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*Neuroendocrine Exam 3 > Test Myself > Flashcards

Test Myself Flashcards

1
Q

A primary growth hormone disorder:

  1. Potential causes
  2. Lab level of GH and IGF-1
  3. Characteristics
A
  1. GH insensitivity at the liver
  2. ↑↑ GH, ↓ IGF-1
  3. Weight gain: ↓ fat and glycogen breakdown and protein synthesis
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2
Q

A secondary growth hormone disorder:

  1. Potential causes
  2. Lab level of GH and IGF-1
  3. Characteristics
A
  1. Pituitary tumor
  2. ↓GH if not making or if not responsive to GHRH/somatostatin, ↓IGF-1, ↑GHRH, ↑somatostatin
    3.
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3
Q

A tertiary growth hormone disorder:

  1. Potential causes
  2. Lab level of GH and IGF-1
  3. characteristics
A
  2. ↓GH, ↓IGF-1
    3.
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4
Q

What would diet low in protein, but adequate carb (w/insulin) due to GH?

  1. symptoms?
  2. Lab values of GH and IGF-1
A
  1. weight gain: ↑carb storage and lipogenesis

2. ↓GH, ↓IGF-1

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5
Q

what would you include in a differential for pituitary enlargement and a high prolactin level?

A

hypothyroidism

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6
Q

Pituitary adenoma, condition for each cell type:

  1. lactotrophs (prolactinoma)
  2. thyrotrophs
  3. corticotrophs
  4. somatotrophs
A
  1. hyperprolactinemia
  2. central hyperthyroidism
  3. cushings disease
  4. Acromegaly/gigantism (high GH)
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7
Q

General symptoms of pituitary adeoma

A
  • headache bitemporal

- hemianopsia b/c compression of optic chiasm (lose peripheral field)

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8
Q

Symptoms of prolactinoma: women vs man

A

women:
- amenorrhea (↓GnRH/LH/FSH)
- galactorrhea
- bone fx (osteoporosis)

male:
- hypogonadotrophic hypogonadism
- decreased libido
- impotence
- infertile

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9
Q

If someone was hypoglycemic, but had adequate protein intake, what symptoms and lab values would that cause?

  1. symptoms?
  2. Lab values of GH and IGF-1
  3. how would you test this?
A
  1. shift metabolism to lipids as energy source: lipolysis, ketogenic metabolism, diabetogenic
  2. ↑ GH, IGF-1
  3. oral glucose test, would fail to suppress GH production (sensitive for acromegaly)
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10
Q

Potential causes for GH deficiency

A
  1. ↓GHRH (hypothalamic dys)
  2. ↓GH secretion
  3. failure to generate somatomedin (IGF-1)
  4. GH or somatomedin resistance (rec def)
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11
Q

primary cause for GH excess

A

GH secreting pituitary adenoma

-could lead to gigantism or acromegaly

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12
Q

PT presents with:

  • increase bone growth
  • increase extremity size
  • HTN
  • hyperglycemia
  • organomegaly
  • deep voice
  • coarsening facial features with age
  • excessive sweating
  • insulin resistance
  1. What do you think the condition is?
  2. Cause of condition
  3. How would you diagnose the patient
  4. What lab values?
A
  1. Acromegaly
  2. Pituitary adenoma
  3. Oral glucose test w/ failure to suppress GH and pituitary mass on MRI
  4. ↑ IGF-1, ↑ GH
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13
Q

Causes of hypopituitarism

A
  1. brain damage: TBI, subarachnoid hmmm, irradiation, stroke
  2. pituitary tumors: adenoma
  3. non-pituitary tumors: carinopharyngioma
  4. infections: meningitis, encephalitis, hypophysitis
  5. infarction: Sheehan syndrome
  6. autoimmune disorder
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14
Q

Hypopituitarism-GH:

A

Children: short stature
Adult: no effect

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15
Q

Hypopituitarism-FSH/LH:

A

infertility
Male: decreased sperm count, hypogonadism
Female: hypogonadism, menstural irregularity

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16
Q

Hypopituitarism-TSH:

A

hypothyroidism

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17
Q

Hypopituitarism-ACTH:

A

loss of pigmentation and hypoadrenalism

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18
Q

Hypopituitarism-ADH:

A

diabetes inspidus

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19
Q

PTH:

  1. Stimulus:
  2. Action on:
    - Bone:
    - Kidney
    - GI:
  3. Overall effect on:
    - Serum Ca:
    - Serum P:
A
  1. ↓ serum Ca
  2. organs
    - Bone: ↑ resorption
    - Kidney: ↑Ca reabsorp, ↓P reabsorption (↑urine cAMP)
    - GI: + Vit D to ↑ Ca reabsorption
  3. ↑ Ca, ↓P
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20
Q

