module 10 Endocrine

Question 1

1. • 2. What are the 2 ways that we get hormonal dysfunction?
2. • 9. How do hormonal alterations occur (the mechanisms)?

Answer 1

1. altered hormonal levels
2. target cell failure
3. Failure of feedback systems
4. Dysfunction of endocrine gland.
5. Secretory cells don’t produce, obtain, or convert hormone precursors.
6. Excess hormonal production or release from endocrine gland.
7. Insufficient production of hormone by endocrine gland.
8. Increased hormone degradation or inactivation.
9. Ectopic hormone release

Question 2

1. If there is a failure at the target cell it can be either at the cell’s ………….. or ……………. .
2. What 5 dysfunctions are associated with the cell surface receptors?
3. What 2 dysfunctions are associated with intracellular disorders?

Answer 2

1. cell’s surface or intracellular.
2. Decrease in number of receptors, Impaired receptor function, Antibodies against receptors, Antibodies that mimic hormone action, Unusual expression of receptor function
3. Defects in post-receptor signaling cascades, Inadequate synthesis of second messenger

Question 3

1. Name the 2 diseases of the poterior pituitary:
2. What is Syndrome of inappropriate antidiuretic hormone secretion (SIADH)?
3. What are the causes of SIADH?
4. What are the clinical manifestations of SIADH?
5. How do we treat SIADH?

Answer 3

1. Syndrome of inappropriate antidiuretic hormone secretion (SIADH), and diabetes insipidus
2. It is the hypersecretion of ADH
3. ectopic ADH production, CNS disorder, surgery, trauma, medications
4. Water retention, Hyponatremia, Serum hypo osmolality
5. Fluid restriction (usually resolves itself within 10 days)– ADH receptor antagonist– Loop diuretics

Question 4

1. What is diabetes insipidus?
2. What are the 3 types of diabetes insipidus and their causes?
3. What are the manifestations?

Answer 4

1. It is the hyposecretion of ADH
2. Neurogenic- In the CNS from idiopathic, head trauma, surgery, or tumor

Nephrogenic (lithium, hyperglycemia)– Inadequate response to ADH

Psychogenic

3. Polyuria and polydipsia, Partial or total inability to concentrate the urine, blood hyperosmolarity, hypernatremia,

Question 5

1. What are the 2 diseases of the anterior pituitary?
2. What causes these 2 diseases?
3. How do we diagnose acromegaly and gigantism?
4. How do we treat these diseases?
5. How does gigantism present?
6. What are the physical characteristics of someone with acromegaly?

Answer 5

1. acromegaly and gigantism
2. a hypersecretion of growth hormone because of a pituitary tumor (in adulthood for acromegaly) and (before puberty in gigantism)
3. measuring IGF-1 and GH levels, or CNS imaging (CT scan or MRI) to detect a pituitary tumor
4. Surgical – transsphenoidal– Radiation therapy– suppress GH secretion– GH receptor blocker
5. Person is big everywhere, yet proportional.
6. Transfrontal scar, frontal bossing, bitemporal hemianopia (visual disturbance in peripheral), papilledema, protruding jaw, large tongue, proximal myopathy, spade-like hands

Question 6

1. What is diabetes mellitus?
2. What 2 things cause the inadequacy of insulin effects?
3. Diabetes results in abnormal …………, …………, and ………. ………… .
4. Which tissues can transport glucose without insulin?

Answer 6

1. inadequate insulin effects in receptor tissues
2. Deficit of insulin secretion, or the production of insulin antagonists
3. carbohydrate, protein, and fat metabolism.
4. CNS, kidney, myocardium, gut, skeletal muscle (still needs insulin at a certain point)

Question 7

1. Type 1 diabetes differs from type 2 in that the patients of type 1 are ………….. weight, and type 2 are …………..
2. Which type of diabetes has circulating islet antibodies?
3. Diabetic ketoacidosis in the absence of insulin happens in which type? What happens in the other type?
4. How would you describe type 1 (as far as beta cells)?
5. How would you describe type 2 (as far as beta cells)?
6. Why is it important to not just assume diabetes with hyperglycemia?

