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mic cabatu Physiology > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

Produces new proteins from DNA

Lipid-soluble

A

Steroid Hormones

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2
Q

Modifies existing proteins

Water-soluble

A

Protein hormones

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3
Q

T3, T4, epinephrine, Norepinephrine

A

Derivative of Tyrosine

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4
Q

Convert hormonal signal into 2nd messenger

A

G proteins

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5
Q

For fat-soluble substances

A

Intracellular Receptors

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6
Q

Acts as transducers

A

G proteins

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7
Q

Is stimulated by Guanine Nucleotide Exchange Factors

A

GTP-activated

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8
Q

Is inhibited by GTPase-Accelerating Proteins, RGS proteins

A

GTP-activated

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9
Q

Activates Adenylate Cyclades converts ATP to cAMP -> activates Protein Kinase A

A

Alpha Subunit of G protein

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10
Q

May regulate ion channels directly

Broken down by cAMP phosphodiesterase

A

cAMP

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11
Q

Regulates effector proteins

A

PKA

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12
Q

Alpha t subunit activates cGMP phosphodiesterase -> decreases cGMP -> closes cGMP-dependent ion channels

A

G protein with alpha t (transducin)

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13
Q

Phospholipids C -> PIP2 -> PIP2 splits into InsP3 or IP3 (releases Calcium from ER) and DAG (activates Protein Kinase C)

A

G-protein with alpha q

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14
Q

Releases calcium from ER

A

IP3

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15
Q

activates Protein Kinase C

A

DAG

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16
Q

Guanylyl Cyclase converts GTP to cGMP -> activates Protein Kinase G -> Phosphorylates Proteins

A

Receptor Guanylyl Cyclases

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17
Q

Example of Receptor Guanylyl Cyclases

A

ANP

NO

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18
Q

Attaches to Type 1 subunit-> Phosphorylates Serine/Threonine residues on Type 2 subunit -> activates effectors

A

Receptor Serine/ Threonine Kinases

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19
Q

Example of Receptor Serine/ Threonine Kinases

A

TGF-Beta

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20
Q

Example of Receptor Tyrosine Kinase

A 
NGF
EGF
PDGF
IGF-1
insulin
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21
Q

No intrinsic tyrosine kinase activity

Associate with proteins that have tyrosine kinases of the Src family and Janus family (JAK)

A

Tyrosine-associated Kinase Receptors

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22
Q

Example of Tyrosine-associated Kinase Receptors

A

EPO

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23
Q

Synthesize in the hypothalamus

A

CRH

Vasopressin/Oxytocin

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24
Q

cAMP - 2ND MESSENGER

A 
DH (V2 receptors)
Angiotensin II (Epithelial cells)
Catecholamines (B1 & B2 Receptors)
ACTH
LH, FSH, TSH
HCG
MSH
CRH
Calcitonin
PTH
Secretin
Somatostatin
Glucagon
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25
Q

IP3/ DAG - Phospholipase C

A 
ADH (V1 receptor)
Angiotensin II (vascular. Smooth muscles)
catecholamines (A1 receptors)
GnRH
TRH
GHRH
Oxytocin
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26
Q

Steroid Hormone

A 
Aldosterone
Cortisol
Testosterone
Progesterone
Estrogen
Vitamin D
Thyroid Hormone
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27
Q

Tyrosine Kinase

A 
LeptinIGF-1
Insulin
EPO
GH
Prolactin
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28
Q

Guanylate Cyclase Mecanism (cGMP)

A

ANP
EDRF
nitric oxide

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29
Q

Transport of steroid hormone

A

Bound to proteins

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30
Q

Active form of steroid hormones

A

Free, unbound form

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31
Q

Main site of inactivation of hormones

A

Liver

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32
Q

Mechanism for removal of hormones

A

Liver

Kidneys

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33
Q

Number of Hormone Receptors - Constant or Variable?

