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AN SCI 373 > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Short term adjustment for low arterial blood pressure

A
  • Low blood pressure detected by baroreceptors
  • increased sympathetic activity which leads to increased cardiac output and increased vasoconstriction
  • Increased vasoconstriction leads to increased total peripheral resistance
  • Cardiac output and peripheral resistance leads to increased arterial blood pressure
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2
Q

Long term adjustment for low arterial blood pressure

A
  • Low blood pressure detected by baroreceptors
  • Leads to increased sympathetic activity which increases arteriolar vasoconstriction which leads to decreased glomerular capillary blood pressure which leads to decreased GFR which leads to decreased urine volume and conservation of salt and fluid
  • this leads to increased arterial blood pressure
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3
Q

What happens when there is low NaCl, ECF volume and arterial blood pressure

A
  • Detected by the juxtaglomerular apparatus
  • Triggers kidney to release renin
  • Liver continually releases angiotensinogen
  • Renin converts angiotensinogen to angiotensin I
  • The lungs release ACE which converts angiotensin I to angiotensin II
  • Angiotensin II triggers thirst (increases ECF volume), an increase in vasopressin (conserves H2O), arteriolar vasoconstriction (helps bp), and the adrenal medulla to release aldosterone
  • Aldosterone acts on the kidney and promotes Na+ reabsorption (Na+ and Cl- conserved which osmotically holds more H2O in ECF which increases H2O conserved)
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4
Q

ACE2

A
  • vasodilator
  • key enzyme in angiotensin pathway
  • receptor for sars
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5
Q

Aldosterone

A

-Stimulates Na+ absorption
- Increases K+ secretion when K+ is high
- Acts in distal tubule and early collecting duct

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6
Q

Proximal tubule function

A

Mostly reabsorption

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7
Q

Loop of Henle function

A

Establishment of osmotic gradient

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8
Q

Distal tubule function

A

K+ and H+ secretion

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9
Q

Collecting duct function

A

Determination of urine osmolarity

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10
Q

Weak osmoconcentrators

A

cortical nephrons

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11
Q

Strong osmoconcentrator

A
  • Desert dwelling mammals
  • Juxtamedullary nephrons
    -elongated medulla leads to exaggerated vertical osmotic gradient
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12
Q

Regulation mechanism of ECF volume

A

-Maintenance of salt balance
- Aldosterone and Na+ secretion

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13
Q

Regulation mechanism of ECF osmolarity

A
  • ADH (excretion of H2O in urine) and free H2O balance
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14
Q

What occurs when there is a loss of H2O and Na+ during severe diarrhea

A
  • Decreased Plasma volume which leads to decreased venous pressure
  • The decrease in venous pressure will lead to two things
  • A decrease in venous return which decreases end diastolic volume, which leads to decreased stroke volume and cardiac output which decreases arterial pressure which decreases glomerular filtration pressure
  • An increase in sympathetic activity which leads to vasoconstriction of afferent arterioles which causes decreased glomerular filtration pressure
  • Decreased glomerular filtration pressure leads to decreased GFR which leads to less Na+ and H2O secreted
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15
Q

Physiologic role of Aldosterone in restoration of plasma volume

A
  • Decrease plasma volume leads to decrease in venous, atrial and arterial pressures
  • Leads to a decrease in GFR and increase of activity of renal sympathetic nerves (which also leads to decrease in GFR) which leads to an increase in renin secretion due to a decrease in flow to macula densa which leads to an increase in angiotensin II which leads an increase in aldosterone from adrenal cortex which leads to an increase in Na and H2O reabsorption which leads to less Na and H2O excreted
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16
Q

What triggers release of ADH

A

Osmoreceptors detect increase in blood osmolarity in hypothalamus trigger release of ADH from pituitary gland

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17
Q

Where is the ADH receptor located

A

basolateral membrane in epithelial cell in collecting duct

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18
Q

Where are AQP 3 and 4 located

A

basolateral membrane

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19
Q

Where do AQP 2 get inserted

A

Luminal membrane

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20
Q

Effect of alcohol on hypothalamus

A

inhibits ADH secretion

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21
Q

Physiologic reflexes to severe sweating

A

Severe sweating leads to loss of hypoosmotic salt solution which leads to two things: a decrease in plasma volume which leads to a decrease in GFR and an increase in Aldosterone which leads to a decrease in Na+ excretion. Also an increase in plasma osmolarity which leads to thirst and an increase of ADH secretion which leads to less H2O secreted

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22
Q

pH

A

=log(1/[H+])

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23
Q

pH of pure H2O at 25 and 37 degrees C

A

7 and 6.81 respectively

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24
Q

pH of arterial blood

A

7.45

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25
Q

pH of venous blood

A

7.35

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26
Q

pH range compatible with life

A

6.8 to 8

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27
Q

Weak acid vs strong acid

A

strong acids have H+ fully dissociated and weak acids have a small amount of H+ dissociated

