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Endocrinology > NON-VASCULAR COMPLICATIONS OF DIABETES > Flashcards

NON-VASCULAR COMPLICATIONS OF DIABETES Flashcards

1
Q

What is Diabetic Ketoacidosis (DKA)?

What is it characterized by?
3

A

An absolute insulin deficiency
Potentially fatal if not treated properly

Characterized by a biochemical triad of hyperglycemia, ketonemia, and anion gap metabolic acidosis
(extra glucose in blood is pulling all the fluid out from your cells)

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2
Q

HOw does DKA usually evolve? (onset)

A

DKA usually evolves rapidly,

over a 24-hour period.

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3
Q

Pathophysiology:

Reduction in what?
Elevation in what? 3

This results in? 3

A

Reduction in net effective concentration of circulating insulin

Elevation of counter-regulatory hormones
Glucagon
Cortisol
Growth hormone

Hyperglycemia
Osmotic diuresis
dehydration

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4
Q

What causes the ketonuria in DKA?

3 steps

A
  1. Insulin deficiency causes the inability to drive glucose into the cells.
  2. Cell starvation so we have to break down fats for energy instead.
  3. These fats are converted to ketone and we make too many
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5
Q

PRECIPITATING FACTORS
The most common events associated with DKA?
4

Other less common?
7

A
  1. inadequate insulin therapy
  2. infection
  3. pneumonia
  4. urinary tract infection
Severe dehydration
Acute major illnesses 
myocardial infarction 
cerebrovascular accident 
pancreatitis
New onset type 1 diabetes
Drugs that affect carbohydrate metabolism
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6
Q 
Diabetic Ketoacidosis (DKA) 
CLINICAL PRESENTATION
A 
Thirst, polydipsia
Polyuria
Nausea, vomiting
Abdominal pain
Weakness
Fatigue
Anorexia
Tachycardia
Orthostatic hypotension
Poor skin turgor
Dry skin and mucous membranes
Kussmaul’s respirations
Fruity breath (ketones)
Altered mental status or coma
Hypothermia
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7
Q 
Diabetic Ketoacidosis (DKA) 
Lab findings?

What will be high? 3
What will be low? 2

A
  1. Blood glucose 250 - 800
  2. Serum osmolality normal to high
  3. Serum K+ high ( >5)
  4. Serum Na+ normal to low (130-145)
  5. Serum Bicarb low 12 meq/L
    pH
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8
Q

Hyperosmolar Hyperglycemic State (HHS) occurs almost exclusively in what type of pts and why?

A

Occurs almost exclusively in Type 2 DM
Elderly and physically impaired
Limited access to free water!!

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9
Q

How is HHS distinguished from DKA?

6

A
  1. Severe hyperglycemia >600
  2. Hyperosmolality
  3. Develops more insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission
  4. Greater degree of dehydration
  5. Relative absence of acidosis and ketones
  6. Mortality rates 5-20%
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10
Q

Hyperglycemia is the constant between HHS and DKA what makes them diiferent according to the medscape chart?
3 things

A

DKA- hyperlipidemia

HHS- hyperosmolarity
absence of ketogenesis

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11
Q

Hyperosmolar Hyperglycemic State causes?

4

A
  1. Catabolic Stress
  2. Infection
  3. Non-compliance
  4. Drugs
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12
Q

Hyperosmolar Hyperglycemic State clinical persentation?

A 
Polyuria
Polydipsia
Weight loss
Vomiting
Dehydration
Weakness
Mental status changes
Slower progression
Tachycardia
Hypotenstion
Severe dehydration
Dry skin and mucous membranes
Extreme thirst
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13
Q

WHat are the neuro signs of HHS?

A 
Neuro signs:
Lethargy to coma
Sensory impairment
Seizures
Hyperthermia
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14
Q

Hyperosmolar Hyperglycemic State lab findings:
What will be high? 3
What will be normal? 4

What can this state be complicated by?

A

Lab findings:

  1. Blood glucose > 600
  2. Serum osmolality >320 (too much solute/sugar in the blood)
  3. Serum Na+ - normal to high (135-145)
  4. Serum K+ - normal (4-5)
  5. Serum Bicarb >20 (no acidosis)
  6. pH > 7.3
  7. 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:
Initial assessment? 3
After that what are the two things that we do? 2

A

Initial assessment:

  1. Airway, breathing, and circulation (ABC) status
  2. Mental status
  3. Volume status
  4. IV fluid and electrolyte replacement
    - -Slower rate and greater volume needed for HHS
  5. Insulin therapy
    - -Insulin replacement starts after rehydration is in progress
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16
Q

HHS vs DKA differ clinically how?

