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Physiology Flashcards

1
Q

What is urine?

A

Remaining water and solutes after the kidneys have filtered the blood plasma

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2
Q

What are 3 things that allow urine to move through the ureters to the bladder?
What prevents backflow?

A
  1. Peristaltic waves
  2. Hydrostatic pressure
  3. Gravity

No backflow = physiological sphinter (bladder filling compresses opening)

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3
Q

What is the input to:

  • The prostatic urethra
  • The spongy urethra
A

Prostatic = urine, secretions from prostate containing sperm, and things to neutralize acidity and contribute to sperm motility/viability

Spongy = urine, mucus, things to neutralize acidity

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4
Q

What is the job of the pontine micturition center? Where does it get its input?

A

Job = regulaiton of micturition and relaxation of urethral sphincter

Input = bladder, medial frontal cortex, insular cortex, hypothalamus, periaqueductal gray

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5
Q

Explain the micturition reflex

A
  1. Urine volume exceeds 200-400mL and we sense fullness
  2. We decide that we will allow urination and relax the pelvic floor muscles
  3. Stetch receptors send an AP to the spinal micturition center
  4. The spinal micturition center inhibits motor neuons of the external sphinter and sends a PNS impulse to the urinary bladder and internal sphincter for bladder contraction and sphincter relaxation
  5. Urination occurs.
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6
Q

What is in the fluid the prostate secretes into the prostatic urethra?

A
  1. Semen (30% of total)
  2. Spermatozoa
  3. Seminal vesicle fluid
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7
Q

What is the renal blood flow? (L/min)

A

1.2 L/min

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8
Q

What are 8 main functions of the kidneys?

A
  1. Regulate water and electrolyte balance
  2. Regulate body fluid volume
  3. Regulate blood osmolarity/electrolyte concentration
  4. Regulate blood pH
  5. Regulate arterial blood pressure
  6. Produce hormones (calcitriol, erythropoietin)
  7. Regulate blood glucose
  8. Excrete waste (ammonia, urea, bilirubin) and foreign substances from the body
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9
Q

What are the 3 processes involved in the formation of urine by the nephron? Define each:

A
  1. Glomerular filtraiton = movement of water and most solutes from blood plasma to Bowman’s capusle and renal tubule
  2. Tubular reabsorption = reabsorption of 99% of water/solutes from the renal tubule back into the blood (peritubular capillaries/vasa recta)
  3. Tubular secretion = secretion of wastes, drugs, and excess ions back into the fluid from the blood (peritubular capillaries/vasa recta)
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10
Q
  1. How much fluid is filtered by the renal corpuscle a day?
  2. How much fluid is excreted in urine a day?
  3. What is the glomerular filtration rate in mL/min?
  4. How much blood flows through the kidney in a minute? What % becomes filtrate?
A
  1. 150 L in females and 180 L in men
  2. 1-2 L
  3. 105 mL/min in females and 125 mL/min in men
  4. About 1L/min; About 20%
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11
Q

What is the filtration fraction?

A

The fraction of blood plasma in afferent arterioles that becomes glomerular filtrate (usually 16-20%)

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12
Q

What are 2 ways that filtration prevents proteins from making it into the filtrate?

A
  1. Endothelial cell fenestration size
  2. Negative charge of the basal lamina between capillary endothelium and podocytes
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13
Q

What is able to make it through the podocyte’s slit membrane?

A

Water, glucose, vitamins, amino acids, small plasma proteins, ammonia, urea, and ions

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14
Q

What 3 forces determine what the net filtration pressure will be?

A
  1. Glomerular blood hydrostatic pressure (~55mmHg)
  2. Capsular hydrostatic pressure (~15mmHg)
  3. Blood colloid osmotic pressure (~30mmHg)

NFP = 10mmHg

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15
Q

What are 6 ways the body regulates glomerular filtration rate?

A
  1. Myogenic mechanism = afferent arteriole stretching leads to vasoconstriction of the afferent arteriole (via prostaglandins/decreased NO)
  2. Tubuloglomerular feedback = increased Na/Cl/water delivery in macula densa causes decreased NO release from JGA and thus vasoconstriction
  3. Macula densa = decreased Na/Cl/water delivery in macula densa causes them to release prostaglandins which causes vasodilation of the afferent arteriole
  4. Epinephrine binding to alpha 1 receptors causes afferent arteriole vasoconstriction
  5. Angiotensin II causes vasoconstriction of afferent and efferent arteriole
  6. ANP = stretch of teh atria leads to relaxation of mesangial cells and increased filtration
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16
Q

What part of the nephron has the biggest role in reabsorption?

What solutes are reabsorbed in the nephron?

What are 2 routes of reabsorption?

A

Proximal convoluted tubule

Glucose, amino acids, urea, sodium, potassium, calcium, chloride, bicarbonate, phosphate, small proteins/peptides

Paracellular reabsorption (between cells) or transcellular reabsorption (passive, primary active, secondary active)

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17
Q

What part of the nephron has the biggest role in secretion?

What solutes are secreted in the nephron?

A

Distal tubule and collecting ducts

Creatinine, certain drugs, hydrogen, potassium, ammonium

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18
Q

What does the proximal convoluted tubule reabsorb (and in what percentages?)

What does the proximal convoluted tubule secrete?

A
  1. Water, Na+ and K+ = 65-70%
  2. Glucose and amino acids = 100%
  3. Cl- and urea = 50%
  4. HCO3- = 80-90%
  5. Ca++, Mg++, HPO4- = variable

Secrete = H+, NH4+

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19
Q

Explain the role of sodium in establishing solute movement in the PCT

A

Sodium is pumped into the interstitium via ATPase powered Na+/K+ pump

This creates a concentration gradient that pulls sodium into the cell from the lumen.

Using symporters, this energy also pulls in 2 glucose, amino acids, phosphate, and citrate. It also pulls out Na+

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20
Q

Explain how the proximal convoluted tubule deals with hydrogen and bicarbonate?

A
  1. HCO3- is filtered into the tubule
  2. In the PCT, H+ is secreted into the lumen
  3. H+ and HCO3- join to form H2O and CO2. The H2O is excreted and the CO2 is absorbed. If there is excess H+ it is excreted. If there is excess HCO3- it is excreted
  4. CO2 once in the cell reacts with H2O in the cell to form HCO3- and H+. HCO3- enters the blood while H+ enters the lumen.
  5. Production of HCO3- can also occur when glutamine is metabolized to NH4+ and HCO3-. The NH4+ is excreted and the HCO3- enters the blood
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21
Q
  1. How much of our body’s fluids are ICF vs. ECF?
  2. Of the ECF, how much fluid is interstitial vs. plasma?
  3. Where else is our body’s fluids located?
A
  1. ICF = 2/3, ECF = 1/3
  2. Interstitial = 80% of ECF, plasma = 20% of ECF
  3. Lymph, CSF, synovial fluid, aqueous humor, vitreous body, endolymph, perilymph, pleural fluid, peritoneal fluid, pericardial fluid
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22
Q

What percent of our body is fluid (vs. solid)

A

55% in women and 60% in men

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23
Q

How is water gained in our body versus lost?

A

Gained = drink liquids, eat moist food, aerobic respiration, dehydration synthesis

Lost = kidney excretion, perspiration, sweat, exhalation, feces, menstrual flow

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24
Q

How does our body ativate the thirst center in the hypothalamus?

A
  1. Increased blood osmolarity detected by hypothalamic osmoreceptors
  2. Angiotensin II from kidney’s sensing low BP –> siganls hypothalamus
  3. Baroreceptors in heart/vessels sensing BP –> signals hypothalamus
  4. Decreased salivary flow sensed by neurons in the mouth –> signals hypothalamus
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25
Q

What causes release of ADH from the posterior pituitary?

What is the effect of ADH on water volume?

A

Release:

  • Increased blood osmolarity
  • Decreased blood volume sensed by baroreceptors in left atrium and vessels

Result:

ADH increases aquaporin-2 along collecting duct’s apical membrane which increases water reabsorption

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26
Q

Fill in the following chart on electrolytes:

A
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27
Q

What does the loop of Henle reabsorb (and in what percentages?)

What does the loop of Henle secrete?

A
  1. Water = 15-20%
  2. Na+ and K+ = 20-30%
  3. Cl- = 35%
  4. HCO3- = 10-20%
  5. Ca++ and Mg++ = variable amount

Secretes = H+ and urea

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28
Q

Fill in the following chart concerning the loop of Henle in the nephron:

A
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29
Q

What is the osmolarity of the filtrate as:

  1. It enters the loop of Henle
  2. It reaches the bottom of the descending limb
  3. It reaches the end of the thick ascending limb
A
  1. 300 mOsm/L (isotonic)
  2. 1200 mOsm/L (hypertonic)
  3. 100-150 mOsm/L (hypotonic)
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30
Q

What is countercurrent multiplication?

