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YEAR 3 - SEMESTER 2 > Case 11 - DKA > Flashcards

Case 11 - DKA Flashcards

1
Q

HHS is more common in Type _ Diabetes

DKA is more common in Type _ Diabetes

A

HHS is more common in Type 2 Diabetes

DKA is more common in Type 1 Diabetes

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2
Q

Name 5 triggers of DKA (the 6 i’s)

A 
Infection
Infarction 
Insulin withdrawal
Intoxication
Intercurrent illness
Iatrogenic (e.g. corticosteroids)
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3
Q

Describe the pathophysiology of polyuria, polydipsia, and glycosuria in DKA

A

Absolute insulin deficit –> Glucose cannot enter cells –> cells starved of glucose, body starts releasing catabolic hormones to try and increase BGL concentration –> inc. gluconeogenesis + glycogenolysis, decreased glycolysis –> polyuria, polydipsia, glycosuria

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4
Q

What leads to ketoacidosis? Describe the pathophysiology.

A

Glucose not entering cells –> lipolysis to use fat as an energy source –> free fatty acids (FFAs) released from adipose tissue –> FFAs undergo ketogenesis in the liver –> ketones released –> fuck shit up

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5
Q

What is the typical biochemistry finding in DKA?

A

Metabolic acidosis with elevated anion gap

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6
Q

What is the PATHOPHYSIOLOGY behind the typical biochemistry finding in DKA?

A

Ketones released after FFA metabolism in the liver –> presence of 2 acidic ketones (acetoacetic acid & beta-hydroxybutyric acid) –> serum bicarbonate consumed to act as a buffer –> HIGH ANION GAP METABOLIC ACIDOSIS (HAGMA)

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7
Q

How does DKA cause hyperkalemia?

A

Ketone bodies give off protons (H+) –> acidosis –> H+ pumped INTO cells whilst K+ is pumped OUT –> K+ accumulates in ECF –> insulin drives Na+ / K+ ATPase pumps, so the lack of insulin means there’s no driving force to bring K+ BACK INTO the cell –> decreased total body K+ and normal or paradoxically INCREASED SERUM K+

https://www.youtube.com/watch?v=jCf7W1U4JKE

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8
Q

List 3 consequences of hyperkalemia

A
  • Arrhythmias (–> palpitations, chest pain)
  • Ileus (–> abdominal pain)
  • Muscles weakness
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9
Q

Describe the characteristic DKA presentation (separate into those shared by DKA & HHS vs. those that are specific to DKA)

A

DKA SPECIFIC: RAPID (<1 day onset), fruity breath (acetone breath), abdo pain, Kussmaul breathing

DKA & HHS: polyuria, polydipsia, recent weight loss, NV, dehydration, altered mental status (drowsiness, confusion, coma)

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10
Q

List 5 important investigations used to assess a hyperglycaemic cr.isis (DKA & HHS)

A
  1. BGL
  2. Ketones (urine & serum)
  3. ABG
  4. BMP
  5. Serum osmolality
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10
Q

List 5 important investigations used to assess a hyperglycaemic crisis (DKA & HHS)

A
  1. BGL
  2. Ketones (urine & serum)
  3. ABG
  4. BMP
  5. Serum osmolality
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11
Q

Differences in the following investigation findings in DKA vs. HHS:

  1. BGL
  2. Ketones (urine & serum)
  3. ABG
  4. BMP
  5. Serum osmolality
A
  1. BGL: in DKA is typically <33.3mmol/L. In HHS typically >33.3mmol/L
  2. Ketones (urine & serum): in DKA moderate-severe ketonuria. In HHS little to no ketonuria.
  3. ABG: in DKA pH<7.30. In HHS ph>7.30
  4. BMP: in DKA will be metabolic acidosis with high anion gap. HHS has normal anion gap
  5. Serum osmolality: normal in DKA. High in HHS.
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12
Q

DKA is the diagnosis in patients with type 1 diabetes who have __________, _________, and ___ anion gap metabolic ________ with decreased ________!

HHS is the diagnosis in type 2 diabetes patients with ___________ and ______________.

A

DKA is the diagnosis in patients with type 1 diabetes who have hyperglycemia, ketonuria, and high anion gap metabolic acidosis with decreased bicarbonate!

