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SRNA3AdvancedPatho2 > EXAM 1 Neuro and Endocrine Pathophysiology > Flashcards

EXAM 1 Neuro and Endocrine Pathophysiology Flashcards

1
Q

Cell communications: What are gap junction?

A

Pores in the cells membrane allowing signaling to move from cell to cell

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2
Q

What are neurotransmitters?

A

Release from neuron to travel across gap to a 2nd cell

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3
Q

What are paracrine hormones?

A

Local hormones secreted into tissue fluids to affect nearby cells

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4
Q

Strict definition of hormones

A

Chemical messengers that travel in the bloodstream and stimulate response in another tissue or organ

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5
Q

What are target cells?

A

They have receptors for hormone

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6
Q

Endocrine hormones

A

Produce hormones

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7
Q

Endocrine system : endocrine organs are

A

Thyroid , pineal, etc

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8
Q

Endocrine system: also produce

A

hormone producing cells organs (Brain, heart, and small intestine)

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9
Q

***Endocrine control : normal homeostatic control of what? MEWGIH

A 
Metabolism
Electrolyte balance (Na, K, Ca2+)
Water retention and BP control
Glucose levels
Inflammation
Healing
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10
Q

Normal vs disease states complicated usually by?

A

Elevated stress of illness/surgery

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11
Q

***Hormone regulation: levels of hormone, what happens?

A

levels maintained within a certain range for normal physiologic function

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12
Q

***Hormone regulation is mainly controlled by what feedback?

A

Negative feedback

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13
Q

What are the environmental factors that can affect levels of hormones? (SSSND)

A 
Stress (both physical and mental) 
Systemic illness
Sleep patterns
Nutritional changes
Day-night cycle
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14
Q

Hormone Regulation: Most pituitary hormones exhibit what?

A

Circadian rhythm

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15
Q

During hormone regulation, it ensure

A

Peak hormone levels at times of greatest demand

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16
Q

When does peak secretion of ACTH and cortisol?

A

Occur early in the morning

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17
Q

What is stress caused by?

A

Any situation that upsets homeostasis via physical or emotional causes

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18
Q

What is general adaptation syndrome?

A

The way the body reacts to stress

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19
Q

What are the 3 stages of general adaptation syndrome?

A

Alarm REACTION
Stage of RESISTANCE
Stage of EXHAUSTION

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20
Q

Alarm reaction is the _________

What happens?

A

Initial response
Increase Epinephrine and norepinephrine levels
HR and BP and blood glucose (NEHBB) (NaH2O
Sodium and water retention (aldosterone)

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21
Q

Stage of Resistance what happens?

GACFatGDS

A 
Glycogen reserves gone
Increase ACTH and cortisol levels
Fat and protein breakdown
Gluconeogenesis 
Depresses immune function
Susceptibility to infection and ulcers
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22
Q

Stage of Exhaustion is defined as

A

stress that continues until fat reserves are gone

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23
Q

What happens during stage of exhaustion? Protein

PL HE HA

A

Protein breakdown and muscle wasting
Loss of glucose homeostasis
Hypertension and electrolyte imbalances (loss of K+H+)
Hypokalemia and alkalosis (can lead to death)

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24
Q

***Effects of stress : What is activated and what does it depend on?

A

Activation of the adaptive processes to stress depends on the severity and or duration of the stressor event

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25
Q

***Effects of stress when adaptive process activated , 3 different outcomes possible

A
  1. Restoration of homeostasis
  2. Inadequate response
  3. Exaggerated response
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26
Q

***Stress response : a modified endocrine response

A

Causing physical and mental changes

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27
Q

***Modified endocrine response: what physical changes occur?

A

There is redirection of blood flow
Decreased to GLK (gut, liver and kidney)
Increased to HBLS (Heart, brain, liver and skeletal muscle)