Vitamin D:

  1. Stimulus:
  2. Action on:
    - Bone:
    - Kidney
    - GI:
  3. Overall effect on:
    - Serum Ca:
    - Serum P:
A
  1. ↑ PTH, ↓P and Ca
    • Bone: ↑ resorption
    • Kidney: ↑Ca reabsorp, ↑P reabsorption (↑urine cAMP)
    • GI: ↑ Ca and P reabsorption
  3. ↑ Ca and P
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21
Q

Calcitonin:

  1. Stimulus:
  2. Action on:
    - Bone:
    - Kidney
    - GI:
  3. Overall effect on:
    - Serum Ca:
    - Serum P:
A
  1. ↑ serum Ca
  2. ↓ resorption
  3. ↓ Ca
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22
Q

Primary hyperparathyroidism

  1. Cause
  2. Lab levels for:
    - PTH:
    - Calcitriol:
    - Bone:
    - Urine:
    - Serum Ca:
    - Serum P:
A
  1. Parathyroid adenoma
    • PTH: ↑
    • Calcitriol: ↑ (PTH + 1a-hydroxylase)
    • Bone: ↑ resorption
    • Urine: ↑ cAMP, P, Ca
    • Serum Ca: ↑
    • Serum P: ↓
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23
Q

Humoral hypercalcemia of malignancy

  1. Cause
  2. Lab levels for:
    - PTH:
    - Calcitriol:
    - Bone:
    - Urine:
    - Serum Ca:
    - Serum P:
A
  1. PTH-related peptide (PTH-rp)
    • PTH: ↓
    • Calcitriol: -
    • Bone: ↑ resorption
    • Urine: ↑ P
    • Serum Ca: ↑
    • Serum P: ↓
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24
Q

Surgical Hypoparathyroidism

  1. Cause
  2. Lab levels for:
    - PTH:
    - Calcitriol:
    - Bone:
    - Urine:
    - Serum Ca:
    - Serum P:
A
  1. thyroidectomy
    • PTH: ↓
    • Calcitriol: ↓
    • Bone: ↓ resorption
    • Urine: ↓ P excretion, ↓ cAMP
    • Serum Ca: ↓
    • Serum P: ↑
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25
Q

Pseudohypoparathyroidism type 1a

  1. Cause
  2. Lab levels for:
    - PTH:
    - Calcitriol:
    - Bone:
    - Urine:
    - Serum Ca:
    - Serum P:
A
    • PTH: ↑
    • Calcitriol: ↓
    • Bone: ↓ (defect Gs)
    • Urine: ↓P and cAMP
    • Serum Ca: ↓
    • Serum P: ↑
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26
Q

Chronic Renal Failure

  1. Lab levels for:
    - PTH:
    - Calcitriol:
    - Bone:
    - Urine:
    - Serum Ca:
    - Serum P:
A
    • PTH: ↑ (secondary)
    • Calcitriol: ↓ (caused from RF)
    • Bone: osteomalacia (↓ D3), ↑ resorption (↑PTH)
    • Urine: ↓P excretion (due ↓ GFR)
    • Serum Ca: ↓ (due to ↓ D3)
    • Serum P: ↑ (↓ P excretion)
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27
Q

Osteoporosis causes:

A

-Age: bone resorption rate>deposition

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28
Q

Hypocalcemia symptoms

A
  • hyperflexia
  • spontaneous twitch
  • muscle cramp
  • tingle, weakness

Chvostek sign: twitch facial muscles from tapping on facial n
Trousseau sign: carpopedal (hand) spasm on BP inflation

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29
Q

Hypercalcemia signs

A
  • decrease QT
  • constipation
  • lack of appetite
  • polyuria
  • polydyspia
  • muscle weakness
  • hyporeflexia
  • lethargy
  • coma
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30
Q

effect of chronic hypercalcemia on PTH

A

↓storage and synthesis

↑b/d of stored PTH and inactive PTH release

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31
Q

effect of chronic hypocalcemia on PTH

A

↑storage and synthesis = hyperplasia of parathyroid gland (secondary hyperpara-)

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32
Q

Patient presents with hypocalcemia and severe hypomagnesemia, what is the physiological basis? What condition is this commonly seen in?

A

Mg acts like Ca+ normally in stimulating PTH when levels are low, but in severely low levels- some Mg+2 is needed for normal functioning of the CaS-Rec
-Abnormal function = surpasses PTH release

Alcoholism

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33
Q

Primary hyperparathyroidism

A

Overactive gland

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34
Q

Secondary hyperparathyroidism

A

Overactive gland due to hypocalcemia

35
Q

Tertiary hyperparathyroidism

A

Renal failure

36
Q

What is the hypothalamus’s role in emotion and what would happen to damage of the area?

