Final Exam Flashcards

0
Q

What are the three layers of the adrenal cortex?

A

Zona Glomerulosa
Zona Fasciculate
Zona Reticularis

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1
Q

Who created a model for “stress adaptation”?

A

Han Selye

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2
Q

What does the zona glomerulosa produce?

A

Aldosterone- a mineralocorticoid responsible for long term BP

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3
Q

What is the functions of Aldosterone?

A

renal reabsorption of sodium and excretion of hydrogen and potassium ions

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4
Q

What does control of secretion for aldosterone?

A

ACTH- adrenocorticotropic hormone- or corticotropin released by the anterior pituitary
Angiotensin II - most powerful- causes vasoconstriction and subsequent increase in BP

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5
Q

What is the function of the Zona Fasciculate?

A

Primary- metabolism of glucose

secondary- increase metabolism

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6
Q

What is produced in the Zona Reticularis?

A

Androstenedione- precursor to testosterone

Dehydroepiandrosterone (DHEA)

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7
Q

What is the function of the adrenal medulla?

A

Secretes catecholamines (Epinephrine/adrenaline and Norepinephrine/noradrenaline)

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8
Q

What is the chemical class for epinephrine & norepinephrine?

A

mono-amino-acid derivatives

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9
Q

What is the control of secretion for epinephrine & norepinephrine?

A

ACTH, STH, T4, Blood glucose, Blood pressure

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10
Q

What adrenal disorder is derived from hyposecretion of the adrenal gland?
Hypersecretion?

A

Addison’s disease

Cushing’s disease

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11
Q

What is the cause of Addison’s disease?

A

too little Cortisol and Aldosterone

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12
Q

Symptoms of Addison’s disease

A

weight loss, decreased appetite, hyperpigmentation, salt craving, muscle or joint pain, body hair loss or sexual dysfunction

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13
Q

Signs of Addison’s disease

A

darkening areas of skin

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14
Q

What is the function of androgens?

A

libido and a sense of well being in both males and females

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15
Q

What is the cause of Addison’s disease (primary and secondary)?

A

Primary adrenal insufficiency- adrenal cortex is damaged

Secondary adrenal insufficiency- pituitary gland diseased. Corticosteroids used for treatment (tx)- Asthma

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16
Q

What is the cause of Cushing’s disease?

A

too much cortisol

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17
Q

Symptoms of Cushing’s disease

A

thinning of skin, bruising, high BP, puffy face- moon face, buffalo hump (back of neck/shoulders), face puffy and rounded

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18
Q

what is the function of the kidneys?

A

regulates BP (maintain sodium and water)
controls thirst
produce 1,25 dyhydroxyvitamin D3, Erythropoietin, Renin

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19
Q

How is thirst controlled?

A

receptor cells in hypothalamus activate when hypertonic conditions and secrete hormones
blood volume increases pressure in atria activating stretch receptors

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20
Q

What hormones control renal function?

A

ADH, Renin-Angiotensin, Parathyroid Hormone, Aldosterone

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21
Q

Function of anti-diuretic hormone (ADH)?

A

control blood pressure/ blood volume

reabsorption of water directly from renal tubules by acting on epithelial cells of distal renal tubule

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22
Q

Another name for ADH?

A

Vasopressin

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23
Q

Purpose of ADH?

A

Limits water lost in urine by reabsorbing to plasma thus increasing sodium/water concentration in urine

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24
Q

Where is aldosterone made?

A

adrenal gland- zona glomerulosa

it is a mineralocorticoid

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25
Q

What is the most abundant hormone from the zona glomerulosa?

A

aldosterone

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26
Q

What is the function of aldosterone?

A

sodium and water reabsorption

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27
Q

What causes an increase is secretion of aldosterone?

A

blood potassium levels increase

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28
Q

What will an increase in sodium reabsorption cause?

A

an increase of fluid in the blood

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29
Q

What is the acronym for Renin-Angiotensin-Aldosterone System?

A

RAAS

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30
Q

What does RAAS regulate?

A

BP (brings up to normal) and fluid balance

Increase filtration of the glomerular system

31
Q

What does RAAS stimulate?

A

norepinephrine

32
Q

What will stimulate the release of renin?

A

Loss of blood volume/pressure –stimulate–> macula densa to signal juxtoglomerular cells to release renin

33
Q

What does the macula densa monitor?

A

sense decrease in BP = decrease in glomerular filtration rate (GRF)

34
Q

What is a function of the macula densa?

A

osmolarity of plasma

35
Q

Plasma renin (from kidneys) activates what?

A

conversion of Angiotensin (liver) to Angiotensin I

36
Q

Angiotensin I is converted to what?

