202 ES - Physiology Flashcards

1
Q

Anterior pituitary secretions (5)

A

Growth hormone
Prolactin
Adrenocorticotropin or corticotropin (ACTH)
Thyrotropin or thyroid-stimulating hormone (TSH)
Gonadotropins (FSH & LH)

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2
Q

Posterior pituitary secretions (2)

A

Anti-diuretic hormone (ADH)

Oxytocin

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3
Q

Secretory cells of pituitary gland & their secretion

A
Somatotropes (Acidophils) - somatotropin (Growth hormone GH)
Corticotropes - corticoropin (ACTH)
Thyrotropes - TSH
Gonadotropes - FSH & LH
Lactotropes - prolactin
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4
Q

Growth hormone (GH)

A

Growth of body

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5
Q

Thyrotropin (TSH)

A

Stimulate thyroid to produce hormones

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6
Q

Corticotropin

A

Stimulates adrenal cortex to produce cortisol

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7
Q

Prolactin

A

Stimulates milk production from breast

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8
Q

FSH & LH

A

Reproductive function in males & females

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9
Q

What controls anterior pituitary secretion?

A

Hypothalamus

- hypothalamic releasing & inhibitory hormones

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10
Q

How do neurons from hypothalamus reach anterior pituitary gland?

A

From hypothalamic nucleus → hypothalamic-hypophyseal portal vessels

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11
Q

Releasing hormones of hypothalamus & affected hormone

A

Thyrotropin-releasing hormone (TRH) - TSH
Corticotropin-releasing hormone (CRH) - ACTH
GH releasing hormone - GH
Gonadotropin-releasing hormone (GnRH) - FSH & LH
Prolactin releasing hormone - prolactin

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12
Q

Inhibitory hormones of hypothalamus & affected hormone

A

GH inhibitory hormone (somatostatin) - GH

Prolactin inhibitory hormone (PIH/dopamine) - Prolactin

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13
Q

Sheehan syndrome

A

Affects women, following post-partum hemorrhage

Reduced blood flow to pituitary → pituitary infarction & necrosis → pituitary hormone insufficiency

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14
Q

Functions of growth hormone

A

Growth
Metabolic
Bone growth

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15
Q

When does the lengthening of bone stop?

A

After fusion of epiphysis with shaft

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16
Q

What is the effect of GH on bones after adulthood?

A

Thickening of bone

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17
Q

Effect of GH on protein

A

↑ cellular protein synthesis; ↓ protein breakdown

Anabolic effect

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18
Q

Effect of GH on adipocytes

A

↑ lipolysis → ↑ free fatty acids

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19
Q

Why does lipolysis cause protein sparing?

A

Lipolysis mobilize free fatty acid, which supplies energy

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20
Q

Protein sparing

A

Body derives energy from sources other than protein

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21
Q

How does GH affect carbs metabolism?

A
  1. Decrease glucose uptake in tissue
  2. Increase glycogenesis
  3. Increase insulin secretion (compensatory)
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22
Q

Diabetogenic effect of GH

A

It mimics insulin’s glucose-lowering effect

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23
Q

GH effect on bone growth

A
  1. Increase protein production by chondrocytic & osteogenic cells
  2. Increased rate of reproduction of these cells
  3. Converting chondrocytes into osteogenic cells → deposition of new cartilage in epiphysis & conversion to bone
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24
Q

Chondrocytic cells

A

Produce and maintain the cartilaginous matrix

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25
Q

Osteogenic cells

A

Only bone cells that divide

Develop into osteoblasts → responsible for forming new bones

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26
Q

How does osteoblast affect bones after adulthood?

A

Increases bone thickness, mainly membranous bones

Protrusion of jaw
Bony protrusions over eyes

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27
Q

Somatomedin C

A

When GH acts on liver/cartilage

aka. insulin-like growth factor 1 (IGF-I)

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28
Q

Factors affecting GH secretion

A

↓ Secretion: Aging

↑ Secretion
Exercise, excitement, trauma
Deep sleep
Ghrelin - produced before meals
Acute hypoglycemia
Chronic protein deficiency - Kwashiorkor
Low free fatty acid
Starvation
Stress
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29
Q

Regulation of GH secretion

A

Secretion: GHRH
Inhibition: GHIH

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30
Q

What happens if there’s excessive GH?

