APPROACH TO

DIABETES
MELLITUS
PATIENT

PRESENTED BY :
Roll No : 648
SHREEJA MAHESHWARI
 Hyperglycemia

 Drowsy
 Flushed
 Thirsty
 Diabetes Mellitus
 HYPERGLYCEMIA: fluid/electrolyte
imbalance.
 Polyuria
• Sodium, chloride, potassium excreted
 Polydipsia from dehydration
 Polyphagia: cells are starving, so person
feels hungry despite eating huge amounts of
food. Starvation state remains until insulin is
available.
Skin problems
-Skin Infections leading to boils,
carbuncles or abscesses.
-Oral & Genital candidiasis
 Diabetes Mellitus
 Major risk factors
 Family history - A history of diabetes in first-degree
relatives is a potent risk factor for diabetes. Type 2
diabetes appears to have a stronger genetic
component than type 1.

Obesity

Origin (Afro-American, Hispanic, Native American,
Asian-American)
 Age (older than 45)
 History of gestational diabetes
 High cholesterol
 Hypertension
 Vascular disease (cerebro-, cardio- or peripheral
vascular )
 DIET & LIFE STYLE HISTORY
• Regularity of meals
• Content of fatty foods
• Content of fruits &
vegetables
• Contents of sugary foods
• Content of salt
• Alcohol intake
• Smoking history
• Occupational history
• Physical activity
 HISTORY IN DIAGNOSED
PATIENTS
• HOME GLUCOSE
TESTING IN PREVIOUSLY
DIAGNOSED PTS.
• INSULIN INJECTIONS –
Ascertain whether the
patient self injects, delivery
device, site chosen, and
whether they experience
any problems.
 SYMPTOMS OF
COMPLICATIONS OF DIABETES
MACROVASCULAR DISEASE
1. CORONARY HEART DISEASE – Pt.
has less severe chest pain symptom
known as silent ischemia due to
autonomic neuropathy. Only symptom
can be breathlessness.
2. PERIPHERAL VASCULAR DISEASE
– Pt. present with claudication. There
may be foot ulceration.
3. CEREBROVASCULAR DISEASE –
Pt. may present with stroke
syndrome. TIA are common.
MICROVASCULAR DISEASE
1. RETINOPATHY – May be asymptomatic until it cause significant
visual loss, acute due to retinal hemorrhage or insidious due to
cataract or maculopathy.
2. NEPHROPATHY – May be asymptomatic until uraemic symptoms
ensues like fatigue, breathlessness, tachypnoea, pleuritic chest
pain and pruritus.
3. NEUROPATHY –
Peripheral sensory neuropathy – numbness, a feeling of walking on
cotton wool and paraesthesias or burning, sharp shooting pains.
Proximal motor neuropathy (Femoral neuropathy) – uncommon but
presents with deep pain and parasthesiae in upper anterior thigh,
followed by wasting of quadriceps muscle.
Mononeuropathies – particularly affecting the median nerve of the hand
(carpal tunnel syndrome ) – This presents with parasthesiae and
numbness in the median nerve distribution of the hand (lateral two-
and-half digits), and is again worse at night. Similar symptoms may
occur in the foot (tarsal tunnel syndrome). Cranial
mononeuropathies are rare
Autonomic Neuropathy- symptoms includes impotence, gustatory
sweating, urinary retention or incontinence, dizziness or syncope
due to postural hypotension, constipation or diarrhoea, and nausea
vomiting due to diabetic gastroparesis.
 EXAMINATION OF
THE DAIBETIC PATIENT
Acute hyperglycemic crises –
1. Severely dehydrated with dry mucous membranes and reduced skin
turgor.
2. Hypotension and tachycardia
3. Signs of diabetic ketoacidosis
Non acute cases :
1. Ascertain BMI
2. Blood pressure – erect and supine
3. Injection sites
4. Dermatological examination
5. Examination of eyes
6. Examination of CVS
7. Examination of Feet
 Dermatological examination
COMMONLY ENCOUNTERED MANIFESTATIONS
 Skin thickening
 Microvascular manifestations in the skin .
 Neuropathy of the foot
 Infection of the skin in diabetes .
 Yellow skin and nails

DISTINCT BUT UNCOMMON MANIFESTATIONS

 Necrobiosis lipoidica
 Necrobiosis lipoidica is a distinct skin manifestation which is more
commonly found in patients who also have diabetes mellitus.
 Diabetic bullae
 With no other apparent cause, diabetics may develop blisters, usually
on the extremities.
 Disseminated granuloma annulare
 Patients who develop disseminated granuloma annulare have been
noted to commonly have diabetes mellitus.
 Kyrle disease

