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LWBK634-c07[01-16].qxd 7/6/10 3:43 PM Page 13 Aptara Inc

D IA B ET ES MEL L ITU S
Definition (Diabetes Care 2003;26:S33 & 2009;32:1327)
• Fasting glc 126 mg/dL 2; random glc 200 mg/dL 2 or 1 if severe
hyperglycemia and acute metabolic decompensation; or 75 g OGTT w/ 2-h glc
200 mg/dL (routine OGTT not recommended)
• Blood glc higher than normal, but not frank DM (“prediabetics,” 40% U.S. population)
Impaired fasting glc (IFG): 100–125 mg/dL
Impaired glc tolerance (IGT): 140–199 mg/dL 2 h after 75 g OGTT
Preventing progression to DM: diet & exercise (58% T), metformin (31% T), TZD (60% T)
• c HbA1C (no accepted criterion yet, 6.5% recommended by intl expert cmte)
Categories
• Type 1 : islet cell destruction; absolute insulin deficiency; ketosis in absence of insulin
prevalence 0.4%; usual onset in childhood but can occur throughout adulthood; c risk
if FHx; HLA associations; anti-GAD, anti-islet cell & anti-insulin autoantibodies
• Type 2: insulin resistance relative insulin deficiency
prevalence 8%; onset generally later in life; cc risk if FHx; no HLA associations
risk factors: age, FHx, obesity, sedentary lifestyle
• Type 2 DM p/w DKA (“ketosis-prone type 2 diabetes”): most often seen in nonwhite,
anti-GAD Ab, eventually may not require insulin (Endo Rev 2008;29:292)
• Mature-Onset Diabetes of the Young (MODY): autosomal dom. forms of DM due to
defects in insulin secretion genes; genetically and clinically heterogeneous (NEJM 2001;345:971)
• Secondary causes of diabetes: exogenous glucocorticoids, glucagonoma (3 Ds
DM, DVT, diarrhea), pancreatic (pancreatitis, hemochromatosis, CF, resection),
endocrinopathies (Cushing’s disease, acromegaly), gestational, drugs (protease
inhibitors, atypical antipsychotics)
Clinical manifestations
• Polyuria, polydipsia, polyphagia with unexplained weight loss; can also be asymptomatic

(NEJM 2007;356:2457; Lancet 2009;373:2125)

DIABETES
7-13
(JAMA 2007;298:1180)
LWBK634-c07[01-16].qxd 7/13/10 2:40 PM Page 14 Aptara Inc

Complications
• Retinopathy
non-proliferative: “dot & blot” and retinal hemorrhages, cotton-wool/protein exudates
proliferative: neovascularization, vitreous hemorrhage, retinal detachment, blindness
treatment: photocoagulation, surgery
• Nephropathy: microalbuminuria S proteinuria nephrotic syndrome S renal failure
diffuse glomerular basement membrane thickening/nodular pattern (Kimmelstiel-Wilson)
usually accompanied by retinopathy; lack of retinopathy suggests another cause
treatment: strict BP control using ACE inhibitors (NEJM 1993;329:1456 & 35:1941; Lancet
1997;349:1787) or ARBs (NEJM 2001;345:851, 861), low-protein diet, dialysis, or transplant
• Neuropathy
symmetric peripheral: symmetric distal sensory loss, paresthesias, motor loss
autonomic: gastroparesis, constipation, neurogenic bladder, erectile dysfxn, orthostasis
mononeuropathy: sudden-onset peripheral or CN deficit (footdrop, CN III VI IV)
• Accelerated atherosclerosis: coronary, cerebral, and peripheral arterial beds
• Infections: UTI, osteomyelitis of foot, candidiasis, mucormycosis, necrotizing external otitis
• Dermatologic: necrobiosis lipoidica diabeticorum, lipodystrophy, acanthosis nigricans
Outpatient screening and treatment goals (Diabetes Care 2009;32:193 & S1:S13)
• ✓ HbA1C q3–6mo, goal 7% for most Pts (NEJM 2008;358:2545, 2560); microvascular &
macrovascular complications T by strict glycemic control in T1D (NEJM 1993;329:997 &
2005;353:2643) & T2D (Lancet 1998;352:837; NEJM 2008;359:1577; Lancet 2009;373:1765; Annals 2009;151:394)
• Microalbuminuria screening yearly with spot microalbumin/Cr ratio, goal 30 mg/g
• BP 130/80; LDL 100,TG 150, HDL 40; benefit of statins even w/o overt CAD
(Lancet 2003;361:2005 & 2004;364:685);ASA if age 50 ( ) or 60 ( ) or other cardiac risk
factors (Circ 2010;121:2694)
• Dilated retinal exam yearly; comprehensive foot exam qy (Diabetes Care 2009;32:51, 513)
Management of hyperglycemia in inpatients
• Identify reversible causes/exacerbaters (dextrose IVF, glucocorticoids, postop, c carb diet)
• Dx studies: BG fingersticks (fasting, qAC, qHS; or Q6h if NPO), HbA1C
7-14

