Lecture 9.2 Highlights

Question 1

List the 2 types of anterior pituitary tumors and their symptoms

Answer 1

1) Hormone secreting = “functional”
-Hormone excess Sx; likely small
2) Non-hormone secreting = “hypofunctioning”
-No hormone Sx, likely large
-Structural Sx: bitemporal hemianopsia

Question 2

What type of anterior pituitary tumor is more likely to have bitemporal hemianopsia?

Answer 2

Non-hormone secreting

Question 3

1) Normal function of prolactin axis: Because prolactin is typically released during pregnancy, the desired effect is to ________ ovulation and _________ lactation
2) Therefore, symptoms of prolactinoma are _________ and _____________.

Answer 3

1) inhibit; stimulate
2) amenorrhea; galactorrhea

Question 4

*List the three cases that increase prolactin levels and their respective pathways (abbreviated version)

Answer 4

1) Pregnancy: disinhibits lactotrophs [inhibits dopamine release]
2) Schizophrenia: disinhibits lactotrophs [and mimics prolactinoma Sx]
3) Hypothyroidism: TRH also stimulates lactotrophs

Question 5

*Prolactinoma pathology of Dx in women :
1) What are the 2 primary Sx?
2) What does the med list NOT include?
3) What is normal?
4) What is elevated?

Answer 5

1) Amenorrhea and galactorrhea
2) Antipsychotics
3) TSH is normal
4) Prolactin is elevated

Question 6

*Prolactinoma
1) Men may present with ___________ Sx.
2) What do men’s labs look like?
3) What are both men and women often treated with?

Answer 6

1) structural
2) Labs should be the same, sans the beta HCG test
3) Dopamine agonists first, resection later

Question 7

Under normal function, hypothalamus stimulates somatotrophs w. the release of GHRH and ___________ them with release of somatostatin

Answer 7

inhibits

Question 8

True or false: IGF-1 normally is like insulin, and most importantly, causes growth

Answer 8

True

Question 9

Pathological IGF-1 levels; describe how they affect the:
1) Heart
2) Bones
3) Liver + spleen
4) Metabolic

Answer 9

1) Diastolic heart failure
2) Hypertrophy and linear growth (if growth plates are not fused)
3) Hepatosplenomegaly
4) HTN, DM, HLD, obesity

Question 10

1) If hypersecreting tumor occurs __________ puberty, pt will be tall, and proportionally developed; this is called “______________”
2) If hypersecreting tumor occurs ___________ puberty, the epiphysial plates will be closed and pt will have bone growth without elongation; this is called “_______________”
3) Both patients will risk what and develop what?

Answer 10

1) before; “gigantism”
2) after; “acromegaly”
3) obesity and develop DM, HTN, hyperlipidemia

Question 11

GH Tumor pathology of Dx:
1) What should you test for?
2) What should you do if this is elevated? Why?
3) What supports Dx?

Answer 11

1) IGF-1
2) “Glucose suppression” f/u test
-Because GH is counter to insulin in its effects, it works as a regulatory hormone
3) Failure to suppress GH with glucose challenge supports diagnosis

Question 12

Describe the Pathology of treatment of a GH tumor

Answer 12

1) Surgery is usually performed first
2) If ineffective, medicinal treatment with octreotide
-Why? This is synthetic somatostatin
-Why? Review axis slide

Question 13

GH Pathology: If there is too little GH, is this achondroplasia?

Answer 13

No

Question 14

1) Adaptation to injury is one cause of what kind of hypopituitarism?
2) Why?

Answer 14

1) Chronic
2) Pituitary will priorities which hormones to secrete

Question 15

Acute Hypopituitarism: List 2 causes and give examples

Answer 15

1) Sheehan’s
2) Adaptation: Hypotension, lethargy, coma, or death

Question 16

SIADH causes __________ urine and _________ blood

Answer 16

concentrated; dilute

Question 17

SIADH pts will have what:
1) Blood concentration?
2) Blood volume?
3) Sodium level?

Answer 17

1) Dilute
2) Normal
3) Low

Question 18

True or false: aldosterone primary impacts volume

Answer 18

True

Question 19

*When patient has low sodium, low serum osmolality, and normal blood volume, they have “euvolemic hypoosmolar hyponatremia”, you should think of what?