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28
Q

***Modified endocrine response: what mental changes occur?

A

Increased alertness and arousal, cognition, analgesia

inhibition of appetite (Improved CAAA IA)

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29
Q

***Hemodynamic & Metabolic Changes in stress leads to redirection of blood flow

A

Increase HR, CO and Metabolism with hyperglycemia (HCML) Lypolysis
Decreased insulin

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30
Q

Neuroendocrine effectors of Stress response: What are the peripheral effectors? (GEN)

A

Glucocorticoids
Epinephrine
Norepinephrine

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31
Q

Neuroendocrine effectors of Stress response: What are the central effectors? (CV)

A

Corticotropin Releasing hormone (CRH): { (CRH –>Pituitary –> ACTH)}
Vasopressin (ADH) Increase BP

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32
Q

Hypothalamic-Pituitary-Adrenal Axis (HPA-axis) stress reaction (CAA)

A

CRH stimulate release of ACTH from hypothalamus
Acts with Vasopressin to control pituitary adrenal axis
ACTH leads to cortisol release

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33
Q

What is the most important regulator of ACTH release?

A

CRH

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34
Q

***What are other components affecting HPA ? What does it depends on ? (CIAL)

A

Depending on the magnitude of the stress, additional factors to enhance HPA response are:
Cytokines (TNF)
Interlukins (IL-6 & IL-1)
Angiotensin II
Lipid mediators of inflammation (Arachidonic acid –>Prostaglandins & Leukotrienes)

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35
Q

***Short term stress (CLR)

A

Cortisol regulates CRH, Vasopressin & ACTH via negative feedback
Limits exposure of tissues to cortisol
Reduces excessive metabolic, CV, and Immune
stress response

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36
Q

***Long Term Stress examples (CAMPA)

A 
Chronic illness/depression
Anorexia nervosa
Malnutrition
Panic disorder
Alcohol withdrawal
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37
Q

***Long term stress Sequela:(GIPI)

A

Increased gluconeogenesis, insulin resistance, protein catabolism, immune depression (GIPI)

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38
Q

Exocrine Glands vs Endocrine glands: Exocrine glands

A

secrete their product through a duct and onto an open surface or organ cavity. Extracellular effects (food digestion)

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39
Q

Exocrine Glands vs Endocrine glands: Endocrine glands

A

Secrete their products directly into the bloodstream, no ducts. Intracellular effects (Alter target cell metabolism)

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40
Q

Nervous vs Endocrine Systems: Communication

A

Nervous : both chemical and electrical

Endocrine: Only CHEMICAL

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41
Q

Nervous vs Endocrine Systems: Speed and persistence of response

A

Nervous: reacts quickly , stops quickly
Endocrine: react slowly . effect may continue for weeks

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42
Q

Nervous vs Endocrine Systems: Adaptation to long term stimuli

A

Nervous: response declines (adapt quickly)
Endocrine: response persists

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43
Q

Nervous vs Endocrine Systems: Area of effect

A

Nervous: Targeted and specific (one organ)
Endocrine: general, widespread effects (many organs)

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44
Q

What are chemical that function as both hormones and neurotransmitters? CANT Do

A 
Cholecystokinin
ADH
NE
Thyrotropin releasing hormone (TRH) 
Dopamine
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45
Q

Some hormones are secreted by neuroendocrine cells

A

Oxytocin and catecholamine

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46
Q

Both Nervous and endocrine systems have

A

overlapping effects on same target cells

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47
Q

Both cause glycogenolysis in the liver

A

NE and Glucagon

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48
Q

Both nervous and endocrine systems can regulate each other, How so?

A

Neurons trigger hormone secretion

Hormones stimulate or inhibit neurons

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49
Q

Hypothalamus description

A

Flattened funnel, forms floor and wall of third ventricle

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50
Q

What is the function of the hypothalamus?

A

Regulates homeostasis mechanisms and some endocrine functions.

