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Flashcards in Exam 2 Deck (229):
1

Overall response of the body to the presence of growth hormone in blood:

Growth of most cells and structures.

2

Anabolic effects of growth hormone:

DNA synthesis, Protein synthesis

3

Long bone growth:

Seen only in children before epiphyses have closed

4

Excess growth hormone causes:

acromegaly, more extreme coarsening of facial features and continued growth of hands and feet

5

Catabolic effects:

glycogenolysis (glycogen-->glucose), Lipolysis of fat--> free fatty acids in blood, preferential use of fat for energy.

6

Growth hormone aka:

protein sparer

7

According to article by Andrew Weil, MD, GH improved:

lean body mass, bone density, and in men: increased alertness and vigor.

8

According to article by Andrew Weil, MD, GH decreased:

percentage of body fat

9

Extensive long term studies have shown that GH increases:

blood pressure, blood glucose, blood cholesterol, heart mass, growth rate of preexisting cancers.

10

GH is only approved to treat:

GH deficiencies, wasting syndrome of AIDS, short bowel syndrome

11

Direct action of GH:

stimulates the liver to produce somatomedins (aka insulin-like growth factors -- IGF's)

12

Direct action of IGF's:

Mediate growth hormone's actions on DNA and protein synthesis, stimulates growth of bones, muscle and internal organs

13

Direct action of GH:

In liver: stimulates glycogenolysis
In Adipose: stimulates lipolysis
In Pancreas: stimulates insulin secretion (diabetogenic effect)
In most tissues: stimulates somatomedin production

Paracrine action : growth, metabolic effects.

14

Growth hormone releasing hormone (GRH) :

raises set point for GH. Acts on Anterior pituitary to stimulate synthesis and release of GH.

15

Somatostatin (Inhibiting hormone):

lowers the set point for GH. Acts on the hypothalamus to decrease GRH release. Acts on the anterior pituitary to inhibit the release of GH.

16

Somatomedins:

exert negative feedback control of GH levels around the set point. a) hypothalamus (inhibit GRH release) b)anterior pituitary (inhibit GH release)

17

Growth hormone:

negative feedback on the hypothalamus, rising levels of GH (above the set point) suppresses GRH release

18

Physiological control of GH controlled by:

Sleep
Diet
Exercise
Mental Stimulation
Extreme Stress
Sex Steroids
Normal Cortisol and Thyroxin

19

Effect of Sleep on GH release:

slow wave (non REM sleep)--> GH release. Acts as serotonin and the limbic system.

20

Effect of diet on GH release:

Norepinepherine and dopamine from the hypothalamus influence GHRH secretion.

High protein meals--> GH secretion

High Carbohydrate (CHO)--> inhibits GH release

Prolonged Starvation--> suppress GH and growth

Protein deficiency-->Kwashiokor-->rise in GH but lack of growth

21

Effect of exercise on GH release:

increases GH

22

effect of mental stimulation (mile stress) on GH release:

increases GH

23

effect of extreme stress on GH release:

inhibits GH

24

psychosocial dwarf:

stress-->high cortisol-->stimulates somatostatin release-->blocks GH release but NOT GH synthesis and storage. Catch up growth occurs when stress is removed.

25

effect of sex steroids on GH release:

promotes pubertal growth spurt. testosterone is more effective than estrogen. testosterone also synergies with GH to promore bone and muscle growth.

26

effects of cortisol and thyroxin on GH hormone:

inhibits growth by blocking GH release and opposing GH action on protein and DNA synthesis

27

What secretes GRH?

arcuate nucleus

28

Failure to grow due to:

genetic defects, inadequate GRH, inadequate GH, inadequate somatomedins, or inability of cells to respond to the above.

29

Excessive GH due to pituitary adenoma:

gigantism in child, acromegaly in adult

30

Acromegaly:

overgrowth of bones other than long bones, diabetes mellitus, and overgrowth of internal organs

31

Pituitary dwarf:

lacks GH, short with normal body proportions, normal intelligence.

