Physiology Exam 1

Front 1

3 ways the Hypothalamus integrates nervous & endocrine systems?

Back 1

1. controls release of hormones in the Anterior Pituitary

2. is an endocrine organ itself

3. controls endocrine cells in the Adrenal Medullae

Front 2

What hormones does the hypothalamus release into the Anterior Pituitary?

Back 2

1. TRH (Thyrotropin Releasing Hormone)
2. CRH (Corticotropin Releasing Hormone)
3. GnRH (Gonadotroping Releasing Hormone)

Front 3

TRH is released by who & does what?

Back 3

TRH is released by hypothalamus w/low blood Thyroid Hormones into the anterior pituitary --> TSH

Front 4

CRH is relased by who & does what?

Back 4

CRH is released by hypothalamus into the anterior pituitary --> ACTH --> causes Adrenal Cortex --> glucocorticoids

Front 5

GnRH is released by who & does what?

(Gonadotropin-Releasing Hormone)

Back 5

GnRH is released by the hypothalamus into the Anterior Pituitary --> release of Gonadotropins
- FSH (Follicle Stimulating Hormone)
- Leuteinizing Hormone

Front 6

how is Prolactin (PRL) regulated

Back 6

PRF (Prolactin Relasing factor)

PIH (Prolactin Inhibiting Hormone)

Front 7

Hypothalamus regulates GH through these regulatory hormones

Back 7

GH-RH (Growth Hormone Releasing Hormone)

GH-IH (Growth Hormone Inhibiting Hormone)

Front 8

Hypothalamus regulates MSH through these regulatory hormones

(Melanocyte Stimulating Hormone)

Back 8

MSH (Melanocyte Stimulating Hormone)

MIH (Melanocyte Inhibiting Hormone)

Front 9

what are the Regulatory Hormones?

Back 9

1. TRH
2. CRH
3. GnRH
4/5 PRF/ PIH
6/7 GH-RH/ GH-IH
8/9 MSH/ MIH

Front 10

hypothalamus controls ____ by release of ___ into the anterior pituitary?

Back 10

controls
PLR by PRF & PIH
2. thyroid hormones by TSH
3. Gonadotropins by GnRH
4. Somatomedins (Insuline-like Growth Factors) by GH-IH & GH-RH

Front 11

Diabetes Insipidus

Back 11

Posterior Pituitary releases too little ADH
--> too much water loss @ kidneys

may need synthetic ADH (desmopressin)

Front 12

high blood PRL -->

low blood PRL -->

cause hypothalamus to release

Back 12

high PRL --> PIH

low PRL --> PRF

Front 13

Diabetes mellitus

Back 13

hyperglycemia --> glycosuria & polyuria

Front 14

What happens w/too much Growth Hormone?

Back 14

Gigantism, acromegaly

excesssive growth

Front 15

ADH is triggered by?

causes?

Back 15

triggered by rising solute in blood or dropping BP

causes reabsorption of water at kidneys & vasoconstricion of peripheral blood vessels

inhibited by alcohol

Front 16

glucocorticoids

Back 16

made by adrenal cortex

release stimulated by ACTH

causes?

Front 17

what 5 hormones are released by the anterior pituitary & cause other hormones to be released?

Back 17

1. TSH --> Thyroid gland to secrete Thyroid hormones
2. ACTH --> Adrenal Cortex to secrete Glucocorticoids
3. FSH --> Ovaries to secrete Estrogen
4. GH --> Liver releases Somatomedins (IGF)
5. LH --> Ovaries to secret Estrogen & Progesterone

Front 18

These Anterior Pituitary hormones have indirect action

Back 18

1. PRL stimulates mamary gland development & makes interstistitial cells more sensitive to LH

2. MSH stimulates skin to produce melanin

Front 19

Thyroid secretes these 2 hormones

Back 19

Thyroid hormones (T4 & T3)

Calcitonin

Front 20

Calcitonin synthesis & release is triggered by what,

Back 20

C cells of the thyroid monitor blood calcium levels

High Blood Ca++ triggers release

Front 21

What can happen if blood Ca++ gets too high?

Back 21

Na+ permeability decreases & membranes become less responsive

Front 22

What happens if blood Ca++ gets low ?

Back 22

Na permeability increases & cells become excitable

even lower --> convulsions, muscular spasms

Front 23

PTH - who makes it & what does it do?

