AMK 3

Question 1

What is Insulin, action and where is secreted?

Answer 1

Insulin- hormone secreted from Beta cells of Islets of Langerhans.

Action - Controls Blood Sugar levels - causes liver, muscle and fat cells to take up glucose from blood.

Question 2

What causes an Insulin Deficiency ?

Answer 2

Increased Insulin demand - 5 I’s
0 Infection
-pneumonia
- UTI’s
- Cellulitis (infection of the skin)
(PUC) - People usually cry
0 Inflammation
- Pancreatitis
- Cholecystitis
0 Iatrogenic
- Corticosteroids - (increased Blood glucose increasing insulin demand)
- Surgery - increase in wound healing increased energy demand and thus glucose demand)
0 Intoxification
- Alcohol
- Cocaine
- Methamphetamines -
0 Infarction
- Acute MI
- Cerebral infarction (CVA)

Decreased insulin supply

• Undiagnosed Diabetic -so not yet taking medication.
• diabetic patient who is not taking their insulin medication - non-compliance.

Question 3

What is Diabetic Ketoacidosis?

Answer 3

People with diabetes have a lack of insulin - causing build up of ketones (causes acidosis)

1. Reduced Insulin
   - Increased demand
   - Decreased Supply
   (Glucose not enter cells - ATP not produced - secondary energy source- Triglycerides -needed )
2. Triglycerides broken down to Free fatty acids + Glycerol
   (Triglycerides also found in Adipose tissue so Lipolysis occurs )
3. Triglycerides converted into Acetyl CoA (by beta oxidation)
4. Krebs cycle overwhelmed with the excessive Acetyl CoA entering so Acetyl CoA shifted to an alternative pathway which synthesises Keto bodies.
5. Build of Ketobodies - Acidosis.

Increased demand due to stress .
- Increased Blood Glucose but insulin is deficient so glucose cannot get into cells . PCT of Kidney cannot reabsorb all the excess glucose so it is excreted into urine - H20 drawn with it - dehydration (osmotic Diuresis).

Osmotic Diuresis - increased urination rate due presence of in the fluid filtered by the kidney causing dehydration.

Question 4

What is Hyperglycaemic Hyperosmolar Syndrome ?

Answer 4

Hyperosmolar hyperglycaemic state - metabolic complication of diabetes mellitus characterized by:
0 severe hyperglycaemia
0 extreme dehydration,
0 hyperosmolar plasma,
0 altered consciousness.
Most common - type 2 diabetes with physiologic stress.

Stress ——-> increased SNS stimulation ——-> increased releases of Adren, Noradrenaline ——> stimulate alpha cells of Islets of Langerhans to produce Glucagon ——–> Increased Glucose production——–> osmotic Diuresis (increased urination because of excess glucose) ———> Dehydration ——- > Hyperosmolarity

          - Glucagon acts and liver and results in conversion of Glycogen to Glucose. Adren and Noradrenaline act on live and promote Gluconeogenesis and Glycogenolysis 

Hyperosmolarity - Dehydration - h20 conc decreases so blood becomes hyperosmolar (more glucose)

osmolarity - conc of dissolved particles of chemical in serum.

Question 5

What is the presentation of diabetic Ketoacidosis ?(Labs)

*for specific numbers look on OneNote

Answer 5

More common in Type 1 diabetics.

 - Ketoacidosis - 
 - Dehydration 

onset of symptoms - within 1 day

Clinical signs

  0 Acidosis - lowered PH - <7.3 
                      (causes low HC03- , H BINDS TO HCO3 TO FORM H2CO3)

  0 Hyperkalemia

  0 increased Anion Gap - above 12 
             - Anion calc = anions (+) - 
              cations (-) , increased H+, K+ 
              causes increased gap. 

  0 increased serum/urine ketones
        -Ketones are high if above 2+ in 
         the urine or above 3 mmol/L in the 
         blood. 
  0 Hyperglycaemia -  11 mmol/L / 198 mg/DL

Question 6

Signs of DKA

Answer 6

Fruity smell of acetone on the breath.

-Acidotic breathing — deep sighing (Kussmaul) respiration.

-Dehydration, which can be classified as:
0Mild — only just clinically
detectable.
0 Moderate — dry skin and mucus
membranes;
reduced skin turgor.
0 Severe — sunken eyes and
prolonged capillary refill time.
0 Shock — the person is severely ill
with:
- Tachycardia,
- poor peripheral
perfusion,
- hypotension (indicating
decreased cardiac
output). - late sign
- Lethargy, drowsiness, or decreased level of consciousness (indicating decreased cerebral perfusion).
Reduced urine output (indicating decreased renal perfusion).

Question 7

How does DKA effect Potassium level?

Answer 7

1. Acidosis - high H+ levels accumulate in ECF. Will diffuse into ICF from high to low.
2. Cells pump out K+ into ECF to maintain ion balance.
3. NA+/K+ pump on cells insulin dependent. insulin deficiency means that K+ is not pump back into Cells and accumulates in the ECF leading to hyperkalaemia.

• hyperkalaemia - leads to
  0 Arrhythmias
  0 ileus - (lack of peristaltic
  activity in a part of the
  small intestine) -
  hyperkalaemia interferes
  with peristaltic activity

Question 8

Treatment of DKA ?

Answer 8

Saline - 0.9 % (NACL )- (saline is salt in water) - dose can changed depending on need.

• Insulin - correct hyperglycaemia
• Potassium (possibly ) -
  (insulin will drive potassium inot cells - if too much - hypokalaemia) - Stop insulin then give potassium to correct this.

Question 9

Effects of HHS ?

Answer 9

1. Hyperosmolar blood passes through organs e.g. brain, muscle
2. h20 drawn out of these cells - causing shrinkage
   CNS cell shrinkage - lead to confusion, lethargic (altered mental state) and long term - coma.

Question 10

What is the presentation of HHS ?(Labs)

Answer 10

0 Hyperosmolarity
0 Dehydration

• Hyperglycaemia - >33.3 mmol/L [>600 mg/dL]
• Hyperosmolarity - >320 mmol/kg [≥320 mOsm/kg]

Absence of significant ketoacidosis (pH >7.3 and HCO3 >15 mmol/L [>15 mEq/L])

Question 11

Effects of Dehydration caused by DKA and HHS ?

Answer 11

Dehydration —– > Low blood volume ——-> reduced renal prefusion ——-> decreased urine output.

Dehydration —-> Baroceptors in carotid sinus and aortic arch detect low BP —– > send less impulses to brain (Nucleus Tractus Solitarii). ——–> NTS/ brain stimulates SNS and inhibits PSNS. ——–> SNS releases adrenaline, noradrenaline and increases SVR and vasoconstriction.

Question 12

What is Cullen’s sign ?

Answer 12

Superficial oedema and bruising around the umbilicus /peri-umbilical region.

Can occur with:

• Acute appendicitis
• Splenic rupture
• perforated ulcer
• splenic rupture
• ruptured etopic pregnancy
• intra- abdominal ulcer
• complication of anti- coagulation