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Endo Flashcards

1
Q

Thyroid hormones

A

T3t4

Parafollicular calcitonin

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2
Q

Proteins and peptides

A

Stored in secretory vesicles until needed

Water soluble

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3
Q

Amines

A

Derived from tyrosine

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4
Q

Steroids

A

Synthesized from cholesterol
Lipid soluble

Not stored

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5
Q

More protein binding

A

Less metabolic clearance long plasma half life

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6
Q

Little protein binding

A

Lots of metabolic clearance

Little protein binding

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7
Q

Adenylate cyclase mechanism

A

ACTH, LH, FSH, TSH, hCG, MSH, CRH, PTH, calcitonin, glucagon

Gs

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8
Q

Phospholipase C

A

GnRH, TRH, GHRH, oxytocin

Gq, a bound to GTP, activate phospholipase C and get PIP2 then get DAG, IP3

DAG-PKC
IP3-ca release from er or sr

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9
Q

Steroid hormone mechanism

A

Thyroid hormones, glucocorticoids, aldosterone, estrogen, testosterone, 1,25 D

Cytoplasmic receptor and into nucleus where dimerize and bind to steroid responsive element

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10
Q

Anterior pituitary embryo

A

Oral ectoderm-epithelial

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11
Q

Posterior pituitary embryo

A

Neuroectoderm

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12
Q

Posterior pituitary nerves

A

PP is a collection of axons whose cell bodies are located int he hypothalamus

-SON, PVN

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13
Q

ADH from

A

SON

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14
Q

Oxytocin from

A

PVN

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15
Q

Anterior pituitary to hypothalamus

A

Neural and hormonal

-hypothalmic release and inhibit hormones into hypothalamic hypophysial portal vessels which go to anterior lobe which release into blood