A

Negative feedback → inhibition & decrease secretion

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31
Q

Panhypopituarism

A

Decreased secretion of all anterior pituitary hormones

  • hypothyroidism, decreased secretion of adrenal hormones, decreased secretion of gonadotropins
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32
Q

Dwarfism causes

A

Decreased GH secretion during childhood
Deficiency of somatomedin C - African pygmies & Levi-Lorain syndrome
Part of panhypopituitarism - sexual maturation also impaired

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33
Q

Gigantism causes

A

Hypersecretion of hormone during childhood

Pituitary tumors → hypersecretion

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34
Q

Acromegaly causes

A

Increased GH secretion after fusion of epiphysis

GH producing tumor in anterior pituitary → increased thickness of bones

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35
Q

Signs of acromegaly

A

Protrusion of jaw - prognathism

Enlarged, hands, feet & membranous bones

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36
Q

Deficiency of GH can lead to?

A

Dwarfism

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37
Q

Excess secretion of GH may lead to?

A

Gigantism

Acromegaly

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38
Q

GH can ______ blood glucose in pt with hypoglycemia, why?

A

increase; due to negative feedback

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39
Q

Where does the anterior pituitary develop from?

A

Rathke’s pouch

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40
Q

Where does the posterior pituitary originate from?

A

Neural ectoderm

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41
Q

Where are hormones produced in?

A

Hypothalamic nuclei (Supraoptic & paraventricular nuclei)

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42
Q

What is posterior pituitary mainly composed of?

A

Pituicytes (glial cells)

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43
Q

Hypothalamic-hypophysial tract

A

How hormones are transported from hypothalamic nuclei to pituitary

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44
Q

What happens if pituitary stalk is cut?

A

Decrease of hormone production, but normal after few days - secreted by the cut ends of the fibers by neurophysins

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45
Q

Where is ADH produced?

A

Suproptic nuclei

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46
Q

Where is oxytocin secreted?

A

Paraventricular nucleus

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47
Q

How are ADH & oxytocin secreted at nerve terminal?

A

Exocytosis

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48
Q

Function of ADH

A

Increases reabsorption of water from DCT & collecting duct

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49
Q

How does ADH increase reabsorption?

A

By inserting aquaporins in epithelium of DCT & collecting ducts - through V2 receptors → concentrated urine

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50
Q

Stimulus for ADH secretion

A

Hyperosmolarity of blood

Decrease in blood volume

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51
Q

Osmoreceptors

A

Sense an increase in blood osmolarity → stimulate ADH secretion

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52
Q

Baroreceptors

A

Sense decrease in bp hence decrease blood volume → stimulate ADH secretion

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53
Q

Inhibition of ADH secretion

A

Alcohol

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54
Q

Diabetes insipidus

A

Secretion of ADH from hypothalamus decrease due to injury, infection, congenital

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55
Q

Signs of diabetes insipidus

A

Pt passes large volumes of dilute urine
Persists even with water deprivation
Results in dehydration
High blood osmolarity

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56
Q

Nephrogenic diabetes insipidus

A

Production of ADH normal, but the kidney is not responding to ADH

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57
Q

Treatment of diabetes insipidus

A

Desmopressin (DDAVP)

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58
Q

Treatment of nephrogenic diabetes insipidus

A

Doesn’t respond to DDAVP

Treat cause

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59
Q

Syndrome of inappropriate ADH secretion (SIADH)

A

Increased secretion of ADH

- causing hyponatremia - water retention & decrease blood osmolarity

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60
Q

Neuroendocrine reflex (oxytocin - contraction of uterus)

A

Positive feedback:

  1. Baby’s head stretches cervix
  2. Cervical stretch excites fundic contraction ( → stimuli reaches hypothalamus → release oxytocin)
  3. Fundic contraction pushes baby down & stretches cervix more
  4. Repeats until expulsion of baby
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61
Q

Main functions of oxytocin

A

Uterine contraction

Milk ejection

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62
Q

Why is T4 converted to T3?