A

hypothalamus in emotional control is largely related to its ability to activate the autonomic nervous system to produce the characteristic changes in pulse, blood pressure, pupils, etc. that we associate with strong emotion (particularly anger, fear, etc.). In a patient with hypothalamic damage (in this case, likely due to the pressure produced by the pituitary adenoma), these physiologic changes will be blunted or absent as the hypothalamus cannot relay the information to the autonomic nervous system. The paraventricular nucleus of the hypothalamus is particularly important in this function.

37
Q

What is in charge of naming emotion?

A

interaction between the limbic association cortex and PTO association cortex

38
Q

what is in charge of recognizing anger?

A

dopaminergic transmission in the amygdala

39
Q

what is in charge of delayed gratification

A

higher cortical function

40
Q

what is in charge of Integration of inputs related to learned fear

A

Lateral nucleus of amygdala

41
Q

what is in charge of Additional processing of learned fear inputs

A

basal nucleus of amygdala

42
Q

what Identifies appropriate responses to fear-producing inputs

A

central nucleus of amygdala

43
Q

the ability to recognize/feel disgust requires normal functioning of what? what condition is this commonly diminished in?

A

putamen, one component of the striatum and is lost early in the development of Huntington disease

44
Q

what changes would you see in Alzheimers disease

A

produces cognitive decline related to the loss of the ability to learn/create memories

45
Q

what changes would you see in Fronto-temporal dementia

A

cognitive decline related to the loss of the highest cortical functions (ex: delayed gratification)

46
Q

what three parts of the brain function together to make decisions when we have sufficient information to make an informed decision?

A
  1. striatum
  2. ventromedial PFC
  3. orbitofrontal cortex
47
Q

What part of the brain allows us the ability to learn from our mistakes? What is the system called? It’s components? And general function?

A

action selection system

  1. Ant cingulate gyrus

encode the value of the results of the decision and detect errors

48
Q

What deficit is a patient likely to show as a result of damage to the anterior mirror neuronal system?

A

Inability to recognize the intent of a motor action (e.g. Dr. Karius is handing you a diet Pepsi as a gift to you)

49
Q

Damage to the posterior mirror neuronal system would result in what?

A

render you unable to recognize the action itself (ex: that Dr. Karius is handing you the Dr. Pepsi).

50
Q

what do the anterior and posterior mirror neuronal systems need in order to successfully function

A

dorsal visual pathway for their visual input

51
Q

what allows us the ability to recognize the emotional content of speech?

A

Prosody in auditory cortex

52
Q

what is the theory of mind?

A

skill that allows people to understand other’s intentions and how another’s beliefs may differ from their own

53
Q

what must be functional for a person to understand the intention’s of another person and why they may differ from our own?

A

amygdala and its connections to the medial temporal lobes and orbitofrontal cortex

54
Q

where is the damage if someone is unable to recognize certain facial expressions in related to emotion?

A

superior temporal sulcus and fusiform gyrus

55
Q

where is the damage if someone is unable to understand certain facial expressions in related to emotion?

A

posterior superior temporal sulcus

56
Q

what type of memory is encoded by post-tetanic?

A

shortest form of memory there is, literally lasting only for seconds.

It results from an increase in neurotransmitter release from the pre-synaptic cell due to higher than normal levels of calcium in the presynaptic terminal. This increase in calcium occurred because the Ca-ATPase could not remove the high amount of calcium that entered the terminal during a period of high activity

57
Q

what type of memory is encoded by long-term potentiation

A

short-term, like remembering a few words for 5 mins

changes in both the presynaptic and post-synaptic responses at a synapse. These changes have to last for hours to even be considered LTP, and are the “gateway” to permanent memories

58
Q

what type of encoding is happening for you to be able to recall that the sweat glands are innervated by sympathetic cholinergic fibers acting on muscarinic receptors on Wednesday’s test.

A

transition of the fact from short-term memory (based on LTP) to permanent memory produced by changes in the physical nature of the synapse. It then will require the transition to the working memory for you to use that fact on the test. Working memory also relies on LTP, just like short-term memory, because working memory is a variety of short-term memory.

59
Q

what type of encoding is happening for you to be able to recall the location of a window in your childhood home

A

function of the space cells in the hippocampus. Spatial memory is a special case of permanent memory because the spatial memory becomes the scaffold by which the hippocampus reconstructs recalled episodic memories.

60
Q

what are the 6 B’s of T3 function?

A
  1. Brain maturation, CNS develop, (adult-memory, attention)
  2. Bone growth (w/GH), ↑ osteoblast
  3. B-adrenergic: ↑Rec = ↑CO,HR,SV
  4. BMR: ↑NaKATPase activity=↑O2 consump,RR,Temp
  5. BG: ↑GNG,glycogenylysis- also ↑EPI/NE, glucagon
  6. Breakdown lipids: ↑ GH activity
61
Q

What does Propylthiouracil (PTU) do?

