Diabetes Mellitus

By Tadesse Dagget (MSc, MPH, Asst. prof)

Feb, 2023
 Pancreas
 Has both exocrine & endocrine gland function

 Endocrine Pancreas

 Islets of langerhans are the cells involved in the endocrine function

 Composed of 3 distinct types of cells

- Alpha cells secret glucagons
- Beta cells secret insulin
- Delta cells secret somatostatin
-Glucagons & insulin have significant effect on carbohydrates, protein & lipids
metabolism
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 Diabetes mellitus(DM)
A chronic metabolic disorder characterized by elevated levels of glucose
in the blood (hyperglycemia) resulting from defects in insulin secretion,
insulin action, or both.

 In diabetes the body’s ability to respond to insulin may be decreased or

the pancreas may stop producing insulin entirely.

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 Diabetes mellitus(DM)….
 Normally a certain amount of glucose circulates in the blood.

 The major sources of glucose

 Absorption of ingested food in the gastrointestinal (GI)

 Formation of glucose by the liver from food substances.

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 Diabetes Mellitus(DM)
 Carbohydrate, lipid & protein metabolism abnormality resulting from
relative or absolute absence of insulin or its cellular metabolism
effect.

 Insulin:- controls the level of glucose in the blood by regulating the

production and storage of glucose.

 Metabolism abnormality leads to hyperglycemia, which results in

1. Acute metabolic complication

2. Long term complications

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 DM…

 Acute metabolic complications;

Diabetic ketoacidosis (DKA) and

Hyperglycemic hyperosmolar nonketotic syndrome (HHNS).

 Long-term effects of hyperglycemia;

 Macrovascular complications (coronary artery disease, cerebrovascular

disease, and peripheral vascular disease),

 Chronic microvascular complications (kidney and eye disease), and

 Neuropathic complications (diseases of the nerves).

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 Classification
A. Type-1
B. Type-2
C. Gestational diabetes mellitus (GDM); Onset during pregnancy, usually in the
second or third trimester.
 Due to hormones secreted by the placenta, which inhibit the action of insulin
D. Diabetes mellitus associated with other conditions or syndromes-
 Accompanied by conditions known or suspected to cause the disease: pancreatic
diseases, hormonal abnormalities, medications such as corticosteroids and estrogen-
containing preparations

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 Type- 1

 5 to 10% of people with DM have type 1 /formerly insulin dependent

diabetes.

 In this form the beta cells of the pancreas that normally produce insulin are
destroyed by an autoimmune process.

 It is characterized by sudden onset usually before the age of 30yrs.

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 Type-2

~ 90 to 95% of people with diabetes

 Results from decreased amount of insulin production

 Occurs most frequently in people who are older than 30yrs of age and

obese.

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 Normal Physiology
 Insulin is secretary by B cells of pancreases

 Insulin is an anabolic or storage hormone it has the following effects.

Stimulate storage of glucose in the liver and muscle (in the form of
glycogen)

Enhance storage of dietary fat in adipose tissue.

Accelerates transport of amino acids in to cells

 Insulin prevents the breakdown of stored glucose, protein and fat.

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 Pathophysiology of Diabetes
Type 1 Diabetes

 Results from β-cell destruction due to immune mediated or idiopathic, causing absolute
insulin deficiency. Inability to produce insulin because pancreatic beta cell has been
destroyed.

 Fasting hyperglycemia

 Post prandial (after meal) hyperglycemia

 Glucose in the urine since the concentration is high in the blood

- Excess glucose excreted in the urine

 Excessive loss of fluids and electrolytes
- Osmotic diuresis – Polyuria
 Polydipsia 11
 Insulin deficiency
 Impaired metabolism of protein and fats

-Weight loss

 Polyphagia – because of the decreased storage of calories

 Further hyperglycemia from – Glycogenolysis

- Gluconeognesis

 Fat break down

 Production of ketone bodies leads to diabetic Ketoacidosis (DKA)

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 Type-2 Diabetes (pathophysiology)
 Due to a progressive insulin secretary defect on the background of insulin

resistanceImpaired insulin secretion

 Insulin resistance -decreased sensitivity of the tissue to insulin

 To overcome insulin resistance and to prevent the buildup of glucose in the

body there must be an increased in the amount of insulin secretion.