32

Pan hypopituitary dwarf:

total pituitary deficiency. short, stocky, short limbs, fail to mature sexually, diminished mental function

33

Hypothyroid:

short and stocky, short limbs, diminished mental function

34

hypocortisol:

short, stocky, malformed limbs

35

problems with administering GH to normal children:

negative feedback by GH-->suppress own GH production and secretion. May increase height by 2 inches. risk of diabetes mellitus, risk of over enlargement of heart, excess GH may also stimulate growth of cancers

36

Thyroid gland

two lobes, usually not large enough to be palpable

37

What may you suspect if the thyroid gland is palpable?

may be compensating for difficulty in making hormones, could be under or over producing hormones if very large

38

T3

triiodothyronine
the active form, binds to the thyroid hormone receptor

39

T4

thyroxin
inactive form, 93% or hormone produced is in this form and converted to T3 by target cells

40

Major actions of thyroid hormones

are on metabolic rate, heat generation, nerve function, needed by essentailly every cell, influences growth, reproduction, heart sensitivity to norepinepherine

41

Calcitonin

involved in calcium homeostasis

42

Thyroid gland organization

into follicles normally filled with colloid which contains thyroglobulin

43

thyroglobulin

33500 MW protein found in the follicles of the thyroid gland
used to create T3 and T4
includes 70 tyrosines in the structure

44

What is the normal orientation of the cells of the follicles in the thyroid gland?

cuboidal epithelial cells

45

what will inactive follicular cells look like?

flat

46

what will overactive follicular cells look like?

larger, and more columnar than normal cells

47

First step in production of T3 and T4

thyroglobulin is made by the follicle cells and secreted into the center of the follicle

48

second step in production of T3 and T4

Iodine trapping
iodine pump takes up about 20% of the iodine in the blood and the thyroid can concentrate 30-250 times the concentration of iodine in the blood

49

Yearly iodine requirement

about 50 mg

50

third step in production of T3 and T4

oxiation of iodine

51

fourth step in production of T3 and T4

tyrosines are iodinated while still part of thyroglobulin

52

Organification of thyroglobulin

should be called orgainification of idoine

53

How long can the store of T3 and T4 in the thyroid gland last?

2-3 months, this is why thyroid deficiency is slow to develop

54

What is the half life of T4?

6 days

55

What is the half life of T3?

1 day

56

What percentage of thyroid hormones are bound to carrier proteins while traveling in the blood?

99%

57

2 structures of the adrenal gland

cortex and medulla

58

Cortex of the adrenal gland:

develops from endothelial cells. Produces steroid hormones (mineralocorticoids- aldosterone and cortisol, glucocorticoids-cortisol, sex steroids- mostly androgens: androstenedione and dehydropiandrosterone, DHEA)

59

Temporary fetal adrenal zone:

decresses/regresses in postnatal life. innermost region of adrenal cortex

60

functions of the fetal adrenal zone:

produces DHEA, important for placenta production of estrogen's during pregnancy, stimulates embryonic and fetal growth.

61

DHEA as a youth hormone:

production declines with age so it's used by some in the hopes of improving muscle strength and libido. Found to stimulate growth of some cancers and inhibit the growth of others.

62

Medulla of the adrenal gland:

derived from neural crest cells. stimulated by preganglionic sympathetic neurons. secret ACH to stimulate production/secretion of monoamines: norepipinephrine and epinephrine

63

Zona Glomerulosa:

produces aldosterone. controlled by renin-angiotensin system and potassium levels in ECF.

64

Corticotrophin (AKA ACTH):

permissive of the function of the zone glomerulosa. Does not stimulate aldosterone secretion.

65

Steroid hormones:

4 rings, 18-21 carbons. Synthesis: Substrate: Cholersterol.

66

How is cholersterol brought to the cells?

From the liver by LDL or made by cells from acetate.

67

Progesterone actions:

promotes body changes to support pregnancy. can bind to adrenal steroid hormone receptors and mimic or antagonize their actions

68

Rate limiting step for production of steroid hormones regulated by:

ACTH/LH stimulation of cyclic AMP production.

