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MS2 Endocrine > 10/15- Acute Complications of Diabetes > Flashcards

10/15- Acute Complications of Diabetes Flashcards

1
Q

What are some acute complications of diabetes?

A
  • Insulin-induced hypoglycemia
  • Diabetic ketoacidosis
  • Hyperosmolar hyperglycemic nonketotic state (HONK)
  • Lactic acidosis
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2
Q

What are some hypoglycemic reactions?

  • Neurogenic
  • Neuroglycopenic
A

Neurogenic (responses of S/PS systems):

  • Sweaty
  • Hungry
  • Tingling
  • Shaky/tremulous
  • Heart Pounding
  • Nervous/anxious

Neuroglycopenic (responses of central NS):

  • Warm
  • Weak
  • Difficulty thinking/confused
  • Tired/drowsy, faint, dizzy
  • Difficulty speaking
  • Blurred vision
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3
Q

What are counterregulatory responses (substances) to hypoglycemia?

A
  • Glucagon* (fastest)
  • Cortisol
  • Growth hormone (slowest)

*(Normally low insulin levels correspond to higher glucagon, which would seem to be protective about hypoglycemia in diabetes… but for some reason, not the case. No surge; it’s an acute response)

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4
Q

What is Diabetic Ketoacidosis?

A

Uncontrolled diabetes leading to:

1. Hyperglycemia:

  • Osmotic diuresis
  • Volume depletion
  • Dehydration

2. Ketogenesis: anion-gap acidosis

3. Other metabolic changes

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5
Q

Difference between volume depletion and dehydration?

A
  • Volume depletion: loss of isotonic fluid
  • Gauged pretty much only clinically: blood pressure, urine production, orthostatic hypotension, mental status, skin turgor…
  • Dehydration: loss of water; hypertonic serum
  • Measured by serum sodium or serum osmolarity
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6
Q

Describe the liver and adipocyte collaborate to produce ketoacidosis?

A
  • Insulin fails to restrain storage of fatty acids in adipocyte
  • FAs released and go to liver
  • Liver has high oxidation and ketone production (faster than ability to esterify fatty acids)

Depends on 2 things:

  • Complete lack of insulin
  • Excess of glucagon
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7
Q

What 2 things are necessary for the regulation of ketogenesis?

A

1. Insulin deficiency

  • Activates lipolysis (fat cells)
  • Increased plasma FFA concentration
  • Increased liver fatty acids
  • Accelerated ketogenesis

2. Glucagon excess

  • Increased hepatic carnitine content with decreased malonyl CoA content (removes inhibition from –)
  • Activation of CPT-1
  • Accelerated ketogenesis
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8
Q

T/F: Massive excess of glucagon, cortisol, GH, and catecholamines (due to increased stress) can also push pt into DKA despite normal (not low) insulin levels

A

False- really never happens

  • If someone comes in with DKA, suspect sudden drop in insulin rather than acute rise in other factors
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9
Q

What are etiologies of DKA?

A

86% of DKA episodes have an identifiable precipitating factor:

  • Alcohol
  • Drugs
  • Infection
  • MI/stroke
  • Trauma
  • Pregnancy
  • Treatment errors
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10
Q

How do trauma, stroke, and pregnancy contribute to DKA?

A

Stress levels (?)

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11
Q

Do people with Type I or Type II DM get DKA more commonly?

A
  • Type I are morel likely to get DKA in black and white populations
  • Type II more commonly get DKA in Hispanic and Asian
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12
Q

What is the cause of hyperglycemia in DKA?

A

Insulin deficiency leading to:

  • Increased hepatic glucose production
  • Decreased peripheral glucose utilization
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13
Q

What are the effects of hyperglycemia in DKA?

A

Osmotic effects

  • H20 from ICF to ECF
  • Osmotic diuresis ECF volume

Renal loss of water > electrolytes

  • Volume depletion
  • Some degree of dehydration
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14
Q

What causes metabolic acidosis in DKA?

A
  • Excess acetoacetic acid and β-OH butyric acid production (ketones)
  • Diminished renal excretion of H+
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15
Q

What are effects of metabolic acidosis in DKA?

A

Buffer of protons and bicarb increases CO2 and H2O production, but ultimate correction of H excess depends on:

  • Oxidation of AAA + βOHB - Renal excretion of H+
  • Exchange of H+ for Na+
  • Ammonia -> ammonium
  • Loss of electrolytes in urine
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16
Q

What causes water and electrolyte imbalance in DKA?

A
  • Osmotic diuresis
  • Vomiting
  • Increased aldosterone
  • ICF – ECF shift (K+3PO4)
17
Q

What are the effects of water and electrolyte imbalance in DKA?

A

10% body weight lost as fluid

  • 50% extracellular
  • 50% intracellular

Significant loss of extra- and intracellular electrolytes

  • K
  • Na
  • PO4
18
Q

What are symptoms of DKA? Signs?