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28
Q

Sources of H+ Gain

A

-Generation of H+ from CO2
- Production of nonvolatile acids from metabolism of proteins or other organic molecules
- Loss of bicarbonate in diarrhea
- Loss of bicarbonate in urine

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29
Q

Sources of H+ Loss

A
  • Utilization of H+ in metabolism
  • Loss of H+ during vomiting
  • Loss of H+ in urine
  • Hyperventilation (respiratory alkalosis)
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30
Q

Characteristics of H+ generation

A

-Unceasing
- Highly variable
- Essentially unregulated

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31
Q

Defense against [H+] changes

A
  • Chemical buffer system
  • Respiratory mechanisms (short term regulation)
  • Excretory mechanisms (long term regulation)
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32
Q

Addition of HCl to a buffered solution

A

Leads to less free H+ than an unbuffered solution

33
Q

Main Chemical Buffer Systems in Vertebrates

A
  1. CO2-HCO3- buffer system
  2. Peptide protein buffer system
  3. Hemoglobin buffer system
  4. Phosphate buffer system
34
Q

CO2-HCO3- buffer system

A

Main ECF buffer for non-carbonic acids

35
Q

Peptide protein buffer system

A

Main ICF buffer

36
Q

Hemoglobin buffer system

A

Main erythrocyte (red blood cell) buffer for carbonic acid changes

37
Q

Phosphate buffer system

A

Secondary ICF and primary urinary buffer system

38
Q

Henderson-Hasselback Equation

A

pH = pKa + log[HCO3-]/[CO2]

39
Q

pKa for bicarbonate system

40
Q

Normal ratio of [HCO3-] to [CO2]

41
Q

What happens to pH when CO2 increases and decreases

A

If more CO2, pH will decrease
If less CO2, pH will increase

42
Q

Excretory Regulation of acid-base homeostasis

A
  1. H+ excretion in urine (get rid of acidosis)
  2. HCO3- excretion in urine (get ride of alkalosis)
43
Q

[H+] excretion in urine

A
  • [H+] concentration in plasma is low so filtration rate is low
  • Most H+ in urine is due to H+ secretion in proximal and distal tubules using K+/H+ ATPase or the Na+/H+ cotransporter
44
Q

[HCO3-] excretion in urine

A
  • High HCO3- (20x H+ concentration in plasma)
  • Each secreted H+ leads to one HCO3+ reabsorbed
  • If Acidosis, more H+ secreted and more HCO3- reabsorbed
  • If alkalosis, less H+ secreted and less HCO3- reabsorbed so bicarbonate in urine
45
Q

Excretory response to acidosis

A
  • Increase in H+ secretion and more HCO3- reabsorbed
  • Plasma [H+] decreases
  • Plasma [HCO3-] increases
46
Q

Reabsorption of bicarbonate

A

-H2O and CO2 in peritubular cell undergo carbonic anhydrase and become H2CO3
H2CO3 breaks apart and becomes H+ and HCO3-
-HCO3- is passively transported to interstitial fluid
- H+ is actively transported into the tubular lumen and filtrate (where HCO3- is already located from being filtered by glomerulus)
- H+ and HCO3- combine to make H2CO3 which breaks down into H2O and CO2 which then both diffuse into plasma
- The role of the H+ is to essentially bring back the HCO3- from the filtrate back to the blood

47
Q

Generation of New Bicarbonate with each H+ excretion

A
  • H2O and CO2 in peritubular cell undergo carbonic anhydrase and merge into H2CO3 which breaks down into H+ and HCO3-
  • HCO3- is passively transported into interstitial fluid
  • H+ is actively transported into tubular lumen and filtrate where HPO42- is already present from being filtered
  • H+ and HPO42- merge to become H2PO4- which is excreted in the urine
  • This actively excretes the free H+ ions
48
Q

Renal response to acidosis

A
  • Sufficient H+ secreted to reabsorb all filtered bicarbonate
  • More H+ secreted creating new bicarbonate in plasma and H+ is secreted bound to urinary buffer (HPO42-)
  • Net result: more bicarbonate added to plasma, plasma bicarbonate is increased, compensating for acidosis, urine pH is acidic
49
Q

Renal response to alkalosis

A
  • Rate of H+ secretion is inadequate to reabsorb all filtered bicarbonate so significant amounts of bicarbonate in urine and little excretion of H+ ion on nonbicarbonate urinary buffers
  • Net result: plasma bicarbonate is decreased thereby compensating for alkalosis. Urine pH is alkaline
50
Q

Ovarian cycles of Cows, mares, ewes and sows

A
  • Long estrus cycle ~3 weeks
  • spontaneous estrus and ovulation
  • If pregnant, CL prolonged
51
Q

Humans and primates ovarian cycle

A
  • Long menstrual cycle ~3-4 weeks
  • Spontaneous ovulation
  • If pregnant CL prolonged
52
Q