Answer 7

1. normal (or underweight before diagnosis), obese
2. type 1
3. type 1. Type 2 have nonketotic hyperosmolar coma
4. beta cell destruction leading to insulin deficiency
5. beta cell dysfunction in combination with insulin resistance
6. Many disorders present with hyperglycemia, like adrenal tumors, cystic fibrosis, pancreatic defects, thyroid issues, cytomegalovirus, phenochromocytoma, cushings etc.

Question 8

1. What does hyperglycemia cause (as far as food consumption, urine output, and fluid ingestion)? Are these classic signs of diabetes? If so, which type?
2. will there be glucosuria? What does this cause and why?
3. Why do diabetics eat so much?

Answer 8

1. polyphagia, polyuria, polydipsia. Classic signs of type 1, but will also present in type 2.
2. yes, dehydration because the excess glucose ends up in filtrate and pulls water towards it. This make more pee and the person feels thirsty.
3. their cells can’t uptake glucose, so they feel hungry

Question 9

1. • 3. How do we diagnose diabetes? Name and describe 3 tests and their appropriate ranges:
2. How do we treat diabetes, and why is exercise important?

Answer 9

1. Fasting blood glucose level: for initial screening/follow up (100-125 = prediabetic, >126= diabetic). If results show hyperglycemia proceed to next tests…..
2. Glucose tolerance test (where you drink the syrup shit and wait) plasma glucose level of 200 mg/dL is diabetic
3. H1Ac - Glycosylated hemoglobin test
   –Monitors glucose levels over several months in rbcs. <5.7% normal, 5.7-6.4 = prediabetes, 6.5% or more = diabetes.
4. Exercise and diet (more fiber, less fat and sugar), Oral medication (to stimulate beta cells to make more insulin for type 2), Add insulin (imperative in type 1, but last resort in type 2).

Question 10

1. Type 1 diabetes is classified in what 2 ways?
2. How do the beta cells get destroyed in type 1?
3. What happens in type 2 as far as why insulin doesn’t have it’s effect?
4. What are the risk factors to type 2?
5. Why would someone with type 2 need insulin added to their treatment down the road?
6. Name some of the manifestations of type 2:

Answer 10

1. autoimmune or idiopathic (hereditary)
2. autoimmunity attacks beta cells
3. failure of target tissue to uptake the insulin (insulin resistance). Can also be due to defects in signalling cascade.
4. Age, Obesity, Hypertension, Physical activity, Family history (both genetic and environmental factors)
5. beta cells become diminished over time
6. Fatigue, Pruritus, Recurrent infections, Visual changes, Neuropathy, Overweight, Dyslipidemic, Hyperinsulinemic, and Hypertensive

Question 11

1. What is Maturity onset diabetes of youth (MODY)?
2. What is gestational diabetes?
3. Name the two acute complications of diabetes 1 and how they happen:
4. what are symptoms of ketoacidosis?
5. Name the acute complications of diabetes 2, and how they happen:
6. What are manifestations of HHNKS?

Answer 11

1. Beta-cell function or insulin action affected by autosomal dominant mutations –Disrupt insulin production. Usually happens before age 30, but can happen before.
2. A type of type 2 diabetes. Any degree of glucose intolerance with onset or first recognition during pregnancy. Baby born large and hypoglycemic

3. Hypoglycemia (from too much insulin, follows exercise, skipping meals, life-threatening) and 
Diabetic ketoacidosis (DKA) - too little insulin in blood, too much unusable glucose in blood, ketones from lipid digestion, acidic environment, comes from infection, stress, dosage error, exercise, alcohol intake

4. dehydration, kussmauls breathing, electrolyte imbalance, acetone breath
5. Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS). Isidious onset, diagnosis easily missed, happens in old people- assumed to be senile,
6. Hyperglycemia, Severe dehydration, Electrolyte imbalances result in: Neurologic deficits