 If the B cells are unable to keep up with the increased demand for insulin,

the glucose level rises.

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 Cont…

 DKA does not occur in type 2 diabetes

 Occurs most commonly in people > 30yrs

 For most pt’s the problem is detected incidentally

 Long term complications are common

 Wt reduction is the primary Rx of type 2 DM and also exercise and diet.

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 Etiology

Type 1 diabetes

 Genetic

 Combination of - Immunology

- Environmental factors

 An abnormal response in which antibodies are directed against normal

tissue of the body responding to tissue as if they are foreign.

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 Type-2 Diabetes

 Exact mechanisms that leads to insulin resistance and impaired secretion

in type 2 DM are unknown.

 But genetic factors play a role in addition age (>65 yrs), obesity, family
history and ethnic group.

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 Diagnostic Evaluation

 3P’s plus

 The presence of abnormally high blood glucose level on at least two

occasions

 Fasting plasma glucose > 126mg /dl (7.0 mmol/L)

 Random plasma glucose >200mg/dl (11.1 mmol/L)

 2hrs Oral glucose tolerance test >200 mg/dl (11.1 mmol/L)

 Hg A1C ≥6.5% (48 mmol/mol)

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 Testing for Type 2 Diabetes and Pre-diabetes in Asymptomatic Adults

Type 2 diabetes screening should be performed in adults of any age who are overweight or
obese, and who have one or more diabetes risk factor

 Testing should begin at age 45

If test is normal? Repeat it at least every 3 years

 Screening for prediabetes can be done using A1C, FPG, or 2-hr PG after 75-g OGTT
criteria

 CVD risk factors should be identified and treated

 Testing may be considered in children and adolescents who are overweight or obese and
have two or more risk factors for diabetes

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 Type 2 Diabetes Risk Factors
 Physical inactivity

 First-degree relative with diabetes

 High-risk race/ethnicity

 Women who delivered a baby >9 lb(4kg) or were diagnosed with GDM

 HDL-C <35 mg/dL ± TG >250 mg/dL

 Hypertension (≥140/90 mm Hg or on therapy)

 A1C ≥ 5.7%, IGT, or IFG on previous testing

 Conditions associated with insulin resistance: severe obesity, acanthosis nigricans, PCOS

 History of CVD
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ADA 2016 Guideline 20
Glycemic Targets

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Type 2 Diabetes Prevention

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 Management
The main goal of the Management

 To normalize insulin activity and blood glucose

 To reduce development of the vascular and neuropathic complications

 Normal blood glucose level without hypoglycemic and without seriously

disrupting the pt usual activity patterns.

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 Cont…
A. Diet
B. Medication
C. Education
D. Exercise
E. Monitoring

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 A. Dietary Mxt

 Constitutes the foundation of diabetes Mxt

 Has the following goals

oProvision of all the essential foods

oMeeting energy needs

oDecrease of blood glucose lipid levels.

 For obese pts wt loss is the key to Rx

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 A. Dietary Mxt….
 Important objective in dietary Mxt of diabetes is control of total calorie
intake to attain or maintain a reasonable body wt and control of
blood glucose level.

 In a young pt with type 1 diabetes, priority should be given to provide a diet

with enough calories to maintain normal growth & dev’t.

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 B. Medication
Insulin Therapy
 Insulin lowers blood glucose level after meals by facilitating the uptake &
utilization of glucose by muscles, fat and liver cells.
 During periods of fasting insulin inhibits the breakdown of stored glucose,
protein & fat.
 In type 1 diabetes exogenous insulin must be administered.
 In type 2 diabetes insulin may be necessary and a long term bases to control
glucose levels if diet and oral agents have failed.

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 Insulin Preparation

A number of insulin preparations are available

 Vary according to four major characteristics

Time course of action

Concentration

Species and source

 Manufactures

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 Time Course

 May be grouped into three main categories based on onset, peak and
duration.

I. Short Acting Insulin

II. Intermediate acting Insulin

III. long acting Insulin

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 Time Course …..

I. Short Acting Insulin

 Regular insulin (marked “R”)

 Onset of regular human insulin action is ½ to 1hr,

 peak 2 to 3 hrs

 duration 4 to 6hrs

 Clear in appearance

 given 20 minutes before food.