Answer 19

SIADH

Question 20

1) Give 2 examples of what causes SIADH
2) What doesn’t cause SIADH? Why?

Answer 20

1) Meds and lung cancer
2) Adenomas; this is neural tissue

Question 21

*In a DI Patient:
1) What will the urine osm. be?
2) What will the serum sodium be?
3) Volume will be ________________.

Answer 21

1) low (i think)
2) elevated (I think)
3) normal

Question 22

*What can help treat DI?

Answer 22

Water depravation

Question 23

What are the 2 main causes of DI? Give examples

Answer 23

highlighted 37

Question 24

1) Give an example of a mineralocorticoid
2) What does it increase?

Answer 24

1) Aldosterone
2) Blood volume

Question 25

1) Give an example of a glucocorticoid 1) List 5 of its effects

Answer 25

1) Cortisol 2) Anti-inflammatory Increase in blood glucose Increase in blood glucose

Question 26

42

Answer 26

Reticularis DHEA is a sex hormone precursor that transforms external genitalia Regulated by ACTH along with cortisol

Question 27

Adrenal medulla

Answer 27

43

Question 28

CAH (congenital adrenal hyperplasia) most common subtype is what?

Answer 28

The enzyme 21-hydroxylase.

Question 29

Adrenogenital syndromes: androgen excess The adrenal cortex can secrete excess androgens in either of two settings

Answer 29

Adrenocortical neoplasms (usually **virilizing** carcinomas) Congenital adrenal hyperplasia (CAH)

Question 30

Under Normal Function: 1) Hypothalamus causes a bunch of steps that ultimately cause the fasciculata to release _____________ 2) Cortisol inhibits ACTH and CRH

Answer 30

cortisol

Question 31

49

Answer 31

Normal ACTH synthesis Pro-opio-melanocortin (POMC) is turned into ACTH in the corticotropes *Note that keratinocytes also

Question 32

*List 3 effects of hypercortisolism

Answer 32

1) HTN 2) DM 3) Obesity

Question 33

1) Patients with ___________ symptoms of HTN, DM, Central obesity should have their ______-night cortisol checked 2) Alternative testing is ______________ collection

Answer 33

refractory; late-night 2) 24-hour urine

Question 34

*1) So, the cortisol is high? Now what do you give? 2) What 2 effects should this suppress? 3) What are the 2 potential outcomes?

Answer 34

1) 2) Hypothalamus and the anterior pituitary 3)) 52 highlight If there is not suppression of cortisol, they have an illness of hypercortisolism If there is suppression of cortisol, they have no illness, and you need to look elsewhere to explain s/s

Question 35

*1) So, the low-dose test didn’t suppress cortisol. Now what? 2) What do you check? What do you know if the result of this is low? -Give an example of a potential cause 3) What if the result is still high? -Give 2 examples of potential causes

Answer 35

1) They have hypercortisolism 2) ACTH; if low, then the axis is responding to suppression, and you know the cortisol is coming from somewhere outside the axis; Adrenal adenoma! 3) If ACTH is still high, then the illness is ACTH dependent Pituitary adenoma Paraneoplastic disease

Question 36

* **So, the ACTH remains high after dexamethasone suppression, now what?** 1) The endocrine axis __________ respond to a high enough dose of counterregulatory hormone. 2) This means that a _________-dose dexamethasone suppression test will cause a drop in ACTH if the source is a _______________. 3) When will the ACTH will high no matter what?

Answer 36

1) will 2) high-dose; pituitary adenoma 3) If the source is a small-cell lung cancer, the ACTH will be high no matter what

Question 37

Primary hypercortisolism: 55 HL

Answer 37

This is the patient with adrenal tumor Because the cortisol is always high, there is consistent negative feedback decreasing CRH and ACTH Because ACTH is therefore low, the remaining adrenal tissue atrophies due to lack of stimulation

Question 38

55 HL

Answer 38

Secondary Hypercortisolism: ACTH dependent illness Whether from pituitary adenoma or malignancy, this patient will have very high levels of ACTH Because ACTH is always high, the adrenal glands will hypertrophy Because ACTH is always high, melanocytes will be stimulated and will demonstrate hyperpigmentation

Question 39

What are the 2 main types of hypercortisolism?