69

Generic names of steroid hormone 21 carbon:

progestins

70

First product produced by cholesterol:

pregnenolone (inactive steroid precursor for all steroid hormones.)

71

Progesterone is secreted by:

ovary, placenta.

72

Progesterone actions:

promotes body changes to support pregnancy.

73

androgenital syndrome:

genetic mutation-->defective enzyme for cortisol production.

decreased cortisol secretion-->inadequate negative feedback by cortisol on ACTH--> increased ACTH secretion-->increased stimulation of cholesterol side chain cleavage-->increased pregnenolone-->adequate cortisol with excessive androgen production.

74

Iodine deficiency in the diet

hypothyroid condition with enlarged thyroid due to large cells, very active enzymes, and a lot of thyroglobulin turnover, but little T3 and T4 production

75

cortisol and progesterone overlap:

have weak mineralocorticoid action.

76

The molecular action of thyroid hormone is similar to what class of hormones?

steroids
T3 enters cells and binds to receptor
hormone/receptor complex then interacts with DNA

77

What must happen to T4 before it can cause changes in a cell?

it must be transformed to T3

78

T3 has influence of what type of genes?

both mitochondrial and nuclear genes

79

What does T3 stimulate the production of?

enzymes that produce ATP in the mitochondria and molecules that require ATP to function (like active pumps)

80

How long does it take to see the physiological effects of T3?

6-12 hours

81

How long does the maximum cellular response to T3 last?

2-3 days, some effects can last weeks

82

cortisol:

glucocorticoid and mineralocorticoid activity

83

aldosterone:

mineralocorticoid

84

19 carbon steroids:

androgens- masculinizing hormones (testosterone)

85

In absence of mineralocorticoids (both aldosterone and cortisol):

die within 3-14 days.

86

Synthetic path of the adrenal:

cholesterol-->pregnenolone-->progesterone-->aldosterone (in the zone glomerulosa)--> 17 OH progesterone-->cortisol, androgens (in the zone reticular and fasciculata only)

87

androgenital syndrome:

genetic mutation-->defective enzyme for cortisol production.

decreased cortisol secretion-->inadequate negative feedback by cortisol on ACTH--> increased ACTH secretion-->increased stimulation of cholesterol side chain cleavage-->increased pregnenolone-->adequate cortisol with excessive androgen production.

88

What are the effects of T3 on mitochondria?`

increased size, increased number of mitochondria, increased ATP production

89

What are the effects of high levels of T3 on the mitochondria?

mitochondria swell, can uncouple oxidative phosphorylation, generating more heat than ATP and increased action of the sodium potassium pump

90

symptoms of excessive androgens:

masculinization of females, pseudo puberty in boys, little effect on adult males except for decreased sperm production due to negative feedback action of androgens causing decreased LH secretion by the anterior pituitary.

91

cortisol and progesterone overlap:

have weak mineralocorticoid action.

92

metabolism steroids:

enzymes in liver, lungs, kidney, blood destroy steroids within 30 minutes-a few hours.

93

How are steroids excreted?

in urine, feces, saliva, sweat

94

what is transcortin?

specific binding protein for adrenal corticoids.

95

what is albumin?

major blood protein. serves as a non-specific binding protein for all steroids.

96

Action of Mineralocorticoids: Aldosterone:

stimulates sodium retention by renal tubules in exchange for potassium and hydrogen

97

What happens when sodium is retained?

water is reabsorbed to maintain osmotic pressure.

