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
