Diabetes

Mellitus

By Rozjanne Chrizsa A. Pahilan

 CASE STUDY
A 56-year-old Hispanic woman presents to
her medical practitioner with symptoms of
fatigue, increased thirst, frequent
urination, and exercise intolerance with
shortness of breath of many months
duration.
She does not get regular medical care and
is unaware of any medical problems. Her
family history is significant for obesity,
diabetes, high blood pressure, and
coronary artery disease in both parents
and several siblings. She is not taking any
medications. Five of her six children had
 CASE STUDY
Physical examination reveals a BMI (body mass
index) of 34, blood pressure 150/90 mmHg and
evidence of mild peripheral neuropathy.
Laboratory tests reveal a random blood sugar of
261 mg/dL; this is confirmed with a fasting plasma
glucose of 192 mg/dL. A fasting lipid panel reveals
a total cholesterol 264 mg/dL, triglycerides 255
mg/dL, high density lipoproteins 43 mg/dL, and low
density lipoproteins 170 mg/dL. What type of
diabetes does this woman have? What further
evaluations should be obtained? How would you
treat her diabetes?
 Overview
Pancreas is both an endocrine gland that
produces the peptide hormone insulin, glucagon,
and somatostatin and an exocrine gland that
produces digestive enzymes
The peptide hormones are secreted from cells
located in the islets of Langerhans ( cells produce
insulin, cells produce glucagon, and cells
produce somatostatin).
These hormones play an important role in
regulating the metabolic activities of the body,
particularly the homeostasis of blood glucose.
 Introduction

Diabetes
Mellitus

refers to a group of common metabolic

disorders that share the phenotype of
hyperglycemia
a heterogeneous group of syndromes
characterized by an elevation of blood glucose
caused by a relative or absolute deficiency of
insulin
 Introduction

factors contributing to hyperglycemia include:

reduced insulin secretion
decreased glucose utilization
increased glucose production

DM is the leading cause of end-stage renal

disease (ESRD), nontraumatic lower extremity
amputations, and adult blindness
 Common Signs and Symptoms

Unusual thirst

Frequent Urination

Weight change (gain or loss)

Extreme fatigue or lack of energy

Blurred vision

Tingling or numbness in the hands or feet

Frequent or recurring infections

 Common Signs and Symptoms

Frequent or recurring infections

Cuts and bruises that are slow to heal

Feeling very tired much of the time

Very Dry skin

 Classification

TYPE 1: INSULIN DEPENDENT DIABETES

TYPE 2: NON-INSULIN DEPENDENT

DIABETES

TYPE 3: OTHER (diabetes due to other causes

for example, genetic defects or medications).

TYPE 4: GESTATIONAL DIABETES

MELLITUS
 TYPE 1: INSULIN DEPENDENT DIABETES

characterized by an absolute deficiency of insulin

caused by massive -cell necrosis
As a result of the destruction of these cells, the pancreas
fails to respond to glucose, and the type 1 diabetic
shows classic symptoms of insulin deficiency
(polydipsia, polyphagia, polyuria, and weight loss).
Type 1 diabetics require exogenous insulin to avoid the
catabolic state that results from and is characterized by
hyperglycemia and life-threatening ketoacidosis.
 TYPE 1: INSULIN DEPENDENT DIABETES

CAUSE: In a normal postabsorptive period, low basal levels of circulating

insulin are maintained through constant -cell secretion. This suppresses
lipolysis, proteolysis, and glycogenolysis. A burst of insulin secretion occurs
within 2 minutes after ingesting a meal, in response to transient increases in the
levels of circulating glucose and amino acids. This lasts for up to 15 minutes
and is followed by the postprandial secretion of insulin. However, having
virtually no functional cells, those with type 1 diabetes can neither maintain a
basal secretion level of insulin nor respond to variations in circulating fuels
TREATMENT:
A person with type 1 diabetes must rely on exogenous (injected) insulin to
control hyperglycemia, avoid ketoacidosis, and maintain acceptable levels of
glycosylated hemoglobin (HbA1c)
The goal in administering insulin to those with type 1 diabetes is to maintain
blood glucose concentrations as close to normal as possible and to avoid wide
swings in glucose levels that may contribute to long-term complications.
 TYPE 2: NON-INSULIN DEPENDENT
DIABETES

influenced by genetic factors, aging, obesity, and

peripheral insulin resistance, rather than by autoimmune
processes or viruses.
CAUSE:
The pancreas retains some -cell function, but variable insulin
secretion is insufficient to maintain glucose homeostasis .The -
cell mass may become gradually reduced in type 2 diabetes.
Type 2 diabetes is frequently accompanied by the lack of
sensitivity of target organs to either endogenous or exogenous
insulin.This resistance to insulin is considered to be a major cause
of this type of diabetes.
 TYPE 2: NON-INSULIN DEPENDENT
DIABETES

Treatment: The goal in treating type 2 diabetes is to:

Maintain blood glucose concentrations within normal limits and to
prevent the development of long-term complications of the disease
Weight reduction, exercise, and dietary modification
decrease insulin resistance and correct the hyperglycemia of type
2 diabetes in some patients.