• Treatment goals: avoid hypoglycemia, extreme hyperglycemia ( 180 mg/dL)

• Modification of outPt treatment regimen: In T1D, do not stop basal insulin (can cause DKA).
In T2D: stopping oral DM meds generally preferred to avoid hypoglycemia or med
DIABETES

interaction (except if short stay, excellent outPt cntl, no plan for IV contrast, nl diet)
• InPt insulin: can use outPt regimen as guide; if insulin naïve:
total daily insulin wt (kg) 2, to start; adjust as needed
give ⁄ of total daily insulin as basal insulin in long-acting form to target fasting glc
give other ⁄ as short-acting boluses (standing premeal & sliding scale corrective insulin)
• Discharge regimen: similar to admission regimen unless poor outPt cntl or strong
reason for .Arrange early insulin and glucometer teaching, prompt outPt follow-up.

DIABETIC KETOACIDOSIS (DKA)

Precipitants (the Is)
• Insulin defic. (ie, failure to take enough insulin); Iatrogenesis (glucocorticoids)
• Infection (pneumonia, UTI) or Inflammation (pancreatitis, cholecystitis)
• Ischemia or Infarction (myocardial, cerebral, gut); Intoxication (alcohol, drugs)
Pathophysiology
• Occurs in T1D (and in ketosis-prone T2D); c glucagon and T insulin
• Hyperglycemia due to: c gluconeogenesis, c glycogenolysis, T glucose uptake into cells
• Ketosis due to: insulin deficiency S mobilization and oxidation of fatty acids,
c substrate for ketogenesis, c ketogenic state of the liver, T ketone clearance
Clinical manifestations (Diabetes Care 2003;26:S109)
• Polyuria, polydipsia, & dehydration S c HR, HoTN, dry mucous membranes, T skin turgor
• Nausea, vomiting, abdominal pain (either due to intra-abdominal process or DKA), ileus
• Kussmaul’s respirations (deep) to compensate for metabolic acidosis with odor of acetone
• MS S somnolence, stupor, coma; mortality 1% even at tertiary care centers
Diagnostic studies
• c anion gap metabolic acidosis: can later develop nonanion gap acidosis due to
urinary loss of ketones (HCO3 equivalents) and fluid resuscitation with chloride
• Ketosis: urine and serum ketones (acetoacetate measured by nitroprusside, but
predominant ketone is -OH-butyrate; urine ketones may be in fasting normal Pts)
• c serum glc; c BUN & Cr (dehydration artifact due to ketones interfering w/ some assays)
• Pseudohyponatremia: corrected Na measured Na [2.4 (measured glc –100)/100]
• T or c K (but even if serum K is elevated, usually total body K depleted); T total body phos
• Leukocytosis, c amylase (even if no pancreatitis)