A

The process by which a progressivley increasing osmotic gradient is formed in the renal medullary interstitium

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31
Q

How do we get angiotensin II in the body?

A
  1. Prorenin in the JG cells is converted to renin in response to a signal
  2. The renin circulates until it reaches the liver
  3. Renin cleaves angiotensinogen into angiotensin I
  4. Angiotensin I circulates until angiotensin-converting enzyme (ACE) in lungs/blood vessels converts it to angiotensin II
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32
Q

What are 7 effects of angiotensin II in the body?

A
  1. Directly increase thirst (hypothalamic center)
  2. Vasoconstriction of systemic blood vessels
  3. Vasoconstriction of renal arterioles (mesangial cell contraction)
  4. Secretion of aldosterone from adrenal cortex (increased Na+ and water reabsorption at the distal tubules; increased K+ excretion at the distal tubules)
  5. Secretion of ADH from posterior pituitary (increased aquaporins at CT causing increased water reabsorption)
  6. Increased Na+/H+ antiporters on apical membrane of PCT causing increased Na+ and water reabsorption
  7. Hypertrophy of renal cells
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33
Q

What 4 body systems are most directly responsible for controlling the body’s blood pressure?

A
  1. Heart
  2. Blood vessel tone (arteries)
  3. Kidneys
  4. Hormones/endocrine/CNS
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34
Q

What does the early distal convoluted tubule absorb (and in what percentages?)

What is it’s main function?

A

5% of filtered Na+

5% of filtered Cl-

10-15% of water (dependent on aldosterone)

Variable amounts of Ca++

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35
Q

What are 3 special characteristics of the (medullary) collecting tubule?

A
  1. Permeability to water is controlled by ADH (reabsorption)
  2. Permeable to urea via urea transporters (reabsorption)
  3. Secretion of H+ ions against a large [C] gradient
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36
Q

What is the normal pH of:

  1. Arterial blood
  2. Venous blood
  3. Interstitial fluid
  4. Intracellular fluid
  5. Urine
  6. Gastric HCl
A
  1. 7.4
  2. 7.35
  3. 7.35
  4. 6.0-7.4
  5. 4.5-8.0
  6. 0.8
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37
Q

What are the body’s 3 main mechanisms for regulation of [H+]/pH? How quickly do they act? How effective are they?

A
  1. Chemical acid-base buffer systems –> immediate; no fix
  2. Respiratory system –> 3-12 minutes; 0.1-0.3 pH alteration
  3. Renal system –> hours to days; powerfully eliminate problem
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38
Q

What are 3 chemical acid-base buffer systems in our body fluids?

A
  1. Bicarbonate bufer =

CO2 + H2O <–CA–> H2CO3 <–> H+ + HCO3-

  1. Phosphate buffer =

HCl + Na2HPO4 <–> NaH2PO4 + NaCl-

NaOH + NaH2PO4 <–> Na2HPO4 + H2O

  1. Protein (for intracellularly)

H+ + Hb <–> H-Hb

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39
Q

What is the role of the PCT in renal acid-base homeostasis?

A
  1. Secretion of H+ (via Na+/H+ antiporter) which neutralizes H2CO3- in lumen, reclaiming bicarbonate and decreasing H+ levels
  2. HCO3- reabsorption (due to the above proess)
  3. Production of HCO3- via glutamine metabolism to 2 NH4+ and 2 HCO3-
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40
Q

What is the role of the thick ascending limb of LOH in renal acid-base homeostasis?

A
  1. Production of HCO3- via glutamine metabolism to 2 NH4+ and 2 HCO3-
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41
Q

What is the role of the (late) DCT and collecting tubules in renal acid-base homeostasis?

A
  1. Secretion of H+ via H+ ATPase or H+/K+ ATPase which neutralizes H2CO3- in lumen, reclaiming bicarbonate and decreasing H+ levels
  2. HCO3- reabsorption (due to the above proess)
  3. Production of HCO3- via glutamine metabolism to 2 NH4+ and 2 HCO3-
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42
Q

What are the 2 buffer systems present in the tubular lumen?

A
  1. Phosphate buffer system = when HCO3- is used up, H+ joins HPO4- becoming H2PO4 which leaves the body
  2. Ammonia buffer system = when HCO3- is used up, H+ joins NH3- becoming NH4+ which is effectively trapped in the lumen
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43
Q

Does an increase or a decrease in the following conditions lead to increased/decreased H+ secretion and HCO3- reabsorption?

A
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44
Q

What is the equation for the anion gap? What is a normal range of values?

A

Na+ - (Cl- + HCO3-)

Normal = 3-12 mmol/L

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45
Q

What is the equation for the urine anionic gap? What is a normal value?

A

UAG = Cl- - Na+ - K+

Normal = negative

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46
Q
  1. How much potassium do we consume a day?
  2. How much intracellular potassium do we normally have?
  3. How much serum potassium do we normally have?
  4. Where is potassium stored in the body?
A
  1. 50-200 mmol/day
  2. 140-150 mmol/L
  3. 3.5-5.0 mmol/L
  4. Red blood cells, muscle, liver, bone
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47
Q

Fill out the following chart regarding regulation of potassium’s concentration in the extracellular fluid:

A
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48
Q

What are the 3 major categories of mechanisms the body uses to regulate K+ serum levels?

A
  1. Cellular buffering
  2. Renal excretion
  3. Fecal excretion
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49
Q

Where is potassium reabsorbed along the nephron and in what percentages?

Where is potassium secreted along the nephron and in what percentages?

A

Absorbed

  • PCT = 65%
  • Thick ascending LOH = 25-30%
  • Late DCT and CT = variable

Secreted

  • Late DCT and CT - 33%
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50
Q

What are the main cells responsible for renal K+ homeostasis?

What happens here with high potassium levels? Low levels?

A

Principal cells in the late DCT and CT

High ECF K+ =

  • Increased activity of Na+/K+ ATPase pump on the principal cells
  • Decreased K+ backflow in the principal cells
  • Increased aldosterone release

Low ECF K+ =

  • Increased H+/K+ ATPase in the intercalated A cells
  • Decreased angiotensin II decreases luminal K+ permeability
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51
Q

What role does potassium play in the body’s:

  1. Cardiac system
  2. Vascular system
  3. GI tract
  4. Kidney
  5. Endocrine system
  6. Muscular system
  7. Skeletal system
  8. Systemically
A
  1. Contraction of the heart
  2. Establishing vascular tone and controlling systemic BP (lowers overall BP)
  3. GI motility
  4. Acid-base homeostasis (increases H+) and urine concentrating
  5. Glucose and insulin metabolism regulation, mineralocorticoid actions
  6. All contraction/relaxation
  7. Bone strength
  8. Fulid and electrolyte balance
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52
Q

What is the filtration fraction?

A

GFR/RPF = fraction of plasma in the glomerular capillary that enters the Bowman’s space. About 1/5

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53
Q

What 3 barriers must fluid pass through in the kidney’s Bowman’s capsule before becoming filtrate?

A
  1. Fenestrations in the glomerular capillary’s endothelium
  2. Negatively charged basement membrane
  3. Slit membranes between negatively charged pedicels of the podocytes
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54
Q

What 3 factors determine GFR?

A
  1. Hydraulic permeability of the capillaries
  2. Surface area of the capillaries
  3. Net filtration pressure
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55
Q

What 3(4) forces determine the net filtration pressure?

What is the average value for the net filtration pressure in the glomerular capsule?

A

Starling forces:

  1. Glomerular capillary hydrostatic pressure
  2. Glomerular capillary oncotic pressure
  3. Bowman’s capsule hydrostatic pressure
    (4. Bowman’s capsule oncotic pressure)

17mmHg

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56
Q

Fill in the following chart:

A
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57
Q

Define pressure natriuresis

A

An increased excretion of salt (and thus water) in response to an increase in blood pressure

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58
Q

What are the 3 ways the renal system auto-regulates urinary excretion volume?

Up to what % decrease in GFR can these mechanisms compensate?

A
  1. Myogenic response
  2. Tubuloglomerular feedback
  3. RAAS

65%

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59
Q

What is a normal serum creatinine?

What is a normal eGFR?

What happens to these values in AKI?

What happens to these values in CKD?

A

Serum creatinine = 74.3-107 uM

eGFR = 90-120 mL/min/1.73m^2

AKI = may not change because it is acute

CKD = creatinine increases, GFR decreases

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60
Q

What is creatinine?

How is creatinine exposed of by the body?

A

An end product of creatine (nitrogenous organc acid used to recycle ATP) metabolism

80-90% is filtered at glomerular capillaries and will never be re-absorbed

10-20% is secreted into the lumen at the PCT

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61
Q

What 3 tubular secretion systems in the kidneys are used for drugs?

A
  1. Organic anion channels
  2. Organic cation channels
  3. Multi-drug efflux pump - p-glycoprotein
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62
Q

What are temporal levels of insulin throughout the day?