HHS is the diagnosis in type 2 diabetes patients with HYPERGLYCAEMIA and HYPEROSMOLALITY

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13
Q

Why is DKA treatment (fluids, K+, insulin) administered gradually? Which complication does this prevent?

A

Cerebral oedema (more common in paediatrics)

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14
Q

The most important findings in DKA are…

DDKAA

A

DDKAA

Delirium/psychosis
Dehydration
Kussmaul respirations
Abdominal pain / nausea / vomiting 
Acetone (fruity) breath
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15
Q

What is the treatment protocol for DKA?

A
  1. Low-dose short-acting IV insulin
  2. IV saline
  3. Electrolyte (particularly K+) repletion once insulin is started
  4. IV bicarbonate (in severe cases of deficiency: <10mmol/L)
  5. Identify and treat underlying cause
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16
Q

When should K+ repletion be initiated BEFORE insulin?

A

When potassium < 3.3mEq/L, give potassium chloride (KCl) before starting insulin

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17
Q

Potassium replacement is initiated immediately if the serum potassium is ____ mEq/L as long as there is adequate urine output

A

Potassium replacement is initiated immediately if the serum potassium is <5.3 mEq/L as long as there is adequate urine output

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18
Q

Low-dose intravenous (IV) insulin should be administered to all patients with moderate-severe DKA who have a serum potassium ≥ ___ mEq/L.

If the serum potassium is less than ___ mEq/L, insulin therapy should be delayed until K+ replacement has begun and the serum concentration has increased.

A

Low-dose intravenous (IV) insulin should be administered to all patients with moderate-severe DKA who have a serum potassium ≥ 3.3 mEq/L.

If the serum potassium is less than 3.3 mEq/L, insulin therapy should be delayed until K+ replacement has begun and the serum concentration has increased

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19
Q

Why is insulin administration delayed in patients with a serum K+ of <3.3mEq/L

A

Insulin will only deplete serum K+ further by driving it into the cells

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20
Q

Why is insulin administration delayed in patients with a serum K+ of <3.3mEq/L

A

Insulin will only deplete serum K+ further by driving it into the cells (Na+/K+ ATPase pumps on cells require insulin to work)

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21
Q

What is the pathophysiology behind kussmaul breathing?

A

Increased protons (H+) in the blood –> stimulates peripheral chemoreceptors –> info travels via vagus & glossopharyngeal nerve to CNS –> stimulates increased respiratory rate in an attempt to breathe off more CO2 and bring the pH back up

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22
Q

What is the pathophysiology behind fruity/acetone breath?

A

Increased protons (H+) in the blood –> stimulates peripheral chemoreceptors –> info travels via vagus & glossopharyngeal nerve to CNS –> stimulates increased respiratory rate in an attempt to breathe off more CO2 and bring the pH back up –> breathing off KETONES in addition to CO2

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23
Q

What is responsible for the reflex tachycardia and sweating seen in DKA?

A

Dehydration –> decreased blood volume –> activation of baroreceptors –> increased SNS activity –> tachycardia, diaphoresis

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24
Q

Why is there no ketone production (and hence no metabolic acidosis & ketonuria) in HHS?

A

A small amount of insulin is still present in the body, inhibiting LIPOLYSIS.

If ketones are detected in a patient with HHS it’s likely due to another mechanism such as starvation.

25
Q

Why does HHS progress more slowly than DKA?

A

Only people with T2DM can develop HHS. This is because there is a RELATIVE insulin deficiency (not absolute), so the small amount of insulin can still allow glucose to enter cells.

Acute hyperglycemia progresses more slowly and serum glucose is significantly elevated compared with patients with type 1 diabetes in DKA
Diabetic ketoacidosis.

26
Q

What is the characteristic manifestation of HHS and why?

A

MARKED dehydration due to hyperglycaemia and osmotic diuresis

27
Q

Ketone levels should be ordered in all patients with high anion gap metabolic acidosis to evaluate for…?

A

Ketone levels should be ordered in all patients with high anion gap metabolic acidosis to evaluate for euglyceemic DKA.

.

