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Physiology > Endo > Flashcards

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
Q

Fasting effect on gh, IGF1 and insulin

A

Increase GH, decrease IGF1, decrease insulin

Increase caloric mobilization

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26
Q

ADH precursor

A

Preprossophysin

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27
Q

Oxytocin precursor

A

Prepro-oxyphysin

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28
Q

ADH action

A

V1-vasoconstriction
V2-increase reabsorption kidney
Urea can pass with water but electrolytes cant

Overall increase bp and blood volume

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29
Q

What causes secretion ADH

A

Plasma osmolarity 1% increase
(>280mOsm)
Decrease bp, by, angII, symp, dehydration

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30
Q

How sense osmolarity

A

Hypothalmic receptors and interneuron send to hypothalamus

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31
Q

How detect arterial stretch (look volume)

A

Atrial stretch receptors to sensory neuron to hypothalamus

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32
Q

How detect bp

A

Cardiac and aortic baroreceptors send sensory neuron to hypothalamus

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33
Q

DI

A

Lack ofAH on renal collecting duct

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34
Q

What causes central DI and how treat

A

Damage to pituitary and destruction of hypothalamus

Desmopressin

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35
Q

What causes nephrogenic DI and how treat

A

Lithium, chronic disorders

No desmopressin

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36
Q

Water deprivation test

A

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

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37
Q

17 a hydroxylase defiency

A

Increase mineralocorticoids, decrease cortisol, decrease sex hormones

High bp
Low K

Decrease androstenedione

Male-undescended testes
Female-lack of secondary sexua development

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38
Q

21 b defiency

A

Decrease mineralocorticoids, decrease cortisol, increase sex hormones,

Decrease bp increase K

Increase renin and 17 hydroxyprogesterone

Salt wasting , precocious puberty, virtualization

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39
Q

11b defiency

A

Decrease aldosterone, increase DOC, decrease cortisol, increase sex hormone, increase bp, decrease k , decrease renin

Virluisation

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40
Q

Cortisol release

A

Cortisol inhibit acth and CRH, long loop negative feedback

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41
Q

When is cortisol secreted

A

Morning

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42
Q

Cushing syndrome

A

Adrenal tumor, increase cortisol

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43
Q

Cushing disesase

A

Pituitary tumor increase cortisol

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44
Q

Addison

A

Autoimmune adrenal gland

Decrease cortisol

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45
Q

Secondary adrenal insuffiency

A

Glucocorticoid drugs suppressing H and P

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46
Q

Primary adrenal excess

A

Increase cortisol, decrease CRH, decrease ACTH, no hyperpigmentation

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47
Q

Secondary cortisol excess

A

Increase cortisol, decrease CRH, increase ACTH, hyperpigmentation

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48
Q

Primary defiency cortisol

A

Decrease cortisol, increase CRH, increase ACTH, hyperpigmentation

49
Q

Secondary defiency

A

Decrease cortisol increase CRH, decrease ACTH, no hyperpigmentation

50
Q

Steroid administration

A

Decrease cortisol but symptoms of excess, decrease plasma CRH, decrease acth, no hyperpigmentation

51
Q

When secrete aldosterone

A

Decrease bp get renin

Stress

Decrease na k in blood,

52
Q

Paracrine mechanisms in pancreas

A

Delta cells send to alpha and beta

Alpha and beta send to each other

53
Q

Explain glucose regulat of insulin

A

Glucose bind glut2 and glycolysis so get ATP which close K channel (inward rectifying k channel), depolarization opens ca channel and exocytosis

54
Q

Sulfonylurea receptor

A

Sulfonylurea drugs (tolbutamide, glyburide) promote closing of the ATP dependent k channel: increase insulin secretions used in treatment of type 2 DM

55
Q

Insulin and insulin receptor

A

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
Q

Insulin on striated muscle

A

Increase glucose uptake

Increase glycogen synthesis

Increase protein synthesis

57
Q

Insulin liver

A

Decrease gluconeogenesis

Increase glycogen synthesis

Increase lipogenesis

58
Q

Insulin on blood glucose

A

Decrease

59
Q

Insulin of glycogen

A

Increase formation

60
Q

Insulin on gluconeogenesis

A

Decrease

61
Q

Insulin on glycogenolysis

A

Decrease

62
Q

Insulin on protein synthesis

A

Increase, decrease aa in blood

63
Q

Insulin on fat deposition

A

Increase, decrease FFA

64
Q

Insulin on lipolysis

A

Decrease, decrease ketoacid

65
Q

Insulin K

A

Increase uptake into cells, decrease K

66
Q

What stimulates insulin

A

Glucose, aa, FA, ketoacid, glucagon, cortisol, GIP, vagal, K, sulfonylurea, obesity, somatotataton, diazoxide, exercise

67
Q

Associated conditions with type 1 DM

A

Autoimmune thyroid disease

Addison’s disease

68
Q

Associated with type 2 DM

A

Obesity, lipid abnormalities, PCOS, NAFLD

69
Q

Glycogen effect

A

Increase lipolysis and inhibit FA synthesis, which shunts substrates toward gluconeogenesis