An uncommon but distinct finding in diabetic patients with renal disease.
 Cutaneous side effects of insulin injection
 Patients who need daily insulin to control their sugar metabolism may
develop secondary skin problems.
 PEBBLES - ACANTHOSIS NIGRICANS

Anterolateral neck region and dorsum of right hand of a diabetic patient

with acanthosis nigricans. It is recognized by the darker velvety skin.
The dorsum of the fingers are similarly involved with velvety skin. It is
associated with increased epidermal thickness.

Velvety appearance consists of

multiple closely spaced
micropapules.
pebbles - thick skin of diabetes
mellitus
Although he does not have acanthosis
nigricans, he does have similar
discrete micropapules located on the
knuckle area of this finger..

Proximal nail fold skin of a diabetic

patient who demonstrates
micropapules or "pebbles" in the
absence of acanthosis nigricans.
Note that the micropapules in this
patient are far less exaggerated than
those which occur in acanthosis
nigricans. .
Distal inter-phalangeal joint and dorsum of the distal aspect
of the left foot diabetic patients demonstrating pebbling.
Clinically thickened skin is common on the dorsum of the
hand (especially over the knuckles) and sometimes even on
the dorsum of the toes.
 DIABETIC
SCLEREDEMA
Occurs in about three
percent of diabetics and
is almost totally limited
to those with adult onset
disease.
There is visible thickening
involving skin on the
back of the neck and the
upper back.
Diabetic Hand Syndrome
Diabetic hand syndrome consists of joint limitations (inability to
fully extend a finger) and thickened skin of the hand, especially
involving the dorsum of the fingers palpably thickened skin
Some patients with diabetes mellitus develop thickening of the
skin on the fingers which is termed "scleroderma-like". This
terminology does not imply that existence of vasculitis, or
Raynaud's phenomenon, only that the skin is thicker.

Joint limitation
In addition to thickened skin, diabetic hand syndrome is
characterized by joint limitation. Often diabetics develop
asymptomatic joint limitations of the fingers. This limitation is
usually minor and not incapacitating. Thick skin and joint
limitation seem to correlate with retinopathy.
 Diabetic Hand Syndrome
The patient's finger on the right is pushing
against the examiner's fingers on the left.
The finger skin is taught and when the
patient pushed, his finger blanched except
.for a periungual blush
The examiner is attempting to tent the dorsal
finger skin which is distal to the proximal
interphalangeal joint of this patient . With non-
diabetic subjects, it is fairly easy to pick up a
fold of skin on the dorsum of the fingers. This
is often not the case in persons with diabetes.

The fifth finger demonstrates a typical minor

joint limitation. The fifth finger cannot fully
. extend
 PRAYER SIGN
(CHEIROARTHROPATHY )

The hands of two patients with diabetes mellitus and the diabetic
hand syndrome. The patients are attempting to fully appose the
palms and fingers. The patient on the left illustrates moderate
limitation. The patient on the right has significant impairment.
PERIUNGUAL ERYTHEMA
Microvascular disease is a major complication of diabetes mellitus.
At the capillary level, this can be due to both a structural (e.g.
thickened capillary wall) and functional problems (increased blood
viscosity). Impaired blood flow due to increased viscosity results in
dilated capillary loops, and such clinical manifestations as facial
blush and periungual erythema.

Erythema of the proximal nail fold.

Shin of a patient demonstrating

hyperpigmented atrophic macules.
The patient relates previous trauma
for each of these spots.
DERMOPATHY
Diabetic dermopathy is a condition characterized by the presence
of multiple hyperpigmented atrophic macules on the legs. Typical
lesions are depressed (atrophic) and appear to have post-
inflammatory hyperpigmentation. The occurrence of 4 or more
such lesions is almost always limited to persons with diabetes.
PIGMENTED PURPURA
Pigmented purpura of the legs is most often encountered in the
elderly diabetic. These areas of spontaneous focal extravasation
from the microcirculation are recognized as brown to red macules
and patches.
Erythematous, brown, and golden macular changes on the
shins. The small erythematous areas, representing recent
vascular hemorrhage gradually enlarge, turn brown, and
coalesce with neighboring lesions.
With resolution, the lesion
have a golden appearance.

