Diabetic ketoacidosis Flashcards
beta oxidation occurs where
Krebs cycle in mitochondria
insulin prevents fatty acids moving into mito
what happens when you inhibit insulin like in type 1
insulin not amiable to prevent beta oxidation leading to lots of palmitoyl coA through that enzyme now free to go inside cell and now used to make energy
3 ketone bodies
acetone - volatile - gas - smell in breath
acetoacetate
beta-hydroxybrutyrate
in dka what do we see
low insulin
no inhibiting of fatty acid transport
low insulin in dka is
going to lead to High glucose so dehydration and osmotic diuresis will occur
potassium goes up in serum, total body potassium depleted though
acidosis
dehydration leading to increase creatine due to renal failure
serum ketones and beta hydrolyse rate
anion gap formula
The anion gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions (e.g. albumin is the main unmeasured anion). The normal anion gap varies with different assays but is typically between 4 to 12 mmol/L.
cause of high include DKA
The anion gap is an artificial measure that is calculated by subtracting the total number of anions (chloride & HCO3–) from the total number of cations (Na+). There are lots of other anions and cations, however, those shown in brackets have the most significant influence, which is why other cations (e.g. K+) and anions (e.g. albumin, phosphate) are not used in the calculation of the anion gap.
Anion gap formula: Na+ – (Cl– + HCO3–)
triad of DKA
this all leads to potassium body depletion leading to dehydration
ketonaemia above 3mmol or significant ketonuiria more than 2 + on stick)
blood glucose above 11 or know diabetes mellitus
bicarb under 15 and or venous pH below 7.3
what is DKA
pathological process resulting from insulin deficiency due t bodies inability to metabolise glucose
newly diagnosed type 1 diabetics often present in DKA
triggers of DKA
Infection, such as flu or a urinary tract infection (UTI) Poor compliance with treatment plan, such as missing doses of insulin Injury or surgery Drugs such as steroids Binge drinking Using illegal drugs Pregnancy Menstruation
alcohol starvation diets such as anti epileptic diets medications toxins
what cause potassium to leave cells
hyperosmolarity
exercise
cell lysis
soft in caused by insulin and beta agonists
i.e. high glucose could be high potassium
so if no insulin more insulin in th e extracellular fluid so high levels of potassium
first ketone produced by the body and created from the breakdown of fatty acids and measure in urien
acetoacetate
most prevalent ketone in our body and the most energy efficient measured directly by blood ketone meter
beta-hydroxybutyrate
what ketone is virtually useless to the body and excreted through the breath measured with an breath meter
acetone
dka
patient with acidic blood
dehydrated
excess potassium in their blood
but a total body potassium deficit
kussmaul breathing
deep and laboured breathing pattern with tachypnoea
ketosis and acidosis and resp comp
what is the treatment for DKA
IV normal saline
metabolic treatment targets for DKA
reduction of the blood ketone conc by 0.5mmol
increase the venous bicarb by 3
reduce cap blood glucose by 3
maintain potassium between 4 and 5.5
As per consensus guidelines on DKA you administer normal saline 1L over 1 hour. You now need to administer insulin, How are you going to do this?
a fixed rate insulin infusion
this will suppress ketogensis and reduce the blood glucose
You repeat a venous blood gas after the second bag of intravenous fluids.
if the potassium drops low what has happened
cellular shift/uptake into the cells
You review Charlie the later in the day.
He has now had 5 litres of fluid including replacement of his potassium and been on a stable fixed rate of insulin for several hours.
Although he is no longer ketotic and his blood sugars below 10 consistently he continues to vomit and has been unable to eat anything
What would you like to do now?
Ng Tube
Continue IV fluids
Variable rate Insulin infusion
DKA treatment complications
hypokalaemia
hypoglycaemia
cerebral oedema
pulmonary oedema
Electrocardiography shows bradycardia,
a prolonged PR interval,
a prolonged QU interval,
ST-segment depression,
T wave inversion,
U waves best seen in the precordial leads (particularly in leads V2–lead 4),
and slurring of T waves into U waves (leads II and III)
John is a 57 year old man with very poorly controlled type 2 diabetes, His most recent HbA1C was 109. He is poorly compliant with treatment and has had bilateral leg amputations due to complications of diabetes.
He has presented to the emergency department with confusion abdominal pain, nausea and vomiting and on arrival his blood sugar is Hi (outside ref range). His ketones are 0.4 and his VBG reveals a pH of 7.36
hyperosmolar hyperglycaemic state
Phillip is a 62 year old man with a diagnosis of type 2 diabetes, he has recently been started on a new diabetes medication by his GP.
He presents to the emergency department with vomiting abdominal pain.
He has a normal glucose but is noted to be acidotic on his blood gas. On capillary ketone measurement his ketones are elevated
What is going on?
SGLT2 inhibitors - prevent reabsorption of glucose from primary urine at the Proximal renal tubules by targeting SGLT2 receptors
Hyperosmolar hyperglycaemic state
Hyperosmolar hyperglycaemic state (HHS) occurs in people with type 2 diabetes. Very high blood glucose levels (often over 40 mmol/L) develop as a result of a combination of illness, dehydration and an inability to take normal diabetes medication due to the effect of illness
how Is DKA different to HHS
DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia
DKA is hyperglycaemia
HSS - severe hyperglycaemia
DKA- metabolic acidosis
HSS - pH > 7.3
DKA - ketonemia ( beta hydroxybutyrate)
HSS - profound vol depletion
DKA- young T1DM
HSS - elderly T2DM
DKA more acute and HSS longer and protracted course of illness
