Diabetes mellitus type 2 Treatment and Management

 

DIABETES MELLITUS TYPE 2

 

Definition:

Diabetes Mellitus is a syndrome causes by the lack or diminished effectiveness of endogenous insulin.  Type 2 DM is caused by insulin resistance in combination with relative insulin deficiency.

 

Clinical Manifestations:

• polyuria
• polydipsia
• polyphagia with unexplained weight loss
• can also be asymptomatic

 

Diagnosis:

• Fasting glucose > 7.0mmol/l or random glucose >11.1mmol/l
• diagnosis requires 1 abnormal glucose value if symptomatic or 2 separate abnormal measurements if pt is asymptomatic

 

Complications:

• Retinopathy

o   non-proliferative: ‘dot and blot’ and retinal hemorrhages, cotton wool/protein exudates

o   proliferative: neovascularization, vitreous hemorrhage, retinal detachment, blindness

o   both treated with photocoagulation

• Nephropathy

o   microalbuminuria -> proteinuria +/- nephrotic syndrome -> eventual renal failure

o   difffuse glomerular basement membrane thickening

o   treatment: strict BP control, ACE-I, low protein diet

• Neuropathy

o   symmetric peripheral: symmetric distal sensory loss, paresthesias, +/- motor loss

o   autonomic: gastroparesis, neurogenic bladder, impotence, orthstatic hypotension

o   mononeuropathy: sudden onset of peripheral or CN deficit (footdrop, CN III>VI>IV)

• Accelerated atherosclerosis

o   coronary, cerebral and peripheral arterial beds (ie: diabetics are at a higher risk for MI, CVA, and foot ulcers)

• Infections

o   candidiasis, mucormycosis, necrotizing external otitis

• Dermatologic

o   necrobiosis lipodica diabeticorum, lipodystrophy, acanthosis nigricans

 

 

Treatment and Management:

• oral agents

o   metformin: decreases hepatic gluconeogenesis and increases insulin sensitivity; side effects include N/V and diarrhea, rarely can cause lactic acidosis; contraindicated in liver or renal failure

o   sulfonylureas: increases insulin secretion at B-cell; side effects include weight gain and hypoglycemia

o   thiazolidinediones: increases insulin sensitivity at adipose and muscles; can cause weight gain, hepatotoxicity, fluid retention and CHF; contraindicated in liver disease and heart failure; monitor LFTs

• Insulin therapy

o   consider starting if mono oral therapy not adequate and definitely start if combo oral therapy not enough.  Start with a short-acting/long-acting mix of insulin at .5 units/kg/day, 2/3 in morning and 1/3 in evening, titrate up as necessary.  Should be given 20 min before breakfast and evening meal

• encourage weight reduction, diet, exercise
• should be on daily ASA unless contraindicated (eg: h/o GI bleed)
• start ACE-I if + microalbuminuria
• strict BP control: goal <130/80, start ACE-I as first line as nephro-protective
• lipid control: goal LDL <100, TG <150, HDL >40; there is a benefit of statins in all diabetics even w/o overt CAD

 

 

Diabetic Follow-Up

Clinic check list:  every 6 months check

• Treatment compliance and glucose control
• BP
• Injection sites
• Feet: pulses, numbness, sores, nail care
• Eyes: acuity, cataracts, retinopathy
• Urine dipstick for albumin 
• +/- serum creat

 

 

DIABETES CASE

 

39yo F with no medical history presents to your clinic with increased fatigue and weight loss. With further questioning, patient states she has been having increased thirst, increased urinary frequency and weakness. She denies fevers/chills, dysuria, abdominal pain, diarrhea, nausea/vomiting, difficulty breathing.

 

FH: unknown

SH: Married with 2 children. No tob/alcohol use

No medications and no drug allergies

 

Physical Exam: T36 BP 108/60 PR 90

Patient is thin, not pale and sitting comfortably.

HEENT: She has dry mucus membranes. No oral lesions

Neck: supple no LAD

CV: RRR nl s1s2 no murmurs, PMI non displaced

Lung: Clear bilaterally

Abdomen: Soft non tender, non distended normal bowel sounds, no organomegaly, no flank tenderness

Ext: no edema, DP pulses equal bilaterally

 

FBG: 26   Urine dip: No ketones, +leukocytes

 

1. You are suspicious for diabetes, what further investigations would you like to do?
2. What distinguishes Type I from Type II Diabetes?
3. What are the acute complications of Type II Diabetes and what are the long term complications?
4. How would you conservatively manage the patient while you await results? How will you initially treat the patient and what will you tell the patient about side effects?
5. How will your management change if the patient had hypertension? Or what about neuropathy?
6. When would you like to see the patient next? What studies will you perform at your next visit to follow the patient?

 

 

Answers:

1.  No further studies required to confirm dx of DM as FBG > 7mmol/L.  Also check urine for microalbuminuria.  Check baseline cholesterol, creatinine & liver function tests.
2. Type I results from an autoimmune destruction of pancreatic islet cells.  It often  initially manifests clinically with a stressor causing diabetic ketoacidosis, usually at an early age.  There is no endogenous insulin production in type 1 diabetics, so they must be treated with insulin.

DM II results from acquired insulin resistance over time.  It is often diagnosed later in life (40s-60s) & is associated with metabolic syndrome (obesity, dyslipidemia, hypertension).  It can initially be treated with oral hypoglycemic agents as there is still endogenous insulin production until late stages.

3. Acute complications: hyperglycemic hyperosmolar nonketotic syndrome

Long-term complications: macrovascular – coronary artery disease, peripheral artery disease, microvascular – nephropathy, retinopathy, neuropathy.  Also increased risk for infections.

4. Oral hydration (evidence of volume depletion from osmotic diuresis on exam), dietary counseling (avoidance of foods with high sugar & high fat content)

Initial pharmacologic therapy: metformin 500mg BD – do not start if patient has liver or kidney failure as can cause lactic acidosis.  Most common side effects are nausea, vomiting, diarrhea.

5. First line agent for HTN would be an ACEI (or ARB) as these agents reduce proteinuria & therefore slow the progression of diabetic nephropathy.  Neuropathy can be treated with gabapentin.  Progression of microvascular complications can be slowed by tightly controlling blood sugar with hypoglycemic agents.
6. See the patient soon after the initial visit (2 wks – 1 month) to assess tolerance of new medications & for improvement of symptoms.   Perform a repeat FBG at this time as medications doses may need to be increased.  Patients will then need to be followed every 6 months.  They should have creatinine checked yearly, as well as a yearly ophthalmologic & podiatric exam to assess for microvascular complications (nephropathy, retinopathy, neuropathy).