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51
Q

Where is the pituitary gland hypophysis

A

Suspended by hypothalamus by stalk (infundibulum)

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52
Q

Where is the pituitary gland located?

A

House in SELLA TURCICA of sphenoid bone

1.3 cm diameter

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53
Q

Where is the Anterior pituitary ?

A

The anterior pituitary (Adenohypophysis) arises from hypophyseal pouch (outgrowth of pharynx)

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54
Q

Where is the Posterior pituitary ?

A

Also called neurohypophysis (arises from brain)

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55
Q

Oxytocin released by

A

Posterior pituitary gland

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56
Q

Pituitary Hormones - Anterior Lobe : What types of hormones?

A

Tropic hormones target other endocrine hormones

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57
Q

What are the Gonadotropins hormones?

A

Target gonads (FSH and LH)

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58
Q

What are the Anterior lobes hormones?

A 
FLAT PG
FSH 
LH
ACTH
TSH
PRL
GH
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59
Q

Axis refer to

A

Way endocrine glands interact

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60
Q

What is the role of FSH?

A

Stimulates production pf egg or sperm cells

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61
Q

What is the role of LH? In female

A

Mainly stimulates hormone production

Female: stimulates ovulation and secretion of estrogen and progesterone

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62
Q

What is the role of LH in males?

A

Stimulates testes to secrete testosterone

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63
Q

What is the role of TSH?

A

Stimulates growth of thyroid and secretion of thyroid hormones

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64
Q

What is the role of ACTH (adrenocorticotropic hormone)

A

Regulates response to stress, stimulates adrenal cortex

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65
Q

What does corticosteroids regulated?

A

Glucose, Fat, and protein metabolism

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66
Q

What is the role of Prolactin (Prolactin releasing factor) ?

A

stimulates anterior pituitary produce it

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67
Q

Prolactin in female

A

Milk synthesis after delivery

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68
Q

Prolactin in male

A

Increase LH sensitivity and increase Testosterone secretion

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69
Q

Growth hormones aka

A

somatotropin

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70
Q

Where is the GH secreted?

A

Anterior pituitary

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71
Q

Growth hormone promotes

A

Tissue growth

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72
Q

Growth hormones promote tissue growth 2 ways

A

Mitosis and cellular differentiation

Stimulates liver to produce IGF-I and II

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73
Q

Growth hormone , liver protein synthesis

A

Increase DNA transcription for Increase mRNA production, proteins synthesized
Enhanced amino acid transport into cells, decrease protein catabolism

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74
Q

Growth hormone , Lipid metabolism how?

A

GW stimulates FFA and glycerol release from adipocytes, protein sparing.

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75
Q

Growth hormone, CHO metabolism

A

Glucose sparring effect = less glucose used for energy

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76
Q

Growth hormone, Electrolyte balance

A

Promotes Na+, K+, Cl- retention, Ca2+ absorption

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77
Q

Growth Hormone and Aging: Childhood and adoslescence

A

Bone, cartilage, and muscle growth

Stimulates growth at Epiphyseal plates

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78
Q

Growth Hormone and Aging: Adulthood

A

Increase osteoblastic activity and appositional growth affecting bone thickening and remodeling.

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79
Q

Growth hormone and aging, what changes occur in concentration

A

Blood concentration decrease by age 75 to 1/4 of that of adolescent.

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80
Q

Levels of GH throughout the day _______

A

fluctuates

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81
Q

GH is higher during (SAV)

A

Sleep, after high protein meals, vigorous exercise

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82
Q

GH is lower

A

After High CHO meals

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83
Q

Posterior Pituitary Hormones produced by

A

Hypothalamus

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84
Q

Posterior Pituitary Hormones are

A

AGO
ADH
GnRN (Gonadotropin-releasing hormone)
Oxytocin

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85
Q

What is the role of ADH?

A

targets kidneys, Increase water retention, reduce urine

Also a neurotransmitter

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86
Q

Acts as both Neurotransmitter and hormones?