A

Angiotensin I converted to Angiotensin II by Angiotensin Converting Enzymes (ACE) found in LUNGS

37
Q

What does angiotensin II cause?

A

vasoconstriction

^^^ leads to release of aldosterone (adrenal cortex)

38
Q

What is the order of the Renin-Angiotensin-Aldosterone system (RAAS)?

A

Kidney -> Liver -> Lungs -> Adrenal

39
Q

What is the site of synthesis of the Parathyroid hormone?

A

the parathyroid glands

40
Q

What is the function of the parathyroid hormone?

A

regulate calcium and phosphate

41
Q

What is the site of synthesis of the Atrial Natriuretic Peptide (ANP)?

A

atria of the heart

42
Q

What is the chemical class of ANP?

A

PPP

43
Q

What is the function of Atrial Natriuretic peptide?

A

stimulates renal excretion of sodium (decrease angiotensin II and aldosterone)

44
Q

What is the control of secretion of Atrial Natriuretic Peptide?

A

BP, Blood Volume, Plasma Concentration

45
Q

When is ANP released?

A

when atria expand when increased blood pressure

46
Q

What causes central diabetes insipidus?

A

decreased output of ADH

47
Q

What will be increased with Central Diabetes Insipidus?

A

excessive urine output & thirst

48
Q

Physical characteristics of Central Diabetes Insipidus

A

polyuria (frequency), dilute urine, hypotension (decrease plasma volume), increased plasma concentration

49
Q

Compensations for central diabetes insipidus

A

increased aldosterone secretion, increased renal reabsorption of sodium, excretion of hydrogen and potassium

50
Q

Cause of nephrogenic diabetes insipidus

A

abnormalities in the kidneys
Lithium
High levels of calcium or low potassium can block ADH

51
Q

What happens in nephrogenic diabetes insipidus?

A

decreased sensitivity to ADH which causes an increase in ADH secretion
kidneys fail to respond to ADH and therefore cannot concentrate urine

52
Q

Is the pituitary gland still releasing ADH?

A

Yes but the kidneys do not respond to the signal

53
Q

What is syndrome of inappropriate ADH secretion

A

excessive release of ADH

Fluid overload in patients- strokes, head trauma, brain tumors

54
Q

Hormones associated with the pancreas

A

insulin

glucagon

55
Q

Where is Insulin made? Chemical class?

What is it’s function?

A

Beta cells- Islets of Langerhans
PPP
Decrease blood glucose

56
Q

Where is glucagon made?

Function?

A

alpha cells- islets of Langerhans
Primary- increase blood glucose
Secondary- decrease plasma calcium

57
Q

What is Type 1 Diabetes?

What happens?

A

Insulin Dependent

Antibodies attack pancreas (beta cells)

58
Q

What is type II diabetes?

What happens?

A

Non-Insulin dependent

Body lacks sensitivity to insulin

59
Q

Diabetes complications

A

Coronary heart disease, diabetic retinopothy, retinal detachment, cataracts & glaucoma, kidney damage, nerve damage

60
Q

Another name for Leutinizing hormone and follicle stimulating hormone

A

gonadotropin

61
Q

General function of LH and FSH?

A

stimulate gonads

essential for reproduction

62
Q

Function of LH?

A

secretes sex steroids, testes- testosterone, ovaries - - estrogen by granulosa cells

63
Q

Function of FSH?

A

stimulates maturation of ovarian follicles (female), sperm cell (male)

64
Q

Increase in gonadotropin releasing hormone (GnRH) will cause…

A

increase in LH = increase in sex steroids

65
Q

Low FSH in males can cause?

A

erectile dysfunction, decreased libido, infertility, low energy

66
Q

High FSH can cause?

A

headaches, hormonal deficiencies

67
Q

What is Clomid?

A

most frequently prescribed fertility drug

68
Q

What happens when taking Clomid?

A

Increase in GnRH leads to increase in LH & FSH
Specifically:
1. hypothalamus release GnRH
2. pituitary increase FSH
3. follicle growth produce estrogen
4. maturing oocyte for ovulation (forced ovulation)

69
Q

Side effects of Clomid?

A

headache

70
Q

Where is Gastrin released?

Function?

A

G Cells in Stomach

Increase gastric acid secretion

71
Q

GI Function of Somatostatin?

A

reduces gastrin and stomach acid

72
Q

Function of Grehlin?

A

stimulates appetite

73
Q

Where is Cholecystokinin (CCK) released?

Function?

A
Dudodenum - Jejunum- I Cells
reduces appetite (satiety)
74
Q

Function of Secretin?

A

Dilution & neutralization of stomach acid

75
Q

Function of Motilin?

A

controls peristalsis- movement