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My Endocrine > Non-vascular Complications of DM > Flashcards

Non-vascular Complications of DM Flashcards

1
Q

DKA

A

absolute insulin deficiency

biochemical triad of hyperglycemia, ketonemia, and acidosis

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2
Q

DKA usually develops over how much time?

A

24 hrs

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3
Q

What is elevated as counter-regulatory hormones in DKA?

A

glucagon, cortisol, GH

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4
Q

Hyperglycemia in DKA leads to dehydration by

A

osmotic diuresis

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5
Q

How does DKA work to produce ketones?

A

Insulin deficiency causes elevation in glucagon which causes free fatty acids to break down to ketones

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6
Q

Most common reasons for DKA

A

-inadequate insulin therapy or infection (pneumonia or UTI)

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7
Q

Other factors causing DKA

A

severe dehydration, MI, cerebrovascular accident, pancreatitis, new onset type 1 DM, drugs affecting carb metabolism (steroids, thiazide diuretics, cocaine)

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8
Q

Signs and Symptoms of DKA

A

same as hyperglycemia + orthostatic hypotension, poor skin turgor, dry skin and mucous membranes (because of dehydration), Kussmaul respirations, fruity breath (from ketones), hypothermia, altered metal status

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9
Q

Labs in DKA

A 
BG=250-800
Serum osmolality= normal to high
Serum Na+= normal to low (130-145)
Serum K+= high (>5)
Serum Bicarb= low (10
pH= < 7.3 acidotic
Ketones=positive
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10
Q

Who does hyperosmolar hyperglycemic state (HHS) happen in?

A

type 2 DM, elderly and physically impaired, limited access to free water

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11
Q

How is HHS different than DKA?

A 
severe hyperglycemia= >600
hyperosmolality
can go several days before needing to be hospitalized
greater degree of dehydration
relative absence of acidosis and ketones
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12
Q

Causes of HHS

A

catabolic stress, insufficient water intake, excess water loss, high sugar intake, drugs

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13
Q

Signs and Symptoms of HHS

A

same as DKA without Kussmaul, fruity breath, and hypothermia

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14
Q

Labs of HHS

A 
Blood glucose= > 600
Serum osmolality= >320
Serum Na+ = normal to high    (135-145)
Serum K+= - normal  (4-5)
Serum Bicarb= >20 (high)
pH= > 7.3
Ketones – negative
--Can be complicated by thromboembolic events arising because of the high serum osmolality.
--Prognosis less favorable than DKA.
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15
Q

Treatment of DKA and HHS

A

medical emergencies!

  • initially: ABC (airway, breathing, and circulation), mental status, and volume status
  • IV fluid and electrolyte replacement (slower rate and greater volume for HHS)
  • insulin therapy after rehydration is in progress
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16
Q

What are the two main clinical differences in DKA and HHS?

A

-ketoacidosis and degree of hyperglycemia

17
Q

Is hypoglycemia more frequent in type 1 or type 2 DM?

A

type 1

18
Q

Neurogenic Symptoms of Hypoglycemia

A

catecholamine mediated/adrenergic: tremors, palpitations, anxiety/arousal
acetylcholine mediated/cholinergic: sweating, hunger, and paresthesias

19
Q

Neuroglycopenic Symptoms of Hypoglycemia

A

cognitive impairment, behavioral changes, psychomotor abnormalities, seizure, coma

20
Q

Signs of Hypoglycemia

A

diaphoresis
pallor
tachycardia
elevated blood pressure

21
Q

Why would hypoglycemia present without symptoms?

A
  • loss of autonomic warning (recent hypoglycemia, prior exercise, or sleep)
  • autonomic neuropathy (epi response diminished or lost)
  • medications (beta-blockers)
22
Q

Treatment of Hypoglycemia

A

outside hospital: oral/SQ/IM glucose

in hospital: IV glucose (D50)

23
Q

Non-Diabetic Hypoglycemia Whipple’s triad

A
  • signs and sx of hypoglycemia
  • low plasma glucose at time of sx
  • resolution of signs and sx after raising plasma glucose
24
Q

Endogenous hypersinsulinemia

A
  • insulin and c-peptide parallel each other because they are secreted in an equimolar fashion
  • due to accidental, surrepitious, or malicious hypoglycemia in well-appearing pt
25
Q

Exogenous insulin factitious hypoglycemia

A
  • plasma insulin high while c-peptide is low

- this is usually due to drugs, critical illness, endocrine deficiency, nonislet cell tumor

26
Q

Why can recovery from hypoglycemic coma be delayed?

A

cerebral edema

27
Q

What defines post-hypoglycemic coma?

A

unconsciousness lasting more than 30 minutes after plasma glucose is corrected

28
Q

What can be used to help treat a post-hypoglycemic coma?

A
  • IV mannitol
  • Glucocorticoids
  • Maintenance of plasma glucose levels
29
Q

What is the dawn phenomenon?

A
  • high morning blood glucose (5am-9am)

- counter regulatory hormones are released

30
Q

What is the somogyi effect?

A

hypoglycemia begets hyperglycemia

  • rebound hyperglycemia
  • -“man made” from poor diabetes management
31
Q

How do you tell whether a high morning blood sugar is caused by the dawn phenomenon or somogyi effect?

A

Check BG around 2-3 am for several nights:

  • if BG is low at that time suspect somogyi
  • if BG is normal to high at that time suspect dawn phenomenon
32
Q

Are neurologic complications higher in DKA or HHS?

A

HHS–because of higher glucose levels and serum osmolality

33
Q

DKA triad

A
  • hyperglycemia
  • anion gap metabolic acidosis
  • ketonemia

My Endocrine (4 decks)

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