Diabetes Flashcards
1
Q
How do we diagnose diabetes?
A
- requires two of the following:
- a fasting glucose greater than 7.0 mmol/L (125 mg/dL)
- a glucose level greater than 11.1 mmol/L (200 mg/dL) two hours after a glucose tolerance test (GTT) is given
- a random glucose greater than 11.1 mmol/L
- an HbA1C greater than or equal to 6.5%
2
Q
Symptoms of Hyperglycemia vs. Symptoms of Hypoglycemia
A
- hyperglycemia: weakness, polyuria, polydipsia, dehydration, altered vision, weight loss (prolonged: Kussmaul hyperventilation, coma, arrhythmia)
- hypoglycemia: palpitations, tachycardia, diapharesis, anxiety, nausea, hyperventilation (prolonged: confusion, behavioral changes, seizures, coma)
3
Q
What is Somogyi syndrome?
A
- a rebound hyperglycemia in response to initial hypoglycemia (AKA post-hypoglycemia hyperglycemia); due to a stress reaction by the body in response to prolonged hypoglycemia, triggering glucagon and stress hormone release to increase BGLs
- occurs in patients taking insulin
- classic situation: insulin taken at night leads to elevated blood glucose levels in the morning
4
Q
What is type I DM? When and how does it classically present?
A
- autoimmune destruction of beta cells via T-cells (type IV), resulting in insulin deficiency and hyperglycemia
- presents in childhood (peak age is 10-14) with hyperglycemia, weight loss, low muscle mass, polyphagia, polyuria, polydipsia, and glycosuria
5
Q
What is T1DM associated with?
A
- genetic association with HLA-DR3 and HLA-DR4
6
Q
What is a major complication of T1DM? When can it often arise? What are the clinical features?
A
- diabetic ketoacidosis (DKA) via an excessive serum level of ketoacids
- often arises during stress (infection, etc) due to elevated epinephrine levels, which increases glucagon secretion
- clinical features: hyperglycemia, anion gap metabolic acidosis, hyperkalemia, Kussmaul breathing, acetone breath, mental status changes
7
Q
Explain the development of hyperkalemia in a patient with DKA.
A
- insulin helps drive K+ into cells to keep serum levels low, so without it, K+ has a tendency to stay outside
- in acidosis, the body is trying to get rid of the acid and increases H+ cell uptake to do so; when H+ comes in, K+ goes out
- serum level of K+ therefore increases, HOWEVER, the total body store of K+ is being depleted, as large amounts of the K+ in the serum will be lost in the urine via osmotic diuresis
8
Q
How do we treat DKA?
A
- with fluids, insulin, and electrolyte replacement (especially K+!)
- when we give the patient insulin, cells will quickly take back up the K+ they lost and the serum K+ level will plummet = risk for arrhythmia
9
Q
What is type II DM? What causes it? How does it usually present? Are patients insulin dependent?
A
- (more common type of DM)
- end-organ resistance to insulin results in hyperglycemia
- obesity results in a loss of insulin receptors
- usually is quite silent, but polyuria, plydipsia, and hyperglycemia are common
- initially, patients are not insulin dependent as they are producing insulin (they just can’t use it effectively), but as the disease progresses the beta cells burn out and stop producing insulin
10
Q
Which type of diabetes is more common? Which has a stronger genetic component?
A
- type II DM is more common
- believe it or not, type II has a stronger genetic component!
11
Q
What is a major complication of T2DM?
A
- hyperosmolar non-ketonic coma (HHS: hyperosmotic hyperglycemic state)
- this is a state of extremely high BGL (over 500 mg/dL; 28 mmol/L), resulting in life-threatening diuresis due to hypotension and coma
- ketones are NOT present
12
Q
What are two major complications of hyperglycemia?
A
- non-enzymatic glycosylation of vasculature
- osmotic damage to the cell types that can take up sugar without insulin
13
Q
Non-Enzymatic Glycosylation
A
- a result of chronic hyperglycemia
- results in atherosclerosis of large vessels (cardiac problems/IHD, gangrene/amputation/PVD, stroke) and hyaline arteriosclerosis of small vessels (retinopathy, neuropathy, nephropathy)
- (N.E.G. of Hb results in HbA1C, so this test tests for the state of glycosylation)
14
Q
Osmotic Damage
A
- a result of chronic hyperglycemia
- occurs in cells that do not rely on insulin to take up glucose from the blood: Schwann cells (neuropathy), cells of the lens (cataracts), pericytes of retinal blood vessels (blindness)
- in these cells, excess glucose is converted into sorbitol via aldose reductase; sorbitol is highly osmotic and drags in tons of water that causes the damage
15
Q
Which five things is diabetes a leading cause of?
A
- blindness, MI, stroke, renal failure, and gangrene