Answer 39

Primary and secondary

Question 40

What causes you to look tan? **need to know**

Answer 40

High ACTH (has nothing to do w cortisol)

Question 41

56 HL

Answer 41

Exogenous use of steroid: These patients have high levels of cortisol This will decrease the hormones produced upstream They will have atrophy of the adrenal glands This is why patients on long term steroids need to be taperedq

Question 42

Primary adrenal insufficiency 1) Primary adrenal insufficiency means what? 2) How does it cause hyperpigmentation? 3) What 2 things does it cause to be low?

Answer 42

1) Adrenal glands not working 2) ACTH rises 3) aldosterone

Question 43

List and name the 2 kinds of hypocortisolism

Answer 43

1) Chronic = Addison’s disease 2) Acute = almost dead

Question 44

Pituitary hypocortisolism: 1) What does it do to ACTH? 2) What abt cortisol?

Answer 44

1) Low ACTH 2) Low cortisol

Question 45

Hypo-functioning adrenal treatment 1) What do you do for low cortisol ? 2) What abt low aldosterone?

Answer 45

Give them what they lack: 1) Low cortisol = hydrocortisone 2) Low aldosterone = fludrocortisone

Question 46

Review: After low GFR or sodium triggers the RAAS, eventually, angiotensin II triggers thirst response, release of ADH, and stimulates the glomerulosa to release the mineralocorticoid called _______________

Answer 46

aldosterone

Question 47

Review: What does aldosterone do?

Answer 47

Through the use of these [ENAC] channels, sodium is absorbed, which increases blood volume, and potassium is excreted

Question 48

Review: Formula?

Answer 48

CO2 + H2O <> H2CO3 <> HCO3- + H+ (carbonic anhydrase helps w. first rxn)

Question 49

Review: Give the short version of what aldosterone does

Answer 49

It increases blood volume with sodium, and “dumps” potassium into the urine It raises the blood pH (more basic)

Question 50

68

Answer 50

This will never be a kidney disorder Why? Look at the mechanisms described above – there is no pathway for decreasing aldosterone production in renal pathology Therefore, the issue will be due to the adrenal gland and its production of mineral corticoid Hypo-functioning of the adrenal gland usually means a deficiency of both cortisol and aldo, which we have already discussed

Question 51

69

Answer 51

This would be a “salt wasting” syndrome Hyponatremia Remember, that ENAC channels also discard potassium Therefore, pts with low aldo will have Hyperkalemia

Question 52

70 *

Answer 52

What will happen to the blood pressure? What will happen to the electrolytes, based on what you know?

Question 53

71 *List and give examples of the 2 main kinds of hyperaldosteronism causes

Answer 53

1) Primary: adenoma; adrenal hyperplasia 2) Secondary: a problem with the kidney

Question 55

1) Which is active, T3 or T4? 2) Which is inactive?

Answer 55

1) T3 = active 2) T4 = inactive

Question 56

Thyroid peroxidase (TPO) and thyroglobulin (TG) work together to oxidize iodide and turn it into ________________

Answer 56

thyroid hormone

Question 57

What 2 things work together to oxidize iodide and turn it into thyroid hormone? **"need to know"**

Answer 57

Thyroid peroxidase (TPO) and thyroglobulin (TG)

Question 58

Thyroid Hormone Release 1) T___ > T___ in the target cells, where it becomes more potent. 2) 3) These hormones increase cellular metabolism  protein synthesis and catabolism as well as triglyceride mobilization

Answer 58

1) T4 > T3 2) These hormones increase cellular respiration  thus increasing ATP consumption and heat

Question 59

HYPERthyroid vs. hypOthyroid 77 *

Question 60

HYPERthyroid vs. hypOthyroid 77 *

Answer 60

The opposite of what I just said. . .

Question 61

*Grave's disease (hyperthyroid): 1) A TSH receptor ___________ (Type II Hypersensitivity) 2) _____________, secondary to antibody causing increased fibroblast activity in the eye

Answer 61

1) antibody 2) Exophthalmos

Question 62

1) In what condition will the pt develop a singular nodule?2) What happens to the remainder of the organ?