Close-up view of the shin demonstrating the

presence of diabetic dermopathy and pigmented
purpura. The dermopathy is distinguished by the
atrophy whereas the changes involved with
pigmented purpura are macular.
SENSORY NEUROPATHY
Another major complication of diabetes mellitus is development
of neuropathy. Relative to the skin, the most common
manifestations involve legs and feet. Sensory neuropathy allows
trauma to occur to the feet from ill-fitting shoes which may then
result in ulceration.

callus and ulcer on the distal multiple erosions on the

aspect of the right second toe. dorsal aspect of the toes.
MOTOR NEUROPATHY
Motor neuropathy results in weakened intrinsic foot muscles. The toes
dorsiflex and the foot splays (becomes wider) on weight -bearing. This new
shape may no longer fit the previous shoes and, along with sensory
neuropathy, may potentiate trauma and ulceration.
CHARCOT FOOT
With loss of sensation and weak intrinsic muscles, the foot may fracture
when stressed. Multiple fractures allowed to heal without realignment result
in the distortion of shape.

The toes are being drawn upward. Sensory and motor neuropathy.
She started to run bare foot and heard the
snapping sound in her feet .
 CANDIDA INFECTION
Candida albicans is a frequent pathogen in the skin of
diabetics usually involving the groin or genital region. Candida
involvement of the groin region and uncircumcised penis tend
to occur in men who have poor control of their diabetes.

the groin region has erythema and erythema of the glans penis
multiple satellite papules
 The hands may also become
involved with Candida. Usual sites
of infection include proximal nail
fold and intertriginous areas which
allow for natural moisture to
accumulate.

MALIGNANT EXTERNAL
OTITIS
External otitis is a common, however
in diabetics it may become a serious
problem. The patient complains of
severe ear pain from the otitis. The
infection, due to Pseudomonas, may
even gain access to cranial nerves.
Examination of the ear canal reveals
polypoid growths.
 STAPHYLOCOCCUS
INFECTION
Abscess involving the left arm of
a diabetic patient. This patient
developed a carbuncle at the site
of insulin injection.

This patient has an ankle ulcer which

developed an erythematous halo and a red
streak going up the leg. This vascular ulcer
is complicated by cellulitis and
lymphangitis
 DERMATOPHYTE INFECTION

annular erythematous scaling plaque of

dermatophyte infection.
 YELLOW NAILS
The skin and nails of
patients with diabetes tend
to take on a yellow hue,
probably due to
metabolism of glucose
which has become linked
to protein.

YELLOW SKIN
Persons with diabetes
often have a yellow hue
to the skin, best seen on
the palms and soles.
Probably due to yellow
glucosylation end-
products
NECROBIOSIS LIPOIDICA
Although necrobiosis is a classic finding in diabetes, it is rather
uncommon (less than one percent) and may also occur in
persons who do not have the disease. Typical involvement
occurs on the legs as bilateral erythematous, brown or yellow
plaques with raised margins and central atrophy. The surface of
a lesion often becomes somewhat transparent and enlarged
blood vessels may be seen in the lesion.

characteristic
the early papule stage translucency and
enlargement of
underlying
cutaneous blood
vessels.
SPONTANEOUS BLISTERS IN DIABETES
Lesions may rupture, develop an ulcer or
become secondarily infected.
 DIABETIC NEUROPATHY
Diabetic Neuropathy is a common complication of DM. It usually includes
micro vascular injury to the small blood vessels leading to your nerves.
Diabetic Neuropathy is damage to nerves caused by the prolonged
effect of high sugar levels in the blood.
Diabetic neuropathy is caused by the walls of the blood vessels that supply
the nerves becoming thicker. The end result of this is less nutrients are
unable to get to the nerves as well as a demyelinization. This slows the
ability of the nerves to conduct impulses back to the brain.
The four types are :
-Peripheral – that affects the extremities of the body, notably the feet
-Autonomic – that affects the autonomic nervous system
-Proximal – the areas affects are the hips, thighs and buttocks
-Focal – a focused group of nerves in any region of the body.
There are two forms of neuropathies that can form with diabetes;
polynueropathies and mononeuropathies.
Polynueropathies are the most common in those with diabetes
and is a bilateral sensory disorder. The symptoms for this form
are most common in the toes and feet and normally appear
there first.
Mononeuropathies are isolated events that affect single
nerves. The symptoms of this form of neuropathy are entirely
dependent on which nerve is affected.
CARPAL
TUNNEL
SYNDROME
 INSULIN INJECTION SITE
LIPOATROPHY AND LIPOHYPERTROPHY
DIABETIC NEPHROPATHY
Diabetic nephropathy
refers to kidney problems
which result from diabetes
mellitus. These include the
excretion of protein in the
urine (proteinuria) and
slowly developing kidney
failure. Diabetes interferes
with the function of the
glomerular tuft. When
enough of these tufts have
been affected, kidney
failure results.
 Proteinuria
Most people with established
diabetic nephropathy have
urine containing large
quantities of protein (known
as proteinuria), which their
doctors can detect using a
dipstick urine test.

