AMK 3 Flashcards
What is Insulin, action and where is secreted?
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.
What causes an Insulin Deficiency ?
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.
What is Diabetic Ketoacidosis?
People with diabetes have a lack of insulin - causing build up of ketones (causes acidosis)
- Reduced Insulin
- Increased demand
- Decreased Supply
(Glucose not enter cells - ATP not produced - secondary energy source- Triglycerides -needed ) - Triglycerides broken down to Free fatty acids + Glycerol
(Triglycerides also found in Adipose tissue so Lipolysis occurs ) - Triglycerides converted into Acetyl CoA (by beta oxidation)
- Krebs cycle overwhelmed with the excessive Acetyl CoA entering so Acetyl CoA shifted to an alternative pathway which synthesises Keto bodies.
- 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.
What is Hyperglycaemic Hyperosmolar Syndrome ?
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.
What is the presentation of diabetic Ketoacidosis ?(Labs)
*for specific numbers look on OneNote
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
Signs of DKA
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).
How does DKA effect Potassium level?
- Acidosis - high H+ levels accumulate in ECF. Will diffuse into ICF from high to low.
- Cells pump out K+ into ECF to maintain ion balance.
- 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
Treatment of DKA ?
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.
Effects of HHS ?
- Hyperosmolar blood passes through organs e.g. brain, muscle
- h20 drawn out of these cells - causing shrinkage
CNS cell shrinkage - lead to confusion, lethargic (altered mental state) and long term - coma.
What is the presentation of HHS ?(Labs)
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])
Effects of Dehydration caused by DKA and HHS ?
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.
What is Cullen’s sign ?
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