Ketoacid are produced from FA

70
Q

Glucagon on glucose, FA, ketoacid

A

Increased, increased, increased

71
Q

Where is most ca

A

Bone

72
Q

Biologically active form Ca

A

Free ionized (50% of total)

73
Q

Sign of hypocalcemia

A

Tetany

Chvostek sign

Trousseau sign

74
Q

Hypercalcemia

A

Long QT, constipation, not hungry, polyuria, polydipsia, weak, hyporeflecia, coma

75
Q

Low Ca

A

Reduces activation threshold for Na

Increases membrane excitability

Tingling numbness and muscle twitches

76
Q

High ca

A

Decrease membrane excitability, reflex response slowed

77
Q

How alter ionized concentration

A

Change fraction bound to albumin

78
Q

Changes in anion concentration

A

If increase phosphate conc, decrease ca concentration

79
Q

Changes in plasma protein conc

A

No change in ionized

80
Q

PTH effect

A

Bone-resorption
Kidney, decrease P reabsorption, increase ca reabsorption, increase urinary camp

Intestine-increase ca ab via vitamin d

81
Q

How parathyroid sense ca

A

CASR

82
Q

CASR

A

Gq, Gi to PTH gene decrease

83
Q

Chronic hypercalcemia

A

Decrease synthesis and storage of PTH, increase breakdown of stored PTH and release of inactive PTH fragment into the circulation

84
Q

Chronic hypoglycemia

A

Increase synthesis and storage of PTH and hyperplasia of parathyroid glands

85
Q

Vitamin d make

A

See

86
Q

Cyp1a

A

1a hydrozylase

87
Q

PTH short term

A

Bone formation, receptors on osteoblasts not osteoclast (direct action on osteoclast)

—-use PTH synthetic in osteoporosis

88
Q

Long term PTH

A

Bone resorption (inc=direct on osteoclasts from cytokines released from osteoclast

89
Q

Vd

A

Stimulate osteoclast

90
Q

PTH kidney

A

Stimulates 1 a hydrozylase

91
Q

How PTH get osteoblast

A

M-CSF, RANKL and OPG production

92
Q

VD

A

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
Q

Hyperparathyroidism

A

Stones, bones, groans(constipation)

94
Q

Primary hyperparathyroidism

A

Increase PTH, increase Ca, decrease Pi, increase VD

95
Q

Secondary hyperparathyroidism

A

Low ca

Renal failure, VD defiency

96
Q

Renal failure vs vitamin d defiency

A

Renal-increase PTH, decrease ca, increase P, decrease VD

VD def-increase PTH, decrease ca, decrease Pi, decrease VD

97
Q

Hypoparathyroidism

A

Decrease PHT, decrease Ca, increase pi, decrease Vd

98
Q

Albright hereditary osteodystrophy(pseudopohypoparathyroidism type 1a

A

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
Q

Phenotype Albright hereditary osteodystrophy

A

Short, short neck, obese, subcutaneous calcification, short metatarsals, and metacarpals

Increase PTH, decrease Ca, increase pi, decrease VD

100
Q

Hypercalcemia of malignancy

A

PTHrP-n terminal to PTH

Decrease PTH, increase Ca, decrease Pi, decrease Vd

101
Q

Familial hypocalcemia hypercalcemia FHH

A

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
Q

Pseudovitamin d deficient rickets or vitamin d dependent rickets type I

A

Decrease 1a hydroxylase

103
Q

Pseudovitamin d deficient rickets or vitamin d dependent rickets II

A

Decrease VD receptor

104
Q

Vd defiency

A

Increase PTH, decrease P, increase urine P and camp, decrease VD< increase osteomalacia and resorption

105
Q

Enough hormone is stored as iodinated TG int he follicular colloid to last the body 2-3 months

A

Iodine is stored iodinated as tyrosine of thyroglobulin

106
Q

Peripheral conversion T4 to T3

A

Deiodinase

107
Q

Defiency of deiodinase

A

Mimics dietary I defiency

108
Q

High levels I

A

Inhibit organification and synthesis of thyroid hormones: Wolff chaikoff effect

109
Q

PTU

A

Effective treatment for hyperthyroidism

110
Q

Transport T3 t4

A

Thyroxine binding protein -synthesized in liver, higher affinity for T2

Trnasytherin

Albumin

111
Q

Hepatic failure

A

Decrease TBG, increase free t2m t4

Inhibition of T2 t4 synthesis from neg feedback

112
Q

Pregnancy tbg

A

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
Q

T3 t4 inhibit

A

TSH

114
Q

Is TSH pulsation Luke gh

A

No steady state

115
Q

Stimulate thyroid

A

TSH, the=triode stimulating immunoglobulins, incrase tbg

116
Q

Inhibit thyroid hormone

A

I defiency, deiodinase defiency, intake I, perchlorate, thiocyanate, PTU, decrease TBG

117
Q

PTU

A

Propylthiouracil

118
Q

Thyroid hormone action

A

Growth, cns maturation, increase BMT, increase metabolism, increase cardiac output and upregulate b1 receptors, diarrhea

119
Q

Goiter

A

Hyper or hypo

Physiology (7 decks)

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