A

Variable

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34
Q

Minimum amount of hormone to produce effect

A

1 pictograms per ml

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35
Q

Onset of Hormone Effects

A

seconds to months

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36
Q

Additive effects of synergistic effects

A

Epinephrine

NE

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37
Q

Complementary Effects of Synergistic Effects

A

FSH

Testosterone on spermatogenesis

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38
Q

Permissive effects

A

Cortisol has permissive effects on Epi & NE with regards to blood vessels
T3 - on Epi with regards to lipolysis

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39
Q

Antagonistic effects

A

Estrogen blocking prolactin effects on the breast during pregnancy

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40
Q

More common

Hormone has biological actions that, directly or indirectly, inhibit further secretion of the hormone

A

Negative Feedback (Self-Limiting)

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41
Q

Rare, exploding

Hormone has biological actions that, directly or indirectly, stimulate further secretion of the hormone

A

Positive Feedback (Self-Augmenting)

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42
Q

Supraoptic Nucleus

A

Vasopressin

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43
Q

Paraventricular Nucleus

A

Oxytocin

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44
Q

Give an example of Negative Feedback that does not utilize HPA

A

Insulin

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45
Q

Give 3 examples of Positive feedback involving hormones

A

Estrogen-induced LH and FSH Surge
Oxytocin during labor
oxytocin during lactation

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46
Q

Decrease in receptor number or receptor affinity

A

Down-regulation of Receptors

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47
Q

Example of Down-regulation of Receptors

A

In uterus, progesterone

T3 down regulates TRH receptors

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48
Q

Increase in receptor number or receptor affinity

A

Up-regulation of Receptors

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49
Q

Example of Up-regulation of Receptors

A

Prolactin increases the number of its receptors in the breast
Growth hormone increases the number of its receptors in skeletal muscle and liver
In the ovary, estrogen up-regulates it’s own receptor and that of LH

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50
Q

Lies in the Sella Turcica

A

Pituitary Gland

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51
Q

Connected to the Median Eminence of the Hypothalamus via pituitary/hypo physical stalk

A

Pituitary gland

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52
Q

Transmit hypothalamic hormones to the pituitary without passing through the systemic circulation

A

Hypothalamic-Hypophysial Portal Blood vessels

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53
Q

Adenohypophysis

A

Anterior Pituitary

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54
Q

Neurohypophysis

A

Posterior Pituitary

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55
Q

Derived from oral ectoderm (rathke’s Pocuh)

A

Anterior Pituitary

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56
Q

Basophils cells of Ant. Pituitary

A 
FSH
LH
ACTH
TSH
MSH
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57
Q

Acidophilus Cells of Ant. Pituitary

A

GH

Prolactin

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58
Q

Derived from neural ectoderm (neural outgrowth of Hypothalamus)

A

Posterior Pituitary

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59
Q

Pituicytes of Post. Pituitary

A

Vasopressin

Oxytocin

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60
Q

Which of the following is a consequence when the anterior lobe of the pituitary gland is resected?

A

Inability to stimulate production of thyroid hormone

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61
Q

4 hormones that increase Blood Glucose Level

A

Epinephrine
GH (acromegaly, gigantism) lead to DM
Cortisol
Glucagon

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62
Q

If pituitary stalk is damaged, all anterior pituitary hormones would decreased, EXCEPT

A

Prolactin

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63
Q

In terms of number, what are the top 2 cells in the anterior pituitary?

