diabetes Flashcards
what is the endocrine function of the pancreas?
the beta cells secrete insulin and the alpha cells secrete glucagon
what does insulin do?
lowers blood glucose as its stimulated by high blood glucose
what does glucagon do?
raises blood glucose stimulated by low blood glucose
What hormone is released at hyperglycaemia?
Blood glucose concentration too high from set point so insulin released
What hormones are released at hypoglycaemia?
Blood glucose comcentration is too low from set point so glucagon and adrenaline are released
What chemical processes occur during hyperglycemia?
glycogenisis = the conversion of glucose to glycogen
- conversion of glucose to lipid
- increased metabolism so increased respiration to reduce blood glcuose levels
What chemical processes occur during hypoglycaemia
glycogenolysis = breakdown of glycogen to glucose
what is polydipsia?
thirst due to fluid loss and increased osmolarity
what defines type 1 diabetes
absolute need for insulin therapyw
what defines type 2 diabetes?
non insulin dependent diabetes and is the most common form of diabetes
what is gestational diabetes?
diabetes that develops during pregnancy and usually disappears after giving birth
what can diabetes be secondary to?
-pancreatic disease
-other endocrine disease e.g. cushings syndrome
-drugs
-abnormalities of insulin/ insulin receptor
-genetic syndromes - cystic fibrosis
for type 1 diabetes (IDDM) what can cause it and how can it be treated?
caused by:
-genetic predisposition
-autoimmune destruction of beta cells
-environmental factors like viruses or chemicals
treated by:
-insulin injections and diet
for type 2 diabetes (NIDDM) what can cause it and how can it be treated?
caused by
-multifactorial inheritance
-down regulation of insulin receptors so they have a reduced response to insulin
treated by
-dietary management and exercise
-oral hypoglycaemic agents
what is the genetic susceptibility of type 1 diabetes associated with?
-HLA
-DR3
-DR4
for type 1 diabetes, what lesions can it cause and what causes them
islet lesions - in early stages these cause inflammation and in later stages cause atrophy and fibrosis
caused by cell autoantibodies
what happens as a result of hyperglycemia?
check screenshots
what lesions are formed in type 2 diabetes?
tissue fibrosis and amyloid
is there HLA association with type 2 diabetes?
no
what do diabetic complications depend on?
-severity and duration of hyperglycaemia
-level of glycaemic control
give 3 acute complications of diabetes type 1 what are the symptoms
hypoglycaemia symptoms
-shaking, sweating, tachycardia
-hunger
-headache
-sudden moodiness
-behaviour changes, confusion
-blurred vision
ketoacidosis (this is worse than the non-ketoic version) where there’s a severe lack of insulin in the body
-blurred vision
-thirsty
-stomach pain
-more frequent urination
-confusion
-tiredness
hyperosmolar non-ketoacidotic coma
-severe hyperglycaemia
-dehydration
-lethargy
give the symptoms of diabetes in the following categories:
-central
-systemiic
-repiratory
-eyes
-breath
-gastric
-urinary
-polydipsia, polyphagia, lethargy and stupor
-weight loss
-hyperventilation
-blurred vision
-smell of acetone in the breath
-nausea, vomiting, abdominal pain
-polyuria, glycosuria
give general complications in diabetes
-reduced immune and poor healing response
-hyperglycemia
-reduced immune cell function
-increased inflammation
-bacterial and fungal infections
give chronic complications in diabetic macrovascular disease
-cardiovascular disease
-peripheral vascular disease
-diabetic foot
give chronic complications in diabetic microvascular disease
-diabetic neurapathy
-diabetic nephropathy
-diabetic cardiomyopathy
-diabetic retinopathy
what are the consequences of atherosclerotic lesions?
-cardiovascular disease
-vascular insufficiency causing brain infarction and gangrene/ ulcers in legs
give two examples of diabetic foot
-ulceration
-gangrene due to ischaemia
how can diabetes cause major vascular disease?
by causing atherosclerotic lesions where the blood vessel is blocked
what does diabetic microvascular disease cause?
