Approach To Endocrine Complaints I

Question 1

What are the classic endocrine glands?

Answer 1

Pituitary, thyroid, parathyroid, pancreatic islets, adrenal glands

Question 2

What is the mechanism of pathology for hormone excess?

Answer 2

Neoplasia, autoimmune disorders, or excess hormone administration

Question 3

What are the mechanisms of pathology for hormone deficiency?

Answer 3

Glandular destruction by autoimmunity, surgery, infection, inflammation, infarction, hemorrhage, tumor infiltration

Question 4

What is the mechanism of pathology for hormone resistance?

Answer 4

Defective hormone action despite increased hormone levels
Rare genetic disorders
Acquired functional resistance (generally reversible) - receptor downregulation and postreceptor desensitization of signaling pathways

Question 5

What is the general rules for tx of hormone excess?

Answer 5

Remove or destroy tumor/gland, block excess hormone, decrease excess hormone

Question 6

What is the general rule for Tx of hormone deficiency?

Answer 6

Replace hormone, ideally as physiologically as possible

Question 7

What is the general rule for Tx of hormone resistance?

Answer 7

Overcome resistance, resensitize target organs

Decrease high hormone levels

Question 8

How should you clinically evaluate endocrine disorders?

Answer 8

Most glands are relatively inaccessible - look for signs/sx of hormone excess/deficiency, recognize patterns
Presenting sx
ROS: when things are vague, go wide
Prior illness, medications
Family and social history
Physical exam clues: directly examine thyroid, gonads; recognize clues (e.g. acanthosis nigiricans)
Appropriate diagnostic testing - usually biochemical testing +/- imaging

Question 9

What is the prevalence of obesity in adults?

Answer 9

36% BMI >30

70% BMI >25

Question 10

What is the prevalence of type 2 DM in adults?

Answer 10

> 8%

Question 11

Describe obesity

Answer 11

Fat cells adapted to store excess energy efficiently
Measuring obesity by BMI (weight/height^2)
Etiology: genetic predisposition + environment, cultural factors, SES factors
Complex neuroendocrine and metabolic systems that regulate energy intake, storage and expenditure

Question 12

What is the prevalence of HLD in adults?

Answer 12

20-25%

Question 13

What is the prevalence of metabolic syndrome in adults?

Answer 13

35%

Question 14

Describe the epidemiology of metabolic syndrome

Answer 14

Other names = syndrome X or insulin resistance syndrome
Greater prevalence with increased age
Prevalence of 33% overall in US

Question 15

What is metabolic syndrome?

Answer 15

Metabolic abnormalities that confer increased risk of CVD and DM

Question 16

What are risk factors for metabolic syndrome?

Answer 16

Overwight/obesity especially central adiposity
Sedentary lifestyle, genetics, aging, DM2, CVD (3x risk of heart attack or stroke), lipid abnormalities
Other associated conditions - fatty liver disease, hyperuricemia, PCOS, OSA

Question 17

What is the criteria for diagnosing metabolic syndrome?

Answer 17

Any 3 or more of the following:
Central obesity (weight circumference >40 for men and >35’ for women)
Abnormal lipids (triglycerides high and high-density lipoprotein low)
BP >130/85
Fasting glucose >100mg/dlL

Question 18

What is the management for metabolic syndrome?

Answer 18

Lifestyle changes such as diet (Mediterranean, DASH) and exercise
Weight reduction is the primary approach (consider weight loss medication, surgery)
Treat comorbidities like impaired fasting glucose (metformin), HTN and lipids

Question 19

Describe type 2 DM

Answer 19

Insulin resistance leading to ineffective transport of glucose out of blood vessels into cells
-also impaired insulin secretion
-increased hepatic glucose production
Glucose levels rise in the blood (hyperglycemia)
Hyperglycemia and increased insulin leading to end organ damage

Question 20

What is the epidemiology of T2DM?

Answer 20

Estimated to effect 9.4% of US population
Prevalence on the rise with increased sedentary lifestyle and obesity
7th leading causing of death
Long asymptomatic period so screening is important (start screening with presence of risk factors)

Question 21

What are the risk factors for T2DM?

Answer 21

Age >45, BMI >25, DM2 in a 1st degree relative, sedentary lifestyle, high risk ethnicity (African-American, Hispanic, Native American, Asian-American, Pacific Islanders)
History of gestational diabetes (insulin resistance as a consequence of hormones of pregnancy)
HTN, dyslipidemia, prediabetes (HbA1c and/or glucose mildly elevated), PCOS and history of vascular disease

Question 22

What is HbA1c?