98

ANH inhibits:

aldosterone release, ADH release, ADH action on kidney, angiotensin II action on vasoconstriction, salt and fluid intakes

99

Excess aldosterone leads to:

increase in H+ excretion-->rise in pH-->alkalosis

100

inadequate aldosterone:

fall in pH=acidosis

101

Examples of thyroid hormone actions

effects on mitochondria, increased metabolic rate, stimulates CHO and fat metabolism, increased appetite, important for normal growth

102

How does T3 influence nerve growth?

influences synapse formation and maintenance, severe mental deficiency in children without it

103

Hypothyroid Children

show failure to grow
cretinism, bone growth retarded more than soft tissues, short stocky child, also shows mental deficiency due to poor neuron growth and synapse formation

104

Hyperthyroid children

tall for their age, but may stop growing at an early age due to effects on epiphyses of bones making them a short adult

105

Where does a fetus get thyroid hormone from?

the mother when it is in utero

106

symptoms of absent mineralocorticoids:

hyponatremia, decreased ECF, retain too much K+ in ECF-->hyperkalemia

heart weakens, cardiac arrhythmia-->decreased cardiac output-->circulatory shock-->death

107

glucocorticoid effects on liver:

enhanced amino acid transport into liver, increased use of amino acids to produce liver proteins and blood protein.

108

Role of aldosterone in starvation or dieting:

1. cells die, release K+ (hyperkalemia)
2. fatty acid metabolism generates chaotic acids-->decreased pH-->acidosis

109

Role of aldosterone in circulatory shock:

absence of aldosterone-->acidosis.

110

acidosis leads to:

nerves decrease ability to funtion

111

Angiotensin II acts on:

adrenal (to stimulate aldosterone production and secretion) and vascular smooth muscle (contraction and increased BP)

112

Renin produced by:

juxta glomerular cells of the kidney

113

Renin secreted in response to:

decreased BP
decreased Na+/K+
decreased Na+/CL-
increased K+
decreased osmotic pressure
sympathetic nerves to kidneys

114

apple shape body:

android shape. more insulin receptors and fewer cortisol receptors on upper body

115

Atrial Natriuretic Hormone:

aka ANH, ANF, ANP

116

ANH produced by:

the atria of the heart

117

ANH is produced because:

increased blood volume in the atria or weak left ventricle

118

ANH inhibits:

aldosterone release

119

Effects of low T3 on nerve function:

required to function, adults with low T3/T4 will show confusion, poor memory, inability to concentrate, depression, sleepy

120

Effects of high T3 on nerve function:

anxiety, inability to sleep even though exhausted, hyperactive

121

Cardiovascular response to T3/T4

enhanced by normal levels, overstimulated in hyperthyroidism and weakened in hypothyroidism

122

What are some consequences of low T3 in the cardiovascular system

arteriosclerosis due to increased blood cholesterol, peripheral vascular disease, deafness and coronary sclerosis

123

What are some consequences of low T3 in the reproductive system?

decreased libido, impotence, irregular periods, may be frequent and heavy or absent

124

Thyrotropin Releasing Hormone

released by hypothalamus
acts on thyrotrophs of the anterior pituitary to stimulate TSH production and release

125

What messenger system does TRH work through?

phospholipase second messenger system, which raises intracellular Ca++

126

How does TRH respond to body/environmental temperature?

increased TRH with cold temperatures
decreased TRH with high temperatures

127

How does TRH respond to stress?

increased stress = depression of TRH sectretion

128

Thyroid Stimulating Hormone

shares structural similarity with FSH and LH
stimulates the follicle cells in the thyroid to divide and increase in size

129

What does TSH stimulate in follicle cells of the thyroid?

division, increase in size
increases production of enzymes for thyroglobulin synthesis, iodine trapping, oxidation of iodine, and iodination of thyroglobulin

130

TSH stimulates the release of what?

T3 and T4 from thyroglobulin and secretion into the blood

131

The negative feedback mechanism of thyroid hormones is primarily controlled by what?

almost exclusively through high levels of T3 causing decreased sensitivity to TRH in the anterior pituitary leading to lower secretion of TSH

132

Physiological results of ANH:

decreased Na+ retention
decreased water retention
decreased blood pressure

133

Glucocorticoids percentages in human:

95% cortisol, 5% corticosterone

134

Physiological action of glucocorticoids:

mobilization of energy stores for survival, maintain glucose supply to brain.