A
  • Inhibits TPO: ↓ T3/T4 from thyroid gland

* Inhibits 5’-deiodinase: ↓ T4 to T3 conversion peripherally

62
Q

what does Methimazole do?

A

• Inhibits TPO: ↓ T3/T4 from thyroid gland

63
Q

Wolff-Chaikoff Effect

A
  • Excessive iodide in diet could lead to hyperthyroidism
  • Thyroid protects itself via Wolff-Chaikoff Effect
  • Organification inhibited by ↑ iodide • Less synthesis of MIT/DIT
64
Q

effect of estrogen, pregnancy, and OCP on TBG and TH

A

increase TBG and increase total T4 levels

65
Q

effects of Liver failure on TBG and TH

A

decrease TBG, decrease T4

66
Q

what would one see in a Pendrin gene mutation? (SCL26A4, PDS)

A

hypothyroidism with goiter

67
Q

what does clinically euthyroid mean?

A

higher than normal levels of TOTAL T3/4 b/c increase in TBG binds more TH = less free TH, so system regulates to increase free production

However, levels of free (physiologically active) TH are normal

68
Q

Causes of hypothyroidism

A
  1. thyroiditis (autoimmune or Hashimoto thyroiditis)
  2. thyroidectomy
  3. I- def
  4. Congenital (creationism)
  5. Decreased TRH/TSH
69
Q

causes of hyperthyroidism

A
  1. Graves disease ( increase TSI)
  2. Thyroid neoplasm
  3. excess TSH excretion
  4. Exogenous T3/4
70
Q

Levels of TSH in hypothyroidism

A
  1. increased (primary disease in thyroid gland)

2. decreased (disease in hypothalamus or A.Pit)

71
Q

Levels of TSH in hyperthyroidism

A
  1. decreased (inhibition of T3)

2. increased (defect in A.Pit)

72
Q

treatment for hyperthyroidism

A
  1. PTU (inhibit peroxidase and TH synthesis)
  2. thyroidectomy
  3. I-131 (destroys thyroid)
  4. B-adrenergic blocking agent
73
Q

Graves: primary hyperthyroidism

  1. clinical signs:
  2. lab values serum and free T4/T3, TSI, and TSH
  3. CLINICAL PEARLS!
  4. Tx:
A
  1. exophthalmos and periorbital edema; goiter; ophthalmophaty
  2. ↑free T3/4, ↑total T3/T4, +TSI, ↓TSH
  3. Issues with eyes and shins
    Exophthalamos and periorbital edema
    non pitting edema of shin
  4. beta blocker, PTU (inhibit peroxidase and 5’ ionidase) to inhibit TH formation; ablation, thyroidectomy
74
Q

secondary hyperthyroidism

  1. cause
  2. lab values
A
  1. TSH secreting tumor

2. ↑TSH, ↑T3/4

75
Q

Primary hypothyroidism

  1. cause
  2. presentation
  3. lab values
A

Hashimoto thyroiditis

  1. gland destruction (thyroidectomy, irration, autoimmune)- impaired TH synthesis because TG/TPO antibodies
  2. cold, everything slows
  3. +TPO, ↓T3,T4, ↓I-, ↑TSH (trophic effect = goiter)
76
Q

goiter

A

high TSH, but inability to produce T3/T4

  • iodine def
  • graves
77
Q

Congenital hypothyroidism (cretinism)

  1. cause
  2. symptoms
A
  1. I- def, mom taking PTU/methimazole (inhibit PTO), impaired thyroid g growth, inherent TH synthesis defect
  2. Symptoms: difficulty feeding, resp difficulty, curse facial feat, growth retardation, mental retardation, jaundice, dry skin
78
Q

secreting pituitary adenoma result on:

  1. lactotrophs
  2. thyrotrophs
  3. corticotrophs
  4. somatotrophs
A
  1. hyperprolactinemia - prolactinoma is most common
  2. central hyperthyroidism
  3. cushings disease
  4. acromegaly/gigantism
79
Q

pleasure and disgust: anatomical structures, role, and damage to that area

A

BG: NA and Putamen
process social cues
Hungtingtons

80
Q

sad: anatomical structures, role

A

lower ant cingulate gyrus

thinking about sad events

81
Q

Surprise: anatomical structures, role

A

parahippocampal gyrus

detect novelty

82
Q

Avoidance:anatomical structures, role

A

lateral post hypothalamus, dorsal midbrain, enterohinal cortex
prevent short term reward when long term = shit

83
Q

anger: anatomical structures, role

A

amygdala

84
Q

fear

A

amygdala

*Neuroendocrine Exam 3 (27 decks)

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