what is Humalog
also called insulin lispro – this is a fast acting inuslin that starts to work about 15 minutes after injection, used to manage blood sugar spikes and might help keep sugar levels in balance, most common side effect of Humalog is hypoglycaemia that can lead to levels of unconsciousness and passing out, should be taken 15 minutes before eating or right after a meal, with type I diabetes Humalog it needs to be used with a longer acting insulin, can also be used in type II
what is glargine insulin
– subcutaneous injection – this is a long acting insulin used in both type I and type II, side effects include oedema, and hypoglycaemia
what is a dipstick urine test
this is a urine test that checks pathological differences in the persons urine, checks can include for protein, glucose, blood, bilirubin, white blood cells, acidity
what is the anion gap
this is the contribution of the unmeasured anions to metabolic acidosis
what is the causes of type I diabetes
- Lack of insulin production, don’t produce any insulin therefore cannot control blood glucose levels
- Can be due to an autoimmune condition where the cells attack the pancreas and the beta cells are therefore cannot produce insulin
- Characterised by immune T cell mediated disruption of the pancreatic beta cells within the islet of Langerhans
- Usually develops by early adulthood
what are the signs and symptoms of type I diabetes
- Feeling thirsty
- Frequent urination particularly at night – billy has this
- Feeling tired
- Losing weight without trying
- Thrush that keeps coming back
- Blurred vision
- Cuts and grazes that are not healing
how do you diagnose type I diabetes
- Dipstick urine test – this can check to see if there is any glucose in the blood
Blood tests –
One abnormal plasma glucose
- (random ≥11.1 mmol/L or fasting ≥7 mmol/L) in the presence of symptoms (thirst, increased urination, recurrent infections, weight loss, drowsiness and coma)
Two fasting venous plasma glucose samples in the abnormal range
- (≥7 mmol/L) recommended in asymptomatic people
HbA1c
- Advantages – reliable measure stable and calculate the glucose over 3 months
- Disadvantages – high cost, Hb traits such as sickle cell influence it as well as conditions affecting the RBC turnover
- Has to be higer than 48 mmol/mol as recommended as the cut of point for diagnosing diabetes
how do you manage diabetes
Fast acting inuslin
- Humalog – patients should eat meal within 5-10 minutes
Long actin basal inuslin
- Glargine
- These are mcirocystals that release insulin slowly, they have a long duration of action of 18-26 horus with no peak
- Trys to mimic insulin secretion of a healthy individual
what are the treatments of hypoglycaemia
Eat or drink something sugary - 3 dextrose or glucose sweets - 5 small sweets likely jelly babies - 1 glass of non diet surgary drink - 1 glass of fruit jucie Emergency - Glucagon injection – this releases glucose from the liver
describe how type I diabetes can effect the social aspect
- Driving
- Alcohol intake
- Managing on their own
what are the causes of DKA
- Caused by if the body starts to run out of insulin
- Lack of inulin – causes carbohydrate unavailability (no glucose enters the cell) therefore minimics starvation state produces ketones
- High levels of glucagon – high levels because alpha cells are not inhibited by beta cells and readily release glucagon this contributes to the starved state
describe the mechanisms of hyperglycaemia
- Lack of insulin – this inhibits glycolysis, stimulates glycolysis and gluconeogenesis
- Excess glucagon – inhibits glycolysis – this is because it inhibits fructose -2,6-bispphoate- regulates phosphofructokinase -1, fructose -6-phosphate to fructose-2.6-bisphopshate which is the rate limiting step in glycolysis
what are the effects of hyperglycaemia
- Hyperosmolarity – causes osmotic diuresis – increased urine and loss of water and electrolytes in the urine
- Glucose in the urine – glucose is freely filtered by the glomerulus and reabsorbed, but when the threshold is reached it is filtered out into the glucose
- Dilutional hyponatremia – low sodium – there is a shift of water form the intracellular to the extracellular compartments due to imbalance of glucose
- Severe dehydration – due to vomiting and later decreasing fluid intake
describe the pathophysiology of DKA
- Arises due to lack of insulin and corresponding levels of glucagon rising
- This leads to an increased of glucose in the liver from glycogen via glycongenolysis and also through gluconeogenssi
- Absence of glucose leads to lipolysis in adipose tissue which are converted to ketones via beta oxidation
- Ketone bodies have a low pKa make the blood acidic
- Leads to metabolic acidosis
- Hyperventilation in order to compensate
- Excess glucagon turns off supply of substrate into the Krebs cycle and causes ketogenesis