However, most patients are dependent on pharmacologic intervention

with oral glucose-lowering agents. As the disease progresses, -cell
function declines and insulin therapy is often required to achieve
satisfactory serum glucose levels
 GESTATIONAL DIABETES

defined as carbohydrate intolerance with

onset or first recognition during pregnancy.
Diet, exercise, and/ or insulin administration
are effective in this condition.
Glyburide and metformin may be reasonably
safe alternatives to insulin therapy for
gestational diabetes. However, larger
randomized studies are needed to fully
assess neonatal outcomes and optimal
dosing regimens
Diagnosis
 Diagnosis
Glucose tolerance is classified into three
categories based on the FPG:
FPG < 5.6 mmol/L (100 mg/dL) is considered normal
FPG = 5.66.9 mmol/L (100125 mg/dL) is defined as
IFG
FPG > 7.0 mmol/L (126 mg/dL) warrants the
diagnosis of DM

Based on the OGTT:

IGT is defined as plasma glucose levels between 7.8
and 11.1 mmol/L (140 and 199 mg/dL)
diabetes is defined as a glucose > 11.1 mmol/L (200
mg/dL) 2 h after a 75-g oral glucose load

The current criteria for the diagnosis of DM

emphasize that the FPG is the most reliable and
convenient test for identifying DM in
asymptomatic individuals
 Screening
Widespread use of the FPG as a screening test for type 2
DM is recommended because:
a large number of individuals who meet the current criteria for DM
are asymptomatic and unaware that they have the disorder
epidemiologic studies suggest that type 2 DM may be present for
up to a decade before diagnosis
as many as 50% of individuals with type 2 DM have one or more
diabetes-specific complications at the time of their diagnosis
treatment of type 2 DM may favorably alter the natural history of
DM
The ADA recommends screening all individuals >45 years
every 3 years and screening individuals at an earlier
age if they are overweight [body mass index (BMI) > 25
km/m2] and have one additional risk factor for diabetes
In contrast to type 2 DM, a long asymptomatic period of
hyperglycemia is rare prior to the diagnosis of type 1
DM
Screening
 LONG TERM TREATMENT
Overall Principles
The goals of therapy for type 1 or type 2 DM are to:
(1) eliminate symptoms related to hyperglycemia,
(2) reduce or eliminate the long-term microvascular and
macrovascular complications of DM, and
(3) allow the patient to achieve as normal a lifestyle as possible

To reach these goals, the physician should:

identify a target level of glycemic control for each patient
provide the patient with the educational and pharmacologic
resources necessary to reach this level
monitor/treat DM-related complications

Symptoms of diabetes usually resolve when the plasma

glucose is <11.1 mmol/L (200 mg/dL), and thus most DM
treatment focuses on achieving the second and third
goals.
 INSULIN PREPARATIONS

A. Rapid-acting and short-acting insulin

preparations
Examples:
Insulin lispro, Insulin aspart, and Insulin glulisine
(Rapid-acting)
Regular insulin (short-acting)
B. Intermediate acting insulin
Examples:
Neutral protamine Hagedorn (NPH) insulin
 INSULIN PREPARATIONS
C. Long-acting Insulin Preparations
Examples:
1. Insulin glargine: The isoelectric point of insulin glargine
(GLARQeen) is lower than that of human insulin, leading to
precipitation at the injection site and extending its action. It is
slower in onset than NPH insulin and has a flat, prolonged
hypoglycemic effect with no peak subcutaneously.
2. Insulin detemir: Insulin detemir (deh-TEE-meer) has a
fatty-acid side chain. This addition enhances association to
albumin. Slow dissociation from albumin results in long-
acting properties similar to those of insulin glargine. Neither
insulin detemir nor insulin glargine should be mixed in the
same syringe with other insulins, because doing so may
alter the pharmacodynamic and pharmacokinetic properties.
 INSULIN PREPARATIONS
D. Insulin combinations
Various premixed combinations of human insulins, such as 70-
percent NPH insulin plus 30-percent regular insulin (see Figure
24.8), 50 percent of each of these, and 75-percent NPL insulin plus
25-percent insulin lispro, are also available

