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ECOS II Midterm > Approach To Endocrine Complaints I > Flashcards

Approach To Endocrine Complaints I Flashcards

1
Q

What are the classic endocrine glands?

A

Pituitary, thyroid, parathyroid, pancreatic islets, adrenal glands

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2
Q

What is the mechanism of pathology for hormone excess?

A

Neoplasia, autoimmune disorders, or excess hormone administration

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3
Q

What are the mechanisms of pathology for hormone deficiency?

A

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

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4
Q

What is the mechanism of pathology for hormone resistance?

A

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

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5
Q

What is the general rules for tx of hormone excess?

A

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

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6
Q

What is the general rule for Tx of hormone deficiency?

A

Replace hormone, ideally as physiologically as possible

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7
Q

What is the general rule for Tx of hormone resistance?

A

Overcome resistance, resensitize target organs

Decrease high hormone levels

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8
Q

How should you clinically evaluate endocrine disorders?

A

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

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9
Q

What is the prevalence of obesity in adults?

A

36% BMI >30

70% BMI >25

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10
Q

What is the prevalence of type 2 DM in adults?

A

> 8%

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11
Q

Describe obesity

A

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

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12
Q

What is the prevalence of HLD in adults?

A

20-25%

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13
Q

What is the prevalence of metabolic syndrome in adults?

A

35%

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14
Q

Describe the epidemiology of metabolic syndrome

A

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

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15
Q

What is metabolic syndrome?

A

Metabolic abnormalities that confer increased risk of CVD and DM

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16
Q

What are risk factors for metabolic syndrome?

A

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

17
Q

What is the criteria for diagnosing metabolic syndrome?

A

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

18
Q

What is the management for metabolic syndrome?

A

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

19
Q

Describe type 2 DM

A

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

20
Q

What is the epidemiology of T2DM?

A

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)

21
Q

What are the risk factors for T2DM?

A

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

22
Q

What is HbA1c?

A

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

23
Q

What is the clinical presentation for T2DM?

A

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

24
Q

What is the criteria for diagnosing T2DM?

A

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

25
Q

Describe a diabetic foot exam

A

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

26
Q

What is the management for T2DM?

A

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

27
Q

What organs/systems are affected by poorly controlled diabetes?

A

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

28
Q

What is the epidemiology for T1DM?

A

Incidence increasing worldwide

One of the most common diseases of childhood

29
Q

What is T1DM?

A

Immune mediated beta cell destruction

30
Q

What are the risk factors for T1DM?

A

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

31
Q

What is the clinical presentation of T1DM?

A

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%

32
Q

What is the diagnostic criteria for T1DM?

A

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

33
Q

What are some associated conditions for T1DM?

A

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

34
Q

How is T1DM managed?

A

Education

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

35
Q

Describe hyperglycemia

A

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
36
Q

What is the management for DKA/HHS?

A

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

37
Q

Describe hypoglycemia

A

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

38
Q

Describe how the brain regulates blood sugar

A

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

39
Q

What are the consequences for hypoglycemia?

A

Consequences are serious

Must avoid hypoglycemic unawareness and serious cardiovascular morbidity/mortality

ECOS II Midterm (10 decks)

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