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 II. Intermediate Acting

 NPH insulin (neutral protamine Hagedorn)

 Lente insulin

 Onset 3-4 hrs,

 peak 4-12 hrs

 duration 16-20 hrs.

 White and milky in appearance

 It is important for the pt to have eaten some food

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 III. Long Acting Insulin

 Ultra lente Insulin (UL)

 Sometimes referred to as “peak less” b/c it tends to have a long, slow,

sustained action rather than sharp peaks in action

 Onset 6-8hrs ,

 duration 20-30hrs

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 Concentration

 The most common conc. of insulin is U-100

- This means 100 units of insulin per ml)

 Also U-40 & U-80 are used

Species

 In the past all insulin were obtained from beef (cow) and pig pancreas.

 Now human insulin is widely available.

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 Insulin regimen
 Vary from one to four injections per day.

 Usually these are a combination of a short acting and long acting insulin

 There are two general approaches to therapy.

• Conventional Regimen

• Intensive Regimen

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 Conventional Regimen

 Simplifying the insulin regimen as much as possible with the aim of avoiding
the acute complications.

 This approach would be appropriate for

Terminally ill

The elderly with limited self care abilities

Pt. completely unwilling or unable to engage in self management.

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 Intensive Regimen

 Uses a more complex insulin regimen to achieve as much control over bgl
as safe.

 Allows pts more flexibility to change their eating and activity patterns.

 Intensive therapy consist

 three or more insulin injections per day,

 Self monitoring of blood glucose concentration

 at least four times per day, and

 frequent contact with a diabetes health care team.

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 Intensive Regimen…

 Pts who may not be appropriate candidate

 Persons with autonomic neuropathy to have hypoglycemic awareness

 with permanent, irreversible complications of diabetes

 who do not take full responsibility in their care

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 Problems with Insulin
1. Local allergic reaction
 Redness, Swelling, tenderness and indurations at the site of injection

 Usually occur during the beginning stages of therapy and disappear with
continued use of insulin.

2. Systemic Allergic Reaction

 First, an immediate local skin reaction that gradually spread into severe &
generalized.

- Rx is desensitization of insulin( by injecting increasing amounts of the

allergen over time)
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 3. Insulin Lipodystrophy
 Lipodystrophy refers to a localized reaction,
occurring at the site of insulin injections.

 Lipoatrophy is loss of subcutaneous fat and

appears as slight dimpling or more serious
pitting of subcutaneous fat.

 The use of human insulin has almost eliminated

this disfiguring complication.

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 3. Insulin lipodystrophy…

 Lipohypertrophy, the development of fibrofatty masses at the injection site,

caused by the repeated use of an injection site.

 If insulin is injected into scarred areas, absorption may be delayed.

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 4. Insulin Resistance

 Clinical insulin resistance is a daily insulin requirement of 200 units or

more.

 Immune antibodies develop and bind the insulin, thereby decreasing the
insulin available for use.

 All animal insulins, as well as human insulins to a lesser degree, cause

antibody production

Rx:- administering a more concentrated insulin preparation, such as U500

 Prednisone is needed to block the production of antibodies.

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 5. Morning hyperglycemia
 An elevated blood glucose level upon arising in the morning caused by an
insufficient level of insulin
1. The dawn phenomenon:- relatively normal bgl until approximately 3 a.m.,
when bgl begin to rise.
 The phenomenon is thought to result from nocturnal surges in growth hormone
secretion that create a greater need for insulin in the early morning hours in
patients with type 1 diabetes.
Rx:-Change time of injection of evening intermediate-acting insulin from dinner
time to bedtime.

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 5. Morning hyperglycemia….

ii. Insulin waning:- the progressive increase in blood glucose from bedtime
to morning.

Rx:-Increase evening (predinner/bedtime) dose of intermediate or long-acting

insulin

iii. Somogyi Effect:-Normal or elevated blood glucose at bedtime, a decrease

at 2–3 [Link] hypoglycemic levels, and a subsequent increase caused by the
production of counter-regulatory hormones

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 5. Morning hyperglycemia….
Rx:-
* Decrease evening (predinner or bedtime) dose of intermediate acting insulin
or
* Increase bedtime snack.

