Path Flashcards

1
Q

“Is the pt unable to make adequate amounts of this hormone?”

What test are we likely to perform?

A

Stimulation test

-Pt receives or does something that should raise levels of the hormone. If response is not adequate, dx is made.

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2
Q

“Is this pt unable to limit production of this hormone to what is appropriate?”

What test are we likely to perform?

A

Suppression test

-Pt receives or does something that should lower levels of the hormone. If response is not adequate, dx is made.

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3
Q

Thyroxine (T4) and tri-iodothyronine (T3) are produced in the thyroid gland.

What hormone (and from where) stimulates their production and secretion?

A

Thyroid stimulating hormone (TSH, thyrotropin) from the anterior pituitary

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4
Q

TSH production and secretion is stimulated by what (and from where)?

A

TSH releasing hormone (TRH) from the brain

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5
Q

Low T4 confirms:

A

HYPOthyroidism

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6
Q

Pts who are HYPOthyroid from thyroid dz will have high TSH. Why?

A

Loss of negative feedback on the pituitary

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7
Q

Pts who are HYPERthyroid from thyroid dz will have low TSH. Why?

A

Strong negative feedback on pituitary

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8
Q

Low T4, high TSH:

A

Hypothyroidism

-mimics depression, mental illness

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9
Q

High T4, low TSH:

A

Hyperthyroidism

-mimics anxiety, mental illness

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10
Q

Labs for 2° hypothyroidism:

Cause of 2° hypothyroidism:

A

Low T4, low TSH.

Pituitary does not produce adequate amount of TSH.

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11
Q

Labs for 2° hyperthyroidism:

Cause of 2° hyperthyroidism:

A

High T4, high TSH.

Overactive pituitary OR a tumor elsewhere producing excess TSH.

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12
Q

Anti-thyroid peroxidase Abs (anti-TPO) target an:

A

Iodine oxidizer

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13
Q

Anti-thyroglobulin Abs target the:

A

Colloidal storage form of thyroid hormone

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14
Q

Anti-TSH receptor Abs (anti-TR, “TRAbs”) are often stimulatory and cause:

A

Hyperthyroidism

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15
Q

Cortisol from the adrenal cortex is the body’s principal glucocorticoid.

Excess cortisol produces what syndrome?

A

Cushing’s

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16
Q

Adrenal or pituitary dz with HYPOadrenocorticism:

A

Addison’s

  • Cannot stimulate cortisol production
  • Mimics depression or anorexia nervosa
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17
Q

Adrenal or pituitary dz with HYPERadrenocorticism:

A

Cushing’s

  • Cannot suppress cortisol production
  • Mimics mental illness and other common problems
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18
Q

Cortisol production by the adrenal cortex is stimulated by:

A

ACTH

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19
Q

A morning serum cortisol > __ ug/dL or a morning salivary cortisol > __ ug/mL basically excludes adrenal insufficiency.

What test would you perform?

A

Serum cortisol > 18 ug/dL
Salivary cortisol > 5.8 ug/mL

ACTH stimulation test.

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20
Q

What is expected in an ACTH stimulation test in primary adrenal cortical insufficiency (due to dz of the gland itself)?

A

Cortisol levels won’t rise despite ACTH administration.

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21
Q

Auto-Abs detected in autoimmune adrenalitis:

A

Anti-21-hydroxylase Abs

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22
Q

Plasma ACTH LOW
Aldosterone LOW
Renin HIGH

Dx:

A

Primary adrenal insufficiency

adrenal gland problem

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23
Q

Plasma ACTH LOW
Aldosterone NORMAL
Renin NORMAL

Dx:

A

Secondary adrenal insufficiency

pituitary problem

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24
Q

In suspected hyperadrenocorticism, screen with:

