1.

DM type 2

-refers to a group of common metabolic disorders that share the phenotype of

hyperglycemia. Several distinct types of DM are caused by a complex interaction of genetics and
environmental factors. Depending on the etiology of the Dm, factors contributing to hyperglycemia
include reduced insulin secretion, decreased glucose utilization and increased glucose production.
- The metabolic dysregulation assocaited with DM causes secondary pathophysiologic
changes in multiple organ systems that impose a tremendous burden on the individual with diabetes
and on the health care system.
Epidemiology

Occurrence in the United States

A 2017 Centers for Disease Control and Prevention (CDC) report estimated that in the
United States, as of 2015, 30.3 million persons of all ages, or 9.4% of the population, had
diabetes (including 30.2 million adults aged 18 years or above, or 12.2% of all US adults) and
84.1 million adults (33.9% of the adult population) had prediabetes.
Prediabetes, as defined by the American Diabetes Association, is that state in which blood
glucose levels are higher than normal but not high enough to be diagnosed as diabetes. It is
presumed that most persons with prediabetes will subsequently progress to diabetes. In 2015,
according to the CDC report, prediabetes was present in 23.1 million persons aged 65 years or
older (48.3%).
A study by Andes et al using a cross-sectional analysis of the National Health and
Nutrition Examination Survey (2005-2016) indicated that in the United States, prediabetes
exists in approximately 1 out of 5 adolescents and 1 out of 4 young adults.
As estimated for 2015, diabetes occurred in 4.6 million adults aged 18-44 years (4.0%),
14.3 million aged 45-64 years (17.0%), and 12.0 million aged 65 years or older (25.2%). Of
those adults with diabetes, however, 7.2 million did not know or did not report that they had the
disease.
In 2014, the CDC reported that about 40% of US adults will develop diabetes, primarily
type 2, in their lifetime, and more than 50% of ethnic minorities will be affected. This is
substantially higher than previous estimates. The central reason for the increase is obesity.
A study by Ludwig et al found that neighborhoods with high levels of poverty are
associated with increases in the incidence of extreme obesity and diabetes. Although the
mechanisms behind this association is unclear, further investigation is warranted\

International occurrence
Type 2 diabetes mellitus is less common in non-Western countries where the diet contains
fewer calories and daily caloric expenditure is higher. However, as people in these countries
adopt Western lifestyles, weight gain and type 2 diabetes mellitus are becoming virtually
epidemic.
 Rates of diabetes are increasing worldwide. The International Diabetes Federation predicts
that the number of people living with diabetes will to rise from 366 million in 2011 to 552
million by 2030. [73] In the United States, the prevalence of diagnosed diabetes has more than
doubled in the last 3 decades, largely because of the increase in obesity.

The top 10 countries in number of people with diabetes are currently India, China, the
United States, Indonesia, Japan, Pakistan, Russia, Brazil, Italy, and Bangladesh. The greatest
percentage increase in rates of diabetes will occur in Africa over the next 20 years.
Unfortunately, at least 80% of people in Africa with diabetes are undiagnosed, and many in
their 30s to 60s will die from diabetes there.
- Pat
hophysiology
- Typ
e 2 DM is characterized by impaired insulin secretion, insulin resistance, excessive hepatic
glucose production and abnormal fat metabolism.
- Ob
esity particularly visceral or central is very common in type 2 DM.
- In
early stages if the disorder, glucose tolerance remains near normal, despite insulin
resitance, because of the pancreatic beta cells compensate by increasing insulin output.
- An
insulin resistance and compensatory hyperinsulinemia progress the pancreatic islets in
certain individuals are unable to sustain the hyperinsulinemia state.
- IG
T, characterized by elevations in postprandial glucose, then develops.
- A
further decline in insulin secretion and an increase in hepatic glucose production lead to
overt diabetes with fasting hyperglycemia.
- Ulti
mately beta cell failure ensues. Although both insulin resistance and impaired secretion
contribute to the pathogenesis if type 2 DM.