A

ADH

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87
Q

Oxytocin role ? Causes

A

Causes uterine contractions and milk ejection (letdown)

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88
Q

Stimulates production of FSH and LH

A

GnRH

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89
Q

Pituitary is under control of

A

Hypothalamic and Cerebral control

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90
Q

Anterior lobe control

A

Releasing hormones and inhibiting hormones of hypothalamus

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91
Q

Posterior lobe control

A

Neuroendocrine reflexes

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92
Q

Posterior lobe control hormone release in response to NS signals

A

hormones release in response to nervous system signals

Sucking infant –> stimulates nerve ending –> Hypothalamus –> posterior lobe –>oxytocin –> milk ejection

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93
Q

Hormone release in response to higher brain centers

A

Milk ejection reflex can be triggered by a baby’s cry

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94
Q

What is negative feedback?

A

Increase target organ hormone levels inhibits release of tropic hormones

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95
Q

What is positive feedback?

A

Stretching of uterus increase Oxytocin release, causes more contraction/stretching uterus until delivery

96
Q

Pineal gland peak secretion ages_____by ______, lower

A

1-5 by puberty 75% lower

97
Q

What does pineal gland produces? day vs night?

A

Serotonin by day

Melatonin at night

98
Q

Melatonin increase in

99
Q

Melatonin decrease in

A

Phototherapy

100
Q

Melatonin increase in

A

Depression, sleepiness, irritability, and carbohydrate craving.

101
Q

*** Thymus is located

A

In mediastinum superior to heart

102
Q

***Involution of thymus happens

A

after puberty

103
Q

***The thymus secretes hormones that regulate development and

A

later activation of T-lymphocytes

T- cells become immunocompetent

104
Q

Largest endocrine gland

A

Thyroid; high rate of blood flow

105
Q

Anterior and lateral sides of trachea 2 larges lobes

connected by___

A

connected by isthmus

106
Q

2 thyroid hormones

A

T3 (triiodothyronine)
T4 (Tetraiodothyronine)
Calcitonin

107
Q

T4 is produced by

A

thyroid follicles filled with colloid and lined with simple cuboidal epitheliar “follicular cells”

108
Q

Effect of T4 physiologic

metabolic rate, O2 consumption, heat production, HR, contraction strength, RR, what happens to appetite

A

Increase metabolic rate, O2 consumption, increase heat production, increase HR, contraction strength, RR
stimulates appetite, and breakdown CHO lipid and proteins

109
Q

What is calcitonin produced by___

A

Parafollicular “c” cells

110
Q

Calcitonin and Ca2+

A

decrease blood calcium levels, promote Ca2+ deposition , antagonistic PTH

111
Q

Parathyroid glands (PIS)

A

Parathyroid glands
Increase Blood Ca2+ Levels
Stimulates osteoclast maturation and mobilization of calcium from bone

112
Q

What promote synthesis of calcitriol ?

3 roles

A

Parathyroid glands
Increase absorption of Ca2+
Decrease urinary excr3etion
Increase bone resorption

113
Q

**Adrenal Gland: Adrenal cortex (GFR)

A 
Zona Glomerulosa (outer)
Zona Fasciculata (middle)
Zona Reticularis (inner)
114
Q

***Adrenal Cortex: Zona Glomerulosis produces_____What do they do?

A

mineralcorticoids

Control electrolyte balance, aldosterone promotes Na+ retention, water reabsorption and K+ excretion

115
Q

***Adrenal Cortex: Zona Fasciculata produces ______What do they do?

A

Glucocorticoids
Cortisol, stimulates fat and protein catabolism, gluconeogenesis (from amino acids and FA) and lipogenesis (release of fatty acids and glucose into blood)

116
Q

***What happens with long term use of Glucocorticoids?

A

Anti-inflammatory effect becomes immune suppression with long term use

117
Q

***Zona Reticularis produces ________ what do they do?

A

Sex hormones

Androgens (including DHEA with other tissues convert to testosterone) and estrogen (important after menopause)

118
Q

*Adrenal medulla sympathetic ganglion innervated by

A

Innervated directly by sympathetic preganglionic fibers

119
Q

Adrenal medulla consists of

A

Modified neurons called CHROMAFFIN CELLS

120
Q

Stimulation causes release of

A

Catecholamines (epinephrine and NE)

121
Q

Hormones effects of Adrenal medulla

What about insulin?