A

Basal insulin levels throughout all 24 hours with increases following meals (sugar intake).

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63
Q

Where in the body are the following synthesized:

  1. Estrogens
  2. Progestogens
  3. Androgens
A
  1. Ovaries, placenta, adrenal glands, breasets, liver, fat tissue
  2. Ovaries, adrenal glands, nervous tissue, fat tissue
  3. Testes, ovaries, adrenal glands, liver, fat tissue
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64
Q
  1. What are unique functions of androgens in males?
  2. What are the functions of androgens in both males and females?
  3. What are the 5 androgens?
A
  1. Development of primary male sex organs and secondary sex characteristics, descent of testes, balding, prostate growth
  2. Sebaceous gland activity, acne, libido and sexual arousal, pubic and body hair, axiallary odor, estrogen precursor
  3. Androstenediol, androstenedione, dehydroepiandosterone, dihydrotestosterone, testosterone
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65
Q
  1. What are unique functions of estrogens in females?
  2. What are the functions of estrogens in both males and females?
  3. What are the 4 estrogens?
A
  1. Development of female secondary sex characteristics (breast, hips, fat distribution), libiod and sexual arousal, vaginal lubrication, uterus lining, menstrual cycle
  2. Bone strength, vessel and skin maintenance, metabolism acceleration, protein synthesis, coagulation, fluid/electrolyte/hormone levels, cholesterol homeostasis
  3. Estradiol, Estetrol, Estriol, Estrone
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66
Q
  1. What are the unique functions of progesterone in females?
  2. What are the functions of progesterone in both males and females?
A
  1. Development of secondary sex characteristics (breasts), menstrual cycle, fertilization and pregnancy, lactation, libido
  2. Brain function, hormone production (estrogens, androgens, MCs, GCs), skin maintenance, bone strength, anti-inflammation
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67
Q

What 2 locations are associated with sex steroid “de novo” synthesis and what 2 locations are associated with sex steroid conversion from other sex steroids?

A

De Novo = Adrenal glands and gonads (ovaries and testes)

Conversion = Liver and fat tissue

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68
Q

What is the function of the following enzymes in steroid hormone synthesis?

  1. Cholesterol desmolase
  2. 17-alpha hydroxylase
  3. 17,20-lyase
  4. 3-beta hydroxysteroid dehydrogenase
  5. 17-beta hydroxysteroid dehydrogenase
  6. 21-hydroxylase
  7. 11-beta hydroxylase
  8. 5-alpha reductase
  9. Aromatase
  10. Aldosterone synthase
A
  1. Cholesterol –> pregnenolone
  2. Pregnenolone / progesterone –> 17alpha-OH pregnenolone / progesterone
  3. 17-alphaOHpregnenolone –> dehydroepiandrosterone

17-alphaOHprogesterone –> androstenedione

  1. Pregnenolone –> progesterone

17alpha-OHpregnenolone –> 17alpha-OHprogesterone

Dehydroepiandrosterone –> androstenedione

Androstenediol –> tesosterone

  1. Dehydroepiandrosterone –> androstenediol

Androstenedione –> testosterone

Estrone –> estradiol

  1. Progesterone –> deoxy-corticosterone

17alpha-OHprogesterone –> 11-deoxycortisol

  1. Deoxy-corticosterone –> corticosterone

11-deoxycortisol –> cortisol

  1. Testosterone –> dihydrotestosterone
  2. Androstenedione –> Estrone

Testosterone –> Estradiol

  1. Corticosterone –> alodsterone
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69
Q
  1. What weeks in embryogenesis does non-sexually differentiated gonad development occur?
  2. At what week does sexual differentiation begin to occur in the embryo?
  3. At what week does phenotypical differentiation of external genital glands occur?
A
  1. Week 5 and 6
  2. Week 7
  3. Week 12
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70
Q

What does SRY stand for and what is its role in sexual differentiation?

A

SRY = Sex-determining region of chromosome Y

Codes for testis-determining factor which initiates formation of testes from the gonads

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71
Q

Describe the sexual differentiation of gonads into hormone secreting testes?

A
  1. Primitive sex cords mature in medullary cords that grow longer, carrying PGCs deeper into the mesoderm
  2. The surface epithelial layer thins out and forms the tunica albuginea
  3. The medullary cords develop into straight tubules, seminiferuos tubules, and rete testis
  4. The PGCs settle in the seminferous tubules and lie dormant (until puberty)
  5. Cells in the walls of the seminiferous tubules differentiate into sertoli cells that secrete anti-mullerian hormone
  6. Cells lying between the seminiferous tubules differentiate into Leydig cells that secrete testosterone
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72
Q

Describe the sexual differentiation of gonads into follicle-containing ovaries

A
  1. No SRY means that no TDF is created
  2. The primitive sex cords extending towards the center of the gonad degenerate
  3. The surface epithelium proliferates and forms cortical cords that project up to the origin of the primitive sex cords
  4. Cortical cords re-arrange to form nests of follicular cells (theca and granulosa) that surround the PGCs
  5. The PGC within the differentiated follicular cells differentiates into an immature oocyte
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73
Q

What are the two nephrogenic cords before sexual differentiation?

Which gives rise to male and which gives rise to female ducts?

Where do they originate from?

A
  1. Wolffian / Mesonephric Duct –> male
  2. Mullerian / Paramesonephric Duct –> female

Intermediate mesoderm

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74
Q

How do gonads develop prior to sexual differentiation?

A
  1. Endoderm cells in the yolk sac differentiate into primordial germ cells
  2. PGCs migrate down the vitelline duct and into the primitive duct
  3. From the primitive duct they travel into the dorsal mesentery until they reach the genital ridge
  4. PGC settle in the epithelial layer of the genital ridge, sending out chemical signals to the cells there
  5. These signals make the cells of the genital ridge self-generate into gonads
  6. The epithelial layer of teh gonad forms primitive sex cords penetrating into the mesodermal layer of the gonad
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75
Q

How does the male genital duct system develop?

A
  1. Mullerian inhibitin factor (anti-mullerian hormone) causes the Mullerian ducts to degenerate into the appendix testes
  2. Testosterone causes the Wollfian ducts to grow long under the influence of testosterone
  3. The Wollfian ducts differentiate into the efferent ductulres, intratesticular straight tubules, epididymis, vas deferens, seminal glands, and ejaculatory ducts
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76
Q

How does the female genital duct system develop?

A
  1. Lack of anti-Mullerian hormone allows the Mullerian duct to remain
  2. Lack of testosterone causes the Wollfian ducts to degenerate
  3. The upper regions of the Mullerian ducts form the fallopian tubes
  4. The lower regions of the Mullerian ducts form the uterus, cervix, and upper 1/3 of the vagina
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77
Q

Describe the external genitalia prior to sexual differentiation?

A
  1. Opening = urogenital sinus
  2. Symmetrical folds around the opening = urethral folds
  3. Symmetrical folds around the urethral folds = labioscrotal swellings
  4. Small tissue above opening = genital tubercle –> primordial phallus
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78
Q

How does the male external genitalia develop?

A
  1. Testosterone levels are secreted from Leydig cells
  2. 5-alpha reductase, present in the perineal skin, converts this testosterone into DHT
  3. DHT causes the phallus to enlarge and causes the urethral folds to zip up over it, trapping the elongating urogenital sinus inside
  4. DHT causes the genital tubercle to become the glans penis and the labioscrotal swellings to fuse into the scrotum
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79
Q

How does the female external genitalia develop?

A
  1. Lack of testes –> lack of Leydig cells –> lack of testosterone –> lack of DHT
  2. The urovaginal septum forms creating a separate urethra and bottom 1/3 of the vagina
  3. The urethral folds remain unfused and form the labia minora
  4. The genital tubercle shrinks and becomes the clitoris
  5. The labioscrotal swellings are fused only anteriorly, forming the labia majora
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80
Q

What is the gubernaculum and what is its job?

A

A fibrous cord connecting the gonads to the labioscrotal swellings

The gubernaculum pulls the testes down into the scrotum and the ovaries down towards the uterus

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81
Q

Describe gonadal descent in males

A
  1. The gubernaculum begins to shorten, pulling the testes down along the posterior of the abdominal cavity
  2. The abdominal cavity creates an outpouching into the scrotum, called the processus vaginalis
  3. The testes are pulled down the processus vaginalis into the scrotum
  4. The vas deferens and testicular artery/vein are pulled along, forming the spermatic cord
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82
Q

Describe gonadal descent in females

A
  1. The gubernaculum begins to shorten, pulling the ovaries downward
  2. The gubernaculum then attaches at its middle to the uterus, forming a superior and inferior portion
  3. The inferior portion becomes the round ligament, anchoring the uterus to the labia majora
  4. The superior portion becomes the ovarian ligament, anchoring the ovaries above and beside the uterus, near the fallopian tubes
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83
Q

What is the role of testosterone in the following:

A
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84
Q

What are 3 exogenous signals that increase GnRH release?