E. Standard treatment versus intensive treatment

For patients with diabetes mellitus who require insulin therapy,
standard treatment involves injection of insulin twice daily. In
contrast, intensive treatment seeks to normalize blood glucose
through more frequent injections of insulin (three or more times
daily in response to monitoring blood glucose levels). The ADA
recommends a target mean blood glucose level of 154 mg/dL or
less (corresponding to a HbA1c of 7 percent or less) for patients
with diabetes, and this is more likely to be achieved with intensive
treatment.
 INSULIN PREPARATIONS
MECHANISM OF ACTION:
-Activate insulin receptor
Effects:
-Reduce circulating glucose
-promote glucose transport and oxidation; glycogen,
lipid, protein synthesis, and regulation of gene expression
Clinical applications: TYPE 1 & TYPE 2
PK, Toxicities, Interactions: Parenteral (SC or IV)
Toxicity: Hypoglycemia, weight gain, lipodystrophy
(rare)
 ORAL AGENTS: INSULIN
SECRETAGOGUES
Useful in the treatment of patients who have type 2 diabetes
but who cannot be managed by diet alone.
Patients who have developed diabetes after age 40 and have
had diabetes less than 5 years are those most likely to respond
well to oral glucose-lowering agents.
Patients with long-standing disease may require a combination
of glucose-lowering drugs with or without insulin to control
their hyperglycemia.
 Sulfonylureas
These agents are classified as insulin secretagogues, because they
promote insulin release from the cells of the pancreas
Mechanism Of Action:
1) Stimulation of insulin release from the cells of the pancreas by
blocking the ATP-sensitive K+ channels, resulting in depolarization
and Ca2+ influx
2) reduction in hepatic glucose production; and
3) increase inperipheral insulin sensitivity.
Effects:In px with functioning beta cells, reduce circulating glucose
increase glycogen, far and protein information gene regulation
Clinical Applications: TYPE 2 Diabetes
PK, Toxicities, Interactions : Orally active duration 10-24 h
Toxicity: Hypoglycemia, weight gain
Examples: Glipizide, Glyburide, Glimipiride
 Glinides
This class of agents includes repaglinide and nateglinide .Although they are not
sulfonylureas, they have common actions.
Mechanism Of Action: Like the sulfonylureas, their action is dependent on
functioning pancreatic cells. They bind to a distinct site on the sulfonylurea
receptor of ATP-sensitive potassium channels, thereby initiating a series of
reactions culminating in the release of insulin. However, in contrast to the
sulfonylureas, the glinides have a rapid onset and a short duration of action. They
are particularly effective in the early release of insulin that occurs after a meal and
are categorized as postprandial glucose regulators.
Effects: In px with functioning beta cells, reduce circulating glucose increase
glycogen, far and protein information gene regulation
Clinical applications: TYPE 2 DIABETES
PK, Toxicities, Interactions :
>Oral very fast onset of action duration 5-8 hrs
Toxicity: Hypoglycemian (Repaglinide)
>OralVery fast onset and short duration (<4h)Toxicity:
Hypoglycemia (Nateglinide)
 ORAL AGENTS:
INSULIN SENSITIZERS
Two classes of oral agents, the
biguanides and
thiazolidinediones, improve insulin
action. These agents lower blood
sugar by improving target-cell
response to insulin without
increasing pancreatic insulin
secretion.
 biguanide
s
Metformin, the only currently available biguanide, is
classed as an insulin sensitizer. It increases glucose uptake and
use by
target tissues, thereby decreasing insulin resistance.
Mechanism of action: The main mechanism of action of
metformin is reduction of hepatic glucose output, largely by
inhibiting hepatic gluconeogenesisMetformin also slows
intestinal absorption of sugars and improves peripheral
glucose uptake and utilization. An important property of this
drug is its ability to modestly reduce hyperlipidemia (low-
density lipoprotein [LDL] and very-low-density lipoprotein
[VLDL] cholesterol concentrations fall, and high-density
lipoprotein [HDL] cholesterol rises).
Metformin may be used alone or in combination with one of
the other agents as well as with insulin. Hypoglycemia may
occur when metformin is taken in combination with insulin.
 biguanide
s
Effects: Decreased endogenous glucose production