135

High level of glucocorticoids see in response to:

stress, starvation, bodily injury

136

Glucocorticoids stimulate:

gluconeogenesis

137

Glucocorticoids decrease:

glucose utilization

138

Excessive levels of cortisol is a cause of:

osteoporosis

139

Glucocorticoid effects of muscle, bone, and other tissue:

decreased amino acid uptake,decreased protein synthesis, increased protein catabolism and release of AA into blood, decrease storage of protein

140

glucocorticoid effects on liver:

enhanced amino acid transport into liver, increased use of amino acids to produce liver proteins and blood protein.

141

glucocorticoid effects on adipose cells:

mobilization of fatty acids
stimulates lipolysis
release free fatty acids into blood

142

glucocorticoid effects on non-neural tissue:

increased use of fatty acid (oxidation) for energy needs to cells

143

Effects of cortisol in relation to obesity:

may stimulate apetite, stimulates fat deposition in chest and head region of body and visceral fat deposits in abdomen.

144

Visceral fat vs. subcutaneous fat:

excess subcutaneous fat on lower body (pear shape) is healthier than excess visceral fat in abdominal region (apple shape)

145

Pear shape body:

gynoid shape. more insulin receptors on lower body and more cortisol receptors on upper body.

146

insulin stimulates:

fat deposition

147

apple shape body:

android shape. more insulin receptors and fewer cortisol receptors on upper body

148

Hyperthyroidism

too much thyroid hormone
could be due to a failure of the negative feedback mechanism to control levels or an enlarged thyroid

149

What are three causes of hyperthyroidism

pituitary adenoma
antibodies against TSH receptors
Thyroid adenoma

150

pituitary adenoma

produces excess TSH
cells are functioning out of control and insensitive to negative feedback
Healthy thyroid gland is overstimulated
you will have high TSH and thyroid hormone levels and an enlarged thyroid

151

Antibodies against TSH receptors on thyroid

Graves disease, toxic goiter, thyrotoxicosis
antibodies bind receptors and stimulate thyroid hormone secretion
low TSH, high T3/T4
enlarged thyroid, exopthalmus

152

Thyroid adenoma

thyroid cells secrete thyroid hormone out of control, do not need TSh to stimulate them
low TSH, high T3/T4
thyroid with multiple enlarged nodules

153

Hypothyroidism

not enough thyroid hormone

154

What are five causes of hypothyroidism

autoimmune destruction, congenital lack of thyroid, inadequate iodine in diet, inadequate enzymes/inhibited enzymes, defective genes for certain thyroid hormones

155

Hashimoto's disease

autoimmune destruction of the thyroid
most commonly antibodies against thyroglobulin are the most common
High TSH, low thyroid hormone
thyroid may be small, normal, or have enlarged nodules

156

What demographic is commonly effected by hashimoto's disease?

women over 50

157

Congenital lack of a thyroid gland

high TSH, low T3/T4

158

Inadequate iodine in the diet

high TSH, low T3/T4
will see an enlarged thyroid gland

159

goitrogenic substances

chemicals found in foods in cluding turnips and cabbage and are used to treat hyperthyroidism

160

thiocyanate

blocks iodine uptake

161

propylthiouracil

blocks oxidation of iodine

162

subclinical hypothyroidism

elevated TSH, normal T3/T4
classical symptoms of hypothyroidism are not obseved
may lead to atherosclerosis and cardiovascular problems if left untreated

163

effects of cortisol on the immune system:

suppresses immune system, immune response, and allergy response.

164

At normal low physiological levels, cortisol:

keeps immune system under control, limits but does not block destructive actions, enhances readiness of immune system

165

at hight levels, cortisol:

associated with stress. inhibits antibody synthesis, lymphocyte proliferation, cytokine production. causes down regulation of substance P receptors, increased rate of substance P metabolism

166

overproduction of substance P:

asthma, RA

167

Cortisol's medical uses:

treat symptoms of RA, suppress immune response for organ transplantation

168

cortisol favors healing of injuries by:

providing amino acids for repair, providing fats for energy, and decreasing inflammation

169

cortisol stimulates RBC production. Excess RBC =

polycythemia.

170

inadequate cortisol =

anemia

171

How does ACTH get stimulated?

