Complications are either… Acute---DKA
---hyperosmolor non ketotic coma
---hypoglycemia
---lactic acidosis Chronic ---macrovascular
---microvascular
Prevalance of complications at the time of diagnosis { UKPDS }
newly diagnosed diabetes
Complications Prevalance %
Any complication 50 %
retinopathy 21 %
Abnormal ECG 18 %
Absent foot pulses
14 %
Macrovascular complication 40-50 % of people with DM die from these
complications Factors that contribute to the ↑ risk include
1-↑ prevalance of hypertension in diabetics
2--↑ lipid profile
3—abnoramlity in clotting system
4—effect of hyperglycemia on progression of atherosclerotic lesions
Coronary artery disease Coronary artery disease accounts for the majority of
diabetic deaths Certain features of CAD in diabetics include: Adjusted for age MI is 2-5 times more frequent in
patients with diabetes Pts with DM who have MI have a lower survival rate
compared to pts without DM ↑ incidence of silent MI –40% Silent MI may present as new onset of CCF Small vessel disease with relatively patent coronary
arteries are more common
Peripheral vascular disease {PVD}Special characteristics of PVDLocation—tibial + popliteal arteries are
common----aorta ,ileal, femoral –rareExtend—multi segmental occlusionProgression—accelerated progression
compared to non diabeticsGangrene---risk ↑ more than non diabetics
over 40 yrs of age
Retinopathy Background—this is the most common
type of retinopathy
--not usually seen untill after 10 yrs of DM
---may be found in 30 % of pts with type 2 DM
Proliferative maculopathy
NephropathyConsists of the following clinical stages: ↑ GFR > 150 mls /min Microalbuminurea 30-300 mg /24 hrs Clinical albuminuria also called
macroalbuminuria > 300 mg/ 24 hrs Worsening of proteinuria , hypertension and
↓GFR Kidney failure occurs when GFR ↓ to ≤
10mls/min
Factors influencing renal function in DM Glomerular basement membrane damage
→ diabetic nephropathy Renal artery stenosis and ischaemia due
to atherosclerosis Ascending infection Renal papillary necrosis
Neuropathy
Different clinical presentations Symmetrical sensory polyneuropathy Mononeuritis multilplex Autonomic neuropathy
Sensory neuropathy Insidious onset of loss of sensation in feet
and hands—gloves and stockings Loss of vibration sense and reduced or
absent ankle or knee jerk Loss of peripheral nerve function results in
wasting of small muscles of feet and hands
Mononeuritis multiplex Nerves commonly affected are 3rd and 6th Amyotrophic motor neuropathy
characterized by unilateral or bilateral pain and weakness of the quadriceps—they often recover spontanously
Median nerve palsy leeds to carpal tunnel syndrome
Peroneal nerve palsy leeds to foot drop
Autonomic neuropathy CVS—loss of vagal { parasympathetic tone} produces --resting tachycardia--loss of sinus rhythm –change in heart rate with
respiration---sinus arrythmia Loss of sympathetic activity in arterioles results in
peripheral vasodilatation and postural hypotension Rx—support stockings --fludrocortisone -alfa blockers
GIT Gastroparesis--Delayed gastric emptying results in early
statiety or recurrent vomiting --treated with –dopamine agonist metochlorpramide domperidone erythromycin Nocturnal diarrhea loperamide Constipation due to colonic atony laxatives
Autonomic bladder Loss of bladder smooth muscle tone
results in incomplete emptying , stasis , and ↑ risk of infection
In severe cases the bladder is persistantly distended—atonic which results in over flow incontinance
sympathomimetics—carbachol antichilinesterase drugs
Gustatory sweating Eating cause excessive facial sweatingAnticholinergic drugs--probantheline