- Ris
k factors
- Phy
sical inactivity
- Fa
mily history of diabetes
- Ob
esity ( BMI > 25 kg/m2 or ethnically relevant definition for overweight)
- Hig
h risk ethnicity ( African American, Latino, Native American, Asian American, Pacific
Islander)
- GD
M or delivery of a baby > 9 lbs (4kg)
 - His
tory of cardiovascular disease or hypertension (140/90 mmHg)
- HD
L cholesterol < 35 mg/dl (0.90 mmol/L) and or triglycerides > 250 mg/dl (2.82
mmol/L )
- Hb
A1C 5.7-6.4 %, IGT or IFG on previous testing
- Co
nditions with insulin resistance ( acanthrosis nigricans, polycystic ovary syndrome)

- Cli
nical Manifestations
- Cla
ssic symptoms:
- pol
yuria
- pol
ydipsia
- pol
yphagia
- noc
turia
- wei
ght loss
-others: fatigue, weakness, blurred vision, frequent superficial infections and
poor wound healing.

* Important: explain why patient experienced occasional constipation (insert

pathophysio of Diabetic Neuropathy and Gastroparesis)
- Dia
gnostic work up- routine labs, screening tests

Glucose Tolerance Fasting Plasma Glucose Glucose After Oral Glucose HbA1c
Challenge

Normal <10 mg/dL (5.6 mmol/L) <140 mg/dL (7.8 mmol/L) < 5.7%
Impaired Glucose 100- 125 mg/dL (5.6-6.9 140-199 mg/dL (7.8 mmol/L) 5.7 - 6.4 %
Homeostasis mmol/L
Diabetes Mellitus > 126 mg/dL (7.0 mmol/L) >200 mg/dL (11.1 mmol/L) >6.5%

Criteria diagnosis
 Either of the following:
• Hemoglobin A1c > 6.5% or
• FPG > 126 mg/dL ( 7.0 mmol/L or
• 2 hour plasma glucose > 200 mg/dL (11.1
mmol/L) during 75 g OGTT, or
• symptoms of DM + RBS >200 mg/dL (11.1
mmol/L)

2. Hypertension

DIAGNOSIS OF HYPERTENSION

Two or more elevated readings on at least 2 clinic visits over a period of one
to several weeks

Definition – adults with:

SBP > 140 mmHg, or o DBP > 90 mmHg

• II. CLASSIFICATION OF HYPERTENSION

• A. Classification as to Etiology

•  Primary / Essential (most common)

• Secondary Hypertension

• B. Clues for Suspecting Secondary Hypertension

• Age of onset <20 or >50 years

• No family history of HPN

•  DBP >100-120 mmHg

• Sudden increase in BP in a patient with stable Stage I HPN

• Poor BP control, despite good compliance

• Systemic findings (e.g. weight loss/gain, potassium abnormalities)

Epidemiology
Hypertension is a worldwide epidemic; accordingly, its epidemiology has been well
studied. Data from National Health and Nutrition Examination Survey (NHANES)
spanning 2011-2014 in the United States found that in the population aged 20 years or
older, an estimated 86 million adults had hypertension, with a prevalence of 34%.
 2017 Data from the Centers for Disease Control and Prevention's (CDC) National
Center for Health Statistics (NCHS) spanning 2015-2016 show a hypertension
prevalence of 29.0% among those aged 18 and older (see the following image). The
following image shows prevalence of hypertension among adults aged 18 and over, by
sex and age: United States, 2015–2016.
 - Pat
hophysiology

- Risk factors
- Cli
nical manifestations
An accurate measurement of blood pressure is the key to diagnosis. Several determinations
should be made over a period of several weeks. At any given visit, an average of 3 blood
pressure readings taken 2 minutes apart using a mercury manometer is preferable. [5, 7] On the
first visit, blood pressure should be checked in both arms and in one leg to avoid missing the
diagnosis of coarctation of aorta or subclavian artery stenosis.
 The patient should rest quietly for at least 5 minutes before the measurement. Blood
pressure should be measured in both the supine and sitting positions, auscultating with the bell
of the stethoscope. As the improper cuff size may influence blood pressure measurement, a
wider cuff is preferable, particularly if the patient’s arm circumference exceeds 30 cm.
Although somewhat controversial, the common practice is to document phase V (a
disappearance of all sounds) of Korotkoff sounds as the diastolic pressure.