Question 12

1. Name the complications of both type 1 and type 2 diabetes:

Answer 12

1. macrovascular disease - atheroscelrosis cvd. , microvascular disease - damages kidneys, retina, and nerves, causes infections (b/c immunocompromised), inflammation, decreased firinolysis, nersous system problems resulting in bad wound healing and gangrenous necrosis

Question 13

1. Name 4 diseases of the adrenal cortex:
2. What is cushing’s disease?
3. What is cushing’s syndrome caused by?
4. What are the manifestations of Cushing’s?

Answer 13

1. Cushing’s disease, Cushing’s syndrome, hyperaldosteronism, and Adrenocortical Hypofunction
2. Excessive anterior pituitary secretion of ACTH
3. Excess cortisol secretion from an adenoma of the adrenal cortex or steroid use.
4. “truncal obesity”, “moon face”, “buffalo hump”, Glucose intolerance and protein wasting, hypotension

Question 14

1. What are the two types of hyperaldosteronism?

2. What are the manifestations of Hyperaldosteronism?

Answer 14

1. Primary: Aka Conn Syndrome: Increased aldosterone secretion from abnormality in adrenal cortex.

Secondary: Extra-adrenal stimulus of aldosterone secretion

2. Retention of sodium causes Hypertension, hypokalemia (low potassium), and hypervolemia

Question 15

1. What are the 2 types of adrenocortical hypofunction:
2. Describe Addison’s:
3. How does Addison’s manifest?
4. Describe secondary hypocortisolism:

Answer 15

1. Primary adrenal insufficiency aka Addison’s Disease. and Secondary hypocortisolism
2. autoimmune attack on the adrenal gland causing hyposecretion of adrenocorticoid
3. decreased blood glucose, inability to tolerate stress, low serum sodium, infections, fatigue, weight loss, high potassium, hyperpigmentation, hypotension
4. adrenal atrophy and decreased ACTH resulting from prolonged exposure to glucocorticoids

Question 16

1. What causes disorders of the adrenal medulla?
2. Name one of these disorders:
3. Describe Pheochromocytoma:
4. What are the manifestations?

Answer 16

1. tumors coming from chromaffin cells of adrenal medulla
2. Pheochromocytoma
3. benign tumor that secretes epinephrine, norepinephrine, and catecholamines on a continuous or episodic basis.
4. Headache, heart palpations, sweating, intermittent or constant anxiety

Question 17

1. Name 3 disorders of hyperthyroidism:
2. Describe Graves disease
3. How does Graves manifest?
4. Describe nodular thyroid disease:
5. Describe Thyrotoxic crisis

Answer 17

1. Graves Disease, Nodular thyroid disease, and thyrotoxic crisis (thyroid storm)
2. autoimmune disease in which thyroid is stimulated by antibodies against TSH receptor. Type of thyrotoxicosis. Causes hypermetabolism
3. Increased body temp., Goiter, Sweating, Soft silky hair and skin, Reduced BMI, Insomnia, Hyperactivity, bulging eyes, tremors, Pretibial myxedema
4. Toxic multinodular goiter or Toxic adenoma causing hyperthyroidism
5. TH levels rise dramatically, can be fatal (thyroid storm)

Question 18

1. What are 2 diseases of hypothyroidism?
2. Describe Hashimoto’s
3. Manifestations of Hashimoto’s
4. Describe cretinism:
5. What other reasons why a person could have hypothyroidism:

Answer 18

1. Hashimoto’s and cretinism
2. Most common in the US –Autoimmune disorder
3. low metabolism, lethargy, cold intolerance, weight increase, slow heart, goiter, myxedema, beefy tongue
4. untreated congenital hypothyroidism. May be related to iodine deficiency during pregnancy. Results in short stature, and severe retardation
5. Iodine deficient (most common world-wide), tumor, or surgical removal or treatment of thyroid gland