A

Increase alertness, anxiety, fear, HR, airflow ,raises metabolic rate.
Insulin secretion inhibited
stimulates GLUCONEOGENESIS and GLYCOGENOLYSIS

122
Q

What causes medullary cells to stimulate cortex

123
Q

***Adrenal Medulla Tumor

A

Pheochromocytomas

Causes by tumors derived from the chromaffin cells of the adrenal medulla

124
Q

***What secretes catecholamines

A

Pheochromocytomas

125
Q

***What are the Clinical manifestations of Pheochromocytomas?

A 
HTN
Diaphoresis
Tachycardia
Palpitations
Severe headaches
126
Q

Is both exocrine and endocrine

127
Q

***Endocrine tissue of Pancreas

A

Clusters of endocrine cells called Islets of Langerhands

128
Q

***The islets include 4 types of cells that secrete different hormones:

A

Alpha cells
Beta cells
Delta cells
F cells

129
Q

*** Alpha cells secrete

130
Q

***Beta cells secrete

131
Q

***Delta cells secrete

A

Somatostatin

132
Q

*** F cells

A

Pancreatic polypeptide

133
Q

Pancreatic hormones

A

1-2 millions islets produce hormones

134
Q

Insulin from Beta cells

A

Secreted after meals with carbohydrates raises blood glucose levels

135
Q

Insulin on glucose and AA

A

stimulate glucose and amino acid uptake

136
Q

Nutrient storage and pancreatic hormones

A

Nutrient storage effect (promotes glycogenesis and lipogenesis)
Antagonizes glucagon

137
Q

Pancreatic hormones glucagon secreted when

A

Blood glucose is low, acts on liver cells to release glycogen, increases blood sugar.

138
Q

Glucagon stimulates

A

Glycogenolysis , fat catabolism (release of FFA) and promote absorption of amino acids for gluconeogenesis

139
Q

Somatostatin secreted when

A

secreted with rise in blood glucose and amino acids after a meal, inhibits GH

140
Q

Somatostatin paracrine secretion

A

Inhibits secretion of insulin, glucagon by alpha and beta cells

141
Q

Hyperglycemic hormones

A

Raise blood glucose (GH, EPi, NE, Corticol, Corticosterone)

142
Q

Hypoglycemic hormones

A

Lower blood glucose (insulin)

143
Q

Endocrine Functions of Other organs: Heart

A

ANP released with an increase in BP

Decrease BV and BP by Increase Na and H2O loss by kidneys

144
Q

Endocrine Functions of Other organs: SKIN

A

Helps produce D3

145
Q

Endocrine Functions of Other organs: LIVER

A

15% of erythropoietin (stimulates bone marrow)

Angiotensinogen (prohormone, precursor of angiotensin II)

146
Q

Liver converts

A

Vitamin D3 to calcitriol

147
Q

Promotes intestinal absorption of iron

148
Q

Produces 85% of erythropoietin

149
Q

Stimulates bones marrow to produce RBCs what hormones

A

Erythropoietin

150
Q

Convert angiotensinogen to angiotensin I

A

Kidneys (renin)

151
Q

Kidneys and calcitriol

A

converts calcidiol to calcitriol (ACTIVE FORM OF VitD)

By increasing absorption by intestine and inhbits loss in the urine; More Ca2+ available for bone deposition

