DM Complications

Question 1

Acute
DKA (DM type? Mortality? Precipitant?)

Answer 1

Usually in pre-diagnosed Type 1 DM, 10% mortality
ABSOLUTE lask of insulin AND increased counter-regulatory hormones
Infx is most common precipitant, often accompanied by misguided omission of insulin

Question 2

Acute

DKA (path?)

Answer 2

Incr FFA from adipocytes, Ketogenesis in liver

WITHOUT INSULIN BOTH GLU AND KETONES ARE OVERPRODUCED AND UNDERUTILIZED

Question 3

Acute

DKA (pres?)

Answer 3

Kussmaul breathing, skin tenting, tachycardia, hypOtension
Polyuria, polydipsia, weight loss, weakness
Nausea, vomiting, abd pain (correlates with severity of acidosis)
Altered mental status (drowsy, stuporous)
Severe dehydration (from osmotic diuresis –> decr GFR and less excretion of glu)

Question 4

Acute

DKA (diagx)

Answer 4

Blood sugar >200 WITH ketones in urine/serum

ABG: pH

Question 5

Acute

DKA (treat)

Answer 5

IV fluids, IV insulin (slow to avoid cerebral edema)

K with Mg (if hypokalemic)

Question 6

Acute
Hypoglycemia (DM type?/cause?/and unawareness?)

Answer 6

Most common complication of DM (more in Type 1)
When trying to control glu with insulin overshoot
Unawreness: so many hypoglycemic episodes that no longer have adrenergic sx when actually hypoglycemic)

Question 7

Acute

Hypoglycemia (hormones?)

Answer 7

All 4 increase glucose in a hypoglycemic states
Glucagon and catecholamines (fast)
Cortisol and growth hormone (slow)

Question 8

Acute

Hypoglycemia (sx?)

Answer 8

Adrenergic (TOO MUCH EPI): sweating, tremor, tachycardia, anxiety, hunger
OR
Neuroglycopenic (CNS dysfxn from hypoglycemia): izzy, HA, confusion, convulsions, LOC

Question 9

Acute

Hypoglycemia (diagnx/treat for unawareness)

Answer 9

Glucose

Question 10

Chronic

Macrovascular

Answer 10

CVD (77% hospitalizations and 80% mortality from DM)
Hyperglycemia –> Endothelial cell dysfxn –> incr risk of atherosclerosis and procoagulation
T2DM often have HTN (not in T1DM until renal dz)
Hyperinsulinemia damages vessel walls and increases CV risk

Question 11

Chronic

Macrovascular (Treat)

Answer 11

Treat DM pats as if they have CV dz

Statins (goal of LDL

Question 12

Chronic

Microvascular (Four Mechs?)

Answer 12

1) Excess glu –> POLYOL PATHWAY –> soribitol –> oxidative damage
2) ADVANCED GLYCOSYLATION END PRODUCTS (AGEs) –>interfere with basement membrane, impair vasodilation, DNA damage
3) AGEs and high sugar –> INCREASE PKC –> BM thickening –> retinopathy and damage
4) Hi ROS –> oxidative damage

Question 13

Chronic
Microvascular
Retinopathy

Answer 13

Leading cause of US blindess
PERICYTE DROPOUT, BM thickens, hemorrhage and exudates –>ischemia leads to dilated vessels and angiogenesis
Treat: EARLY intervention can prevent, tight glycemic control, panretinal photocoag +/- intravitreal drugs (eg anti-VEGF)

Question 14

Chronic
Microvascular
Nephropathy

Answer 14

DM is leading cause of renal failure/dialysis and transplant in US (5-10% of DM require dialysis)
HYPERFILTRATION (hgih GFR) due to increased osmotic load –> intrarenal HTN –>BM thickens –> glomerular obilteration
Screen for urine albumin (GFR not good as affected too late)
Treat: Anti-HTN (ACEi) and glycemic control (also protein restriction)

Question 15

Chronic
Microvascular
Neuropathy (four types)

Answer 15

1) Mononeuritis multiplex (reversible)
2) Distal symmetric polyneuropathy (common - “stocking glove”): treat with foot care, examination, education
3) Autonomic neuropathy (most fatal, increased risk of MI - includes gastroparesis, sexual dysfxn, orthostatic hypotension, hypoglycemia unawareness)
4) Diabetic amyotrophy (18-24 months of truncal wasting, resolves)