A

bc T3 is more potent than T4

It has a shorter life and less amount, but more active than T4

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63
Q

Difference between T3 & T4

A

T3 - active thyroid hormone

T4 - precursor of the thyroid hormone

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64
Q

What do thyroid follicles contain?

A

Filled w colloid made of glycoprotein thyroglobulin

Lined by cuboidal epithelium

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65
Q

C cells

A

between follicles; secrete calcitonin

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66
Q

Calcitonin

A

Lower blood calcium

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67
Q

Synthesis of thyroid hormones

A
  1. Thyroglobulin synthesis
  2. Iodide trapping - sodium-iodide symport pump
  3. Oxidation of iodide - by peroxidase
  4. Transport of iodine into follicular cavity - by iodide-chloride pump - “pendrin”
  5. Iodination of tyrosine (organification) - iodine binds with thyroglobulin
  6. Coupling reactions
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68
Q

Coupling reactions of thyroid hormones

A

2 DIT - T4

MIT + DIT = T3

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69
Q

Release of thyroid hormones

A
  1. Thyroglobulin w hormone is taken up by epithelial cells by endocytosis
  2. Vesicles fuses w lysosomes
  3. Lysosomal enzymes cleave the hormone
  4. Hormone exits cell through basolateral side into blood
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70
Q

Deiodinase

A

Remove iodine from MIT & DIT for reuse

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71
Q

Deficiency in deiodinase will result in?

A

Hypothyroidism

  • bc iodine from MIT & DIT cannot be reused
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72
Q

How is thyroid hormone transported?

A

By binding to plasma proteins - thyroxine-binding globulin

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73
Q

MOA of thyroid hormones

A

Genomic - slower

Non-genomic - faster

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74
Q

Thyroid hormone effect on metabolism

A

↑ metabolic activity

↓ body weight

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75
Q

______ can cause diabetes mellitus

A

Hyperthyroidism

  • Hyperthyroidism is typically associated with worsening glycemic control and increased insulin requirements.
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76
Q

______ have high blood cholesterol

A

Hypothyroidism

  • hypothyroidism LDL cholesterols not removed quickly, LDL accumulates
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77
Q

______thyroidism causes weight gain;

______thyroidism causes weight loss & increased appetite

A

Hypothyroidism; Hyperthyroidism

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78
Q

Thyroid hormone effect on growth

A

Important for skeletal growth & brain development

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79
Q

Why does hypersecretion of thyroid hormone cause reduced height?

A

Due to early fusion of epiphysis

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80
Q

Thyroid hormone effect on CVS

A
↑: 
CO
HR
Force of contraction
↑ Systolic ↓ Diastolic
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81
Q

Thyroid hormone effect on GI

A

↑ GI secretion & motility

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82
Q

Diarrhoae in ______;

Constipation in ______

A

hyperthyroidism; hypothyroidism

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83
Q

Thyroid hormone effect on CNS

A

Increase cerebration - working of the brain

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84
Q

Does hyperthyroidism or hypothyroidism cause extreme worry?

A

Hyperthyroidism

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85
Q

Thyroid hormone effect on hormones

A

↑ insulin secretion - bc hyperglycemia from carb metabolism

↑ PTH - bc ↑ skeletal growth

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86
Q

Thyroid hormone effect on sexual function

A

Hyposecretion - ↓ libido (M & F)
Hypersecretion - impotence (M)

Hypersecretion & hyposecretion - menstrual abnormalities (F)

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87
Q

Regulation of thyroid hormone secretion

A

Negative feedback:

  1. Hypothalamus secretes TRH, stimulate anterior pituitary
  2. Anterior pituitary secretes TSH, stimulate thyroid gland
  3. Thyroid gland secretes thyroid hormones, ↑ in thyroid hormones → ↓ TSH & TRH
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88
Q

Goiter

A

Enlargement of thyroid gland indicating ↑ TSH

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89
Q

Antithyroid drugs - Thiocyanate

A
  1. Bind to sodium-iodide transporter & inhibits the uptake of iodine
  2. Thyroglobulin formed normally
  3. Iodination & formation of thyroid hormones ↓
  4. Lack of negative feedback → ↑ TSH → goiter
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90
Q

