WK 6: Endocrine Flashcards
What are cells three sources of glucose?
- ingestion of food
- glycogenolysis (breakdown of glycogen to glucose )
- gluconeogenesis (breakdown of fat to glucose)
How is glucose used in the body?
Glucose is an energy source for cells in the body. In the cell, glucose undergoes a chemical reaction to form ATP.
What counterregulatory hormones does glucose fluctuate in response to?
- insulin
- glucagon
How does glucose enter cells?
Though facilitated diffusion by carrier proteins in the cell membrane as it is moving against a concentration gradient.
Describe insulin, where it is produced, its action/role, major sites of action and its other functions.
= an anabolic hormone
Produced by: the islets of Langerhans in the pancreas
Role: 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.
Major sites of action: liver, muscles and fat tissue.
An increase in glucose levels results in an increase in insulin production, and vice versa when glucose levels decrease.
Additional function: Insulin also transports K+ into the cell.
Define diabetes, state the types and their defining characteristic
= 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
Explain the pathophysiology of hyperglycemia and the flow on effects it has.
=a lack of insulin
-> glucose cannot enter the cells and accumulates in the blood (hyperglycaemia)
-> blood becoming hyperosmolar (due to increased concentration of glucose)
-> fluid shifts from cells to the IV space
-> renal threshold is exceeded resulting in glucose being passed in the urine (glycosuria)
-> cells become dehydrated and thrist response is stimulated (polydipsia)
-> increased fluid volume-> diuresis (polyuria)
-> fluid shifts and diuresis results in large losses of electrolytes (K+ and Na+)
Glucose can not enter cells they become starved-> hunger feeling stimulated (polyphagia)
= body looks for other ways to get glucose
-> breakdown of glycogen to glucose in liver (glycogenolysis)
-> breakdown of fats to glucose (gluconeogenesis)
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+
What is DKA? and who is most at risk?
= Diabetic ketoacidosis is the accumulation of ketones (the by-product of gluconeogenesis) making it acidic and thus contributing to electrolyte imbalances.
- T1DM pts are most at risk
- life-threatening complication
- onset can be rapid and can be within sever within hours
What are some common causes of DKA?
- imbalance in insulin and glucose
- stress (physical and psychological)
- infection
- AMI
What are some complications of DKA?
- acidosis
- dehydration
- electrolyte imbalances
What 3 states need to be present to diagnose DKA?
- hyperglycemia
- ketosis
- acidosis
What investigations are used to diagnose DKA and identify the underlying condition?
- blood glucose level (BGL)
- blood ketone level
- venous blood gas
- pathology - venous blood gas, U&E, FBC
- MSU
- CXR
- blood cultures (if febrile)
What are some clinical manifestations of DKA?
- 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
What are the critical differences in HHS that aren’t in DKA?
- degree of insulin deficiency
- degress of fluid deficit
- non to limited ketone production (minimal acidosis evident)
What diabetes population does HHS typically affect? and what specific population groups within this type are at greater risk?
= T2DM
Other risk factors
- elderly
- co-morbid
- sicker
**making managing the illness challenging
What is the onset time of HHS in comparison to DKA?
= days to weeks
recall: DKA is within hours
What are common causes of HHS?
- infection
- stroke
- AMI
- some medications such as diuretics and steroids.
What are the investigations for HHS?
- blood glucose level
- blood ketones
- pathology - venous blood gases, U&E, FBC
- MSU
- CXR
- blood cultures (if febrile)
What are the clinical manifestations of HHS?
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
Explain the pathophysiology of DKA and HHS, particularly the fluid and electrolyte shifts when a pt begins to be hypoglycemic.
-> Insulin is needed to open carrier proteins in cell walls to allow glucose in.
-> without insulin glucose remains in IV space= hyperosmolar state
-> body attempts to compensate for this and return to homeostasis
-> fluid is drawn from cells into IV system + stimulates thirst response (polydipsia)
-> eventually fluid is in over supply in IV space
-> body-initiated diuresis (polyuria) and carrier molecules are oversaturated so cant keep glucose in body so it is excreted (glycosuria)
-> with loss of fluid, cells shrivel
-> hunger response is initiated (polyphasia) as cells are still starving
-> hyperglycemia compounds with ingested glucose
-> with the fluid shifting to IV system, Na+ and K+ concentration is lesser
-> body thinks it is hypovolemic so draws K+ out of cells to equalise concentration.
