Week 7 Flashcards
what do the islets of langerhans in the pancrease do?
secrete
hormones directly into the blood
(endocrine function)
What do alpha cells in pancreas produce?
Glucagon
what do beta cells in the pancreas produce?
Insulin
what do delta cells in the pancreas do?
somatostatin (inhibits
insulin and glucagon secretion)
What are the metabolic effects of insulin?
Release is stimulated by increase in blood glucose levels.
Insulin facilitates diffusion of carbohydrates into cells.
Causes excess carbohydrate to be stored as glycogen, mainly in liver and skeletal muscle.
Spare carbohydrate converted to fat (triglycerides) and stored in adipose tissue, particularly when glycogen stores are exceeded.
Promotes up take of amino acids by cells for conversion into proteins needed for anabolic metabolism.
Inhibits gluconeogenesis – creation of glucose from new sources.
Circulates in the blood in unbound form. Plasma half life of ≈15 minutes (rapid onset and short duration).
Degraded by insulinase, mainly in the liver.
how does insulin affect carbohydrate metabolsim?
Increase in BSL causes an increase in insulin production.
Insulin activates membrane receptors on target cells causing most body cells to become highly permeable to glucose.
Muscles either use glucose (when active) or store it as glycogen (to be used later).
Liver stores glucose as glycogen. Up to 6% of liver mass is glycogen. This can be transformed into glucose again when needed.
how does insulin affect fat metabolsim?
Insulin decreases the utilisation of fat for energy (carbohydrate is used instead).
Inhibits the release of fat from adipose tissue.
Fat breakdown and use is enhanced in the absence of insulin.
– Lack of insulin causes hydrolysis of stored
triglycerides, releasing lots of free fatty acids, which become the primary source of energy for cells.
– Fatty acids are also converted by the liver to cholesterol and phospholipids.
how does insulin affect protein metabolsim?
Insulin causes proteins to be stored in cells by increasing uptake of amino acids;
Promotes protein synthesis by increasing the translation of messenger RNA;
Inhibits protein catabolism.
what is the function of GLUCAGON?
Released in response to LOW BSL.
Rapidly converts liver glycogen to
glucose (glycogenolysis).
Increases gluconeogenesis - through
the transport of amino acids to liver,
stimulates conversion to glucose.
Most of the blood glucose available
between meals is used by the brain.
It is important that insulin is not
released during this time.
Define diabetes mellitus
A deficiency of insulin production, or insulin action, or both.
What causes diabetes type 1
Usually autoimmune destruction of pancreatic beta cells that produce absolute deficiency in insulin production
-> peak incidence between 9 months and 14 years
What is the cause of Type 2 diabetes
- Associated with ‘insulin resistance’
- may initially have increased plasma insulin levels
- associated with obesity, hypertension, elevated blood triglycerides, sedentary lifestyle
How does obesity impact type 2 diabetes?
decreases the relative number of insulin receptors on target cells, hence insulin still released but less effective
What are the AUTONOMIC clinical findings of Hypoglycaemia?
– Hunger (Ach) – Tremor (SNS) – Anxiety (SNS) – Nervousness (SNS) – Palpitations (SNS) – Tachycardia (SNS) – Sweating (SNS) – Diaphoresis (Ach) – Pallor (SNS) – Paraesthesia (Ach) – Pupil dilation (SNS)
What are the CEREBRAL/CNS clinical findings of Hypoglycaemia?
– Headache – Irritability – Confusion – Stupor – Dysphonia – Ataxia – Diplopia – Hemiparesis – Seizures – Coma – Brain damage–death (if left untreated)
How do you treat Hypoglycaemia?
Diabetes education to patients to consume fast acting glucose: – 100 ml Lucozade – 5 jelly beans – 150 ml soft drink – Glucagon IM
Prehospital management:
– Glucose paste
– Glucagon IM
– Dextrose IV
“Neuronal store of glycogen is
depleted in 2 min, after which the
brain is susceptible to damage”
What is Hypoglycaemic-associated autonomic failure (HAAF)
A condition that may develop in T1 and some T2 diabetics
– Causes reduced sympathoadrenal responses to hypoglycaemia.
– > risk for patients with absolute loss of endogenous insulin and
autonomic neuropathy
It a decrease in adrenaline release and sympathetic responses
– Results in defective glucose counter-regulation
– Patients are unaware of hypoglycaemia.
HAAF has cardiovascular implications including reduced baroreflex
sensitivity, predisposing patients to ventricular arrhythmias.
Basically they get used to hypoglycaemia, and are unaware they have it due to reduced adrenaline and autonomic symptoms
What are the risk factors for gestational diabetes?
> 30 years of age
Have a family history of type 2 diabetes
Overweight
From an indigenous Australian or Torres strait islander background
From a Vietnamese, Chinese, middle eastern, Polynesian or Melanesian background
Gestational diabetes during previous pregnancies
how does diabetic ketoacidosis work?
- lack of insulin (or insulin effectiveness) results in INCREASED BGL
- Fatty acids are released from adipose tissue -> unsuppressed lipase activity of triglyceride breakdown
- INCREASED fatty acid levels -> increased ketone production by liver
What are the 3 states of DKA?
- hyperglycaemia
- Ketosis
- Metabolic acidosis
what is the pathophys of DKA
Hyperglycaemia
– Osmotic diuresis => dehydration
=> electrolyte imbalance
Ketosis
– Metabolic break down of stored
fat, results in build up of ketones
Metabolic acidosis
– Increased accumulation of keto
acids resulting in low blood Ph
value
DKA is the most common cause of
death in newly diagnosed diabetes
what are the clinical features of DKA?
– Slow onset – days – Tachycardia – Hypotension (due to severe dehydration) – Hyperventilation (Kussmaul respiration) – Frequent vomiting – Polyuria – Polydipsia (thirst) – Fatigue – Abdominal pain/tenderness (without associated disease/ issue) – Weight loss (fluid, muscle, fat) – Acetone detected on breath – Altered consciousness – BSL > 13mmol/L
What is Hyperosmolar Hyperglycemic state (HHS)?
Hyperglycemic Hyperosmolar Non-ketotic Coma (HHNC)
aka Hyperosmolar Hyperglycemic State (HHS)
- More common among Type II diabetics (the elderly)
- No hyperventilation
- Significant dehydration (increased BSL)
- High mortality
What is the pathophys of Hyperosmolar Hyperglycemic state (HHS)?
Insulin deficiency is enough that hyperglycaemia (> 33mmol/L)
develops but not enough to promote metabolism of fatty acids,
therefore no production of ketones
Excessive diuresis results in severe hyperosmolarity and dehydration
Most common in elderly Type 2 patients
Can mimic a stroke
Precipitated by
- Increased resistance to effect of insulin
- Excessive carbohydrate intake
What are the clinical features of Hyperosmolar Hyperglycemic state (HHS)?
- Dehydration – Thirst – Seizures – Hemiparesis – Aphasia – Muscle twitching – Hyperthermia - Visual hallucinations
What are some complications of diabetes mellitus?
Arterioles - Hyaline Arteriolosclerosis > hardening
Capillary – basement membrane thickens > diffusion
Arteries - Atherosclerosis > deposits (stroke and (S)MI)
Diabetic Retinopathy > blindness
Kidney damage > Nephrotic syndrome > dialysis
Peripheral neuropathy > numbness in hands and feet > ulcers