Antithyroid drugs - Propylthiouracil

A
  1. Inhibits iodination & coupling
  2. ↓ thyroid hormone secretion
  3. ↓ negative feedback → ↑ TSH → goiter
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91
Q

Antithyroid drugs - Iodides

A

Given in high amounts can reduce thyroid secretory activity

Reduces size of thyroid gland & vascularity
Given 2-3 weeks before surgery to reduce bleeding

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92
Q

Grave’s disease

A

Antibody against TSH receptor; increase secretion of thyroid hormones

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93
Q

Expothalamos

A

Protrusion of eyeballs

Seen in hyperthyroidism

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94
Q

Hyperthyroidism:

______ thyroid hormones; ______ TSH

A

Increase; reduced

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95
Q

How to distinguish between Grave’s disease & adenoma?

A

Grave’s disease: the presence of antibodies

Adenoma: antibody absent

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96
Q

Hyperthyroidism treatment

A

Surgical removal - adenoma
Antithyroid drugs
Radioactive iodine

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97
Q

Hashimoto’s disease

A

Autoimmune thyroiditis

Decrease secretion of thyroid hormones

98
Q

Hypothyroidism:

______ thyroid hormones; ______ TSH

A

Low; elevated

99
Q

Treatment of hypothyroidism

A

Thyroxine (T4) tablets

100
Q

Cretinism

A

Congenital hypothyroidism
Affects growth and mental development

矮呆病

101
Q

How is cretinism prevented?

A

By measuring TSH immediately after birth

102
Q

What is important in thyroid hormone synthesis?

A

Iodine

103
Q

Deficiency of thyroid hormone in childhood may lead to?

A

Crenism w short stature & mental retardation

104
Q

Cause of hyperthyroidism

A

Grave’s disease

Adenoma

105
Q

Cause of hypothyroidism

A

Iodine deficiency

106
Q

What is parathyroid hormone important for?

A

Maintaining blood calcium

↑ calcium ↓ phosphate

107
Q

Normal volume of calcium

A

9-11 mg/dL

108
Q

Uses of ionized calcium

A

Contraction of skeletal, cardiac, smooth muscle
Blood clotting
Transmission of nerve impulses

109
Q

Hypocalcaemia can cause?

A

Tetany

110
Q

Hypercalcemia can cause?

A

Depression

111
Q

Daily intake of calcium

A

~1000 mg/day

112
Q

What controls calcium & phosphate absorption from intestine?

A

Vitamin D

113
Q

How is calcium excreted?

A

Mainly feces

114
Q

Calcium absorption from kidney is from?

A

PCT
DCT
Collecting duct

115
Q

What are bones made of?

A

70% salts & 30% matrix

Newly formed bone more matrix

116
Q

Bone matrix contains?

A

Mainly collagen

Also proteoglycans - chondroitin sulfate & hyaluronic acid

117
Q

Bone salts are?

A

Calcium & phosphate in hydroxyapatite crystal form

118
Q

Collagen give ______ strength;

Hydroxyapatite crystals give ______ strength.

A

tensile; compressional

119
Q

Mechanism of Bone Calcification

A
  1. Osteoblast secrete collagen molecules → form osteoid
  2. Osteoblast gets trapped in osteoid → form osteocytes
  3. Calcium & phosphate start precipitating (non-crystalline - amorphous) → forms hydroxyapatite crystals
120
Q

Regulation of Bone Calcification

A

Normally inhibited by: pyrophosphate

Osteoblasts secretes tissue non-specific alkaline phosphatase (TNAP) to inhibit pyrophosphate

121
Q

______ bone formation can cause ______ TNAP (Tissue Nonspecific Alkaline Phosphatase) in blood.

A

Increased; increase

122
Q

Site of abnormal calcification

A

Blood vessels (atherosclerosis)
Old clots
Degenerating tissues

123
Q

Osteoblasts

A

Help in formation of new bone

124
Q

Osteoclasts

A

Cause resorption of bones under influence of PTH

125
Q

PTH action of osteoblasts

A

Secrete RANKL, inhibit OPG

126
Q

RANKL

A

Activates osteoclasts

127
Q

OPG

A

Inhibits activation of osteoclasts

128
Q

Oestrogen ______ OPG (osteoprotegerin) production, why?

