Diabetic ketoacidosis

Question 1

beta oxidation occurs where

Answer 1

Krebs cycle in mitochondria

insulin prevents fatty acids moving into mito

Question 2

what happens when you inhibit insulin like in type 1

Answer 2

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

Question 3

3 ketone bodies

Answer 3

acetone - volatile - gas - smell in breath
acetoacetate
beta-hydroxybrutyrate

Question 4

in dka what do we see

Answer 4

low insulin

no inhibiting of fatty acid transport

Question 5

low insulin in dka is

Answer 5

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

Question 6

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

Answer 6

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–)

Question 7

triad of DKA

this all leads to potassium body depletion leading to dehydration

Answer 7

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

Question 8

what is DKA

Answer 8

pathological process resulting from insulin deficiency due t bodies inability to metabolise glucose
newly diagnosed type 1 diabetics often present in DKA

Question 9

triggers of DKA

Answer 9

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

Question 10

what cause potassium to leave cells

Answer 10

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

Question 11

first ketone produced by the body and created from the breakdown of fatty acids and measure in urien

Answer 11

acetoacetate

Question 12

most prevalent ketone in our body and the most energy efficient measured directly by blood ketone meter

Answer 12

beta-hydroxybutyrate

Question 13

what ketone is virtually useless to the body and excreted through the breath measured with an breath meter

Answer 13

acetone

Question 14

dka

Answer 14

patient with acidic blood
dehydrated
excess potassium in their blood
but a total body potassium deficit

Question 15

kussmaul breathing

Answer 15

deep and laboured breathing pattern with tachypnoea

ketosis and acidosis and resp comp

Question 16

what is the treatment for DKA

Answer 16

IV normal saline

Question 17

metabolic treatment targets for DKA

Answer 17

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

Question 18

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?

Answer 18

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.

Question 19

if the potassium drops low what has happened

Answer 19

cellular shift/uptake into the cells

Question 20

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?

Answer 20

Ng Tube

Continue IV fluids

Variable rate Insulin infusion

Question 21

DKA treatment complications

Answer 21

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)

Question 22

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

Answer 22

hyperosmolar hyperglycaemic state

Question 23

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?

Answer 23

SGLT2 inhibitors - prevent reabsorption of glucose from primary urine at the Proximal renal tubules by targeting SGLT2 receptors

Question 24

Hyperosmolar hyperglycaemic state

Answer 24

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

Question 25

how Is DKA different to HHS

Answer 25

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