High blood pressure

Another related condition of diabetic nephropathy is high blood
pressure (hypertension). Hypertension will speed up existing kidney
disease, so treatment of even mild hypertension is necessary for those
with diabetes. Because the function of the kidney deteriorates and
protein is lost, puffy swelling of the body tissues, especially the legs,
can occur. This is called the nephrotic syndrome.
MOUTH COMPLICATIONS
Periodontal disease is infection and inflammation of the gums. It can
cause gum recession, bone and tooth loss. High blood sugars cause
inflammation of the gums and promote infection.
Periodontal disease
Common signs of periodontal disease are gums that are swollen and
bleed easily. Chronic high blood sugar can also cause yeast infections
in the mouth and dental caries.
 Heart Disease & Stroke
Vascular disease can affect all blood vessels in
the body. Blocked arteries in the brain can lead
to a TIA (transient ischemic attack) or stroke.
Blocked arteries in the heart can lead to chest
pain (e.g., angina) or a heart attack. Blocked
arteries in the legs can cause problems with
circulation and walking. Erectile problems also
can be due to blocked arteries.
Vascular disease
It is caused by stiffening and clogging of
arteries (atherosclerosis). In diabetes, when the
blood sugar is chronically high, excessive
amounts of glucose attach to the inner walls of
the blood vessels, decreasing their elasticity.
Elevated blood sugars also cause
atherosclerosis by promoting plaque
formation.
 DIABETIC RETINOPATHY
People with diabetes have an increased chance of developing a variety
of eye problems, including cataracts and glaucoma. Typically,
changes begin to take place in the retina after a patient has been
living with diabetes for 10 to 15 years. The effect of diabetes on the
retina and vitreous is called diabetic retinopathy.
In the earliest phase of the disease, known as background diabetic
retinopathy, the arteries in the retina become weakened and leak,
forming small, dot-like hemorrhages. These leaking vessels often
lead to swelling or edema in the retina, which may result in
decreased vision.
The next stage is known as proliferative diabetic retinopathy. In this
stage, circulation problems lead to oxygen-deprivation in some areas
of the retina. New, fragile, blood vessels develop as the circulatory
system attempts to maintain adequate oxygen levels within the
retina. This is called neovascularization. The delicate vessels
hemorrhage easily and blood may leak into the retina and vitreous,
causing spots or floaters, and an overall decrease in vision.
As the disease progresses even further, continued abnormal vessel
growth and scarring can result in serious problems such as retinal
detachment and glaucoma.
Signs and Symptoms
•Blurred vision - often linked to blood sugar levels
•Floaters and flashes
•Sudden loss of vision

DIABETIC CATARACT
 Investigations for Diabetes Mellitus
Glucose can be estimated chemically and enzymatically. If the fasting blood glucose value
is more than 126 mg/dl or the random blood glucose value is more than 200 mg/dl, then
it is considered to be a case of diabetes.
Glucose Tolernce Test: (GTT)
This test is used to measure the glucose tolerance in a person. The blood is drawn at
intervals of 30 mins each. The first sample is fasting, at 30 mins, 60 min, 120 mins and
180 mins. In all five samples are collected.
The most important role of GTT is to help in the investigation of symptomless glycosuria.

