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N398 Exam 2 > Endocrine Patho > Flashcards

Endocrine Patho Flashcards

1
Q

What do cells need/use as a source of energy?

A

Glucose

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2
Q

What is a hormone that increases the amount of glucose in your blood?

A

Glucagon

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3
Q

What is a hormone that decreases the amount of glucose in your blood?

A

Insulin

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4
Q

What produces insulin?

A

B cells in the pancreas

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5
Q

What patient population typically has Type 1 DM?

A
  • Once of most common childhood diseases
  • Peak onset = 11-13 years
  • 1.5-2x higher in whites
  • Genetic component: 5-10% risk to siblings and 2-5% to offspring
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6
Q

What is the pathophysiology of Type 1 DM?

A
  • Absolute insulin insufficiency
  • Autoimmune attack on the beta cells of the pancreas
  • Typically destroy 90% of B cells before s/s occur
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7
Q

3 Major clinical manifestations of Type 1 DM

A
  1. Polyuria: increased pee because sugar in urine and water follows sugar
  2. Polydipsia: increased thirst, hypovolemic
  3. Polyphagia: increased hunger, weight loss r/t fluid loss, fat/protein store breakdown
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8
Q

Other clinical manifestations of Type 1 DM

A

Fatigue, weakness, blurred vision, nausea, slow wound healing, tingling in hands, increased infection

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9
Q

Evaluation of Type 1 DM

A
  • History and physical
  • Ketones and glucose in urine
  • Blood glucose
  • HgA1C over 6.5
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10
Q

How do we evaluate blood glucose?

A
  1. Random sampling of blood glucose above 200 mg/dl with classic s/s of diabetes
  2. Fasting blood glucose over 126 mg/dl
  3. Blood glucose concentration over 200 mg/dl 2 hours after 75 g oral glucose load
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11
Q

Type 1 DM Treatment

A
  • Insulin therapy: main treatment
  • Diet/meal planning
  • Activity and exercise
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12
Q

Monitor for complications of Type 1 DM

A
  • Acute hyperglycemia
  • Diabetic ketoacidosis
  • Hypoglycemia
  • Chronic changes
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13
Q

Hypoglycemia

A 
T: tachycardia
I: irritable
R: restless
E: excessive hunger
D: diaphoresis and depression
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14
Q

Diabetic Ketoacidosis

A
  • One of most common reasons for diabetic hospitalization
  • Causes: stress, ineffective management of diabetes
  • Result of increased lipolysis and conversion to ketone bodies
  • Clinical symptoms: metabolic acidosis (increased breathing and depth of breathing, fruity smelling breath, hyperkalemia)
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15
Q

Patient population with Type 2 DM?

A
  • Accounts for most cases of diabetes
  • Mostly non-caucasian (especially blacks and native Americans) and elderly
  • Risk factors: aging, sedentary, obesity, genetics, metabolic syndrome, HTN, dyslipidemia
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16
Q

Pathophysiology of Type 2 DM

A
  • Body is resistant to the action of insulin on peripheral tissues
  • Requirement for more insulin and glucose utilization is lowered
17
Q

Evaluation of Type 2 DM

A
  • H and P but more subtle
  • Glucose in urine
  • Blood glucose
  • HgA1C above 6.5
18
Q

Treatment of Type 2 DM

A
  • Primarily lifestyle changes: diet, exercise, weight loss improve glucose tolerance
  • Meds: oral, insulin over time
19
Q

Monitor for complications of Type 2 DM

A
  • Chronic changes from hyperglycemia

- Eyes, kidneys, CV, cerebrovascular, neuropathy, peripheral vascular, infection

20
Q

What is gestational diabetes?

A

Glucose intolerance during pregnancy

21
Q

What causes gestational diabetes?

A
  • Placental hormones and weight gain during pregnancy cause insulin resistance and inability to produce increased amount of insulin needed during pregnancy
  • Risk factors: advanced maternal age (35-40+), family history of diabetes, previous GDM, previous LGA babies
  • All pregnant women screened around 28 weeks
22
Q

Treatment of GDM

A
  • Nutritional counseling and exercise

- Insulin if not controlled with above

23
Q

Complications of GDM

A
  • Babies: weight over 4 kg, neonatal hypoglycemia, stillbirth
  • Mom: higher chance of developing DM in next 10-20 years
24
Q

What are the adrenocortical hormones?

A

Produced by adrenal cortex (too much or too little)

  • Glucocorticoids: cortisol (energy, immune response, inflammatory, stress)
  • Mineralocorticoids: aldosterone (retain sodium and fluids)
  • Androgens: sex hormones
25
Q

What is Addison’s disease?

A
  • Adrenal insufficiency
26
Q

What are causes of Addison’s disease?

A
  • Destruction of adrenal cortex leads to decreased secretion of adrenal hormones
  • Causes: removal of adrenal gland, autoimmune disease (most common), Neoplasms, TB, histoplasmosis, cytomegalovirus
27
Q

What are clinical manifestations of Addison’s disease?

A
  • Decreased cortisol: hypoglycemia
  • Decreased aldosterone: sodium and water loss = hypotension
  • Hyperkalemia = acidosis
  • Decreased androgens: changes in body hair distribution
  • ACTH not suppressed: pigmentation changes
28
Q

What is evaluation of Addison’s disease?

A
  • History and physical
  • Labs: plasma cortisol level
  • ACTH stimulation test: would cause cortisol in normal person but no or little rise in person with this
29
Q

How do we treat Addison’s disease?

A
  • Replacement hormones

- Stress dosing: increase during times of stress

30
Q

What is Cushing’s disease?

A
  • Cluster of clinical abnormalities caused by excessive adrenocortical hormones or related corticosteroids
  • Excess of cortisol
31
Q

What are causes of Cushing’s disease?

A
  • Pituitary hypersecretion of ACTH
  • Tumor
  • Administration of synthetic glucocorticoids or steroids
32
Q

What are clinical manifestations of Cushing’s disease?

A
  • Moon face
  • Fat deposits on back of shoulders
  • Na and H2O retention
  • Edema
  • HTN
  • Mood changes: depression
  • Hyperglycemia
33
Q

What is evaluation of Cushing’s disease?

A
  • History and Physical

- Dexamethasone suppression test: cortisol stays high

34
Q

How do we treat Cushing’s disease?

A
  • Surgery/radiation for tumors

- Pharm: Anti-HTN, K+, diuretics

N398 Exam 2 (6 decks)

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