- Ciritic acid is used up and there is a decrease of malonyl CoA in the liver, this turns off carnitine acyl transferase 1 and turns on ketogenesis as free fatty acids enter the liver – this is used for ketogenesis
what are the signs of DKA
- Needing to pee more than often
- Feeling thirsty
- Being sick
- Tummy pain
- Breath that smells fruity
- Deep or fast breathing
- Feeling very tired or sleepy
- Confusion
- Passing out
how do you diagnose a DKA
- Check blood sugar level and check ketone level
- If blood sugar level is greater than 11 mmol/L then do ketone check , if ketone is 0.6-1.5 slightly increased risk of DKA and if it is 1.6-2.9 mmol then it means that you have an increased risk of DKA, if greater than 3mmol/L means that you have a very high risk of DKA
what are the causes of a DKA
- Infection
- Injury
- Not following treatment plan
- Taking certain medications
- Binge drinking
- Illegal drugs
- Pregnancy
- Having your period
what is the treatment of a DKA
- Insulin given through a vein
- Fluid given into a vein to rehydrate the body
- Nutrients to replace any you have lost
can type 2 diabetics get DKA
- Insulin is present but resistance or not enough, these usually suppress ketogenesis
- Can occur and it is called ketosis-prone type 2 diabetes
what are the effects of DKA
- Increased anion gap – metabolic acidosis can cause an increase anion gap, bicarbonate is excreted therefore other ions need to rise in order to maintain electroneurtrality
- Vomiting -c auses a loss of potassium and sodium
- Hyperosmolarity – causes osmotic diuresis as ketoacid are osmotically active (acetoacetate can influence fluid shifts across a semipermeable membrane)
- Initial increase in serum potassium – due to acidosis pulling intracellular potassium out of the cell then lost through the urine causing hypokalaemia
- Enzyme ineffective – becomes infective and worsens ketoacidosis
- Hyperntesion – increased respiratory compensation
what are the effects of alcohol on type 1 diabetics
- You can drink alcohol if you are diabetic
- Show be prepared and get diabetes kit and hypo treatments ready and check your blood sugar level before you start to drink, don’t drink on an empty stomach – eat foods that have carbs in them
- Carry snacks with you and eat before you go to bed
- Dancing is exercise so it can make your blood sugar level drops if you are walking from venue to venue
- Beer and sweet wine has sugar in it
- Alcohol may increase triglyceride levels
- Moderate amounts of alcohol can cause it to raise, excess amounts of alcohol can cause it to drop
- Common to get hypo during the night as they do not take additional carbohydrate before going to bed
describe the mechanism of alcohol break down
- Accumulation of NAD+ to NADH this inhibits cytoplasm malate dehydrogenae which is used gluconeogenesis therefore this is inhibits gluconeogenssi
- This results in a reduction in the glucose in the blood
- Which results in hypoglycaemia
- More important at night and more common to lead to hypoglycaemia at night as the body uses carbohydrate stores
- Can lead to anaerobic respiration and lactic acid
- This produced a metabolic acidosis and prevents production of ADH
explain the blood results
glucose
- High – lack of inuslin means that process such as gluconeogenesis are not inhibited, therefore glycerol, fatty acids, proteins are all being converted to glucose in order to supply the brain with glucose, when in high concentration this can be present in the glucose as the glucose can not be filtered out
- This also increased if you decrease ultilzation
- Increase in lipid breakdown, protein breakdown
sodium
- Low - leads to hyperosmolarity this is because he is urinating more easily therefore sodium which is excreted in the urine is being lost
potassium
- Normal but high – sodium and potassium are exchange, tyring to excrete hydrogen ions may replace the missing hyodrgne ions
chloride
- This is normal – shows that he does not have normal anion metabolic acidosis and there are other anions that are replacing the missing ones caused by the loss of bicarbonate
Ketones
- High
- Ketone acidosis
- Gluconeogenesis is impaired
pH
- Acidosis
HCO3-
- Low – due to ketoacidosis
pO2
- Normal but high
pCO2
- Low – respiratory compensation caused by the hyperventilation which blows of more carbon dioxide in order to get oxygen and lowers
Anion gap
- 30.9
- Has a high anion gap
Causes of anion gap
- Ketoacidosis – in our case DKA causes the high anion gap
- Lactic acidosis
- Renal failure
- Toxic ingestions
explain ketosis
Ketosis
- This occurs when there is elevated levels of ketone bodies in the blood
- Normal response to low glucose availability
- Produced mianly in the mitochondria of the liver cells
- HMG -CoA synthase helps turn them into ketones
- acetylCOa COMBIEND TO FORM acetoocteyl CoA
- turned into acetoacetate and this can split inot acetone and beta hydroxylburate
