Lopez: Endocrine Review Flashcards
(107 cards)
1
Q
What correlates with plasma half-life and metabolic clearance of hormones?
A
- the degree of protein binding
- the thyroid hormones do this a lot
2
Q
What kind of mechanism does ACTH, LH, FSH, TSH, and glucagon use?
A
the adenylyl cyclase mechanism -Gs ptn -ATP to cAMP -activation of PKA ...
3
Q
What mechanism does GnRH, TRH, GHRH, and oxytocin use?
A
PLC mechanism
- Gq ptn
- activates PLC
- makes DAG and IP3
- DAG gets PKC
- IP3 releases Ca2+ from ER
4
Q
What mechanism do Thyroid hormones, glucocorticoids, aldosterone, estrogen, and testerone use?
A
the steroid hormone MOA
- binds cytoplasmic receptor
- dimerizes
- goes to nucleus
- gets the SRE… gene transcription
5
Q
What is the connection between the hypothalamus and the posterior pit?
A
-just neural
6
Q
connection b/w hypothalamus and ant pit
A
- neural and endocrine
- via the hypothalamic-hypophysial portal vessels
7
Q
What is a primary endocrine disorder
A
-low or high levels of hormone due to defect in the peripheral endocrine gland
8
Q
What is a secondary endocrine disorder?
A
-low or high levels of hormone due to defect in the pituitary gland
9
Q
What is a tertiary endocrine disorder
A
low or high levels of hormone due to defect in the hypothalamus
10
Q
Ant pit hormones
A
- TSH
- FSH
- LH
- ACTH
- GH
- Prolactin
11
Q
What will PRL excess give us clinically?
A
- galactorrhea and hypogonadism
- it inhibits LH and FSH as well
12
Q
Where does somatostatin and PIF (dopamine) come from?
A
the hypothalamus
13
Q
difference between a functioning and non functioning pituitary adenoma?
A
- functional: releases active hormone…. lots of it
- non functional: doesn’t
14
Q
Prolactinoma
A
-hypogonadism and galactorhea
15
Q
excess GH symptoms
A
Acromegaly in adults and gigantism in children
16
Q
Cushing’s disease
A
-pituitary tumor w/ an overproduction of cortisol
17
Q
What syndrome do pituitary adenomas show up in?
A
MEN1 patients (25% of the time)
18
Q
What does PRL excess do to LH ad FSH?
A
lowers them both
19
Q
What are the two hormones released from the post pit?
A
ADH and oxytocin
20
Q
Which hypothalamic nucleus releases ADH?
A
-Supraoptic nuclei
21
Q
Which nucleus releases oxytocin?
A
paraventricular nuclei
22
Q
What kind of hormones are ADH and oxytocin
A
neuropeptides
23
Q
What is secretion of ADH most sensitive to?
A
plasma osmolarity changes
-gets V1 and V2 receptors
24
Q
What are the triggers of ADH release?
A
- high plasma osm
- low BP
- low BV
- high ANGII
- sympathetic stimulation
- dehydration
25
What is Diabetes insipidus?
- lack of an effect of ADH on the renal collecting duct
- fequent urination
- large volume of urine is dilutes
26
Central DI
- lack of ADH... so low ADH
| - results from damage to pituitary or destruction of hypothalamus
27
Tx of Central DI?
- desmopressin
| - drug that prevents water excretion
28
NEphrogenic DI
-kidneys are unable to respond to ADH... so high plasma ADH
29
Causes of Nephrogenic DI?
- drugs like lithium
- Chronic disorders (PCKD, SSA)
- *desmopression tx does not work*
30
What is the water deprivation test for DI?
- cut off fluids
- weigh pt every 1-2 hrs for 8 hrs
- measure plasma osmolarity and urine
- if looks like DI, allow pt to drink, administer desmopressin
- then measure plasma and urine osmolality again
31
SIADH
- excessive secretion of ADH
- excessive water retention
- hypoosmolarity fails to inhibit ADH release
- wathc for sodium below 120.... hyponatremic encephalopathy
32
What does the adrenal cortex secrete?
- Aldosterone
- Cortisol
- Androgens
33
What does the adrenal medulla secrete?
E and NE
34
From outside to inside, name the layers of the adrenal gland and the hormones they secrete
- GFRM
- Glomerulosa: Mineralocorticoid (aldosterone)
- Fasciculata: Glucocorticoids(cortisol), androgens
- Reticularis: Glucocorticoids and androgens again
- Medulla: E and NE (catecholamines)
35
What is the first step in synthesis of steroid hormones?
- Cholesterol to pregnenolone
- mediated by cholesterol desmolase
- then we split three ways to make Aldosterone, cortisol, or androstenedione
36
how is Aldosterone made?
- Pregenolone, progesteron, Deoxycorticosterone (DOC), Corticosterone, Aldosterone!
- 3B, 21, 11, aldosterone synthase
37
How is cortisol made?
- Pregnenolone, 17-OH Pregnenolone, " " progesterone, 11-deoxycortisol, cortisol!
- 17, 3B, 21, 11
38
How are androgens made?