28
Q

Describe the following biochemistry findings in DKA and HHS

  1. Sodium
  2. Potassium
  3. Phosphorous
  4. Magnesium
  5. BUN & creatinine
A
  1. Sodium: hyponatremia
  2. Potassium: normal or high in DKA despite total body deficit
  3. Phosphorous: falsely elevated despite total body deficit
  4. Magnesium: typically low (due to osmotic diuresis)
  5. BUN & creatinine: elevated (suggests AKI due to dehydration)
29
Q

What is the criteria for resolution of DKA?

A

BGL <11.1mmol/L with AT LEAST 2 of the following:

  • pH >7.30
  • Serum bicarbonate >15mEq/L
  • Anion gap <12mEq/L
30
Q

What is the criteria for resolution of HHS?

A
  • Normal mental status

- Serum osmolality <320mOsm/kg

31
Q

How can alcohol perpetuate hypoglycaemia?

A

The liver is responsible for releasing glucose at a steady rate.

  • Alcohol reduces glycogen breakdown and glucose release
  • Alcohol also impairs gluconeogenesis
32
Q

What is the dominant ketoacid in alcoholic ketoacidosis? Why might this be an issue for diagnosis?

A

The dominant ketoacid is BETA-HYDROXYBUTYRATE. This is not detected by urine dipstick and serum measurements must be taken

33
Q

How does management of alcoholic ketoacidosis vary from DKA?

A

ALCOHOLIC KETOACIDOSIS: NO INSULIN. Just fluid resus w/ saline & dextrose

34
Q

What effect does acidosis have on O2 saturation?

A

Acidosis increases O2 offloading from Hb

35
Q

Name 3 physiological systems that are important for maintaining pH, and state what they are effective against

A
  1. Buffering: both
  2. Respiratory compensation: metabolic
  3. Renal compensation: respiratory
36
Q

Name 2 important buffers in the ECF and ICF

A

EXTRACELLULAR FLUID: HCO3-, ionised plasma proteins (e.g. albumin)

INTRACELLULAR FLUID: Hb, ionised proteins

37
Q

Describe the respiratory compensatory mechanism

A

Regulation of carbonic acid concentration through respiratory rate and depth:

More CO2 in blood –> reacts w/H2O to form carbonic acid (H2CO3) –> decreased blood pH –> increased depth and rate of respirations to try and blow off more CO2 –> loss of CO2 reduces H2CO3 levels –> adjusts pH back to normal levels

https://open.oregonstate.education/aandp/chapter/26-4-acid-base-balance/

38
Q

Describe the renal compensatory mechanism

A

Increased CO2 in body –> converted into carbonic anhydrase (H2CO3) –> H2CO3 circulates around the body –> reaches renal tubular cells, which convert it into HCO3- and H+ ions –> H+ excreted in urine, HCO3- retained in body

39
Q

Give an example of a chronic condition that requires renal compensation and describe how this affects the compensatory mechanisms

A

EXAMPLE: COPD

CO2 retention –> converted into carbonic anhydrase (H2CO3) –> H2CO3 circulates around the body –> reaches renal tubular cells, which convert it into HCO3- and H+ ions –> H+ excreted in urine, HCO3- retained in body

In the short-term, this won’t affect HCO3- levels but chronic conditions may cause a rise in bicarbonate levels

40
Q

List the 3 pH compensatory mechanisms and their speed of onset

A
  1. Buffering: immediate onset
  2. Respiratory: onset minutes-hours (this has the largest capacity)
  3. Renal: days
41
Q

Describe the ABG findings in an acute metabolic acidosis

A
  • Low pH
  • Normal CO2
  • Low HCO3-
42
Q

Describe the ABG findings in an acute RESPIRATORY acidosis

A
  • Low pH
  • High CO2
  • Normal HCO3-
43
Q

Describe the ABG findings in a CHRONIC RESPIRATORY acidosis

A
  • Low pH
  • High CO2
  • High HCO3- (due to chronic renal compensation)
44
Q

Describe the ABG findings in a mixed respiratory/metabolic acidosis

A
  • Low pH
  • High CO2
  • Low HCO3-
45
Q

Describe the causes of metabolic acidosis

A
  1. TOO MUCH ACID: increased production (e.g. sepsis), decreased excretion (e.g. renal tubular acidosis), ingestion (rare)
  2. NOT ENOUGH bicarbonate: increased loss (e.g. diarrhoea), decreased production (e.g. renal problems)
46
Q

Which additional measurement helps determine the CAUSE of acidosis in the body?