Ambulatory or home blood pressure monitoring provides a more accurate prediction of

cardiovascular risk than do office blood pressure readings. [53] "Nondipping" is the loss of the
usual physiologic nocturnal drop in blood pressure and is associated with an increased
cardiovascular risk.

A study by Wong and Mitchell indicated that independent of other risk factors, the
presence of certain signs of hypertensive retinopathy (eg, retinal hemorrhages,
microaneurysms, cotton-wool spots) is associated with an increased cardiovascular risk (eg,
stroke, stroke mortality). [54] Consequently, perform a funduscopic eye evaluation to identify
any signs of early or late, chronic or acute hypertensive retinopathy, such as arteriovenous
nicking or vessel wall changes (eg, copper/silver wiring, hard exudates, flame-shaped
hemorrhages, papilledema). Acute or chronic ocular changes can be the initial finding in
asymptomatic patients that requires a primary care referral. Alternatively, a symptomatic
patient may be referred to the ophthalmologist for visual changes due to hypertensive changes.

Palpation of all peripheral pulses should be performed. Absent, weak, or delayed femoral
pulses suggests coarctation of the aorta or severe peripheral vascular disease. In addition,
examine the neck for carotid bruits, distended veins, or enlarged thyroid gland. [5, 7] Listen for
renal artery bruit over the upper abdomen; the presence of a bruit with both a systolic and
diastolic component suggests renal artery stenosis.

A careful cardiac examination is performed to evaluate signs of LVH. These include

displacement of apex, a sustained and enlarged apical impulse, and the presence of an S4.
Occasionally, a tambour S2 is heard with aortic root dilatation.
* Important: explain why patient experienced dizziness

2.Metabolic Syndrome
 Metabolic abnormalities that confer an increased risk of cardiovascular disease and
diabetes mellitus

• Insulin resistance: most accepted an unifying hypothesis in metabolic

syndrome

•  Hypertriglycerides is an excellent marker of insulin resistance

• Other associated conditions: non-alcoholic fatty liver, hyperuricemia,

polycystic ovarian syndrome and obstructive
sleep apnea

Epidemiology
Occurrence in the United States
Metabolic syndrome is increasing in prevalence, paralleling an increasing epidemic
of obesity. In the United States, almost two thirds of the population in 2008 was
overweight or obese, with more than one fourth of the population meeting diagnostic
criteria for metabolic syndrome. [29] 2004 Data from a 1999-2000 survey showed that
the age-adjusted prevalence of metabolic syndrome among US adults aged 20 years
or older had risen from 27% (1988-1994 data) to 32%. [30] 2011-2014 National Health
and Nutrition Examination Survey (NHANES) data showed a crude estimate of 36.5%
for the prevalence of adult obesity (32.3% in adults aged 20-39 years; 40.2% in those
aged 40-59 years; 37.0% in those aged ≥60 years). [20] There was a 38.3% overall
prevalence of obesity in women and a 34.3% in men. Among youth aged 2-19 years,
there was a 17% prevalence of obesity over the same period (8.9% in those aged 2-5
years; 17.5% in those aged 6-11 years; 20.5% in those aged 12-19 years).
Fortunately, since peaking in 2001-2002, the overall prevalence of metabolic
syndrome in the United States has fallen, primarily due to decreases in the
prevalences of hypertriglyceridemia and hypertension—and in spite of increases in the
prevalences of hyperglycemia and obesity/waist circumference. [31] Data from the
2009-2010 NHANES showed that the age-adjusted prevalence of metabolic syndrome
had fallen to approximately 24% in men and 22% in women.