Back 23

made by chief cells in the Parathyroid gland

1. inhibits osteoblasts --> inhibits bone formation
2. increases osteocast #'s --> more release of Ca++ from bone
3. enhances reabsoption of Ca++ at kidneys
4. stimulates synthesis & release of Calcitriol at kidneys

Front 24

are released when blood Ca++ is too low

Back 24

PTH
1. inhibits bone mineralization & increases Ca++ release
2. Enhances Reabsorption of Ca++ by kidneys
3. releases Calitriol by kidney
Calcitriol
same as PTH but also stimulates digestive tract to absorb Ca++ & phosphate

Front 25

are released when blood Ca++ is too high

Back 25

Calcitonin from C cells of Thyroid

Front 26

how are glucocorticoids regulated?

Back 26

negative feed back
Glucocorticoids inhibit CRH

Front 27

diabetes insipidus: 2 causes

Back 27

1. Posterior Pituitary can't releases enough ADH

2. Kidneys can't respond to ADH

Front 28

Adrenal Cortex makes what?

Back 28

1. Mineralocorticoids (Aldosterone)
2. Glucocorticoids (cortisol)
3. Androgens

Front 29

Adrenal Medulla makes ?

Back 29

Epinephrine & Norepinephrine

Front 30

in this type of diabetes:
- normal/high insulin production
- tissue doesn't respond normally

Back 30

type 2 Diabetes Mellitus

Front 31

what triggers Aldosterone release?

Back 31

drop in blood: Na+/pressure/volume

increase in blood K+

Angiotensin II

Front 32

Glucocrticoids

Back 32

glucose sparing effect
-synthesis of glucose & Glycogen
- release of FFA & AA for fuel

anti-inflammatory
_ inhibits WBC --> stops histamine release & others that promote inflammation

Front 33

Epinephrine & Norepinephrine
effects

Back 33

Muscle: mobilize glycogen & incresses ATP production -> stronger & longer
Fat cells: release & breakdown of fat
Liver: breakdown release of glycogen/glucose
Heart: increased heart rate & force of contractions

Front 34

what hormones does the hypothalamus synthesize?

Back 34

1. CRH (Corticotropin Releasing Hormone)
2. PIH (Prolactin Inhibiting Hormone) aka dopamine
3. GnRH
4. GH-RH
5. GH-IH (Somatostatin)
6. TRH (Thyrotropin-releasing hormone)
7. ADH
8. Oxytocin

Front 35

1. ____ can drop blood glucose & is made by the Adrenal 2. _____

Back 35

1. Glucocorticoids (Cortisol)

2. Adrenal Cortex

Front 36

1. ____ can increase blood glucose & is made by the Adrenal _____

Back 36

1. Epinephrine

2. Adrenal Medulla

Front 37

the hypothalamus controls this part of the Adrenal gland through direct neural control

Back 37

Pre ganglionic motor fibers control Adrenal Medulla

Front 38

Pineal Gland

Back 38

produces Melatonin

Front 39

what does Melatonin do

Back 39

1. inhibits premature puberty by reducing GnRH
2. antioxidant in CNS
3. Circadian Rhythms- higher Melatonin @ night

Front 40

Exocrine pancreas

Back 40

Pancreatic acini

produces digestive

Front 41

Endocrine pancreas

Back 41

islets of Langerhans

Front 42

what are the cell types of Islets of Langerhans & what do they do?

Back 42

alpha cells: glucagon
Beta cells: insulin
Delta cells: GH-IH that inhibits alpha/beta from releasing glucagon & insulin & slows absorption & enzyme secretion in GI
F cells: Pancreatic Polypeptide (PP) inhibits gallblader contractions

Front 43

high blood Somatomedins (IGF) pathway -->

Back 43

1. hypothalamus responds by releasing GH-IH into anterior pituitary
2. Anterior Pituitary stops/reduces GH release

Front 44

low blood Somatomedins (IGF) pathway -->

Back 44

1. hypothalamus responds by releasing GH-RH into anterior pituitary
2. Anterior Pituitary releases GH
3. liver releases IGF (somatomedins)

Front 45

too little GH

Back 45

Pituitary growth failure

--> retarded growth

--> abnormal fat distrobution

--> low blood Glucose hours after meal

Front 46

low ADH or low AVP

Arginine Vasopressin

Back 46

--> Diabetes insipidus

Front 47

these Hormones activate the GPCR pathway

G-pro -> AC-> cAMP pathway

Back 47

Nor/Epinephrine
calcitonin
TSH, PTH
ADH
ACTH
FSH, LH & glucagon

Front 48

too much ADH or AVP

(Arginine Vasopressin)

Back 48

Syndrome of Inappropriate ADH secretion (SIADH)

--> increased body weight/water

Front 49

why do you pee so much when you drink?