What are 4 exogenous signals that decreased GnRH release?

A

Increase = leptin, glutamate, kisspeptin

Decrease = GABA, dopamine, beta-endorphins, grehlin

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85
Q

What is puberty?

What are the normal ages of puberty in boys and girls?

What is happening physiologically to “cause” puberty?

A

Puberty is the process of physical changes allowing a child’s body to mature and become capable of sexual production

Girls = 8-13; Boys = 9-14

Baseline GnRH becomes nocturnal pulsatile release and finally increases to a continuous pulsatile level throughout the day. GnRH receptors also become more sensastive. This leads to increased LH and FSH (with LH>FSH)

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86
Q

What is adrenarche? What is happening physiologically during it?

A

Early sexual maturation starting before puberty

The zona reticularis of the adrenal gland develops causing increased androgen secretion (DHEA, DHEAS).

This can cause development of pubic hair, body odor, skin oiliness, and acne (but not sexual reproductive abilities)

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87
Q

Fill in the following chart for how LH and FSH affect males and females reproductive cells

A
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88
Q

During puberty what happens to female primary sex characteristics? (5)

A
  1. Keratinization of perineal skin for infection resistance
  2. Thicker multi-layered vaginal mucosa with superficial squamous cells
  3. Increased glycogen content in the vaginal epithlium to help with vaginal pH regulation
  4. Increased size of uterus, ovaries, and follicles
  5. Menstruation
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89
Q

During puberty what happens to female secondary sex characteristics? (9)

A
  1. Widening of lowerhalf of pelvis and hips to prepare a birth canal
  2. Increased stature
  3. Increased fat tissue and distribution to breasts, hips, butts, thighs, upper arms, pubis
  4. Body odor
  5. Increased oil from skin and acne
  6. Growth and darkening of the labia minora and majora
  7. Development of pubic and axiallary hair
  8. Breast and nipple development
  9. Clitoral enlargement
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90
Q

During puberty what happens to male primary sex characteristics? (7)

A
  1. Testicular enlargement
  2. Increased length and shaft of penis
  3. Glans penis enlargement
  4. Growth of seminiferous tubules
  5. Maturation of sperm
  6. Erections (spontaneous and explained)
  7. Foreskin retraction
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91
Q

During puberty what happens to male secondary sex characteristics? (9)

A
  1. Increased skeletal muscle (lean muscle)
  2. Widening of the shoulders and jaw
  3. Increased stature
  4. Fat pads of the male breat tissue and nipples develop
  5. Body odor
  6. Increased oil from skin and acne
  7. Development of pubic and axillary hair
  8. Devlopment of other body and facial hair
  9. Voice lowering and increased size of Adam’s apple
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92
Q

What things are scaled via Tanner staging in:

  1. Boys
  2. Girls
A
  1. Testicular volume, penis size, scrotum presentation, pubic hair
  2. Breat development, pubic hair
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93
Q

What are the ages and associated changes of Tanner stages 1-5 in males?

A
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94
Q

What are the ages and associated changes of Tanner stages 1-5 in females?

95
Q

What are the ages and associated stages of Tanner stages 1-5 for pubic hair in males and females?

96
Q

What is thelarche?

A

The onset of secondary breast development

97
Q

Please list the 3 types of estrogens.

  1. What is the principal estrogen secreted by the ovaries?
  2. Which is the principal estrogen in pregnancy?
  3. Which one is mostly derived in the liver?
  4. Which one is mostly derived in peripheral tissues?
A

Beta-estradiol, estrone, estriol

  1. Beta-estradiol
  2. Estriol
  3. Estriol
  4. Estrone
98
Q

What are 5 organs that produce estrogen?

Which produces the majority of estrogen? (non-pregnancy)

A
  1. Ovaries
  2. Adfrenal cortex
  3. Fat cells
  4. Bone
  5. Placenta

Majority = ovaries

99
Q

What is a basic overview of the synthesis of estrogens?

A
  1. Cholesterol –> pregnenolone
  2. Pregnenolone –> progesterone
  3. Progesterone –> androstenedione and testosterone
  4. Androstenedione and testosterone –> estrogens via aromatase
100
Q

How is estrogen carried throughout the blood?

A

Bound to plasma albumin and specific estrogen-binding globulins such as SHBG

(Bound loosely –> rapid release)

101
Q

What are 4 functions of estrogen during the first 14 days of the menstrual cycle?

A
  1. Thickening of the endometrium and formation of its progesterone receptors
  2. Growth of the follicles
  3. Negative feedback to the AP to decrease FSH (and thus select a dominant follicle)
  4. Positive feedback to the AP to increase LH and FSH (and thus lead to ovulation)
102
Q

What are 8 local effects of estrogen on the primary and secondary sex organs in females?

A
  1. Enlargement of the internal genitalia (ovaries, fallopian tubes, uterus, vagina)
  2. Enlargement of the external genitalia
  3. Conversion of vaginal epithelium from cuboidal to stratified
  4. Proliferation of glandular tissue in the fallopian tubes
  5. Increased ciliated epithelial cells lining fallopian tubes and increased cilial activity
  6. Widening of the hips
  7. Growth of the breasts and their ductile system
  8. Fat distribution to buttocks, hips, thighs, and breasts
103
Q

What are 10 systemic effects of estrogen on the body?

A
  1. Protecting the CV system (blood vessel wall flexibility and decreased LDL)
  2. Sustained bone density (inhibited osteoclasts, increased OPG)
  3. Epiphyseal closure
  4. Increase in total body protein
  5. Increasd whole-body metabolic rate
  6. Increased fat deposition in subcutaneous tissue
  7. Softening and thickening of skin with increased vasculature
  8. (Slight) water and sodium retention
  9. Increased libido
  10. Neuroprotective effect for memory
104
Q

What are the three types of estrogen receptors?

A
  1. Nuclear estrogen receptor alpha
  2. Nuclear estrogen receptor beta
  3. Membrane estrogen receptors
105
Q

What is perimenopause?

A

1-2 years prior to menopause; remaining follicles have decreased sensitivity to LH and FSH leading to oligomenorrhea (or menorrhagia) and some early menopausal symptoms

106
Q

What is menopause?

How is it diagnosed?

When does it usually occur?

A

A natural halting of the menstrual cycle due to a lack of ovarian follicles and an accompanying drop in estrogen levels

Diagnosed by amenorrhea for 1 year

Usually occurs around age 50

107
Q

How does menopause occur?

A
  1. As we mature, we cycle through ovarian follicles, expelling or degenerating most of our follicles
  2. The remaining follicles in perimenopausal have weaker receptors and fewer attempt to become dominant with each cycle
  3. This leads to decreased estrogen/progesterone and increased LH/FSH –> oligomenorrhea
  4. Eventually no more follicles are left (that will respond to LH/FSH) and the menstrual cycle stops altogether
  5. Over time, hormone levels return to normal
108
Q

What causes the symptoms of menopause?

List 15 symptoms of menopause

A

Cause = erratic hormone levels and overall decreased estrogen

  1. Hot flashes and night sweats –> trouble sleeping
  2. Vaginal atrophy/dryness –> discomfort, itching, dyspareunia, bleeding after sex
  3. Decreased libido
  4. Altered vaginal pH and flora –> frequent UTIs
  5. Increased urinating urgency/frequency/dysuria/incontinence
  6. Fatigue
  7. Memory loss
  8. Irritability and mood swings
  9. New onset depression, anxiety, and/or OCD
  10. Weight gain and bloating
  11. Mastodynia
  12. Headaches
  13. Joint pain
  14. CV disease from decreased protection
  15. Osteoporosis / decreased strength from decreased bone density
109
Q

Fill in the following chart regarding management options for women experiencing symptoms of menopause:

110
Q

During menopause, what would you expect for:

  1. Estrogen levels
  2. Inhibin levels
  3. FSH and LH levels
  4. Ovarian U/S
A
  1. Decreased
  2. Decreased
  3. Elevated (more FSH than LH)
  4. No follicles
111
Q

The X chromosome:

  1. What % of the human genome is located on the X chromosome?
  2. What % of human protein coding genes are located on the X chromosome?
  3. What % of Mendelian diseases are X-linked?
112
Q

What are pseudoautosomal regions (PARs)? What is their function? (3)

A

Areas of homology between X and Y chromosomes

  1. These allow X and Y to pair up in meiosis and undergo cross-over
  2. These allow daughter cells to inherit allele’s on a father’s Y chromosome or a son to inherit allele’s from both his mother’s X chromosomes
  3. These allow for double dosing of important hormones in both males and females
113
Q

Give 4 examples of more prevalent X-linked diseases and describe what happens:

A
  1. Klinefelter = XXY male; interferes with male sexual development causing tall stature, lowered IQ, and reduced fertility
  2. Trisomy X = XXX female; taller stature and lower IQ but normal fertility
  3. Turner syndrome = XO female; missing X chromosome causing short stature and infertility
  4. XX male syndrome = XX males; SRY region of the Y chromosome is translocated to an X chromosome
115
Q

What is X-inactivation?