Answer 62

1) Toxic adenoma 2) Remaining thyroid will become **less** active

Question 63

Toxic Multinodular Goiter: ________ nodules formed by receptor or second messenger mutations in several cells

Answer 63

many

Question 64

Give examples of hyperthyroid causes

Answer 64

1) Grave's disease 2) Toxic adenoma 3) Toxic Multinodular Goiter 4) Factitious 5) Stroma Ovarii

Question 65

81 Give 2 other hyperthyroid causes

Answer 65

1) Factitious 2) Stroma Ovarii

Question 66

Other thyroid disorders: 1) Subacute thyroiditis, also called “granulomatous,” also called ______________ 2) Is this condition painful?

Answer 66

1) De Quervain’s 2) Thyroid hurts the whole time

Question 67

*Thyroid Cancer: List 4 different kinds in order of freq

Question 68

Calcium and Vit D: 1) Which is the Vit D you eat? 2) UV light creates D3 - Vit D precursor in your skin Liver takes both forms and makes 25 Vit D, which is still an intermediate form Kidney turns 25 Vit D into 1, 25 Vit D in the proximal convoluted tubule

Answer 68

1) D2 UV light creates D3 - Vit D precursor in your skin Liver takes both forms and makes 25 Vit D, which is still an intermediate form Kidney turns 25 Vit D into 1, 25 Vit D in the proximal convoluted tubule

Question 69

1) In a healthy parathyroid, what does PTH do? 2) List the 3 target organs of PTH

Answer 69

1) Raises Ca+ when it's low 2) Bone GI tract Kidney

Question 70

Normal PTH activitiy 1) Kidney PTH Signals the release of 1, 25 Vit D and tells kidney to resorb Ca and ELIMINATE Phosphate

Answer 70

1) eliminate 2) Serum Ca++ is HIGH and Phosphate is LOW 3) Increase in URINE Calcium

Question 71

*HYPERparathyroid: 1) Bones: Osteoclast activity increased  watch for _________ and _________________ 2) Stones: 3) Abdominal groans Increased Ca  constipation and pain 4) Psychic moans Ca  encephalopathy

Answer 71

1) osteopenia and bone pain 2) Urine Calcium UP, urine phosphate UP  calcium phosphate and calcium oxalate kidney stones

Question 72

Hypoparathyroid: 1) The ________ tried to resect some of the thyroid and cut out parathyroid glands or cut their vascular supply. . . _________ calcium

Answer 72

1) surgeon; LOW Hyperactive nerves Calcium is not available to block sodium channels on neuron, increasing total activity

Question 73

In the _____________ of glucose, the pancreas releases insulin

Answer 73

presence

Question 74

The chief trigger for pancreas to release insulin is what?

Answer 74

Glucose

Question 75

Differentiate between fasting and non-fasting states

Answer 75

1) Fasting state: Low insulin and high glucagon > hepatic gluconeogenesis and glycogenolysis (glycogen breakdown) > we prevent hypoglycemia 2) Non-fasting state: pancreas releases insulin

Question 76

Islets of Langerhans: ___________ cells (70%) release Insulin

Answer 76

Beta (B)

Question 77

*Type I diabetes: 1) A __________ disease that's a failure of self of tolerance in __________ specific for ______________. 2) Progressive destruction of islet beta cells → leading to absolute insulin deficiency.

Answer 77

1) Autoimmune disease; T cells; beta cell antigens 2)

Question 78

*Type 2 diabetes 94

Answer 78

94 1. Peripheral Insulin resistance 2. Inadequate insulin section (beta cells) even with insulin resistance and ↑ blood glucose

Question 79

95

Answer 79

Pancreatogenic diabetes Gestational diabetes

Question 80

What are 2 kinds of Multiple Endocrine Neoplasia?

Answer 80

1) MEN 1 2) MEN 2

Question 81

MEN 1: List the 3 Ps

Answer 81

1) Parathyroid 2) Pancreas 3) Pituitary

Question 82

MEN 2: 1) List 3 examples of type 2A 3) List 3 examples of type 2B

Answer 82

1) Pheochromocytoma Medullary Thyroid Cancer Parathyroid tumor 2) Pheochromocytoma Medullary Thyroid Cancer Neuronal Tumors

Question 83

Differentiate between the inheritance of MEN 1 and MEN 2

Answer 83

MEN 1 is germline, MEN 2 is inherited autosomal dominant