q

What are the principles behind DKA and HHS management?

A

Rehydration and correction of electrolyte imbalances
Correction of hyperglycaemia and acidosis
Identify and correct the underlying cause

21
Q

List the prioritisation of management of DKA and HHS

A
  1. IV Normal Saline (correct dehydration)
  2. IV short acting insulin (usually Actrapid) on a sliding scale (correct hyperglycaemia)
  3. IV potassium (correct hypokalaemia)
  4. IV glucose (correct hypoglycaemia)
22
Q

List some management considerations for DKA/HHS

A

1/24 BGL and blood ketone monitoring
1/24 electrolyte checks (consider venous blood gases)
Oxygen therapy (if required)
Keep patients NBM for at least 24 hours
1/24 urine measurements with strict FBC
Cardiac monitoring (especially if altered potassium)
MSU, ECG and other pathology (e.g. FBC) to identify any source of infection
Vital sign monitoring

23
Q

What is the difference between DKA and HHS?

A

DKA is associated with hyperglycemia and ketoacidosis, whereas HHS mainly has severe hyperglycemia and hyperosmolarity (no ketoacidodis)
DKA usually affects type 1 diabetes, HHS usually affects type 2 diabetes