A

Somatotropin (40%)

Corticotropes (20%)

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64
Q

What are the 3 families of hormones in the anterior pituitary

A

TSH, LH, FSH ( same alpha unit, unique beta unit)
MSH, ACTH ( derived from POMC)
GH, Prolactin

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65
Q

Both catabolic and anabolic

A

Growth hormone

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66
Q

Released in pulsatilla fashion (every 2 hours)

Nocturnal Peak: 1 hours after stage 3 or 4 sleep

A

Growth hormone

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67
Q

Growth hormone

A

Somatotropin

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68
Q

Stops growth hormone

A

Somatostatin

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69
Q

IGF

A

Somatomedin

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70
Q

Mcc of dwarfism

Defect in FGF receptor 3

A

Achondroplasia

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71
Q

Increased GH

With skeletal deformities

A

Gigantism

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72
Q

Actions of Prolactin

A

Lactogenesis
Lactation amenorrhea
Breast development

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73
Q

What is one possible side effects of anti-psychotic drugs that involve Prolactin?

A

Amenorrhea-Galactorrhea

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74
Q

Prolactin is stimulated by the following

A 
Pregnancy(ESTROGEN)
breast ending
Sleep
Stress
TRH
Dopamine antagonist
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75
Q

Prolactin is inhibited by

A

Dopamine, Bromocriptine
Somatostatin
Prolactin (negative feedback)

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76
Q

Aka as ADH or AVP

A

Vasopressin

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77
Q

Secreted by Supraoptic Nuclei of the hypothalamus

A

Vasopressin

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78
Q

Responds to ECF changes detected by osmoreceptors in the Organum Vasculosum

A

Vasopressin

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79
Q

Most potent stimulus of Vasopressin

A

Increased plasma osmolality

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80
Q

Vasoconstrictor

A

V1 blood vessels

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81
Q

Water permeability

A

V2 kidneys

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82
Q

Central DI

A

URine volume: high
Urine osmolarity: low
ADH levels:low
Treatment: DDAVP (ADH analog)

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83
Q

Peripheral DI

A

URine volume: high
Urine osmolarity: low
ADH levels: high
Treatment: thiazides diuretics

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84
Q

SIADH

A

URine volume: low
Urine osmolarity: high
ADH levels: high
Treatment:Demeclocycline (ADH antagonist)

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85
Q

In SIADH, the brain reduces intracellular osmolytes to prevent cell swelling. What happens if you rapidly correct the Hyponatremia?

A

Osmotic Demyelination Syndrome (esp. In the pons)

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86
Q

From Paraventricular nuclei of the hypothalamus

A

Oxytocin

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87
Q

Synthesized by the follicular epithelial cells of the thyroid

A

Thyroid Hormone

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88
Q

T4

A 
93%
More half life (6 days)
More affinity for binding plasma protein
Less (10% of the receptors) binding to nuclear receptor
Onset of action: 4x slower (2 days)
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89
Q

T3

A 
7% synthesized
Less half life (1 day)
Less affinity
More (90%) binding receptor)
4x faster (12 hours) onset of action
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90
Q

Thyroxine Binding Globulin (TBG

A

70%

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91
Q

Transthyretin or Thyroxine Binding Prealbumin (TBPA)

A

20%

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92
Q

Thyroxine Binding Albumin

A

10%

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93
Q

Free Thyroxine

A

0.03%

94
Q

MIT + DIT

A

= T3

95
Q

DIT + DIT

A

= T4

96
Q

Iodine trapping

A

I2

97
Q

Organic action

A

MIT & DIT

98
Q

Coupling

A

MIT + DIT = T3

DIT + DIT = T4

99
Q

Storage

A

Thyroglobulin

100
Q

Secretion

A

TSH binding & TSH Receptor

101
Q

Bone maturation

Bone formation

A

Thyroid hormone
Growth hormone
IGF 1

102
Q

Regulation of thyroid hormone secretion is mediated by

A

TRH & TSH levels

103
Q

Hyperthyroidism symptoms

A 
Increased basal metabolic rate
Weight loss
Negative nitrogen balance
Increased cardiac output
Dyspnea (shortness of breath)
Tremor, muscle weakness
Exophthalmos - deposition of GAGs and fat
Goiter
Tibial edema
104
Q