-> now it is in IV space, body thinks there is to much K+ so it is excrete-> eventually leading in hypovolemia.
-> body is still hungry so initiated gylconeogensis= producing ketones= keto acidosis
-> H+ collects in IV space
-> H+ is stashed in cell to relieve acidosis-> as + ion goes in another had to go out so more K+ leaves the cell= furthering hyperolemia
-> diuresis is further increased to overcome increased hypervolemia.
What are the four key aspects or end states/symptoms of a pt who has had DKA or HHS?
- acidotic
- hyperglycemia
- dehydrated
- Hypokalaemic and electrolyte imbalances
For cells in a normal state, where are K+, Na+ and glucose located?
- K+ predominately intracellular
- Sodium predominantly extracellular
- Glucose an initially extracellular molecule
In diabetes, how does the body attempt to correct hyperglycemia and what are the flow on effects of these actions?
- draws fluid from cells to extracellular spaces to equalise the concentration of glucose.
- initiate the thirst response (polydipsia) to dilute glucose in the blood.
= increased vascular volume= polyuria and diuresis
= fluid shifts making cells dehydrated and shrinking
Although the body makes attempts to overcome hyperglycemia, if glucose is still unable to enter the cells what occurs?
- cells remain ‘hungry’
-> causing an increase in oral intake of
food (polyphagia) - further increase hyperglycaemia
- leading to more fluid shifting and
diuresis
Define glycosuria and how does it occur?
- number of glucose molecules in urine exceeds the number of carrier
molecules - carrier molecules are required to reabsorb glucose in kidneys-> glucose being excreted in urine
Explain the electrolyte imbalances that occur when the body attempts to correct hyperglycemia
- Fluid shifting from cells to IV space results in dilution of not only the glucose but sodium and potassium
- Body interprets this as decreased
potassium (hypokalaemia)
-> Resulting in K being drawn out of the cells to IV space to increase
concentration
Explain how the bodys correct mechanisms for hyperglycemia initiate a negative feedback loop?
Negative feedback loop created with
ongoing/increasing hyperglycaemia, fluid shifting, diuresis and electrolyte deficits
When hyperglycemic, however still without insulin, how does the body fuel its cells for ATP?
-> breakdown fats (gluconeogenisis)
-> Fat breakdown results in by-product of ketones (hydrogen [H] molecules)
-> Ketones accumulate in blood and patients become acidotic (ketoacidosis)
How does the body attempt to correct metabolic acidosis secondary to ketone production?
-> moves H ions into cells in exchange for K+ molecules
- results in further exacerbation of hypokalemia
-> excess H+ ions are excreted in urine
- results in exacerbation of diuresis
What are the key principles of managing DKA and HHS?
- Rehydration
- correction of electrolyte imbalances
- Correction of hyperglycaemia
- correct acidosis
- Identify and correct the underlying cause
Prioritise your management actions for hyperglycemia and in what order?
- IV Normal Saline
- correct dehydration
- relativley quickly in adults, risk of cerebral odema in paeds if given to quickly - IV short-acting insulin (usually Actrapid) * Insulin will generally be given IV- however, in HHS it may be given S/C
- to correct hypoglycemia
- usually a sliding scale insulin infusion - IV potassium (ensure it goes back into the cells and do that K+ doesn’t rush into the cells leaving them hpoykalaemic)
- correct electrolytes
- with the knowledge that we have lost K+ in in diuresis and that insulin will take K+ with it into the cells so they can get more hypokalemic - IV glucose
- eventually will become hypoglycemic (when BGL gets to around 10-20mmol/L) - What is the cause!!
- investigation such as ECG, urinalysis, CXR, blood cultures.
**acidosis will correct itself when all these infusions are running
**if you know the pt has normal or high potassium levels then follow this, if not then prioritise K+ so that they don’t have arrhythmias.
What is the impact insulin has on serum K+?
= the presence of insulin encourages transport of potassium INTO the cells and OUT of the blood serum. If the patient is already hypokalaemic, administering insulin will lower the blood potassium level even further, putting them at risk of life-threatening cardiac arrhythmias.
**A potassium level MUST be available before we start our insulin infusion/administration in DKA/HHS.
What are some key points of management you need to consider while and after commencing initial care of a pt with DKA or HHS?
- 1/24 BGL and blood ketone monitoring
- 1/24 electrolyte checks (consider venous blood gases or full pathology)
- Oxygen therapy (if required)
- Keep patients nil by mouth (NBM) for at least 24 hours to control glucose
- 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