Administering Insulin Injection

- Selection and rotation
- The four main area for injection are the abdomen, arms, thighs and the hip.
- Speed of absorption is in the abdomen and decrease progressively in the arm, thigh
and hip.

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 5. Morning hyperglycemia….

 Systematic rotation of injection site with anatomic areas is recommended to

prevent localized changes in fatty tissues (lipodystrophy)

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 Oral Anti diabetic/hypoglycemic Agents

 Are effective for type II diabetic pts.

 They cannot be used during pregnancy.

 Oral agents include – Sulfonylureas -Tolazamide

- Biguanides -Metformin

Sulfonylureas

 Exert their primary action by directly stimulating pancreas to secret insulin

 Additionally improve insulin action at the cellular level

 Also decrease glucose production by the liver

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 C. Patient Education

Pt should follow regular pattern

of eating, administering insulin
and exercise.

 Routine blood glucose tests

 Identification tag

 Pt should know potential

symptoms of hypoglycemia

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 D. Exercise
 Regular exercise is important to promote

 overall health and

to reduce cardiovascular complications.

reduce overall insulin requirements by further enhancing insulin sensitivity

Through accelerated insulin absorption

 increased muscle glucose consumption

 Duration: 30 minutes

 Frequency: at least 3 days per week

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 E. Self-monitoring of Blood Glucose Concentration

 It actively involves patients in the treatment process,

 allows more rapid treatment adjustments, and reinforces dietary changes

 Encouraged to monitor

Before each meal

At bedtime and

Whenever symptoms occur.

 Before, during, and after exercise

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Acute complications
 Three major acute complications of glucose
imbalance

 Hypoglycemia

 DKA

 Hyperglycemic Hyperosmolar non ketotic

syndrome.(HHNKS)

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Hypoglycemia (Insulin Reaction)
 Occurs when bgl falls below 50 to 60 mg /dl

Can be caused by

 Too much insulin, oral hypoglycemic agents

 Too little food

 Excessive physical activity.

 Occurs at any time of the day or night

Hypoglycemia can be Mild
Moderate
Severe
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 Severe hypoglycemia
 CNS function is so impaired that the pt needs the assistance of another
person for Rx

 Disoriented behaviors, seizures, difficulty arousing from sleep or loss of

consciousness.

 Immediate Rx must be given

 Usual recommendation 10 to 15 gm of fast acting sugar orally.

 N.B Golden advice – diabetic pts must carry some form of simple sugar
with them all the times
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Severe Hypoglycemia
For unconscious pt

 40 % DW IV

 Injection glucagon 1Gm IM

 Simple sugar dissolved (NGT)

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Impaired function of CNS
 Inability to concentrate

 Headache, light headedness

 Confusion, memory lapses

 Numbness of the lips & tongue

 Slurred speech to coordination

 Emotional Change

 Irrational Behavior

 Double vision & drowsiness

Mx – Fast Acting Sugar 58
 Diabetic Ketoacidosis

 Caused by an absence or markedly inadequate amount of insulin

 Result in disorder of metabolism of carbohydrate, Protein & fats.

Cause of DKA

 Decreased or missed dose of insulin

 illness or infection

 Initial manifestations of undiagnosed and untreated diabetes.

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DKA…
 The three main clinical features of DKA

- Hyperglycemia

- Dehydration & Electrolyte loss

- Acidosis (pH < 7.30)

Pathophysiology of DKA

 Break down of fat / lipolysis /

 Free fatty acid & glycerol

 Ketone bodies (Acid)

 Metabolic acidosis 60
 Clinical Manifestation
 Polyuria & Polydipsia

 Blurred vision, weakness & headache

 Orthostatic Hypotension

 Weak rapid pulse

 GI Symptoms - Anorexia
- Nausea – vomiting
- Abdominal pain.
- Acetone breath
 Kussmaul respirations

 Mental Status Change (Alert/Lethargic /Comatose) 61

Dx of DKA
 Clinically

 Glucose levels greater than 250mg/dl,

 Serum bicarbonate concentration drops below 18 meq/L

 ph range from 7.20 to 7.30; in severe cases, it can fall

below 7.00

 Urine or serum ketone = +ve

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 Treatment:
 Aimed at correction of three main problems

 Dehydration

 Electrolyte loss

 Acidosis

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 Rehydration

 Rehydration is important for maintaining tissue perfusion.