A

The process of inactivating one of the two X chromosomes in females via packaging it into heterochromatin

116
Q

Describe the general process of X-inactivation.

A
  1. Initial X-inactivation of the mother is reversed in the inner mass cells so that both express weak levels of Xist and Tsix (RNA strands)
  2. At the early blastocyst stage (100 cells), the X(active) continues to express only Tsix while the X(silent) continues to express only Xist (this is a random process occurring separately in each cell)
  3. Tsix acts as a limiting block factor on its X(active) while Xist RNA coats its entire X(silent)
  4. This leads to high DNA methylation and low histone acetylation –> heterochromatin (Barr Body)
  5. All daughter cells will carry the X-inactivation of their parent cell
117
Q

What percent of genes will escape X-inactivation?

118
Q
  1. How many follicles are present at birth?
  2. How many follicles are present at the time of puberty?
  3. How many follicles will end up becoming mature?
A
  1. 200,000 to 2,000,000
  2. 40,000
  3. 400
119
Q

What is the average length of the menstrual cycle?

What are the 2 ovarian phases and what is their average length?

What days do menstruation take place on?

A

28 days

Follicular phase = day 1-14

Luteal phase = day 15-28

Menstruation = 1-4/7

120
Q

Understand the menstrual cycle.

A

Formation of a new layer of endometrium with associated growth of spiral arteries/uterine glands and production of fertile cervical mucus

Corresponds to day 4-14

121
Q

What are the 3 endometrial phases of the menstrual cycle and what days do they correspond to?

A
  1. Menstrual phase = day 1-4
  2. Follicular phase = day 4-14
  3. Secretory phase = day 14-28
122
Q

What is meisosis and what does it result in?

A

Division of a diploid eukaryotic cell into 4 haploid and genetically different daughter cells

123
Q

Describe what happens in interphase, meiosis I, interkinesis, and meiosis II

A

Interphase = replication of all DNA to form sister chromatids; production of proteins/enzymes needed for replicaiton

Meiosis 1 = chromosomes condense and cross over with homologous chromosomes; homologous chromosomes line up and separate to opposite poles; cytoplasm divids

Interkinesis = nucleur membrane forms to create two haploid cells with sister chromatids

Meiosis 2 = chromosomes condense and line up; sister chromatids separate; cytoplasm divides to form 4 haploid cells

124
Q

What is mitois and what does it result in?

A

The division of a eukaryotic cell into two identical diploid daughter cells

125
Q

Describe what happens in interphase, mitosis, and cytokinesis?

A

Interphase = replication of all DNA to form sister chromatids; production of proteins/enzymes needed for replicaiton

Mitosis = chromosomes condense and line up; sister chromatids separate and move to opposite sides

Cytokinesis = cytoplasm/organelles divide; membrane forms around two separate cells

126
Q

What are the 6 organs of the female reproductive system?

What are the 4 organs of the male reproductive system?

A

Female:

  1. Ovaries
  2. Fallopian/uterine tubes
  3. Uterus
  4. Vagina
  5. Vulva (pudnedum)
  6. Mammary glands

Male:

  1. Testes
  2. Ductal system (epididymis, vas deferens, ejacultory ducts, urethra)
  3. Accessory sex glands (seminal vesicles, prostate, bulbourethral glands)
  4. Supporting structures (scrotum, peni)
127
Q

What are the 2 main functions of the ovaries?

A
  1. Produce gametes (secondary oocytes)
  2. Produce hormones (progesterone, estrogens, inhibin, relaxin)
128
Q

What are the 2 main functions of the fallopian tubes?

A
  1. Location for fertilization
  2. Route for sperm to reach ovum and ovum to reach uterus
129
Q

What are 5 functions of the uterus?

A
  1. Route for sperm to reach ovum
  2. Implantation of fertilized ovum
  3. Location for fetal development
  4. Contractions during labor
  5. Production of cervical mucus to impede or help sperm
130
Q

What are 3 functions of the vagina?

A
  1. Receptacel for penis during sex
  2. Outlet for menstrual flow
  3. Passageway for childbirth
131
Q

What are 2 functions of the scrotum?

A
  1. Hold the testes
  2. Move the testes closer or further from the body to regulate their temperature
132
Q

What are 2 functions of the testes?

A
  1. Produce sperm
  2. Produce testosterone
133
Q

What are 3 functions of the epididymis?

A
  1. Location for sperm maturation
  2. Helps propel sperm into vas deferens during sexual arousal (peristaltic contraction)
  3. Stores sperm for up to several months
134
Q

What are 2 functions of the vas deferens?

A
  1. Helps move sperm from epididymis to urethra (peristaltic contractions)
  2. Stores sperm for up to several months
135
Q

What is 1 function of the ejaculatory ducts?

A
  1. Carry sperm/seminal vesicle secretions into the urethra
136
Q

What is the function of the seminal vesicel?

A

Create alkaline fluid containing fructose (energy for sperm), prostaglandins (sperm motility and viability, female tract contraction), and clotting factors (coagulate semen) that can neutralize the female tract’s acidity

137
Q

What is the function of the prostate?

A

Produce milkly acidic fluid containing citric acid (energy for sperm), proteolytic enzymes (break down clotting proteins), acid phsophatase, and seminal plasmin (antibiotic)

138
Q

What are 2 functions of the bulbourethral glands (Cowper’s glands)?

A
  1. Secrete alkaline fluid into urethra during sexual arousal to neutralize any acids from urine
  2. Secrete mucus to lubricate the end of the penis and urethral lining
139
Q

What is the function of the penis?

A

Passageway for ejaculation of semen and excretion of urine

140
Q

What is the blood-testis barrier and what is its function?

A

Tight junctions between Sertoli cells of the seminiferous tubules of the testes

Separates sperm from blood to avoid an immune response

141
Q

When spermatogenesis begin and end?

When does oogenesis begin and end?

A

Spermatogenesis = early puberty –> death

Oogenesis = fetus –> age ~50

142
Q

Describe the process of spermatogenesis.

A
  1. Spermatogonia (stem cells) in seminiferous tubules undergo mitosis to increase numbers
  2. At puberty, spermatogonia move through sertoli cells, differentiating into primary spermatocytes as they move
  3. Primary spermatocytes undergo meiosis I becoming secondary spermatocytes
  4. Secondary spermatocytes undergo meiosis II becoming spermatid
  5. Spermatid mature into sperm (spermiogenesis) as they near the lumen
  6. Sperm release from their connections to Sertoli cells (spermiation) and enter the lumen
143
Q

What happens to spermatid for it to mature into sperm during spermiogenesis?

A
  1. Elongation
  2. Acrosome formation atop the nucleus
  3. Condenstion and elongation of nucleus
  4. Development of flagellum
  5. Multiplication of mitochondira
  6. Excess cytoplasm sloughed off and disposed by Sertoli cells
144
Q

Label the following image of sperm:

145
Q

How do spermatogonia/oogonia form?

A
  1. Primoridal germ cells migrate from yolk sac to urogenital ridge
  2. PGC migrate from urogenital ridge into embryonic gonad
  3. PGCs differentiate into gonocytes
  4. Gonocytes differentiate into spermatogonia
146
Q

Describe the process of oogenesis.

A
  1. Oogonia undergo mitosis to produce millions of themselves
  2. Most degenerate as the fetus develops but 2 hundred thousand to 2 million differentiate into primary oocytes surrounded by follicular cells (primordial follicle)
  3. Primary oocytes enter meiosis I and arrest in prophase I
  4. During puberty to menopause, primordial follicles are selected to grow into primary follicles and then secondary follicles and then graafian follicles
  5. As the follicle matures, the primary oocyte finishes meiosis I and becomes a secondary oocyte and first polar body
  6. The secondary oocyte begins meiosis II and arrests in metaphase
  7. Ovulation and fertilization occur
  8. A fertilized secondary oocyte finishes meosis II becoming a second polar body and ovum.
147
Q
  1. What happens for a primordial follicle to become a primary follicle?
  2. What happens for a pimary follicle to become a secondary follicle?
  3. What happens for a secondary follicle to become a graavian/mature follicle?
A
  1. Zona pellucida forms, follicular cells become granulosa cells, thecal cells form
  2. Thecal cells become interna (estrogens) and externa; antrum forms with follicular fluid; innermost granulosa attach to zona pellucida becoming corona radiata
  3. Grows larger
148
Q

Compare oogenesis and spermatogenesis:

149
Q

What is emission?

