WK 6: Endocrine

Question 1

What are cells three sources of glucose?

Answer 1

• ingestion of food
• glycogenolysis (breakdown of glycogen to glucose )
• gluconeogenesis (breakdown of fat to glucose)

Question 2

How is glucose used in the body?

Answer 2

Glucose is an energy source for cells in the body. In the cell, glucose undergoes a chemical reaction to form ATP.

Question 3

What counterregulatory hormones does glucose fluctuate in response to?

Answer 3

• insulin
• glucagon

Question 4

How does glucose enter cells?

Answer 4

Though facilitated diffusion by carrier proteins in the cell membrane as it is moving against a concentration gradient.

Question 5

Describe insulin, where it is produced, its action/role, major sites of action and its other functions.

Answer 5

= 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.

Question 6

Define diabetes, state the types and their defining characteristic

Answer 6

= 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

Question 7

Explain the pathophysiology of hyperglycemia and the flow on effects it has.

Answer 7

=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+

Question 8

What is DKA? and who is most at risk?

Answer 8

= 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

Question 9

What are some common causes of DKA?

Answer 9

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

Question 10

What are some complications of DKA?

Answer 10

• acidosis
• dehydration
• electrolyte imbalances

Question 11

What 3 states need to be present to diagnose DKA?

Answer 11

• hyperglycemia
• ketosis
• acidosis

Question 12

What investigations are used to diagnose DKA and identify the underlying condition?

Answer 12

• blood glucose level (BGL)
• blood ketone level
• venous blood gas
• pathology - venous blood gas, U&E, FBC
• MSU
• CXR
• blood cultures (if febrile)

Question 13

What are some clinical manifestations of DKA?

Answer 13

• 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

Question 14

What are the critical differences in HHS that aren’t in DKA?

Answer 14

• degree of insulin deficiency
• degress of fluid deficit
• non to limited ketone production (minimal acidosis evident)

Question 15

What diabetes population does HHS typically affect? and what specific population groups within this type are at greater risk?

Answer 15

= T2DM

Other risk factors
- elderly
- co-morbid
- sicker
**making managing the illness challenging

Question 16

What is the onset time of HHS in comparison to DKA?

Answer 16

= days to weeks

recall: DKA is within hours

Question 17

What are common causes of HHS?

Answer 17

• infection
• stroke
• AMI
• some medications such as diuretics and steroids.

Question 18

What are the investigations for HHS?

Answer 18

• blood glucose level
• blood ketones
• pathology - venous blood gases, U&E, FBC
• MSU
• CXR
• blood cultures (if febrile)

Question 19

What are the clinical manifestations of HHS?

Answer 19

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

Question 20

Explain the pathophysiology of DKA and HHS, particularly the fluid and electrolyte shifts when a pt begins to be hypoglycemic.

Answer 20

-> 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.

Question 21

What are the four key aspects or end states/symptoms of a pt who has had DKA or HHS?

Answer 21

• acidotic
• hyperglycemia
• dehydrated
• Hypokalaemic and electrolyte imbalances

Question 22

For cells in a normal state, where are K+, Na+ and glucose located?

Answer 22

• K+ predominately intracellular
• Sodium predominantly extracellular
• Glucose an initially extracellular molecule

Question 23

In diabetes, how does the body attempt to correct hyperglycemia and what are the flow on effects of these actions?

Answer 23

• 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

Question 24

Although the body makes attempts to overcome hyperglycemia, if glucose is still unable to enter the cells what occurs?

Answer 24

• cells remain ‘hungry’
  -> causing an increase in oral intake of
  food (polyphagia)
• further increase hyperglycaemia
• leading to more fluid shifting and
  diuresis

Question 25

Define glycosuria and how does it occur?

Answer 25

• 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

Question 26

Explain the electrolyte imbalances that occur when the body attempts to correct hyperglycemia

Answer 26

• 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

Question 27

Explain how the bodys correct mechanisms for hyperglycemia initiate a negative feedback loop?

Answer 27

Negative feedback loop created with
ongoing/increasing hyperglycaemia, fluid shifting, diuresis and electrolyte deficits

Question 28

When hyperglycemic, however still without insulin, how does the body fuel its cells for ATP?

Answer 28

-> breakdown fats (gluconeogenisis)
-> Fat breakdown results in by-product of ketones (hydrogen [H] molecules)
-> Ketones accumulate in blood and patients become acidotic (ketoacidosis)

Question 29

How does the body attempt to correct metabolic acidosis secondary to ketone production?

Answer 29

-> 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

Question 30

What are the key principles of managing DKA and HHS?

Answer 30

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

Question 31

Prioritise your management actions for hyperglycemia and in what order?

Answer 31

1. IV Normal Saline
   - correct dehydration
   - relativley quickly in adults, risk of cerebral odema in paeds if given to quickly
2. 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
3. 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
4. IV glucose
   - eventually will become hypoglycemic (when BGL gets to around 10-20mmol/L)
5. 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.

Question 32

What is the impact insulin has on serum K+?

Answer 32

= 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.

Question 33

What are some key points of management you need to consider while and after commencing initial care of a pt with DKA or HHS?

Answer 33

• 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