Hyperthyroidism causes

A

Graves’ disease
Thyroid neoplasm
Excess TSH secretion
Exogenous T3 or T4

105
Q

Hyperthyroidism TSH levels

A

Decreased (feedback inhibition of T3 on the anterior lobe)

Increased (if defect is in anterior pituitary)

106
Q

Hyperthyroidism treatment

A

Propylthiouracil
Thyroidectomy
I132
Beta adrenergic blocking agents

107
Q

Hypothyroidism symptoms

A 
Decreased basal metabolic rate
Weight gain
Positive nitrogen balance
Decreased heat production
Cold sensitivity
Decreased cardiac output
Hypoventilation
Lethargy, mental slowness
Drooping eyelids
Myxedema
Growth retardation
Mental retardation
108
Q

Hypothyroidism causes

A 
Thyroiditis
Surgery for hyperthyroidism
I deficiency
cretinism
Decreased TRH or TSH
109
Q

Hypothyroidism TSH levels

A

Increased (by negative feedback if primary defect is in thyroid gland)
Decreased ( if defect is in hypothalamus or anterior pituitary)

110
Q

Hypothyroidism treatment

A

Thyroid hormone replacement therapy

111
Q

RDA of Iodine per day

A

150 nanograms

112
Q

High levels of Iodine inhibiting organize action and iodine thyroid hormone synthesis

A

Wolf-Chaikoff Effect

113
Q

Bone age < Chronological Age

A

Hypothyroidism

114
Q

Liver and Kidney Failure: TBG levels

A

Decreased TBG

115
Q

Estrogen or Pregnancy: TBG levels

A

Increased TBG

116
Q

Enzyme that converts T4 to T3

A

5’ iodinase

117
Q

T4 can also be converted to

A

RT3 (inactive)

118
Q

Aldosterone (mineralocorticoid)

A

Zone Glomerulosa

119
Q

Cortisol, corticosterone (Glucocorticoids)

A

Zone Fasciculata

120
Q

De-hydro-Epi-androsterone (DHEA) and Androstenedione (weak androgens)

A

Zone Reticularis

121
Q

Epinephrine - 80%

NE - 20%

A

Adrenal medulla

122
Q

Right adrenal kidney

A

Pyramidal

123
Q

Left renal kidney

A

Crescent shape

124
Q

Inhibits 11beta-hydroxylase

A

Metyrapone

125
Q

Inhibits Desmolase

A

Ketoconazole

126
Q

Adrenal androgens in males

A

Insignificant

127
Q

Adrenal androgens in females

A

Significant

128
Q

Need ACTH for 1st step, but otherwise controlled by RAAS

A

Aldosterone

129
Q

Diabetogenic Hormones

A

Cortisol
GH
Glucagon
Epinephrine

130
Q

Increases Na reabsorption in the kidneys, sweat glands, salivary glands and colon
Increase K secretion in the kidneys and colon
Increases H secretion in the kidneys

A

Aldosterone

131
Q

Oscillates with circadian rhythm

A

Cortisol

132
Q

Carbohydrate Effects of Cortisol

A

Stimulate gluconeogenesis
Increases protein catabolism in muscles
Decreases glucose utilization and insulin sensitivity of adipose tissue

133
Q

Protein effects in Cortisol

A

Reduces cellular proteins (except liver)
Increases blood amino acids
Increases liver and plasma proteins

134
Q

Fat effects of Cortisol

A

Increases lipolysis

Moon face and buffalo hump

135
Q

Anti-inflammatory effects of Cortisol

A

Induces synthesis of lipocortin which inhibits Phospholipase A2 needed for PG and LT synthesis
Stabilizes lysosomal membranes
Decreases migration and phagocytosis of WBC
Suppression of T-lymphocytes
Reduces IL-1, IL2
Increases resolution of inflammation
Blocks inflammatory response to allergies
Decreases eosinophils and lymphocytes
Inhibits histamine and serotonin
Increases RBCs