Glycosylated Haemoglobin
Of all the glycated forms of Hb, HbA1c is the most stable. More than 80 per cent of the
glycated form is the HbA1c. Hence, its measurement is taken to be the ideal parameter
to understand the “Long term diabetic control”. This is the most important tool for
monitoring diabetes. This test refers to the hemoglobin component formed by interaction
with glucose, since half life of RBCs is approximately 120 days; a single HbA1c
determination can give information about glycemic control in the preceding 8-12 weeks.
It is estimated by HPLC method, which is considered to be gold standard. The advantage is
that this test does not require any dietary preparations, has low sensitivity but high
specificity compared to oral glucose tolerance test.
Microalbumin (MAU)
MAU as the name suggests, is the first warning signal to an impending
“Nephropathy” - if attention is not paid to keep diabetes under control. Patients with
microalbuminuria have a greater risk for developing renal failure, vascular damage
and risk for cardiovascular damage. It can be estimated by immunoturbidometry and
nephelometry:

Insulin
This test is used for determination of concentration of bioavailable insulin in the
patients. Total insulin exists in free and bound form. In patients without insulin
antibodies, total and free levels are similar, but in patients with insulin antibodies
total insulin levels are dependant on the binding capacity of the circulating
endogenous insulin antibody and availability of insulin to bind to antibody sites. This
test is used to determine dosage of IDDM with insulin antibodies.

Insulin Antibodies
Most common antibodies are IgG, IgM, IgA & IgE Abs have been reported. These
antibodies are generally seen in pre-Type I DM as well as DM pts with exogenous
bovine or human porcine insulin.
Free Insulin
Increased levels of free insulin are seen:
Exogenous insulin
Insulinoma
Insulin resistance
Type II DM.

Proinsulin
Proinsulin is produced in beta cells of pancreas and cleaved into insulin and C-peptide
before release into circulation.
Increased levels are seen in
Insulinomas
Severe hypoglycemic hypoinsulinomas
Hyperproinsulinemia.
Proinsulin inhibits hepatic production of glucose thus useful in type II DM.TG & HDL
concentrations improve with proinsulin
GAD Antibodies
GAD-65 Antibodies: GAD is known as Glutamic Acid Decarboxylase. They are detected
in approximately 90 per cent of patients who are newly diagnosed of Type I DM and 80
per cent of pre-diabetic individuals and first degree relative of patients with IDDM.
C-Peptide
C-peptide is cleaved from proinsulin and released into circulation in the course of insulin
biosynthesis. C-peptide is used for assessment of pancreatic islet cell function.
 Testing :
Fasting Plasma Glucose Test Oral Glucose Tolerance Test
(FPG) - (cheap, fast) (OGTT)
*fasting B.G.L. 100-125 mg/dl *tested for 2 hrs after
signals pre-diabetes glucose-
*>126 mg/dl signals diabetes rich drink
*140-199 mg/dl signals pre-
diabetes
*>200 mg/dl signals diabetes

A.K.A.: Glycated Hemoglobin tests

A1C

♦ 80 to 90 mg per 100 ml, is the normal fasting blood glucose

concentration in humans and most mammals which is
associated with very low levels of insulin secretion.
 Triad of Treatment
Diet

Medication Exercise
Oral hypoglycemics
Insulins
 Diabetes treatment
 Diet
 Lower calorie

Fewer foods of “high glycemic index”
 Spread meals evenly

 Exercise
 Under physician supervision
 Check glucose prior
Diabetes – Oral Medications

6 Classes :
 Sulfonylureas
 Biguanides
 Sulfonylureas and biguanide combination
drugs
 Thiazolidinediones
 Alpha-glycosidase inhibitors
 Meglitinides
 Sulfonylureas
 Stimulate pancreas to secrete insulin

Glyburide (Diabeta) [Prototype Pro p 393]
• Diabenese (chlorpropamide)
• Glucotrol (Glipizide), Gliclazide, Glibenclamide

 Mechanism of Action
 Sulfonylureas interact with receptors on pancreatic β -cells to block
ATP-sensitive potassium channels
 This, in turn, leads to opening of calcium channels
 Which leads to the production of insulin
 Adverse reactions

Hypoglycemia

Water retention/edema

Photosensitivity
 Biguanides
 Decreases liver production of glucose
 Decreases intestinal absorption of glucose
 Improves cell sensitivity to insulin

 Example: Metformin
 GI upset, flatulence
 Cardiac (CHF, MI)
 Thiazolidinediones
 Increase cellular sensitivity to insulin
 Pioglitazone (Actos)
 Rosiglitazone (Avandia)

Patient should have liver enzymes

checked periodically
 D-Phenylalanine derivatives

 Nateglinide (Starlix)

 Rapid onset, short half-life

 Good for those with rapid post prandial rise in
blood glucose
 Combinations
 Glucovance
 Glyburide and Metformin

 Avandamet
 Avandia and Metformin
 Αlpha – glycosidase inhibitors
Block enzymes that help digest starches  slowing the
rise in B.G.L.
- Precose ® (acarbose),