Clinical applications: TYPE 2 DIABETES
PK, Toxicities, Interactions :
OralMaximal plasma concentration in 2-3 h
Toxicity: Gastrointestinal symptoms, lactic acidosis
(rare) cannot use if impaired renal/hepatic
function Congestive heart failure (CHF),
hypoxic/acidotic states, alcoholism
Other uses: In addition to the treatment of type 2
diabetes, metformin is effective in the treatment of
polycystic ovary disease. Its ability to lower
insulin resistance in these women can result in
ovulation and, therefore, possibly pregnancy.
 Thiazolidinediones
(glitazones)
Another group of agents that are insulin
sensitizers are the thiazolidinediones (TZDs),
also called the glitazones.
Although insulin is required for their action,
these drugs do not promote its release from
the pancreatic cells, so hyperinsulinemia is
not a risk.
Troglitazone was the first of these to be
approved for the treatment of type 2 diabetes
but was withdrawn after a number of deaths
from hepatotoxicity were reported.
 Thiazolidinediones
(glitazones)
Mechanism of action: Although the exact mechanism by which
the TZDs lower insulin resistance remains to be elucidated, they
are known to target the peroxisome proliferatoractivated receptor-
(PPAR), a nuclear hormone receptor. Ligands for PPAR regulate
adipocyte production and secretion of fatty acids as well as glucose
metabolism, resulting in increased insulin sensitivity in adipose
tissue, liver, and skeletal muscle. Hyperglycemia, hyperinsulinemia,
hypertriglyceridemia, and elevated HbA1c levels are improved.
Effects: Reduces insulin resistance
Clinical Applications: Type 2 diabetes
PK, Toxicities, Interactions :
Oral, long acting(>24h)
Toxicity: Fluid retention, edema, anemia, weight gain, macular
edema, bone fractures in women, cannot use if CHF, hepatic
disease
Examples: Pioglitazone and Rosiglitazone
 ALPHA GLUCOSIDASE
INHIBITORS
Mechanism Of Action
These drugs are taken at the beginning of meals. They act by
delaying the digestion of carbohydrates, thereby resulting in lower
postprandial glucose levels. Both drugs exert their effects by
reversibly inhibiting membrane-bound -glucosidase in the intestinal
brush border. This enzyme is responsible for the hydrolysis of
oligosaccharides to glucose and other sugars. Consequently, the
postprandial rise of blood glucose is blunted. Unlike other oral
glucose-lowering agents, these drugs neither stimulate insulin
release nor increase insulin action in target tissues.
Effects: Reduce conversion of starch and disaccharides to
monosaccharides Reduce post-prandial hyperglycemia
Clinical applications: TYPE 2 DIABETES
PK, Toxicities, Interactions :
OralRapid onset
Toxicity: Gastrointestinal symptoms cannot use if impaired
renal/hepatic function, intestinal disorders
Examples: Acarbose, Miglitol
 DIPEPTIDYL
PEPTIDASE-IV
INHIBITORS
Mechanism of Action:These drugs inhibit the enzyme DPP-IV,
which is responsible for the inactivation of incretin hormones such
as glucagon-like peptide-1 (GLP-1). Prolonging the activity of
incretin hormones results in increased insulin release in response to
meals and a reduction in inappropriate secretion of glucagon
Effects: Reduces post-meal glucose excursions: Increases
glucose-mediated insulin release, lowers glucagon levels, slow
gastric emptying, decreases appetite
Clinical applications: Type 2 Diabetes
PK, Toxicities, Interactions :
Oral half-life-12 hr 24 hr duration of action
Toxicity: Rhinitis, Upper respiratory infections, headaches, pancreatitis,
rare allergic reactions
Examples: Sitagliptin, Saxagliptin
 INCRETIN MIMETICS;
Glucagon-Like Polypeptide-1
(GLP-1) Receptor Agonist
Oral glucose results in a higher secretion of insulin than
occurs when an equal load of glucose is given IV. This
effect is referred to as the incretin effect and is
markedly reduced in type 2 diabetes. The incretin
effect occurs because the gut releases incretin
hormones, notably GLP-1 and glucose-dependent
insulinotropic polypeptide, in response to a meal.
Incretin hormones are responsible for 60 to 70 percent
of postprandial insulin secretion.
These agents may be used as adjunct therapy in
patients who have failed to achieve adequate glycemic
control on a sulfonylurea, metformin, a glitazone, or a
combination thereof.
 INCRETIN MIMETICS; Glucagon-
Like Polypeptide-1 (GLP-1)