A

Symptoms:

  • Nausea/vomiting
  • Polyuria/polydipsia
  • Abdominal pains
  • Mental changes (lethargy to near-coma)

Signs:

  • “Fruity” breath (due to acetone)
  • Kussmaul’s respirations (rapid, deep breaths)
  • pH of less than 7.2 (sharp inflection point)
  • Signs of volume depletion (tachycardia, orthostatic hypotension)
  • Signs related to precipitating factors (infection, MI, trauma, etc.)
19
Q

What are lab tests that may be done for the diagnosis of DKA?

A
  • Elevated blood glucose
  • pH < 7.35
  • Low HCO3-
  • High anion gap
  • Positive serum ketones!
20
Q

How to calculate corrected serum sodium concentration? Why do you want this?

A
  • Corresponds to initial state of sodium depletion/volume depletion (?)
21
Q

How to calculate anion gap?

What is normal?

Why do you want this?

A

AG = Na - (Cl + HCO3)

Normal value = 8-12 (+/-2)

  • This can tell you if something else is going on (simple or complex acid-base disorder)
22
Q

What is the treatment for DKA?

A
  • Mainly isotonic fluid!!
  • Insulin!!
  • Reverses ketosis and acidosis
  • Potassium
  • HyperK due to lack of insulin, but overall body is actually K-depleted (will be seen when volume corrected)
  • MONITOR
  • very rapidly; don’t stop insulin when glucose is approaching normal, just add glucose drip (takes longer to correct ketogenesis and acidosis)
  • Normalization is marked by disappearance of ketones or normalization of pH
  • Treat precipitating cause(s)
23
Q

What is “HONK”

  • Characteristics
A

Aka HHNS

  • Hyperosmolar hyperglycemic nonketotic state

Characteristics:

- Extreme hyperglycemia

  • Poorly treated/undetected diabetes
  • Renal insufficiency
  • Age/mental obtundation -> decreased oral fluids

- Absence of ketosis:

  • Insulin is not totally deficient

- Severe dehydration and volume depletion

- Coexisting chronic illnesses

- High mortality

24
Q

What is the critical calculation that should be done if you suspect HONK? Why?

  • How to calculate
  • Normal values
  • HONK values
A

Serum osmolality

  • Grade of consciousness of patient is quite related to serum osmolality
  • Mortality is in turn related to the grade of consciousness

Calculation: 2Na + glucose/18 + BUN/2.8

  • Normal is 290-300 mOsm
  • HONK is >> 300 mOsm
25
Q

What is the treatment for HHNS/HONK?

A

Mainly want to correct fluid-volume situation (first!)

  • Isotonic and hypotonic fluids
  • Correct volume status first (normal saline); although even normal saline may be somewhat hypotonic compared to their blood
  • Correct serum osmolality (hypernatremia and dehydration) next; do so very carefully to avoid bad brain effects

Then:

  • MONITOR
  • Electrolyte replacement
  • Insulin
  • Treatment
26
Q

In what settings does lactic acidosis occur?

A
  • With hypoxemia/shock (“Type A”)
  • Without hypoxemia/shock (“Type B”)
  • Illnesses
  • Toxins
  • Hereditary
  • Miscellaneous
27
Q

What diabetic conditions may contribute someone to developing lactic acidosis?

A
  • Hypotension (acute GI hemmorrhage, sepsis, pancreatitis
  • Less organ perfusion -> hypoxia -> anaerobic respiration -> lactic acid
  • Arterial oxygen desaturation
  • (same mechanism as above)
  • Decreased cardiac output
  • Regional hypoperfusion
  • Drugs (Metformin)
28
Q

What is the upper limit of normal of lactic acid?

A

1 mmol (after intense exercise… normally much lower)

29
Q

What is the most concerning ASE of Metformin?

A

Lactic acidosis

30
Q

What part of respiration is diverted/altered that increases lactic acid?

A
  • Normally, at the end of glycolysis, pyruvate goes into the citric acid cycle
  • If oxygen depleted, converted instead to lactate (this allows regenration of NAD and some slight energy production with continued glycolysis)
31
Q

What is the treatment for lactic acidosis?

A

1. Correct hypoxia (most important)

  • Give oxygen
  • Fix problem (e.g. ischemic liver)

2. Remove toxins

3. Bicarbonate (cautiously!!)

4. Dichloroacetate

32
Q

What is the risk of giving bicarbonate in lactic acidosis?

A
  • Heart not pumping well; less O2 delivery to tissues, which are depending on lactic acid production in respiration
  • Increase amount of CO2 to breath out in lungs and help compensate in acidosis (removes H+ and HCO3- substrtes)
  • CO2 builds up in cells due to excess production, causing a drop in pH and resultant decrease in contraction/function
  • Could make heart function even worse by giving more bicarb (more CO2)

MS2 Endocrine (25 decks)

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