A

stimulates;

prevents osteoporosis in women

129
Q

Steps of bone remodelling

A
  1. Osteoclast eats bone & create tunnel
  2. Osteoblast take over & deposit new bone in concentric circles - “lamellae”
  3. Deposition continues until blood vessel reach - which runs through Haversian canal
130
Q

Osteon

A

Area of new bone formation

131
Q

Callus

A

New bone formation after fracture

132
Q

Formation of Vitamin D

A
  1. 7-dehydrocolestrol → Vitamin D3 (UV, skin)
  2. Vitamin D3 → 25(OH)D (liver)
  3. 25(OH)D → 1,25(OH)2D3 (kidney)
133
Q

Functions of Vitamin D

A

↑ calbindin (calcium bindng) protein in intestinal epithelium
↑ phosphate absorption
↑ calcium & phosphate absorption from kidney

134
Q

What are calcium sensing receptor (caSR)?

A

Sense calcium levels in blood, located on chief cells

↓ Calcium ↑ PTH

135
Q

PTH action on bone

A

↑ bone resorption

136
Q

PTH action on kidney

A

↑ calcium absorption
↑ phosphate excretion
↓ phosphate reabsorption from PCT

137
Q

PTH action on intestine

A

↑ calcium & phosphate reabsorption

138
Q

Where is calcitonin produced?

A

C cells

139
Q

Function of calcitonin

A

↓ blood calcium levels

↑ calcium ↑ calcitonin

140
Q

Signs of Hypoparathyroidism

A

↓ blood calcium levels → tetany

Chvostek sign - contraction of facial muscles provoked by lightly tapping over the facial nerve anterior to the ear as it crosses the zygomatic arch

Trousseau sign - carpopedal spasm

141
Q

Chvostek sign

A

Tapping of facial nerve in front of tragus of ear causes contraction of facial muscles

Seen in hypoparathyroidism

142
Q

Trousseau sign

A

Spasm of hand muscle on inflating BP cuff

Seen in hypoparathyroidism

143
Q

Treatment of hypoparathyroidism

A

PTH
Vitamin D
Calcium injection

144
Q

Signs of Hyperparathyroidism

A

↑ osteoclastic activity

↑ calcium ↓ phosphate

145
Q

Cause of primary hyperparathyroidism

A

Adenoma of parathyroid gland secreting PTH

146
Q

Cause of secondary hyperparathyroidism

A

Vitamin D deficiency

Renal disease

147
Q

Vitamin D deficiency in children causes?

A

Rickets

148
Q

Vitamin D deficiency in children causes?

A

Osteomalacia

軟骨病

149
Q

Adrenal medulla produces which 2 hormones?

A

Epinephrine

Norepinephrine

150
Q

Adrenal cortex produces which hormones?

A

Corticosteroids

151
Q

What does zona glomerulosa produce?

A

Mineralocorticoid - aldosterone

152
Q

What stimulates secretion of zona glomerulosa?

A

Angiotensin II

Potassium

153
Q

What does zona fasciculata produce?

A

Glucocorticoid - cortisol

154
Q

What stimulates secretion of zona fasciculata?

A

ACTH

155
Q

What does zona reticularis produce?

A

Adrenal androgens - dehydroepiandrosterone (DHEA) & androstenedione

156
Q

Synthesis of adrenal hormones

A
  1. Synthesised from LDL cholesterol
  2. LDL cholesterol is taken up by cells - receptor-mediated endocytosis
  3. Converted to pregnenolone by cholesterol desmolase in mitochondria
157
Q

Function of aldosterone

A

Cause sodium & water reabsorption in kidney

158
Q

Main stimuli for aldosterone

A

High blood potassium & angiotensin II

159
Q

Function of glucocorticoid

- Carbohydrate metabolism

A

↑ gluconeogenesis

160
Q

Functions of glucocorticoid

A
Carbohydrate metabolism 
Protein metabolism
Fat metabolism
Stress
Inflammation
161
Q

Function of glucocorticoid

- Protein metabolism

A

↓ protein synthesis & ↑ protein catabolism

162
Q

Function of glucocorticoid

- Fat metabolism

A

↑ lipolysis

163
Q

What happens w excess cortisol?

