Diabetes mellitus

and causes of
hyperglycemia
 Diabetes mellitus
DM is a systemic disease affecting many
organ systems, among them the pancreas
which becomes incapable of producing
insulin.
 Classifications
• Insulin dependent DM (IDDM type I).
• Non insulin dependent DM (NIDDM, type II)
• Gestational
• Pre-diabetes: blood glucose levels are higher
than normal but not high enough to be
diagnosed as diabetes.
• Another classification:
– Primary DM
– Secondary diabetes
 Classification
• Type 1: if insulin is withdrawn, ketosis and
eventually ketoacidosis develop.
• These patients are dependent on exogenous
insulin and carbohydrate for survival.
• Patients with type 2 diabetes may not need any
treatment for hyperglycemia during periods of
fasting or decreased oral intake.
 Modes of inheritance/transmission
• Not a transmitted disease

• For Type I
– Genetic predisposition
– Trigger

• Type II
– Weight gain/obesity
– Excess sugar in bloodstream
 Risk factors
• Family history of diabetes
• Older than 30 years of age
• Lack of physical activity (Sedentarism )
• Excessive weight
• Lack of knowledge on the disease
• No health care access
• Consumption of alcohol and drugs
• Smoking
IDDM

Treated by insulin

Ketosis prone

Less than 30y

male +

marked and progressive

inability of the pancreas to
secrete insulin
NIDDM

Oral hypoghlycemic, diet

Not ketosis prone

Middle to old age

Female +

Deficient production or
improper utilization of
insulin
 Diabetes complications
• Retinopathy (blindness?)
• Nephropathy (kidney problems)
• Foot ulceration and/or amputations
• Hypertension
• Hyperlipidemia
• Erectile Dysfunction
• Diabetic Ketoacidosis
• Diabetic coma
• Hypoglycemic coma
• Most of the
complications are
similar regardless
of the type of
diabetes,including:
– microvascular,
– macrovascular,
and
– neuropathic,
 Diagnosis

• Symptoms
(suggest possible diabetes)
• High glucose in blood
(confirm if higher than 126 mg/dl)
• Glucose in hemoglobin
(indicates quality of diabetes control -
higher than 7 mmol)
 Management
• Monitor blood glucose levels

• Diet, exercise, medications

• Type I: Daily insulin injections

• Type II:
– Weight reduction
– Oral hypoglycemic drugs
Oral hypoglycemic
drugs
Physical Activity

Benefits:
 Lowers glucose levels in blood
 Improves blood circulation in the entire
body
 Contributes to weight loss
 Improves physical and mental wellbeing
 Helps the body to utilize insulin more
efficiently
 Causes of Hyperglycemia

• Diabetes if uncontrolled

• Eating more than you usually do at a

particular meal.

• Physical Stress

• Emotional Stress

• Lack of physical exercise

 Diabetic Ketoacidosis (DKA)
• Diabetic ketoacidosis is a state of :
– Absolute or relative insulin deficiency
– Aggravated by ensuing :
• Hyperglycemia
• Dehydration
• Acidosis
• The most common causes are:
– Underlying infection
– Disruption of insulin treatment
– New onset of diabetes.
• Diabetic ketoacidosis is typically
characterized by:
– Hyperglycemia over 300 mg/dL,
– Low bicarbonate level (<15 mEq/L), and
– Acidosis (pH <7.30)
– Ketonemia and ketonuria.
– Mental status changes
Pathophysiology
• The initial symptoms of DKA :hyperglycemia
• Abdominal pain, altered mental function,
or frank coma may ensue.
• Symptoms of associated infections and
conditions
 Physical signs
• Kussmaul respirations and an acetone
odor on the pt’s breath.
• Volume depletion can lead to dry mucous
membranes, tachycardia, and
hypotension.
• Fever and abdominal tenderness may also
be present
 Laboratory Studies
• Hyperglycemia
• Ketosis (β-hydroxybutyrate >
acetoacetate)
• Metabolic acidosis (arterial pH 6.8–7.3)
• Despite a total-body potassium deficit, the
serum potassium at presentation may be
normal or mildly high as a result of
acidosis.
• Leukocytosis
• Hypertriglyceridemia,and
hyperlipoproteinemia are common.
• Hyperamylasemia is usually of salivary
origin but may suggest a diagnosis of
pancreatitis.
• The measured serum sodium is reduced
as a consequence of hyperglycemia

Repeat laboratory tests are critical.

