Non-vascular complications of DM

Question 1

What is DKA?

Answer 1

• an acute metabolic complication of diabetes
• an absolute insulin deficiency
• potentially fatal if not tx properly
• characterized by biochemical triad of hyperglycemia, ketonemia, and anion gap metabolic acidosis
• usually evolves rapidly, over a 24 hr period

Question 2

Pathophys of DKA?

Answer 2

• reduction in net effective concentration of circulating insulin
• elevation of counter regulatory hormones: glucagon (stimulates free FAs into ketones), cortisol, GH
• hyperglycemia: osmotic diuresis (water and electrolyte loss) and dehydration

Question 3

process of DKA?

Answer 3

• beta cell dysfunction in pancreas seen in type 1 DM leads to insulin deficiency which results in:
• resultant elevation in glucagon - free fatty acid conversion to ketones - ketonuria
• inability to drive glucose into cells which leads to cell starvation and breakdown of fats for energy - leads to free fatty acid conversion to ketones - to ketonuria

Question 4

Precipitating factors of DKA?

Answer 4

• most common events associated with DKA:
  inadequate insulin therapy, infection (pneumonia, and UTI)
• other factors include: severe dehydration, acute major illnesses (MI, CVA, pancreatitis)
• new onset type 1 diabetes
• drugs that affect carbohydrate metabolism

Question 5

Clinical presentation of DKA?

Answer 5

• thirst, polydipsia
• polyuria
• N/V
• abdomincal pain
• weakness
• fatigue
• anorexia
• tachycardia
• orthostatic hypotension
• poor skin turgor
• dry skin and mucous membranes
• Kussmaul’s respirations (acidotic response)
• fruity breath (ketones)
• altered mental status or coma
• hypothermia

Question 6

Lab findings in DKA?

Answer 6

• blood glucose: 250-800
• serum osmolality normal to high
• serum Na+ normal to low (130-145) pulling Na into vasculature and urinating it out
• serum K+ high (greater than 5, glucose is going to pull K+ out of cells)
• serum bicarb low, less than 20
• serum anion gap is greater than 12 meq/L
• pH is less than 7.3, acidotic
• ketones + positive

Question 7

What is a hyperosmolar hyperglycemic state (HHS)?

Answer 7

• occurs almost exclusively in type 2
• elderly and physically impaired
• limited access to free water

Question 8

How is HHS distinguished from DKA?

Answer 8

• severe hyperglycemia (greater than 600)
• hyperosmolality (induced hepatic outpt of glucose -kidneys can’t get rid of glucose fast enough)
• develops more insidiously with polyuria, polydipsia, and wt loss, often persisting for several days before hospital admission
• greater degree of dehydration: relative absence of acidosis and ketones, mortality rates 5-20%

Question 9

Causes of HHS?

Answer 9

• catabolic stress
• infection
• non-compliance
• drugs

Question 10

Clinical presentation of HHS?

Answer 10

• polyuria
  -polydipsia
• wt loss
• vomiting
• dehydration
• weakness
• mental status changes
• slower progression
• tachycardia
• hypotension
• severe dehydration: dry skin and mucous membranes, and extreme thirst
• Neuro signs (not in DKA):
  lethargy, sensory impairment, seizures, hyperthermia

Question 11

HHS lab findings?

Answer 11

• blood glucose greater than 600 (higher than in DKA)
• serum osmolality: greater than 320
• serum Na+ normal to high (135-145)
• serum K+ normal (4-5)
• serum bicarb: greater than 20 (high)
• pH greater than 7.3
• ketones are negative
• can be complicated by thromboembolic events arising because of high serum osmolality
• prognosis less favorable than DKA

Question 12

Tx for DKA and HHS?

Answer 12

• medical emergencies that require prompt recognition and management
• initial assessment: ABC status, mental status, volume status
• IV fluid and electrolyte replacement: slower rate and greater volume needed for HHS, insulin replacement starts after rehydration is in progress
• insulin therapy (want to make sure K is higher than 3.3 before insulin, if not insulin will push K back into cell and pt becomes hypokalemic).

Question 13

Differences in HHS and DKA?

Answer 13

• DKA and HHS differ clinically according to presence of ketoacidosis and usually degree of hyperglycemia
• significant overlap b/t DKA and HHS has been reported in more than 1/3 of pts
• in HHS: amino acids are being broken down and used in gluconeogenesis, and glycogenesis is occuring this leads to hyperglycemia and osmotic diuresis (dehydration)
• in DKA: adipose tissue releases free fatty acids and liver breaks them down into keton bodies and this leads to hyperketonemia - decreased alkaline buffer - acidosis

Question 14

Where is hypoglycemia seen the most?