Ovarian cycle of rats, mice, and hamsters

A
  • Short estrous cycle ~3-5 days
  • Spontaneous ovulation
  • If bred - pseudopregnancy
  • If pregnant CL prolonged
53
Q

Ovulation cycle of rabbit, cat, mink, ferret, alpaca, llama

A
  • Induced ovulation
  • If bred- pseudopregnancy
  • If pregnant - CL prolonged
54
Q

Hypothalamus

A

GnRH- Pulses vs Surge

55
Q

Anterior Pituitary

A

Gonadotropins (LH and FSH)

56
Q

Ovary

A
  • Steroid Hormones (E2 and P4)
57
Q

Hypothalamic - Pituitary -Gonadal Axis

A

-Tonic GnRH Pulse Center in Hypothalamus signals to anterior pituitary to release LH pulses which signal to the dominant follicle to grow (grew from follicle via FSH)
- Dominant follicle becomes preovulatory follicle signals to GnRH surge center in hypothalamus to start a GnRH/LH surgve via E2 Positive feedback
- This surge causes ovulation and the development of the Corpus Luteum which releases progesterone and negatively regulates the Tonic GnRH Pulse Center and estradiol

58
Q

Follicle diameter and days from ovulation

A
  • Right after ovulation, there is a non-dominant follicle wave in which the diameter is low and stays low (~6mm diameter) until menses
  • Menses occurs roughly 14 days after ovulation and the follicle diameter dips than skyrockets until it becomes the ovulatory follicle right before ovulation (~20 mm diameter)
59
Q

CL area and days from ovulation

A
  • At ovulation, CL is high and increases a bit and then starts decreasing as menses approaches ~14 days after ovulation
  • Continues to steadily, yet more slowly decrease until ovulation
60
Q

When does menstruation occur

A

After CL regression (decrease in progesterone and estradiol)

61
Q

E2 concentration and days from ovulation

A

-After ovulation, E2 is somewhat raised from presence or large CL
- Decreases during menses and stays low until it rapidly increases from circulating E2 before ovulation

62
Q

Progesterone and Estradiol concentrations vs days onset of menstration

A

-Both are low during menstruation
- Estradiol has a sharp increase and decrease 14 days after menses (ovulation) and then a more prolonged period of a higher concentration up until the next menstruation
- Progesterone stays low until it starts to increase around 14 days after menstruation (ovulation)

63
Q

FSH and LH vs days onset of menstration

A
  • FSH surge at menstruation, then again 13 days after (during ovulation)
  • LH surge 14 days after menses (ovulation)
64
Q

Follicle size and days onset of menstration

A
  • Day 4: many follicles largest around 8mm
  • Day 13: one follicle is largest ~20 mm
    ovulation occurs
  • Day 21: Many follicles largest ~8 mm, and Large CL ~20 m
  • Day 28: regressed CL ~10mm
65
Q

Progesterone (P4) concentrations in bovine cycle

A
  • Steadily increases after estrus and then sharply decreases before estrus
66
Q

Two follicular waves

A
  • Recruitment, selection and dominance occur twice, but the first time leads to follicle death since there is no ovulation and the second time leads to ovulation
67
Q

Bovine P4 and E2 vs days from onset of estrus

A
  • at Estrus, there is a spike in estradiol
  • At estrus there is low progesterone, after estrus there is a steady increase in progesterone until it sharply decreases
68
Q

Bovine LH and FSH

A
  • At Estrus, there is a spike in LH and FSH
  • Shortly after estrus there is a second spike in FSH and before the next estrus there is a larger spike in FSH
69
Q

Estradiol

A

-Produced by follicle
- Causes estrus, Tone, GnRH/LH surge

70
Q

Progesterone

A
  • Produced by corpus luteum
  • Maintains pregnancy and inhibits estrus and tone
71
Q

Follicle stimulating hormone (FSH)

A
  • Produced by pituitary
  • Causes growth of follicles
72
Q

GnRH

A
  • Produced by Hypothalamus (Brain)
  • Causes LH surge
73
Q

LH (Luteinizing hormone)

A
  • Produced by Pituitary
  • Causes ovulation
74
Q

Prostaglandin

A

-Produced by non-pregnant uterus
- Regresses CL

75
Q

If uterus is removed from cow

A

No CL regression (as opposed to CL regression at 18-19 days)

76
Q

If uterus is removed from woman

A

Regression of CL happens at a similar time

77
Q

Luteolysis in primates

A
  • Does not involve PGF secretion from non-pregnant uterus
  • Involves a loss of adequate LH/PKA stimulation
78
Q

In women, why do follicles only grow large after regression of CL

A
  • The CL produces estradiol and inhibin
79
Q

What causes menstration

A
  • Due to CL regression and decrease in progesterone and estradiol

AN SCI 373 (9 decks)

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