 Enhances the excretion of excessive glucose by the kidneys.

 Requires 6 -10 liters of IV fluid to replace fluid losses caused by polyuria,

hyperventilation, diarrhea, and vomiting.
 Initially, 0.9% NaCl is administered at a rapid rate( 0.5-1 L /hour for 2 to 3
hours.
 (0.45%NaCl) hypotonic used for patients with hypertension or
hypernatremia or those at risk for heart failure.

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 Rehydration…
 After the first few hours, half-normal saline solution is the fluid of choice for
continued rehydration, if BP is stable and the sodium level is not low.

 Moderate to high rates of infusion (200 to 500 mL/ hr) may continue for
several more hrs.

 When the bgl reaches 300 mg/dL or less, the IV fluid may be changed to
dextrose 5% in water (D5W) to prevent a precipitous decline in the blood
glucose level

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Rehydration…
 Monitor fluid volume status involving frequent
measurement of

- Vital sign (BP,PR,RR)

- Input & out put

- Lung assessment

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 Restoring electrolytes
 The major electrolyte of concern during treatment of DKA is potassium.

 Although the initial plasma concentration of potassium may be low, normal,

or even high, there is a major loss of potassium from body stores and an
intracellular to extracellular shift of potassium.

 Further, the serum level of potassium drops during the course of treatment
of DKA as potassium re-enters the cells

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 Factors related to treating DKA that reduce the serum
potassium concentration
 Rehydration leads to increased plasma volume

 Rehydration leads to increased urinary excretion of potassium.

 Insulin administration, which enhances the movement of potassium from

the extracellular fluid into the cells.

 Cautious but timely potassium replacement is vital to avoid dysrhythmias.

 Up to 40 mEq per hour may be needed for several hours.

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 Acidosis

 Ketone bodies accumulate as a result of fat breakdown.

 The acidosis that occurs in DKA is reversed with insulin, which inhibits fat
breakdown, thereby stopping acid buildup.

 Insulin is usually infused intravenously at a slow, continuous rate 5 units per

hour).

 Hourly bgl values must be measured.

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 3 . Hyperglycemic hyperosmolar nonketotic syndrome

 HHNS is a serious condition in which hyperosmolarity and hyperglycemia

predominate, with alterations of sensorium.

 The basic biochemical defect is lack of effective insulin.

 The patient’s persistent hyperglycemia causes osmotic diuresis, resulting

in losses of water and electrolytes.

 To maintain osmotic equilibrium, water shifts from the intracellular fluid

space to the extracellular fluid space.

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HHNS…
 With glucosuria and DHN, hypernatremia and
increased osmolarity occur.

 HHNS can be traced to a precipitating event such as an

acute illness (eg, pneumonia or stroke), medications
that exacerbate hyperglycemia (thiazides).

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HHNS…
 Patients may tolerate polyuria and polydipsia until
neurologic changes or an underlying illness (or family
members or others) prompts them to seek
treatment.

 Because of possible delays in therapy, hyperglycemia,

dehydration, and hyperosmolarity may be more
severe in HHNS.

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Clinical Manifestations
 Hypotension

 Profound DHN (dry mucous membranes, poor skin

turgor)

 Tachycardia

 Variable neurologic signs (eg, alteration of sensorium,

seizures, hemiparesis).

 The mortality rate ranges from 10% to 40%, usually

related to an underlying illness.
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 Assessment and Diagnostic Findings
 Serum osmolality: exceeds 350 mOsm/kg.

 The bgl is usually 600 to 1,200 mg/dL

 Electrolyte and BUN levels are consistent with the clinical picture of severe
dehydration.

 Mental status changes, focal neurologic deficits, and hallucinations are

common secondary to the cerebral dehydration that results from extreme
hyperosmolality.

 Postural hypotension accompanies DHN

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 Medical Management
 The overall approach to the treatment of HHNS is similar to that of DKA:

 Fluid replacement

 Correction of electrolyte imbalances, and

 Insulin administration.