A

Discharge of a small volume of semen before ejaculation, due to peristaltic contractions in epididymis, vas deferens, seminal vesicles, ejaculatory ducts, and prostate

Functions to propel semen into the spongy urethra prior to ejaculation

150
Q

Define the embryonic vs. fetal period of development.

A

Embryonic = fertilization –> week 8

Fetal period = week 9 –> birth

151
Q

Define fertilization. Where in the female reproductive tract does this take place?

A

The process leading to fusion of the genetic material from a haploid sperm cell and a haploid secondary oocyte into a single diploid nucleus.

Takes place (usually) in the ampulla of one of the fallopian tubes.

Includes sperm entrance, sperm capacitation, egg penetration, membrane fusion, and syngamy

152
Q

What forces help sperm reach oocytes?

A
  1. Sperm’s beating flagella
  2. Semen’s prostaglandin stimulating uterine/fallopian tube contractions.
  3. Oxytocin from female orgasm stimulating uterine/fallopian tube contractions
153
Q

What is capacitation?

A

Physical and functional changes to the sperm within the female tract preparing it for fertilization of a secondary oocyte.

  • Sperm’s tail beats more vigorously
  • Sperm’s plasma membrane changes to prepare for fusion
  • Sperm gains the ability to respond to chemical factors
154
Q

How does the sperm penetrate:

  1. The corona radiata?
  2. The zona pellucida?
A
  1. Enzymes from the acrosome; strong tail movement
  2. ZP binds sperm –> triggers acrosomal reaction –> released acrosomal enzymes that digest a path; strong tail movement
155
Q

Define syngamy.

A

The actual fusion of the male pronucleus and female pronucleus into a single diploid nucleus.

At this point the fertilized ovum is a zygote.

156
Q

What are 2 mechanisms in place to avoid polyspermy?

A
  1. Fast block = depolarization of oocyte membrane when sperm’s membrane fuses
  2. Slow block = exocytosis molecules from depolarization hardens the ZP to other sperm.
157
Q
  1. Sperm need ___ hours once inside the vagina before they can penetrate the oocyte?
  2. Sperm can survive up to ___ hours once they enter the vagina?
  3. Oocytes can survive up to ___ after ovulation?
  4. Fertilization usually occurs ___ hours after fertilization?
A
  1. 7
  2. 48
  3. 24
  4. 12-24
158
Q

Define zygote vs. morula vs. blastocyst? At what times are each in existence?

A

Zygote = fusion of the sperm and egg –> morula = Day 1-4

Morula = solid sphere of 8-64 cells entering the uterine cavity = Formed by day 4/5

Blastocyst = 100s of cells with outer trophoblast cells, inner embryoblast cells, and a fluid filled blastocoel cavity = formed by day 5/6

159
Q

What is uterine milk and what is it used for?

A

A glycogen rich secretion from the endometrium

Used to nourish the morula cells at about the 32 cell stage.

160
Q

What is compaction mean in reference to blasotcyt formation?

A

The original zygote becomes hundreds of cells without changing the overall size

This occurs because the blastomeres (cells) become progressively smaller and align tightly together.

161
Q

What do the trophoblast cells of the blastocyst develop into?

What do the embryoblast cells of the blastocyst develop into?

A

Trophoblast = outer chorionic sac, fetal portion of the placenta

Embryoblast = embryo/fetus

162
Q

What is the implantation window

A

A 4 day time period, about 7-9 days post ovulation, when the endometrium is ready to receive an implanting blastocyst.

163
Q

What changes occur during pre-decidualization that allow blastocyst implantation? (3)

A
  1. Proliferation of the endometrium
  2. Production of decidual cells
  3. Vascularization and increased gland secretion in the endometrium
164
Q

Desceribe the process of implantation

A
  1. The uterine cavity swells, moving the blastocyst close to the wall
  2. The blastocyst loosely attaches to the endometrium at day 6 with the ICM facing the endometrium
  3. The blastocyst firmly attaches to the endometrium at day 7 via integrin
  4. The blastocyst’s trophoblast cells secrete enzymes to digest the endometrium, allowing it to burrow INTO the endometrium until it is completely surrounded
165
Q

What is the decidua?

A

The endometrium post-implantation

166
Q

What are the 3 separate regions of decidua called? What is each of their functions?

A
  1. Decdiua basalis = endometrium surrounding the implanted side of the embryo = becomes maternal placenta and provides glycogen/lipids to embryo/fetus
  2. Decidua capsularis = endometrium covering the lumen-facing side of the embryo = encloses embryo IN the endometrium
  3. Decidua parietalis = endometium lining the non-invovled areas of the uterus = fuses with decidua capsularis so that there is no empty uterine spae
168
Q

What are 4 (general) functions of the placenta?

A
  1. Fetal-maternal blood communication (nutrients, temperature, waste, gas)
  2. Fights against intenal infection
  3. Produces hormones that support pregnancy
  4. Metabolizes certain substances and releases end-products
169
Q

What maternal tissue develops into placenta?

What fetal tissue develops into placenta?

A

Maternal = decidua basalis (endometrium)

Fetal = chorion frondosum (trophoblasts)

170
Q

Describe the formation of the placenta.

A
  1. Trophoblastic cells differentiate into inner (single-cell layer) cytotrophoblasts and outer (thick layer) syncytiotrophoblasts
  2. Cytotrophoblasts proliferate and migrate into the syncytiotrophoblast layer. They lose their cell membranes and form a multi-nucleated mass
  3. Syncytiotrophoblasts send out projections for firm embedding
  4. Spaces form within the syncytiotrophoblast layer
  5. Cytotrophoblasts release enzymes to degrade endometrium. The spaces thus are filled with maternal blood and endometrial glandular secretions.
  6. Blood filled spaces fuse
  7. Cytotrophoblasts grow projections that penetrate into the syncytiotrophoblast layer –> primary chorionic villi
  8. Extra-embryonic mesoderm grows into these villi –> secondary chorionic villi
  9. Embryonic blood vessels form, branching into the villi –> tertiary chorionic villi
  10. Cytotrophoblasts grow completely through the syncytiotrophoblast layer to form a cytotrophoblastic shell
  11. Capillary networks form at the terminal ends of the now branched chorionic villi
171
Q

Fill in the following charts:

172
Q

What are 2 ways that oxygen transport from maternal to fetal blood is enhanced?

What are 2 ways that CO2 transport from fetal to maternal blood is enhanced?

A

Oxygen:

  1. Double Hb [C] in fetal blood
  2. Fetal hemoglobin has greater affinity to oxygen

CO2:

  1. Decreased CO2 in maternal blood from altered respiratory center
  2. Decreased CO2 in maternal blood from decreased tidal volume
173
Q

What fetal waste diffuses easily through the placenta and what doesn’t diffuse easily?

A

Easy = urea/uric acid

Difficult = creatinine

174
Q

What is the luteal placental shift and when does it take place? What triggers it?

A

The shift from the corpus luteum producing hCG/estrogen/progeterone to the placenta producing these hormones

Happens between week 13 and 17

Triggered by decreasing hCG levels from syncytiotrophoblasts

175
Q

What are 6 hormones produced by the placenta?

A
  1. Human chorionic gonadotropin
  2. Estrogens
  3. Progesterone
  4. Human placental lactogen (aka hCS = somatomammotropin)
  5. Relaxin
  6. CRH
176
Q

What is the function of hCG from the placenta? (4)

A
  1. Prevents corpus luteum involution up until the luteal-placental shift takes place
  2. Causes stimulation of Leydig cells to produce testoterone so that a male fetus’ testes can descend
  3. Increases maternal thyroxine production
  4. Signals the release of relaxin from ovaries and placenta
177
Q

What is the function of estrogens from the placenta? (6)

A
  1. Enlargement of the uterus
  2. Enlargerment of the mother’s breasts and growth of the breast ductal structure
  3. Enlargement of the mother’s external genitalia
  4. Relaxation of the pelvic ligaments (sacroiliac joints, symphysis pubis)
  5. Cellular reproduction in growing early embryo
  6. Inhibits release of LH and fSH from mother’s pituitary
178
Q

What is the function of progesterone from the placenta? (4)

A
  1. Development of decidual cells in the uterine endometrium –> nutrition
  2. Decreased contractility of uterus to prevent abortion
  3. Helps prepare breasts for lactation
  4. Inhibits release of LH and FSH from mother’s pituitary
179
Q

What is the function of human placental lactogen from the placenta? (4)

A
  1. Partial development of breasts
  2. Formation of protein tissues
  3. Decreased insulin sensitivity and glucose use in the mother, increases maternal blood glucose levels
  4. Promotes release of FFA from mother’s fat stores for an alternative maternal energy source
180
Q

What is the function of relaxin from the placenta? (2)

A
  1. Weak relaxation of ligaments of symphysis pubis
  2. Softening of the cervix at time of delivery
181
Q

What is the function of CRH from the placenta?