152
Q

Stomach and small intestines and endocrine

A

10 enteric hormones

Coordinate digestive motility and secretion

153
Q

Placenta and endocrine

A

secretes estrogen, progesterone, and others

regulates pregnancy, stimulates development of fetus and mammary glands

154
Q

Fat Soluble vs Water soluble : Steroids

A

Derived from cholesterol

Sex steroids, corticosteroids

155
Q

Fat Soluble vs Water soluble : Peptides and Glycoproteins

A

Oxytocin and ADH: all releasing and inhibiting hormones of hypothalamus: most of anterior pituitary hormones

156
Q

Fat Soluble vs Water soluble :Monoamines (biogenic amines)

A

Derived from amino acids

Catecholamines (Ne, Epi, Dopa and thyroid hormones)

157
Q

Hormones synthesis: Steroid hormones synthesized from

A

Cholesterol : differs in functional groups attached to 4- rings steroid backbone

158
Q

Hormones synthesis : Peptides -> Cellular steps

A

Rough ER removes segment, forms prohormones
Golgi complex further modifies it into hormones
(e.g. insulin formation preproinsulin converted to proinsulin in RER) proinsulin split into insulin and C peptide in Golgi complex).

159
Q

Hormone synthesis: Monoamines: All are synthesized from

160
Q

What is the only monoamines not synthesized from tyrosine?

A

Melatonin (synthesized from tryptophan)

161
Q

Thyroid hormones is unusual why?

A

Composed of 2 tyrosine molecules

Requires a mineral, iodine

162
Q

Thyroid Hormone Synthesis

A
  1. Iodide absorption and oxidation
  2. Thyroglobulin synthesis and secretion
  3. Iodine added to tyrosines and thyroglobulin
  4. Thyroglobulin uptake and hydrolysis
  5. Release of T3 and T4 into the blood
163
Q

T3 and T4 synthesis

A

Follicular cells
Absorb iodine from blood and store in lumen as Iodine
Synthesize thyroglobulin and store in lumen (contains tyrosine)
Tyrosine and iodine form T3 and T4

164
Q

TSH

A

Stimulates follicular cells to remove T3 and T4 from Thyroglobulin for release into plasma

165
Q

Hormones transport: Monoamines and peptides are (hydrophobic or hydrophilic)

A

Hydrophillic

166
Q

How are protein hormones transported?

A

Transported in the bloodstream, transported free unbound as water soluble form

167
Q

Steroids and thyroid hormones are

(hydrophobic or hydrophilic) what must they do?

A

Hydrophobic

They must bind to transport protein for transport

168
Q

When bound hormone by to protein what happens?

A

Bound hormones attached to transport protein, prolongs half life to weeks and protect from enzymes and kidney filtration

169
Q

What happens to unbound hormones?

A

Unbound hormones leave capillary to reach target cell (half life a few minutes)

170
Q

Transport proteins in plasma

A

Albumin and TGB (thyroxine binding globulin)bind to thyroid hormones

171
Q

Steroid hormones bind to

172
Q

Aldosterone and transport protein

A

NO transport protein , 20 min half life

173
Q

Hormones receptors are located on

A

plasma membrane, mitochondria, other organelles or in nucleus

174
Q

Hormone binding turns

A

metabolic pathway on or off

Exhibit specificity and saturation

175
Q

How does hydrophobic hormones exert their actions

A

They penetrate plasma membrane and bind to intracellular receptors such as estrogen, T3 and aldosterone.

176
Q

How does hydrophilic hormones exert their actions?

A

Must bind to cell surface receptors (such AS epinephrine)

177
Q

Thyroid hormone effects : TH binds to receptors on mitochondria and

A

Increase rate of aerobic respiration

178
Q

Thyroid hormone effects : TH binds to receptors on ribosomes and chromatin and

A

Increase protein synthesis

179
Q

Thyroid hormones effects Na Na ATPase produced

A

Generates heat.