CRH acts on anterior pituitary.

172

CRH acts on anterior pituitary to stimulate:

pro-opiomelanocortin synthesis

173

Pro-opiomelanocortin =

pre-prohormone
processed by enzymes to release several hormones

174

How does congenital adrenal hyperplasia alter the function of the adrenal cortex?

The adrenal cortex fails to produce sufficient Cortisol to exert complete negative feedback regulation of the Hypothalamus and Anterior Pituitary

175

What is the response of the hypothalamus and anterior pituitary to inadequate production of cortisol?

Negative feedback is insufficient to suppress the hypothalamic secretion of CRH and the Anterior Pituitary's secretion of Corticotrophin (aka ACTH), thus increased amounts of both ACTH and CRH are secreted into the blood

176

what is the end result of Congenital adrenal hyperplasia?

overproduction of androgens with adequate production of cortisol

177

What is the effect of CAH on females?

the female body is masculinized, with increased muscle mass, and increased body hair, ect
in extreme cases a female with a uterus and ovaries can outwardly appear to be a fully developed male

178

What is the effect of CAH on males?

may exhibit psuedopuberty at an early age, with suppressed testicular function due the to ability of androgens to suppress the release of gonadotrophin lutenizing hormone

179

acini

glandular tissue that secretes digestive enzymes and buffer into the pancreatic duct

180

Islets of Langerhans

contains alpha, beta, and delta cells
surrounded by capillaries, which are important for diffusing of nutrients and hormones

181

Alpha cells

release glucagon to the blood

182

Beta cells

release insulin to the blood

183

Delta cells

release somatostatin which has local actions on the alpha and beta cells

184

Paracrine action of Somatostatin

inhibits release of both insulin and glucagon

185

Paracrine action of insulin

inhibits glucagon secretion

186

Paracrine action of glucagon

triggers insulin secretion
the two hormones work together as glucagon stimulates glucose release from the liver and insulin drives it into the muscle, adipose, and other cells

187

Insulin promotes:

anabolic reations
carbohydrates to glycogen and fatty acids
fatty acids to adipose stores
amino acids to proteins

188

Insulin opposes

catabolic reactions
lipolysis, glycogenolysis, glycolysis, proteolysis, and gluconeogenesis

189

insulin half life in the blood

6 minutes

190

Big Insulin

insulin is synthesized as a pre-pro-hormone
11,000 MW, large molecule
must be processed by enzymes to be active

191

Insulin receptor

in the cell membrane
4 subunits held together by di-sulfide bridges
2 alpha and 2 beta

192

Alpha subunits of the insulin receptor

on the outside of the cell membrane
bind insulin

193

beta subunits of the insulin receptor

extend through the cell membrane
have tyrosine kinase enzyme activity inside the cell

194

At time when insulin levels are naturally low:

muscle, liver, and other tissues (besides neurons) use fat for energy unless stimulated by insulin to use glucose

195

When do neurons use fat for energy?

during prolonged periods of starvation
cortisol induces

196

How does muscle react to high levels of insulin?

stimulated to actively take up glucose, use glucose for energy, and store glucose as glycogen

197

How does the liver react to high levels of insulin?

It is stimulated to use glucose to synthesize glycogen
synthesizes fatty acids when the glucose uptake exceeds the livers ability to synthesize glycogen

198

How does adipose tissue respond to high levels of insulin?

actively takes up glucose and fatty acids to synthesize triglycerides for storage

199

Which ions does insulin stimulate the uptake of?

K+, PO4--, and Mg++

200

How does the kidney respond to insulin?

stimulated to retain K+ and phosphate

201

What happens when insulin is given to a patient experiences diabetic ketoacidosis?

extreme drop in plasma levels of K+, PO4, and Mg++
need to give IV infusions of these vitamins

202

What occurs in the body in the absence of insulin?

lipolysis- increased FFA's and glycerol in blood
use of FFA's instead of glucose for energy
Decreased uptake of glucose leading to elevated blood glucose
increased amino acids and ketoic acids in the blood leading to acidosis

203

What can the hypothalamus not detect without insulin?

hyperglycemia
thinking the body is in hypoglycemia it will release cortisol and epinephrine and cause further hyperglycemia as these hormones raise blood glucose levels

204

Which hormones can Pro-opiomelanocortin be processed to create?