A

24 hour urinary cortisol

Cushing’s pts have > 3x the upper limit of ref range

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25
For borderline hyperadrenocorticism, what test is used?
Dexamethasone suppression test
26
Explain dexamethasone suppression testing. If cortisol is still high: If ACTH is still high:
Pt is given 2mg of dexamethasone... If cortisol is still high, 1° or 2° hyperadrenocorticism is likely. If ACTH is still high, it is likely 2° (comes from pituitary).
27
Too much aldosterone is responsible for: How is it screened? Consider screening pts with: (3)
Hypertension Screened through spot plasma aldosterone + plasma aldosterone / renin ratio (both will be high). Consider screening pts with hypokalemia, severe refractory HTN, or a known adrenal tumor.
28
Low aldosterone is familiar as:
Renal tubular acidosis, type IV
29
Low usable levels of growth hormone before closure of the epiphyses results in: High levels produces _________ in children/teens and _________ in adults.
Low GH >> Permanent short stature (i.e., dwarfism) High GH >> GIGANTISM in children/teens, ACROMEGALY in adults.
30
How is GH measured?
IGF-1 in the liver
31
To screen for acromegaly, measure:
Serum IGF-1
32
Acromegaly is most often caused by:
Pituitary adenoma
33
IGF-1 and IGFBP-3 are both low in deficiency of:
hGH
34
- Children who grow up in a neglectful/non-nurturing environment produce insufficient hGH and develop short stature as a result. Remember this when working up "pituitary GH deficiency." - When removed from environment, pts exhibit catch-up growth. Dx:
Psychosocial dwarfism
35
Prolactin is produced in the pituitary in response to absence of:
Dopamine | inhibits production and secretion of prolactin
36
- Woman with galactorrhea / amenorrhea or who doesn't have a normal cycle - Loss of libido, infertility, "trouble seeing" High values (> 10x the top of ref range) suggest:
Prolactinoma
37
- Released from posterior pituitary | - Allows reabsorption of water by renal collecting ducts
ADH (aka vasopressin)
38
Too little ADH. | Clinical syndrome is:
Diabetes insipidus | polyuria without glycosuria, SG < 1.020
39
The distinction between pituitary and nephrogenic diabetes insipidus is usually made by injecting:
Desmopressin (synthetic ADH)
40
Too much ADH (SIADH) usually results from: (2) | Pts have low levels of:
- Ectopic ADH secretion by a tumor, often oat cell lung cancer - Porphyria (from the brain) Low sodium (pt is hyponatremic)
41
Abnormal serum calcium levels on routine screening and/or passing a calcium kidney stone should raise suspicion for:
Hyperparathyroidism
42
Dx of hyperparathyroidism is based on:
Elevated serum PTH
43
When low calcium levels are detected, screen for:
Hypoparathyroidism - DiGeorge syndrome – no parathyroids - Autoimmune parathyroiditis - Post-thyroid surgery
44
The best known marker for type I diabetes is Abs against:
Gamma-glutamyl decarboxylase
45
Pts with hypoglycemia, measure: (2)
- Insulin | - C-peptide (production accompanies production of insulin)
46
- Pts appear anxious - Intermittent or persistent HTN - Sweating attacks - Severe headaches Dx:
Pheochromocytoma
47
Best screen for pheochromocytoma:
24 hour urinary fractionated catecholamines and metanephrines
48
- Common origin = adrenal medulla | - Increased dopamine and/or homovanillic acid (HVA) and vanillylmandelic acid (VMA) in urine
Neuroblastoma
49
- Ulcers and/or diarrhea prompt consideration for: | - Caused by:
Zollinger-Ellison syndrome | Caused by an endocrine tumor in the pancreas or duodenum producing excess gastrin (gastrinoma)
50
Elevated gastrin levels are also seen in:
- Achlorhydria from dz (atrophic gastritis) | - Meds (antacids)
51
What stimulates the release of gastrin from gastrinomas but suppresses it from normal G-cells?
Secretin
52
What is the marker in medullary thyroid cancer?
Calcitonin
53
-Wheezing, flushing, diarrhea Think...
Carcinoid syndrome
54
Carcinoid syndrome is due to production of _________ by the tumor.
Carcinoid syndrome is due to production of SEROTONIN by the tumor.
55
A screen for carcinoid is:
5-hydroxy-indole acetic acid (major metabolite of serotonin) in urine
56
- Boy who doesn't undergo puberty when it's time - Grown man who is troubled by infertility, erectile dysfxn, or "loss of energy" What is ordered?
Serum testosterone, FSH and LH levels
57
- Often unrecognized XXY - Testosterone is low - FSH and LH are high
1° hypogonadism
58
- Problem is in the brain / hypothalamus - Most often "idiopathic" - Testosterone, FSH and LH are all low
2° hypogonadism
59
- Pituitary adenomas (usually prolactinomas) - Parathyroid adenomas / hyperplasias - Pancreatic endocrine tumors (gastrinomas, etc) Think...
MEN-I
60
- Caused by mutated RET - Features medullary thyroid cancer and pheochromocytomas Think...
MEN-II
61
- Mutant RET | - Parathyroid adenomas / hyperplasias
MEN-IIa
62
- Mutant RET - Marfanoid habitus - Mucosal neuromas
MEN-IIb