 Close monitoring of volume and electrolyte status is important for

prevention of fluid overload, heart failure, and cardiac dysrhythmias.

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 Cont…

 Fluid treatment is started with 0.9% or 0.45% NS, depending on the

patient’s sodium level and the severity of volume depletion.

 Potassium is added to IV fluids when urinary output is adequate

 Extremely elevated bgl drop as the patient is rehydrated.

 Insulin plays a less important role in the treatment of HHNS because it is

not needed for reversal of acidosis.

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 Cont…

 Insulin is usually administered at a continuous low rate to treat

hyperglycemia

 Replacement IV fluids with dextrose are administered when the glucose

level is decreased to the range of 250 to 300 mg/dL

 Treatment is continued until metabolic abnormalities are corrected and

neurologic symptoms clear.
• It may take 3 to 5 days for neurologic symptoms to resolve

 Treatment of HHNS usually continues well beyond the time when

metabolic abnormalities are resolved. 77
 Long-Term Complications of Diabetes
 Long-term complications are becoming more common
as more people live longer with diabetes.

 The long-term complications of diabetes can affect

almost every organ system of the body.
 The general categories of chronic diabetic
complications are
 Macrovascular disease,
Microvascular disease, and

Neuropathy.
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Long Term Complications…
 Increased bgl may play a role in neuropathic disease,
microvascular complications, and risk factor
contributing to macrovascular complications.

 HTN may also be a major contributing factor, especially

in macrovascular and microvascular diseases.

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 Macrovascular complications
 Result from changes in the medium to large blood vessels.

 Blood vessel walls thicken, sclerose, and become occluded by plaque that
adheres to the vessel walls. Eventually, blood flow is blocked.

 Coronary artery disease, cerebrovascular disease, and peripheral vascular

disease are the three main types of macrovascular complications that occur
more frequently in the diabetic population.

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 Macrovascular complications…
 Myocardial infarction is twice as common in diabetic men and three times as
common in diabetic women.

 Coronary artery disease may account for 50% to 60% of all deaths in patients
with diabetes.

 One unique feature of coronary artery disease in patients with diabetes is that the
typical ischemic symptoms may be absent.

 This lack of ischemic symptoms may be secondary to autonomic neuropathy .

 Cerebral blood vessels are similarly affected by accelerated atherosclerosis.

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 Macrovascular complications…

 Occlusive changes or the formation of an embolus elsewhere in the

vasculature that lodges in a cerebral blood vessel can lead to transient
ischemic attacks and strokes.

 Atherosclerotic changes in the large blood vessels of the lower extremities

are responsible for the increased incidence (two to three times higher than
in nondiabetic people) of occlusive peripheral arterial disease in patients
with diabetes.

82
Signs and symptoms
 Diminished peripheral pulses

 Intermittent claudication (pain in the buttock, thigh, or

calf during walking).

 The severe form of arterial occlusive disease in the

lower extremities is largely responsible for the
increased incidence of gangrene and subsequent
amputation in diabetic patients.

 Neuropathy and impairments in wound healing also

play a role in diabetic foot disease 83
 Management
 Prevention and treatment of the commonly accepted risk factors for
atherosclerosis.

 Diet and exercise are important in managing obesity, hypertension, and

hyperlipidemia.

 The use of medications to control hypertension and hyperlipidemia .

 Smoking cessation is essential.

 Control of bgl may reduce triglyceride levels and can significantly reduce
the incidence of complications.
84
 Cont…

 When macrovascular complications do occur, treatment is the same as with

nondiabetic patients.

 In addition, patients may require

increased amounts of insulin or

switch from oral antidiabetic agents to insulin during illnesses.

85
 Microvascular complications
 Unique to diabetes

 Diabetic microvascular disease is characterized by capillary basement

membrane thickening.

 Two areas affected by these changes are the retina and the kidneys.

 Diabetic retinopathy is the leading cause of blindness in both type 1 and

type 2 diabetes.

86
 Microvascular complications …

 Retinopathy is caused by changes in the small blood vessels in the retina, the
area of the eye that receives images and sends information about the images
to the brain.