Anterior pituitary is a collection of endocrine cells

Connected t hypothalamus by hypothalamic hypophysial portal vessels

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16
Q

Primary, secondary, tertiary disorders

A

Primary peripheral endocrine gland

Secondary pituitary

Tertiary hypothalamus

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17
Q

What are the families of anterior lobe hormones

A

ACTH

TSH, fsh, lh

GH, prolacitn

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18
Q

Growth hormone is secreted in a pulsation manner, when is most secreted

A

Sleep

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19
Q

Who is GH secretion higher in

A

Pubertal growth than in kids and adults

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20
Q

Describe GH secretion

A

Increased by GHRH , inhibited by somatostatin

Get IGF which - anterior pituitary

IGF and GH + hypothalamus

GHTH - hypothalamus

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21
Q

What does GH hormone do

A

Diabetogenic effect

Increase protein synthesis and organ growth

Increase linear growth

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22
Q

Diabetogenic effect GH

A

Increase blood glucose

Insulin resistance

Decrease glucose uptake, increase lipolysis in adipose tissue

INCREASE BLOOD INSULIN

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23
Q

GH increase protein synthesis and organ growth

A

Increase uptake of aa

Stimulate synthesis of DNA, RNA and protein

done by IGF-1

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24
Q

GH increase linear growth

A

Stimulates DNA, RNA protein synthesis

Increase metabolism inc artilage forming cells and chronrocytes proliferation

Done by IGF-1

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25
Fasting effect on gh, IGF1 and insulin
Increase GH, decrease IGF1, decrease insulin Increase caloric mobilization
26
ADH precursor
Preprossophysin
27
Oxytocin precursor
Prepro-oxyphysin
28
ADH action
V1-vasoconstriction V2-increase reabsorption kidney Urea can pass with water but electrolytes cant Overall increase bp and blood volume
29
What causes secretion ADH
Plasma osmolarity 1% increase (>280mOsm) Decrease bp, by, angII, symp, dehydration
30
How sense osmolarity
Hypothalmic receptors and interneuron send to hypothalamus
31
How detect arterial stretch (look volume)
Atrial stretch receptors to sensory neuron to hypothalamus
32
How detect bp
Cardiac and aortic baroreceptors send sensory neuron to hypothalamus
33
DI
Lack ofAH on renal collecting duct
34
What causes central DI and how treat
Damage to pituitary and destruction of hypothalamus Desmopressin
35
What causes nephrogenic DI and how treat
Lithium, chronic disorders No desmopressin
36
Water deprivation test
For DI Allow fluids overnight before test and give breakfast with no fluid Weigh Allow no fluid for 8 hours, every 1-2 hours weigh (stop test is drop more than 5%) Measure urine volume and osmolarity Measure plasma osmolarity (stop if over 300 ) If indicate DI give after and desmopressin Measure plasma and urine osmolarity urine volume
37
17 a hydroxylase defiency
Increase mineralocorticoids, decrease cortisol, decrease sex hormones High bp Low K Decrease androstenedione Male-undescended testes Female-lack of secondary sexua development
38
21 b defiency
Decrease mineralocorticoids, decrease cortisol, increase sex hormones, Decrease bp increase K Increase renin and 17 hydroxyprogesterone Salt wasting , precocious puberty, virtualization
39
11b defiency
Decrease aldosterone, increase DOC, decrease cortisol, increase sex hormone, increase bp, decrease k , decrease renin Virluisation
40
Cortisol release
Cortisol inhibit acth and CRH, long loop negative feedback
41
When is cortisol secreted
Morning
42
Cushing syndrome
Adrenal tumor, increase cortisol
43
Cushing disesase
Pituitary tumor increase cortisol
44
Addison
Autoimmune adrenal gland Decrease cortisol
45
Secondary adrenal insuffiency
Glucocorticoid drugs suppressing H and P
46
Primary adrenal excess
Increase cortisol, decrease CRH, decrease ACTH, no hyperpigmentation
47
Secondary cortisol excess
Increase cortisol, decrease CRH, increase ACTH, hyperpigmentation
48
Primary defiency cortisol
Decrease cortisol, increase CRH, increase ACTH, hyperpigmentation
49
Secondary defiency
Decrease cortisol increase CRH, decrease ACTH, no hyperpigmentation
50
Steroid administration
Decrease cortisol but symptoms of excess, decrease plasma CRH, decrease acth, no hyperpigmentation
51
When secrete aldosterone
Decrease bp get renin Stress Decrease na k in blood,
52
Paracrine mechanisms in pancreas
Delta cells send to alpha and beta Alpha and beta send to each other
53
Explain glucose regulat of insulin
Glucose bind glut2 and glycolysis so get ATP which close K channel (inward rectifying k channel), depolarization opens ca channel and exocytosis
54
Sulfonylurea receptor
Sulfonylurea drugs (tolbutamide, glyburide) promote closing of the ATP dependent k channel: increase insulin secretions used in treatment of type 2 DM
55
Insulin and insulin receptor
When bind, autophosphorylation and other proteins (insulin receptor substrate) which activate MAP PI3K which mediate the metabolic and mitogenic activities Internalized Insulin downregulates its own receptor
56
Insulin on striated muscle
Increase glucose uptake Increase glycogen synthesis Increase protein synthesis
57
Insulin liver
Decrease gluconeogenesis Increase glycogen synthesis Increase lipogenesis
58