Back 49

ADH is inhibited by alcohol which inhibits your body's ability to accurately maintain blood osmolarity, pressure, & volume by decreasing urine output & vassoconstriction

Front 50

too little T4, T3

Back 50

Myxedma, Cretinism

--> low metabolic rate/temp

--> impaired physical & mental development

Front 51

Oxytocin

Back 51

Women: uterin contractions, milk ejection from mammary glands

Men: prostate gland
both: rises during sex

Front 52

too much T4, T3

Back 52

Hyperthyroidism, Graves Disease

High metabolic rate & body temp

Front 53

too little PTH

Back 53

hypoparathyroidism

muscular weakness, neurological problems
dense bones, tetany due to low blood Ca++

Front 54

too much PTH

Back 54

hyperparathyroidism

Neurological, mental, & muscle problems b/c high Ca++ blood concentration

brittle bones

Front 55

too much Mineralocoticoids

Back 55

Hypoaldosteronism

Polyuria, low blood volume, High K+/low Na+

Front 56

too much mineralocorticoids

Back 56

Aldosteronism

increased body weight/water b/c Na+/water retension
low blood K+

Front 57

too little Glucocorticoids

Back 57

Addison disease

inability to tolerate stress, mobilizes energy, or maintain normal blood glucose

Front 58

too much Glucocorticoids

Back 58

Cushing disease

excessive breakdown of tissue proteins & lipid reserves

impaired glucose metabolism

Front 59

Too much Epinephrine/norepinephrine

Back 59

Pheochromocytoma

High metabolic rate/temp, & heart rate
elevated blood glucose

Front 60

too little Estrogens in women

too little Androgens in men

Back 60

hypogonadism

sterile, lack 2nd sex characteristics

Front 61

What is the major difference btw PTH & Calcitriol

Back 61

Calcitriol stimulates absorption of Phosphate & Ca++ by the digestive tract

Chief cell monitor blood Ca & release PTH when too low

Kidney releases Calcitriol b/c PTH

Front 62

Addison Disease

Back 62

too little glucocorticoids & mineralocorticoids

inability to mobilize energy & maintain normal blood glucose

Front 63

Cretinism

Back 63

Congenital Hypothyroidism

inadequate skeletal & nervous system development
low metabolic rate

Front 64

Cushing Disease

Back 64

caused by hypersecretion of glucocorticoids

excessive breakdown--> relocation of lipid reserves & protein

Front 65

General Adaption Syndrome

Back 65

pattern of hormonal & hysiological adjustments with which the body responds to all forms of stress

Front 66

Myxedema

Back 66

severe hyposecretion of thyroid hormones

subcutaneous swelling, hair loss, dry skin, low temp, muscle weakness, & slow reflexes

Front 67

Mineralocorticoids

Back 67

increrase reabsorption of Na & Water at kidney
increase salt sensation --> eat more salt

increase renal loss of K+

Triggered by angiotensin II

Example: Aldosterone

Front 68

in this type of diabetes:
- inadequate insulin production by beta cells of pancreatic islets

Back 68

Type 1 Diabetes Mellitus

Front 69

Seasonal Affective Disorder (SAD)

Back 69

linked to elevated melatonin levels in individuals exposed to only short periods of daylight

depression, lethargy, can't concentrate, & altered sleep/eating

Front 70

overuse of Glucocorticoids can lead to

Back 70

diabetes

Front 71

Thyrotoxicosis

Back 71

caused by hyperthyroidism

increased:metabolic rate, blood pressure, heart rate
excitabiity & emotional instability
lowered energy reserves

Front 72

Seasonal Affective Disorder can be caused by

Back 72

too much melatonin

not enough light --> causes increased melatonin levels

changes in mood, eating, & sleep

Front 73

What hormones does the kidney secrete?

Back 73

Erythropoietin

Calcitriol

Renin

Front 74

Erythropoietin (EPO)

Back 74

Trigger: low O2

causes: increased RBC production

Front 75

Calcitriol

Back 75

causes Ca++ release from bone
absorption of Ca & phosphate from GI
inhibits PTH secretion

Front 76

Renin:
Triggers?

Back 76

Renin secretion is triggered by
• Sympathetic stimulation
• Low bp
• Low filtrate osmolality

Front 77

Renin Causes

Back 77

Angiotensinogen --> (blood) Angiotensin I --> (lungs) Angiotensin II

stimulates ADH from Posterior Pituitary
stimulates Aldosterone from Adrenal Cortex

Front 78

Heart makes what hormone

Back 78

ANP (Atrial natriuretic peptide)

Front 79

what triggers ANP

Atrial Natriuretic Peptide

Back 79

High Blood Pressure that stretches endocrine cardiac muscle cells

Front 80

ANP acts against the functions of ?