ACTH, alpha and gamma MSH, Beta endorphin, lipotrophin

205

Which membrane enzymes does ACTH work through

activated through G proteins
adrenal cyclase
phospholipase C
guanyl cyclase

206

MSH

melanocyte stimulating hormone
responsible to level of melanin in skin

207

MSH action in humans

Causes darkening of the skin with excess ACTH production as it is produced as well
also released in emotional situations and enhances mental arousal, motivation, attention span, memory retention, learning ability

208

Stimuli that trigger CRH-ACTH secretion

blood glucose levels and sudden temperature change perceived by hypothalamus
pain, emotions, and frightening stimuli communicated to hypothalamus

209

Negative feedback of CRH-ACTH is mainly controlled by what:

cortisol
suppressed ACTH and CRH release and also diminishes emotional response from limbic system

210

Adrenal androgens are synthesized in response to what?

ACTH stimulation

211

Adrenogenital syndrome

excess androgen production masculinizes female, premature pseudo puberty in males

212

Addisons Disease

total destruction of the adrenal corten usually due to autoimmune attack
loss of both cortisol and aldosterone actions

213

Symptoms

elevated acth (with MSH activity)- unexplained darkening of the skin
lack of cortisol and mineralocorticoids

214

What does lack of mineralocorticoids with addisons disease cause

decreased extracellular volume
difficulty regulating osmotic pressure- risk of water intoxication
hyperkalemia and acidosis

215

What does lack of cortisol with addisons disease cause

hypoglycemia
decreased response to epinephrine and norepinephrine-difficulty regulating BP, increased risk of circulatory shock
muscle weakness, anemia, decreased GI mobility, decreased iron and B12 absorption, decreased appetite w wt loss, susceptible to depression

216

Cushings Syndrome

adrenocortical excess due to excessive cortisol exposure
primary- due to adrenal tumor, can be from pharmacological use of cortisol

217

Cushing Disease due to ACTH secreting tumor

darkening of the skin
excess cortisol and androgens

218

Symptoms of excess cortisol

increased appetite, hyperglycemia, insulin resistance, abdominal fat accumulation, type two diabetes, loss of muscle and fat from limbs, hypokalemia, polycythemia, osteoporosis

219

Psychologial disturbances with Cushing Disease

anxiety depression euphoria poor concentration

220

Excessive androgens in cushings disease

hirsuitism, male pattern baldness, clitoral enlargement, acne

221

Conn's Disease

primary hyperaldosteronism
due to aldosterone secreting tumors

222

Symptoms of Conn's disease

sodium retention leading to hypertension, atrial natriuretic hormone release and polyuria
potassium and hydrogen loss
hypokalemia
alkalosis

223

Catecholamines

epinephrine and norepinephrine synthesized from tyrosine

224

Control of catecholamine secretion

activation of the sympathetic nervous system
stress/excitation, low BP, inadequate oxygen, low blood sugar, pain, injury, ect

225

What enzymes destroy catecholamines

monoamine oxidase and catechol-o-methyl transferase
MAO in nervous system and COMT in blood

226

effects of norepinephrine on the immune system

low levels- act on alpha receptors to increase lymphocyte proliferation
high levels- act on beta receptors to decrease lymphocyte proliferation

227

effects of epinephrine on the immune system

mobilizes preformed neutrophils and lymphocytes
low levels- stimulate monocyte fn
high levels- inhibit monocyte fn

228

Pheochromocytoma

tumor that secretes excess norepinephrine, epinephrine, and dopamine
often episodic in catecholamine production- have periods without symptoms

229

Symptoms of pheochromocytoma

hypertension, palpitations, chest pain, headache, nervousness, anxiety, visual disturbances, abdominal pain, nausea, vomiting

can lead to MI and intracranial hemorrhage