Erectile dysfunction impotence
Can we prevent type 2 DM Before pts develop DM ,they almost
always have “ pre diabetes” Clinical trails have documented that
dietary changes and regular exercise prevent or delay the development of overt DM in individuals at high risk
Risk factors for type 2 DM Age > 45 1st degree relative with type 2 DM History of gestational diabetes or delivery of
infant >9 lbs PCO Abdominal obesity CVD, hypertension ,dyslipidemia ,other
metabolic syndrome features
Prediabetes
Defined as- IFG—FBS =100 -125 mg/dl…5.6 - 6.9
mmol / l Impaired glucose tolerance---plasma
glucose level 140 – 199 mg/dl …7,8 – 11.0 mmol / l, 2 hrs after 75 gms of glucose
Evaluation and treatment FBG HbA1c Serum electrolytes Urine for protein and microalbuminuria ECG Fasting lipid profile
Treatment Diet Exercise Stop smoking Treat hyperlipidemia ---statin group Treat hypertension—mainly ACEI Prevent proteinuria by prescribing ACEI Start ASA as prophylaxis for IHD OHG Insulin
ADA Rx goals for glycemic control
glycemia normal goal Further action required
Average preprandial glucose mg / dl
< 110 80 - 120 > 140
Average pp glucose < 140 < 160 > 180
HbA1c < 6 < 7 > 8
OHG Biguanides— Suppress hepatic glucose production Decrease intestinal glucose absorption Improve insulin sensitivity metformin Sulphonylurea Increase pancreatic insulin secretion —glimepiride ---glipizide ---glyburide ---chlorpropamide
Cont..Alfa glucosidase inhibitors— ↓post prandial hyperglycemia by decreasing GIT
carbohydrate absorption arcaboseMeglitinides--- Increase pancreatic insulin secretion through
different glucose binding sites than used by sulphonylureas
repaglinide
Insulin therapy in type 2 diabetes Don,t wait forever Don,t be afraid of hypoglycemia Consider combination therapy Don,t under insulinize Consider insulin pump therapy
Risk factors for DKA Results from absolute or relative insulin
deffeciency Missing the dose of insulin Infection Increase food intake Stress like MI or surgery
Diagnosis
Triad of. Hyperglycemia—glucose more than
15mmol /l Metabolic acidosis—PH < 7.2
---HCO3 <17 mmol /l Ketones in the urine
Principles of management Rehydration Insulin Correction of K+ Correction of acidosis + / - antibiotics
Rehydration 1 litre NS over 30 min 1 litre over 1 hr 1 litre over 1 hr 1 litre over 2 hrs 1 litre over 4 hrs I litre over 6 hrs
Change ½ saline once BS reaches 13 mmol / l
Insulin therapy 10 -20 units of RI is given IM stat 4 - 6 units / hr by IV infusion untill BS ↓ to
10 – 15 mmol/l then ↓ to 1 - 4 units / hr Aim to ↓ BS 3 – 6 mmol / hr Change to SC once BS ↓13 mmol / l
Potassium replacement 1st 30 min if K+ > 5.5 mmol/l– no K+ If 3.5 5.5 --give 20 meq in the 1st litre If < 3.5 --give 40 meq in the 1st litre Continue K+ infusion 20 meq in each litre
to maintain K+ at the level of 3.5 – 4. 5
Bicarbonte replacement
Bicarbonate is replaced when the PH is between 7.0 – 7.1
Antibiotics
These are used when there is strong suspicion of infection
HYPOGLYCEMIACauses Missed delayed or inadequate meal Unaccustomed exercise Alcohol Increase dose of drugs ..insulin or OHG Gastroparesis Malabsorption factitious
NON KETOTIC HYPEROSMOLAR DIABETIC COMA
Characterized by Severe hyperglycemia--> 50 mmol / l No ketones in the urine Severe dehydration Occurs in the elderly Risk of thrombosis is high Mortality is high
Management
Differs from DKA in the following Very sensitive to insulin so very small
dose should be started Calculate osmolality and start either ½ or
¼ saline
Plasma osmolality =2Na + 2K + glu + urea=280 - 295