-increased thickness of capillary basement membrane
-arteriolosclerosis
-vascular occlusion
-defective healing in chronic ulcers
-major complications in kidney and retina
-nerve damage
what is diabetic nephropathy? what does it cause?
a renal faliure that mainly occurs in IDDM over NIDDM
-necrotising papillitis
-diabetic glomerulosclerosis
what is diabetic glomerulosclerosis?
an end stage renal disease causing chronic renal faliure due to the BM changing and renal hyperfusion
what is diabetic neuropathy? what does it cause?
-thickened capillaries and ischaemia
it causes:
-glycosylated nerve proteins
-axonal degeneration
-loss of myelination causing reduced conduction velocity
-reduced sensation
-muscle weakness, atrophy, wastage
-ptosis which is the 3rd cranial nerve palsy
give some common occular complications of diabtes
-cataracts
-background diabetic retinopathy
-serious diabetic retinopathy
-endstage diabetic retinopathy
what are the stages in diabetic retinopathy?
- microaneurysms
- haemorrhages
- exudates
- proliferative DR
what does background diabetic retinopathy look like
scattered microaneurysms and dot haemorrhages
what does serious diabetic retinopathy look like?
-cotton wool spots
-hard exudates
-haemorrhages
-venule bleeding
-vessel breakage
what does end stage diabetic retinopathy consist of?
-uncontrolled new vessel growth
-fibrous tissue contraction
-retinal traction
-retinal detachment
-visual loss
How is the increase in blood glucose regulated?
- Stimulus of the increased blood glucose concentration is detected as the input signal by the receptors being beta cells in the pancreas
- The output signal triggers insulin release which is a polypeptide hormone so a chemical messenger
- Effectors = liver/ muscle tissue
- Insulin binds to the protein receptor in the cell surface membrane of liver / muscle cells.
- Tertiary protein structure changes shape and the cells insert carrier proteins through which the glucose can enter the cell via facilitated diffusion
- Glucose is polymerised into glycogen
- Response is triggered of blood glucose concentration being lowered
- Negative feedback
How is a decrease in blood glucose concentration regulated?
- Stimulus of the decreased blood glucose concentration is detected as the input signal by the receptors being alpha cells in the pancreas
- The output signal triggers glucagon release which is a polypeptide hormone so a chemical messenger
- Effectors = liver
- Glucagon binds to the protein receptor in the cell surface membrane of liver cells.
- Tertiary protein structure changes shape and the cells insert carrier proteins
- Glycogen glycosidic bonds are hyrolysed to release alpha glucose which moves out if tge carrier proteins by facilitated diffusion
- Response is triggered of blood glucose concentration being increased
- Negative feedback
What three factors influence blood glucose concentration?
- glucose from hydrolysis of consumed carbohydrates such as starch
- glycogenolysis
- gluconeogenisis
give 2 oral hypoglycaemic agents
-sulfonylureas which stimulate insulin production
-metformin which inhibits liver glucose production
what is necrobiosis lipoidica diabeticorum?
a skin condition mainly seen in women as a result of diabetes that causes severe ulceration
what are the two types of diabetes mellitus?
-insulin dependent diabetes mellities - type 1
-non insulin dependent diabetes mellitus type 2
what are the two mechanisms that are involved in the chronic complications of diabetes?
-polyol pathway: glucose is absorbed into tissue and converted into sorbitol
-protein glycosylation: releases advanced glycation end -products which inactivates protein and increases BM thickness
why is cardiovascular disease a major cause of death in patients with diabetes?
due to accelerated atherosclerosis causing
-coronary artery disease
-ischaemic heart disease
-myocardial infarction
why is wound healing compromised in diabetics?
-compromised immune cell function causing a decreased immune response
-compromised blood flow reduces o2 supply and reduced metabolites delays healing