 Other Tests
 Electrocardiography (ECG)
• Chest X-ray
 MANAGEMENT OF DIABETIC
KETOACIDOSIS
• Supportive care:
– Give oxygen (35% or more, as needed) if
arterial oxygen saturation is <92%
– Place a nasogastric tube if the patient is too
drowsy to answer questions or there is a
gastric succussion splash. Aspirate the
stomach and leave on continuous drainage.
Inhalation of vomit is a potentially fatal
complication of DKA
– Airway intubation as needed
– Put in a bladder catheter if no urine has been
passed after 4 h, or if the patient is
incontinent, but not otherwise
– Use graduated compression stockings and
prophylactic low molecular weight heparin to
reduce the risk of deep vein thrombosis
Focused care:
1. Assess patient: What precipitated the
episode? Maintain extreme vigilance for
any concomitant process such as:
– Infection & sepsis
– CVA & MI
– DVT
– Noncompliance, cocaine
– Trauma
2. Initiate appropriate workup for
precipitating event (cultures, CXR, ECG).
3. Admit to hospital; intensive-care setting
may be necessary for frequent
monitoring or if :
– pH < 7.00 or
– unconscious.
4. Measure:
– Capillary glucose
every 1–2 h;
– Electrolytes
(especially K+,
bicarbonate,
phosphate) every 4 h
for first 24 h.
5. Monitor every 1–4h:
– blood pressure
– Pulse
– Respirations
– Mental status
– Fluid intake and output
6. Replace fluids: isotonic saline
solution should be initiated early
7. Administer short-acting insulin
• Insulin should be started about an hour
after intravenous fluid replacement is
started to allow for checking potassium
levels and because insulin may be more
dangerous and less effective before some
fluid replacement has been obtained.
8. Administer intermediate or long-acting
insulin as soon as patient is eating.
9. Potassium replacement: started with
initial fluid replacement if potassium
levels are low.
10.Bicarbonate: not replaced since acidosis
will improve with the above treatments
alone
 Hypoglycemia
• Plasma glucose level <2.5–2.8 mmol/L
(<45–50 mg/dL) [although the absolute glucose level at
which symptoms occur varies among individuals]

• Whipple’s triad :
– Symptoms consistent with hypoglycemia,
– A low plasma glucose concentration
measured by precise method
– Relief of symptoms after the plasma glucose
level is raised.
• Glucose is an obligate metabolic fuel for
the brain. Hypoglycemia should be
considered in any patient with confusion,
altered level of consciousness, or
seizures.
• Counter-regulatory responses to
hypoglycemia include:
– insulin suppression
– the release of :
• Catecholamines
• Glucagon
• Growth hormone
• Cortisol.
 Causes of hypoglycemia
• In patients with diabetes
– Excess insulin, excess sulfonylurea (most
common cause)
– Development of renal failure (with reduced
clearance of insulin and sulfonylurea)
– Development of other endocrine disorder
(adrenal insufficiency,hypothyroidism,
hypopituitarism)
– Gastroparesis and malabsorption
• In patients with or without diabetes
– Alcoholic binge , Starvation, Severe liver
disease , Sepsis , Salicylate poisoning
– Adrenal insufficiency , Hypopituitarism,
Insulinoma
– Falciparum malaria, Quinine/quinidine for
malaria
– Pentamidine for Pneumocystis pneumonia
– Error with substitution of sulfonylurea
 CLINICAL
FEATURES

autonomic neuroglycopenic
• Autonomic:
– adrenergic:
• palpitations
• tremor, and
• anxiety
– cholinergic:
• sweating
• hunger, and
• paresthesia
• Neuroglycopenic symptoms: 997
– behavioral changes,
– confusion,
– fatigue, seizure,
– loss of consciousness, and,
– if hypoglycemia is severe and prolonged:
death
• Recurrent hypoglycemia shifts thresholds
for the autonomic symptoms and counter-
regulatory responses to lower glucose
levels, leading to hypoglycemic
unawareness. The first manifestation of
hypoglycemia is neuroglycopenia, placing
patients at risk of being unable to treat
themselves.
 Physical examination
• Tachycardia & bounding pulse
• Elevated systolic blood pressure
• Pallor
• Diaphoresis
 Lab investigations
• blood should be
drawn at the time of
symptoms, whenever
possible before the
administration of
glucose, to allow
documentation of the
glucose level.
• Other lab tests include
– Insulin level
– Sulfonylurea levels
– Cortisol
– Ethanol
• In the absence of documented spontaneous
hypoglycemia, overnight fasting or food
deprivation during observation in the outpatient
setting.
 Treatment
• Acute therapy of
hypoglycemia
requires:
– Administration of:
• Oral glucose or
• 25 g of a 50% solution
IV
– Followed by a constant
infusion of 5 or 10%
dextrose if parenteral
therapy is necessary.
• Hypoglycemia from
sulfonylureas is often
prolonged, requiring
treatment and
monitoring for 24 h or
more.
• Subcutaneous or
intramuscular glucagon
can be used in diabetics.
• Prevention of recurrent hypoglycemia
requires treatment of the underlying cause
of hypoglycemia, including:
– Discontinuation or dose reduction of offending
drugs
– Treatment of critical illnesses
– Replacement of hormonal deficiencies
– Surgery of insulinomas or other tumors.
.

• Treatment of other
forms of
hypoglycemia is
dietary:
– Avoidance of
fasting
– Ingestion of
frequent small
meals.
.