136
Q

Dexamethasone Test Cushing syndrome

A

Cortisol level not suppressed either by low or high dose

137
Q

Dexamethasone Test Cushing Disease

A

ACTH and cortisol suppressed by high dose but not low dose

138
Q

Addison’s disease

A

Primary adrenocortical insufficiency

139
Q

Addison’s disease

A 
Hypoglycemia
Anorexia, weight loss, vomiting, nausea
Weakness
Hypotension
Hyperkalemia
Metabolic acidosis
Decreased pubic and auxiliary hair in females
Hyper pigmentation
140
Q

Addison’s disease ACTH levels

A

Increased (negative feedback effect of decreased cortisol)

141
Q

Addison’s disease treatment

A

Replacement of glucocorticoids and mineralocorticoids

142
Q

Cushing syndrome

A

Ex. Primary adrenal hyperplasia

143
Q

Cushing syndrome

A 
Hyperglycemia
Muscle wasting
Central obesity
Round face, supraclavicular fat, buffalo hump
Osteoporosis
Striae
Virilization and menstrual disorders in females
Hypertension
144
Q

Cushing syndrome ACTH levels

A

Decreased (negative feedback effect of increased cortisol)

145
Q

Cushing syndrome treatment

A

Ketoconazole

metyrapone

146
Q

MCC of exogenous dose of steroid

A

Cushing syndrome

147
Q

Cushing disease

A

Excess ACTH

148
Q

Cushing disease

A 
Hyperglycemia
Muscle wasting
Central obesity
Round face, supraclavicular fat, buffalo hump
Osteoporosis
Striae
Virilization and menstrual disorders in females
Hypertension
149
Q

Cushing disease ACTH levels

A

Increased

150
Q

Cushing disease treament

A

Surgical removal of ACTH-secreting tumor

151
Q

Conn Syndrome

A

Aldosterone-secreting tumor

152
Q

conn syndrome

A

Hypertension (inc ECF vol)
Hypokalemia (inc K secretion)
Metabolic acidosis ( inc H secretion)
Decreased renin levels ( inc ECF levels)

153
Q

Conn syndrome treatment

A 
Aldosterone antagonist (spironolactone)
Surgery
154
Q

21 beta-hydroxylase deficiency

A

Virility ton in females
Early acceleration of linear growth
Early appearance of public and axillary hair
Symptoms of deficiency of glucocorticoids and mineralocorticoids

155
Q

21 beta-hydroxylase deficiency ACTH levels

A

Increased (negative feedback effect of decreased cortisol)

156
Q

21 beta-hydroxylase deficiency treatment

A

Replacement of glucocorticoids and mineralocorticoids

157
Q

17alpha-hydroxylase deficiency

A

Lack of pubic and axillary hair in females
Symptoms of deficiency of glucocorticoids
Symptoms of excess mineralocorticoids
Hypoglycemia

158
Q

17alpha-hydroxylase deficiency ACTH levels

A

Increased (negative feedback effect of decreased cortisol)

159
Q

17alpha-hydroxylase deficiency treatment

A 
Replacement of glucocorticoids
Aldosterone antagonist (spironolactone)
160
Q

Which of the following statements are true of Cushing’s syndrome except?
A. Pituitary tumors are the most common cause of Cushing’s disease
B. ACTH secreting Tumors can be suppressed by high dose Dexamethasone
C. Exogenous steroids are the most common cause of Cushing’s syndrome
D. NOTA

A

NOTA

161
Q

What is the predominant mechanism of hypotension in Addison’s disease?

A

Decreased responsiveness of Arterioles to catecholamines

162
Q

Which of the following are expected effects/manifestation of a patient with conn’s syndrome?