180
Q

Hydrophillic hormones : Mode of Action

A

cAMP as second messenger i.e epinephrine

181
Q

Hydrophillic hormones steps (HAPPAM)

A
  1. Hormone binding activates G protein
  2. Activate adenylate cyclase
  3. Produces cAMP
  4. Activates Kinases
  5. Activates enzymes
  6. Metabolic reactions: Synthesis, secretion, change membrane potentials.
182
Q

Hormones may use

A

Different second messengers in different tissues

183
Q

Hormones clearance signals must be

A

turned off

184
Q

Hormone clearance take UP AND degraded by

A

Liver and kidney

185
Q

Hormones excreted in

A

bile or urine

186
Q

Metabolic clearance rate

A

Half time required to clear 50% of hormone

187
Q

***Modulation of target cell sensitivity : Upregulation (LIS)

A

Low receptor density Weak response
Increase receptor density : Increase sensitivity
Stronger response

188
Q

***Modulation of target cell sensitivity : Downregulation (HRD)

A

High receptor density Strong response
Reduced receptor density : Reduced sensitivity
Diminished response

189
Q

Long term use of high pharmacological doses

A

Bind to receptor sites of related hormones

Target cell may convert to different hormone

190
Q

Hormones interactions 3 (SPA)

A

Synergistic effects
Permissive effects
Antagonistic effects

191
Q

What is permissive effects

A

One hormone enhances response to a second hormone

192
Q

Chemical messengers that diffuse short distances and stimulates nearby cells

193
Q

Unlike neurotransmitters, paracrine secretions are

A

not produces in neurons

not transported in blood

194
Q

Examples of paracrine and their functions

Histamine

A

Histamine (from mast cells of Connective tissue)

causes relaxation of blood vessel smooth muscle

195
Q

Examples of paracrine and their functions: Nitric oxide

A

From endothelium or blood vessels, causes vasodilation

196
Q

Examples of paracrine and their functions: Somatostatin

A

From gamma cells, inhibits secretions of alpha and beta cells

197
Q

Examples of paracrine and their functions: Catecholamines

A

Diffuse from adrenal medulla to cortex

198
Q

Paracrine secretion :

A

Eicosanoids

199
Q

Paracrine secretion: Eicosanoids: Leukotrienes

A

Converted from arachidonic acid (by lipoxygenase) mediates allergic and inflammatory reactions)

200
Q

Paracrine secretion: Eicosanoids: Prostacyclin

A

By cyclooxygenase, inhibits blood clotting and vasoconstriction

201
Q

Paracrine secretion: Eicosanoids: Thromboxane

A

by cyclooxygenase: Produces by blood platelets after injury; override prostacyclin, stimulates vasoconstriction and clotting

202
Q

Paracrine secretion: Eicosanoids: Prostaglandins PGE

A

by cyclooxygenase:

PGE: Relaxes smooth muscles in bladder, intestines, bronchioles, uterus and stimulates contraction of blood vessels.

203
Q

Paracrine secretion: Eicosanoids: Prostaglandins PGF

A

Opposite effects

204
Q

Endocrine disorders characterized by

A

too much or too little

205
Q

Hyposecretion

A

Inadequate hormone release
Tumor or lesion destroys glands For example head trauma affects pituitary gland ability to secrete ADH
DI = chronic poyluria

206
Q

Hypersecretion

A 
Excessive hormone release
Tumors or autoimmune disorder
Toxic goiter (Graves disease) antibodies mimic effect of TSH on the thyroid
207
Q

Hypersecretion of growth hormones: Gigantism

Dwarfism

A

If oversecretion Gigantism

if Undersecretion Dwarfism

208
Q

Hypersecretion of GH

A

Acromegaly

Thickening of the bones and soft tisses

209
Q

Congenital Hypothyroidism (Decreased TH) cretinism

A

infant suffers abnormal bone development , thickened facial features, low temperature, lethargy and brain damage