- pregnenolone, 17-OH pregnenolone, DHEA, Androstenedione (androgens!)
- 17, 17+20, 3B
39
How can you tell a 21 vs and 11 deficiency?
- in 11 deficiency, there will be increased BP due to the mineralocorticoid effect of DOC that builds up
- that doesn't happen with 21 deficiency because we never get to the DOC point
40
What does Aldosterone do?
- increases sodium concentration in the blood
| - raises BP
41
What will we have a lot of if there is a 17 alpha deficiency?
- mineralocorticoids
- they will be totally fine because we don't need 17 for aldosterone synthesis
- that is 3B, 21, 11, aldosterone synthase
42
What will we have a lot of if there is a 21B deficiency?
- Sex hormones!
- they don't need 21
- they are just 17, 17+20, 3B
43
What will we have a lot of in 11B deficiency?
- Sex hormones again!
- again, they don't need 11
- remember though, there will be high BP b/c of DOC creation
- 21 still works well :)
44
Which one is the most common deficiency?
- 21B
- high Renin activity for some reason
- also high 17-hydroxyprogesterone
45
What is Cushing's syndrome
- high cortisol due to an ADRENAL tumor
| - there is just high cortisol... lower down the chain
46
What is Cushing's disease?
- high ACTH which leads to high cortisol
| - caused by a PITUTARY tumor
47
What is Addison's disease?
- caused by autoimmune disease of the adrenal gland
| - so... low cortisol, high ADH and high CRH... the adrenal gland is where the problem is at
48
What is Secondary adrenal insufficiency?
- caused by glucocorticoid drugs suppressing H and P
| - everything is low
49
If we have high ACTH, what else will we have besides high plasma cortisol?
-hyperpigmentation
50
If we have a primary excess, where is the problem?
the adrenals... so high cortisol, low everything else
51
If we have a secondary excess, where is the problem?
the pituitary, so high ACTH, pigmentation, and cortisol elevated
-these same things go for deficiency
52
What is ANGII's effect on the adrenal cortex?
-makes it secrete aldosterone
53
Which zone makes aldosterone?
Glomerulosa
54
What do pancreatic B cells secrete?
insulin
| -located more toward the center of the islets of Langerhans
55
What do alpha cells make?
glucagon
56
What do the delta cells secrete?
-somatostatin
57
What is glucagon's effect on insulin secretion?
increases it
| -weird because insulin from B cells will decrease the glucagon from delta cells
58
What can be use as a long-term marker of endogenous insulin secretion?
C peptide
| -it's secreted in equimolar amounts with insulin
59
What do the sulfonylurea do the the ATP-dependent K+ channels?
closes them... K+ is stuck in the cell now
- makes the cell depolarize
- Ca2+ channels open
- Ca2+ comes in
- Exocytosis of insulin... yay
- hypokalemia
60
What kind of receptor does insulin bind?
RTK
- autophosphorylates itself
- insulin down-regulates its own receptor
61
What are the effects of insulin?
- we start storing stuff
- increased glycogen/lipid/protein synthesis
- decreased lipolysis
- cell growth and differentiation
- decreased gluconeogenesis
62
When in doubt, what does insulin do to things in the blood?
lowers them!
- increased glucose uptake... low glucose
- increased Ptn synth.... low aa's
- Increased fat deposition.... low FA;s
- decreased lipolysis.... low ketoacids
- increased K uptake into cells... low K+
63
What is Type 1 DM?
-inadequate insulin secretion
-destruction of B cells, often as the result of autoimmune disease
-no symptoms until 80% of symptoms are gone
-kids
-ketosis
-
64
What is Type 2 DM?
- Insulin resistance
- more common type
- progressive exhaustion of active B cells
- pts can make insulin, but no enough to overcome insulin resistance
- adults
- family Hx
- fat ppl
65
If we are given the mmol/L of glc, how do we get the concentration of glucose in mg/dL?
multiply by 18
66
What does Glucagon do?
-increases lipolysis and inhibits GA synthesis , which shunts substrates towards gluconeogenesis
67
What are produced from FA?
Ketoacids!
68
Where is the vast majority of calcium stored in our body?
-bones and teeth
69
What does PTH and Vit D do to bone resorption?
increases it
- gives us more Ca2+ in blood
- PTH also helps us reabsorb the Ca2+ from the kidneys
70
What must the kidneys do to maintain Ca2+?
excrete the same amount of Ca2+ that is absorbed by the GI tract
71
How is extracellular Pi related to Ca2+ levels?
- inversely related!
| - extracellular concentration of Pi is regulated by the same hormones that regulate Ca2+ concentration
72
What wil PTH do to Pi?
- decrease its reabsorption from the kidney
- so we get phophaturia
- we will also have very high cAMP urine levels for some reason
73
So, if we have a high serum Ca2+ level, what will that do to our PTH?
inhibit it
74
What does Vit D do genetically?
