Week 6- endocrine Flashcards
(17 cards)
Insulin
Insulin is an anabolic hormone produced by the islets of Langerhans in the pancreas.
Insulin regulates the metabolism of carbohydrates, fats and proteins, and facilitates the transport of glucose into the cell by activating carrier proteins in the cell membrane.
Diabetes
Diabetes is a chronic disease resulting in metabolic disturbances of carbohydrate, fat and protein metabolism.
Related to a lack of insulin or insulin resistance.
Diabetes is classified as:
* Type 1 - absolute lack of insulin
* Type 2 - predominantly due to insulin resistance
* Type 2 - insulin requiring
* Induced - onset due to management e.g. drugs such as corticosteroids
* Gestational - when diabetes occurs during pregnancy
Pathophysiology of diabetes- Hyperglycaemia
- Lack of insulin means glucose cannot enter the cells and accumulates in the blood (hyperglycaemia)
- Hyperglycaemia results in blood becoming hyperosmolar (due to increased concentration of glucose) resulting in fluid shifting from the cells to the intravascular space
- Renal threshold is exceeded resulting in glucose being passed in the urine (glycosuria).
Pathophysiology of diabetes- Fluid shift
- 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+)
Pathophysiology of diabetes- Alternate sources of glucose
- 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 (glycogenolysis)
○ breakdown of fats to glucose (gluconeogenesis)
Pathophysiology of diabetes- Acidosis develops
- 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+
Diabetic ketoacidosis (DKA)
Diabetic ketoacidosis (DKA) is a life threatening complication of diabetes. Usually associated with Type 1 diabetics.
Onset of DKA is rapid and can be severe within hours.
The common causes of DKA are:
* imbalance in insulin and glucose
* stress (physical and psychological)
* infection
* AMI
DKA results in acidosis, dehydration, and electrolyte imbalances.
DKA is diagnosed when three (3) states are present:
* hyperglycaemia
* ketosis
* Acidosis
Investigations for DKA
The following investigations are used to diagnose DKA and identify any underlying conditions (e.g. infection) which may have caused the illness:
* blood glucose level (BGL)
* blood ketone level
* venous blood gas
* pathology - venous blood gas, U&E, FBC
* MSU
* CXR
* blood cultures (if febrile)
The clinical manifestations of DKA include the following:
- 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
Hyperglycaemic Hyperosmolar Syndrome (HHS)
Similar to DKA, HHS has some critical differences:
* degree of insulin deficiency
* degree of fluid deficit
* none to limited ketone production (minimal acidosis evident)
Usually affects Type 2 diabetics.
Onset of HHS is days to weeks (within hours for DKA).
Common causes of HHS are infection, stroke, AMI and some medications such as diuretics and steroids.
Patients with HHS are generally older, sicker and have more co-morbidities which adds to the challenge of managing the illness.
Investigations for HHS
- blood glucose level
- blood ketones
- pathology - venous blood gases, U&E, FBC
- MSU
- CXR
- blood cultures (if febrile)
Patients with HHS have the same clinical manifestations 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
Pathophysiology – DKA & HHS
Normal state of cells
▪ Potassium predominantly intracellular electrolyte
▪ Sodium is predominantly an extracellular electrolyte
▪ Glucose is an initially extracellular molecule
Altered metabolism in diabetes
Diabetes is caused by a lack of insulin, causing hyperglycemia, diuresis, fluid shifting, and cell dehydration. This leads to increased fluid intake, glycosuria, and hypokalemia. The body creates a negative feedback loop, leading cells to break down fats and proteins into glucose, resulting in ketones. This leads to acidosis and further exacerbation of hypokalaemia and diuresis.
The principles of management for DKA/HHS are:
- Rehydration and correction of electrolyte imbalances
- Correction of hyperglycaemia and acidosis
- Identify and correct the underlying cause
Management of DKA and HHS is prioritised and commenced in the following order:
- IV Normal Saline
- IV short acting insulin (usually Actrapid) * Insulin will generally be given IV- however in HHS it may be given S/C
- IV potassium
- IV glucose
After commencing the prioritised care you need to consider:
- 1/24 BGL and blood ketone monitoring
- 1/24 electrolyte checks (consider venous blood gases)
- Oxygen therapy (if required)
- Keep patients nil by mouth (NBM) for at least 24 hours
- 1/24 urine measurements with strict fluid balance chart
- Cardiac monitoring (especially if altered potassium)
- MSU, ECG and other pathology (e.g. FBC) to identify any source of infection
- Vital sign monitoring