210
Q

Myxedema (adult hypothyroidism) decrease TH

A

Low metabolic rate slugglishnes, sleepiness, weight gain, bradycardia, constipation, dry ksin

211
Q

Endemic goiter

A

Dietary iodine deficiency , no TH ,no feedback, increased TSH

212
Q

Toxic goiter

A

Graves disease

Antibodies mimic TSH, increase TH, exophthalmos

213
Q

Hyperthyroidism aka ________ is a condition that results from any cause of

A

Thyrotoxicosis

increase levels of thyroid hormones. Excess amount of thyroid hormones are secreted from the thyroid gland

214
Q

Clinical manifestation of Hyperthyroidism

A

Increase metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by the SNS : Enlargement of the thyroid gland

215
Q

Treatment of hyperthyroidsim

A

Methimazole or Propylthiouracil
Radiactive iodine therapy
Surgery

216
Q

Parathyroid disorders: Hypoparathyroid

A

Surgical excision during thyroid surgery

Fatal tetany 3-4 days

217
Q

Parathyroid disorders: Hyperparathyroid

A

Excess PTH secretion
tumor in gland
Increase Ca2+ –> Renal Calculi

218
Q

Cushing syndrome

A

Excess cortical secretion

219
Q

S/S of Cushing syndrome

A

Hyperglycemia, HTN, Weakness, edema
Muscle and bone loss
Buffalo hump and MOON FACE (fat deposition between shoulders)

220
Q

Adrenogenital syndrome

A

Adrenal androgen hypersecretion: Accompanies cushing
Enlargement of external sexual organs in children and early onset of puberty
Masculinizing effects of women (deeper voice and beard growth)

221
Q

Diabetes Mellitus S/S

A

Hyposecretion of insulin
Polyuria, polydipsia and polyphagia
Hyperglycemia, glycosuria, ketonuria
osmotic diuresis

222
Q

What is osmotic diuresis

A

Blood glucose levels rise above transport maximum of kidney tubules, glucose remains in urine (ketones also present) Increased osmolarity draws water into urine

223
Q

Type I DM

A

IDDM
10%
Autoimmune destruction of B cells diagnosed about age 12

224
Q

Type I Treated with

A

Diet, exercise, monitoring of blood glucose and periodic injections of insulin

225
Q

Type II

A

NIDDM
90%
Insulin resistance: Failure of target cell to respond to insulin

226
Q

What are the 3 major risk factors for NIDDM

A

Heredity, age and Obesity

227
Q

NIDDM treated with

A

Weight loss program diet and exercise

Oral medication improve insulin secretion or target cell sensitivity

228
Q

Acute pathology of Diabetes

A

Cells cannot absorb glucose, rely on fat and proteins (weight loss, weakness)

229
Q

Fat catabolism and diabetes

A

FAT catabolism increase FFA in blood and ketone bodies

230
Q

Ketonuria and diabetes

A

Ketoacidosis occurs as ketones decrease blood pH

If continued causes dyspnea and eventually diabetic coma

231
Q

Chronic pathology of Diabetes

A

Chronic hyperglycemia lead to neuropathy and CV damage from atherosclerosis
Retina and kidneys damage common in type I
Atherosclerosis leads to heart failure common in type II and GANGRENE

232
Q

Hyperinsulinism

A

From excess insulin injection or pancreatic islet tumor

233
Q

Hyperinsulinism causes

SIA

A

hypoglycemia, weakness and hunger

Triggers secretion of epinephrine, GH and glucagon (SE: anxiety, sweating and increase HR)

234
Q

Insulin shock (DUC)

A

Uncorrected hyperinsulinism with Disorientation
Unconsciousness
Convulsion

235
Q

Tropic Hormones TAPGG

A 
TSH
ACTH
PRL
Gonagotropins (FSH, LH)
GH

SRNA3AdvancedPatho2 (15 decks)

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