Endocrinology Flashcards
What hormones control Glucose levels?
After meal?
Insulin is a hypoglycaemic hormone. Polypeptide hormone from beta cells in Islets of Langerhans in the Pancreas. Secreted in response to hyperglycaemia. Allows glucose into cells and promotes fat and protein synthesis
Hyperglycaemics:
Glucagon,- produced by alpha cells in IOLs. Opposes insulin
Cortisol-promotes gluconeogenesis
Catecholamines- secreted by adrenal medulla as a response to stress, raising blood glucose levels.
Growth Hormone
After meal, glucose stored as glycogen in fat and in the liver
What is DM?
Diabetes mellitus refers to a group of conditions characterised by chronic hyperglycaemia resulting from relative insulin deficiency, peripheral tissue resistance, or both.
Can also occur secondary to pancreatitis/pancreatectomy, Cushings disease, acromegaly, drugs (steroids/thiazide diuretics).
Other type of Diabetes is Diabetes Insipidus which occurs due to diuresis when theres a lack of ADH. No water uptake results in a relative increase in blood glucose conc.
2 types of DM
Type 1
Insulin dependent (IDMM)
Younger pts, lean and DM usually causes weight loss
Acute Onset
LOW/NO INSULIN
due to autoimmune disorder of pancreatic Beta cells
Type 2
Non-insulin dependent (NIDDM)
older pts, often obese, very rarely get associated weight loss
Chronic
Only partially Insulin deficient, peripheral tissue becomes insulin resistant
Beta cell mass reduced 50%
Symptoms of Hyperglycaemia
Excess blood glucose beyond renal re-absorption limit so enters urine, osmotic diuretic effect –> polyuria and thirst as excess fluid and electrolytes lost by due diuretic effect.
Weight loss and lethargy: fluid depletion and fat/protein breakdown as cells can’t use serum glucose
Management of DM
Get sugar down and control it as near normal as possible (mimick normoglycemia) to delay/minimise severity + likelihood of complications.
- Diet Advice
Drugs
Oral Hypoglycaemics
Most common type is Metformin which decreases gut glucose absorption, increases peripheral tissue insulin sensitivity (insulin helps glucose enter cells and thus leave blood).
Also have:
Sulphonylureas: Increase Beta cell insulin secretion and reduces peripheral insulin resistance
Glibenclamide: long acting. Tolbutamide: short acting
Insulin
Main problem with insulin is that it is a short chain protein which the body is very good at digesting, therefore insulin has to be administered bypassing GI tract
3 Types
1. Actrapid- fast acting (15-60mins), lasts 4-6 hours. Used in multi-injection regimes, surgery and A + E
2. Monotard/insultard- longer acting (12-24hours/24hours plus)
3. Mixtard- mixture of long and short acting, smooth effects
When injecting insulin always make sure you are also eating as injecting insulin but not eating can lead to Hypoglycaemic event.
BUT be aware, if patient is ill and off food, don’t stop insulin- pt will have a raised metabolism to fight the illness therefore will need more insulin. reducing their insulin can kill them by leading to hypohypoglycaemia
Measuring Glycaemic Control
Fingerprick Glucose Tests. Best for knowing current sugar state. Random test >11mmol/l is DM. Fastes test >6.7 is DM)
HbA1C Test: measures level of glycosylated Hb present. Provides long term control review (average life of each Hb molecule 6 weeks). Normal level 4-6%
Also have:
Urine Dipstix: crude test as glucose will only appear if exceeding renal threshold for the individual and urine levels will often lag behind blood levels so info out of date
Lab serum : most accurate test but have to wait for results to return form Lab.
Diabetic Emergency- Acute Hyperglycaemia
Blood Glucose drops 2.2mmol/l<
Causes:
Frequent complication of insulin therapy- pt self management problems (reduces food intake/skips meal leads to risk of relative overdose and hypoglycaemia risk)
Excess alcohol inhibits hepatic gluconeogenesis and enhances insulin sec’
Insulinomas producing excess insulin
Addison’s Disease causing low cortisone production impairing gluconeogenesis
S/S
Increased sympathetic tone: Hunger, Sweating, Palor, Tachychardia
Peripheral tingling + altered sensations
Fitting, hemiparesis and eventually coma will supervene
Tx
If patient conscious, rapid ingestion of sugar
if unconscious/depressed gag reflex then IV glucose (50ml, 50pc dextrose) or Glucagon 1mg IM
If in doubt to what is happening, always give dextrose, never give insulin. If they are hypo and u give insulin –> fatality.
Diabetic Emergency- Diabetic Ketoacidosis
Typically occurs in; Undiagnosed Diabetic. Insufficient/missed insulin dose.
Pathophysiology
Insulin deficiency –> cells can’t access glucose
Unrestrained Hepatic Gluconeogenesis –> more glucose pouring into blood stream
These two things lead to high blood glucose levels.
Leads to: Glycosuria, Osmotic Diuresis, Dehydration
Due to inaccessibility to glucose, cells use alternate sources of energy;
Get peripheral lipolysis + proteolysis –> production of free fatty acids –> liver degrades these into Acidic Ketones hence ‘ketoacidosis’
Stress hormones, catecholamines glucagon and cortisol accelerate this process.
Clinical Features:
Profound Dehydration due to water and electrolyte loss. Typically adult can lose 6L of water, 500mmol Na, 400mmol K
Low BP and Kussmaul’s Respiration (deep laboured) to compensate for metabolic acidosis.
Breath smells of acetone
Investigations Blood Glucose >20 Plasma: High in Ketones Urine Dipstix: Glycosuria, Ketonuria Serum: High Urea + Creatinine, Low K + Na.
Treatment Restore fluid and electrolytes Give insulin to reduce blood glucose Supply extra K as serum levels will plummet as glucose returns to cells Restore acid-base balance
Diabetic Emergency: Hypersmolar Non Ketotic State (HONK)
severe hyperglycaemia without significant ketosis
seen more in type 2
manage same as DKA but ignoring acidosis measures
If serum Na is high, half normal saline for fluid replacement
Complications of Diabetes
Complications can be split into Macrovascular and Microvascular
Macrovascular
Hyperglycaemia –> Non-enzymatic glcyolysation of blood + storage of glucose as fat –> damaged to vessel walls –> accelerated atherosclerosis –> CVD, Atheroma, Stroke, Peripheral Vascular Disease (Gangrene)
Microvascular Diseases
Occurs body wide
Certain areas of increased danger
Hyperglycaemia –> excesss glucose, converted in cells to sorbitol.
Certain cells have insufficient enzyme to break sorbitol down leading to osmotic imbalance, water uptake and cell lysis
These cells are:
Schwann Cells
Pericytes
Lens Cells
Leads to:
Diabetic Neuropathy- irreversible glove and stocking loss or peripheral sensation and autonomic system failures i.e. impotence, loss of joint + position sense. Can get mononeuropathies i.e. of CN III and VI