 Nearly all patients with type 1 diabetes and more than 60% of patients with
type 2 diabetes have some degree of retinopathy after 20 years.

 Retina is richly supplied with blood vessels of all kinds: small arteries and
veins, arterioles, venules, and capillaries.

87
 Nephropathy
 Renal disease secondary to diabetic microvascular changes in the kidney, is a
common complication of diabetes.

 About one in every four individuals starting dialysis has diabetic

nephropathy.

 People with diabetes account for nearly half of new cases of endstage renal
disease (ESRD) each year and about a quarter of those requiring dialysis or
transplantation each year.

88
 Medical Management

 To achieving and maintaining near-normal bgl, management for all patients

with diabetes include careful attention to the following:

 Control of hypertension (use of [ACE] inhibitors, captopril

 Prevention or vigorous treatment of UTI
 Avoidance of nephrotoxic substances
 Adjustment of medications as renal function changes
 Low-sodium diet
 Low-protein diet

89
 Cont…

 Lower BP and reduce microalbuminuria and therefore protect the kidney.

 In chronic or end-stage renal failure:

 Hemodialysis and transplantation from a relative or a cadaver.

90
 Diabetic neuropathies
 Refers to a group of diseases that affect all types of nerves, including
peripheral (sensorimotor), autonomic,and spinal nerves.

 The disorders appear to be clinically diverse and depend on the location of

the affected nerve cells.

 The prevalence increases with the age of the patient and the duration of the
disease

 may be as high as 50% in patients who have had diabetes for 25 years.

91
 Diabetic neuropathies…
 Elevated bgl over a period of years have been implicated in the etiology of
neuropathy.

 The pathogenesis of neuropathy may be attributed to either a vascular or a

metabolic mechanism or both.

 Capillary basement membrane thickening and capillary closure may be present.

 Demyelination of the nerves, which is thought to be related to hyperglycemia.

Nerve conduction is disrupted when there are aberrations of the myelin sheaths.

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 Diabetic neuropathies…

 Control of bgl to normal or near-normal levels was shown in the study to

decrease the incidence of neuropathy by 60%.

 The two most common types

 Sensorimotor polyneuropathy

 Autonomic neuropathy.

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 Cont…
 Peripheral neuropathy most commonly affects the distal portions of the nerves,
especially the nerves of the lower extremities.

 It affects both sides of the body symmetrically and may spread in a proximal
direction.

 Decreased sensations of pain and temperature place patients at increased risk for
injury and undetected foot infections.

 Deformities of the foot may also occur with neuropathy-related joint changes .

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 Autonomic Neuropathies
 Results in a broad range of dysfunctions affecting every organ system of the body.

 Three manifestations of autonomic neuropathy are related to the cardiac, GI, and
renal systems

 Cardiovascular symptoms range from fixed, slightly tachycardic heart rate;

orthostatic hypotension; to silent, or painless, myocardial ischemia and infarction.

 Delayed gastric emptying may occur with the typical symptoms of early satiety,
bloating, nausea, and vomiting.

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 Cont…

 Urinary retention, a decreased sensation of bladder fullness, and other

urinary symptoms of neurogenic bladder result from autonomic neuropathy.

 Patients with a neurogenic bladder are predisposed to developing urinary

tract infections due to inability to completely empty the bladder.

 This is especially true in patients with poorly controlled diabetes, because

hyperglycemia impairs resistance to infection

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 Hypoglycemic unawareness

 Autonomic neuropathy of the adrenal medulla is responsible for diminished

or absent adrenergic symptoms of hypoglycemia.

 Patients report that they no longer feel the typical shakiness, sweating,
nervousness, and palpitations associated with hypoglycemia.

 Strict blood glucose monitoring is recommended for these patients. Their

inability to detect and treat these warning signs of hypoglycemia puts them
at risk for developing dangerously low bgl.

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 Sexual dysfunction
 Impotence in men, is a complication of diabetes

 The effects of autonomic neuropathy on female sexual functioning are not

well documented.

 Reduced vaginal lubrication, decreased libido and lack of orgasm.

 Vaginal infection, increased in incidence in women with diabetes, may be

associated with decreased lubrication and vaginal itching and tenderness.

 Urinary tract infections and vaginitis may also affect sexual function

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