Diabetes Flashcards
T1D diagnosis
Hyperglycaemic (random plasma glucose less than 48mmol/L) and symptoms
Adults
Ketosis
Rapid weight loss
Under 50 yrs old
BMI under 25
Personal/ family history of autoimmune disease
Kids
Polyuria ( increased urinarion)
Polydipsia ( increased thirst)
Weight loss
Excessive tiredness
T1D monitoring
Clinical monitoring
- HBA1c every 3-6 months
- urine glucose
Self monitoring
- Capillary blood monitoring (BM)
- ketone test strips
BM
4 x daily
6-8 when I’ll, driving, sport, pregnant, frequent hypos
Waking - 5-7 mmol
Bf meals 4-7 mmol
After meals 5-9 mmol
Flash monitoring & continuous monitoring
First line insulins for T1D
Multiple daily injections basal-bolus insulin regiment
Basal -twice daily insulin Detemir (long acting)
- or once daily glargine
- or degludec if nocturnal hypos or health care administers
AND bolus - rapid acting insulin injections befor meals
(Lispro, aspart, glulusine)
Rapid acting
Given before meals, onset 5-15 mins
Example lispro
Amino acid sequence is altered
Amino acid chain sequence differs from human insulin because position B28 the proline is replaced by lysine and lysine position B29 is replaced by proline
This change in sequence gives it a monomer formation, preventing it forming into a hexamer or dimer
The chain no longer attracts another insulin
This means it is easily released giving it a rapid fast acting
Short acting
Examples - actrapid, humlin S
Taken 15-30 min before food
Not altered, amino acid sequence is the same as normal insulin
Action is slower then lispro as it has a hexmeric structure
Intermediate
Amino acid change is not altered but the insulin is bound to proteins
When injected, enzymes break down to hexamers then nexamers are broken down into monomers
Due to this the onset is delayed
Long acting
Example- glargine
It’s amino acid is changed
2 arginine are inserted to chain B
Glycine is substituted by asparagine at chain A21 position
This change makes it more soluble in acidic conditions
Micro precipitates in blood
What do islets do (a,b,delta)
Alpha cells
- secrete glucagon
- raised blood glucose
- located at periphery of the islet
Beta cells
- secretes insulin
- lowers blood glucose
- mainly found in core of islets
Delta cells
- produce gastrin and somatostatin
- somatostatin inhibits secretion of glucagon and insulin
What occurs in the body when there is low blood glucose (hypoglycaemia)
Alpha cells secrete glucagon, they act on hepatocytes to convert glycogen to glucose and form glucose from lactic acid and certain amino acids
Release of glucose by hepatocytes increase blood glucose levels to normal, if blood glucose continues to rise, hyperglycaemia inhibits glucagon secretion
What happens in the body when there is high blood glucose (hyperglycaemia)
Beta cells secret insulin. Insulin speed facilitated diffusion of glucose into cells, increase conversion of glucose to glycogen increases uptakes if amino acids and protein synthesis, increase synthesis of fatty acids, decreases glycogenolysis and gluconogensis
Which lowers blood glucose levels
If blood glucose continues to decrease hypoglycaemia inhibits the release of insulin
Insulin action on glucose levels (normal)
Pancreas detects glucose in blood through GLUT2 transporters causes a release in insulin
1. Insulin binds insulin receptors (activated)
2. Receptor is phosphorylased
3. Activates cell signaling
4. Releases glucose transporter GLUT4 (activates)
5. GLUT4 imports glucose
6. Lowers blood glucose
What does GLUT4, GLUT2 and GLUT1 do
GLUT4
Insulin dependant glucose transporter for skeletal muscle and adipose tissue. Active when insulin causes it to move from inactive sites in the cell membrane
GLUT2
Major transporter of glucose into beta cells and liver cells, low affinity for glucose and acts when glucose plasma levels are high
GLUT1
Present in all tissue. Does not require insulin. Important for transport of glucose into the cells of the nervous system
Mechanism of B cell destruction
- Tcells React against b-cell antigens resulting in cell damage
- t helpers activate macrophages directed at B cells
- cytotoxic T cells directly kill B cells
2.locally produced cytokines damage B cells
T2D Signs and symptoms
Polydipsia (increases thirst)
Polyuria (increased urination)
Blurred vision
Unexplained weight loss
Recurrent infections (UTI)
Tiredness
Skin condition - darkening of folds
T2D diagnosis
HBA1c of OVER 48 mmol/mol
Fasting plasma glucose OVER 7 mmol/L
Random plasma glucose OVER 11.1
(And in presence of symptoms)
- no features of T1D (childhood, ketosis, insulin dependant)
Diabetic ketoacidosis (DKA) symptoms
Symptoms
Polyuria
Polydipsia
Rapid weight loss
Nausea / vomiting
Abdominal pain
Fast breathing
Sleepinesss
Sweet smelling breath / metallic taste
Reduced consciousness
DKA causes
Infection
New onset diabetes
Medication (SGLT2 - flozin, corticosteroids)
Management of DKA
Fluid replacement
Correct hypertension
Counteract osmotic
Correct electrolyte
Potassium to prevent hypokalemia
Fixed rate infusion 0.1 unit /kg/hr made up to 50 ml with 0.9 NaCl
Hypoglycaemia symptoms and management
Hunger
Anxious/irritable
Palpitations
Tingling lips
Sweating
Weakness
Confusion
Visually disturbance
Loss of consciousness
Death
Management
10-20g of fast acting carbohydrate
- 2-6 glucose tablets
- 180 ml pop or juice
- 4 jelly baby’s
- 1-2 tubes of dextrogel
Recheck blood glucose levels after 10-15 mins
No response - repeat and check 15 min
Unconscious or unable to swallow (severe)
- IM glucagon administered ASAP
No response - A&E
Which oral drug causes Weight Gain and HIGH hypo risk
Sulfonylurea
Gliclazide
Metformin SERIOUS SE
REPORT severe nausea, vomiting, abdominal pain - lactic acidosis
Metformin CI and cautions
STOP eGFR below 30
Reduced dose in CKD max 1g eGFR below 45
SGLT2 (flozins) SERIOUS SE
UTI
REPORT - DKA sweet smelling /metallic taste, fast breathing, nausea vomiting
REPORT severe pain, tenderness swelling in genital area - Fournier gangrene
STOP if ulcers on feet - lower limb amputation
Exebatide SERIOUS SE
REPORT panceritis