A

Anion gap

  • High anion gap metabolic acidosis (HAGMA)
  • Non anion gap metabolic acidosis
47
Q

4 causes of HAGMA

A
  1. Lactic acidosis (shock of any cause) - due to poor O2 delivery to tissues, requiring anaerobic respiration (e.g. shock, MI, PE)
  2. Ketoacidosis (DKA)
  3. Renal (AKI - high urea)
  4. Toxins (metformin, methanol, iron, CO, cyanide)
48
Q

4 causes of normal anion gap metabolic acidosis (NAGMA)

A
  1. GI causes (vomiting, diarrhoea)
  2. Cl- excess (too much saline)
  3. Diuretics (acetazolamide)
  4. Addison’s disease
  5. Renal (bicarbonate loss)
49
Q

4 causes of respiratory acidosis

A
  • Airway obstruction
  • Chest wall abnormalities (e.g. flail chest)
  • Pulmonary (e.g. severe COPD, severe pulmonary oedema, pulmonary fibrosi)
  • CNS (e.g. head trauma, respiratory depressants such as alcohol + opioids)

can think about Respiratory acidosis anatomically: CNS (most acute), pulmonary (most chronic)…etc.

50
Q

How is K+ level corrected in states of acidosis?

A

0.5mmol/L of K+ for each 0.1 decrease in pH

EXAMPLE: someone has a pH of 6.9 with a K+ level of 5.5
= 5.5 - (0.5 x 5)
= 3.0

Actually low total body potassium

51
Q

In alcoholic ketoacidosis, BGL rarely rises above…

A

In alcoholic ketoacidosis, BGL rarely rises above 15.3mmol/L

52
Q

How are sodium levels corrected in DKA?

A

Corrected Na+ can be approximated by adding 2 mEq/L to the plasma Na+ concentration for each 5.5 mmol/L increase above normal in glucose concentration

53
Q

Why do sodium levels require correction in DKA?

A

Increase in plasma osmolality created by hyperglycaemia draws water out of the cells and dilutes Na+ concentration

54
Q

Why is K+ administered even though the patient’s K+ levels may be above normal range?

A

Will become hypokalemic if you don’t administer K+ because it’s all rushing back into the cells once insulin is administered

55
Q

Why is a lactate level useful in evaluating DKA?

A

Remember the 5 i’s of DKA.

If lactate is normal, it helps rule out some of the causes (e.g. infarction, ischaemia) which would cause increased anaerobic respiration and hence raise lactate levels

56
Q

What are ‘basal’ and ‘bolus’ insulin regimes?

A

BASAL = background insulin. Long/intermediate-acting insulin that is injected 1-2 times per day. Helps keep blood glucose levels at consistent levels during periods of fasting.

BOLUS = short-acting insulin, taken before, during, or after a meal to keep BGL in control after a meal.

57
Q

Why does severe (alcohol-induced) ketoacidosis only occur after alcohol consumption has ceased?

A

During active ethanol ingestion, ethanol METABOLISM generates acetate and acetyl-CoA, which inhibits lipolysis and delivery of fatty acids to the liver

57
Q

Why does severe (alcohol-induced) ketoacidosis only occur after alcohol consumption has ceased?

A

During active ethanol ingestion, ethanol METABOLISM generated acetate and acetyl-CoA, which inhibits lipolysis and delivery of fatty acids to the liver

58
Q

Name 3 illnesses that can lead precipitate DKA and explain why

A

Infections: UTI, pneumonia, cellulitis
Infarction: MI

Stress –> increased SNS –> release of epinephrine, norepinephrine, and glucagon –> increased INSULIN DEMAND (and these 3 hormones can also generate lipolysis pathway) –> DKA

59
Q

How can corticosteroids precipitate DKA?

A

Corticosteroids raise BGL –> increased insulin demand

YEAR 3 - SEMESTER 2 (12 decks)

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