- Glyset ® (miglitol)

Meglitinides
Stimulate more insulin production ;
dependant upon level of glucose present
- Prandin ® (repaglinide)

- Starlix ® (nateglinide)
 Insulin
 Made in beta cells of the pancreas
 Moves glucose into cells (thus acts
like growth hormone in a way)
 Moves potassium into cells (can
buy time in emergencies)
Who need insulin medicine
 Type I diabetes patients whose
body produces no insulin.
 Type 2 diabetes patients that do
not always produce enough
insulin.
Treatment
 subcutaneous injection
Insulin drug evolution
Stage 1 Insulin was extracted from the glands of
cows and pigs. (1920s)

Stage 2 Convert pig insulin into human insulin by

removing the one amino acid that distinguishes them
and replacing it with the human version.
 Stage 3 Insert the human
insulin gene into E. coli and
culture the recombinant E.coli
to produce insulin (trade name
= Humulin®). Yeast is also
used to produce insulin (trade
name = Novolin®) (1987).

Recombinant DNA technology has also made it possible to

manufacture slightly-modified forms of human insulin that
work faster (Humalog® and NovoLog®) or slower
(Lantus®) than regular human insulin.
Types of insulin

• Regular insulins

• Insulin analogs

• Pre-mixed insulin

Short peptide mimics

SITES OF INJECTION
Regular insulins:

 Human insulin: Humulin® (from E.coli),

Novalin® (from yeast)
 NPH - neutral protamine Hagedorn (NPH),
protamine mixed.
 Lente® insulin / Ultralente® insullin-
zinc added
Insulin Analogs:

 Fatty Acid Acylated insulins

 Insulin Lispro (Humalog®) (1996)

 Insulin Aspart (NovoLog®) (2000)

 Insulin Glargine (Lantus®) (2002)
 Insulin Detemir (Levemir®) (Jun.,2005)
 Insulin Glulisine (Apidra®) (Jan., 2006)
 Insulin preparations
given ONLY with syringes marked in “units”

 Rapid acting (lispro,

asparte)
 Short acting (regular)
 Intermediate acting
(NPH)
 Long acting

Ultralente

[Glargine/Lantus]
 Rapid acting insulin
 Lispro (Humolog, Novolog Aspart)
 Onset of action
• “15-30” minutes [may come on in 5 minutes…]

 Peak of action
• 1 - 2 hours

 Duration
• 3 – 4 hours
 Short acting insulins
 Regular (clear so can be given IV)
 Onset of action
• 0.5 to 1 hour

 Peak of action
• 2 – 4 hours

 Duration of action
• 6 – 8 hours
 Intermediate acting insulins
 NPH, Lente (chemicals added. Cloudy)
 Onset of action
• 1 – 4 hours

 Peak of action
• 4 – 12 hours

 Duration of action
• 18 – 24 hours
 Long acting insulins
 Ultralente
 Onset of action
• 4 – 8 hours

 Peak of action
• 18 hours

 Duration of action
• 24 – 36 hours
 Once a day insulin
 Glargine/Lantus
 Cannot be diluted or mixed in syringe with any
other insulin

Slow, steady release
 Daily dosing [usually at bedtime]
 Refrigerated or tosses every 14 days
 Combination insulins
 70/30 (70% NPH and 30% regular)
 Humolog 70/30 (Humolog and regular)

 Fewer injections
 Rotate sites to decrease lipodystrophy
 Miscellaneous
 Byetta for type II Diabetics taking
sulfonylureas or combination
 Mimics physiologic glucose control
• Inhances insulin secretion only in presence of
hyperglycemia
• Insulin secretion decreases as blood glucose
approaches normal

 Neutontin for Diabetic nerve pain

 Amino Acid Substitutons
A- B- chain Position
chai
n
Position
Source/ A21 B3 B28 B29 B30 B31
Type And
B32
Human Asn Asn Pro Lys Thr

Aspart Asn Aspartic Lys Thr

acid
Lispro Asn Lys Pro Thr rapid-acting
Glulisin Asn Lys Pro Glu Thr
e
Glargine Gly Pro Lys Thr Arg
long-acting
Detemir Lys Myristic
acid
Dawn Phenomenon vs Somogyi’s effect
 Dawn phenomenon
Blood sugar rises in early morning

 Somogyi’s (rebound) effect

Blood sugar rise in morning as reaction to
hypoglycemic episode due to
counterregulatory hormone release.