A

Turns on the fetal pituitary production of ACTH which then stimulates the adrenal glands to make DHEAS and cortisol

(Some goes to mother)

182
Q

Know this image:

183
Q

What are 5 different categories of contraceptives?

A
  1. Natural
  2. Barrier
  3. Intrauterine device
  4. Hormonal
  5. Emergency
184
Q

What are 3 examples of natural contraceptives? Pros and Cons of each?

A
  1. Periodic abstinence using ovulation assessment methods
    - Pro = religious reasons
    - Con = motivation, requires regular cycles
  2. Coitus interruptus
    - Pro = religious reasons
    - Con = self-control
  3. Lactational amenorrhea (prolactin-induced GnRH inhibition)
    - Pro = religious reasons
    - Con = can only use for 6 months
185
Q

What are 5 examples of barrier contraceptions? Pros and Cons of each?

A
  1. Male condoms
    - Pro = cheap and available, STI protection
    - Con = reaction to material, decreased sensation
  2. Female condoms
    - Pro = female control, STI protection
    - Con = bulk, costly
  3. Vaginal diaphragm
    - Pro = female control
    - Con = side effects (bladder irritation, UTI, TSS), costly, 2 year replacement
  4. Cervical caps
    - Pro = put in 6 hours prior to sex and left up to 1-2 days after
    - Con = clinician has to fit cap, dislodgement, not ideal if given birth before
  5. Spermicide
    - Pro = Available and cheap
    - Cons = irritation, mess, increased STI susceptibility
186
Q

What are 2 examples of intrauterine devices?

How do they work?

What are general pros and cons for IUDs?

A
  1. Intrauterine copper TIUD (ParaGard)
  2. Levonorgestrel Intrauterine system (Mirena)

IUDs create a sterile inflammatory response that englufs and immbolizes sperm.

They may reduce tubal motility.

Mirena release progesterone to thickn cervical mucus and atrophy the endometrium

ParaGard uses copper to hamper sperm motility and capacitation

  • Pros = effective, long-lasting, reversible, safe in breastfeeding women, decreases menorrhagia/dysmenorrhea, can treat endometriosis and cancer, PID protection
  • Cons = needs a prescription and clinician insertion/removal, monthly string check, increased risk of ectopic, possible pain/bleeding/perforation/infection
187
Q

What are 3 ways to take hormonal E&P contraceptives?

What are 3 ways to take P only contraceptives?

Pros and Cons of each?

A

E&P

  1. Oral pill (pro = efficient; con = weight gain, nausea, headache)
  2. Transdermal patch (pro = weekly self admin; con = DVT/PE risk, skin irritation)
  3. Vaginal ring (pro = less hormones; con = discomfort, expulsion, discharge)

P only

  1. Oral pill (pro = nursing; con = follicular cysts, acne, breast tenderness)
  2. IM injection (Pro = 3 month admin; Con = depression, amenorrhea, weight gain)
  3. Implantable subdermal rod (Pro = 3 years; Con = headaches, clinician insertion)
188
Q

What are 2 types of oral E&P contraceptive pills?

A
  1. Monophasic Combination Pills (Fixed-Dose) = active pill has the same E&P amount
  2. Multiphasic Combination Pills (Dose-Varying) = active pill has varying doses of E&P to mimic the natural cycle

Both involve an active pill for 21-24 days and a placebo pill for 4-7 days.

189
Q

What are 3 examples of emergency contraceptives? Pros and Cons of each?

A
  1. Morning After Pill (E&P or P only)
    - Pro = effective and safe
    - Con = short window of time (2 doses within 72 hours)
  2. Copper T IUD
    - Pro = effective, long-lasting, decreases amenorrhea/dysmenorrhea
    - Con = risk of ectopic, possible pain/bleeding/perforation/infection
  3. Ulpristal (progesterone receptor modulators)
    - Pro = more effective in the 72-120 hour window, 1 dose
    - Con = pregnancy test required, headahce, bleeding, nausea, stomach pain
190
Q

What are 3 abortion options in first trimeter?

What are 2 abortion options in second trimester?

When is the latest they can each be performed?

A

First trimester = suction curettage (12), manual vacuum aspiration (12), medical (mifepristone or methotrexate) (9)

Second trimester = surgical evacuation (24), medical induction of labour (26)

191
Q

Explain the process of suction curettage or manual vacuum aspiration abortion. What are possible complications?

A
  1. Prophylactic antibiotics
  2. Paracervical anesthetic block
  3. Mechanical dilation of cervix
  4. Suction or vacuum to remove products
  5. Sharp curettage to finish if done with suction

Complications = infection, hemorrhage, uterine perforation, incomplete, Asherman’s if done 3+ times

192
Q

Explain the process of surgical evacuation abortion. What are possible complications?

A
  1. Paracervical block
  2. Gradual dilation of cervix (manual, osmotic, prostaglandins
  3. Breakage of products within the uterus
  4. Large suction cannula inserted to extract pieces
  5. Forceps if GA > 16 weeks

Complications = cervical laceration, hemorrhage, uterine perforation, infection, retained tissues, mortality

193
Q

Explain the process of labour induction abortion. What are possible complications?

A
  1. Give feticidal agents (ex. intraamniotic saline/digoxin + KCl)
  2. Give cervical ripening agents and perform an amniotomy
  3. Give high-dose IV oxytocin infusion

Complications = retained placenta, uterine rupture, hemorrhage, infection, live birth, nausea/vomiting, mortality

194
Q

What are 5 assessment and 3 educational components of an initial prenatal visit?

A
  1. Comprehensive History
  2. Breast and pelvic exam
  3. Screening for social risk factors
  4. Lab studies
  5. Assessment of GA
  6. Education of routine prenatal care
  7. Education on warning signs and contact information
  8. Education on nutritional and social services
195
Q

What are 9 important lab results to get during the first trimester of pregnancy?

A
  1. CBC
  2. Rubella immunity
  3. Hep B testing
  4. STD screen
  5. Antibody screen
  6. Toxoplasmosis testing
  7. Glucose levels
  8. Hormone levels
  9. Blood typing
196
Q

What are 3 ways to assess for gestational age?

A
  1. Naegele rule = add 7 days and substract 3 months from first day of last normal menstruation
  2. U/S = length of crown to rump (mm) + 6.5 equals GA from week 8-18
  3. Fundal height = GA from week 18-36
197
Q

What is the frequency of antenatal visits?

A

Every 4 weeks for the first 27 weeks.

Every 2 weeks from week 28-36.

Every week from week 37-birth.

198
Q

What are 5 typical things checked during an antenatal visit?

A
  1. History
  2. Blood pressure
  3. Urinalysis
  4. Weight
  5. Obstetrical physical exam (fundal height, FHR, Leopold maneuvers)
199
Q

What are 3 ways to assess fetal well-being?

A
  1. U/S (normal and doppler for umbilical artery blood flow)
  2. Subjective maternal perception of activity (kick counts)
  3. Electronic fetal monitoring (non-stress test, contraction test)
200
Q

Fill in the following chart for weight gain in pregnancy:

201
Q

Why is there a hypercoagulable state in pregnancy?

A
  1. Altered plasma levels of clotting factors (increased fibrinogen, thrombin, factor 5/7/8/9/10/12, decreased protein S and C)
  2. Plasminogen activator inhibitor-2 made by placenta
  3. Hormones enhance vessel wall compliance increasing venous stasis
  4. Gravid uterus compresses veins increasing venous stasis
202
Q

Describe what happens to the levels of the following hormones over the course of pregnancy:

  1. hCG
  2. Estrogen
  3. Progesterone
  4. Human placental lactogen
A

hCG increases and peaks during the first trimester and then declines.

Estrogen, progesterone, and hPL continually increase throughout pregnancy.

203
Q

What are the cardiovascular changes during pregnancy? (3)

A
  1. Increased CO
    - HR increases 20bpm
    - Transient hypertrophy
    - Greater BV (30-50% increase)
  2. Decreased BP until 20 weeks and then increased until term
    - Progesterone and NO mediate vasodilation
    - Vessels less responsive to angiotensin II
  3. Displacement of heart upwards and to the left (left axis deviation on ECG)
  4. Supine hypotension later in pregnancy
    - Fetal compression if IVC
204
Q

What are the respiratory changes during pregnancy? (4)

What 2 things do not change?