A

Cortisol ↑ glucose uptake

Excess cortisol → hyperglycaemia → diabetes

164
Q

Buffalo hump

A

↑ fat deposition in certain areas of the body

165
Q

Moon face

A

↑ fat deposition in face

166
Q

What happens to glucocorticoid levels during stress?

A

Cortisol ↑ during physical & mental stress

as it ↑ blood glucose, a.a., f.f.a. may be useful in stress

167
Q

Glucocorticoid role on inflammation

A

Blocks inflammation

168
Q

Regulation of cortisol secretion

A

Controlled by ACTH (anterior pituitary), which is controlled by CRH (hypothalamus)

CRH (hypothalamus) → ACTH (anterior pituitary) → Cortisol (adrenal cortex)

169
Q

What causes release of CRH?

A

Hypertrophy of zona fasciculata & reticularis
Pain stimuli reaches hypothalamus through brainstem
Mental stress activating limbic system

170
Q

↑ cortisol causes ______ feedback ↓ of ACTH & CRH

A

negative

171
Q

Cortisol levels are ______ during early morning.

A

higher

172
Q

Effect of adrenal androgens in male

A

Early development of sex organs

173
Q

Effect of adrenal androgens in female

A

↑ Libido

Growth of axillary & pubic hair

174
Q

What happens with excess ACTH?

A

Have MSH like activity - stimulation of melanocytes in skin & ↑ pigmentation

175
Q

Causes of primary hypoadrenalism

A

Adrenal insufficiency/Addison’s disease
Autoimmune destruction
Tuberculosis
Cancer invasion

176
Q

Causes of secondary hypoadrenalism

A

↓ ACTH production by anterior pituitary

177
Q

Clinical features of hypoadrenalism

A

Lack of mineralocorticoids

Lack of glucocorticoids

178
Q

Treatment of hypoadrenalism

A

Mineralocorticoids

Glucocorticoids

179
Q

Cushing’s disease

A

↑ secretion of ACTH secretion from anterior pituitary tumor → hyperadrenalism

180
Q

Causes of hyperadrenalism

A

Adenoma of adrenal cortex
↑ secretion from other tumors
↑ CRH secretion from hypothalamus
↑ secretion of ACTH secretion from anterior pituitary tumor - Cushing’s disease

181
Q

Suppression of Cushing’s disease

A

High doses of dexamethasone

182
Q

Cushing’s syndrome

A

Hyperadrenalism - ↑ secretion of cortisol

183
Q

Cushing’s syndrome vs Cushing’s disease

A

Syndrome - hyperadrenalism

Disease - cause of hyperadrenalism

184
Q

Clinical features of Cushing’s syndrome

A
↑ facial hair & acne
Androgenic effects
Mineralocorticoid action
Muscle weakness
Purplish striae - tear of subcutaneous tissue
185
Q

Treatment of Cushing’s syndrome

A

Surgical removal of the tumor

- drug treatment if surgery not feasible

186
Q

Causes of hyperaldosteronism

A

Primary hyperaldosteronism - aka Conn’s syndrome - caused by tumor of zona glomerulosa

187
Q

Clinical features of hyperaldosteronism

A

Hyperkalaemia

Metabolic alkalosis

188
Q

Treatment of hyperaldosteronism

A

Surgical removal of tumor

Aldosterone receptor blocker - spironolactone

189
Q

Adrenogenital syndrome

A

Excess adrenal androgen production

190
Q

Clinical features of adrenogenital syndrome - female

A

Growth of beard, deep voice, baldness
↑ body hairs
Enlargement of clitoris
↑ muscle mass

191
Q

Clinical features of adrenogenital syndrome - male

A

Growth of beard, deep voice, baldness
↑ body hairs
↑ muscle mass
Enlargement of penis

192
Q

Diagnosing feature of adrenogenital syndrome

A

↑ excretion of 17 ketosteroid in urine

193
Q

What is cortisol important for?

A

Metabolism & stress response

194
Q

Diabetes mellitus

A

A chronic disease that occurs when the pancreas is no longer able to make insulin (type 1) or when the body cannot make good use of insulin it produces (type 2)

195
Q

The pancreas is made up of collections of cells called?

