L4 Diabetes and Obesity Flashcards
(47 cards)
what are the two metabolic states? explain them.
Absorptive State:
• After a meal: absorption of nutrient from diet (into the blood stream)
• Excess nutrients are stored in the body (used or stored)
Post-absorptive State:
• Between meals
• Stored energy is mobilised for use (energy supplied back into blood stream)
Note: blood concentration of nutrients (e.g. glucose) remain fairly stable during these states
define glucose
a monosaccharide (simple sugar) = only made up of one sugar
why is glucose control important
• Blood glucose levels are maintained between 70-110mg/100ml of plasma
• Most tissues can also generate ATP (cellular energy) from fats (adipose tissue)
• During starvation, we can break down proteins (muscle) to make ATP
BUT the brain can only get ATP from glucose SO blood glucose levels must be maintained
define glycogenesis & will it increase or decrease the blood glucose levels
glycogenesis: Building glycogen from glucose (glucose -> glycogen)
decrease blood glucose
define glycogenolysis & will it increase or decrease the blood glucose levels
glycogenolysis: Breaking down glycogen to release glucose (glycogen -> glucose)
increase blood glucose
define gluconeogenesis & will it increase or decrease the blood glucose levels
gluconeogenesis: Making new glucose molecules (amino acids -> glucose)
increase blood glucose
The breakdown of glycogen into glucose is called _______ whereas the production of glycogen from glucose is called _______. _______ is the creation of new glucose from non-carbohydrates.
The breakdown of glycogen into glucose is called GLYCOGENOLYSIS whereas the production of glycogen from glucose is called GLYCOGENESIS. GLUCONEOGENESIS is the creation of new glucose from non-carbohydrates.
_____ produces hormones to control blood glucose
PANCREAS produces hormones to control blood glucose
what are the effects of insulin on glucose
• Insulin favours glucose uptake and storage
o Facilitates glucose transport from blood into body cells (especially skeletal muscle and adipose tissue)
o Stimulates glycogenesis in liver and skeletal muscle
o Inhibits glycogenolysis and gluconeogenesis
• Promotes storage of fats (triglycerides) in adipose tissue
• Stimulate protein synthesis
what are the effects of glucagon on glucose
• Glucagon factors the release of glucose into the blood= stimulates glycogenesis, stimulates gluconeogenesis, inhibits glycogenesis
• Breakdown of stored fats
• Breakdown of proteins in live
• Insulin and glucagon have opposite effects on blood glucose
o Insulin: released during absorptive state when blood glucose is increased
o Glucagon: released during post absorptive state when blood glucose is decrease
what is hyperglycaemia
high blood glucose
what is hypoglycaemia
low blood glucose
describe glucose homeostasis
Increased blood glucose -> pancreas produces insulin -> stimulate glucose uptake by cell and stimulate glycogen formation by liver (increase glycogenesis) -> blood falls to normal range
Decreased blood glucose -> pancreas produces glucagon -> stimulates glycogen breakdown (increase glycogenolysis) -> blood glucose rises to normal range
what is diabetes mellitus
Impaired ability to utilise blood glucose = characterised by hyperglycaemia (high blood glucose)
regarding type 1 diabetes, describe the following:
- old classification
- % of cases
- peak age of onset
- pathophysiology
- level of insulin
- treatment
- old classification: insulin-dependent diabetes mellitus (IDDM); juvenile onset
- % of cases: 10-15% of diabetes cases (least common)
- peak age of onset: < 20 years (children and adolescents)
- pathophysiology: autoimmune destruction of B cells (produce antibodies that attack and destroy B cells) = inability to produce insulin
- level of insulin: none or almost none
- treatment: insulin injections, dietary management, exercise
regarding type 2 diabetes, describe the following:
- old classification
- % of cases
- peak age of onset
- pathophysiology
- causes
- level of insulin
- treatment
- old classification: non-insulin-dependent diabetes mellitus (NIDDM); adult onset
- % of cases: 85-90% (most common)
- peak age of onset: over 35-40
- pathophysiology
3 metabolic abnormalities
1. Insulin Resistance: insulin is produced but insulin receptors are unresponsive or insufficient in number; pancreas compensates by increasing insulin production
2. Decreased production of insulin: beta cells become fatigued; hyperglycaemia
3. Inappropriate glucose production: liver releases glucose when not needed - causes: genetics; environmental factors (obesity, poor diet, lack of exercise); often associated with hypertension and hyperlipidaemia
- level of insulin: may be normal or exceed normal
- treatment: dietary control and weight reduction, exercise, oral hypoglycaemic drugs
what are the three methods for diagnosis
- Fasting plasma glucose (glucose levels after fasting): ≥ 7mmol/L
- Random plasma glucose: ≥ 11.1 mmol/L (also manifestations – symptoms – of diabetes: polyuria, polydipsia, weight loss)
- Two-hour oral glucose tolerance test (OGTT): plasma glucose ≥ 11.1 mmol/L (glucose load after fasting
describe the oral glucose tolerance test
- Patients consume 150g of carbohydrates/day for 3 days prior
- Fast over night
- On following morning: measure fasting plasma glucose
- Ingest 75g glucose drink
- Measure plasma glucose after 2 hours
T/F: Type 1 diabetes experience insulin resistance
F (type 2)
T/F: Type 1 diabetes is due to autoimmune destruction of pancreatic alpha cells
F (B cells)
what is prediabetes
intermediate stage of disordered carbohydrate metabolism
what are the acute consequences of diabetes
glycosuria (glucose in the urine), polyuria (excessive urination), polydipsia (excessive thirst), polyphagia (excessive hunger), weight loss, fatigue, diabetic acidosis (if untreated: coma and death)
(for type I and II but type II is a slower progression and type I is quicker)
describe what hyperglycaemia does to damage the blood vessels
- Hyperglycaemia causes endothelial cells of blood vessels take in glucose and form glycoproteins by glycosylation (advanced glycation end products- AGEs) (protein + sugar = glycated protein)
- These damages the basement membrane leading to microvascular and macrovascular disease
describe what retinopathy is
- Retinal capillaries become leaky and develop microaneurysms
- Microaneurysms can haemorrhage causing bleeding in the retina
- Lack of oxygen to retina is compensated by growth of new blood vessels (neovascularisation)
(microvascular disease)