A

Decreased plasma renin level

163
Q 
All of the following substances are decreased in 21 beta-hydroxyl asedeficiency except?
A. Deoxycorticosterone
B. Aldosterone
C. Androgens
D. Cortisol
A

C. Androgens

164
Q

Glucagon is Synthesizedand secreted by

A

Alpha cells

165
Q

Glucagon functions

A

Mirror image of insulin
Hormone of starvation
Promotes storage of metabolic fuels, mobilization and utilization
Synthesized as pre-glucagon

166
Q

Glucagon actions

A

Increase and maintain blood glucose concentration

167
Q

Major factor stimulating the secretion of decrease blood glucose level

A

Glucagon

168
Q

Glucagon secretes what AA?

A

Arginine and Alanine

169
Q

Glucagon

A

CCK - fasting and increase exercise

170
Q

2nd messenger of Glucagon

A

CAMP

171
Q

Delta cells

A

Somatostatin

172
Q

Secretion inhibited by insulin via intraislet paracrine mechanism
Inhibit secretion of insulin and glucagon
Modulate or limit the response of insulin and glucagon to ingesting of food

A

Somatostatin

173
Q

21 - beta - hydroxylase

A 
Aldosterone: dec
COrtisol: dec
Androgens: inc
ACTH: inc
Blood pressure: dec
Accumulating substance: 17-hydroxyprogesterone
174
Q

11 - beta- hydroxylase

A 
Aldosterone: dec
COrtisol: dec
Androgens: inc
ACTH: inc
Blood pressure: inc
Accumulating substance: 11-deoxy-corticosterone
175
Q

17-alpha-hydroxylase

A 
Aldosterone: inc
COrtisol: dec
Androgens: dec
ACTH: inc
Blood pressure: inc
Accumulating substance: pregnenolone
176
Q

Secretes insulin and Aylin

A

Beta cells (60%)

177
Q

Secretes glucagon

A

Alpha cells (25%)

178
Q

Secretes Somatostatin

A

Delta Cells (10%)

179
Q

Secrete Pancreatic Polypeptide

A

F cell / PP Cell (5%)

180
Q

Actions of Insulin

A 
Increases:
glucose uptake into the cells
Glycogen edits
Amino acid uptake into the cells. (For protein synthesis)
Lipogenesis and uptake fat deposition
Potassium uptake into the cells
181
Q

Actions of Insulin

A

Decreases:
Gluconeogenesis
Glycogenolysis
Lipolysis

182
Q

Actions of glucagon

A

Increase blood glucose (inc glycogenolysis, gluconeogenesis)
Inc Blood fatty acid and ketoacids
Inc Urea production
Inc Insulin

183
Q

Actions of Somatostatin

A

Inhibits both glucagon and insulin to modulate their effects
Inhibits all GI hormones
Stimulated by all types of nutrients
Decreases motility of stomach, duodenum and gallbladder
Decreases both absorption and secretion in the GIT

184
Q

Side effect of Metformin

A

Lactic Acidosis

185
Q

Type 1 crisis

A

DKA

186
Q

Type 1 treatment

A

Insulin

187
Q

Type 2 crises

A

HHHS

188
Q

Type 2 treatment

A 
Weight loss
Thiazolidinediones
Metformin
Sulfonylureas
Insulin
189
Q

Effect of insulin on the brain

A

None

190
Q

Insulin: 2nd messenger

A

Tyrosine Kinase

191
Q

Glucagon: 2nd messenger

A

cAMP

192
Q

Marker for endogenous insulin

A

C peptide

193
Q

When proinsulin becomes insulin, what part is cleaved off?