- goes in and stops PTH gene and upregulates CaSR gene
| - the CaSR will respond to the high calcium levels and also inhibit PTH
75
What is the active form of Vit D
1,25 cholecalciferol
| -24,25 is the inactive form
76
Where does Vit D get converted into its active form?
the renal prosimal tubule
| -by 1 alpha hydroxylase... makes sense
77
Where does Vit D (cholecalciferol) get the 25 hydroxyl group slapped onto it?
the liver
- that happens first
- so that is the main circulating form of Vit D
78
Where are the PTH receptors located?
- on the OsteoBLASTS... not clasts
- so, short term, it will increase bone formation via direct action on osteoblast
- basis for use of intermittent synthetic PTH administration in osteoporosis tx
79
What is the long term actions of PTH?
- high bone resorption
- indirect action on osteoclasts mediated by cytokines released from osteoblast
- Vit D acts synergistically with PTH to stimulate osteoclast activity and bone resorption
80
At what part of the renal tubule is Ca2+ reabsorbed because of PTH?
- Thick ascending limb
| - PTH also gets the 1 alpha hydroxylase... activates Vit D
81
Vit D effects on Small intestine?
-increase Ca2+ and Pi absorption by increasing calbindin expression
82
Vit D effects on bone
- sensitizes osteoblasts to PTH
| - regulates osteoid production and calcification
83
Vit d effects on kidney
- promotes Pi reabsorption by proximal nephrons (PTH does opposite)
- minimal actions on Ca2+
84
Vit D effects on parathyroid gland?
- Directly inhibits PTH gene expression
| - Directly stimulates CaSR gene expresion
85
Primary hyperparathyroidism?
-lots of Pi, cAMP, Ca2+ excretion
-Stone, bones, and groans
-hypercalciuria... stones
-high bone resorption...
-constipation... groans
tx usually requires parathyroidectomy
-HYPERCALCEMIA/HYPOPHOSPHATEMIA
86
Lab values for hyperparathyroidism?
- PTH: high
- Ca2+: high
- Pi: low
- Vit D: high
87
Secondary hyperthyroidism?
- increase in PTH levels secondary to low Ca2+ in blood
| - causes: renal failure, Vit D deficiency
88
lab values for Secondary hyperparathyroidism due to renal failure?
- PTH: high
- Ca2+: low
- Pi: high
- Vit D: low
89
lab values for secondary hyperparathyroidism due to Vitamin D deficiency?
-PTH: high
-Ca2+: low
Pi: low
-Vit D: low
90
Hypoparathyroidism?
- PTH isn't made anymore!
- no Vit D
- No Ca2+
- no Pi excretion
- Hypocalcemia/Hyperphosphatemia
91
lab values for hypoparathyroidism?
- PTH: low
- Ca2+: low
- Pi: high (PTH normally promotes Pi excretion)
- Vit D: low
92
What is Albright hereditary osteodystrophy?
- inherited autosomal dominant disorder, Gs for PTH in bone and kidney is defective
- Hypocalcemia and hyperphosphatemia develop
- high PTH levels..... so it's a psuedohypoparathyroidism
- administration of exogenous PTH won't do shit
93
lab values for Pseudohypoparathyroidism?
- PTH: high
- Ca2+: low
- Pi: high
- Vit D: low
94
what is the phenotype for albright hereditary osteodystorphy?
-short stature, short neck, obesity, subcutaneous calcification, shortened metatarsal and metacarpals
95
What is PTHrP
-secreted by tumor cells.... acts like PTH
96
lab values for humoral hypercalcemia of malignancy
- PTH: low
- Ca2+: high
- Pi: low
- VitD: low (apparently doesn't activate that one enzyme...)
97
Familial hypocalciuric hypercalcemia (FHH)
- auto dominant
- Mutations inactivate CaSR in PT glands
- decreased urinary Ca2+ excretion and increased serum Ca2+
98
Rickets type 1 and 2
- congenital disorders
- Vit-D deficiency (kinda)
- type 1: no 1 alpha hydroxylase
- type 2: no vitamin D receptor
- lots of Pi and cAMP in the urine
99
how long does the body have enough Thyroglobulin for if everything were to shut down?
-2 to 3 months
100
What enzyme is involved with the peripheral conversion of T4 to T3?
-deiodinase
101
When the availability of iodide is restricted, what is favored more? T3 of T4?
T3
| -makes sense because that takes less iodine >
102
What drugs will inhibit the sodium idodide symporter?
- perchlorate
- thiocynate
- PTU is an effective treatment for hyperthyroidism
103
What will oddly inhibit organification and synthesis of thyroid hormones?
high levels of Iodide
- this is called the Wolff-Chaikoff effect
- it's wierd because either too much or too little Iodine will inhibit Thyroid hormone
104
How are thyroid hormones transported?
in the bloodstream either bound to plasma proteins or free
| -mostly bound to ptns (TBG)
105
What is TSH regulated by?
- TRH
| - Free T3
106
What is something that makes TSH secretion different from GH secretion?
-TSH secretion occurs at a steady rate
107
Most common cause of thyrotoxicosis?
Graves disease
- Thyroid stimulating Ig's (TSI) stimulate TSH receptor without TSH hormone
- TSH levels are low because of high circulating levels of thyroid hormones inhibits TSH secretion!
- exophthalmos