Answer 22

A simple blood test that measures average blood sugar levels over the past 3 months

Question 23

What is the clinical presentation for T2DM?

Answer 23

Polyuria, polydipsia, polyphasic, rapid weight loss, increased hunger, weight gain, dehydration, fatigue, blurry vision, impaired healing, acanthosis nigricans, fruity breath, recurrent UTIs, Candidal vulvovaginitis, tingling pain numbness in extremities

Question 24

What is the criteria for diagnosing T2DM?

Answer 24

HbA1c >6.5%
Fasting glucose >126
2 hour glucose >200 on oral glucose tolerance test
Random glucose >200 with classic sx of hyperglycemia

Question 25

Describe a diabetic foot exam

Answer 25

At each visit/at least once per year Inspection: examine for skin breaks, red or calloused areas, pallor, areas of dryness, pattern of hair growth, deformity, nails ingrown, infected, too long? Palpation: feel for pedal pulses, capillary refill, temperature Special testing: evaluate for protective sensation with 10g monofilament and vibratory sensation with 128 Hb tuning force

Question 26

What is the management for T2DM?

Answer 26

Lifestyle management: self management, nutrition therapy, psychosocial care Oral metformin unless contraindicated - decreases hepatic glucose production, improves peripheral glucose uptake slightly Other oral agents, insulin Check HbA1c every 3 months while adjusting tx then every 6 months when stable Smoking cessation, BP control, HLD control

Question 27

What organs/systems are affected by poorly controlled diabetes?

Answer 27

Eye, kidney, nervous system, CVS, skin, teeth, genitourinary system

Question 28

What is the epidemiology for T1DM?

Answer 28

Incidence increasing worldwide | One of the most common diseases of childhood

Question 29

What is T1DM?

Answer 29

Immune mediated beta cell destruction

Question 30

What are the risk factors for T1DM?

Answer 30

Genetic susceptibility - increased risk of T1DM is believed to reflex the frequency of high risk HLA alleles among ethnic groups in different geographic locations Environmental trigger - may precede onset of diabetes by years Leads to immune mediated destruction of pancreatic beta cells resulting in insulin deficiency

Question 31

What is the clinical presentation of T1DM?

Answer 31

Polydipsia, polyuria, blurred vision, fatigue/weakness, weight loss with hyperglycemia and ketonemia or ketonuria, DKA (diabetic ketoacidosis) which is the initial presentation in 20-25%

Question 32

What is the diagnostic criteria for T1DM?

Answer 32

Age of onset = throughout childhood (after puberty for T2) Insulin secretion: decreased/absent Insulin sensitivity: normal when controlled Insulin dependence: permanent Pancreatic antibodies present

Question 33

What are some associated conditions for T1DM?

Answer 33

Autoimmune thyroiditis - autoimmune mediated destruction of thyroid gland Celiac disease - autoimmune mediated sensitivity to gluten Addison’s disease - autoimmune mediated destruction of adrenal gland

Question 34

How is T1DM managed?

Answer 34

Education | Insulin - the advent of continuous glucose monitoring and insulin pumps has revolutionized management

Question 35

Describe hyperglycemia

Answer 35

Assess individuals with either DM I or II if glucose is higher than 250 for status of mentation or hydration DKA: insulin deficiency + glucagon excess leads to gluconeogenesis, glycogenolysis, and ketone body formation in liver (T1DM) (more acid production = decreased pH) Hyperglycemic hyperosmolar state (HHS): relative insulin deficiency + inadequate fluid intake, resulting in severe dehydration (T2DM) - extra sugar in plasma spills into urine, water follows leading to dehydration - severe electrolyte loss also occurs

Question 36

What is the management for DKA/HHS?

Answer 36

Admit to hospital Generally need IV fluids, IV insulin and potassium replacement, other electrolytes Do not manage as an outpatient

Question 37

Describe hypoglycemia

Answer 37

Most commonly caused by drugs used to treat DM especially with certain medications **should be considered in any pt with confusion, altered mental status, or seizure** Usually <70 but can have sx at high BS in pts with chronic hyperglycemia

Question 38

Describe how the brain regulates blood sugar

Answer 38

Brain requires continuous supply of glucose Complex neurohormonal regulation to prevent running out of gas Glucagon released Sympathetic outflow: ACh increases in sympathetic neurons leading to cholinergic sx such as sweating, hunger, paresthesia Adrenal response stimulated: epinephrine, NE, cortisol all increase leading to adrenergic sx such as palpitations,tremor, anxiety

Question 39

What are the consequences for hypoglycemia?

Answer 39

Consequences are serious | Must avoid hypoglycemic unawareness and serious cardiovascular morbidity/mortality