A

C peptide

194
Q

GLUT transport is found in Beta Cells

A

Glut 2

195
Q

Oral vs IV Glucose: great insulin secretion

A

Oral glucose

196
Q

Is more powerful stimulant for insulin secretion because it stimulates the GIP (gastric inhibitory peptide)

A

Oral Glucose

197
Q

Type 1

A

Inadequate secretion:
Inc blood glucose conc
Inc blood fatty acid and ketoacids conc
Inc blood AA conc

198
Q

Type 2

A

Down-regulation of insulin receptor on target tissues

Insulin resistance

199
Q 
All of the following insulin secretion EXCPET?
A. Hyperglycemia
B. Glucagon
C. Cholecystokinin
D. Alpha adrenergic stimulation
E. Gastric inhibitory peptide
A

D. Alpha adrenergic stimulation

200
Q

ECF + Chondroitin Sulfate + Hyaluronic Acid

Gelatinous medium

A

Ground Substance of Organic Matrix

201
Q

95% of organic matrix

for Tensile Strength

A

Collagen Fibers

202
Q

secrete collagen & Ground Substance where calcium precipitates

A

Osteoblast

203
Q

Bone Remodelling

A

Osteoblast

204
Q

Bone Resorption

A

Osteoclast

205
Q

secrete Lysosomal enzymes, citric acid and lactic acid

A

osteoclast

206
Q

calcium intake > calcium excretion

A

Positive Calcium Balance

207
Q

calcium intake < Calcium excretion

A

Negative Calcium Balance

208
Q

hyperreflexia, spontaneous twitching, muscle cramps, and tingling and numbness

A

Hypocalcemia

209
Q

constipation, polyuria, polydipsia and neurologic signs of hyporeflexia, lethargy, coma, and death

A

hypercalcemia

210
Q

signs of hypocalcemia

A

chvostek & Trousseau sign

211
Q

what is the location of PTH receptors

A

osteoblast

212
Q

would thyroidectomy cause hypercalcemia due to absent calcitonin?

A

no, since calcitonin does NOT participate in minute-to-minute calcium regulation

213
Q

what is the secreted by osteoblast to inhibit osteoclastic activity in hyperparathyroidism?

A

Alkaline Phosphate

214
Q

Vitamin D comes from?

A

Cholesterol

215
Q

1st activation of vitamin D synthesis

A

Liver

216
Q

2nd activation of Vitamin D synthesis

A

Kidney

217
Q

secreted by chief cells of the parathyroid gland

A

PTH

218
Q

stimulated by hypocalcemia

A

PTH

219
Q

also stimulated by hypomagnesemia, except hypomagnesemia caused by alcoholism

A

PTH

220
Q

secreted by Parafollicular Cells (C Cells) of the thyroid gland

A

Calcitonin

221
Q

PTH in the kidney

A

increases calcium reabsorption (DT)

decreases phosphate reabsorption (PCT)

increases active vit D

222
Q

PTH in intestine

A

none

223
Q

PTH in bone

A

increased calcium

decreased phospate

224
Q

vit D in intestine

A

increases calcium & phosphate absorption

225
Q

vit D in Kidney

A

increases calcium & phosphate reabsorption

increases urinary calcium

226
Q

vit D in bone

A

at normal levels: calcium and phosphate deposition

at high toxic levels: calcium & phosphate resorption

227
Q

PTH net effect on serum levels

A

increased calcium

decreased phosphate

228
Q

Vit D net effect on serum levels

A

increased calcium

increased phosphate

229
Q

what is the treatment for Humoral Hypercalcemia of Malignancy?

A

Furosemide ( inhibits renal Ca reabsorption)

Etodronate ( inhibits bone resorption)

230
Q

presents with short stature, short neck, obesity, subcutaneous calcification, and shortened fourth metatarsals and metacarpals?

A

Albright Hereditary Osteodystrophy (Pseudohypoparathyroidsm Type Ia)

231
Q

vitamin D resistance is seen in which condition?

A

chronic Renal Failure

232
Q

Which of the following is an action of parathyroid hormone (PTH) on the renal tubule?

a. stimulation of adenylate cyclase
b. inhibition of distal tubule K secretion
c. inhibition of distal tubule ca reabsorption
d, stimulation of proximal tubular phosphate reabsorption
e, inhibition of production of 1,25-dihydroxycholecalciferol

A

a. stimulation of adenylate cyclase

mic cabatu Physiology (12 decks)

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