Answer 14

• in type 1 diabetics, especially in pts receiving intensive therapy
• plasma glucose concentrations may be less than 50 to 60 mg/dL as much as 10% of the time
• type 1’s suffer an average of 2 episodes of symptomatic hypoglycemia per week, one episode of severe hypoglycemia per year
• hypoglycemia is less frequent in type 2
• overall event rate for severe hypoglycemia (requiring assistance of another individual) in insulin tx type 2 is approx 30% of that in type 1

Question 15

Classification of hypoglycemia?

Answer 15

• functional: fasting and postprandial (reactive)

Question 16

Causes of hypoglycemia?

Answer 16

• insulin injections
• oral hypoglycemic agents
• hepatic and renal dysfunction
• malnutrition
• cahnging of injection site
  hypoglycemia not in diabetics: alcohol, insulinoma, wt loss and infection

Question 17

Clinical presentation of hypoglycemia?

Answer 17

• rapid onset and progression
• neurogenic sxs: catecholamine-mediated/adrenergic: tremor, palpitations, and anxiety/arousal
  acetylcholine-mediated/cholinergic: sweating, hunger and paresthesias
• neuroglycopenic sxs: cognitive impairment, behavioral changes, psychomotor abnormalities, and at very low plasma glucose, seizure and coma

Question 18

Signs of hypoglycemia?

Answer 18

• diaphoresis
• pallor
• tachycardia
• elevated blood pressure

Question 19

What is hypoglycemia unawareness in diabetes?

Answer 19

• absent sxs of hypoglycemia, which is thought to be the result of reduced of sympathoadrenal, predominantly sympathetic neural, responses to a given degree of hypoglycemia caused by:
• loss of autonomic warning: recent antecedent hypoglycemia, prior exercise, or sleep
• autonomic neuropathy: epi response diminished or lost
• meds: beta blockers

Question 20

Management of hypoglycemia?

Answer 20

outside hospital: oral, SQ/IM

hospital: IV, 1 amp of D50 (20-50 ml)

Question 21

What is non-diabetic hypoglycemia? and what is it based upon?

Answer 21

• based upon presence of whipple’s triad
• sxs and signs consistent with hypoglycemia, a low plasma glucose at time of sxs, and resolution of those signs and sxs after raising the plasma glucose
• in individuals w/o diabetes hypoglycemia is most often due to a drug, less common causes include critical illness, endocrine deficiency, or a nonislet cell tumor
• endogenous hyperinsulinism or accidental, surreptitious or malicious hypoglycemia are more likely in well appearing pt

Question 22

What is surreptitiously induced hypoglycemia?

Answer 22

factitious hypoglycemia occurs secondary to surreptitious use of insulin or insulin secretagogues. The term factitious hypoglycemia has been used in medical palance to imply covert human activity

• insulin and C peptide are secreted in an equimolar fashion, as a result, the plasma concentrations of these 2 peptides parallel each other in pts with endogenous hyperinsulinemia
• in contrast, the plasms concentrations of 2 peptides are inversely related in pts with exogenous insulin factitious hypoglycemia: plasma insulin will be high while C peptide is low
• this observation applies to both nondiabetic pts and to those with type 2 DM
• pts with type 1 diabetes are characteristically severely insulin deficient and have low or undetectable plasma concentrations of C peptide

Question 23

What is hypoglycemia coma?

Answer 23

• recovery from hypoglycemia may be delayed, because of cerebral edema
• unconsciousness lasting more than 30 minutes after plasma glucose is corrected is called post-hypoglycemic coma

Question 24

Tx for hypglycemic coma?

Answer 24

• IV mannitol for cerebral edema
• glucocorticoids (dexamethasone)
• or both can be used along with maintenance of normal plasma glucose levels

Question 25

What is the dawn phenomenon?

Answer 25

high morning blood glucose
- between 5 and 9 am: counter-regulatory hormones are released

• don’t have hypoglycemia at all, just hyperglycemia in the morning

Question 26

What is the somogyi effect?

Answer 26

• hypoglycemia begets hyperglycemia
• rebound hyperglycemia: iatrogenic, too much insulin because in middle of night will have low sugars and in morning sugars will rebound and will be high, the body is overcompensating for low blood sugars and hormones cause an increase in blood sugar

Question 27

How do you tell the difference between somogyi and dawn phenomenon?

Answer 27

• to sort out whether an early morning hifh blood sugar level is caused by dawn phenomenon or somogyi effect, check blood sugar levels around 2 to 3 am for several nights
• if blood sugar level is low at 2 to 3 suspect somogyi effect
• if blood sugar level is normal or high at 2 to 3 its likely the dawn phenomenon

Question 28

Triad of DKA?

Answer 28

• hyperglycemia
• anion gap metabolic acidosis
• ketonemia

Question 29

Most common precipitating event ID in pts with DKA or HHS?

Answer 29

• infection or inadequate insulin therapy

Question 30

What should be included in the intial eval of pts with hyperglycemic crises?

Answer 30

• assessment of cardiorespiratory status
• volume status
• mental status