Back 80

opposes actions of Angiotensin II

Front 81

ANP causes what to happen?

Back 81

loss of Na+ & water at kidneys
suppress thirst
prevent Angiotensin II & norepinephrine from raising BP
inhibits release of Renin & Angiotensin II, ADH, & Aldosteron

Front 82

These hormones play a role in growth & development

Back 82

GH
Thyroid Hormones
Insulin
PTH
Calcitriol
Reproductive hormones

Front 83

Role of hormones in Growth: an adult can be normal with low GH, but needs these other hormones to be normal

Back 83

1. T4
2. Insulin
3. Glucocorticoids

Front 84

Role of hormones in Growth:
too little Thyroid hormones

Back 84

1st year --> neurological & mental retard

b/f puberty --> normal skeletal development will not continue

Front 85

Role of hormones in Growth:
reproductive hormones cause what in development?

Back 85

cause gender related skeletal proportions & secondary sex characteristics

Front 86

General Adaption Syndrome: stress response

Back 86

Alarm Phase

Resistance Phase

Exhaustion Phase

Front 87

Alarm Phase

Back 87

1st phase of stress response

-Fight/Flight

Dominant Hormone: Epinephrine

Front 88

What are the characteristics of the Alarm phase?

Back 88

1. increased mental alertness
2. increased energy consumption by skeletal muscles
3. mobilization of energy reserves (Glycogen & lipids)
4. increased blood flow to muscles/reduced to skin, kidneys, & Digestive organs
5. reduction in digestion & urine
6. increased sweat
7. increased BP, HR, Respiratory Rate

Front 89

what other hormones play a supporting role in the alarm phase?

Back 89

ADH- reduction of water loss
aldosterone if blood loss

Front 90

Resistance Phase: basics

Back 90

if stress lasts longer than a few hours

Long term metabolic adjustment

Dominant Hormone: Glucocorticoids

Front 91

Resistance Phase: characteristics

Back 91

1. Mobilize remaining energy: lipids & AA released
2. Conservation of Glucose for neural tissues - peripheral tissue breaks down lipids for energy
3. Elevation of glucose: liver synthesizes Gluc from CHO, AA, Lipids
4. Conservation of salts & water, Loss of K+ & H+

Front 92

Resistance phase hormones

Back 92

GH
Glucocorticoids
Glucagon
Mineralocorticoids
ADH

Front 93

what hormones are involved in the Resistance Phase?

What do they do?

Back 93

GH-
1.mobilize AA & lipids for Energy
2. Conserve Glu

Glucocorticoids
1. AA & Lipids
2. Conserve Glu
3. liver to synth Glu

Glucagon
2. Conserve Glu
3. liver to synth

Mineralocorticoids & ADH
4. conserve water

Front 94

Resistance Phase:
1. Mobilize lipids & AA

Back 94

hypothalamus produces GH-RH & CRH --> GH & ACTH
ACTH --> Glucocorticoids

Adipose: responds to GH & Glucocorticoids by --> FA
Skeletal Muscle: responds to Glucocorticoids --> AA

Front 95

Resistance Phase:
2. Conserve Glu

Back 95

Glucocorticoids & GH have glucose sparing effects in most tissue; NOT NEURAL TISSUE

Front 96

Resistance Phase:
3. Elevate & Stabilize Blood Glu

Back 96

Glucagon & Glucocorticoids stimulate liver to synthesize Glucose from AA, FA, & other CHO like glycerol

Front 97

Resistance Phase:
4. Conserve water, salts & loose K+

Back 97

ADH & aldosteron

Front 98

Whats the bad thing about the resistance phase?

Back 98

glucocorticoids are anti-innflamatory & slow healing & increase likely hood of infection

ADH & aldosteron promote high BP-stresses heart

adrenal cortex may no longer be able to synthesize glucocorticoids

Front 99

Exhaustion Phase:

Back 99

breakdown of homeostatic regulation

Direct Renal Effect: as the body's K+ declines, neurons & muscle cells malfunction

Front 100

Lacking these hormones would inhibit skeletal formation

Back 100

GH
Thyroid hormone
PTH
Gonadal hormones

Front 101

Disscuss the relationship btw endocrine system & muscles

Back 101

endocrine hormones adjust muscular metabolism, energy production & growth
regulate Ca & Phosphate levels necessary for muscle function