A

Islets of Langerhans

196
Q

4 major cell types in islets of Langerhans & their secretion

A

Alpha - glucagon
Beta - insulin
Delta - somatostatin
PP cell - pancreatic polypeptide

197
Q

Where is insulin synthesized?

A

rER

198
Q

Steps in insulin synthesis

A

Preproinsulin → proinsulin (contains B chain, A chain, C peptide) → excise C peptide → insulin

199
Q

What stimulates insulin secretion?

A

Stimuli that ↑ cAMP levels

  • probably by ↑ intracellular Ca2+
200
Q

2 incretin hormones

A

Glucose-dependent insulino-tropic polypeptide (GIP)

Glucagon-like peptide (GLP-1)

201
Q

The function of incretin hormones

A

Enhance the rate of insulin release from the pancreatic β cells in response to an ↑ in plasma glucose.

202
Q

Where is GIP (Gastric inhibitory polypeptide) synthesized?

A

K cells of duodenum

203
Q

Where is GLP-1 synthesized?

A

L cells in ileum & colon

204
Q

What type of receptor is an insulin receptor?

A

Enzyme-linked receptor

205
Q

Subunits of insulin receptor

A

206
Q

Is insulin anabolic or catabolic?

A

Anabolic

  • ↑ storage of glucose, f.a. & a.a.
207
Q

Under what conditions are large amounts of glucose used by muscle?

A
  1. Moderate/heavy exercise

2. Few hours after meal

208
Q

Transporters for glucose

A

GLUT1 - BBB & erythrocytes
GLUT2 - renal tubular cells, liver cells, pancreatic beta cells
GLUT3 - neurons & placenta
GLUT4 - adipose tissue & striated muscle

SGLT1 - ~10% - distal proximal tubule (S3)
SGLT2 - ~90% - early proximal tubule (S1&S2)

209
Q

Actions of insulin on carbohydrate metabolism

A
  1. It ↑ the rate of transport of glucose across the cell membrane in adipose tissue and muscle
  2. It ↑ the rate of glycolysis in muscle and adipose tissue
  3. It stimulates the rate of glycogen synthesis in adipose tissue, muscle, and liver.
  4. ↓ the rate of glycogen breakdown in muscle and liver
  5. It inhibits the rate of glycogenolysis and gluconeogenesis in the liver.
210
Q

GLUT1 is insulin-______;

GLUT4 is insulin-______

A

independent; dependent

211
Q

What happens to insulin actions on GLUT4 (insulin-dependent) in DM?

A

Intracellular glucose deficiency

↑ protein catabolism

212
Q

What happens to insulin actions on GLUT1 (insulin-independent) in DM?

A

Intracellular hyperglycemia

Non-enzymatic glycosylation

213
Q

Effects of hyperglycemia

A

High intracellular glucose levels → Aldose reductase (enzyme) activation → Sorbitol formation → ↓ Na+/K+ ATPase activity

Glucose attaches (non-enzymatically) to the protein amino groups → amadori products → Advanced glycosylation end products (AGEs) → cause cross-linkage of matrix proteins → Damage to blood vessels

↑ Sorbitol and fructose in Schwann cells → disruption in their structure and function

214
Q

What is the renal threshold for glucose?

A

180 mg/dL

215
Q

What happens if plasma glucose exceeds threshold?

A

Glucose appears in the urine

Polyuria, polydipsia

216
Q

What is the effect of insulin on lipid metabolism?

A

↓ FFA conc in plasma

  • Stimulates synthesis of triglycerides in the liver & adipose tissue
  • Stimulates lipoprotein lipase – Increased uptake of FFA into the adipose tissue
  • Inhibits hormone-sensitive lipase
217
Q

What happens to lipid metabolism during insulin deficiency (DM)?

A

Causes lipolysis of storage fat and release of FFA

  • bc hormone-sensitive lipase strongly activated
218
Q

What happens with excess FFA during DM?