Insulin on blood glucose
Decrease
59
Insulin of glycogen
Increase formation
60
Insulin on gluconeogenesis
Decrease
61
Insulin on glycogenolysis
Decrease
62
Insulin on protein synthesis
Increase, decrease aa in blood
63
Insulin on fat deposition
Increase, decrease FFA
64
Insulin on lipolysis
Decrease, decrease ketoacid
65
Insulin K
Increase uptake into cells, decrease K
66
What stimulates insulin
Glucose, aa, FA, ketoacid, glucagon, cortisol, GIP, vagal, K, sulfonylurea, obesity, somatotataton, diazoxide, exercise
67
Associated conditions with type 1 DM
Autoimmune thyroid disease | Addison’s disease
68
Associated with type 2 DM
Obesity, lipid abnormalities, PCOS, NAFLD
69
Glycogen effect
Increase lipolysis and inhibit FA synthesis, which shunts substrates toward gluconeogenesis Ketoacid are produced from FA
70
Glucagon on glucose, FA, ketoacid
Increased, increased, increased
71
Where is most ca
Bone
72
Biologically active form Ca
Free ionized (50% of total)
73
Sign of hypocalcemia
Tetany Chvostek sign Trousseau sign
74
Hypercalcemia
Long QT, constipation, not hungry, polyuria, polydipsia, weak, hyporeflecia, coma
75
Low Ca
Reduces activation threshold for Na Increases membrane excitability Tingling numbness and muscle twitches
76
High ca
Decrease membrane excitability, reflex response slowed
77
How alter ionized concentration
Change fraction bound to albumin
78
Changes in anion concentration
If increase phosphate conc, decrease ca concentration
79
Changes in plasma protein conc
No change in ionized
80
PTH effect
Bone-resorption Kidney, decrease P reabsorption, increase ca reabsorption, increase urinary camp Intestine-increase ca ab via vitamin d
81
How parathyroid sense ca
CASR
82
CASR
Gq, Gi to PTH gene decrease
83
Chronic hypercalcemia
Decrease synthesis and storage of PTH, increase breakdown of stored PTH and release of inactive PTH fragment into the circulation
84
Chronic hypoglycemia
Increase synthesis and storage of PTH and hyperplasia of parathyroid glands
85
Vitamin d make
See
86
Cyp1a
1a hydrozylase
87
PTH short term
Bone formation, receptors on osteoblasts not osteoclast (direct action on osteoclast) —-use PTH synthetic in osteoporosis
88
Long term PTH
Bone resorption (inc=direct on osteoclasts from cytokines released from osteoclast
89
Vd
Stimulate osteoclast
90
PTH kidney
Stimulates 1 a hydrozylase
91
How PTH get osteoblast
M-CSF, RANKL and OPG production
92
VD
SI-increase ca and P absorption Bone-sensitize osteoblast to pth, regulates osteodystrophy production and calcification Kidney-P reabsorption proximal tube by NPT2a expression, PTH-inhibits PTH gene expression and stimulates CASR
93
Hyperparathyroidism
Stones, bones, groans(constipation)
94
Primary hyperparathyroidism
Increase PTH, increase Ca, decrease Pi, increase VD
95
Secondary hyperparathyroidism
Low ca | Renal failure, VD defiency
96
Renal failure vs vitamin d defiency
Renal-increase PTH, decrease ca, increase P, decrease VD VD def-increase PTH, decrease ca, decrease Pi, decrease VD
97
Hypoparathyroidism
Decrease PHT, decrease Ca, increase pi, decrease Vd
98
Albright hereditary osteodystrophy(pseudopohypoparathyroidism type 1a
AD, Gs for PTH in bone and kidney defective Hypocalcemia and hyperphosphatemia Increase PTH -give pth no phosphaturic response and no increase in urinary camp
99
Phenotype Albright hereditary osteodystrophy
Short, short neck, obese, subcutaneous calcification, short metatarsals, and metacarpals Increase PTH, decrease Ca, increase pi, decrease VD
100
Hypercalcemia of malignancy
PTHrP-n terminal to PTH Decrease PTH, increase Ca, decrease Pi, decrease Vd
101
Familial hypocalcemia hypercalcemia FHH
AD, mutation in CaSR in parathyroid and ascending limb of kidney -decrease urinary Ca excretion and increase serum ca Maybe increase PTH, incrase Ca serum, decrease urine ca, no change in p or VD
102
Pseudovitamin d deficient rickets or vitamin d dependent rickets type I
Decrease 1a hydroxylase
103
Pseudovitamin d deficient rickets or vitamin d dependent rickets II
Decrease VD receptor
104
Vd defiency
Increase PTH, decrease P, increase urine P and camp, decrease VD< increase osteomalacia and resorption
105
Enough hormone is stored as iodinated TG int he follicular colloid to last the body 2-3 months
Iodine is stored iodinated as tyrosine of thyroglobulin
106
Peripheral conversion T4 to T3
Deiodinase
107
Defiency of deiodinase
Mimics dietary I defiency
108
High levels I
Inhibit organification and synthesis of thyroid hormones: Wolff chaikoff effect
109
PTU
Effective treatment for hyperthyroidism
110
Transport T3 t4
Thyroxine binding protein -synthesized in liver, higher affinity for T2 Trnasytherin Albumin
111
Hepatic failure
Decrease TBG, increase free t2m t4 Inhibition of T2 t4 synthesis from neg feedback
112
Pregnancy tbg
Increase Decrease free Increase in secretion and synthesis t2 t4 Increase total levels of T3 and t4 but levels of free physiologically active thyroid hormones normal (clnicalll. Euthyroid)
113
T3 t4 inhibit
TSH
114
Is TSH pulsation Luke gh
No steady state
115
Stimulate thyroid
TSH, the=triode stimulating immunoglobulins, incrase tbg
116
Inhibit thyroid hormone
I defiency, deiodinase defiency, intake I, perchlorate, thiocyanate, PTU, decrease TBG
117
PTU
Propylthiouracil
118
Thyroid hormone action
Growth, cns maturation, increase BMT, increase metabolism, increase cardiac output and upregulate b1 receptors, diarrhea
119
Goiter
Hyper or hypo

Physiology (7 decks)

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