Receptor Agonist
Mechanism of Action: The incretin mimetics are analogs of GLP-1
that exert their activity by acting as GLP-1 receptor agonists. These
agents not only improve glucose-dependent insulin secretion but
also slow gastric emptying time, decrease food intake, decrease
postprandial glucagon secretion, and promote -cell proliferation.
Consequently, weight gain and postprandial hyperglycemia are
reduced, and HbA1c levels decline.
Effects: Reduces post meal glucose excursions, Increases
glucose-mediated insulin release, lowers glucagon levels, slows
gastric emptying, decreases appetite
Clinical Applications: Type 2 Diabetes
PK, Toxicities, Interactions :
Parenteral (SC) half-life-2,4 h
Toxicity: Nausea, headache, vomiting, anorexia mild weight loss,
pancreatitis
Examples: Exenatide and Liraglutide
 OTHERS: (According to Katzung)
Subclass MOA Effects Clinical PK,
applications Toxicities,
Interactions
AMYLIN Analog of Reduces post- Type 1 and Parenteral
ANALOG amylin:Binds meal glucose type 2 (SC) rapid
Pramlintid to amylin excursions: diabetes onset half-
e receptors Lowers life- 48 min+
glucagon Toxicity:
levels, slows Nausea,
gastric anorexia,
emptying, hypoglycemia
decreases headache
appetite
BILE ACID Bile acid Lowers Type 2 Oral 24-h
SEQUESTRAN binder glucose diabetes duration of
T through action
Colesevela unknown Toxicity:
m HCl mechanisms Constipation,
indigestion,
flatulence
 LONG TERM TREATMENT
Insulin Secretagogues
stimulate insulin secretion by interacting with the ATP-sensitive
potassium channel on the beta cell
most effective in individuals with type 2 DM of relatively recent onset
(<5 years), who have residual endogenous insulin production
reduce both fasting and postprandial glucose
Repaglinide and nateglinide are not sulfonylureas but also interact with
the ATP-sensitive potassium channel