International occurrence
Metabolic syndrome is a burgeoning global problem, with an increasing prevalence
in urban populations of some developing countries. [10, 21] Approximately one fourth
of the adult European population is estimated to have metabolic syndrome, with a
similar prevalence in Latin America. [29] It is also considered an emerging epidemic in
developing East Asian countries, including China, Japan, and Korea. The prevalence
of metabolic syndrome in East Asia may range from 8-13% in men and from 2-18% in
women, depending on the population and definitions used.
 In Japan, the Ministry of Health, Labor, and Welfare has instituted a screening and
interventional program. [36] Metabolic syndrome has been recognized as a highly
prevalent problem in many other countries worldwide.
Pathophysiology
Target organ damage occurs through multiple mechanisms in metabolic
syndrome. The individual diseases leading to metabolic syndrome produce adverse
clinical consequences. For example, hypertension in metabolic syndrome causes left
ventricular hypertrophy, progressive peripheral arterial disease, and renal dysfunction.
However, the cumulative risk for metabolic syndrome appears to cause microvascular
dysfunction, which further amplifies insulin resistance and promotes hypertension.

Metabolic syndrome promotes coronary heart disease through several

mechanisms. It increases the thrombogenicity of circulating blood, in part by raising
plasminogen activator type 1 and adipokine levels, and it causes endothelial
dysfunction. Metabolic syndrome may also increase cardiovascular risks by increasing
arterial stiffness. Additional mechanisms include oxidative stress, which has been
associated with numerous components of metabolic syndrome.
- risk factors
-Clinical manifestations

Approach Considerations
Initial laboratory studies in patients suspected of having metabolic syndrome should include
standard chemistries to assess for hyperglycemia and renal dysfunction and lipid studies to assess
for hypertriglyceridemia or low HDL levels.
 If a family history of early coronary or other atherosclerotic disease is present, consider
including, in addition to HDL-C and low-density lipoprotein cholesterol (LDL-C), studies of
lipoprotein(a), apolipoprotein-B100, high-sensitivity C-reactive protein (CRP), and (if the patient
does not already merit the lowest LDL-C target [< 70]), homocysteine and fractionated LDL-C.

In view of the various associations between metabolic syndrome and other conditions discussed
elsewhere in this article, additional helpful blood tests may include thyroid and liver studies,
hemoglobin-A1C levels, and uric acid. Increased thyroid stimulating hormone (TSH) has been
linked to a higher prevalence of metabolic syndrome. Hyperuricemia appears to be much more
common in patients with metabolic syndrome than in the general population, and this is attributed to
the inflammatory effects of metabolic syndrome. [82] Further studies should be pursued as clinical
findings dictate.

Imaging studies
Imaging studies are not routinely indicated in the diagnosis of metabolic syndrome. However, they
may be appropriate for patients with symptoms or signs of the many complications of the syndrome,
including cardiovascular disease. Complaints of chest pain, dyspnea, or claudication may warrant
additional testing with electrocardiography (rest/stress ECG), ultrasonography (vascular or
rest/stress echocardiography), stress single-photon emission computed tomography (SPECT),
cardiac positron emission tomography (PET), or other imaging studies.

Testing for sleep-related breathing disorder

Investigation into other causes or exacerbating factors should be considered. For example, sleep-
related breathing disorders, such as obstructive sleep apnea, are becoming increasingly relevant and
novel risk factors for metabolic syndrome. [4]

The difficulty in clarifying the associations between obstructive sleep apnea and metabolic
syndrome lie in part with the confounding effect of obesity. [83] Nevertheless, patients reporting
significant sleep disturbances, snoring, possible pauses, and/or daytime drowsiness may benefit
from further investigation for a treatable sleep-related breathing disorder, including through
polysomnography.
Cardiovascular risk assessment
New guidelines on the assessment of cardiovascular risk, released in late 2013 by the American
Heart Association/American College of Cardiology (AHA/ACC), recommend use of a revised
calculator for the risk of developing a first atherosclerotic cardiovascular disease (ASCVD) event,
which is defined as one of the following in a person who was initially free from ASCVD :

• No
nfatal myocardial infarction
•
• Dea
th from coronary heart disease
•
• Str
oke (fatal or nonfatal)