A

FFA are catabolized to acetyl CoA → excess acetyl CoA → ketone bodies

219
Q

Diabetic ketoacidosis

A

When there’s excess ketone bodies in blood causing acidosis

220
Q

Kussmaul breathing

A

Rapid, deep breathing caused by metabolic acidosis

221
Q

Effects of insulin on protein metabolism

A
  • Stimulates transport of FAA across the plasma membrane in liver and muscle.
  • Stimulates protein synthesis and reduces release of a.a. from muscle
222
Q

Consequences of disturbed protein metabolism

A
  • ↑ protein breakdown → muscle wasting
  • ↓ protein synthesis
  • ↑ plasma amino acids and nitrogen loss in urine → negative nitrogen balance and protein depletion.
  • Protein depletion is associated with poor resistance to infections.
223
Q

Signs of diabetes mellitus

A
Hyperglycemia
Glucosuria
Polydipsia
Polyuria
Polyphagia
Ketosis, acidosis, coma
224
Q

Macrovascular & Microvascular complications of DM

A

Macrovascular:

  • Stroke
  • Peripheral vascular disease
  • Myocardial infarction

Microvascular:

  • Retinopathy
  • Nephropathy
  • Neuropathy
225
Q

Cause of hypoglycemia

A

Drug overdose
Missing meals
Excercise

226
Q

Adrenergic & Neuroglycopenic symptoms of hypoglycemia

A

Adrenergic symptom - palpitation, tremor, anxiety

Neuroglycopenic symptoms - confusion, fatigue, lethargy, loss of co-ordination, seizure, coma

227
Q

Body response to hypoglycemia

A
  1. Inhibition of insulin secretion
  2. Secretion of glucagon, epinephrine & growth hormone
  3. Secretion of cortisol
228
Q

What controls growth?

A

Mainly hormones
Genetic factors
Environmental factors - nutrition
Involves cell division & protein synthesis

229
Q

What is the bone matrix made up of?

A

Collagen, which is mostly calcium phosphate

230
Q

How does elongation of bone occur?

A
  1. On the epiphyseal growth plate, active proliferating cartilages are present
  2. Osteoblasts convert the cartilage into bone, Chondrocytes produce cartilage
  3. The simultaneous action causes growth plate widens
231
Q

How does growth hormone work?

A
  1. For the initial 1-2 years - GH ↑ cell division (mitogen); and ↑ maturation and cell division of chondrocytes
  2. Causes widening of growth plate & lengthening of the bone
232
Q

How does IGF-1 work with growth hormone?

A
  1. GH acts on growth plate & converts prechondrocytes into chondrocytes
  2. Mature cells secrete IGF-1 & produce receptors for IGF-1
  3. IGF-1 undergo autocrine/paracrine action to stimulate cell division
233
Q

Hormonal pathway controlling GH & IGF-1 secretions

A

Stimulus
→ Hypothalamus - ↑ GHRH & ↓ SST
→ Anterior pituitary - ↑ GH
→ Liver & others - ↑ IGF-1 secretion

234
Q

When does GH cause greatest growth?

A

Adolescence

235
Q

Role of IGF-1 in foetal growth

A

Important for pre-natal growth, esp nervous growth

Stimuli for secretion: placental lactogen

236
Q

List the hormones that affect growth

A
Growth Hormone & IGF-1
Thyroxine
Insulin
Sex hormones 
Cortisol
237
Q

How is thyroid hormone involved in growth?

A

Facilitates synthesis of growth hormone
Stimulates chondrocyte differentiation
Stimulates growth of new blood vessels in developing bone
↑ responsiveness of bone to fibroblast-derived growth factor

238
Q

Cretinism

A

Physical deformity & learning disabilities that is caused by congenital thyroid deficiency.

239
Q

How is insulin involved in growth?

A

Stimulates cell division & differentiation during fetal period & childhood
Anabolic effect of insulin
↑ glucose & a.a. uptake by insulin-sensitive cells
↑ fat storage
↑ protein synthesis & ↓ protein breakdown

240
Q

How are sex hormones involved in growth?

A

Testosterone & oestrogen

↑ growth of long bones & vertebrae
Stimulate secretion of GH & IGF-1

Stop growth by causing epiphyseal closure

241
Q

How is cortisol involved in growth?

A

↑ protein catabolism
Inhibits bone growth & ↑ bone breakdown
↓ DNA synthesis
↓ secretion of GH & IGF-1

242
Q

How is testosterone involved in growth?

A

Causes protein synthesis in non-productive organs & tissue

↑ muscle mass