have the potential to cause profound and persistent hypoglycemia,

especially in elderly individuals

their use in individuals with significant hepatic or renal dysfunction is

not advisable

Weight gain, a common side effect of sulfonylurea therapy

 LONG TERM TREATMENT
Biguanides
Metformin is representative of this class of agents
It reduces hepatic glucose production through an undefined
mechanism and improves peripheral glucose utilization
slightly
Metformin reduces fasting plasma glucose and insulin levels,
improves the lipid profile, and promotes modest weight loss
Gastrointestinal side effects:
Diarrhea
Anorexia
Nausea
metallic taste
The major toxicity of metformin, lactic acidosis
Metformin should be discontinued in patients who are
seriously ill, in patients who can take nothing orally, and in
those receiving radiographic contrast material
 LONG TERM TREATMENT
-Glucosidase Inhibitors
Acarbose and Miglitol
reduce postprandial hyperglycemia by delaying glucose
absorption; they do not affect glucose utilization or
insulin secretion
reduce glucose absorption by inhibiting the enzyme that
cleaves oligosaccharides into simple sugars in the
intestinal lumen
The major side effects (diarrhea, flatulence, abdominal
distention) are related to increased delivery of
oligosaccharides to the large bowel and can be
reduced somewhat by gradual upward dose titration
This class of agents is not as potent as other oral agents
in lowering the hemoglobin A1C but is unique because
it reduces the postprandial glucose rise even in
individuals with type 1 DM
 LONG TERM TREATMENT
Thiazolidinediones
reduce insulin resistance
bind to the PPAR- (peroxisome proliferator-activated receptor-)
nuclear receptor
The PPAR- receptor is found at highest levels in adipocytes but
is expressed at lower levels in many other tissues
Thiazolidinediones promote a redistribution of fat from central
to peripheral locations
Circulating insulin levels decrease with use of the
thiazolidinediones, indicating a reduction in insulin resistance
Thiazolidinediones are associated with weight gain, a small
reduction in the hematocrit, and a mild increase in plasma
volume
Peripheral edema and CHF may occur and is more common in
individuals also treated with insulin
These agents are contraindicated in patients with liver disease
or CHF (class III or IV)
 LONG TERM TREATMENT
Agents that Enhance GLP-1 Receptor Signaling
"Incretins" amplify glucose-stimulated insulin secretion
Agents that either act as a GLP-1 agonist or enhance endogenous
GLP-1 activity have become available and are under development
Exenatide, is an analogue of GLP-1
Has prolonged GLP-1-like action by binding to GLP-1 receptors found
in islets, the gastrointestinal tract, and the brain
Exenatide increases glucose-stimulated insulin secretion, suppresses
glucagon, and slows gastric emptying
Exenatide does not promote weight gain; in fact, most patients
experience modest weight loss
It appears that GLP-1 agonists also suppress appetite
The A1C reductions with exenatide are modest compared to those
with some oral agents
Agents that Enhance GLP-1 Receptor Signaling
Exenatide should not be used in patients taking insulin
The major side effects are nausea, vomiting, and diarrhea; some
patients taking insulin secretagogues may require a reduction in
those agents to prevent hypoglycemia
 LONG TERM TREATMENT
Agents that Enhance GLP-1 Receptor
Signaling
DPP-IV inhibitors represent a new class of oral agents
that inhibit degradation of native GLP-1 and thus
enhance incretin effect
These agents promote insulin secretion in the absence of
hypoglycemia or weight gain, and appear to have a
preferential effect on postprandial blood glucose
The FDA has approved the first DPP-IV inhibitor,
sitagliptin, for use with diet and exercise to improve
glycemic control in adult individuals with type 2 DM
It can also be used in combination with metformin or a
thiazolidinedione
Renal function should be assessed prior to initiation of
sitagliptin therapy and periodically thereafter
 EMERGING THERAPIES
Whole pancreas transplantation (performed concomitantly with a
renal transplant) may normalize glucose tolerance and is an
important therapeutic option in type 1 DM, though it requires
substantial expertise and is associated with the side effects of
immunosuppression
Pancreatic islet transplantation has been plagued by limitations in
pancreatic islet isolation and graft survival and remains an
area of clinical investigation
Many individuals with long-standing type 1 DM still produce very
small amounts of insulin or have insulin-positive cells within the
pancreas
This suggests that beta cells are slowly regenerating but are
quickly destroyed by the autoimmune process
Thus, efforts to suppress the autoimmune process and to
stimulate beta cell regeneration are underway both at the time of
diagnosis and in years after the diagnosis of type 1 DM
Closed-loop pumps that infuse the appropriate amount of insulin in
response to changing glucose levels are potentially feasible
now that continuous glucose-monitoring technology has been
 Complications of Therapy for
Diabetes Mellitus
Side effects of intensive treatment include:
an increased frequency of serious hypoglycemia
most serious complication
weight gain
occurs with most (insulin, insulin secretagogues,
thiazolidinediones) but not all (metformin, - glucosidase
inhibitors, exenatide) therapies that improve glycemic
control
increased economic costs
greater demands on the patient

As discussed previously, transient worsening of

diabetic retinopathy or neuropathy sometimes
accompanies improved glycemic control
 CASE STUDY
Subjective Data
symptoms of fatigue, increased thirst, frequent
urination, and exercise intolerance with shortness
of breath of many months duration.
Does not get regular medical care and is unaware
of any medical problems.
Family history is significant for obesity, diabetes,
high blood pressure, and coronary artery disease
in both parents and several siblings.
She is not taking any medications.
Five of her six children had birth weight of over 9
pounds.
 CASE STUDY

Objective Data
Physical Examination
Laboratory tests
- Random blood sugar of 261 mg/dL;
-Fasting plasma glucose of 192 mg/dL.
-Fasting lipid panel reveals:
>a total cholesterol 264 mg/dL
>triglycerides 255 mg/dL
>high density lipoproteins 43 mg/dL
> low density lipoproteins 170 mg/dL
 CASE STUDY
ANSWER
This patient has multiple risk factors for type 2 diabetes.
Although she does not have a prior history of fasting
hyperglycemia, glucose intolerance, or gestational diabetes,
other risk factors are present.
Further evaluations that should be obtained include HbA1c
concentration dilated retinal examination, baseline laboratory
tests, spot urine test for microalbumin/creatinine ratio, plasma
creatinine level, and neurologic examination. The patient
should be taught how to use a glucose meter and monitor her
fingerstick blood glucose level, referred to a nutritionist for
dietary instruction and given diabetes self-management
education. Assuming she has no renal or hepatic impairment,
hygienic interventions (diet and exercise) and metformin would
be first line of treatment. If she is unable to achieve adequate
glycemic control on metformin, an additional agent such as
insulin secretagogue (ie, sulfonylureas, meglitinide, or
nateglinide), insulin, or another antidiabetic medication could