A
  1. Decreased residual volume/functional residual capacity/total lung capaciy
    - Diaphragm 4cm higher
  2. Increased resting minute ventilation and tidal volume
    - Progesterone enhances respiratory drive
    - Progesterone relaxes ligaments allowing more AP/lateral rib flaring
  3. Decreased PaCO2
    - Progesterone lowers CO2 threshold
    - Increased tidal volume contributes
  4. Nasal stuffiness, sinus congestion, nosebleeds
    - Estrogen increases vascularization

Respiratory RATE and vital capacity do not change

205
Q

What are the renal changes during pregnancy? (6)

A
  1. Fluid retention
    - Progesterone lowers osmotic threshold for thirst
  2. Increased GFR by 50%
  3. Increased RAAS activation and ADH secretion
  4. Increased excretion of glucose, amion acids, calcium, bicarbonate
  5. Dilation of ureters and renal pelvis
    - Progesteron mediates smooth muscle relaxation
    - Compression on ureters by fetus
  6. rigone becomes deeper and wider
206
Q

What are the blood changes during pregnancy? (4)

A
  1. Hemodilution with increasing hematopoiesis not matching increasing plasma levels
  2. Lower blood osmolarity causing increased edema
  3. Immune depression (TH1)
  4. Augmented caogulation/fibrionolysis
207
Q

What are the GI changes during pregnancy? (5)

A
  1. Increased GERD
    - Progesterone lowers esophageal sphinter tone
    - Growing fetus pushes up on the stomach
  2. Constipation
    - Progesterone relaxes small bowel motility
    - Estrogen causes NO release
  3. Hemorrhoids
    - Increased portal venous pressure from fetal compression
    - Inreased BP overall
  4. Cholestasis
    - Progesterone relaxes muscles of gallbladder
    - Estrogen inhibits intra-ductal bile acid transport
  5. Nausea from hormones
208
Q

What are the endocrine changes during pregnancy? (6)

A
  1. AP secretion of prolactin
  2. Thyroid hyperplasia
  3. Hyperparathyroidism
    - Protection against calcium loss
  4. Increased serum cortisol/aldosterone
  5. Peripheral insulin resistance and suppression of glucagon increasing total blood glucose
209
Q

What are the female reproductive changes during pregnancy? (6)

A
  1. Muscular hypertrophy and increased elasticity of uterine wall
    - Estrogen and growing fetus
  2. Increased vascularity and edema of cervix
    - Estrogen and relaxin
  3. Proliferation of cervical glands and production of mucous plug
    - Estrogen and relaxin
  4. Cessation of follicular development/ovulation
  5. Vagina and perineum have hyperemia, connective tissue softening, and smooth muscle hyperplasia
    - Estrogen and relaxin
210
Q

What are the dermatological changes during pregnancy? (5)

A
  1. Hyperpigmentation of skin (umbilicus, nipples, linea nigra, chloasma)
  2. Spider angiomas
  3. Palmar erythema
  4. Abdominal striae
  5. Increased cutaneous blood flow
211
Q

What breast changes occur during pregnancy? (2)

A
  1. Production of colostrum/milk
  2. Tender enlarged breasts
212
Q

What are the musculoskeletal changes during pregnancy? (2)

A
  1. Progressive lumbar lordosis to accomodate shifting centre of gravity
  2. Increased mobility of symphysis pubis and sacroiliac joint –> waddle
213
Q

What are the mood changes during pregnancy? (2)

A
  1. Increased irritability/anxiety/depression
  2. Mental fogginess/decreased concentration
214
Q

Fill in the following chart regarding contractions in early vs. late labour.

215
Q

What are different fetal presentations at birth? (7)

What are different fetal positions at birth?

A

Presentation:

  • Cephalic vertex, cephalic face, cephalic brow
  • Breech frank, breech complete, breech incomplete
  • Shoulder

Position:

  • Occiput relative to maternal spine = L/R, A/P/T
  • Tilt or no tilt
  • Flexion or extension
216
Q

Label the following fetal presentations:

217
Q

What are 4 possible pelvic shapes? Name and define.

A
  1. Gynecoid = wide pubic arch with straight side walls, a curved sacrum, and non-prominent ischial spines
  2. Android = narrow pubic arch with convergent side walls, an anteriorly inclined sacrum, and prominent ischial spines
  3. Anthropoid = long AP diameter with a narrow transverse diameter
  4. Platypelloid = short AP diameter with a wide trasnverse diameter
218
Q

What are 3 hypotheses for triggers of labour?

A
  1. Infection = phospholipase from bacteria cause membranes to release arachidonic acid which is a substrate for prostaglandin production
  2. Placental clock = CRH synthesis increases causing cortisol production in the mom and baby which goes on to mature lungs and increase prostaglandin synthesis
  3. Stretch/distention of uterus increases oxytocin/prostaglandin receptors on uterus and prostaglandin production
219
Q

What are the 3 stages of labour?

A
  1. Cervical dilation
  2. Delivery of baby
  3. Delivery of placenta
220
Q

Define true labour.

Define false labour.

A

True = uterine contractions causing cervical change

False = irregular spontaneous contractions that do not lead to cervical change (and are aka Braxton Hicks contractions)

221
Q

Describe the process of labour induction.

A
  1. Progesterone receptors decrease, inhibiting progesterone’s relaxing effect
  2. Maternal estrogen levels rise which increases oxytocin receptors on uterus and oxytocin synthesis fromp ituitary
  3. Oxytocin increases transmission of current between uterine myocytes and stimulates placental production of prostaglandins
  4. Prostaglandins stimulate more uterine contractions, promote cervical ripening, and further increase oxytocin and prostaglandin production
222
Q

What are 6 signs of true labour?

A
  1. Cervical change
  2. Patient discomfort
  3. Bloody show
  4. Nausea/vomiting
  5. Palpable contractions
  6. Pain in back and upper abdomen
223
Q

Explain the 2 components of the first stage of labour.

A

Latent:

Irregular contraction leading to cervical softening, effacement, and 3-4cm dilation

Active:

Strong regular contractions of progressive intensity, with cervical dilation greater than 4cm

224
Q

Explain the 2 components of the second stage of labour.

A

Passive:

Descent of the baby’s head without maternal pushing

Active:

The sensation of an uncontrollable urge to push; pushing the baby throughout the pelvic canal

225
Q

What are the 7 changes in a baby’s position as it passes through the pelvis and into the world.

A
  1. Engagement = BPD of fetal head passes through pelvic inlet
  2. Descent = downward movement of baby
  3. Flexion = head meets pelvic floor causing flexion (chin to chest)
  4. Internal rotation = turning of head so occiput is anterior; descent through plane of midpelvis
  5. Extension of fetal head = occiput contacts symphysis pubis and baby’s head meets mulva, extending to pass through the vaginal outlet
  6. External rotation = body rotates to align shoulders with the AP diameter of the pelvic outlet
  7. Expulsion = delivery of shoulders and rest of baby
226
Q

Explain the third stage of labour

A
  1. The uterus contracts down causing the placenta to buckle.
  2. The uterus separates from the placenta at the decidua spongiosa
  3. The uterus contracts around the maternal blood sinuses to prevent hemorrhage
227
Q

What are 3 indications that the placenta is ready to be delivered?

A
  1. Uterus becomes globular and firm, rising in the abdomen
  2. There is a sudden gush of blood
  3. Umbilical cord protrudes farther out of the vagina
228
Q

What does stage 4 of labour refer to?

A

The 2 hours post-birth in which you are inspecting the birth canal, palpating the uterus to make sure its contracted, and monitoring for blood loss/complications

229
Q

Fill out the following chart for how long each stage takes during labour:

230
Q

What are 3 ways to track labour progress

A
  1. Cervical dilation
  2. Fetal station (cm above/below ischial spines with negative above and positive below)
  3. Partograph (chart noting FHR, colour of AF, fetal skull bones, cervical dilation, contractions, etc.)
231
Q
  1. What is meconium aspiration syndrom?
  2. What causes it?
  3. How does it present? (7)
  4. What is the treatment? (3)
  5. What are complications? (3)
A
  1. Inhalation of meconium due to its presence in the amniotic fluid before birth
  2. Mature digestive system, distress (hypoxia), vagal response to umbilical cord compression
  3. Wet crackles in lungs, hypercapnia, hypoxia, patchy/streaked lungs on CXR, hyperinflation of lungs, flat diaphragm, caridomegaly
  4. Ventilatory support, surfactant, suction
  5. Pneumothorax, persistent pulmonary hypertension, respiratory acidosis
232
Q

What are the normal causes of pain and nerve routes for pain during:

  1. The first stage of labour
  2. The second stage of labour
A
  1. Cervical dilation, uterine contractions (myometrial ischemia); sympathetic nerves joning thoracic spinal nerves T10-T12
  2. Distention of pelvic floor/vagina/perineum; sensory pudendal nerve joining the sacral nerves S2-S4
233
Q

What are 6 types of non-pharmacologic pain management strategies during labour?

A
  1. Psychological support
  2. Transcutaneous electrical nerve stimulation
  3. Supportive techniques (bath, massage, breathing, doula)
  4. Acupuncture
  5. Hypnosis
  6. Aromatherapy
234
Q

What is a normal fetal heart rate?

How can it be assessed?

A

110-160 bpm

Electornical fetal monitoring or doppler stethoscope

T9 MF3 (6 decks)

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