A

according to the presence of ketoacidosis and usually the degree of hyperglycemia
Significant overlap between DKA and HHS has been reported in more than one-third of patients

HHS has some insulin although minimal

17
Q

What biochemical processes are involved with HHS? (what does this lead to?)

What biochemical processes are involved with DKA 1? (what does this lead to? 2)

A

Glycogenolysis and gluconeogenesis leading to hyperglycemia causing osmotic diuresia and dehydration

Ketone body production leading to hyperglycemia causing decreased alkaline buffer and acidosis

18
Q

Hypoglycemia as a side effect is more common in what kind of DM?

A

Type 1, especially those receiving intensive therapy

19
Q

What are the two kinds of functional hypoglycemia?

A

Fasting

Postprandial (reactive)

20
Q

Hypoglycemia causes?

5

A
  1. Insulin injections
  2. Oral hypoglycemic agents
  3. Gastroparesis
  4. Hepatic and renal dysfunction
  5. Malnutrition
21
Q

Hypoglycemia Clinical Presentation onset:

Neurogenic symptoms from what and what do they cause? 2

Neuroglycopenic symptoms? 5

A
  1. catecholamine-mediated/adrenergic
    - –Tremor, palpitations, and anxiety/arousal
  2. acetylcholine-mediated/cholinergic
    - -sweating, hunger, and paresthesias
  3. cognitive impairment,
  4. behavioral changes,
  5. psychomotor abnormalities and,
  6. at very low plasma glucose,
  7. seizure and coma
22
Q

Hypoglycemia Clinical Presentation signs?

4

A
  1. Diaphoresis
  2. Pallor
  3. Tachycardia
  4. Elevated blood pressure
23
Q

Hypoglycemia Unawareness in Diabetes is what?

A

Absent symptoms of hypoglycemia, which is thought to be the result of reduced sympathoadrenal, predominantly sympathetic neural, responses to a given degree of hypoglycemia

24
Q

What is Hypoglycemia Unawareness caused by?

3

A
  1. Loss of autonomic warning
    - –caused by recent antecedent hypoglycemia, prior exercise, or sleep
  2. Autonomic neuropathy
    - – so the epinephrine response diminished or lost
  3. Medications
    - -Beta-Blockers (lowers HR, blood pressure etc, tired, fatigued)
25
Q

Management of Hypoglycemia
Outside the hospital? 2
Hospital setting? 2

A

Oral
SQ/IM

IV
1 amp of D50 (20-50mL)

26
Q

In the patient without diabetes, the definition of hypoglycemia is based upon the presence of what?
3

A

Whipple’s triad:

  1. Symptoms and signs consistent with hypoglycemia
  2. a low plasma glucose at the time of symptoms
  3. and resolution of those signs and symptoms after raising the plasma glucose
27
Q

Surreptitiously Induced Hypoglycemia or Factititious hypoglycemia occurs secondary to what?

What levels will be low and high in this type?
(who will also be like this?)

A

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

plasma insulin is high while C-peptide is low
(Type 1)

28
Q

What levels will be almost undetectable in Type 1 pts?

A

C-peptide levels

29
Q

What causes hypoglycemic coma?

How long does it have to last to be called a coma?

A

Recovery from hypoglycemia may be delayed, because of 1. cerebral edema.

Unconsciousness lasting more than 30 minutes after plasma glucose is corrected is called post-hypoglycemic coma

30
Q

When does the dawn phenomenon occur?

A

Between 5 and 9am

Counter-regulatory hormones released

31
Q

How to tell the difference between Dawns and Somogyi?

A

if the blood sugar level is low at 2 a.m. to 3 a.m., suspect the Somogyi effect.

If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it’s likely the dawn phenomenon.

32
Q

Although part of a spectrum of diabetic complications DKA and HHS primarily differ according to what?

A

the presence of ketoacidosis and the degree of hyperglycemia.

33
Q

Neurologic complications, related to higher glucose levels and serum osmolality, are more common which, HHS or DKA?

A

HHS

34
Q

The triad of DKA consists of what?

A

hyperglycemia, anion gap metabolic acidosis, and ketonemia.

35
Q

A precipitating event can usually be identified in patients with DKA or HHS. The most common are what? 2

The initial evaluation of patients with hyperglycemic crises should include assessment of what?
3

A
  1. infection or
  2. inadequate insulin therapy.
  3. cardiorespiratory status,
  4. volume status, and
  5. mental status.

Endocrinology (23 decks)

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